Earlier this month, the United States Food and Drug Administration authorized the first at-home tests for chlamydia and gonorrhea. The Simple 2 Test is available over-the-counter and costs between $58 and $99 per kit. Results are returned within a week and officials with the FDA hope that it helps curb the country’s STI epidemic.

[Related: A guide to preventing, spotting, and managing STIs.]

Bacteria causes both gonorrhea and chlamydia. While HPV is a more prevalent STI, chlamydia and gonorrhea are the most commonly reported STIs in both the US and other countries. According to the FDA, roughly 1.6 million cases of chlamydia and over 700,000 cases of gonorrhea were reported in 2021. The STIs cause painful urination and bleeding between menstrual periods. They are generally easily treated with antibiotics, but if left unattended, both gonorrhea and chlamydia can cause serious health complications, including infertility.

Rates of gonorrhea, chlamydia, and syphilis have skyrocketed over the past 20 years. The increase is at least partially driven by a lack of funding of the Centers for Disease Control and Prevention’s budget to fight the spread of STIs. Public health officials believe that easy and more accessible testing for STIs is one of the necessary tools needed to combat the country’s STI crisis.

“This authorization marks an important public health milestone, giving patients more information about their health from the privacy of their own home,” Doctor Jeff Shuren, director of the FDA’s Center for Devices and Radiological Health, said in a press release on November 15. “We are eager to continue supporting greater consumer access to diagnostic tests, which helps further our goal of bringing more health care into the home.”

The Simple 2 Test kit can be purchased online at LetsGetChecked’s website. It comes with tools to collect urine specimens or vaginal swabs. The patient then uses a prepaid shipping label to send the specimens to a lab. Users also must complete an online questionnaire. After two to five days, the patient can view the results online. If the test is positive or the results are invalid, users can arrange a telehealth consultation with a healthcare provider.

Doctor Matthew Golden, Director of the  Seattle King County public health departmen’s HIV and STI control program, told NBC News that FDA is catching up on regulating an industry that has grown since the COVID-19 pandemic began.

[Related: This ‘morning after’ pill could prevent STIs from unprotected sex.]

“At some level, the horse has left the barn,” said Golden. He noted that self-testing kits have been widely used for years, but “some of those tests, how well they perform is not well known. So cleaning this up makes sense.”

University of Hawaii STI expert and medical consultant at the Hawaii State Department of Health’s Diamond Head STI/HIV Clinic Alan Katz told Stat News that the Simple 2 Test uses the same investigative procedure that clinicians use to diagnose chlamydia and gonorrhea.

“This option is exceptionally useful for individuals who live in rural areas or are geographically distanced from a clinic where STI testing can be done and there is no telehealth option available,” Katz said. “If a person screens positive, they can then contact a healthcare provider for further evaluation and treatment.”

While unapproved home tests for chlamydia and gonorrhea have already been on the market, The Simple 2 Test is the first to go through the FDA’s approval process. The approval could potentially make it easier for future such tests to clear the FDA’s regulatory pathway.

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Adding liquid soap can boost the potency of some of the pesticides used on malaria-carrying mosquitoes. The discovery is detailed in a study published November 17 in the journal PLOS Neglected Tropical Diseases and offers a tool in the fight against the disease.

[Related: New four-dose malaria vaccine is up to 80 percent effective.]

Malaria is most prevalent in Asia, Latin America, and sub-Saharan Africa and is caused by several species of parasites that are transmitted by the bites of infected female Anopheles mosquitoes. It causes severe fatigue, fever, headaches, and chills and can be fatal. When it is treated with the right medication, such as artemether-lumefantrine, it can be cured and the malaria parasites can be completely cleared from the body. The United States Centers for Disease Control and Prevention estimates that there were 241 million cases of malaria worldwide and 627,000 deaths in 2020. 

While the first malaria vaccines were approved and recommended in 2021, the mosquitoes that carry malaria are becoming more resistant to insecticides. 

“Over the past two decades, mosquitoes have become strongly resistant to most insecticides,” study co-author and University of Texas at El Paso (UTEP) evolutionary biologist Colince Kamdem said in a statement. “It’s a race now to develop alternative compounds with new modes of action.”

Before coming to UTEP, Kamdem worked at Cameroon’s Centre for Research in Infectious Diseases, where he first saw soap’s potential potency during some routine insecticide testing. A special class of insecticide called neonicotinoids have shown to be a potential alternative that targets the mosquito populations that show resistance to current insecticides. However, they can have negative effects on bees if not used carefully and neonicotinoids do not kill some mosquito species unless their potency is boosted. 

World Health Organization protocols recommend adding a seed-oil based product to insecticides to test a mosquito’s susceptibility. When the compound was added, Kamdem noticed that it was more effective than when the insecticide was used on its own.

“That compound belongs to the same class of substances as kitchen soap,” Kamdem said. “We thought, ‘Why don’t we test products that have same properties?’”

The team selected three inexpensive, linseed-oil based soaps that are readily available in sub-Saharan African countries. They added the soaps to four different neonicotinoids. In every case, the potency was increased. 

[Related: Mosquitoes are becoming resistant to our best defenses.]

“All three brands of soap increase mortality from 30 percent to 100 percent compared to when the insecticides were used on their own,” study co-author Ashu Fred said in a statement. Fred is a PhD student at the University of Yaoundé I in Cameroon. 

They also tested a class of insecticides called pyrethroids. This class did not see the added benefits of the boost from soap. They hope to conduct additional testing to see exactly how much soap is needed to enhance insecticides. 

“We would love to make a soap-insecticide formulation that can be used indoors in Africa and be healthy for users,” Kamdem said. “There are unknowns as to whether such a formulation will stick to materials like mosquito nets, but the challenge is both promising and very exciting.”

Malaria was once endemic in the US, but was eradicated by the 1970s. However, the CDC issued a health advisory in June after at least four people in Florida and one in Texas contracted homegrown cases of malaria. The disease is most common in warm climates and some scientists worry that as global temperatures continue to rise, more regions will be affected by malaria. A 2022 study published in Nature found that climate change can exacerbate a full 58 percent of the infectious diseases that humans come in contact with worldwide.

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OUR EYES, unlike other organs hidden deep within our bodies, sit in plain sight. They have been inspirations for artists, symbols for the superstitious, and objects of scientific fascination for centuries. In ancient Greece, medical pioneers cut them open in public dissections, revealing delicate layers of retina, cornea, and iris. In the early 10th century, Persian physician al-Razi discovered that the pupil dilates and contracts to control the amount of light that enters. Six centuries later, the Renaissance-era anatomist Vesalius sketched a cross-section of the orb—with some errors. But eyes themselves are imperfect: Just one fault could cause the whole organ to glitch or break down. 

It turns out that flaws are common in our vision. More than 7 million Americans have some form of vision loss, which can include partial or full blindness, according to a 2021 analysis of 25 years of data from the US Census, the Centers for Disease Control and Prevention, and others. Many of these conditions are present from birth. Mutations in particular regions of DNA can lead to incorrectly formed optical parts. This can distort a person’s sight, especially if the issues are in the retina, the layer of cells at the back of the eye that captures incoming light and transmits it to the brain. But what if we could give someone with limited vision a corrected version of their genetic material to fix the malfunctioning parts?

Currently, there is no way to fully reverse inherited forms of blindness, which are traditionally managed with adaptations rather than treatments. “I speak to a lot of parents who are really frustrated about the lack of standard of care,” says Shannon Boye, a professor in the pediatrics department at the University of Florida. “They’re desperate for cures.”

But understanding the genetic roots of the disability helps. In theory, if scientists can pinpoint the problematic or missing DNA that’s hampering a person’s vision, they can design a rectified copy. The new genetic code is loaded into harmless viruses that deliver therapeutic genes to selected cells, and the viruses are then injected into the affected eye. There, the replacement DNA instructs the eye to make the proteins it needs to see again. 

In practice, it’s not so easy. The Food and Drug Administration (FDA) has approved only one gene therapy to treat a form of blindness—the first gene therapy the agency ever greenlit. Called Luxturna, it was OK’d in the US in 2017 to treat patients with mutations that lead to Leber congenital amaurosis (LCA). In people with this uncommon flaw, light-detecting photoreceptor cells in the retina develop incorrectly, become malformed, or die, leading to rapid vision loss early in life. Luxturna provides the correct version of the gene, partially restoring vision.

“This was a godsend scenario,” says Claudio Punzo, an expert in vision genetics at the University of Massachusetts Chan Medical School. There are several types of LCA, but the retina degrades more slowly in the form of the disease that Luxturna treats, which creates a larger window for the gene therapy to work. What’s more, people with the condition are often completely blind, so even a small improvement in their sight is life changing.

After that first FDA approval, “Unfortunately, the field hit a lull,” Boye says. But she is confident that with new genetic tools, Luxturna’s success story can be replicated on a much larger scale. 

One big step has been designing better couriers for the corrected code. Many gene therapies use naturally harmless adeno-associated viruses, which researchers modify to home in on retinal photoreceptors or other key cell types. Boye imagines a modular system using a suite of viral vessels designed for different destinations, in which any gene can be loaded as cargo. 

“Will we get it to work for everyone? With every mutation? Most likely, yes, at some point,” says Punzo. “It just becomes a logistical problem.” There are hundreds of different mutations that can cause blindness, and finding the right gene to fix in the right cell is no small task. For genes that are too large to fit inside a virus, CRISPR editing technology might offer an alternative method to correct the mutation directly in the patient’s DNA. In 2022, biotech company Editas tried using CRISPR to treat a form of LCA by removing a mutation in the retinal gene CEP290, but it paused the trial when vision in only three out of the 14 participants improved.

For people with visual disabilities, the invasiveness of current treatments is another major hurdle. These methods typically require surgeries to deliver the gene close to the retina, a process that itself can cause mild retinal damage. For someone with a less severe disease, such as night blindness or color blindness, the risks may not be worth the modest benefit. Shots in parts of the eye farther from the retina would be less invasive, but they are not yet standard for gene therapy. Another appealing option would be eyedrops, which were recently used for the first time in an experimental treatment at the University of Miami on a 14-year-old boy with corneal scarring. After months of the topical treatment, his sight returned to near-normal levels.

Cost is another obstacle. When Luxturna first hit the market in 2018, its price tag was $425,000 per eye. In part, the expense comes from the meticulous process of making a virus that won’t harm a patient. But the other part of the equation is the biotech industry’s irresistible pitch: We can help you see again. For people who are progressively losing their vision, even slowing down the process could be priceless—or so gene therapy companies hope. 

Most major insurers cover one dose of Luxturna per eye for patients whose retinas are intact enough to heal. But the hopefuls may still be on the hook for out-of-pocket costs associated with the procedure, or the cost of travel to one of 14 certified treatment centers in the US. “[It’s] an insanely expensive treatment,” Punzo says. “If there are cheaper drugs that would work, I think it will change the market.”

Currently, dozens of gene therapy clinical trials for hereditary forms of blindness are in progress, and many more are in the planning stages. They span diverse conditions, including Stargardt disease (which causes fat to build up in the eye), achromatopsia (a form of color blindness), and retinitis pigmentosa (which makes the retina break down). But progress is slow: Many have been at it for more than a decade with years to go.

Boye knows this firsthand. She co-founded a company called Atsena Therapeutics that is currently conducting a clinical trial for a virus-delivered code to correct an LCA-causing mutation. Her confidence that gene therapies can reverse blindness stems from both data and patients’ stories. She recalls a young girl who got the corrective treatment: As her vision improved, the child was able for the first time to see snowflakes—delicate, magical, and unlike anything she had experienced in her life.

Read more PopSci+ stories.

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Today, the United Kingdom became the first country to give regulatory approval to a medical procedure that uses CRISPR gene editing. The Medicines and Healthcare products Regulatory Agency (MHRA) approved Casgevy, a therapy that will be used to treat sickle cell disease and beta thalassemia (also called β -thalassaemia). 

[Related: CRISPR breaks ground as a one-shot treatment for a rare disease.]

What are sickle cell disease and beta thalassemia? 

Both diseases are painful, life-long genetic conditions that are caused by errors in the genes for a protein called hemoglobin. Red blood cells use hemoglobin to carry oxygen around the body. Sickle cell disease is particularly common among people with Caribbean or African ancestry. The abnormal hemoglobin makes the blood cells crescent-shaped and hard. The misshapen cells then clump together and block the flow of oxygen to the organs, which causes extreme pain. The cells can then die off early, which leads to anemia. 

Beta thalassemia primarily affects patients with Mediterranean, south Asian, southeast Asian, and Middle Eastern backgrounds. It also causes anemia since the mody cannot make as much hemoglobin.  

Casgevy was developed by Boston’s Vertex Pharmaceuticals and Switzerland’s Crispr Therapeutics and could be used to replace bone marrow transplants. The companies estimate that roughly 2,000 people in the UK are now eligible for the therapy.

“I am pleased to announce that we have authorized an innovative and first-of-its-kind gene-editing treatment called Casgevy, which in trials has been found to restore healthy hemoglobin production in the majority of participants with sickle-cell disease and transfusion-dependent beta thalassaemia, relieving the symptoms of disease,” interim executive director of healthcare quality and access at the MHRA Julian Beach said in a statement. 

How does Casgey use CRISPR gene editing?

The new treatment uses the CRISPR-Cas9 gene editing technique, which enables scientists to make precise alterations to human DNA. French microbiologist, geneticist and biochemist Emmanuelle Charpentier and American biochemist Jennifer A. Doudna, who shared the 2020 Nobel Prize in Chemistry for their work. 

Casgevy uses stem cells taken from a patient’s bone marrow. The cells are then brought into a lab and the genes that are meant to switch on a functioning version of hemoglobin are edited with CRISPR. According to the MHRA, patients must then go through a “conditioning treatment.” This can involve taking a drug that suppresses the immune system, radiotherapy, or chemotherapy to get the body ready for an infusion of CRISPR-modified cells back into the body. The new treatment does not come with the risk of graft versus host disease the way that a traditional bone marrow transplant does.

[Related: These organisms have a natural gene-editing system that could be more useful than CRISPR.]

After the infusion, patients may need to remain in a hospital facility for at least a month. During this time, the treated cells will begin to “take up residence” in the bone marrow and make red blood cells that have a stable form of hemoglobin.

While seeking regulatory approval, the researchers performed a clinical trial of 45 patients with sickle-cell disease. Of this group, 29 patients have been in the trial long enough for the researchers to gauge how effective Casgevy is. Of these eligible patients, 28 were free of severe pain crises for at least 12 months after treatment.  

In the clinical trial of 54 patients with transfusion-dependent beta thalassemia, 42 patients have been in the trial long enough to determine efficacy. Of these, 39 did not require a red blood cell transfusion for at least 12 months after the treatment. The remaining three had more than a 70 percent reduction in the need for red cell transfusions. 

“This is a great step in the advancement of medical approaches to tackle genetic diseases we never thought would be possible to cure,” University of Hertfordshire geneticist Alena Pance said a statement released by the Science Media Centre. “Modifying the stem cells from the bone marrow of the patient avoids the problems associated with immune compatibility, i.e. searching for donors that match the patient and following immunosuppression, and constituting a real cure of the disease rather than a treatment.”

The United States Food and Drug Administration is evaluating this same treatment. On October 31, an advisory committee to the FDA said that treatment was safe for patients. It is expected to make a decision by December 8. 

A price for the therapy has not been announced, but it will likely be expensive. 

Previously

Despite its potential for good, CRISPR has been tainted with controversy and ripe for debate over the fear of being able to pick and choose genes for so-called “designer babies.” In 2018, Chinese scientist He Jiankui announced that he had created the first gene-edited babies in the world. He was found guilty of conducting “illegal medical practices” and sentenced to 3 years in prison. This work furthered the debate of how to best regulate this powerful technique, with many saying that it shouldn’t be used to edit human genes that will be passed down to the next generation. 

Other experiments and trials with using the gene editing technique on rare diseases have continued. In 2021, a clinical trial for a drug called NTLA-2001 began, researchers attempted to treat six people with a rare genetic disease called transthyretin amyloidosis with a technology that delivers CRISPR directly to cells in the liver. The FDA cleared the trial to enter its critical third phase in October.

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New research from Oxford University and the University of Adelaide found that asbestos exposure has led to a higher incidence of asbestos-related lung cancers in British and Australian naval personnel. The study published November 14 in the journal Scientific Reports estimates that the proportion of lung cancers related to onboard asbestos exposure was 27 percent in Australian naval personnel and 12 percent in British servicemembers.

[Related: The US never banned asbestos. These workers are paying the price.]

Toxic exposure

This study is a reminder of the continuing need for protections against exposure to harmful airborne dusts and other dangerous substances from sources like toxic burn pits. According to the United States Department of Veterans Affairs, nearly 300,000 United States veterans have reported exposure to pollution from burn pits since the early 2000s. The chemical pollutants that were released during these burns include volatile organic compounds associated with cancer, kidney disease, and nervous system damage. In August 2022, President Joe Biden signed the PACT Act into law to address the health concerns related to burn pits like these.

Illnesses related to asbestos exposure persist, despite the mineral being a known carcinogen. Asbestos has been used in a wide variety of building materials for their strength, flexibility, and electrical and heat resistant properties. Breathing it in can cause mesothelioma, lung cancer, and a non-cancerous condition called asbestosis. About 1,290 Americans die annually from asbestos-related causes, according to the Centers for Disease Control and Prevention (CDC).

Australia currently has a ban and strict control on asbestos-containing materials, they still pose a risk to some workers. A 2021-2022 New South Wales Dust Disease Register report found that there were 142 cases of asbestosis and 111 deaths related to the illness. 

In the United States, asbestos use is not completely banned. The Environmental Protection Agency (EPA) proposed another ban in April of 2022 that has yet to be finalized. 

An increased risk to sailors

For this study, researchers collected data from 30,085 United Kingdom and Australian personnel who served during the 1950s and 1960s. During this time period, asbestos-containing materials were still present in British and Australian naval vessels. Earlier studies of one Australian and two British cohorts also involved in this new research found that increased rates of lung cancer could not be attributed to radiation exposure from nuclear testing. The team used a separate study of Australian Korean War veterans as a comparison in this new research.

The team found that all four cohorts had an elevated incidence of mesothelioma among naval veterans. This same rate was not not statistically significant among sailors from the Korean War. British and Australian personnel involved in nuclear testing also saw higher rates of lung cancers.

Additionally, the rates of pulmonary disease and heart disease were similar between naval and army personnel. This suggests that smoking was not driving higher lung cancer rates among sailors.

[Related: The PACT Act will take the burden of proof off US veterans exposed to burn pits.]

“We found the lung cancer rate was higher overall in naval personnel than in the other armed services, and, while smoking remains the dominant cause of lung cancer, it is unlikely the excess could be explained by a higher smoking rate in the navy,” study co-author and University of Adelaide medical doctor Richard Gun said in a statement.  “Although actual measurements of airborne asbestos levels were not available, and estimates are difficult, we have concluded that the higher lung cancer rate in sailors was most probably caused by onboard asbestos exposure.”

The high occurrence of deaths in sailors from asbestosis also strengthened the team’s conclusion. The team believes that the effects of asbestos exposure are likely underestimated, unless lung cancer is considered alongside mesothelioma and asbestosis.

“Although it remains true that smoking causes most lung cancers, other agents such as asbestos can contribute to the incidence of cancer in an exposed population,” Gun said. “Moreover, we know from other studies that the combination of smoking and asbestos exposure has an enhanced influence on lung cancer risk; this interactive effect would have contributed to the observed lung cancer excess.”

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You’ve probably heard a lot about Ozempic and Wegovy, the semaglutide wonder drugs for weight loss. Their newfound popularity with prescribers and online pharmacies has sparked a global shortage. Other diabetes medications are now also being repurposed for weight loss: On Wednesday, the FDA approved Zepbound, another version of Mounjaro, for chronic weight management.

While Ozempic and Wegovy have different ingredients than Mounjaro and Zepbound, they work in a similar way. Semaglutide mimics a hormone called GLP-1 that’s usually released when the body detects carbohydrates, proteins, and other lipids after a meal. This sends a message to the brain that you’ve eaten, changing hunger signaling activity. When the body thinks it’s full, GLP-1 activates other systems to slow down muscle contractions that would usually move food out of the stomach.

A weekly injection might seem like an easy option to shed pounds, but doctors warn these medications are not a perfect weight-loss solution. Semaglutide carries a number of side effects that range from uncomfortable to life-threatening, which can be even worse with off-label use of Wegovy or Ozempic.

What are the common side effects of semaglutide?

Since semaglutide has a direct effect on the GI tract, a majority of the side effects are gastrointestinal-related. Mir Ali, a bariatric surgeon and medical director of MemorialCare Surgical Weight Loss Center in California, says about 50 percent of people taking Wegovy or Ozempic experience nausea. Other common side effects include constipation, diarrhea, or cramping. People who overeat while on the regimen might experience more severe nausea and even vomiting. Additionally, while not as common as the other GI side effects, Ali mentions there is a chance of dizziness while taking Ozempic. This may stem from the blood sugar-lowering effects of the drug. 

What are the more dangerous side effects?

Since large numbers of people started using semaglutide for off-label weight loss, doctors have been documenting more troubling reactions. New research published in the Journal of the American Medical Association links Ozempic to gastroparesis, a chronic condition that severely weakens the muscles in the stomach wall, making it harder to push food over to the small intestine. The inability to empty stomach contents can delay the digestive process and induce regular episodes of nausea and diarrhea. While there are surgical and non-surgical ways to manage gastroparesis, there’s currently no cure for it. 

Considering that there have only been a few documented cases of gastroparesis with Ozempic use, Ali says the chances of this happening are relatively rare and “not something you typically see in patients.” But as demand for the drug continues to soar, more cases may come to light. Along with stomach paralysis, other limited but severe side effects of Ozempic involve pancreatitis, kidney issues, and gallbladder issues.

Can semaglutide cause suicidal thoughts?

A growing number of people worldwide have also reported suicidal thoughts while taking Ozempic. After receiving 150 reports of suicidal ideation and self-injury, the European Medicines Agency is reviewing the safety data on the diabetes drug. The United Kingdom is also reviewing all drugs classified as GLP-1 agonists, including Ozempic, after an uptick in incidences of self-harming thoughts. In the US, individuals have spoken out about experiencing suicidal ideation while taking Ozempic, despite having no history of self-harm. 

Some of the mental health concerns have precedent. The US Food and Drug Administration (FDA) requires any chronic weight management medication that works on the central nervous system to carry a warning about suicidal behavior and ideation. Wegovy has a warning for suicidal ideation but Ozempic—intended only to control blood sugar levels in people with type 2 diabetes—does not. It’s not clear what the link is between these drugs and suicidal thoughts, but it’s assumed the neuropsychiatric side effects emerge when semaglutide interacts with the brain to control appetite. 

“The question becomes, should the same medication under a different name carry the same caution regarding suicidal ideation?” says Joseph Barrera, an endocrinologist and associate medical director of Providence Mission Hospital in California. He adds that the likelihood of developing self-harming thoughts while taking Ozempic seems to occur more in people with a history of depression or other psychological issues—a possible safety concern as some psychiatrists are now prescribing Ozempic for depression. 

Overall, cases of suicidal ideations are largely anecdotal and relatively rare. As of September 2023, of the 23,845 reports of adverse reactions with semaglutide in the US, there have been 144 cases of suicidal ideation and 2 deaths by suicide. As Barrera points out, it’s still unclear how many of these cases involved Ozempic versus Wegovy.

What to consider if taking Ozempic or Wegovy for weight loss

Barrera has one piece of advice for people considering using Ozempic or Wegovy off-label: Don’t. The risks of taking the drug, including suicidal ideation, are too high. What’s more, Barrera warns some individuals have been paying providers and clinics for “compounded semaglutide,” which involves mixing multiple medications together. According to the FDA, people making compounded semaglutide are using a salt form, such as semaglutide sodium or semaglutide acetate, that doesn’t contain the same active ingredient as Ozempic and Wegovy. 

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On November 8, the United States Food and Drug Administration (FDA) approved a Type 2 diabetes drug called tirzepatide for use in chronic weight management. It has been sold under the brand name Mounjaro for treating diabetes, but it will be called Zepbound when prescribed for weight loss. The drug is made by pharmaceutical company Eli Lilly and doses should be available after Thanksgiving.

[Related: 6 Ozempic facts that make sense of social media hype.]

How Zepbound works

The medicine is a weekly injectable medication and the main ingredient is called tirzepatide. It mimics two hormones called glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Both are naturally produced in the body and the drug targets receptors in the brain for these hormones.

Both GIP and GLP-1 bind to receptors in the brain that tell the body it is full. GLP-1 also slows digestion to make people feel fuller longer and with smaller portions. American Board of Obesity Medicine medical director Kimberly Gudzune told The Washington Post that GLP-1 targets the receptors in the brain that decrease appetite and it slows digestion to make people feel fuller longer and with smaller portions. Additionally, GLP-1 increases the amount of insulin that the pancreas releases after eating, which slows down the rise in blood sugar.

GIP meanwhile works in the brain to decrease appetite and may also improve how the body breaks down fats and sugars.

Who is eligible for Zepbound?

The FDA cleared Zepbound for adults 18 and older considered obese (a body mass index of at least) or overweight (a body mass index of 27 or more) with at least one weight-related health condition. The FDA also said that it should be taken with exercise and a reduced-calorie diet.

What is a ‘weight-related condition’?

Weight-related conditions are medical complications that can arise from being overweight or obese. According to the Centers for Disease Control and Prevention (CDC), they include high blood pressure (hypertension), high LDL cholesterol, high levels of triglycerides, and Type 2 diabetes. 

Roughly 70 percent of American adults are considered overweight or obese by body mass index, according to the FDA. However, body mass index (BMI) is an imperfect metric for measuring health that has been questioned by the American Medical Association. Losing five to 10 percent of body weight with diet and exercise has been associated with a reduced risk of cardiovascular disease in adults who are overweight or obese

“Obesity and overweight are serious conditions that can be associated with some of the leading causes of death such as heart disease, stroke and diabetes,” director of the FDA’s Division of Diabetes, Lipid Disorders, and Obesity John Sharretts, said in a statement. “In light of increasing rates of both obesity and overweight in the United States, today’s approval addresses an unmet medical need.”

[Related: TikTokers are taking a diabetes drug to lose weight. Now it’s in short supply.]

How effective is Zepbound?

The FDA’s approval comes on the heels of a phase 3 clinical trial. All of the participants in the study had obesity or were overweight and had at least one weight-related condition.

At the highest dosage of tirzepatide (15 milligrams) participants saw an average weight loss 22.5 percent body weight, or about 52 pounds, over a period of 72 weeks. At a 10 mg dose, the average weight loss was about 21.4 percent (48 pounds). At only five milligrams, average weight loss was about 16 percent (35 pounds).

How does it compare to Ozempic or Wegovy?

Ozempic and Wegovy contain an ingredient called semaglutide. It works by suppressing the appetite by mimicking GLP-1, a hormone that signals to the brain that the stomach is full. In similar clinical trials, semaglutide has been shown to reduce body weight by roughly 15 percent (34 pounds) after 68 weeks.

By comparison, the tirzepatide in Mounjaro and Zepbound works on both the GLP-1 and GIP pathways.

While those taking tirzepatide lost more weight than those taking semaglutide in separate trials, the data is not comparable due to potential differences in study length and population. More data is needed that compares both drugs at the higher doses needed for weight-loss, so it is too early to say if one is more effective than the other.

[Related: Fatphobia and medical biases follow people after death.]

What are the potential side-effects?

In studies, the main side effects were gastrointestinal issues like nausea, vomiting, constipation, and diarrhea. The FDA says that Zepbound’s label will contain warnings for inflammation of the pancreas, gallbladder problems, low blood sugar, acute kidney injury, diabetic retinopathy, and suicidal behavior or thinking.

How much will Zepbound cost?

A one month supply of Zepbound is estimated to cost about $1,060. While it is less than Wegovy’s $1,300 price tag, both drugs may be too expensive for many that are eligible. Ozempic costs $936 per month before insurance.

Many insurance companies do not cover weight loss medication that is intended to treat Type 2 diabetes, but that could change with the FDA’s approval. Medicare and Medicaid are currently barred by law from covering weight loss medications. 

According to Eli Lilly, patients can sign up on its website for a copay, or a discount card program. The company also said that those who can get Zepbound through commercial insurance may pay as little as $25 for a one-month or three-month supply. It is unclear what will happen after that period as far as coast and weight staying off. Those who are commercially insured, but don’t have coverage for Zepbound, might be eligible to pay as little as $550 for a one-month prescription.

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Americans consume billions of pounds of meat each year. And yet, there’s a plethora of research showing that copious amounts of meat can be unhealthy, both for the Earth and our bodies.  

The question of how to steer consumers toward healthier and more sustainable plant-based foods is a tricky one. Warning labels, similar to the ones found on cigarette packs, could be one way to raise awareness about the negative impacts of meat and perhaps sway consumer choices. But they’re still completely experimental.

In a new study published in the journal Appetite, psychologists in the UK created an online food-selection task where about 1,000 participants—all of whom ate meat—had to choose between a meat-based, fish-based, vegetarian, or vegan meal 20 times. A quarter of these participants based their decisions on images of each of the dishes. The remaining participants were randomly assigned to also see a warning label about the impact of meat on health, climate change, or the risk of future pandemics (researchers and organizations like the United Nations have linked high meat consumption with risk of infectious diseases). The team found that each warning label type reduced the subjects’ desire to eat meat: by 9 percent with health labels, 7 percent with climate labels, and 10 percent with pandemic labels. The individuals also viewed the climate label as the most credible of the three and the pandemic label the least, but potentially had a stronger emotional response to the latter.

One reason these warnings might work is because people see a negative outcome attached to meat, so they have a gut reaction and opt for a different food, says Jack Hughes, a psychology researcher at Durham University in England and lead author on the new paper. Another explanation could just be that the extra information gets people to think more consciously about their decisions, he explains. 

[Related: How to enjoy fake meat in a way that actually helps the planet]

The results of the study are “very in line with what we’ve seen with regards to labeling efforts and their effect on consumer behavior,” says Lindsey Smith Taillie. “They have a small to moderate effect on consumer choices.” Taillie, a nutrition epidemiologist at the University of North Carolina who studies how policies affect food choices, notes that the inclusion of pandemic-related labels is a first for this kind of research, at least to her knowledge. She would be especially interested to see how consumers in the US would react to that kind of messaging given the different political and cultural climate.

There are many factors that could influence the effectiveness of a warning label on a product. For example, as basic as it sounds, pictures make a difference. “We do know for tobacco in the UK that when images became mandatory alongside the text, labels got more effective,” Hughes explains. In two prior studies, Taillie and her collaborators found that text-only labels cautioning of health and environmental impacts of meat consumption only mildly reduced people’s carnivorous intentions, if at all. 

But not all images are the same. Take the case of high sugar content: A photo of teaspoons full of sugar is more factual and informative than a visual of a diseased heart, Taillie says. Regardless, “graphic labels are generally considered to be the most effective type,” she adds.

With warning labels, the goal is to grab people’s attention and get them thinking about their food’s footprint. But it ends up being counterproductive if the message makes the consumer feel angry or restricted, Taillie adds. One 2022 study out of Europe found that eliciting disgust by adding graphic images to packaging can both increase and decrease the likelihood of individuals choosing meat products, depending on whether they felt manipulated. Another recent European study found that meat-shaming messages on products can have paradoxical effects on buying habits.

The next step for this sort of research, says Taillie, would be to see how such labels affect choices in real-world settings—when factors like smells, prices, and peer pressure might influence consumer decisions. It’s also probably easier to choose the plant-based option when it’s a hypothetical online task and you don’t actually have to eat the food, she adds.

[Related: When faced with tough choices, your brain secretly tips the scales]

But choosing a meat-free diet can be an incredibly impactful way for individuals to reduce their carbon footprint, and this research can help nudge people in that direction. “In the UK, the Climate Change Committee says that meat consumption in the country needs to be reduced by 20 percent by 2030 [to meet carbon emission goals],” Hughes says. His team’s work shows that one simple and cheap action could change minds in a portion of the population. 

Would that be in the case in the US as well? Taillie sees a parallel with graphic tobacco warnings, which were adopted by European countries but have stalled in the state due to lawsuits. With meat labels, she says, “I think we’re looking at a timespan of decades.”

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At this time of year, it can feel like everyone around you has a head cold. Decongestant medicine, tissues, and runny noses close in on all sides. But why does your nose run in the first place?

The immune system at work

When you’re sick, it’s because pathogens have gotten past the mucus lining. To protect your body, the immune system kicks into action. Small proteins called cytokines deploy T cells and B cells to seek out and destroy the pathogens. Those same protein messengers instruct cells in the nose to generate more mucus in order to clear the cell lining of other potentially harmful bacteria or viruses. As mucus goes into overdrive, your mucus lining swells and your nasal cavity fills with excess fluid. This can drip out of the nose itself—a medical condition known as rhinorrhea, which the rest of us call a runny nose. Once your body clears the pathogens, your immune system will decrease its panic signals and your mucus lining returns to its usual level.

Generally, Lee says, the immune system in your nose is very adept at identifying cells that the body makes to create your tissues and fluids (those are usually safe) from foreign cells that that need to be attacked. Sometimes, however, that system is not so great at knowing when to shut off its response, or at identifying which cells it should be attacking. Over-active or misdirected immune responses cause conditions like allergies or asthma—the body launches a full-scale attack at something that wouldn’t really harm it, which causes damage to the body’s own tissues.

Go easy on the tissues

All in all, having a runny nose might be annoying, but it’s a good sign. It means your immune system is doing its job. You’re welcome.

This story has been updated. It was originally published on January 27, 2016.

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Thousands of years ago, ancient Egyptians used moldy bread to heal infected cuts and wounds. They may not have realized it, but their bizarre medical practice relied on fungi to create chemicals that kill infection-causing bacteria. This, in other words, was a very rough draft of an antibiotic drug. These types of molds helped Alexander Fleming discover penicillin centuries later. And now, to fight off superbugs, scientists are increasingly turning to another unorthodox source of germ-killers: healthy poop.

Specifically, fecal microbiota transplants are safe and effective in stopping the growth of antibiotic-resistant bacteria, according to a small study published today in Science Translational Medicine. If additional clinical trials prove to be successful, poop transplants could be a promising method in populations at risk of resistant infections, such as patients who get organ transplants. 

Antibiotics have saved millions from deadly infections, and human life expectancy jumped dramatically after their discovery. But their overuse has caused some bacterial strains to develop methods of protection against the medications. Antibiotic-resistant strains are a global problem that was responsible for 5 million deaths in 2019. On top of that is the concerning rise of superbugs, strains of bacteria with the highest resistance to multiple drugs. 

[Related: FDA approves first fecal transplant pill]

Once a patient is infected with antibiotic-resistant bacteria, “there’s not really a way to get rid of colonization,” says Michael Woodworth, an assistant professor of medicine at Emory University School of Medicine and lead author of the new study. “Right now, there are no FDA approved therapies.” In the past, clinicians tried to get rid of superbugs with additional antibiotics, which can set up a “vicious cycle” in which medication promotes the growth of even stronger antibiotic-resistant bacteria.

The idea to use poop transplants to defeat superbugs came after a growing body of evidence shows they can help treat tough C. difficile infections, a germ that patients can get in a hospital. In people who had received poop transplants, it looked as though they had fewer chances of catching the antibiotic-resistant bacteria. 

The new research was a Phase 1 clinical trial that enrolled 11 people awaiting kidney transplants. Organ recipients typically receive preventative antibiotics after their transplants, but this has not stopped an increasing amount of antibiotic-resistant UTI infections in this population.

In the study, people were randomly selected to receive a poop transplant immediately after getting a kidney, or a poop transplant later on if their stool samples showed positive signs of antibiotic-resistant bacteria after day 36. If people continued to be positive for the microbes, they had a second poop transplant. The authors used an enema to administer all the poop transplants, a route the study notes would have the lowest rate of side effects. To reduce the risk of passing harmful bacteria through the fecal transplants, screening tests checked for pathogens known to be resistant. 

The research team detected significant results in the two groups, despite the small number of participants (COVID disrupted patient enrollment in the study). All treatments were safe for people who received one or two poop transplants. Additionally, eight out of nine people were negative for antibiotic-resistant bacteria after 36 days.

Genetic analysis of the stool samples showed that the poop transplants helped reduce the number of superbugs. This decolonization of bacteria, while it was not directly tested, may help in preventing recurrent antibiotic-resistant infections. 

[Related: Finding the world’s super poopers could save a lot of butts]

“This provides the ground to start a large, randomized, controlled study to assess the effect of [fecal microbiota transplants] on decolonizing multi-drug-resistant organisms,” says Seifeldin Hakim, a gastroenterologist with Memorial Hermann in Houston who was not involved in the study. Theoretically, it would make sense that lowering the number of antibiotic-resistant bacteria in the gut would decrease the chances of clinical infection or sepsis, Hakim says, but more evidence-based results are needed to support this.

Woodworth says poop transplants provide a mix of “good” bacteria to improve colonic health and strengthen the gut barrier. It’s also possible that another biological mechanism is at work. Woodworth hypothesizes that the poop transplants might have driven competition between antibiotic-resistant bacteria and non-resistant germs of the same species. This may have contributed to bacterial strains becoming more susceptible to antibiotics.

Because the trial was an early phase test, there are many more questions to answer, Woodworth says, such as figuring out the proper dose. His team is currently conducting two other clinical trials to research wider applications for fighting drug-resistant pathogens. They are currently planning a larger follow-up study, too, among people who received kidney transplants to better understand how competition between strains might reduce bacteria colonization.

There are still some kinks to work out with using fecal transplants, says Woodworth. However, he hopes this study can act as a jumping off point for inspiring other microbiome-related treatments to fight off antibiotic-resistant bacteria. To guide the next generation of therapies, poop may be our society’s moldy bread.

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In 2017 news broke in North Carolina that the water downstream of the Fayetteville Works Plant, owned by the Chemours Company (a spin-off of DuPont), and public water systems reliant on the Cape Fear River contained high levels of per-and poly-fluoroalkyl substances (PFAS). These contaminants, which are common in everyday products like adhesives, food packaging, and cookware, are dubbed “forever chemicals” because they don’t break down easily in the environment and can linger in the body while causing numerous health problems. And indeed, in the years after the positive PFAS tests, evidence emerged on suspected thyroid cancer clusters in local communities.

The Cape Fear River remains tainted to this day, and many of the residents of southeast North Carolina feel its presence in their lives. “We have a lot of pockets of strange illnesses,” says Dana Sargent, executive director of the nonprofit advocacy group Cape Fear River Watch. She notes that people in the area still buy bottled water and are anxious about the pervasive pollution.

[Related: 2 ways of knowing if there are PFAS in your drinking water]

Chemours has been sued multiple times for dumping chemicals in public waterways. But scientists and environmental groups are still investigating the extent of the contamination.  In recent research using novel chemical-analysis tools published in the journal Science Advances, scientists from the University of North Carolina at Chapel Hill and North Carolina State University found 11 types of PFAS in the Cape Fear River that were previously undetected in those waters. Even worse, eight of those 11 compounds had never been reported to the Environmental Protection Agency (EPA), marking them as new forever chemicals. While it’s incredibly difficult to detect and identify toxins scientists aren’t aware, the study authors says this is a crucial step to studying and regulating PFAS that are still under the radar.

“The goals with this project were twofold,” says Kaylie Kirkwood-Donelson, one of the main contributors on the paper. Kirkwood-Donelson, now a chemist at the National Institute of Environmental Health Sciences, was a graduate student and research assistant at North Carolina State University while conducting this work. “One was to work on a method we could use to identify new PFAS and get more information about their chemical structures than we’d typically get. The second was to apply that method.”

To identify the previously undocumented chemicals, the team established four points of testing. The first three were pretty standard—they assessed each chemical’s mass, size, and polarity. Kirkwood-Donelson then used a relatively novel technique: ion mobility spectrometry, a method that reveals electric activity in the target molecule to help narrow down and pinpoint what you’re looking at. The process was fruitful. In total, she and her colleagues found 47 different forever chemicals in the Cape Fear River, including eight that weren’t already on the EPA’s “CompTox PFAS Master List,” which already covers some 14,000 compounds. 

Despite decades of monitoring, PFAS can be challenging to catalog. To validate the ID, you’re supposed to check that your analyses match those of a “standard” sample of the substance that you either purchase or synthesize, says Erin Baker, an associate professor of chemistry at the University of North Carolina at Chapel Hill and an author on the new study. But standard samples don’t exist for most PFAS yet, and many are too difficult or expensive to synthesize in labs. Creative techniques give researchers more power to identify the mysterious characteristics of these chemicals, Baker says.

The ion mobility spectrometry method the team used “is an amazing method,” says EPA chemist Mark Strynar. “I think it’s the wave of the future.” While the agency has its own process for identifying new PFAS, he adds that it won’t be long before experts start asking, “why isn’t everyone doing this?” He just acquired the equipment needed for ion mobility spectrometry tests in his own lab last week. 

[Related: The US might finally regulate toxic ‘forever chemicals’ in drinking water]

When investigating chemicals as toxic pollutants, the EPA typically assesses them as individual molecules, not classes of chemicals as a whole. It also won’t work toward stronger regulations or a ban until the chemical has proven to be damaging in some way. “We’re hoping that by introducing these new technologies we can speed up the discovery of novel PFAS,” Baker says. But right now, completing the process and validating groundbreaking findings can take an incredibly long time, during which potential toxins remains in the water. “That’s a huge barrier,” says Kirkwood-Donelson. Her Cape Fear research, for example, took six years to finalize. 

On the bright side, now that these new kinds of PFAS have been detected, “other researchers will use this information to see if these chemicals exist across the US and across the world,” Kirkwood-Donelson says. If they’re widespread, toxicologists can begin to assess potential adverse effects. 

Sargent, from Cape Fear River Watch, hopes the EPA will make strong and swift rules limiting PFAS use, starting with the Fayetteville Works Plant. But a recent letter from the agency shows that it authorized Chemours to import up to 4 million pounds of waste material containing the PFAS GenX from the company’s Netherlands facility to North Carolina. GenX has been at the center of several cancer and other health studies.

What’s frustrating is that instead of taking action to reduce PFAS in the environment, the EPA is “actually now just doing the exact opposite, which is huge,” says Sargent. “This issue is not going away,” she adds, and “we need to pay attention.”

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If the existence of a cheap, easy-to-use “Invisible Mask” device that generates a three-foot radius of protection against COVID-19 sounds too good to be true—well, that’s because it is. And the Federal Trade Commission is making sure nobody will continue to profit from this ruse.

Bogus science

According to an October 24 announcement, the FTC recently sued four defendants behind KW Tech, the company hawking the “1 Virus Buster Invisible Mask.” After “attach[ing] a small pouch of [unspecified] ingredients and hang[ing] the badge around the neck,” the Invisible Mask makers claimed it protected wearers against “99.9 percent of all viruses and bacteria,” including multiple variants of COVID-19. The Invisible Mask was marketed as effective in public spaces and crowded areas, as well as on public transit like buses and subways. After 30 days of use, KW Tech advised Invisible Mask owners to discard their device and purchase a new one.

[Related: How to avoid getting COVID again.]

Claiming to employ “a unique combination of compounds” from a design utilizing “IBM’s Quantum Computer,” the Virus Buster Invisible Mask was described as generating an invisible, three-foot “protective gaseous barrier” using something called “ion exchange science.”

“When certain ions collide with other ions, a reaction takes place. This reaction omits [sic] an invisible gas, the point of collision,” KW Tech’s website falsely claimed, as cited in the FTC complaint. “Lighter than air, this gas collects in a tight area close to your face and neck. When this thin layer of gas gets in contact with floating elements like common germs, viruses, and pathogens, it kills them before they are able to get into the nose, mouth, and eye.”

Though this may sound entirely like a word salad, a real technique called “ion exchange” exists, often used to extract mineral impurities from drinking water. However, it requires a physical filter, such as a resin, to collect impurities, and isn’t used against germs. A gas that is lighter than air would diffuse, rise, and not hang out near someone’s mouth.

They’ve been warned before

For $29.99, customers received their Invisible Mask alongside a fake “Certificate of Registration” featuring an image of the FDA logo. Perhaps unsurprisingly, KW Tech never received any approvals from the regulatory body, according to the FTC. Despite “no reliable scientific evidence” supporting their claims, makers of the Invisible Mask continued to deceptively peddle their product, even though they vowed to stop after receiving an FTC warning letter in July 2020—amassing “at least” $100,000 in gross revenue from sales in the process since the FTC’s initial admonishment.

Three of the four defendants have already agreed to settle the complaint, which entails a ban on “advertising, promoting, or selling any product claiming to prevent or treat COVID-19, unless the claims are true and supported by scientific evidence.” The order also bars them from misrepresenting government approval claims for products, alongside a $150,000 penalty.

“The defendants’ claims that their products can stand in for approved COVID-19 vaccines are bogus,” Samuel Levine, Director of the FTC’s Bureau of Consumer Protection, said via the October 24 announcement. “The FTC will use every tool it has at its disposal to stop false and unsubstantiated health claims that endanger consumers.”

Experts continue to agree that proper masking, social distance guidelines, vaccines, and boosters remain the best preventative measures against the contraction and spread of COVID-19.

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This article originally appeared in Knowable Magazine.

Back at the turn of the 21st century, Valley fever was an obscure fungal disease in the United States, with fewer than 3,000 reported cases per year, mostly in California and Arizona. Two decades later, cases of Valley fever are exploding, increasing more than sevenfold and expanding to other states.

And Valley fever isn’t alone. Fungal diseases in general are appearing in places they have never been seen before, and previously harmless or mildly harmful fungi are turning deadly for people. One likely reason for this worsening fungal situation, scientists say, is climate change. Shifts in temperature and rainfall patterns are expanding where disease-causing fungi occur; climate-triggered calamities can help fungi disperse and reach more people; and warmer temperatures create opportunities for fungi to evolve into more dangerous agents of disease.

For a long time, fungi have been a neglected group of pathogens. By the early 2000s, researchers were already warning that climate change would make bacterial, viral and parasite-caused infectious diseases like cholera, dengue and malaria more widespread. “But people were not focused at all on the fungi,” says Arturo Casadevall, a microbiologist and immunologist at the Johns Hopkins Bloomberg School of Public Health. That’s because, until recently, fungi haven’t troubled humans much.

Our high body temperature helps explain why. Many fungi grow best at around 12 to 30 degrees Celsius (roughly 54 to 86 degrees Fahrenheit). So, while they find it easy to infect trees, crops, amphibians, fish, reptiles and insects — organisms that do not maintain consistently high internal body temperatures — fungi usually don’t thrive inside the warm bodies of mammals, Casadevall wrote in an overview of immunity to invasive fungal diseases in the 2022 Annual Review of Immunology. Among the few fungi that do infect humans, some dangerous ones, such as species of Cryptococcus, Penicillium and Aspergillus, have historically been reported more in tropical and subtropical regions than in cooler ones. This, too, suggests that climate may limit their reach.

Fungi on the move

Today, however, the planet’s warming climate may be helping some fungal pathogens spread to new areas. Take Valley fever, for instance. The disease can cause flu-like symptoms in people who breathe in the microscopic spores of the fungus Coccidioides. The climatic conditions favoring Valley fever may occur in 217 counties of 12 US states today, according to a recent study by Morgan Gorris, an Earth system scientist at the Los Alamos National Laboratory in New Mexico.

But when Gorris modeled where the fungi could live in the future, the results were sobering. By 2100, in a scenario where greenhouse gas emissions continue unabated, rising temperatures would allow Coccidioides to spread northward to 476 counties in 17 states. What was once thought to be a disease mostly restricted to the southwestern US could expand as far as the US-Canadian border in response to climate change, Gorris says. That was a real “wow moment,” she adds, because that would put millions more people at risk.

Some other fungal diseases of humans are also on the move, such as histoplasmosis and blastomycosis. Both, like Valley fever, are increasingly seen outside what was thought to be their historical range.

Such range extensions have also appeared in fungal pathogens of other species. The chytrid fungus that has contributed to declines in hundreds of amphibian species, for example, grows well at environmental temperatures between 17 and 25 degrees Celsius (63 to 77 degrees Fahrenheit). But the fungus is becoming an increasing problem at higher altitudes and latitudes, likely because rising temperatures are making previously cold regions more welcoming for the chytrid. Similarly, white pine blister rust, a fungus that has devastated some species of white pines across Europe and North America, is expanding to higher elevations where conditions were previously unfavorable. This has put more pine forests at risk. Changing climatic conditions are also helping drive fungal pathogens of crops, like those infecting bananas, potatoes and wheat, to new areas.

A warming climate also changes cycles of droughts and intense rains, which can increase the risk of fungal diseases in humans. One study of more than 81,000 cases of Valley fever in California between 2000 and 2020 found that infections tended to surge in the two years immediately following prolonged droughts. Scientists don’t yet fully understand why this happens. But one hypothesis suggests that Coccidioides survives better than its microbial competitors during long droughts, then grows quickly once rains return and releases spores into the air when the soil begins to dry again. “So climate is not only going to affect where it is, but how many cases we have from year to year,” says Gorris.

By triggering more intense and frequent storms and fires, climate change can also help fungal spores spread over longer distances. Doctors have observed unusually large outbreaks of Valley fever just after dust storms or other events that kick up clouds of dust. Similarly, researchers have found a surge in Valley fever infections in California hospitals after large wildfires as far as 200 miles away. Scientists have seen this phenomenon in other species too: Dust storms originating in Africa have been implicated in moving a coral-killing soil fungus to the Caribbean.

Researchers are now sampling the air in dust storms and wildfires to see if these events can actually carry viable, disease-causing fungi for long distances and bring them to people, causing infections. Understanding such dispersal is key to figuring out how diseases spread, says Bala Chaudhary, a fungal ecologist at Dartmouth College who coauthored an overview of fungal dispersal in the 2022 Annual Review of Ecology, Evolution, and Systematics. But there’s a long road ahead: Scientists still don’t have answers to several basic questions, such as where various pathogenic fungi live in the environment or the exact triggers that liberate fungal spores out of soil and transport them over long distances to become established in new places.

Evolving heat tolerance

Helping existing fungal diseases reach newer places isn’t the only effect of climate change. Warming temperatures can also help previously innocuous fungi evolve tolerance for heat and become deadlier. Researchers have long known that fungi are capable of this. In 2009, for example, researchers showed that a fungus — in this case a pathogen that infects hundreds of insect pests — could evolve to grow at 37 degrees Celsius, five degrees higher than its previous upper thermal limit, after just four months. More recently, researchers grew a dangerous human pathogen, Cryptococcus deneoformans, at both 37 degrees Celsius (similar to human body temperature) and 30 degrees Celsius in the lab. The higher temperature triggered a fivefold rise in mutations in the fungus’s DNA compared to the lower temperature. Rising global temperatures, the researchers speculate, could thus help some fungi rapidly adapt, increasing their ability to infect people.

There are examples from the real world too. Before 2000, the stripe rust fungus, which devastates wheat crops, was restricted to cool, wet parts of the world. But since 2000, certain strains of the fungus have become better adapted to higher temperatures. These sturdier strains have been replacing the older strains and spreading to new regions.

This is worrying, says Casadevall, especially with hotter days and heatwaves becoming more frequent and intense. “Microbes really have two choices: adapt or die,” he says. “Most of them have some capacity to adapt.” As climate change increases the number of hot days, evolution will select more strongly for heat-resistant fungi.

And as fungi in the environment adapt to tolerate heat, some might even become capable of breaching the human temperature barrier.

This may have happened already. In 2009, doctors in Japan isolated an unknown fungus from the ear discharge of a 70-year-old woman. This new-to-medicine fungus, which was given the name Candida auris, soon spread to hospitals around the world, causing life-threatening bloodstream infections in already sick patients. The World Health Organization now lists Candida auris among its most dangerous group of fungal pathogens, partly because the fungus is showing increasing resistance to common antifungal drugs.

“In the case of India, it’s really a nightmare,” says Arunaloke Chakrabarti, a medical mycologist at the Postgraduate Institute of Medical Education and Research in Chandigarh, India. When C. auris was first reported in India more than a decade ago, it was low on the list of Candida species threatening patients, Chakrabarti says, but now, it’s the leading cause of Candida infections. In the US, cases rose sharply from 63 between 2013 and 2016 to more than 2,300 in 2022.

Where did C. auris come from so suddenly? The fungus appeared simultaneously across three different continents. Each continent’s version of the fungus was genetically distinct, suggesting that it emerged independently on each continent. “It’s not like somebody took a plane and carried them,” says Casadevall. “The isolates are not related.”

Since all continents are exposed to the effects of climate change, Casadevall and his colleagues think that human-induced global warming may have played a role. C. auris may always have existed somewhere in the environment — potentially in wetlands, where researchers have recovered other pathogenic species of Candida. Climate change, they argued in 2019, may have exposed the fungus to hotter conditions over and over again, allowing some strains to become heat-tolerant enough to infect people.

Subsequently, scientists from India and Canada found C. auris in nature for the first time, in the Andaman Islands in the Bay of Bengal. This “wild” version of C. auris grew much slower at human body temperature than did the hospital versions. “What that suggests to me is that this stuff is all over the environment and some of the isolates are adapting faster than others,” says Casadevall.

Like other explanations for C. auris’s origin, Casadevall’s is only a hypothesis, says Chakrabarti, and still needs to be proved.

One way to establish the climate change link, Casadevall says, would be to review old soil samples and see if they have C. auris in them. If the older versions of the fungus don’t grow well at higher temperatures, but over time they start to, that would be good evidence that they’re adapting to heat.

In any case, the possibility of warmer temperatures bringing new fungal pathogens to humans needs to be taken seriously, says Casadevall — especially if drug-resistant fungi that currently infect species of insects and plants become capable of growing at human body temperature. “Then we find ourselves with organisms that we never knew before, like Candida auris.”

Doctors are already encountering novel fungal infections in people, such as five new-to-medicine species of Emergomyces that have appeared mostly in HIV-infected patients across four continents, and the first record of Chondrostereum purpureum — a fungus that infects some plants of the rose family — infecting a plant mycologist in India. Even though these emerging diseases haven’t been directly linked to climate change, they highlight the threat fungal diseases pose. For Casadevall, the message is clear: It’s time to pay more attention.

Editor’s note: This story was updated on September 27, 2023, to correct a mischaracterization of malaria. It is caused by a parasite, not a virus or a bacterium as was originally stated.

10.1146/knowable-092623-2

Shreya Dasgupta is an independent science journalist based in Bangalore, India.

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.

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We’re closer than ever to mapping the entire brain to the microscopic level. Hundreds of neuroscientists across the world recently characterized more than 3,000 human brain cell types as part of the National Institute of Health’s BRAIN Initiative Cell Census Network, publishing almost two dozen papers in four Science journals today. This super-focused attention to detail could unlock many mysteries surrounding that complex organ, such as what happened in our brains to distinguish us from other primates. 

“This is the first large-scale, detailed description of all the different kinds of cells present in the human brain,” says Rebecca Hodge, an assistant investigator at the Allen Institute in Seattle who co-authored multiple studies in the paper package. Her hope is that this brain atlas provides a community resource for scientists to explore how the wide variety of brain cells contribute to health and disease.

Mark Mapstone, a professor of neurology at University of California, Irvine School of Medicine, who wasn’t involved with these studies, likened the new data about the brain to a tourist’s guide. “Imagine navigating an unfamiliar city with a roughly drawn street map containing only the major streets of the downtown compared to navigating the same city with a detailed map extending beyond the downtown to the suburbs and including all highways, two-way and one-way streets, alleyways, sidewalks, location of street signs and traffic signals, speed limits, and location of coffee shops and restaurants,” he says. “Cleary, the latter would make navigation and understanding the city much easier.” This first suite of studies shows three main ways the brain map can be used for biology and medicine.

An evolving brain

A human brain atlas can teach us about our evolutionary history. One study published today in Science used single-nucleus RNA sequencing to measure the gene expression of individual brain cells in humans and five other primate species, including chimpanzees and gorillas. In this method, scientists pull out individual cells from a piece of tissue, break them open to expose the genetic messengers inside, then use tags akin to tiny barcodes to identify that material. “This is the main technology used in some of these papers that are coming out and it’s a technique that’s only been around for the past 10 years,” Hodge says. Getting this genetic profile allows researchers to group clusters of cells into specific types. 

[Related: Psychedelics and anesthetics cause unexpected chemical reactions in the brain]

Our cells’ composition and organization is similar to those of our close relatives. However, the biggest differences seemed to occur in a brain region called the middle temporal gyrus, which is involved in processing semantic memory and language. Humans had higher numbers of projecting neurons in this area compared to other species. What’s more, the researchers highlighted a difference in gene expression that promoted synaptic plasticity, which is the ability of neurons to strengthen brain connections. This feature is an important component for learning and memory, and it might explain how humans developed complex cognitive skills.

There was some variation within humans, too. Another study found the most differences across humans in immune cells called microglia as well as deep-layer excitatory neurons, which are involved in the communication between distant brain regions. Researchers are not quite sure why—one theory is that deep-layer excitatory neurons develop earlier and are more exposed to environmental factors that could diversify their gene patterns. “Everyone’s brain is largely similar. Even though we have the same building blocks, it’s the small number of differences that matter,” says Jeremy Miller, a senior scientist at the Allen Institute, and co-author of the study. “We’re now starting to understand how important these changes are and figuring out what makes us uniquely human.”

Animal models

Because human brains share many features with other mammals, neurologists frequently use the small brains of mice to study diseases. The one problem, Miller says, is that mice don’t naturally develop neurodegenerative diseases common in humans. Scientists who want to study Alzheimer’s disease, for example, would need to manipulate multiple mouse genes to cause the kind of brain pathology seen in older people. This requires a comprehensive understanding of how cell types in the brain work together and how they change in the context of disease. 

[Related: How your brain conjures dreams]

Much brain research in mice focuses on the neocortex, responsible for higher cognitive function. It might seem reasonable to assume that much of the brain’s cellular complexity appears here. But this doesn’t seem to be the case. In one of the first studies to create a cell map of the entire adult brain, neuroscientists have found high levels of diversity in older evolutionary structures such as the midbrain, which is involved in movement, vision, and hearing, and the hindbrain, which governs vital bodily functions such as breathing and heart rate. In subcortical areas, there also appears to be a supercluster of cells called splatter neurons that control innate behaviors and physiological functions. Replicating the complexity of these particular brain regions in animal models could help better identify the cellular origins of human diseases. 

Personalized medicine

Imagine a future where treatments are tailored to someone’s specific needs. To do that, scientists would use a person’s genetic profile, rather than characteristics such as weight or age, to inform any medical decisions. Clinicians could also use this genetic information to identify the risks of potential diseases and provide early preventative measures. 

“A detailed brain atlas can help us understand what successful brain function looks like so we can maximize brain cells and circuits that promote brain heath,” Mapstone says. “Addressing brain disease and promoting brain health can be more easily accomplished if we know how these cells are organized. “

Doctors are already using people’s genetic information to assess whether patients would be good candidates for a particular cancer treatment or to find the proper dose of a drug. This may soon include testing for neurological conditions. One study, which analyzed 1.1 million cells in 42 brain regions of neurotypical adults, identified specific neuronal cell types—mainly in the basal ganglia, a region involved in addictive behaviors—that were linked to 19 neuropsychiatric disorders and traits. Those conditions included schizophrenia and bipolar disorder as well as alcohol and tobacco use disorder.

This project is a step in the right direction for advancing research in personalized medicine, says Miller, though he warns this is only one of many to make this a reality for everyone. 

Miller and Hodge are optimistic there will be other versions of the human brain atlas completed in the next five years, as other groups wrap up similar projects. 

But there’s a possibility that we’ll never get the full picture. While Miller finds a half-decade timeframe reasonable, he says there’s always a chance science develops a new technology that could unearth something unexpected about the brain. “We can always do more,” he says.

This post has been updated.

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Gregory Breed doesn’t remember exactly when he began suffering from symptoms of a chronic prostate infection. The 62-year-old estimates they began when he was in his mid-20s. By his early 30s, he was taking painkillers for lower back pain, a common outcome of the disease. Over the years, his doctors put him on course after course of oral antibiotics: trimethoprim-sulfamethoxazole and levofloxacin. But a few months after he stopped taking the drugs, his infection would return.

Prostate infections or prostatitis, one of the most common urinary tract issues in adults, are notorious for recurrence as antibiotics often can’t penetrate tissue deep enough to kill all the bacteria. Over time, with repeated exposure to medicine, the E. coli causing Breed’s infection was becoming increasingly drug-resistant, meaning the bacteria developed the ability to evade and survive treatment. To make matters worse, Breed’s immune response was growing more severe. Between 2000 and 2010, he was hospitalized with sepsis, a life-threatening condition caused by the immune system’s overreaction to an infection, at least five times. Each time he would recover, only to battle another flare-up.

“Greg was constantly in the practice,” Ismail Jimada, Breed’s doctors between 2018 and 2022, says. “We were running out of solutions.”

Breed routinely maxed out his health insurance, paying thousands of dollars out of pocket for his medical bills. The infections took a toll on his loved ones and work life. “I have a very supportive family, but it was hard,” Breed recalls. “There were a lot of years there I didn’t get to be around my family near what I would have liked to.” Some days he struggled to get up and manage his small business selling pipes for oil wells. With limited options for medical care in rural Wyoming, he sought out infectious disease specialists across the country. But with the E. coli in his prostate already resistant to many go-to antibiotics, they didn’t have many treatments to offer him.

Breed’s infection was just one of more than 2.8 million cases of drug-resistant infections recorded by the Centers for Disease Control and Prevention in the US each year. Illnesses that defy antibiotics, antifungals, or other antimicrobials are challenging, if not altogether impossible to treat. More than 35,000 Americans die from drug-resistant infections annually. Globally, that number likely exceeds one million. In 2021 the World Health Organization declared antimicrobial resistance “one of the top 10 global public health threats facing humanity.” Antibiotics are a cornerstone of modern medicine; as pathogens like E. coli , Candida auris, and HIV develop a tolerance to the remedies, common infections, routine dental procedures, and surgeries could become life-threatening. Just in time, however, scientists and physicians are turning to an obscure, decades-old antidote to get drug-resistant infections back under control.

A race to replace antibiotics

Antimicrobial resistance is just another consequence of evolution: Bacteria, fungi, and other microorganisms are constantly adapting unique survival mechanisms to keep up with humans and a changing world. Still, researchers believe the overuse and misuse of antimicrobials in medicine and agriculture is accelerating the emergence and spread of resistance. New drugs capable of killing these evolving microbes could stave off the problem—but it takes millions of dollars and more than a decade of research and development to put out such a product. There hasn’t been a novel class of antibiotics since the 1980s, in part because most major pharmaceutical companies have stopped trying to discover one.

Out of desperation, Breed began scouring the internet for alternative treatments. Sometime in late 2017 or early 2018, he stumbled across a Ted talk by UC San Diego epidemiologist Steffanie Strathdee. In it, Strathdee describes an ill-fated trip to Egypt in 2015 where her husband, Tom Patterson, contracted a drug-resistant infection caused by Acinetobacter baumannii. When they arrived home in California, Patterson fell into a coma; his organs began to shut down. The bacteria behind his infection was already resistant to all known antibiotics.

Strathdee also turned to the internet and found a glimmer of hope: a treatment first discovered in 1917 that had been used in the Soviet Union for decades but largely overlooked by the rest of the world. The method taps bacteriophages, a type of virus that infects and kills bacteria, to combat infections. Scientists have long known that there are billions of different bacteriophages, or “phages,” on the planet. They often live in sewers and other germ-filled places and are highly specific, killing only one or sometimes a few strains of bacteria with no documented harm to humans.

Strathdee reached out to scientists publishing phage research at the time. She thought if they could find a virus that could infect and kill the specific A. baumannii strain causing her husband’s infection, then he might have a chance to survive. Researchers at Texas A&M University immediately responded to her urgent e-mail and started hunting for the right type to combat the culprit. After just a few weeks, they found a few candidate specimens and mailed them to California. The treatment would be experimental—there were no known cases of intravenous phage therapy in the US at the time, according to Strathdee—so Patterson’s clinical team requested emergency use authorization from the Food and Drug Administration (FDA). It was granted within a day. At the UC San Diego Medical Center, doctors injected the phages into Patterson’s abdomen, and a few days later, directly into his bloodstream. Less than a week after the treatment began, Patterson woke up, kissed his daughter’s hand, and went on to make a full recovery.

Building a new path

In 2018, Strathdee co-founded the Center for Innovative Phage Applications and Therapeutics, or IPATH, at UC San Diego to further develop phage therapy for drug-resistant infections. Later that same year, Breed e-mailed the group inquiring if method might also work for his chronic prostate infection. The IPATH team got to work sending specimens of Breed’s E. coli to a network of phage researchers around the country, searching for an effective phage match for much of 2019. It was ultimately provided by the TAILOR lab at the Baylor College of Medicine, which creates “customized phage cocktails for no-hope cases when antibiotics and standard of care have failed,” its founder Anthony Maresso says. Then it took just about one day to receive compassionate use authorization from the FDA.

In January 2020, Breed and his wife flew to San Diego to begin the phage treatment, which IPATH provided for free. “I was excited but extremely nervous about it. When you think about putting the substance they tell you the phage is derived from into your body, it’s not a real good thought,” Breed says. (He’s referring to sewage, the most common source for effective phages.) “Especially when they hook you up and say, ‘Okay, we’re gonna watch and see what happens,’ and you know there’s not a whole lot of people ahead of you who have done it. It’s a really scary situation to be in.”

The IPATH team injected phages into Breed’s catheter. For the next two weeks, he continued with the procedure twice a day, according to Saima Aslam, an infectious diseases physician and IPATH’s clinical lead. Breed’s symptoms—pain, fever, and urinary problems—faded. After six months, laboratory tests confirmed there was no detectable E. coli in his prostate. It has remained that way ever since, and Breed has not suffered any adverse effects from the undertaking.

In high demand

A separate study published in 2023 reported that 11 of 20 patients in the US who received phage therapy for infections caused by mycobacterium had favorable clinical responses. The IPATH team itself has treated 18 patients, including Breed, with phage therapy in the past five years and has had a success rate of 82 percent, Aslam says. She and other physicians and phage researchers are calling for additional research and clinical trials to better understand phage therapy and set forth best practices. There are more than 20 ongoing clinical trials—many for people with cystic fibrosis or prosthetic joint infections—–registered with the US government now.

The current ad-hoc model of sending samples to researchers across the country in hopes for a phage match often delays time to treatment. It usually takes about four to six months to scour repositories—or sewers—for a good phage match, Aslam explains, which means that patients should be in somewhat stable condition to be a candidate. (The FDA typically approves phage therapy for critically ill patients within 24 hours and for more stable patients within 30 days.) The method is also not sustainable for large-scale use. The US government and several universities around the world are working to compile databases that list their discovered phages and the bacterial strains they target. Several biotechnology companies with private collections have also sprung up in recent years; some researchers are even developing and patenting genetically modified phages that are shelf stable or can target more than one type of infection-causing bacteria.

While there is still a long road ahead, phage therapy is one of the few tested solutions for drug-resistant infections—and could some day be comparable, if not cheaper, to the cost of antibiotics. Aslam envisions that in the future, different phage products will be available at pharmacies just like other medicines. But for now, the therapy is proving lifesaving and life changing for lucky individuals like Breed and Patterson. “I have three young grandkids … I was to the point that I was wondering if I really was gonna enjoy the time with them,” Breed says. While he still has some lingering side effects from such prolonged antibiotic use, in terms of quality of life, “it is a thousand times better than it was” before the phages entered the battle.

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This article is republished from The Conversation.

Centenarians, once considered rare, have become commonplace. Indeed, they are the fastest-growing demographic group of the world’s population, with numbers roughly doubling every ten years since the 1970s.

How long humans can live, and what determines a long and healthy life, have been of interest for as long as we know. Plato and Aristotle discussed and wrote about the ageing process over 2,300 years ago.

The pursuit of understanding the secrets behind exceptional longevity isn’t easy, however. It involves unravelling the complex interplay of genetic predisposition and lifestyle factors and how they interact throughout a person’s life. Now our recent study, published in GeroScience,, has unveiled some common biomarkers, including levels of cholesterol and glucose, in people who live past 90.

Nonagenarians and centenarians have long been of intense interest to scientists as they may help us understand how to live longer, and perhaps also how to age in better health. So far, studies of centenarians have often been small scale and focused on a selected group, for example, excluding centenarians who live in care homes.

Huge dataset

Ours is the largest study comparing biomarker profiles measured throughout life among exceptionally long-lived people and their shorter-lived peers to date.

We compared the biomarker profiles of people who went on to live past the age of 100, and their shorter-lived peers, and investigated the link between the profiles and the chance of becoming a centenarian.

Our research included data from 44,000 Swedes who underwent health assessments at ages 64-99—they were a sample of the so-called Amoris cohort. These participants were then followed through Swedish register data for up to 35 years. Of these people, 1,224, or 2.7 percent, lived to be 100 years old. The vast majority (85 percent) of the centenarians were female.

Twelve blood-based biomarkers related to inflammation, metabolism, liver and kidney function, as well as potential malnutrition and anaemia, were included. All of these have been associated with ageing or mortality in previous studies.

The biomarker related to inflammation was uric acid—a waste product in the body caused by the digestion of certain foods. We also looked at markers linked to metabolic status and function including total cholesterol and glucose, and ones related to liver function, such as alanine aminotransferase (Alat), aspartate aminotransferase (Asat), albumin, gamma-glutamyl transferase (GGT), alkaline phosphatase (Alp) and lactate dehydrogenase (LD).

We also looked at creatinine, which is linked to kidney function, and iron and total iron-binding capacity (TIBC), which is linked to anaemia. Finally, we also investigated albumin, a biomarker associated with nutrition.

Findings

We found that, on the whole, those who made it to their hundredth birthday tended to have lower levels of glucose, creatinine and uric acid from their sixties onwards. Although the median values didn’t differ significantly between centenarians and non-centenarians for most biomarkers, centenarians seldom displayed extremely high or low values.

For example, very few of the centenarians had a glucose level above 6.5 earlier in life, or a creatinine level above 125.

For many of the biomarkers, both centenarians and non-centenarians had values outside of the range considered normal in clinical guidelines. This is probably because these guidelines are set based on a younger and healthier population.

When exploring which biomarkers were linked to the likelihood of reaching 100, we found that all but two (alat and albumin) of the 12 biomarkers showed a connection to the likelihood of turning 100. This was even after accounting for age, sex and disease burden.

The people in the lowest out of five groups for levels of total cholesterol and iron had a lower chance of reaching 100 years as compared to those with higher levels. Meanwhile, people with higher levels of glucose, creatinine, uric acid and markers for liver function also decreased the chance of becoming a centenarian.

In absolute terms, the differences were rather small for some of the biomarkers, while for others the differences were somewhat more substantial.

For uric acid, for instance, the absolute difference was 2.5 percentage points. This means that people in the group with the lowest uric acid had a 4 percent chance of turning 100 while in the group with the highest uric acid levels only 1.5 percent made it to age 100.

Even if the differences we discovered were overall rather small, they suggest a potential link between metabolic health, nutrition and exceptional longevity.

The study, however, does not allow any conclusions about which lifestyle factors or genes are responsible for the biomarker values. However, it is reasonable to think that factors such as nutrition and alcohol intake play a role. Keeping track of your kidney and liver values, as well as glucose and uric acid as you get older, is probably not a bad idea.

That said, chance probably plays a role at some point in reaching an exceptional age. But the fact that differences in biomarkers could be observed a long time before death suggests that genes and lifestyle may also play a role.

Karin Modig is an associate professor of epidemiology at the Karolinska Institutet.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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This article was originally featured on Hakai Magazine, an online publication about science and society in coastal ecosystems. Read more stories like this at hakaimagazine.com.

Eight years ago, I first met with researchers from the Save the Tasmanian Devil Program (STDP) in Tasmania, Australia, to learn about their work to protect the endangered marsupials. Since then, I’ve continued to follow this story, including tracking how the Forestier Peninsula devils—the focus of my original article published in late 2015—fared in their “new life.”

Contagious cancers like devil facial tumor disease (DFTD) are virtually unheard of in vertebrates, yet understanding how they’re transmitted and how they evade immune systems has implications for both conservation and oncology. For that research to take place, there needs to be a healthy population of Tasmanian devils. That’s why in late 2015 and early 2016, the STDP released 49 devils bred in captivity on the isolated Forestier Peninsula, to join the estimated 30 wild devils already living on the adjacent Tasman Peninsula. Establishing a new, managed, disease-free population of devils (with another already existing on Maria Island, located just off the east coast of Tasmania) would buy researchers more time to develop a vaccine.

Their release should have been a moment of hope for the endangered species, but it was marred by a discovery some 50 kilometers west, across the sea, on another Tasmanian peninsula. A local spotted a devil with a large facial tumor: the calling card of DFTD.

Routine tests returned an unsettling result—it was a new cancer.

Called DFT2, the new disease is genetically distinct from DFT1 (the original cancer). Its method of transmission and symptoms are the same, and it poses a severe additional threat to the species.

The discovery of DFT2, however, provides a critical clue to the cancer’s puzzle. Devils, it turns out, aren’t victims of bad luck—they are particularly prone to DFTD. There are three known wild infectious cancers in vertebrates in the world, and Tasmanian devils have two of them.

“It was a big surprise. We thought that transmissible cancers were really rare—like lightning striking—and that devils were just a very unfortunate species,” says Elizabeth Murchison, who researches genetic and transmissible cancers at the University of Cambridge in England. It’s likely that DFT1 and DFT2 weren’t the first cancers to emerge in devils and are unlikely to be the last.

The habit the devils have of biting each other helps spread the disease, and their low genetic diversity creates ideal conditions for the cancers to evade the marsupial’s immune system. Another factor in the devils’ inability to fight the infections could be an issue with their peripheral nervous systems, where both DFT1 and DFT2 seem to originate. What’s likely not to blame, however, is environmental pollutants as suggested in my original article. According to Murchison, the imprint mutations left on devil DNA indicate the two cancers are natural occurrences. “There’s nothing to suggest any external exposure to a chemical or radiation or anything like that,” she says.

Fortunately, the discovery of the second cancer hasn’t slowed vaccine development. Andrew Flies—a senior research fellow at the University of Tasmania’s Menzies Institute for Medical Research—says the cancers have similarities that will make it easier for his team to develop a vaccine for both. In 2024, tests on an experimental DFT1 vaccine will begin, with the development of a vaccine that targets both cancers already underway. To reach devils, officials will distribute bait drops containing the vaccine through Tasmania’s vast wilderness.

Rollout is still several years away, but devils no longer appear to be at imminent risk of extinction. Exact numbers are unknown, but thanks in part to pilot projects to improve genetic diversity through the release of healthy devils, their population is holding strong in many areas—at least for now.

“Disease doesn’t really make a species go extinct. Diseases push the species to the very edge, and then everything else just comes along and takes them out,” says Carolyn Hogg, a researcher at the University of Sydney, who has been working with threatened species in Australia, including Tasmanian devils, for over 25 years.

For devils, “everything else” includes low genetic diversity, loss of habitat, and road fatalities. The nocturnal scavengers can’t resist the lure of rotting roadside carcasses, easy pickings in the roadkill capital of the world. In 2021, motorists killed more than 100 devils on just one 25-kilometer stretch of road in northwest Tasmania.

“If you’ve only got five breeding females in a small population and two get hit by cars on the road, you’ve lost 40 percent of your breeding population in one event,” says Hogg.

That’s exactly what happened to the Forestier Peninsula devils I wrote about in my original article. Drivers killed 16 of the 49 individuals within six weeks of their release. Through subsequent tracking, Hogg and her team discovered that devils raised in captive facilities for generations were more likely to use roadways than wild devils.

“You can’t release them anywhere near any major road systems, because behaviorally they’re used to the sound of vehicles,” says Hogg.

Since then, the STDP has done 11 more releases of healthy Tasmanian devils throughout the state to improve genetic diversity of existing wild populations. What’s changed is that instead of releasing devils bred in captivity, it now relies on the wild offspring of the disease-free population on Maria Island. A national park where there are no cars (save for those used by park rangers), Maria Island has wild devils that aren’t habituated to the sound of traffic and are more likely to survive.

Relying on Maria Island’s wild devils is the best option for building up a population of wild devils until a vaccine is developed. But the introduction of the marsupials to the island—which was devil-free until 2012—still has critics, much as it did back in 2015. In 2021, BirdLife Tasmania reported that over a decade, the introduced devils wiped out the island’s 3,000 breeding pairs of little penguins. Little penguins are found in abundance in the wild: Tasmania has hundreds of offshore islands, with an estimated 110,000 to 190,000 breeding pairs.

“We knew that was going to happen,” says Hogg. A risk assessment, she says, determined that the benefits of having a place to breed wild devils disease-free and improve their genetic diversity was “greater than the loss of the birds.”

The news, however, is not all bad. Researchers believe that introducing the carnivore has allowed Maria’s population of eastern barred bandicoots—listed as an endangered species on the mainland—to thrive, by pushing predatory possums up into trees. Cape Barren geese—which dropped in numbers following the marsupial’s introduction—have also learned to coexist with devils. As for the population of little penguins? The Maria Island population began to decline around the same time as one on a neighboring island, suggesting additional environmental factors were likely at play.

Yet, the conservation of endemic species and how to best manage them—from little penguins to Tasmanian devils—remains both a controversial and emotional topic in Australia. It’s rumored that conservation “vigilantes” are covertly rewilding Australia’s mainland with devils smuggled from Tasmania. But Hogg says any mainland devils are just as likely to develop a new cancer, given how susceptible they are to the disease. And without the protection of natural barriers that isolate populations of devils—like the narrow isthmuses on the Forestier and Tasman Peninsulas or the waters around Maria Island—preventing the cancer from spreading is impossible.

For now—until a vaccine is deployed—Maria Island’s disease-free population will be what stands between the devils and extinction.

This article first appeared in Hakai Magazine and is republished here with permission.

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The threat of avian influenza (H5N1) continues to be a serious health and economic issue. As of September, almost 60 million birds have been affected in the United States since the latest outbreak began in January 2022. There are currently 839 known H5N1 outbreaks around the world.

[Related: Thriving baby California condor is a ray of hope for the unique species.]

Earlier this month, France began Europe’s only mass-vaccination campaign against avian influenza. The country plans to vaccinate roughly 64 million ducks at 2,700 farms over the next year as an effort to end mass culls. Drastic actions like the culls cost the poultry industry millions of dollars every year. 

“Vaccination should mean we only face individual cases, avoiding the tidal waves sweeping through farms,” poultry chief at the SNGTV farm vets’ association Jocelyn Marguerie told DW News. 

To reduce the risk of more Highly Pathogenic Avian Influenza (HPAI) spreading in the US, the Department of Agriculture’s Animal and Plant Health Inspection Service has barred poultry imports from France and its European Union trading partners including Iceland, Switzerland, Liechtenstein, and Norway. The ban covers live ducks, duck eggs, and unmitigated/untreated duck products in addition to poultry products and is due to their recent vaccination campaign. 

According to a press release, the agency is concerned that the vaccines may mask that the virus is already circulating in poultry, as the vaccinated birds may not show any signs of infection and could lead to the contaminated animals being brought into the US. 

In France, the vaccine will be given in two doses and is obligatory for ducklings as young as 10 days old being raised on farms that have more than 250 birds. It will cost close to 100 million euros ($105 million) and 85 percent of the cost will reportedly be financed by the French government.

“Typically, animal vaccines in the US take approximately 3 years to develop and get FDA approval. Even though vaccination reduces mortality significantly, there is still concern that vaccinated birds can become infected and shed the virus,” Michelle Hawkins, an ABVP certified veterinarian at the University of California, Davis and the director of the California Raptor Center tells PopSci. “This is the main concern regarding France authorizing a vaccine. Ducks often carry avian influenza viruses without showing any clinical signs when infected.”

Hawkins also cited a concern about how quickly HPAI can mutate which could potentially reduce the vaccine’s efficacy.

[Related: One way to fight off bird flu: extra-CRISPRed chicken.]

Recently, commercial flocks have been culled in South Africa to stop the spread and the virus which has been detected in at least 67 countries. It has also been found in domestic cats in Poland and has even jumped from wild birds into seals on the East and West Coasts of the US. 

While vaccination is not enough to completely stop the disease yet, the jabs are a tool in fighting it. The Department of Agriculture began evaluating four HPAI vaccine candidates for animals and began some trials in April 2023. Other countries including Egypt, China, Mexico, and Vietnam have been vaccinating flocks for years. 

Currently, the risk of avian flu to humans is low, with only one reported human case of this virus in the US. There are trials underway of vaccines for humans if the virus mutates to become more of a threat to people. Researchers in the United Kingdom have also isolated a gene called BTN3A3 that could keep the virus from infecting humans. 

In the meantime, vigilance from bird owners and other protective measures including avoiding contact with wild birds and reporting dead birds to the proper authorities remain crucial. 

“It is critical that bird owners look at what they can do immediately to protect their flocks– now,” says Hawkins. 

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This article was originally published on Undark.

Growing up, Julian Meeks knew what a life without a sense of smell could look like. He’d watched this grandfather navigate the condition, known as anosmia, observing that he didn’t perceive flavor and only enjoyed eating very salty or meaty foods.

The experience influenced him, in part, to study chemosensation, which involves both smell and taste. Meeks, now a professor of neuroscience at the University of Rochester, told Undark that neither gets much attention compared to other senses: “Often, they’re thought of as second or third in order of importance.”

The pandemic changed that, at least somewhat, after it left millions of people without a sense of smell, albeit some temporarily. In particular, more researchers started looking at a specific type of condition called acquired anosmia. Common causes include traumatic brain injury, or TBI, neurodegenerative diseases like Parkinson’s or Alzheimer’s, or following a viral infection like Covid-19. Due to the pandemic, “many people found it scientifically interesting to focus their research on smell,” said Valentina Parma, the assistant director of the Monell Chemical Senses Center, a nonprofit research institute in Philadelphia. By one account, NIH funding of anosmia research nearly doubled between 2019 and 2021.

But many of the research findings do not apply to those who have lacked the ability to smell since birth: congenital anosmics. And, despite the increased attention to smell loss more broadly, some researchers still face challenges in funding studies. In March 2023, for instance, Meeks received a peer review for a small grant, of less than $275,000, from the National Institutes of Health, with which he had planned to look into anosmia in the context of TBI.

For Meeks, the response was frustrating. One expert reviewer in particular “didn’t really understand why there would be any need to establish a preclinical model of anosmia with TBI,” he said, noting that the reviewer also wrote that because anosmia is not a major health problem, the value of the research was low. The comment, Meeks added, was “quite discouraging.”

In response to a request for comment on that decision, Shirley Simson, a spokesperson for NIH’s National Institute on Deafness and Other Communication Disorders, or NIDCD, which funds smell and taste research, replied that “NIH does not discuss the peer review process for individual grant applications.” She noted in a separate email that “all NIH grant applications, including those submitted by investigators to NIDCD, undergo the same review process.”

THE SENSE OF SMELL IS complicated, and not fully understood. Jay Piccirillo, an otolaryngologist at Washington University School of Medicine in St. Louis, likens its complexity, with its many neuronal connections, to Times Square. Compared to the nose, the eye looks relatively simple, he told Undark.

There are a few basic steps, however, on which researchers do agree. Humans smell by detecting molecules, or odorants, in the environment around them. These odorants latch on to one of 400 receptors in the nose, called olfactory receptor neurons, which then send a signal the brain. The result: a dizzying array of odors.

“We can smell and discriminate tens of thousands or maybe billions or trillions of smells,” said Hiroaki Matsunami, an olfaction researcher at Duke University who, along with colleagues, recently published a study on how one of these receptors works.

Both congenital and acquired smell loss can either entail complete loss (anosmia) or minimal loss (hyposmia). Some people also have a distorted sense of smell, a condition known as parosmia, or perceive odors that aren’t there, known as phantosmia. And because of the connection between smell and taste, sometimes smell loss is accompanied by the inability to taste, or ageusia, as it did for many Covid patients.

Any form of anosmia can have a broad effect on daily function. For one, it can be a safety hazard, since affected people may not be able to detect a fire, gas leak, or spoiled food. Smell loss is also associated with depression, and because of the close link between smell and taste, the condition can affect appetite and, by extension, nutritional health.

The cause of anosmia isn’t entirely known. For congenital anosmia, researchers suspect a genetic link or developmental abnormalities. As for acquired anosmia, an injury or illness appears to disrupt the transmission of an odorant to the brain, but the exact spot of that break isn’t clear — and it may vary, depending on the cause. When it comes to Covid, for instance, some researchers initially suspected that the virus was killing the cells that transmit the odorant signal to the brain. More recent research suggests that, instead, it could be because of inflammation or damaged supporting cells.

It’s also not entirely clear how many people have anosmia. In 2012, research analyzing the U.S. National Health and Nutrition Examination Survey estimated that 23 percent of Americans over the age of 40 report some alteration to their sense of smell. A 2016 paper that examined results from a later version of same survey estimated that more than 12 percent of American adults had some sort of olfactory dysfunction. And Fifth Sense, a charity for smell and taste disorders, estimates that 1 in 10,000 people have congenital anosmia.

The numbers are uncertain in part because, compared to other sensory dysfunctions like vision or hearing loss, experts say there are fewer resources or people involved in smell research. And prior to the pandemic, anosmia research was typically relegated to smell and taste research centers or otolaryngologists (also known as ear, nose, and throat doctors). “It was like a niche,” said Thomas Hummel, a smell and taste disorder researcher at the University of Dresden in Germany. Studying smell loss, he added, wasn’t “in the foreground of research.”

When anosmia was reported as a symptom of Covid-19, there was a switch. Smell and taste researchers were suddenly inundated with requests. For Hummel, who works in a clinic, the phone didn’t stop ringing from patients. Others were similarly in demand. “We were flooded with emails, with calls by patients and reporters,” said Parma. “It was the time I gave the most interviews in my entire career.”

While NIH did not provide Undark with statistics detailing exactly how much the field of smell loss research grew, a search for the word “anosmia” on their online database turned up 35 distinct projects, totaling more than $14.6 million in funding for the 2019 fiscal year. In the 2021 fiscal year, that number grew to $28.5 million in funding for 63 projects.

As a result, experts say, the anosmia research community began collaborating more, wanting to use their knowledge and skills to help in whatever way they could. Many researchers, including Parma, developed smell tests that could gauge a user’s sense of smell and, by extension, to see whether they had a Covid-19 infection at a time when PCR and antigen tests were limited. Some conducted longitudinal surveys where they could track reported progression of smell loss and quality of life among Covid-19 patients. Others started exploring potential treatments of Covid-19-linked anosmia, such as olfactory training and topical steroids.

“We were flooded with emails, with calls by patients and reporters. It was the time I gave the most interviews in my entire career.”

While the effectiveness of such treatments is still unclear, more than three years later, interest in such scientific collaborations is still going strong. “Even if that’s not your primary area of research, many people are at least considering the question or reaching out to other investigators that are experts on taste and smell disorders to ask ‘What is a question I can add in my research?’ or ‘Can we collaborate?” said Paule Joseph, a researcher at NIH’s Division of Intramural Clinical and Biological Research within the National Institute on Alcohol Abuse and Alcoholism.

Despite the interest, some scientists, like Meeks, are still running into the same problems they had before the pandemic: It’s difficult to capture funding and attention related to smell and smell loss. When Meeks took to X, the platform formerly known as Twitter, to lament the discouraging peer feedback on his grant proposal for traumatic brain injury and anosmia, he said, the responses were telling.

“There were several people who responded that they had received similar critiques on their own research grants or their scientific research by whoever was evaluating the research or the grant proposal,” he told Undark. “Although it was nice to know we weren’t singled out, it was a moment where I became a little bit more conscious of the need for greater communication with the broader public and with other scientists.”

Parma thinks some may be dubious to invest in research given the lack of sufficient treatments. “The biggest counterargument is: We don’t know how to treat this, so therefore it’s okay for us not to care about it,” she said. And when there are successes in the field, it’s difficult to implement them on a larger scale. Although Parma’s group has received NIH funding for their smell test, for instance, smell tests are often not covered by insurance.

But research, many scientists in the field say, is not just about developing tests or finding a cure. It’s also about informing and understanding the anosmia experience. This is especially important because not all anosmia affects the olfactory system in the same way — and it is not always treatable. A recent survey found that within a sample of nearly 30,000 Americans who were infected with Covid-19, for instance, 60 percent lost some sense of smell and taste. Among those, a quarter didn’t fully recover.

In one longitudinal survey to assess people who contracted the virus and lost their sense of smell, researchers from Virginia Commonwealth University found that among 267 people, more than half reported partial recovery and 7.5 percent reported none over a two-year period. And out of 946 people who had lost their sense of smell for at least three months, more than half reported partial recovery, and more than 10 percent reported no improvement at all.

“It depends on how severe the damage is,” said Richard Costanzo, director of research at the Smell and Taste Disorders Center at VCU and an author of the study, noting that if there is damage in certain regenerative cells in the nose, there is a lower likelihood of recovery.

While recent studies that focus on Covid-19 anosmia can be applied to other forms of acquired smell loss, one group has largely been left out of research: congenital anosmia. The condition is a different, and understudied, form of anosmia.

“It’s like the community of woodworking but the whole world only knows about wooden bowls,” said Sam Lenarczak, a Seattle-based 23-year-old with the condition. And congenital anosmics, like Lenarczak, want to be understood.

“Every time I look to see if I can get involved in research, they’re recruiting very specific people,” said Charlotte Atkins, who also has congenital anosmia and lives in the U.K. Those studies, she added, are nearly always about acquired smell loss, so she’s unable to participate.

Atkins acknowledges that acquired anosmia can be treated. The culprit, especially in the case of Covid-19, can be known. But she is concerned about what treatment for those conditions could mean for congenital anosmics like her — or really anyone who hasn’t had a successful recovery. “I worry that with a cure comes no more help with living,” she said, “which is what a lot more people need.”

Some smell loss scientists are still running into the same problems they had before the pandemic: It’s difficult to capture funding and attention.

Joseph, the NIH researcher, agreed that much of anosmia research focuses on smell loss — and she sees qualitative studies of other anosmics as a next step. By understanding the lived experience, she said, researchers can develop interventions that could help people with smell loss navigate day-today life: “We need evidence to be able to develop policies, to develop guidelines, to just have a way to inform patients of what is the latest thing that could be helpful to them. We need the science.”

Still, there are some Covid-era innovations that may be repurposed. Parma is among a group of researchers pushing to implement testing more universally so that the inability to smell can be gauged earlier on, as many congenital anosmics don’t realize their condition until they start school — or even much later. In Europe, Hummel has received funding for research in olfactory dysfunction more generally, not just reserved to Covid-19 patients.

Meeks is also looking to the future, and determined to push back against the idea that smell is just a luxury and its loss pales in comparison to the loss of any other sense or bodily function. To him, it’s a “dated and narrow-minded view” that needs to be broken if the field wants to keep making progress. And despite the initial pushback from the grant reviewers, Meeks is determined to continue his research. In July, he submitted a new grant application on the topic.

“We’re not going to stop,” he said. “We’re going to keep going as long as we can.”

Hannah Docter-Loeb is a freelance writer based in Washington D.C. Her writing has appeared in the Washington Post, National Geographic, Scientific American, and more.

This article was originally published on Undark. Read the original article.

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The 2023 Nobel Prize in medicine was awarded to Katalin Karikó and Drew Weissman, two of the scientists whose work helped pave the way for mRNA vaccines against COVID-19. Karikó is a biochemist from Sagan’s University in Hungary and an adjunct professor at the University of Pennsylvania. Karikó was also senior vice president and head of RNA protein replacement at BioNTech until 2022 and has been an advisor for the company. Weissman is a vaccine researcher at the University of Pennsylvania’s Perelman School of Medicine and Director of the Penn Institute for RNA Innovations.

[Related: How does an mRNA vaccine work?]

The prize is awarded by the Nobel Assembly of Sweden’s Karolinska Institute medical university and comes with its signature gold medicine and about $1 million (11 million Swedish crowns). 

“Through their groundbreaking findings, which have fundamentally changed our understanding of how mRNA interacts with our immune system, the laureates contributed to the unprecedented rate of vaccine development during one of the greatest threats to human health in modern times,” the panel wrote in a press release. 

A potential game changer for vaccines

Previously, growing viruses, or at least pieces of viruses, were necessary to make a vaccine. The viruses were often cultivated in giant vats of cells or in or in chicken eggs, like the majority of flu shots. The viruses are then purified before being made into a vaccine.  

Using messenger RNA (mRNA) in vaccines is very different. It starts with a snippet of genetic code that brings instructions for making proteins. If the right virus protein is selected for the vaccine, then the body produces its own defenses against the virus. 

Genetic information encoded in DNA is transferred to mRNA, which is used as a blueprint for protein production in our cells. During the 1980s, efficient methods for producing mRNA without cell culture began. This process, called in vitro transcription, accelerated the development of molecular biology applications to several fields, but using mRNA technologies for vaccines had several roadblocks. In vitro transcribed mRNA was considered unstable and challenging to deliver since it required scientists to develop sophisticated carrier lipid systems to enclose the mRNA and produced some early inflammatory reactions. 

[Related: The FDA just green-lit America’s first COVID vaccine.]

Karikó was devoted to the idea of using mRNA for vaccines and other therapeutics during the 1990s when she became colleagues with Weissman. Weissman was interested in dendritic cells, which are important for immune surveillance and triggering vaccine-induced immune responses. 

The breakthrough

The two began to focus on how different RNA types interact with the immune system and noticed that the dendritic cells recognize in vitro transcribed mRNA as a foreign substance. This leads to their activation and release of inflammatory signaling molecules.mRNA from mammalian cells did not give rise to the same reaction,  the panel wrote. Different types of mRNA, therefore, must be distinguishable.

RNA contains four bases that are abbreviated A, U, G, and C. These letters correspond to the letters of genetic code in DNA A, T, G, and C. Karikó and Weissman knew that bases in RNA from mammalian cells are often chemically modified, and in vitro transcribed mRNA is not. They then wondered if the absence of altered bases in the in vitro transcribed RNA could explain unwanted inflammatory reactions. 

To learn more, they created different variants of mRNA which had unique chemical alterations at their bases. They delivered these to dendritic cells and the results were huge.  

The inflammatory response was almost wiped out when these base modifications were included in the mRNA. This was a seismic shift in scientific understanding of how cells recognize and respond to different forms of mRNA. . Their results were published in 2005.

COVID-19 and The Future

Interest in mRNA technology began to accelerate with their discovery. In 2010 several companies were working on developing the method for viruses such as Zika virus and MERS-CoV.

[Related: White House invests $5 billion in new COVID vaccines and treatments as national emergency ends.]

After the COVID-19 pandemic began, two base-modified mRNA vaccines encoding the SARS-CoV-2 surface protein were developed at a breakneck pace. Two highly effective vaccines were approved in December 2020.

One of the major advantages of mRNA technology was that vaccines could be made in extremely large quantities since their main components are made in laboratories, Exeter University infectious disease expert Bharat Pankhania told the Associated Press.  mRNA tech could be used to refine vaccines for diseases including Ebola, malaria, and dengue, as well as help immunize people against auto-immune diseases like lupus and even some types of cancer.

The laureates will receive their awards at ceremonies on December 10. The 2022 medicine prize was awarded to Svante Pääbo for sequencing the genome of the Neanderthal. Other past winners include Karl Landsteiner in 1930 for the discovery of human blood groups and co-winner Alexander Fleming for the discovery of penicillin in 1945.

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Sci-fi author Brian Herbert once wrote, “The only guarantee in life is death, and the only guarantee in death is its shocking unpredictability.” These words ring true to researchers who investigate what happens in a person’s final moments—and the frustration that comes with these studies. One big problem almost always gets in the way: How do you ask people what dying feels like when they’re no longer here? 

Because we haven’t yet figured out how to communicate with the dead, the best-case scenario is talking to people who have had a close brush with death. They often mention seeing bright lights, their life flashing before their eyes, or visions of deceased loved ones. Some have even reported spotting the Grim Reaper by their bedside. It’s a paradoxical situation, says Kevin Nelson, a professor of neurology at the University of Kentucky: A few perceptions are common—a shining light, for instance—but the near-death experience is unique to each individual.

There’s still a lot of mystery when it comes to the cause, but the field is progressing thanks to people who have allowed scientists to study their brains in these situations. People who have survived these close calls say the encounter can be life-changing. One thing is certain: medical experts say near-death experiences are not a figment of the imagination. 

And figuring out the mechanisms behind this phenomenon goes beyond general curiosity. One goal is to better understand how cardiac arrests happen. It could also potentially save lives, because doctors would have more knowledge for when to continue resuscitations after a patient’s heart stops.

“The research not only benefits our understanding of consciousness, but also in understanding the importance of the heart, lung, and brain in our everyday physiology,” says Jimo Borjigin, an associate professor of neurology at the University of Michigan Medical School.

Unreal recall

A near-death experience can happen to anyone. In fact, 1 in 10 people have reported sharper senses, slowed time, out-of-body sensations or other features associated with near-death, despite not being in grave danger. Research shows that near-death experiences come in four types: emotional, cognitive, spiritual and religious experiences, and supernatural. Of the four, people often recall supernatural activity, particularly the feeling of detaching from a physical body.

About 76 percent of people report an out-of-body experience during a near-death experience. While some people may attribute this to a spiritual experience, this is actually a sensory deception caused by the brain, which scientists have successfully replicated in people who are asleep. Research has shown that direct electrical stimulation of a brain area normally inactive in REM sleep can provoke an out-of-body experience. “Like a flip of a switch, you can literally throw somebody out of their body and back into their body,” Nelson says.

[Related: CPR can save lives. Here’s how (and when) to do it.]

Often, though, people with cardiac arrest will recall near-death experiences. “About a quarter of people who suffer and survived cardiac arrest have memories about some aspect of near-death experience, Borjigin says. This is because people with cardiac arrest have decreasing blood pressure, she says. With the heart unable to pump properly, oxygen is unable to travel to the rest of the body, which is essential for every single cell in your body to survive. When a brain is alerted to a sudden decline in oxygen, your brain undergoes certain changes that contribute to the perceptual distortions that accompany a near-death experience. 

Electrical surges in the brain

Ten years ago, Borjigin and her team observed that rats in simulated cardiac arrest still had fully active brains even 30 seconds after their hearts stopped. What’s more, their brains increased in electrical activity. To confirm whether this happens in humans, Borjigin recently tested the brains of four people who were critically ill and removed from life support.

When these comatose patients were taken off their ventilators, they could not breathe on their own. But, using EEGs, Borjigin noticed two people showed a surge in gamma brainwaves as their bodies started shutting down. Gamma brainwaves are usually a sign of consciousness, because they are mostly active when someone is awake and alert. 

“We’ve shown the brain has a unique mechanism that deals with a lack of oxygen because oxygen is so essential for survival that even an acute loss massively activates the brain and could lead to a near-death experience,” Borjigin explains. 

The boost in gamma waves occurred in a brain area called the temporo-parieto-occipital (TPO) junction. This is responsible for blending information from our senses, including touch, motion, and vision, into our conscious selves. It’s impossible to know if the increased brain activity was related to any visions they may have had, because, sadly, the two patients died. But Borjigin suggests activation of this area suggests people may likely pick up sounds and understand language. “They might hear and perceive the conversation around them and form a visual image in their brain even when their eyes are closed.” 

Hidden consciousness

In one of the largest studies of near-death experiences, an international team of doctors has linked the surge in brain activity to what they called a hidden consciousness immediately following death. In the study, people who were brought back to life through CPR after cardiac arrest could recall memories and conversations while they were seemingly unconscious. 

Between May 2017 and March 2020, the team tracked 567 people who underwent a cardiac arrest. They used EEGs and cerebral oxygenation monitoring to measure electrical activity and brain oxygen levels during CPR. To study auditory and visual awareness, the team used a tablet showing one of 10 images on the screen, and five minutes after, it would play a recording of fruit names: pear, banana, and apple, for another five minutes. 

Only 53 people of the original 567 participants were successfully resuscitated. Initially, they showed no signs of brain activity and were considered dead. But during the CPR, the team noticed bursts of activity. These spikes included gamma waves and others: delta, theta, alpha, and beta waves—all electrical activity that signals consciousness. 

[Related: How your brain conjures dreams]

Twenty-eight of those 53 patients were cognitively capable of having an interview. Eleven people recalled being lucid during CPR, being aware of what was happening or showing perceptions of consciousness like an out-of-body experience. No one could recall the visual image but when asked to randomly name three fruit, one person correctly named all the fruits in the audio recording—though the authors note this could have been a random lucky guess. 

The study authors also included self-reports of 126 other survivors of cardiac arrests not involved in the study and what they remembered from almost dying. Common themes included the pain and pressure of chest compressions, hearing conversations from doctors, out-of-body experiences, and abstract dreams that had nothing to do with the medical event.

The findings debunk the idea that an oxygen-deprived brain stays alive for only five to ten minutes. They also raise the question whether doctors can save people already determined to be dead. “These patients were actually alive within, as seen in the positive waves on the EEG, but externally they were dead,” says Chinwe Ogedegbe, an emergency trauma center section chief and coauthor of the study. 

Beyond the brain’s resilience to the lack of oxygen, the authors propose an alternative “braking system” that could explain the distorted perceptions of consciousness. The brain normally filters and inhibits unneeded information when you’re awake. In this unconscious state, however, the braking system is gone, which could allow dormant brain pathways to activate and access a deeper realm of consciousness containing all of your memory, thoughts, and actions. “Instead of being hallucinatory, illusory or delusional, this appears to facilitate lucid understanding of new dimensions of reality,” the authors write in their paper.

Unfortunately, with only a small number of participants surviving their cardiac arrest, it’s unclear whether this altered consciousness is more visual or auditory. Ogedegbe is working to increase the number of participants in the next trial to 1,500. Doing so will give researchers a better idea of the type of brain activity that goes on when someone is at death’s door, and potentially provide comfort that their loved ones can sense them in their final moments.

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Needles are one of the best ways to quickly deliver a drug, but for many, getting jabbed is an unpleasant experience. One in four adults has an intense fear of needles, which could deter people from vaccines or treatments. In some cases—like those with diabetes—skipping out on insulin shots could be life-threatening. While there are other routes of administration, such as through the mouth, drugs containing proteins or large molecules may not be absorbed as well orally. Or they wind up digested in the gastrointestinal tract. Scientists are eager to find less invasive alternatives to needles that still get drugs where they need to go.

Jean-Christophe Leroux, a professor in drug formulation and delivery at ETH Zurich in Switzerland, has one idea: transform an injectable into an oral drug absorbed through the buccal mucosa, the lining of the inner cheek. However, past research attempts at using cheek patches were foiled by the mouth’s wet surface, which weakened adhesion. For inspiration, Leroux and his colleagues turned to a master of underwater suction—the octopus.

In a new study published today in Science Translational Medicine, senior author Leroux and his team replicated the suckers found at the end of an octopus’s arms. Using 3D printing, they created a rubbery but strong suction patch that delivers drugs through the inner cheek. The majority of participants in a small human trial reported that the suction patch was a comfortable fit and they would prefer this method to needle injections. 

“We have developed a very simple and easy to apply delivery system that could potentially replace injectables for several kinds of drugs,” Leroux says.

Octopuses use their grippy suckers to stay anchored in churning oceans or grab squirming prey.  “The starting point was mimicking the good suction these creatures had to strongly stick to wet surfaces,” Leroux adds.

Their sucker-based model has a few advantages over swallowing a pill. Because the delivery system is placed in a cheek for absorption over time, the patch can be removed if needed. The domed cup also protects the drugs inside from dissolving in saliva. 

A small trial in dogs showed drugs delivered by suction patch were effectively absorbed. The team applied patches, loaded with a diabetes tablet called desmopressin, to the mouths of three beagles. This peptide drug—a chain of amino acids—is poorly absorbed when taken orally. But after placing the suction patch, the researchers found higher concentrations of the drug in the dogs’ bodies. “We were really impressed by the level of absorption that we would get with such a simple system,” Leroux says. 

[Related: This pill delivers medication days or weeks after it’s swallowed]

Still, when compared with drug concentrations in the dogs after injections, the patches weren’t quite as effective. One upside, however, was that the dogs appeared to be more comfortable with the patch, which remained on their cheeks for three hours without falling off or causing irritation.

The research makes a significant advance in using the inner cheek as an administration site for peptides, says David Brayden, a professor of advanced drug delivery in the University College Dublin in Ireland who was not affiliated with the study. Previous attempts to apply drugs via cheeks mostly used doses of small molecules that are easily absorbed, but not larger peptides. “No buccal formulation or device has ever been approved for peptide administration, despite a 20-year effort,” he says.

Humans seemed to tolerate the patches, too. Forty adult volunteers wore  suction patches (loaded with water, not drugs) for 30 minutes. They added a strand of dental floss tied to the patch and people’s clothes to prevent  accidental swallowing. During that half-hour, the volunteers walked, talked, and rinsed their mouths. Thirty-five of the 40 patches stayed on; the study authors say the fallen five were probably placed improperly. 

An hour after applying the patch, 75 percent of people said they felt no discomfort. Examining  the inner cheeks with an endoscopic camera, the researchers saw no scarring or changes to the mouths’ tissue. About 92 percent of people found the suction patch generally comfortable. And nearly 83 percent said if they had to take a drug daily, they’d prefer using the patch over a needle.

[Related: This drug-delivery soft robot may help solve medical implants’ scar tissue problem]

“These are innovative studies that seek to identify new feasible methods and sites for [non-oral] drug delivery,” says Daniel Drucker, a professor of medicine at the University of Toronto in Canada who was not involved in the study. The canine trials showed the patch still has a pretty poor absorption of peptide drugs overall, he notes, but because people tolerated it so well, it could be an important foundation for  future approaches to chronic disease therapies. 

Larger safety trials—including wearing the device for longer than a half hour—will help refine how well people tolerate the patch. The researchers also need to show patients can wear it for simulated daily or weekly treatments. Once they have completed a larger safety trial, the next phase will be to test the effectiveness of the drug-loaded patch in people to assess how it compares with the absorption of pills and tablets. 

This drug delivery system could be publicly available in a few years, if all goes well, Leroux says. Or sooner: “We could potentially be even faster because of the simplicity of the technology and because we can use drugs that are already approved.”

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Treating substance use disorders is incredibly challenging. One reason is that the brain scans showing abnormalities in those with addiction often include a lot of varying results and lack of connections. Now, a study published September 25 in the journal Nature Mental Health found that the brains of those with a substance use disorder have a connected circuit, giving researchers some potential places to target in future clinical treatments.

[Related: A powerful combo of psilocybin and therapy might help people overcome alcohol use disorder.]

According to the United States Substance Abuse and Mental Health Services Administration, substance use disorders occur when someone’s recurrent use of alcohol and/or drugs causes them significant health problems, including “disability, and failure to meet major responsibilities at work, school, or home.” In the United States, more than 20 million individuals are estimated to have substance use disorders and some common disorders are opioid use disorder, nicotine use disorder, and alcohol use disorder.

Brain scans or neuroimaging can help inform treatment options, since abnormalities in brain scans are associated with substance use disorders. Some newly developed approaches to study the brain’s role in addiction include a process called brain lesion network mapping. Brain lesions are areas of brain tissue that show damage from injury or disease. Lesion network mapping examines how two lesions in two different sites can cause the same issues. 

“We can think of that as an average wiring diagram of the human brain in order to show how two lesions in two different sites that both cause the same issue actually share connectivity to the same region,” study co-author and University of British Columbia medical student Jacob Stubbs tells PopSci. 

The mapping helped researchers to notice that this network was common across people who have been consuming different addictive substances including alcohol, cocaine, heroin, or nicotine. According to Stubbs, the team was actually quite surprised to find this common circuit across substances given the limitations and amount of diversity in decades of data.

Some of the study’s limitations are that the data all came from previous research and that the findings are correlative. The authors could not conclude any causation or if this circuit is hereditary or environmental. Additionally, there are multiple ways to study brain imaging, which can make looking at the data even more complicated and noisy.

A 2022 study mapped brain lesions to a circuit in the brain that can actually make the lesions go away in the brains of some cigarette smokers. This new study used that data to evaluate this newly discovered brain circuit and areas where the brain had atrophied, or shrunk. It evaluated data from 144 studies on addiction and found that abnormalities across substance use disorder are in a common brain network. The studies primarily looked at alcohol, cocaine, heroin, or nicotine addiction. 

“Our study found that different brain regions implicated in addiction are all a part of a common brain circuit,” study co-author Michael Fox, founding director of the Center for Brain Circuit Therapeutics at Brigham and Women’s Hospital, said in a statement. “Consistency across different papers means we now have a brain circuit to target addiction with treatments, rather than just a region.” (Fox is a consultant for Magnus Medical, Solaris, and Boston Scientific and has intellectual property using connectivity imaging to guide brain stimulation.)

[Related: We probably have big brains because we got lucky.]

The team reviewed data involving more than 9,000 participants. The newly uncovered connection suggests a potential brain circuit that could be targeted neurostimulation therapies to treat substance use disorders. 

The circuit involves five primary areas of the brain–the anterior cingulate, insula, dorsolateral prefrontal cortex, thalamus, and medial prefrontal cortex.

“The five regions that pop up are places that actually do make some amount of intuitive sense. The medial prefrontal cortex is the strip of cortex that goes right down the front of your brain and it’s important because it’s been a target for successful neurostimulation trials,” says Stubbs.

While clinical applications using this circuit are still several years away, it offers some promise.

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You’re once again be able to order four free COVID-19 tests from the US government, and you may want to, given that people tend to get sick with respiratory infections as the temperature drops. At the very least, it’s good to be prepared.

Starting today, you’ll be able to ship rapid antigen tests to every residential address in the US, Puerto Rico and other US territories, as well as those linked to overseas military and diplomatic personnel. The tests will detect currently circulating COVID-19 variants and are intended for use through the end of 2023.

And if you still have unused COVID-19 tests, don’t throw them out—use the Food and Drug Administration’s searchable at-home test database to see if their expiration dates have been extended. Studies have shown that repeat COVID-19 infections increase the risk of hospitalization and death and that the effects of Long COVID might rival heart disease and cancer, so it’s worth hanging onto as many usable tests as you can. It’ll help you avoid spreading the disease among your family, friends, and community.

The program is a continuation of the long-running initiative the Biden-Harris administration shut down earlier this year when the COVID-19 federal public health emergency ended. Now they’re restarting it by giving a dozen US manufacturers $600 million to manufacture over-the-counter rapid tests. 

How to order free at-home COVID tests

Placing an order for your free COVID tests is easy: Go to the special USPS website, enter your name, provide your shipping address (even if it’s a residential P.O. box), and hit Check Out Now under the order summary that confirms the delivery is entirely free. You can also provide an email address if you want to get shipment notifications, but you don’t have to.

Those living in multi-family, co-living, or other shared living spaces can place more than one order for free COVID tests as long as the USPS knows the address houses multiple unrelated families, but may be unable to if the government doesn’t know several families live there. If that happens, you can file a service request or call the USPS help desk at 1-800-ASK-USPS (1-800-275-8777) to try to get it fixed.

If you need help placing an order, you can call 1-800-232-0233 Monday through Friday between 8 a.m. and midnight Eastern Time, seven days a week, for assistance in English, Spanish, and more than 150 other languages. There’s also a teletype (TTY) or text telephone number at 1-888-720-7489 and the aforementioned USPS help desk.

People with disabilities can call the disability information and access line at 1-888-677-1199 between 8 a.m. and midnight ET, seven days a week, or email DIAL@usaginganddisability.org.

If you provide an email address when you order, you will get shipping notifications and can track the package on the USPS website. You can’t pick the tests up anywhere, even your local post office—they will always come to the address you provided, the agency says.

When to take a rapid antigen test

When you receive your tests, the package will display an expiration date, but the FDA has extended most of these beyond what may appear on the label. As mentioned above, you can use the agency’s database to check your tests’ actual expiration dates. This is especially important given the USPS has noted that some people may receive free COVID tests featuring a printed expiration date that has already passed.

[Related: Why some long COVID clinics fail chronic illness patients]

As long as your tests haven’t expired, the government recommends you take them if you begin having COVID symptoms like a fever, sore throat, runny nose, or loss of taste or smell; at least five days after you are in close contact with someone who has since tested positive for COVID; or before you gather with a group, especially if that group includes people at risk of severe disease or who aren’t up to date on their vaccinations (keep in mind that you may not know who’s at risk, either).

It’s also worth noting that you should let your tests come to room temperature before using them—especially if they were delivered in freezing or blistering hot temperatures. Although the tests are built to survive a range of conditions, they might not work as well if they’re cold, the government says. Generally, rapid antigen tests are meant to be used in an environment that’s somewhere between 59 and 86 degrees Fahrenheit (15 to 30 degrees Celsius), but your tests should come with specific instructions about this. The government recommends letting the unopened package sit indoors for at least two hours before opening and using any of the tests inside.

How to take a rapid antigen test

Each test kit comes with directions for how to use it, and they all involve swabbing the inside of your nose. You should get results within 30 minutes and you won’t have to leave your home. If you don’t follow the instructions, the result could be wrong. For visual learners, the Centers for Disease Control and Prevention has a how-to video, and it also has one for people who use American Sign Language.

How to interpret COVID test results

Your test will also tell you how to interpret the results, and what to do afterward, but if you test positive you very likely have COVID. You should follow the CDC’s latest guidance, which suggests you isolate for at least five days, even from people in your home. You may also want to talk to your doctor, and definitely should if you have a weakened immune system, other health conditions like cancer and diabetes, or increased risk due to a factor like smoking or obesity, the government says.

[Related: The Postal Service helps keep millions of Americans alive and well]

If the results come out negative, the test didn’t find COVID in your body, and you might have a lower risk of spreading the disease. It’s worth noting that these at-home antigen tests generally aren’t as accurate as PCR tests, for example, which are processed by laboratories. So if you think you got a false negative, the government suggests testing again within a few days, leaving at least 24 hours between tests.

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After getting bit by a bat bug at a recent conference, Armin Scheben had a literal and figurative itch to study bats. The blood-sucking insect is one of many disease-causing parasites that latch themselves onto the flying mammals—yet, bats rarely get sick in the same way humans do. 

Mammalian immune systems evolve fast as species are always challenged with new pathogens in their environment. “You need to constantly keep pace with new bad guys that are trying to infect and hurt you,” says Scheben, who is a postdoctoral fellow in population genomics at Cold Spring Harbor Laboratory (and has since recovered from the bite). And while he has studied the genetic adaptations of several mammals, they pale in comparison to the ones that have given bats the ability to fight off infections so effectively.

In a new study published today in the journal Genome Biology and Evolution, Scheben and his team have identified the genes that have contributed to bats’ rapidly evolving immune system and their unique ability to evade deadly viruses and even cancer. Understanding how bats survive diseases could inspire new immune treatments for humans and potentially help prevent another pandemic. 

[Related: A ‘living’ cancer drug helped two patients stay disease-free for a decade]

The authors analyzed the DNA of 15 different bat species to get a clearer picture of how their genes evolved over time. They fully sequenced the genomes of two bat species, the Jamaican fruit bat and the Mesoamerican mustached bat, and gathered the other species from preexisting datasets. 

They then compared the bat genomes to that of humans, mice, and other cancer-susceptible mammals, focusing their attention on the sequences that encode proteins responsible for causing or preventing diseases. To start, they lined up the homologous genes, or shared genes among different species inherited from a shared evolutionary ancestor. (It’s like comparing apples with apples, explains Scheben.) With each homologous gene, they hypothesized two scenarios: if bats lost it or if it mutated. If the flying mammals completely lost the gene, it suggests that the omission is important in fighting disease. But if it remained with subtle changes in the DNA sequence that are only found in bats, it could show a change in gene function that somehow helps the group stay healthy.

In the end, the most striking changes the team detected were in type one interferon (IFN) genes, which are important for controlling inflammatory responses to infections. Specifically, they observed a shift in the number of antiviral IFN-α and IFN-ω genes. For instance, three bat species seemed to have lost all of their IFN-α while increasing the number of IFN-ω genes.

According to Scheben, the most surprising finding was observing the loss of IFN-α and addition of more IFN-ω genes, “which hadn’t been reported at all before.” The results suggest the new IFN-ω and missing IFN-α genes are important in bats for resisting viral infections while preventing overactive inflammatory responses—a feature that has made inflammation a double-edged sword in humans.

But while the findings have put geneticists one step closer to understanding how bats evolved their unique ability to resist cancer and viruses, it doesn’t paint a complete picture. The study focuses only on the genetics of innate immunity (the immediate immune response to infected cells), says Tony Schountz, a professor at the Center of Vector-Borne Infectious Diseases at Colorado State University, who was not involved in the study. It does not include information about bats’ adaptive immunity, which consists of the antibody and T-cell responses that many mammals use to fight diseases. “These are two very different, but complementary components of immunity,“ Schountz explains. “Nearly all of the focus on bat immunity to date has been on innate immunity, principally because the study of adaptive immunity requires live animals, which few groups have and is much more complicated.”

Even without a full set of information, understanding the changes in the bats’ innate immune system could help scientists develop genetic treatments for humans that decrease susceptibility to certain illnesses. We can also learn which genes drive bats’ 20- to 30-year lifespans, or how their bodies have adapted to process sugar-rich foods without developing the negative consequences seen in people with diabetes. 

[Related: What bats and metal vocalists have in common]

And though bats have gained a notorious reputation for their purported role in spreading COVID, Scheben hopes that these new findings could point researchers in the right direction in understanding how the animals host such potent viruses and parasites without getting very sick. One day, he says, that information could be used to prevent our species from suffering major symptoms when infected. “It’s absolutely not misplaced to believe that studying bats could help us prevent another pandemic.”

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Adequately treating high blood pressure, or hypertension, would save 76 million lives between this year and 2050, according to a new report from the World Health Organization (WHO). About 1 in 3 adults around the world have this condition, which can lead to stroke, heart attack and failure, kidney damage, and other health problems. And the majority of those with hypertension—about 4 out of every 5 people—are not treated through timely diagnosis, lifestyle changes, medication, or a combination of all three, according to the first-of-its-kind report.

[Related: Why scientists are still on the quest to build an artificial heart.]

Although low-cost medications such as amlodipine or losartan can control high blood pressure, it’s still responsible for roughly 10 million deaths per year. “Hypertension control programs remain neglected, under-prioritized, and vastly underfunded,” WHO director-general Tedros Adhanom Ghebreyesus, said in a news release accompanying the report. This report, released during the 78th Session of the United Nations General Assembly, is WHO’s first on the global impact of high blood pressure. 

“Strengthening hypertension control must be part of every country’s journey towards universal health coverage, based on well-functioning, equitable and resilient health systems, built on a foundation of primary health care,” Ghebreyesus added.

More than half of those with hypertension, defined as a blood pressure of 140/90 mmHg, don’t know they have it. During a standard check-up in a doctor’s office, a blood pressure test measures the pressure in a patient’s arteries when their heart beats (which is the first number in a reading) and when the heart rests (the second number.) Increasing access to healthcare could help increase diagnosis and get effective treatments to those in need. Medication can help lower high blood pressure; those taking drugs prescribed for hypertension doubled between 1990 and 2019.

“Treating hypertension through primary health care will save lives, while also saving billions of dollars a year,” said Michael R. Bloomberg, a WHO ambassador and former New York City mayor, in a statement. In addition to proper screening, preventative measures include eating a balanced diet, avoiding alcohol and tobacco, regular exercise, and weight management.

Governments also have a critical role in keeping their citizens healthy and blood pressures normal. According to WHO’s report, South Korea and Canada have delivered comprehensive national hypertension treatment programs with positive results. Both nations have surpassed the 50 percent mark for controlling blood pressure in adults with hypertension. Additionally, more than 40 low- and middle-income countries have used WHO’s HEART’S package to strengthen their nations’ hypertension and cardiovascular care. Through the program, which does what in a phrase, more than 17 million people in countries including Bangladesh, Cuba, India, and Sri Lanka, have been enrolled in hypertension treatment programs. 

[Related: Reducing sodium in packaged foods could reduce disease and save lives.]

One focus of programs to avoid high blood pressure is to reduce daily sodium intake. “Most heart attacks and strokes in the world today can be prevented with affordable, safe, accessible medicines and other interventions, such as sodium reduction,” Bloomberg added.

The daily recommended amount of sodium varies between countries, but WHO recommends less than 2,000 milligrams a day. However, the organization estimates that the global average is more than twice that amount. In the United States, the Centers for Disease Control and Prevention (CDC) recommends an intake of less than 2,300 mg of sodium a day. Americans consume over 3,400 mg of sodium daily on average, and hypertension affects roughly about 32 percent of Americans ages 30 to 79.

“It’s great to see the WHO taking this issue head-on. Heart disease and stroke are the leading causes of death worldwide and hypertension is a major driver of those deaths,” says primary care physician Nate Favini, the chief medical officer of Forward, a preventative healthcare startup uses a doctor-led 12 week program and at-home biometric monitoring to help patients manage their blood pressure.

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Nurses, researchers, and workplace safety officers worry new guidelines from the Centers for Disease Control and Prevention might reduce protection against the coronavirus and other airborne pathogens in hospitals.

A CDC advisory committee has been updating its 2007 standards for infection control in hospitals this year. Many health care professionals and scientists expressed outrage after the group released a draft of its proposals in June.

The draft controversially concluded that N95 face masks are equivalent to looser, surgical face masks in certain settings—and that doctors and nurses need to wear only surgical masks when treating patients infected by “common, endemic” viruses, like those that cause the seasonal flu.

The committee was slated to vote on the changes on Aug. 22, but it postponed action until November. Once the advice is final, the CDC begins a process of turning the committee’s assessment into guidelines that hospitals throughout the United States typically follow. After the meeting, members of the public expressed concern about where the CDC was headed, especially as covid-19 cases rise. Nationwide, hospital admissions and deaths due to covid have been increasing for several consecutive weeks.

“Health care facilities are where some of the most vulnerable people in our population have to frequent or stay,” said Gwendolyn Hill, a research intern at Cedars-Sinai Medical Center in Los Angeles, after the committee’s presentation. She said N95 masks, ventilation, and air-purifying technology can lower rates of covid transmission within hospital walls and “help ensure that people are not leaving sicker than they came.”

“We are very happy to receive feedback,” Alexander Kallen, chief of the Prevention and Response Branch in the CDC’s Division of Healthcare Quality Promotion, told KFF Health News. “It is our goal to develop a guideline that is protective of patients, visitors, and health workers.” He added that the draft guidelines are far from final.

In June, members of the CDC’s group—the Healthcare Infection Control Practices Advisory Committee—presented a draft of their report, citing studies that found no difference in infection rates among health providers who wore N95 masks versus surgical masks in the clinic. They noted flaws in the data. For example, many health workers who got covid in the trials were not infected while wearing their masks at work. But still, they concluded the masks were equivalent.

Their conclusion runs contrary to the CDC’s 2022 report, which found that an N95 mask cuts the odds of testing positive for the coronavirus by 83%, compared with 66% for surgical masks and 56% for cloth masks. It also excludes a large clinical trial published in 2017 finding that N95 masks were far superior to surgical masks in protecting health workers from influenza infections. And it contradicts an extensive evaluation by the Royal Society, the United Kingdom’s national academy of sciences, finding that N95 masks, also called N95 respirators, were more effective against covid than surgical masks in health care settings around the world.

“It’s shocking to suggest that we need more studies to know whether N95 respirators are effective against an airborne pathogen,” said Kaitlin Sundling, a physician and pathologist at the University of Wisconsin-Madison, in a comment following the June meeting. “The science of N95 respirators is well established and based on physical properties, engineered filtered materials, and our scientific understanding of how airborne transmission works.”

Her assertion is backed by the California occupational safety agency, Cal/OSHA, whose rules on protecting at-risk workers from infections might be at odds with the CDC’s if the proposals are adopted. “The CDC must not undermine respiratory protection regulation by making the false and misleading claim that there is no difference in protection” between N95 masks and surgical masks, commented Deborah Gold, an industrial hygienist at Cal/OSHA, at the August meeting.

Researchers and occupational safety experts were also perplexed by how the committee categorized airborne pathogens. A surgical mask, rather than an N95, was suggested as protection for a category they created for “common, endemic” viruses that spread over short distances, and “for which individuals and communities are expected to have some immunity.” Three committee representatives, researchers Hilary Babcock, Erica Shenoy, and Sharon Wright, were among the authors of a June editorial arguing that hospitals should no longer require all health care workers, patients, and visitors to wear masks in hospitals. “The time has come to deimplement policies that are not appropriate for an endemic pathogen,” they wrote.

However, in a call with KFF Health News, Kallen clarified that the committee put coronaviruses that cause colds in that category, but not yet the coronavirus causing covid.

The committee’s next tier consisted of viruses in a “pandemic-phase,” when the pathogen is new and little immunity through infection or vaccination exists. It recommended that health workers wear an N95 mask when treating patients infected by bugs in this category. Its third, highest tier of protection was reserved for pathogens like those causing measles and tuberculosis, which, they claimed, can spread further than lower-tier threats and require an N95.

Virologists said the committee’s categories hold little water, biologically speaking. A pathogen’s mode of spreading isn’t affected by how common it is; common viruses can still harm vulnerable populations; and many viruses, including SARS-CoV-2, can travel significant distances on microscopic droplets suspended in the air.

“Large COVID outbreaks in prisons and long-term health care facilities have demonstrated that the behavior of infectious aerosols is not easily classified, and these aerosols are not easily confined,” wrote the deputy chief of health at Cal/OSHA, Eric Berg, in a letter of concern to the CDC committee, obtained by KFF Health News.

The committee pitted its assessment of N95 masks against their drawbacks. Its draft cites a study from Singapore in which nearly a third of health care personnel, mostly nurses, said wearing such masks negatively affected their work, causing acne and other problems exacerbated by hot and humid conditions and prolonged shifts. Rather than discard the masks, the authors of that study recommend better-fitting masks and rest breaks.

Noha Aboelata, a doctor and the CEO of Roots Community Health Center in Oakland, California, agrees. “There are other strategies to bring to bear, like improved mask design and better testing,” she said, “if we decide it’s unacceptable to give a patient covid when they go to the hospital.”

Aboelata is one of hundreds of doctors, researchers, and others who signed a letter to CDC Director Mandy Cohen in July, expressing concern that the CDC committee will weaken protections in hospitals. They also warned that scaling back on N95 masks could have repercussions on emergency stockpiles, rendering doctors and nurses as vulnerable as they were in 2020 when mask shortages fueled infections. More than 3,600 health workers died in the first year of the pandemic in the United States, according to a joint investigation by KFF Health News and The Guardian.

The concerned clinicians hope the committee will reconsider its report in light of additional studies and perspectives before November. Referring to the draft, Rocelyn de Leon-Minch, an industrial hygienist for National Nurses United, said, “If they end up codifying these standards of care, it will have a disastrous impact on patient safety and impact our ability to respond to future health crises.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—the independent source for health policy research, polling, and journalism.

The post Why healthcare workers are worried about possible changes to masking protocols in hospitals appeared first on Popular Science.

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This article is republished from The Conversation.

Edmund K. LeGrand is an adjunct professor of biomedical and diagnostic sciences at the University of Tennessee and Joe Alcock is a professor of emergency medicine at the University of New Mexico.

When you’re sick with a fever, your doctor will likely tell you it’s a sign that your immune system is defending you against an infection. Fever typically results from immune cells at infected sites sending chemical signals to the brain to raise the set point of your body’s thermostat. So, you feel chills when the fever starts and feel hot when the fever breaks.

However, if you were to ask your doctor exactly how fever protects you, don’t expect a completely satisfactory answer.

Despite scientific consensus that fever is beneficial in fighting infections, exactly how is contentious. We are a veterinary pathologist and an emergency physician interested in applying evolutionary principles to medical problems. The evolution of fever is a classic conundrum because fever’s effects seem so harmful. Besides making you feel uncomfortable, you may also worry you’ll dangerously overheat. It is also metabolically costly to generate that much heat.

In our research and review, we propose that since fever occurs throughout much of the animal kingdom, this costly response must have benefits or it never would have evolved or been retained across species over time. We highlight several important but rarely considered points that help explain how the heat of fever helps your body fight infections.

How fever fights infection

Infections are caused by pathogens. Pathogens can be microbes such as certain species of bacteria, fungi or protozoans. If microbes or viruses have infected your cells and are using them to replicate, your own cells can also be considered pathogens and are treated that way by your immune system.

The main explanation for how fever helps control infections is that higher temperatures put heat-induced stress on pathogens, killing them or at least inhibiting their growth. But why would the somewhat higher body temperatures of fever—an increase of about 1.8 to 5.4 degrees Fahrenheit (1 to 4 degrees Celsius)—which can’t even kill your own healthy cells, harm such a wide variety of pathogens?

Immunologists have noted that slight heat makes immune cells work better. The implication is that fever is needed to enhance their defensive function. However, from an evolutionary perspective, it seems strange to require the massive energy cost of generating a fever just to get more activity from immune cells, especially since there are already plentiful and faster molecular signals available to activate them.

In addition to heat, slightly low oxygen levels and slight acidity also boost immune cell function. Since these stressful conditions also occur at infected sites, it makes sense that immune cells evolved to have their maximum functionality match their stressful working conditions. In fact, since anything in a state of growth is inherently vulnerable to stress—and pathogens are typically growing—researchers, including one of us, have proposed that a function of immune cells is to actively make local conditions stressful to preferentially harm the growing pathogens.

Heating up pathogens locally

Inflammation is a local defensive response to infection. It typically involves heat, pain, redness and swelling in the areas where the immune system is most active. While some scientists are aware that infected sites generate heat, many believe that the feeling of warmth from inflammation is only from dilated blood vessels bringing in warmer blood from core body tissues.

However, researchers have found that inflamed tissues, even in core body tissues, are up to 1.8 to 3.6 degrees F (1 to 2 degrees C) warmer than adjacent normal tissues, so warmth is not just a byproduct of more blood flow. Much of that extra heat is coming from the immune cells themselves. When they generate reactive oxygen species to kill pathogens in a process known as the respiratory burst, substantial heat is also produced. To date, however, the temperatures involved have not been measured.

While cells can tolerate a wide range of temperatures, all cells experience a sharp decline in their ability to grow and survive at higher temperatures. For mammalian cells, and presumably the pathogens that infect them, even a single degree or two above temperatures around 113 degrees F (45 degrees C) is almost always deadly. So the heat of fever adds to already warmer local temperatures.

There is evidence that pathogens are exposed to temperatures that are much higher than the body temperature routinely measured with a thermometer in the emergency department. A 2018 study finding that local temperatures can be as high as 122 degrees F (50 degrees C) in mitochondria—the powerhouse of the cell—came as a surprise to researchers. The heat mitochondria generate is put to good use in warming the body and for fever. Likewise, we suggest that the local heat the respiratory burst produces at the surface of immune cells helps kill pathogens.

Heat and other stressors

Immune cells target pathogens with a variety of stressors meant to kill or inhibit them. These include reactive oxygen species, toxic peptides, digestive enzymes, high acidity and nutrient deprivation. Most chemical reactions are sped up by increased temperatures, so it isn’t surprising that heat enhances these defenses.

Researchers have shown heat to be synergistic with low oxygen and acidity in killing pathogens. Notably, neither febrile temperatures nor iron restriction on their own were able to inhibit the growth of the infectious bacteria Pasteurella multocida, but they could when combined. The stress of heat doesn’t act alone when controlling infections.

The standard view that the heat of fever kills pathogens and enhances immune responses is correct but incomplete. Fever’s ability to control infections comes from the few extra, but critical, degrees it adds to enhance existing locally generated heat to harm vulnerable growing pathogens. And fever also always acts with other defenses, never alone.

At more than 600 million years old, fever is an ancient feature of life on this planet that deserves respect. In fact, you owe it to infection-fighting heat that you are still here—alive—to read this. Something to think about the next time you’re sick.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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The small medical sensors known as continuous glucose monitors, or CGMs, were first developed to track the blood sugar levels of people with diabetes. But they have recently expanded to several other uses—they’re not just for humans anymore. Veterinarians are repurposing the devices to monitor their furry patients and help regulate diabetes with medication. 

Diabetes is fairly common in dogs and cats, occurring in about 1 in 300 patients. The biggest problem with this disease in pets isn’t its scale, though, but the burden of care, says Chen Gilor, a veterinarian and diabetes specialist at the University of Florida. Animals with diabetes require daily medication such as insulin, which needs regular monitoring to get the doses right. 

That can be tricky for vets and owners. “The question is, how do you make it easier?” says Gilor, who researches veterinary diabetes and has worked with several pharmaceutical companies that manufacture diabetes products. CGMs, he says, might offer a better alternative.

Traditionally, veterinarians measure blood sugar levels in pets using a technique called glucose curves, in which vets periodically take blood samples over roughly 12 hours and manually plot the data. The labor-intensive tool may not give an accurate picture of typical glucose levels because situations that cause anxiety in pets, like going to the vet, skew blood sugar. 

“It’s stressful. It’s expensive. And, the biggest problem is: It’s a lot of variability,” says Catharine Scott-Moncrieff, a veterinarian at Purdue University who specializes in small animal endocrinology. Blood sugar varies daily, so it’s difficult for vets to make treatment decisions based on just a few hours of data. Because CGMs measure glucose levels every few minutes, they can give vets a better sense of fluctuations and daily averages. 

[Related: Declawing cats is harmful. Do this instead.]

The monitors consist of two main parts: an electrode coated in enzymes, which is inserted under the skin with a guide needle, and an inch-long sensor, adhered to a shaved patch of skin on a pet’s upper back. Rather than directly reading blood sugar, the electrode measures glucose in interstitial fluid—the liquid surrounding the body’s cells—which slightly lags behind changes in blood. Veterinarians usually place the devices in their office and then send their patients home, where the CGMs collect data, transmitted to a smartphone or monitor via Bluetooth.

The sensors typically last up to two weeks—if they aren’t scratched off before then. (Even if a pet yanks out the device in this way, the electrodes are too thin to cause any harm.) Gilor says that while dogs tend not to mind the devices, cats are less tolerant. More finicky patients may have to wear jackets to prevent this preemptive removal. 

CGMs are most useful initially for determining insulin dosages, especially for newly diagnosed patients, says Scott-Moncrieff. Then, vets can apply a new CGM every few months to check in and see whether adjustments are needed.

Gilor also highlights the efficiency of regulating his patients’ diabetes with the monitors. While it might take months to regulate a dog or cat with glucose curves, he says vets can adjust insulin to the right levels in a matter of weeks when using a CGM. 

Although the devices are becoming common in veterinary practices, animal-specific devices are not currently available on the market. Instead, vets prescribe human CGMs off-label. Abbott’s Freestyle Libre is most popular, says Scott-Moncrieff. Without insurance, the newest version retails at about $75 per sensor. (By comparison, a glucose curve may cost owners well more than $100.)

Several studies of the Freestyle Libre in dogs and cats found the device reliably measured normal and high blood sugar levels, though it showed more variation for animals with low blood sugar. Additional studies are evaluating newer versions of the monitor, which is already in its third generation. “You really have to stay up to date on the technology, because it’s always changing,” says Scott-Moncrieff.

Despite its promise, using this human technology for pets comes with some hurdles. For example, the adhesive isn’t intended for animal skin, so vets often use extra, which can sometimes cause irritation. 

[Related: Should pets wear Halloween costumes? Your furry friend can help you decide.]

One diabetes management company, ALR Technologies, is developing a CGM specifically for cats and dogs. It decided to expand into the animal health space after noticing a lack of tools for veterinarians. “They’re just in such a need for a better way to check blood sugar,” says Joe Stern, who heads ALR’s animal health division.

The device, called GluCurve, uses a pet-friendly adhesive and applicator. Its software, which includes a specialized dose calculator for insulin treatment, is designed to share data across a veterinary practice. GluCurve was soft-launched in January and is now off the market while the company modifies the hardware design. It plans to begin selling the product again in the next few months, according to Stern. 

Monitoring blood sugar with any type of CGM requires involvement from a pet’s owner and veterinarian, and it often falls to vets to teach themselves and their clients how to use the tech. “It can be quite intense for veterinarians to have to manage all this additional information. There’s always a downside to technology,” says Scott-Moncrieff, which in this case is mostly time and education. Fluctuations in blood sugar are normal—but concerned owners might need reassurance. She also emphasizes that it’s important for owners to consult with vets before making any treatment decisions. With that in mind, Scott-Moncrieff says, “it’s really powerful technology.” 

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This article was originally published on KFF Health News.

Everyone over the age of 6 months should get the latest covid-19 booster, a federal expert panel recommended Tuesday after hearing an estimate that universal vaccination could prevent 100,000 more hospitalizations each year than if only the elderly were vaccinated.

The Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices voted 13-1 for the motion after months of debate about whether to limit its recommendation to high-risk groups. A day earlier, the FDA approved the new booster, stating it was safe and effective at protecting against the covid variants currently circulating in the U.S.

After the last booster was released, in 2022, only 17 percent of the U.S. population got it—compared with the roughly half of the nation who got the first booster after it became available in fall 2021. Broader uptake was hurt by pandemic weariness and evidence the shots don’t always prevent covid infections. But those who did get the shot were far less likely to get very sick or die, according to data presented at Tuesday’s meeting.

The virus sometimes causes severe illness even in those without underlying conditions, causing more deaths in children than other vaccine-preventable diseases, as chickenpox did before vaccines against those pathogens were universally recommended.

The number of hospitalized patients with covid has ticked up modestly in recent weeks, CDC data shows, and infectious disease experts anticipate a surge in the late fall and winter.

The shots are made by Moderna and by Pfizer and its German partner, BioNTech, which have decided to charge up to $130 a shot. They have launched national marketing campaigns to encourage vaccination. The advisory committee deferred a decision on a third booster, produced by Novavax, because the FDA hasn’t yet approved it. Here’s what to know:

Who should get the covid booster?

The CDC advises that everyone over 6 months old should, for the broader benefit of all. Those at highest risk of serious disease include babies and toddlers, the elderly, pregnant women, and people with chronic health conditions including obesity. The risks are lower—though not zero—for everyone else. The vaccines, we’ve learned, tend to prevent infection in most people for only a few months. But they do a good job of preventing hospitalization and death, and by at least diminishing infections they may slow spread of the disease to the vulnerable, whose immune systems may be too weak to generate a good response to the vaccine.

Pablo Sánchez, a pediatrics professor at The Ohio State University who was the lone dissenter on the CDC panel, said he was worried the boosters hadn’t been tested enough, especially in kids. The vaccine strain in the new boosters was approved only in June, so nearly all the tests were done in mice or monkeys. However, nearly identical vaccines have been given safely to billions of people worldwide.

When should you get it?

The vaccine makers say they’ll begin rolling out the vaccine this week. If you’re in a high-risk group and haven’t been vaccinated or been sick with covid in the past two months, you could get it right away, says John Moore, an immunology expert at Weill Cornell Medical College. If you plan to travel this holiday season, as he does, Moore said, it would make sense to push your shot to late October or early November, to maximize the period in which protection induced by the vaccine is still high.

Who will pay for it?

When the ACIP recommends a vaccine for children, the government is legally obligated to guarantee kids free coverage, and the same holds for commercial insurance coverage of adult vaccines. For the 25 to 30 million uninsured adults, the federal government created the Bridge Access Program. It will pay for rural and community health centers, as well as Walgreens, CVS, and some independent pharmacies, to provide covid shots for free. Manufacturers have agreed to donate some of the doses, CDC officials said.

Will this new booster work against the current variants of covid?

It should. More than 90% of currently circulating strains are closely related to the variant selected for the booster earlier this year, and studies showed the vaccines produced ample antibodies against most of them. The shots also appeared to produce a good immune response against a divergent strain that initially worried people, called BA.2.86. That strain represents fewer than 1% of cases currently. Moore calls it a “nothingburger.”

Why are some doctors not gung-ho about the booster?

Experience with the covid vaccines has shown that their protection against hospitalization and death lasts longer than their protection against illness, which wanes relatively quickly, and this has created widespread skepticism. Most people in the U.S. have been ill with covid and most have been vaccinated at least once, which together are generally enough to prevent grave illness, if not infection—in most people. Many doctors think the focus should be on vaccinating those truly at risk.

With new covid boosters, plus flu and RSV vaccines, how many shots should I expect to get this fall?

People tend to get sick in the late fall because they’re inside more and may be traveling and gathering in large family groups. This fall, for the first time, there’s a vaccine—for older adults—against respiratory syncytial virus. Kathryn Edwards, a 75-year-old Vanderbilt University pediatrician, plans to get all three shots but “probably won’t get them all together,” she said. Covid “can have a punch” and some of the RSV vaccines and the flu shot that’s recommended for people 65 and older also can cause sore arms and, sometimes, fever or other symptoms. A hint emerged from data earlier this year that people who got flu and covid shots together might be at slightly higher risk of stroke. That linkage seems to have faded after further study, but it still might be safer not to get them together.

Pfizer and Moderna are both testing combination vaccines, with the first flu-covid shot to be available as early as next year.

Has this booster version been used elsewhere in the world?

Nope, although Pfizer’s shot has been approved in the European Union, Japan, and South Korea, and Moderna has won approval in Japan and Canada. Rollouts will start in the U.S. and other countries this week.

Unlike in earlier periods of the pandemic, mandates for the booster are unlikely. But “it’s important for people to have access to the vaccine if they want it,” said panel member Beth Bell, a professor of public health at the University of Washington.

“Having said that, it’s clear the risk is not equal, and the messaging needs to clarify that a lot of older people and people with underlying conditions are dying, and they really need to get a booster,” she said.

ACIP member Sarah Long, a pediatrician at Children’s Hospital of Philadelphia, voted for a universal recommendation but said she worried it was not enough. “I think we’ll recommend it and nobody will get it,” she said. “The people who need it most won’t get it.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

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Marin Hambley was working as a groundskeeper in Chico, California, when the first plumes of what would become the deadliest fire in the state’s history appeared on the horizon. It was Nov. 8, 2018.

Initially, all Hambley could see of the Camp Fire was a “little puff of cloud”—a sight not uncommon in the northeastern reaches of the Sacramento Valley, where summer temperatures routinely surpass 100 degrees Fahrenheit. But by midafternoon, “the sky was totally black and just dropping chunks of ash,” said Hambley. 

Many residents evacuated; Hambley chose to stay. This area had been heavily impacted by the opioid crisis, and Hambley’s experience with harm reduction, a practice centered on minimizing the negative outcomes of drug use, made them acutely aware of the need to help people with substance abuse disorders. Additionally, their perspective as a queer and trans person led them to believe that they could be especially helpful to the marginalized populations that are often overlooked during disasters. 

Since 2006, Butte County, where Paradise and Chico are located, has consistently been among the top three counties in the state for hospitalizations from opioid-related overdoses, with an annual rate between 2.75 and 5 times the state’s average. 

In the hours after the plumes first appeared, Hambley heard about a pop-up encampment in an empty lot wedged between a busy throughway and the local Walmart. Hundreds of mostly low-income people had flocked there, fleeing the fire, and community organizers were distributing food, water and clothing. Meanwhile, those with means stayed in hotel rooms and Airbnbs or left the area entirely. 

At the time, the county lacked official harm reduction infrastructure. Hambley and other organizers had to locate and distribute supplies on their own. Without the required certification, their activities weren’t technically legal, but Hambley said that was a risk they were willing to take. While the group had received a grant for purchasing Narcan—the overdose-preventing nasal spray approved for over-the-counter use last March—they had to obtain syringes, needles, cotton swabs and fentanyl test strips from groups elsewhere in the state. “We were all kind of underground,” Hambley said, noting that they smuggled backpacks stuffed with Narcan into Red Cross-operated shelters, where drug use was prohibited, though widely practiced. 

At the Walmart encampment and other shelters, Hambley witnessed a disturbing rise in overdoses following the colossal Camp Fire, which ultimately killed at least 85 people and devoured nearly 240 square miles. A local paramedic noted that in the weeks following the fire, overdoses went from being a weekly occurrence to a daily one. And with a rate of 17 deaths per 100,000 residents, for the first time the Paradise area experienced a higher rate of opioid-related overdose deaths in 2018 than any other zip code in Butte County. Hambley said that’s because disasters cause both acute stress and chronic uncertainty, which can lead to more reactive and less managed drug use. “The chaos around you often precedes more chaotic (drug) use,” they said.

Across the Western U.S., climate disasters compound the devastation already caused by the deepening addiction crisis. Wildfires and floods breed anxiety, despair and isolation, all of which can exacerbate substance use. “Your house burns down, your community burns down, your school burns down—of course, you look for an escape,” said Sarah Windels, a co-founder of Bridge, a California-based program that promotes access to substance-use disorder treatment.

Beyond that, climate disasters halt addiction treatment programs and derail critical medication supply chains—all factors that heighten the risk of overdose, including for people who legally use opioids. This is especially true in rural areas, where fewer health-care providers are available, and patients often need to travel substantial distances to receive care. After a massive fire or flood, when local pharmacies and clinics may be closed, a person who is prescribed opioids for chronic pain or who is undergoing medication-assisted treatment (MAT) to curb their addiction may be forced to acquire a substitute illegally. If that supply has a higher potency than they are used to or, as is increasingly common, is laced with fentanyl, that individual is at a high risk of overdosing. 

“Your house burns down, your community burns down, your school burns down — of course, you look for an escape.”

The data suggests that the connection between climate-induced disasters and overdoses is neither occasional nor individual, but seasonal and increasingly predictable. For instance, overdose rates are increasing every year across the nation, but in California, at least, they peak at the height of fire season. According to the California Overdose Surveillance Dashboard, emergency department visits for opioid-related overdoses have topped out during the third quarter of every year since 2018. And in 2020, the counties most affected by the vast August Complex Fire saw a surge in overdose deaths while the wildfire burned. 

From the foothills of the California Sierras, to the floodplains of New Mexico, to the high Rockies in Colorado, these events are also forcing harm reduction workers to adapt their approaches to match their specific surroundings. 

In Albuquerque, New Mexico, for example, extreme weather during the summer months accelerates overdose rates, said Ashley Charzuk, the executive director of the New Mexico Harm Reduction Collaborative, although the reasons differ from those in regions affected by wildfires. In Charzuk’s experience, people who use intravenous drugs can find veins more easily when it’s hot, owing to vasodilation, and this can lead to more frequent and potent use. What’s more, those who use stimulants are at greater risk of overamping, which is different from overdosing. “Your body temperature goes up when you’re using methamphetamine,” said Charzuk. When paired with high environmental temperatures, Charzuk said, overamping can lead to heart attack, stroke or other complications.

As heat waves get more extreme, Charzuk and her colleagues prioritize educating people about the risks of drug use when it’s hot out. 

“We remind people … that heat plays into so many different metabolic factors,” said Charzuk. “If you’ve been out in the heat all day and you’ve been sweating, then you are going to be dehydrated, and anything that impacts your body like that is going to give you less of a defense.” 

In 2020, overdose-related emergency room visits in New Mexico peaked in July at 255, and in 2021, they peaked in June at 260.

As someone who uses drugs and has experienced homelessness in the past, Charzuk has “met some of the same challenges that (program) participants meet on a daily basis,” she said. 

Harm reduction workers are also at risk. In the summer of 2021, while handing out water in a local park, Charzuk was overcome by symptoms of heat stroke that kept her out of the field for days. “I feel like I learned a little bit more on how to take care of the people that are on my team as well as myself,” she said. 

For Hambley, such incidents speak to how important it is for harm reduction workers to think about their own physical and mental health during crises, “or else everyone will burn out,” they said. 

That tension came to a head for Arianna Campbell in the summer of 2021, when the Caldor Fire threatened to raze her community in Placerville, California, 90 miles southeast of Chico. As the flames approached, Campbell’s husband, a retired firefighter, suggested Campbell pack a go box. It was the first time he had ever done so. 

“He had some indications that this was going to be a very big one,” said Campbell; in fact, the fire would go on to burn over 200,000 acres and more than 1,000 buildings. 

But Campbell, a physician assistant, knew that she would be needed at the local hospital. Crises like wildfires strain emergency departments, Campbell explained, which are flooded by people with injuries, respiratory problems or other medical issues. This is especially likely for those who lack stable housing or have a substance use disorder. “If you’re someone who uses drugs, you may not necessarily have a lot of options,” Campbell said. 

In Placerville, Campbell helped her hospital become one of the country’s first rural sites to offer buprenorphine, a medication that helps curb opioid addiction. “If someone is being treated on buprenorphine and there is a lapse in treatment, they are at close to three times the risk of dying,” she said, “because it puts them at such high risk of return to use and overdose.”

Maggie Seldeen, who describes herself as a practicing drug user, founded High Rockies Harm Reduction to address the dearth of safe injection supplies in the region surrounding Aspen, Colorado. Overdoses from opioids, most notably fentanyl, have skyrocketed in the state since the start of the pandemic. For Seldeen—who used cocaine and heroin intravenously for years, starting as a freshman in high school, and who has seen numerous friends contract hepatitis—practicing harm reduction through the use of clean needles and fresh syringes is critically important. But more frequent wildfires and landslides affected the area’s already strained supply chain. 

“A lot of people of color, a lot of queer and trans folks, a lot of poor folks already understand the ways the system fails them.” 

That puts the lives of people who use drugs at risk, she said. In 2020, for instance, the Grizzly Creek Fire meant that I-70 in Glenwood Canyon—45 miles north of Aspen, and a critical juncture on the route from Aspen to Denver, more than a three-hour drive away—was closed for two weeks.  

“It gets really scary,” said Seldeen, who spoke about how the anxiety provoked by wildfires can push her and others to use substances as coping mechanisms. 

Now, Seldeen always has a go bag in her car when she is in the field in the summer months. It holds important personal documents, water, Narcan and first aid supplies, in case she encounters people who need help using drugs safely or reversing an overdose during an evacuation. Her hope is to create a network of people in the Rockies who are knowledgeable about—and prepared for—reducing the risks of drug use. Those connections, she says, will become increasingly important in a future that involves more climate events.

Seldeen isn’t alone in seeing the importance of community in facing the dueling crises of addiction and climate change. Back in Chico, Hambley now chairs the Northern Valley Harm Reduction Coalition, which Hambley helped grow in the wake of the Camp Fire, determined to continue the collective approach to harm reduction that came out of that disaster. “This is a community response,” they said. “The networks that we have are strong.” 

The embers of the Camp Fire had barely cooled in March 2020, when the Chico network had to mobilize once again to prevent overdoses during the statewide COVID-19 lockdown.

“This is a marathon,” Hambley said, explaining how their queer identity and personal experience living on the margins have given them the tools to build a community that will rise to the challenge. 

“A lot of people of color, a lot of queer and trans folks, a lot of poor folks already understand the ways the system fails them,” Hambley said. “As a queer trans person, I’ve already learned how to create family and community and networks outside of my home. Those are skills I live with every day, so in moments of crisis, our skill sets actually become incredibly valuable.”   

Robin Buller is a freelance journalist based in Oakland, California. She writes about health, equity and climate. Email her at robinmbuller@gmail.com.

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Turmeric seems to be everywhere these days—on spice shelves, sprinkled on lattes, in beauty products. While the beloved golden spice has long been touted for health benefits, albeit not always backed up by extensive research, a new study in BMJ Evidence-Based Medicine found that turmeric shows signs of being just as or more effective for indigestion than some conventional over-the-counter drug options.

The study, led by Krit Pongpruil, an associate professor of preventative and social medicine at Thailand’s Chulalongkorn University, randomly assigned 206 patients between the ages of 18 and 70 with recurrent upset stomachs into three treatment groups. One group got two large capsules of curcumin, a naturally active component to turmeric and a dummy capsule, another got a small omeprazole capsule and two summy capsules four times a day, and the last group got omeprazole and turmeric capsules. 

Omeprazole is a common treatment for stomach problems such as acid reflux and ulcers. It works as a proton pump inhibitor, which reduces the amount of acid made by stomach glands, but can also cause health concerns after long term use, like micronutrient deficiencies and fracture risks, according to the study authors. 

[Related: For decades, turmeric’s ultra-golden glow had a deadly secret.]

Assessments were taken after days 28 and 56, and the researchers found that the results between the three groups were similar, which points to the efficacy of turmeric, according to the authors. “The strength of the study lies in its relevance to daily clinical practice, providing additional drug options in addition to PPIs alone, without added side effects,” they wrote in their findings. 

Of course, this study should be taken with a grain of salt, especially since the group of patients was so small. “I don’t think this one study alone is enough for me to say, ‘I recommend this,’” Yuying Luo, a gastroenterologist and assistant professor of gastroenterology at the Icahn School of Medicine at Mount Sinai, told CNN. “Proceed with caution.” It’s crucial to also check with your doctor to make sure that turmeric doesn’t interact poorly with any other medicines before taking it—some case studies have linked curcumin and liver injury, Luo told CNN.

Further studies are needed to see if a taste of turmeric could replace or supplement medicines to help with gastrointestinal issues and more (and if you need to take it in pill form for the effects to kick in). Until then, enjoy your favorite heartily-spiced, turmeric-filled foods, but don’t expect them to make your stomach problems vanish.

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Samuel Hanke is a pediatric cardiologist in Cincinnati, but when you ask him for his title, he follows it by saying: “Most importantly, I’m Charlie’s dad.”

Hanke remembers the night 13 years ago when Charlie, then 3 weeks old, was fussier than usual, so he picked him up to soothe him back to sleep. With Charlie still in his arms, he sat on the couch, turned on the TV, and nodded off.

“We were kind of chest to chest, the way you see in pictures a lot,” Hanke said. But he didn’t realize Charlie’s airways were blocked. Too young to turn his head, too squished to let out a cry, Charlie died silently. The next morning, Hanke woke up to his worst nightmare. Years of medical school weren’t enough to prevent Hanke from losing Charlie to accidental suffocation.

Sudden infant death syndrome, a well-known term that describes unexplained but natural infant deaths resulting from an unknown medical abnormality or vulnerability, is the leading cause of unexpected deaths among infants in the U.S. It has long been among new parents’ greatest fears.

Rates for SIDS have declined since the 1990s, but a different cause of infant death — accidental suffocation or strangulation — has also been a persistent problem. That national rate for the past decade has hovered between 20 and 25 infant deaths per 100,000 live births, accounting for around a fifth of all unexpected infant deaths, according to the Centers for Disease Control and Prevention. Accidental suffocations and strangulations aren’t necessarily happening more often, some experts say; rather, fatality review teams have become better at identifying causes of death.

And the trend remains steady despite decades of public information campaigns imploring parents to take steps to keep their babies safe while sleeping.

In the mid-1990s, the National Institute of Child Health and Human Development launched its “Back to Sleep” campaign, to teach parents to lay infants on their backs to sleep. “There were tremendous results after ‘Back to Sleep,’” said Alison Jacobson, executive director of First Candle, a Connecticut-based nonprofit group focused on safe sleep education. Unexpected infant deaths dipped about 40% from 1990 levels, which was before that campaign launched, according to the CDC. “But then it plateaued,” Jacobson said.

The NICHD eventually broadened this message with other ways to limit risks beyond a baby’s sleep position with the “Safe to Sleep” initiative.

Some clear warnings from it: Infants shouldn’t sleep with blankets, stuffed toys, or bumpers that “can potentially lead to suffocation or strangulation,” said Samantha St. John, program coordinator for Cook Children’s Health Care System in Fort Worth, Texas. They also should sleep in cribs or bassinets — not on beds with siblings or in parents’ arms.

But these public health messages — contradicted by photos or videos circulating in movies and social media — don’t always find traction. Professional photos of infants, for example, too commonly show them peacefully snoozing surrounded by plush animals and blankets. St. John added that parents sometimes have preconceived ideas of how infants’ sleeping spaces should be decorated. “When you think of cribs and nurseries and things like that, you imagine the pictures in the magazines,” St. John said. “And those are beautiful pictures, but it doesn’t keep your baby safe.”

St. John said many parents know that babies should be on their backs to sleep, but warnings about strangulation by blankets or suffocation by sharing a bed with them sometimes fall through the cracks.

For instance, new parents, especially single parents, are more likely to accidentally fall asleep with their infants because of exhaustion, said Emily Miller, a neonatologist at Cincinnati Children’s Hospital.

The idea that sleeping with one’s baby is dangerous can also be counterintuitive to a new parent’s instinct. “We feel like being close to them, being able to see them, being able to touch them and feel that they’re breathing is the best way we can protect them and keep them safe,” said Miller, who is also an assistant professor at the University of Cincinnati’s Department of Pediatrics.

Organizations across the country are working to help parents better understand the true risks. Hanke and his wife, for instance, channeled their grief into Charlie’s Kids, a nonprofit focused on safe sleep practices for infants. The Hankes also wrote a book, “Sleep Baby, Safe and Snug,” which has sold about 5 million copies. The proceeds are used to continue their educational efforts.

Ohio, where Charlie’s Kids is based, in 2020 saw 146 sudden unexpected infant deaths, a classification that includes SIDS, accidental suffocation and strangulation, and other instances in which the cause is undetermined. That’s about a death for every 1,000 live births, according to the state’s health department. Thirty-six percent of those deaths were attributed to accidental suffocation or strangulation. Nationally, the rate of these unexplained deaths has declined since the 1990s, but, according to the CDC, significant racial and ethnic differences continue.

The particular risks for an infant’s accidental suffocation in many respects are situational — and often involve people at the lower end of the income scale who tend to live in close quarters. People who live in a small apartment or motel often share sleep space, said St. John.

Tarrant County has one of Texas’ highest rates of infant deaths — three to four each month — attributed to accidental suffocation.

So, organizations like the Alliance for Children in Tarrant County, which serves Fort Worth and parts of Dallas, have been providing free bassinets and cribs to those in need.

County representatives spoke during the state’s Child Fatality Review Team meeting in May and focused on the prevalence of infant deaths linked to accidental suffocation. For the past decade, data shows, the county has averaged 1.05 sudden unexpected infant deaths per 1,000 births, which is higher than both the state and national averages of 0.85 and 0.93, respectively. During a 15-month period starting in 2022, Cook Children’s Medical Center saw 30 infants born at the hospital die after they left because of unsafe sleeping environments.

Sometimes parents’ decisions are based on fears that stem from their environments. “Parents will say ‘I’m bringing my baby into bed because I’m afraid of gunshots coming through the window, and this is how I keep my baby safe’ or ‘I’m afraid rats are going to crawl into the crib,’” said First Candle’s Jacobson.

She understands these fears but stresses the broader context of safe sleep.

The key to educating parents is to begin when they are still expecting because they receive “a load of information” in the first 24 or 48 hours after a baby is delivered, said Sanjuanita Garza-Cox, a neonatal-perinatal specialist at Methodist Children’s Hospital in San Antonio. Garza-Cox is also a member of the Bexar County Child Fatality Review Team.

And once a child is born, the messaging should continue. In Connecticut, for instance, First Candle hosts monthly conversations in neighborhoods that bring together new parents with doulas, lactation consultants, and other caregivers to discuss safe sleep and breastfeeding.

And both Tarrant and Bexar counties are placing ads on buses and at bus stops to reach at-risk parents and other caregivers such as children, relatives, and friends. Parents are very busy, Garza-Cox said. “And sometimes, multiple children and young kids are the ones watching the baby.”

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Merkel cell carcinoma, the skin cancer that killed beloved Margaritaville singer Jimmy Buffett on September 1, is rare. But it may become more common in the coming decades. Every year the US diagnoses 3,000 new cases of this disease—a number that is estimated to increase to 3,250 cases by 2025. As the US population ages and global warming influences ultraviolet radiation, dermatologists suspect this caseload will only continue to get higher.

“We know that Merkel cell carcinoma occurs in sun-exposed areas and that UV, in particular, is a risk factor,” says Eva Parker, an assistant professor of dermatology at Vanderbilt University Medical Center who has studied climate change’s impact on skin cancer. “I believe we will continue to see increasing rates of both common and less common types of skin cancer.” She pointed to two contributing trends: the delayed period over which skin cancer develops, plus the growing effects of climate change that includes continued pressure humans are placing on the protective ozone layer in the stratosphere.

The relationship between climate change and skin cancer is complex. On one hand, ultraviolet radiation from the sun contributes to skin cancer, because this light can damage our cells’ DNA. And ultraviolet radiation exists regardless of climate change. 

On the other hand, there’s circumstantial evidence that factors related to climate change—stratospheric ozone depletion, heat, and air pollution—are likely contributing to the increasing incidence for melanoma and non-melanoma skin cancer. (Fast-growing Merkel cell carcinomas are a subtype of non-melanoma skin cancer.) Research suggests an average global warming of 3.6 degrees Fahrenheit is associated with an 11 percent rise in all skin cancers worldwide. The world is already on track to reach this number by 2050. 

[Related: Why doctors almost never say cancer is ‘cured’]

The problem with establishing a direct link to climate change and increasing skin cancer cases is that most of the data is based on animal studies and computer modeling. To definitively say that climate change causes skin cancer, Parker says more epidemiological data on humans is needed. Though she explains how climate change may directly or indirectly contribute to rising skin cancer cases.

One reason is likely because of stratospheric ozone depletion. Think of the ozone layer as a giant hat that covers Earth and blocks out ultraviolet and UVB radiation, which is associated with many forms of skin cancer including Merkel cell carcinoma. In the 1970s, scientists started noticing holes in the ozone layer. Further investigation showed that artificial compounds such as chlorofluorocarbons were destroying ozone. “They’re potent greenhouse gases and incredibly long-lived in the atmosphere,” explains Parker. “The implication is that stratospheric ozone depletion will be ongoing for many decades, even though chlorofluorocarbons have been regulated for some time.” 

With less ozone absorbing UVB radiation, people are more exposed to the radiation’s damaging effects on skin cells, leading to an increasing risk of skin cancer. Fortunately, phasing ozone-depleting chemicals has helped to repair this layer, though the healing process has been slow. Environmental scientists estimate it will take until 2040 for ozone to return to the levels they were in the 1980s. 

[Related: Wind turbines do not cause cancer]

Missing ozone is one climate-related contributor to skin cancer. Heat is another possible culprit, Parker says. Ultraviolet radiation needs heat to activate its tumor-forming ability. Excess heat could indirectly create an ideal environment for cancer to flourish. And, when combined with high humidity, it messes with the body’s way of regulating body temperature. When a body can’t cool itself down through sweating, this could lead to physiological dysfunctions, including issues with gene expression while increasing inflammation and oxidative stress. Lastly, when it’s hot outside, people usually wear less clothing, which heightens their UV exposure and skin cancer risk.

There is one silver lining: While Merkel cell carcinoma is more aggressive than melanoma, it is curable if caught early and treated successfully, says Ling Gao, an associate professor of dermatology at the University of California, Irvine. “For all skin cancers, early diagnosis greatly improves outcomes.”

You’re better off, though, by preventing skin cancer from appearing altogether. The first step is to identify when you’re most exposed to the sun, says David Leffell, a professor of dermatology  at Yale School of Medicine and a fellow of the American Academy of Dermatology. Next, you’ll want to take steps to minimize that exposure. If you often go for a 15-minute walk around the block, stay in the shade and avoid peak hours like noon when the sun is at the highest point in the sky. When you do go outside, shield yourself from ultraviolet rays with SPF 50 sunscreen. What you wear helps, too: A brimmed hat and specialized clothing, such as UPF rated shirts and pants, can block out the sun’s rays. 

If you’re unsure whether you should go outside today, consider downloading an app that rates the UV index. Similar to checking weather forecasts, a UV index will tell you whether it’s safer to stay indoors or to pack some sunscreen before heading out.

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With the changing weather comes virus season. Throughout the pandemic, infectious disease experts have seen an uptick in COVID cases during the fall and winter as more people stay indoors. The latter half of the year is also the time when SARS-CoV-2 mutates into other variants. And this year is no exception. Researchers are keeping an eye on the new variant BA.2.86, or Pirola, as it spreads in multiple countries. Meanwhile, back in August, the Centers for Disease Control and Prevention (CDC) announced a new Omicron variant called Eris had become the dominant coronavirus strain in the US.

“The Eris variant appears to be more transmissible compared to prior variants, which may mean that it will be easier for more people to get infected from a given exposure. Also, people who have previously been infected or vaccinated may get infected with this new variant,” says Sherrill Brown, a medical director of infection prevention at AltaMed in California. 

Though Eris has been responsible for an increasing number of COVID hospitalizations in the US, infectious disease experts have not seen signs yet that it causes more severe illness. In fact, Brown says the Eris variant appears no more dangerous than the ones we’ve faced in the past.

With long COVID complications and immunocompromised individuals in mind as well, it doesn’t hurt to stay prepared if cases surge through the end of 2023. Like the flu and other respiratory viruses, some health experts are now calling COVID endemic—the average person will probably get it several times in their life. But the good news is the US is in a much better position now than three years ago with a range of preventative methods, from medical-grade masks and antiviral treatments to updated vaccine formulas. In mid-September, the Food and Drug Administration approved new booster shots, which are tweaked to defend against XBB.1.5, an Omicron variant.

Following an advisory committee vote in favor of this Omicron-targeting vaccine, the CDC is encouraging everyone who is eligible to get a shot for the upcoming fall and winter season. “We have more tools than ever to prevent the worst outcomes from COVID-19,” said CDC director Mandy Cohen in a news release. “CDC is now recommending updated COVID-19 vaccination for everyone 6 months and older to better protect you and your loved ones.”

Is it time to mask up again?

The US government has lifted all masking mandates, so there is no requirement to wear one in public anymore. That said, private businesses and hospitals may demand face coverings on their property if there is another COVID wave.

For the most part, the decision to mask is personal. Sarah Hochman, the section chief of infectious diseases at NYU Langone Tisch Hospital, says people need to evaluate how far they’re willing to risk getting sick. A person who is immunocompromised or has other lung conditions like asthma, for example, may want to start masking up again because the risk of COVID complications in this group is higher. If you’re planning to see friends and family this season, a properly placed mask would tremendously reduce the risk of infection. “It has been a personal choice for the past year and a half and everyone has their own threshold on where they are concerned enough to mask in situations,” Hochman notes. Masking is also helpful in general for protecting against other respiratory viruses such as the flu and RSV.

[Related: Masks can work—even if you’re the only one wearing them]

A good way to evaluate your individual risk is to check the latest numbers of COVID hospitalization in your local area. Hochman says hospital data is a more reliable source of information given that the CDC and local health departments have not been reporting recently as much on case numbers; people can find these stats on their local state or county health department’s website. Additionally, regional or national data could be inaccurate because more people are doing home tests or not testing at all. In most places, however, hospitalized patients are still being tested for the virus. “It’s really more of a tip of the iceberg type of measure because you’re only measuring COVID in the sickest patients, but it can still indicate what’s going on,” Hochman explains.

When will new COVID boosters be available?

The Biden administration is looking at a mid-September rollout date for the new boosters. The bivalent COVID shot currently protects against the original coronavirus and two Omicron variants, BA.4 and BA.5. With the new update, the vaccine will include protection against the Omicron variant XBB.1.5. 

Eris is a close but not exact match to XBB.1.5 as it is a descendent of XBB.1.9.2. Still, infectious disease experts have a strong suspicion the new shots will provide some protection against this new variant. “Most of the circulating variants are still related to the XBB.1.5 strain, so there should be fairly good protection from severe disease with this updated vaccine,” says Brown.

Once the booster becomes publicly available, you can get it in the same places you received your prior vaccines, including doctor’s offices, pharmacies, and local health clinics. Some states and counties may have websites set up to help people find a vaccine administration center close to them. Remember that all COVID vaccines should still be free, regardless of insurance or immigration status. 

What happens if you get COVID again?

Masks and boosters cut your risk for re-infection, but they won’t completely prevent it. To prepare, make sure to keep some at-home rapid test kits on hand. Hochman recommends having one to two tests for every person in the household. 

[Related: How to check if your at-home COVID test has expired]

If you test positive, notify your doctor immediately. They can prescribe you the antiviral pill Paxlovid, which is most effective within five days of developing symptoms. You’ll also want to take time off work and other obligations to rest and drink enough fluids for a proper recovery. 

Isolate from others at home for at least five days to avoid spreading the virus. If you need to go out or see other people, make sure to wear a high-quality mask.

This post has been updated to include more regulatory information about this fall’s COVID boosters. It was originally published on September 5.

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This article is from a partnership that includes WBUR, NPR, and KFF Health News.

An important email appeared in the inboxes of a small group of health care workers north of Boston as this summer started. It warned that local temperatures were rising into the 80s.

An 80-plus-degree day is not sizzling by Phoenix standards. Even in Boston, it wasn’t high enough to trigger an official heat warning for the wider public.

But research has shown that those temperatures, coming so early in June, would likely drive up the number of heat-related hospital visits and deaths across the Boston region.

The targeted email alert the doctors and nurses at Cambridge Health Alliance in Somerville, Massachusetts, got that day is part of a pilot project run by the nonprofit Climate Central and Harvard University’s Center for Climate, Health, and the Global Environment, known as C-CHANGE.

Medical clinicians based at 12 community-based clinics in seven states — California, Massachusetts, North Carolina, Oregon, Pennsylvania, Texas, and Wisconsin — are receiving these alerts.

At each location, the first email alert of the season was triggered when local temperatures reached the 90th percentile for that community. In a suburb of Portland, Oregon, that happened on May 14 during a springtime heat wave. In Houston, that occurred in early June.

A second email alert went out when forecasts indicated the thermometer would reach the 95th percentile. For Cambridge Health Alliance primary care physician Rebecca Rogers, that second alert arrived on July 6, when the high hit 87 degrees.

The emails remind Rogers and other clinicians to focus on patients who are particularly vulnerable to heat. That includes outdoor workers, older adults, or patients with heart disease, diabetes, or kidney disease.

Other at-risk groups include youth athletes and people who can’t afford air conditioning, or who don’t have stable housing. Heat has been linked to complications during a pregnancy as well.

“Heat can be dangerous to all of us,” said Caleb Dresser, director of health care solutions at C-CHANGE. “But the impacts are incredibly uneven based on who you are, where you live, and what type of resources you have.”

The pilot program aims to remind clinicians to start talking to patients about how to protect themselves on dangerously hot days, which are happening more frequently because of climate change. Heat is already the leading cause of death in the U.S. from weather-related hazards, Dresser said. Letting clinicians know when temperatures pose a particular threat to their patients could save lives.

“What we’re trying to say is, ‘You really need to go into heat mode now,’” said Andrew Pershing, vice president for science at Climate Central, with a recognition that “it’s going to be more dangerous for folks in your community who are more stressed.”

“This is not your grandmother’s heat,” said Ashley Ward, who directs the Heat Policy Innovation Hub at Duke University. “The heat regime that we are seeing now is not what we experienced 10 or 20 years ago. So we have to accept that our environment has changed. This might very well be the coolest summer for the rest of our lives.”

The alerts bumped heat to the forefront of Rogers’ conversations with patients. She made time to ask each person whether they can cool off at home and at work.

That’s how she learned that one of her patients, Luciano Gomes, works in construction.

“If you were getting too hot at work and maybe starting to feel sick, do you know some things to look out for?” Rogers asked Gomes.

“No,” said Gomes slowly, shaking his head.

Rogers told Gomes about early signs of heat exhaustion: dizziness, weakness, or profuse sweating. She handed Gomes tip sheets she’d printed out after receiving them  along with the email alerts.

They included information about how to avoid heat exhaustion and dehydration, as well as specific guidance for patients with asthma, chronic obstructive pulmonary disease (COPD), dementia, diabetes, multiple sclerosis, and mental health concerns.

Rogers pointed out a color chart that ranges from pale yellow to dark gold. It’s a sort of hydration barometer, based on the color of one’s urine.

“So if your pee is dark like this during the day when you’re at work,” she told Gomes, “it probably means you need to drink more water.”

Gomes nodded. “This is more than you were expecting to talk about when you came to the doctor today, I think,” she said with a laugh.

During this visit, an interpreter translated the visit and information into Portuguese for Gomes, who is from Brazil and quite familiar with heat. But he now had questions for Rogers about the best ways to stay hydrated.

“Because here I’ve been addicted to soda,” Gomes told Rogers through the interpreter. “I’m trying to watch out for that and change to sparkling water. But I don’t have much knowledge on how much I can take of it.”

“As long as it doesn’t have sugar, it’s totally good,” Rogers said.

Now Rogers creates heat mitigation plans with each of her high-risk patients. But she still has medical questions that the research doesn’t yet address. For example: If patients take medications that make them urinate more often, could that lead to dehydration when it’s hot? Should she reduce their doses during the warmest weeks or months? And, if so, by how much? Research has yielded no firm answers to those questions.

Deidre Alessio, a nurse practitioner at Cambridge Health Alliance, also has received the email alerts. She has patients who sleep on the streets or in tents and search for places to cool off during the day.

“Getting these alerts makes me realize that I need to do more homework on the cities and towns where my patients live,” she said, “and help them find transportation to a cooling center.”

Most clinics and hospitals don’t have heat alerts built into electronic medical records, don’t filter patients based on heat vulnerability, and don’t have systems in place to send heat warnings to some or all of their patients.

“I would love to see health care institutions get the resources to staff the appropriate outreach,” said Gaurab Basu, a Cambridge Health Alliance physician who co-directs the Center for Health Equity Advocacy and Education at Cambridge Health Alliance. “But hospital systems are still really strained by covid and staffing issues.”

This pilot program is an excellent start and could benefit by including pharmacists, said Kristie Ebi, founding director of the Center for Health and the Global Environment at the University of Washington.

Ebi has studied heat early-warning systems for 25 years. She says one problem is that too many people don’t take heat warnings seriously. In a survey of Americans who experienced heat waves in four cities, only about half of residents took precautions to avoid harm to their health.

“We need more behavioral health research,” she said, “to really understand how to motivate people who don’t perceive themselves to be at risk, to take action.”

For Ebi and other researchers, the call to action is not just to protect individual health, but to address the root cause of rising temperatures: climate change.

“We’ll be dealing with increased exposure to heat for the rest of our lives,” said Dresser. “To address the factors that put people at risk during heat waves, we have to move away from fossil fuels so that climate change doesn’t get as bad as it could.”

This article is from a partnership that includes WBUR, NPR, and KFF Health News.

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

Subscribe to KFF Health News’ free Morning Briefing.

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The dietary supplement market in the US is valued at more than $50 million dollars. One slice of that—fish oil supplements—has been growing in popularity in recent years, thanks to the many health benefits touted on their labels. However, medical research has not been able to confirm that consuming the omega-3 fatty acids in them offer many cardiovascular benefits. Despite this lack of hard evidence, fish oil marketers continue to make outsized claims about the supplement’s benefits, according to a study published on August 23 in the journal JAMA Cardiology.

[Related: Do you need a daily multivitamin? Probably not, says national health task force.]

Fish oil contains two omega-3 fatty acids, EPA and DHA, which are found in flax seeds, walnuts, and fatty fish such as salmon. Higher levels of EPA and DHA have been associated with a lower risk of cardiovascular disease; however, these observational findings are based on patients getting them naturally from their diet and not supplemental use. A 2021 study from the National Institutes of Health also showed that general over-the-counter fish oil supplements do not actually improve cardiovascular outcomes. Additionally, a randomized trial of more than 15,000 patients with diabetes found that the risk of a serious cardiovascular event was not significantly different between participants who were and weren’t taking an omega-3 supplement.

In this new paper, a team from the University of Texas Southwestern Medical Center in Dallas analyzed health claims on the labels of 2,819 fish oil supplements taken from the National Institutes of Health Dietary Supplement Label Database. 

More than 80 percent of the supplements in the study used a structure and function claim. These types of claims vaguely describe the role that omega-3 fatty acids play in the body, like “supports heart, mind, and mood” or “promotes heart health.” 

The study also reviewed qualified health claims and found them on only 19 percent (399) of the labels: 394 relating to coronary heart disease, three for blood pressure, and two relating to both. These claims are related to the supplement’s potential to help in the treatment or prevention of a disease and are made by the US Food and Drug Administration (FDA), but only following an evidence review.

Currently, there are only two cardiovascular-related qualified health claims for fish oil, one that relates to coronary heart disease and the other to blood pressure. In 2019, the FDA wrote, “Supportive but not conclusive research shows that consumptions of EPA and DHA omega-3 fatty acids may reduce the risk of coronary heart disease.”

However, the agency also states that structure and function claims cannot say that a supplement has the power to prevent, treat, or cure any illness or disease. They simply “describes the role of a nutrient or dietary ingredient intended to affect the structure or function in humans.’’

In response to Popular Science’s request to comment on fish oil supplement labels, an FDA spokesperson wrote: “In general, the FDA does not comment on specific studies, but evaluates them as part of the body of evidence to further our understanding about a particular issue and assist in our mission to protect public health. The FDA is reviewing the findings of the paper.”

[Related: Viagra shows promise in extending men’s lives, among other areas.]

“It is true that omega-3 fatty acids are present in the brain and are important for all sorts of brain functions,” study co-author and cardiology professor Ann Marie Navar told The Washington Post. “What has not been consistently shown with high-quality trials is that taking more of it in the form of a fish oil supplement leads to improved performance or prevention of disease.” Navar also added that she was “alarmed” to learn that fish oil supplement labels often include claims that imply health benefits for a wide range of organ systems (brain, heart, and eyes) while conducting the study.

The team did recognize several limitations in their analysis. Companies submit label information to the NIH Dietary Supplement Label Database on a volunteer basis, so the paper was not all-inclusive. What’s more, the authors only assessed supplements from the 16 largest fish oil brands and the health claims on their labels, not promotional materials.

“Nutrition studies are notoriously difficult to conduct in the right way,” certified clinical nutritionist and board-certified holistic nutritionist Megan Lyons told Healthline. “Humans have so many variables at play: different health conditions, diverse dietary intake, varying movement patterns, and distinct sleep and stress patterns—all contributing to our overall health.”

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Three years into the global COVID-19 pandemic, an estimated four million Americans report that long COVID is severely impacting their daily lives. Scientists are still trying to better understand the condition that brings with it severe brain fog, blood clots, and a whole host of awful medical conditions that don’t go away. Now, a study published August 21 in the journal Nature Medicine found fallout from COVID-19 can persist even two years after infection. 

[Related: What patients find at long COVID clinics: rejection, outdated therapies, and unanswered questions.]

Some of the health problems associated with long COVID in this study include blood clots, diabetes, heart issues, blood clots, diabetes, neurologic complications, gastrointestinal disorders, fatigue, and difficulties with mental health.

The researchers found that people who had COVID, including patients hospitalized within the first 30 days and those who were not, were still at an elevated risk of developing these conditions two years out.   

“For far too many people, the continuing and enduring risk of long COVID and its long-term, adverse effects on health are sober reminders that the pandemic is not in the rearview mirror,” study author and Washington University clinical epidemiologist Ziyad Al-Aly said in a statement. “The continuous struggles of people with long COVID are vivid, daily reminders of the detrimental and long-lasting legacy of COVID-19.”

In the study, researchers looked at the de-identified medical records of nearly 140,000 veterans who survived for 30 days after contracting COVID-19 in 2020. They compared their health outcomes to close to 6 million other patients within the VA health system who did not have evidence of infection. No one in the study was vaccinated, as the vaccines had not been developed yet, and antiviral treatments targeting to COVID-19 were also not available. 

The authors applied statistical models to examine the health risks that were associated with the virus two years post-infection. Within that time frame, they collected data from those who had COVID-19 and from the non-infected control group at five different periods in time to see if and when the risks of 80 long COVID-related conditions declined or equalized.

When compared with the control group, post-infection risks of death and hospitalization among those who were not hospitalized decreased and became on par with the non infected control group at six months and 19 months. 

For those hospitalized for COVID-19, risk of death and hospitalization remained elevated two years post infection. The risk for 52 of the 80 long COVID-related conditions in the study also remained elevated.

“This suggests a difficult and protracted road to recovery among those whose disease was sufficiently severe enough to necessitate hospitalization while infected with the virus,” Al-Aly said.

[Related: Getting COVID more than once might be even worse than we thought.]

The team also tallied the risks for over 80 different complications that are associated with long COVID and turned it into a health metric called a disability adjusted life year (DALY). Each DALY stands for one year of typically healthy life lost to illness. The team found that long COVID created over 80 DALYs, for every 1,000 people who weren’t hospitalized due to their initial infection.

Based on the Institute for Health Metrics and Evaluation’s Global Burden of Disease study, long COVID creates a higher burden of disability per every 1,000 Americans than cancer (roughly 50 DALYs) or heart disease (about 52 DALYs). 

“Our findings highlight the substantial cumulative burden of health loss due to long COVID and emphasize the ongoing need for health care for those faced with long COVID,” said Al-Aly. “It appears that the effects of long COVID for many will not only impact such patients and their quality of life, but potentially will contribute to a decline in life expectancy and also may impact labor participation, economic productivity, and societal well-being.”

Some important caveats to the study are that typically VA patients are older, in their 60s, and roughly 90 percent of patients were male. 

The team noted one encouraging note that the risks of death or hospitalization to those who were not sent to the hospital—the majority of people infected with the virus— declined and became insignificant at six and 19 months.

Decreasing the risk of long COVID should be a focus of public health policy, according Al-Aly. “Reducing the risk of infection and transmission with updated vaccines — including vaccines that block transmission — may be a critical strategy to reduce the risk of long-term health problems,” he said. “We also need an urgent, coordinated approach that matches the scale and gravity of long COVID to find treatments as soon as possible.”

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The World Health Organization (WHO) and Centers for Disease Control and Prevention (CDC) are tracking and studying a highly mutated new variant of the virus that causes COVID-19. Officially titled BA.2.86 and nicknamed Pirola on social media, the WHO has designated it as a “variant under monitoring.” This status applies to variants that have an unusually large number of mutations that call for monitoring as they spread.  

[Related: What to know about the newly dominant ‘Eris’ COVID variant.]

According to Fred Hutchinson Cancer Center evolutionary biologist Jesse Bloom, BA.2.86  has more than 30 amino acid changes in its spike protein, compared with its next closest ancestor (Omicron’s BA.2 subvariant). 

“We have not seen a new variant [in humans] with this many new spike mutations happening all at once since the emergence of the original Omicron,” Bloom told NBC News. “Based on the sequence, I think we can be very confident this [variant] is going to be relatively good at evading the antibodies that most people have from prior infections and vaccinations. What we still don’t know is, is this variant good enough at transmitting that it will really be able to spread widely around the world?”

So far, only six sequences BA.2.86 have been reported in the United States, United Kingdom, Israel, and Denmark, but epidemiologists are concerned that it is circulating in more places since monitoring COVID-19 variants has dropped.

“It is unusual for corona to change so significantly and develop 30 new mutations. The last time we saw such a big change was when Omicron appeared,” Morten Rasmussen, a senior researcher at the Statens Serum Institut (SSI) in Denmark, said in a statement.

SSI scientists stressed that it is currently too early to say if this new variant is more contagious or severe and that they are in the process testing it against human antibodies.

The CDC will keep monitoring BA.2.86, but did not say it is not currently a cause for alarm. According to the CDC’s variant tracker, the XBB descendant EG.5 (nicknamed Eris) is causing roughly 20 percent of all new COVID-19 cases in the US and is the dominant variant.  The next most common variant is FL.1.5.1, causing about 13 percent new cases. 

[Related: Your guide to COVID testing for the unforeseeable future.]

“I think what we are seeing is our detection mechanisms that we’ve put in place are working, right?” CDC Director Mandy Cohen told CNN. “We are more prepared than ever to detect and respond to changes in the COVID-19 virus.”

As the fall and winter virus season approaches, COVID-19 cases are expected to continue to climb around the US. The Food and Drug Administration (FDA) is expected to authorize updated booster shots soon, with signoff from the CDC expected by mid-September. The new boosters won’t include the specific EG.5 subvariant or BA.2.86, but will target the XBB strains.

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There are now two morning after pills you can pick up after a night of intimacy. Everyone’s familiar with the emergency contraceptive Plan B, but doctors are also pushing for a new treatment called Doxy-PEP to stop the spread of bacterial sexually transmitted infections (STIs) right after unprotected sex.

“In the old days when you had unprotected sex, most worries were on getting pregnant, so you took the morning after pill. This is kind of like the morning after pill, but to prevent getting specific STDs,” says Adi Davidov, an OBGYN at Staten Island University Hospital at Northwell Health.

The US is long overdue for a new STI-prevention strategy. The latest numbers from the Centers for Disease Control and Prevention (CDC) report more than 2.5 million new cases of chlamydia, gonorrhea, and syphilis in 2021. Syphilis, in particular, rose 32 percent from the year prior. 

“The STIs have really been exponentially increasing across the US for the last decade,” says Philip Chan, an infectious disease physician and the medical director for the Rhode Island-based health clinic Open Door Health. Recent studies on Doxy-PEP have shown it prevents certain bacterial infections; Chan is using this data to help the CDC develop guidelines on prescribing the drug and address concerns of antibiotic resistance and superbugs. 

[Related: A guide to preventing, spotting, and managing STIs]

Doxy-PEP is currently available as a prescription medication for anyone in the US. But just like Plan B, it’s only effective if you understand how to use it properly.

What is Doxy-PEP and how does it work?

Doxy-PEP stands for doxycycline post-exposure prophylaxis. It’s a one-time pill that contains 200 milligrams of the widely approved antibiotic doxycycline. In general, the drug wipes out bacterial infections by keeping germs from producing the essential proteins they need to survive.

The most ideal time to get treated with Doxy-PEP is within 24 hours of having sex. Jeffrey Klausner, an infectious disease specialist at the Keck School of Medicine of USC who has spearheaded multiple studies on STIs, says the current research estimates a 70 percent reduction in the risk of infection when taking the pill. “The studies went up to 72 hours, so we don’t really know what the long window is [for effectiveness]. The sooner you take it, the better.” 

Experts agree Doxy-Pep should be used as a contingency rather than as an alternative to condoms. Klausner says this is a medium-term solution until vaccines for STIs like gonorrhea and syphilis bring an end to these nuisances.

What are the side effects of Doxy-PEP?

Since 1967, doxycycline has been a popular antibiotic for getting rid of various disease-causing bacteria, from urinary tract infections to gum disease. But it’s not a perfect remedy. For example, the drug causes the user’s skin to become more sensitive, increasing the likelihood of a severe sunburn when outside.

In very rare situations, Klausner warns that Doxy-PEP can get stuck in a person’s food pipe, “particularly if you take it right before you go to bed.” If it does not travel all the way to the stomach, it can irritate the esophagus and potentially cause a hole or ulcer. To minimize this risk, take the pill at least half an hour before bed and with a full glass of water. You’ll also want to avoid alcohol when taking Doxy-PEP as it can lower the effectiveness of the antibiotic.

To be on the safe side, get a prescription if you’re worried about a possible infection after unprotected sex. Just be aware there are some side effects and precautions you need to follow when using the medication.

Who can take Doxy-PEP?

Anyone who’s had unprotected sex, had experiences with STIs in the past, or had multiple partners could benefit from Doxy-PEP. While there are no age restrictions, parental consent might be required for minors, just like with STI testing. The pill may be especially useful for gay and bisexual men: According to the CDC, this population makes up a disproportionate amount of STI cases. 

The treatment can also help give peace of mind to people who are trying to get pregnant and not using condoms, but still worried about STIs, says Davidov. However, he emphasizes it’s better to have sex with a partner who has tested negative for STIs.

Keep in mind Doxy-PEP only works on bacterial infections like gonorrhea, syphilis, and chlamydia, not viral ones like herpes or HIV. The pill also does not work on individuals who’ve already tested positive for those conditions.

Where to find Doxy-PEP

Like with any antibiotic, you need a prescription to get Doxy-PEP. But your primary care doctor might not be familiar with it, Chan explains. He recommends visiting a sexual health clinic that may be more well-versed in the latest treatment options. 

Some clinics will give out Doxy-PEP for free; if they don’t, insurance will likely cover the cost of the preventative treatment. Even if there is a co-pay or deductible, Klausner says it should not be financially burdensome as doxycycline is one of the cheapest antibiotics available.

Will Doxy-PEP make antibiotic resistance worse?  

The World Health Organization lists antibiotic resistance as one of the top 10 global health problems. Resistance to doxycycline in particular would be a major blow, in particular, because it might limit the ability to treat other infections like malaria and Lyme disease.

A study published this year in the New England Journal of Medicine looked at Doxy-PEP’s effectiveness and safety among men who had sex with men and transgender women who took the medicine within 72 hours of unprotected sex. While doxycycline reduced the risk of bacterial STIs by two-thirds, the authors did observe a few signs of antibacterial resistance. Notably, they found that some gonorrhea strains survived the antibiotic treatment. Doxy-PEP also cut the number of Staphylococcus aureus, a bacterium commonly found in the skin, in half. However, the germs that did persist grew to be antibiotic-resistant a year later—a concern given that doxycycline is usually prescribed to treat Staphylococcus aureus skin infections.

“It’s really about weighing the pros and the cons, and with the increasing incidence of STIs over the last decade, it’s clear we need to do something,” Chan explains. 

[Related: Why the FDA finally approved a condom for anal sex]

For now, the research linking antibiotic resistance to Doxy-PEP is still under investigation. But there is one silver lining: Clinical trials and real-life observations on the pill show that it works well and could improve the sexual health of millions. Just be sure to save it for emergencies.

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What if you could walk into a grocery store, scan the barcode on a Rice Krispie treat, and find out how it would affect your blood sugar before buying it? That’s the promise of January, a virtual continuous glucose monitor (CGM) system that the company describes as a “24/7 AI health coach to change the way you live.”

As a middle-aged woman with a family history of diabetes and a pizza weakness, I’ve wanted to try a CGM. After more than a week of testing the January AI system, I found it to be an effective tool that gave me more insight into my metabolic health and actually helped me lose a few pounds. It’s a sizeable investment but can return equally valuable insights if you sign up for a subscription and keep a few things in mind.

SEE IT

Overview

• After filling out your health history in an online telehealth session, if you’re approved, January will send you a CGM
• Once you attach the CGM to your arm, you log the food you’ve eaten, scan the sensor with your phone, and the January app shows your glucose levels in real-time
• You must also sync with an Apple Watch or an Oura Ring to record your activity levels
• After five days, January will provide detailed recommendations for foods to eat and activities, taking your preferences into account
• A one-month subscription costs $288, and an annual subscription is $380

Pros

• Provides feedback in real-time on how various foods will affect your glucose levels
• Includes a comprehensive database of foods. You can also enter using a QR code on-site in a store
• Fun to use
• Recommends activity to counteract high glucose levels
• Provides meal plans and activity recommendations based on your nutritional needs and preferences

Cons

• Somewhat expensive
• Might not be good for someone with a history of disordered eating around calorie restriction
• Sensor came out somewhat easily

Verdict: If you’re concerned about your risk of diabetes because of family history, physical health, or age, or you just want personalized recommendations on how to live healthier, the January AI system is a useful and fun tool.

What is a continuous glucose monitor (CGM)?

Continuous glucose monitors were originally developed in the 1980s to help diabetics keep tabs on their blood glucose, or blood sugar, levels. People with diabetes have trouble making insulin, a hormone secreted by the pancreas that allows glucose to be used by cells for energy. Glucose then remains in the bloodstream, keeping blood sugar levels high over time. Chronic high blood sugar can also damage the kidneys, heart, and nervous system.

While CGMs used to require users to prick their fingers to test their blood sugar, newer CGMs include a small sensor that goes under the skin. The sensor will then transmit readings of your glucose levels to a device that will analyze them. Pioneering CGM makers include Dexcom, which made the first CGM that didn’t require a finger pricking and got FDA approval for diabetics in 2016.

Increasingly, people who aren’t diabetic, including elite athletes, are using CGMs to get a more granular sense of their metabolic health. Other popular CGMs that keep popping up in my Instagram feed include Nutrisense and Levels. Tech sites have speculated for years about Apple’s possible plan to build a CGM into the Apple Watch. However, CGMs still require a medical prescription, and their use by people who haven’t been diagnosed with diabetes has generated debate in the medical community. One perspective published in the journal JAMA described CGMs for non-diabetics as a “waste of time and money.” 

Other doctors point to the more than 120 million Americans who either already have diabetes or are prediabetic. Peter Attia, M.D., who co-authored the bestselling book, Outlive: The Science and Art of Longevity, makes the case that the typical blood sugar tests that patients get annually don’t reveal daily spikes that can signal a brewing problem.

“In the vast majority of cases, today’s normal individual is tomorrow’s diabetic patient if something isn’t done to detect and prevent this slide,” Attia writes. Fluctuating glucose levels have also been associated with an increased risk of heart disease, cancer, and Alzheimer’s disease, he notes.

While I’m generally healthy, I was interested in learning more about my blood sugar levels and how they might affect my life. My parents had been diagnosed with Type II diabetes in their 40s, so I checked the family history box. After losing weight early in the pandemic, I put on some pounds last year. And despite training for my first marathon, I found that all the exercise wasn’t helping get me into better shape as easily as running did when I was younger. 

True, the lab results from the last time I was tested after a visit to my primary care doctor in September 2022 passed muster. My glucose level of 87 milligrams per deciliter (mg/dL) was in the middle of the normal range, but my hemoglobin A1C—the standard test that measures the average of blood glucose over 90 days—was 5.5%, on the high side of normal.

According to the CDC,  a reading of 99 mg/dL or lower is normal for fasting blood sugar, while 100 to 125 mg/dL signals that you’re prediabetic, and 126 mg/dL or higher indicates you have diabetes. Would seeing those spikes on my phone just after eating help me make better decisions?

The background

Monitoring daily fluctuations in blood sugar can provide a much better window into your metabolic health, says Noosheen Hashemi, January’s co-founder and CEO. She became passionate about a more holistic approach to health care after learning the truth about her parents’ medical conditions. Doctors failed to diagnose her father with prostate cancer while he was being treated for another cancer. And her mother’s heart failure was misdiagnosed as asthma.

“Once you fall into that sick journey, all sorts of things can happen to you,” Hashemi says. “So I became obsessed with: ‘How can we know sooner, what can we know, and why do we know so little?’”

She teamed up with Michael Snyder, Ph.D., chair of Genetics and Director of Genomics and Personalized Medicine at Stanford School of Medicine. Snyder was conducting research that revealed a population of people who looked to have healthy blood sugar levels actually frequently had spikes in which their glucose reached diabetic levels.

“He believed this was a ticking time bomb and that we should look into it,” Hashemi says. “That’s how we got started.”

That was more than five years ago. They’ve since used machine learning to develop a library of foods complete with nutritional information and incorporated data from their clinical studies and thousands of users to develop and refine models for predicting glucose spikes.

They also realized that most of the their users were not diabetics, but instead what Hashemi describes as “optimizers and discoverers”: fit people looking to optimize their health or people who had potential risk factors, such as a family history, like me. Hashemi is optimistic that the FDA will approve CGMs for non-diabetics next year.

The setup

People interested in using January have to complete a telehealth evaluation online. The process involves filling out an online form, not a virtual interaction with a live healthcare professional.

For $288 ($260 for the gear and $28 for the membership), you get a Freestyle Libre CGM, access to January AI’s glycemic food database and recommendations through its app, and $40 off an Oura Ring (Gen 2 or Gen 3) to track your activity. (You can also use an Apple Watch, which I did.) If you’re approved, the Freestyle Libre will arrive in the mail shortly. 

Easy-to-follow videos on the Freestyle LibreLink app showed me how to apply the CGM sensor. I felt a slight pin prick and mild soreness when I installed the sensor on my left upper arm. The app is connected to a medical practice based in California. After agreeing to use of my health data, I was up and running. 

Then using the January app, I was instructed how to scan the sensor with my phone and sync my Apple Watch. Once the sensor is active, it’s ready to deliver real-time glucose readings after each scan. Over the next five days, January’s AI would analyze my glucose levels, activity, and what I was eating and compare it to its thousands of users to predict my body’s response to various foods and exercise. “It takes inputs from your heart rate monitor and your food log and your CGM to build a digital twin for you,” Hashemi says. 

The performance

I began using January at the end of June, logging my meals and scanning the CGM. I found the food database reasonably comprehensive, although sometimes it took some scrolling down to find the exact food.

I was warned that the initial glucose levels could be either high or very low within the first 24 to 48 hours as the CGM calibrated to my system. My first blood sugar reading was very low—58 mg/dL—which got me googling hypoglycemia. 

Then I ate a small bowl of vegetable ramen leftover from a night out at a restaurant the night before. I scanned the CGM with my phone about 5 minutes after eating and found my glucose was in the normal range: 90 mg/dL.

The January app provides reports on the previous day in three categories: Nourish (calories, fiber intake, and macros); Move (post-meal activity, time exercised, and calories burned); and Recharge (fasting period, last-meal sleep gap, and sleep duration). After the five initial days of analysis, January’s AI notified me that it had created my digital twin and began making recommendations for food choices and activity.

I’ve never stuck with food logs in the past, but the ability to quickly see how specific items affected my blood sugar became something I looked forward to testing. I also discovered that requirement to log what I was eating provided additional incentive to eat better. I had been prioritizing protein over refined carbs over the past few months and was glad to see that eating Greek yogurt, flax seeds, and blueberries for breakfast got me a shoutout for protein and fiber goals. I also dialed back on the snacking that’s too easy to do when working from home about six feet from the fridge.

I felt compelled in the name of science to see how a slice of pesto pizza and a Rice Krispie treat would affect my readings. As expected, these foods spiked my blood sugar more than my virtuous breakfast. When I had a high reading, the app recommended a walk after the meal. The January app also provided alternatives based on your preferences (although I was wasn’t excited to replace chia seeds with dried spirulina).

You can also reach out through the app to a virtual health coach named Jan, who provides chatbot answers on everything from what you should eat for lunch to creating a new exercise plan. The company is also in the process of adding more FAQs, such as what is a normal glucose level. Hashemi is quick to point out, however, that January is not a healthcare provider, but it does provide lifestyle recommendations based on their (and your) data. 

In fact, January has explicit behaviors that it’s leading users toward, including adopting intermittent fasting, increasing fiber consumption, aligning calorie intake with activity level, getting post-meal movement, and reducing glucose-spiking foods.

I was doing reasonably well with all of these, but unfortunately, after eight days of testing, I accidentally dislodged my sensor while getting dressed. But January’s AI still provided plenty of valuable insights during the time I used it. My blood sugar was mostly low to normal, but I did see a few spikes that took me out of my normal range. And I did lose a few pounds and came to appreciate the importance of better discipline and regular meals. I did wish there was more information for people with readings on the low side.

But while the nudge toward intermittent fasting might be helpful for many (myself included), I saw how it could also cause problems for people with a propensity for disordered eating around calorie restriction. It concerned me that after I stopped logging meals, the app indicated on days when I didn’t enter food that the number of calories I consumed was “excellent.”

So, who should buy the January system?

Yes, $288 for a month’s subscription sounds expensive. But if you generally eat the same things, 30 days will give you plenty of time to analyze your health data and see how different foods affect you. I’m hopeful that glucose level monitoring will become more accessible and affordable, bearing in mind the estimated 96 million Americans over age 18 characterized as prediabetic.

Technological advances have made it possible for us to see our heart rate with a quick glance at our wrist, a luxury many of our parents didn’t have. Now, the ability to test our blood sugar is now almost as frictionless as posting on Instagram. If you’re concerned about your glucose levels due to family history or just want to fine-tune your health, January’s AI can help with daily insights and personalized recommendations. Just remember that it’s a tool and doesn’t replace regular visits to your healthcare provider. 

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Gary Flook served in the Air Force for 37 years, as a firefighter at the now-closed Chanute Air Force Base in Illinois and the former Grissom Air Force Base in Indiana, where he regularly trained with aqueous film forming foam, or AFFF—a frothy white fire retardant that is highly effective but now known to be toxic.

Flook volunteered at his local fire department, where he also used the foam, unaware of the health risks it posed. In 2000, at age 45, he received devastating news: He had testicular cancer, which would require an orchiectomy followed by chemotherapy.

Hundreds of lawsuits, including one by Flook, have been filed against companies that make firefighting products and the chemicals used in them.

And multiple studies show that firefighters, both military and civilian, have been diagnosed with testicular cancer at higher rates than people in most other occupations, often pointing to the presence of perfluoroalkyl and polyfluoroalkyl substances, or PFAS, in the foam.

But the link between PFAS and testicular cancer among service members was never directly proven — until now.

A new federal study for the first time shows a direct association between PFOS, a PFAS chemical, found in the blood of thousands of military personnel and testicular cancer.

Using banked blood drawn from Air Force servicemen, researchers at the National Cancer Institute and Uniformed Services University of the Health Sciences found strong evidence that airmen who were firefighters had elevated levels of PFAS in their bloodstreams and weaker evidence for those who lived on installations with high levels of PFAS in the drinking water. And the airmen with testicular cancer had higher serum levels of PFOS than those who had not been diagnosed with cancer, said study co-author Mark Purdue, a senior investigator at NCI.

“To my knowledge,” Purdue said, “this is the first study to measure PFAS levels in the U.S. military population and to investigate associations with a cancer endpoint in this population, so that brings new evidence to the table.”

In a commentary in the journal Environmental Health Perspectives, Kyle Steenland, a professor at Emory University’s Rollins School of Public Health, said the research “provides a valuable contribution to the literature,” which he described as “rather sparse” in demonstrating a link between PFAS and testicular cancer.

More studies are needed, he said, “as is always the case for environmental chemicals.”

Not ‘Just Soap and Water’

Old stocks of AFFF that contained PFOS were replaced in the past few decades by foam that contains newer-generation PFAS, which now also are known to be toxic. By congressional order, the Department of Defense must stop using all PFAS-containing foams by October 2024, though it can keep buying them until this October. That’s decades after the military first documented the chemicals’ potential health concerns.

A DoD study in 1974 found that PFAS was fatal to fish. By 1983, an Air Force technical report showed its deadly effects on mice.

But given its effectiveness in fighting extremely hot fires, like aircraft crashes and shipboard blazes, the Defense Department still uses it in operations. Rarely, if ever, had the military warned of its dangers, according to Kevin Ferrara, a retired Air Force firefighter, as well as several military firefighters who contacted KFF Health News.

“We were told that it was just soap and water, completely harmless,” Ferrara said. “We were completely slathered in the foam — hands, mouth, eyes. It looked just like if you were going to fill up your sink with dish soap.”

Photos released by the Defense Visual Information Distribution Service in 2013 show personnel working in the foam without protective gear. The description calls the “small sea of fire retardant foam” at Travis Air Force Base in California “non-hazardous” and “similar to soap.”

“No people or aircraft were harmed in the incident,” it reads.

There are thousands of PFAS chemicals, invented in the 1940s to ward off stains and prevent sticking in industrial and household goods. Along with foam used for decades by firefighters and the military, the chemicals are in makeup, nonstick cookware, water-repellent clothing, rugs, food wrappers, and a myriad of other consumer goods.

Known as “forever chemicals,” they do not break down in the environment and do accumulate in the human body. Researchers estimate that nearly all Americans have PFAS in their blood, exposed primarily by groundwater, drinking water, soil, and foods. A recent U.S. Geological Survey study estimated that at least 45% of U.S. tap water has at least one type of forever chemical from both private wells and public water supplies.

Health and environmental concerns associated with the chemicals have spurred a cascade of lawsuits, plus state and federal legislation that targets the manufacturers and sellers of PFAS-laden products. Gary Flook is suing 3M and associated companies that manufactured PFAS and the firefighting foam, including DuPont and Kidde-Fenwal.

Congress has prodded the Department of Defense to clean up military sites and take related health concerns more seriously, funding site inspections for PFAS and mandating blood testing for military firefighters. Advocates argue those actions are not enough.

“How long has [DoD] spent on this issue without any real results except for putting some filters on drinking water?” said Jared Hayes, a senior policy analyst at the Environmental Working Group. “When it comes to cleaning up the problem, we are in the same place we were years ago.”

On a Mission to Get Screening

The Department of Veterans Affairs does not recommend blood testing for PFAS, stating on its website that “blood tests cannot be linked to current or future health conditions or guide medical treatment decisions.”

But that could change soon. Rep. Dan Kildee (D-Mich.), co-chair of the congressional PFAS Task Force, in June introduced the Veterans Exposed to Toxic PFAS Act, which would require the VA to treat conditions linked to exposure and provide disability benefits for those affected, including for testicular cancer.

“The last thing [veterans] and their families need to go through is to fight with VA to get access to benefits we promised them when they put that uniform on,” Kildee said.

Evidence is strong that exposure to PFAS is associated with health effects such as decreased response to vaccines, kidney cancer, and low birth weight, according to an expansive, federally funded report published last year by the National Academies of Sciences, Engineering, and Medicine. The nonprofit institution recommended blood testing for communities with high exposure to PFAS, followed by health screenings for those above certain levels.

It also said that, based on limited evidence, there is “moderate confidence” of an association between exposure and thyroid dysfunction, preeclampsia in pregnant women, and breast and testicular cancers.

The new study of Air Force servicemen published July 17 goes further, linking PFAS exposure directly to testicular germ cell tumors, which make up roughly 95% of testicular cancer cases.

Testicular cancer is the most commonly diagnosed cancer among young adult men. It is also the type of cancer diagnosed at the highest rate among active military personnel, most of whom are male, ages 18 to 40, and in peak physical condition.

That age distribution and knowing AFFF was a source of PFAS contamination drove Purdue and USUHS researcher Jennifer Rusiecki to investigate a possible connection.

Using samples from the Department of Defense Serum Repository, a biobank of more than 62 million blood serum specimens from service members, the researchers examined samples from 530 troops who later developed testicular cancer and those of 530 members of a control group. The blood had been collected between 1988 and 2017.

A second sampling collected four years after the first samples were taken showed the higher PFOS concentrations positively associated with testicular cancer.

Ferrara does not have testicular cancer, though he does have other health concerns he attributes to PFAS, and he worries for himself and his fellow firefighters. He recalled working at Air Combat Command headquarters at Joint Base Langley-Eustis in Virginia in the early 2010s and seeing emails mentioning two types of PFAS chemicals: PFOS and perfluorooctanoic acid, or PFOA.

But employees on the base remained largely unfamiliar with the jumble of acronyms, Ferrara said.

Even as the evidence grew that the chemicals in AFFF were toxic, “we were still led to believe that it’s perfectly safe,” Ferrara said. “They kept putting out vague and cryptic messages, citing environmental concerns.”

When Ferrara was working a desk job at Air Combat Command and no longer fighting fires, his exposure likely continued: Joint Base Langley-Eustis is among the top five most PFAS-contaminated military sites, according to the EWG, with groundwater at the former Langley Air Force Base registering 2.2 million parts per trillion for PFOS and PFOA.

According to the EPA, just 40 parts per trillion would “warrant further attention,” such as testing and amelioration.

The Defense Department did not provide comment on the new study.

Air Force officials told KFF Health News that the service has swapped products and no longer allows uncontrolled discharges of firefighting foam for maintenance, testing, or training.

“The Department of the Air Force has replaced Aqueous Film Forming Foam, which contained PFAS, with a foam that meets Environmental Protection Agency recommendations at all installations,” the Air Force said in a statement provided to KFF Health News.

Both older-generation forever chemicals are no longer made in the U.S. 3M, the main manufacturer of PFOS, agreed to start phasing it out in 2000. In June, the industrial giant announced it would pay at least $10.3 billion to settle a class-action suit.

Alarmed over what it perceived as the Defense Department’s unwillingness to address PFAS contamination or stop using AFFF, Congress in 2019 ordered DoD to offer annual testing for all active-duty military firefighters and banned the use of PFAS foam by 2024.

According to data provided by DoD, among more than 9,000 firefighters who requested the tests in fiscal year 2021, 96% had at least one of two types of PFAS in their blood serum, with PFOS being the most commonly detected at an average level of 3.1 nanograms per milliliter.

Readings between 2 and 20 ng/mL carry concern for adverse effects, according to the national academies. In that range, it recommends people limit additional exposure and screen for high cholesterol, breast cancer, and, if pregnant, high blood pressure.

According to DoD, 707 active and former defense sites are contaminated with PFAS or have had suspected PFAS discharges. The department is in the early stages of a decades-long testing and cleaning process.

More than 3,300 lawsuits have been filed over AFFF and PFAS contamination; beyond 3M’s massive settlement, DuPont and other manufacturers reached a $1.185 billion agreement with water utility companies in June.

Attorneys general from 22 states have urged the court to reject the 3M settlement, saying in a filing July 26 it would not adequately cover the damage caused.

For now, many firefighters, like Ferrara, live with anxiety that their blood PFAS levels may lead to cancer. Flook declined to speak to KFF Health News because he is part of the 3M class-action lawsuit. The cancer wreaked havoc on his marriage, robbing him and his wife, Linda, of “affection, assistance, and conjugal fellowship,” according to the lawsuit.

Congress is again trying to push the Pentagon. This year, Sen. Jeanne Shaheen (D-N.H.) reintroduced the PFAS Exposure Assessment and Documentation Act, which would require DoD to test all service members — not just firefighters — stationed at installations with known or suspected contamination as part of their annual health checkups as well as family members and veterans.

The tests, which aren’t covered by the military health program or most insurers, typically cost from $400 to $600.

In June, Kildee said veterans have been stymied in getting assistance with exposure-related illnesses that include PFAS.

“For too long, the federal government has been too slow to act to deal with the threat posed by PFAS exposure,” Kildee said. “This situation is completely unacceptable.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

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As summer winds down, there’s a new COVID variant on the rise. EG.5.1, nicknamed the “Eris” variant, has become the dominant strain in the US, making up 17.3 percent of cases in the US. 

The variant is a descendant of the Omicron, which itself had become the dominant COVID subtype by fall 2022. There’s not a lot of data right now on how severe or infectious this subvariant is compared to its parent strain or the other ones we’ve faced in the past. But based on its increasing caseloads, experts like Scott Roberts, an infectious disease specialist at Yale University, predict this one will stick around through the winter. “The question is how long will it stay, and will [Eris] continue to evolve in a few months.”

Fortunately, this isn’t 2020. We’re more prepared to treat COVID. Updated vaccine boosters are on the way this fall that will provide immune defenses against these types of strains. “We are optimistic that the new, updated boosters will offer ample protection against this current variant,” as Roberts says.

Where did Eris come from?

The EG.5.1 variant has been unofficially called Eris on social media after the Greek goddess of chaos, strife, and discord. Genetic sequencing suggests it is a descendant of an Omicron subvariant called XBB1.5, which was responsible for an outbreak of COVID infections earlier this year. “It’s part of this ongoing evolutionary tree from Omicron,” Roberts explains. Eris differs somewhat from others in the XBB lineage because there are new mutations on its spike protein, the part of the virus that lets it latch to and infect cells. 

Where is Eris spreading?

The World Health Organization has labeled Eris as a “variant of interest” as it spreads worldwide. Recently, it has caused COVID cases to spike in the UK. In the US, the latest CDC numbers show Eris is concentrated on both coasts. States like New York have been the hardest, with a 55 percent surge in COVID infections caused by the Eris variant above the previous week. Overall, though, the national test positivity rate is down to 9 percent, when it was nearly 14 percent this time last year, according to the CDC. 

[Related: Your guide to COVID testing for the unforeseeable future]

Linda Yancey, an infectious disease specialist at Memorial Hermann Health System in Houston, says health agencies likely noticed the outbreak in these two countries thanks to aggressive surveillance. “If we could expand out to the rest of the world, the picture would almost certainly look the same,” she says. There have been reports of Eris traveling through Asia, too, and possibly through Australia. 

Is Eris more contagious or dangerous?

The new variant still acts very similar to all the other Omicron strains, says Yancey. Evidence so far does not seem to suggest that it causes more severe illness, and the number of COVID deaths has not increased. The symptoms reported in Eris infections are familiar signs of COVID, including fever, cough, fatigue, and headaches.

In general, Omicron strains cause less severe disease because the virus doesn’t reach most people’s lungs, Yancey says. “So: Yay, they tend to cause less serious illness,” she says. “But, boo, they also tend to cause asymptomatic disease, so people don’t know they are infected and don’t isolate or wear masks.” No official studies have yet calculated Eris’s rate of transmission, and Yancey says that as a new strain it would make sense that it would at least be more contagious. “New strains have to out-compete old strains so the new ones are generally a little bit more easy to transmit.”

Do the vaccines protect against Eris?

There are no vaccines that specifically target EG.5, and scientists are still unsure whether these mutations help Eris bypass vaccine-induced immunity. However, since there are spike protein mutations and an increase in COVID hospitalizations, Roberts says the new variant is likely capable of thwarting some immune defenses. Still, he says, “we predict that vaccine immunity will still hold up quite well against this new Eris variant.” 

From his experience, the ones who remain most at risk appear to be the unvaccinated. “In our hospital, we have seen almost a tripling or quadrupling over the past several weeks,” Roberts adds, though cases remain “well below what we saw last summer and winter.” People who are not vaccinated or have not received all of the shots make up the majority of those hospitalizations. 

[Related: What’s the difference between COVID, flu, and cold symptoms?]

For people who are unvaccinated, Roberts advises not to wait and to get last year’s bivalent booster. He says it should still provide some protection against this current variant, because it is a descendent of Omicron, which that vaccine has shown to protect against. 

Those who are up to date on their vaccinations do not need to re-up again and should instead wait for October’s booster. The new booster won’t include the specific EG.5 subvariant, but it will target the XBB strains. Both Roberts and Yancy recommend getting the booster when it rolls out this fall.

How concerned should we be?

Both infectious disease experts agree people need to be aware of—but not worried about—Eris. Expect to see a wave of cases as the US enters the winter months, but it should not be as big as those in past years. “We have a lot of herd immunity now compared to where we were a year ago,” says Roberts. “Every year as we go on, we’ll see successive decreases in the severity of waves.”

Beyond getting an updated booster, Roberts says to assess your personal risk tolerance levels. While we shouldn’t foresee any mask mandates, if you fall under the high-risk category, it’s a good idea to mask up when in crowds or indoor spaces with poor ventilation. You’ll want to keep some rapid COVID tests at home in case you need to test. Continue washing your hands and staying home when you’re sick to avoid getting and spreading Eris to others.

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The Centers for Disease Control and Prevention (CDC) is recommending that all infants under eight months old should get a new antibody shot aimed to protect the body against severe cases of respiratory syncytial virus (RSV). The agency’s Advisory Committee on Immunization Practices (ACIP) voted unanimously on August 3 to recommend the injection to protect babies beginning this fall. 

[Related: FDA approves long-acting medication to protect babies from RSV.]

In July, the Food and Drug Administration approved nirsevimab, which is the first long-acting medication to protect babies and toddlers from RSV. The lung-attacking virus sends about 58,000 children under five to the hospital, and kills 100 to 300 infants every year in the United States. RSV season typically lasts from November through March.

CDC director Mandy Cohen signed off on the recommendation and it will be added to the CDC’s childhood immunization schedule. ACIP also unanimously recommended that certain infants between the ages of eight to 19 months should receive a second dose of nirsevimab to help them stay healthy during their second RSV season if they have any underlying health issues that put them at a higher risk of hospitalization. 

“As we head into respiratory virus season this fall, it’s important to use these new tools available to help prevent severe RSV illness,” Cohen said in a statement. “I encourage parents of infants to talk to their pediatricians about this new immunization and the importance of preventing severe RSV.”

In a second unanimous vote, ACIP also recommended that certain infants ages eight to 19 months get a second dose of nirsevimab to help them through their second RSV season, if they have underlying health issues that put them at higher risk for hospitalization.

Vaccines for older adults were FDA approved in May, but there are currently no vaccines for babies. The FDA is expected to make a decision on an RSV vaccine for pregnant people, with the goal of passing along protection on to newborns, later in August.

Importantly, nirsevimab is not a vaccine for RSV. It is a lab-made antibody for babies that helps their immune systems fight off the virus and is also the first first form of passive immunization added to the routine childhood immunization schedule. Passive immunizations do not require the body to manufacture antibodies against pathogens the way that vaccines do. Instead, they sent protective antibodies to attack the virus.

[Related: How our pandemic toolkit fought the many viruses of 2022.]

ACIP voted to add the antibody shot to the federally funded Vaccines for Children Program. This program provides free immunizations to children who may have difficulty accessing them. 

Nirsevimab was developed by AstraZeneca and Sanofi and is expected to be ready for the fall RSV season and will be sold under the brand name Beyfortus. Sanofi reportedly said that if this shot is recommended for all infants, it will cost $495 per dose for private payers and $395 through Vaccines for Children. 

The cost of the drug could make it difficult for some doctors to stock up on nirsevimab and complicate billing. However, getting this recommendation from ACIP means that families will not pay an out-of-pocket cost due to the Affordable Care Act. It may take up to 18 months for this coverage to kick-in, as insurers have a year to add implement coverage of new treatments that will then take effect in the new plan year. 

According to CBS News, director of the National Center for Immunization and Respiratory Diseases José Romero closed the meeting by saying, “I would be remiss if I didn’t say that today is a historic event. I think that we will look back on this, in a short period of time, and see what a major impact this vote has had on the health and wellbeing of children in the United States. I think that this will mark one of the major accomplishments of the ACIP.”

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The next time you go grocery shopping, don’t forget to pick up a case of kombucha. Tea lovers have long hailed the funky, fermented drink for keeping the gut healthy and running smoothly, and now we can tack on diabetes management to the list of potential benefits.

A small study published on August 1 in the journal Frontiers in Nutrition found kombucha stopped spikes in blood sugar levels for adults with Type 2 diabetes. With the number of Americans with diabetes tripling in the last three decades, the beverage could potentially help lower blood sugar levels and prevent the condition from worsening in pre-diabetics. While the authors have several ideas on how this works, they haven’t found a clear answer or connection just yet.

Kombucha, which is cultured with bacteria and yeast, has been around for centuries but has grown in popularity around the world in the last two decades. “Consuming one to two 8-ounce servings of kombucha daily offers health benefits while keeping sugar and calorie intake in check,” explains Kelsey Costa, a registered dietitian nutritionist at the National Coalition on Healthcare who was not involved in the study. Most brands sold in stores are typically packaged in 16-ounce bottles, making up two servings.

A first-of-its-kind human trial 

Chagai Mendelson, a medical resident at MedStar Georgetown University Hospital and lead author of the new research, came up with the trial idea after speaking with diabetic patients on ways to cut sugar from their diet. His standard medical advice would involve drinking more water and less sugary beverages, but after noticing that more people were drinking kombucha, he was unsure whether the slightly sweet tea was safe to drink. When diving into the research, he noticed several animal studies where kombucha improved glycemic function or helped regenerate beta cells (cells in the pancreas that produce insulin, but can be overworked to the point of death in people with diabetes) Yet he could not find any clinical trials looking at how kombucha affected diabetic individuals in a real-world setting. 

So, Mendelson and his team recruited 12 diabetic patients for a four-month-long pilot study. Finding volunteers was challenging, he says, because there was no funding to pay the subjects for their time and the criteria was highly selective—they had to have Type 2 diabetes and zero history of drinking kombucha. There was also attrition, where people dropped out in the middle of the study or did not respond during follow-up attempts. Ultimately, only seven participants completed the experiment.

[Related: 2 easy homemade electrolyte drinks that actually work]

To compensate for the small numbers, the authors took a crossover-trial approach. Each participant served as their own control to allow the team to look at the difference in sugar levels when they drank kombucha versus when they didn’t. Half of the volunteers drank one daily cup of kombucha for four weeks, while the other six drank fizzy non-fermented ginger water that acted as the placebo. They then went through a two-month “wash-out period” where the effects of kombucha would go away, allowing people’s metabolisms to reset. Afterward, the group switched roles; neither half knew which drink they were receiving at any point in the trial. “Even though there’s fewer participants, we get two data points from each one. And it also allows us to make sure that some of that variability is accounted for,” Mendelson explains.

How kombucha might affect blood sugar

After four weeks of drinking kombucha, people went from an average blood sugar level of 164 milligrams per deciliter to 116, which falls well within the American Diabetes Association’s healthy range recommendations. Some individuals were also taking insulin when their blood sugar levels were measured, and could have been on restricted diets.

Mendelson has several thoughts about why regular kombucha intake might make a difference. The first is the substitution theory, where the tea is simply replacing sugary drinks like soda and fruit juice that people typically pair with their meals. The second is the microbiome theory. Kombucha is a great source of probiotics and drinking it helps build a diverse and healthier gut bacteria that aid in processing nutrients and food. “As you’re taking more probiotics, your gut is able to digest carbohydrates in a way where they are released to the blood in a more steady flow,” Mendelson says. “That helps to avoid having high blood sugar after a meal.”

[Related: Kombucha may have a surprising new use in tech]

The third but less popular explanation is that the ingredients in kombucha are helping to create new beta cells. Studies on diabetic rats have shown beta cells can be regenerated by potentially blocking certain enzyme activity in the pancreas that would normally promote carbohydrate digestion, but it’s less clear whether that would translate in humans. The final hypothesis is that when patients have more acetic acid—the chemical compound responsible for kombucha’s acidic taste and smell—in their gut, it causes their digestive system to slow down. That leads to slower absorption of carbohydrates and a gradual, not rapid, increase in blood sugar.

The tea is not a cure

While kombucha is a healthy alternative to sweeter drinks, Mendelson cautions people not to think of it as some magic cure-all. The trial does not provide enough evidence to definitively say it will work better than medication and other healthy dietary habits for reducing blood sugar. 

It’s also possible that kombucha may not help at all. Jorge Moreno, an obesity medicine specialist at Yale Medicine who was not involved in the study, notes two major concerns with the trial. First, the small sample size increases the margin of error and inflates the chances of a false connection between kombucha and blood sugar levels. Second, nine of the 12 participants were using insulin, and their doses could have fluctuated. (Mendelson says people were asked to self-report any changes with their insulin use.) “If the dosage of insulin increased for these participants, that would also lower the glucose blood level and affect their results. More research is needed,” Moreno notes.

[Related: FDA approves first drug that can delay onset of Type 1 diabetes]

Kombucha may not help everyone with Type 2 diabetes, but the trial shows it’s one of the better drinks they can choose from. If you do want to test the benefits out yourself, Mendelson suggests pairing your diabetes medication with the tea to avoid dangerous blood sugar spikes and lulls.

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Tick season is not only starting sooner—it’s becoming a year-round event. While April through September are usually the most active months, the pesky eight-legged parasites are biting people and animals much earlier in the year than expected. The increasing tick bites are leading to a rise in a variety of tick-borne diseases, including some that were previously uncommon.

One reason for the hike in tick-transmitted illnesses like alpha-gal, Lyme, and babesiosis is because humans are expanding towns and cities into previously forested areas. Andrew Handel, a pediatric infectious disease specialist in Stony Brook Medicine, says cutting down forests creates an edge habitat—when one habitat type meets another—which presents more opportunity for common tick hosts such as deer and mice to interact with humans. 

[Related: A guide to the tick species every American should know]

Climate change is another culprit. Changes in rain and temperature have morphed regions with low rates of tick-borne diseases into a more palatable place for the parasites to live. What’s more, warmer conditions are getting ticks to wake up earlier from their winter sleep and have more time to bite nearby mammals. “As we see more mild winters, we’re absolutely going to see more tick-borne diseases,” says Handel.

The best thing to do is to stay aware of how ticks are circulating in your area. Even if you don’t live in the Northeast, you may be at risk for other tick-borne diseases. Knowing what to watch out for in spring, summer, and even other seasons can help treat and potentially prevent future tick bites—and the diseases that follow.

Alpha-gal syndrome

A bite from the lone star tick can make you allergic to red meat for life. The unusual condition takes root when someone becomes highly sensitive to a sugar molecule called alpha-gal that’s found in most mammals. People who develop the allergy cannot eat red meat (fish and birds are safe to consume) or mammal-based products like dairy and gelatin. They may also be restricted in using certain medication such as heparin, which uses pig intestines. An allergic reaction can range from hives and nausea to more life-threatening reactions like anaphylactic shock.

Alpha-gal syndrome has been a rare but increasing tick-borne condition. In 2009, there were only 24 alpha-gal cases reported in the US. By 2021, the number was estimated to be around 34,000. And even newer surveys estimate that around 450,000 Americans might be living with the diagnosed or undiagnosed condition.

While saliva from the lone star tick seems to trigger the mammalian allergy, deer tick bites are suspected of also causing it. According to the CDC, lone star ticks have concentrated in large numbers across the country. They are found in the southeastern, eastern, and south-central US states extending from Maine to central Texas and Oklahoma. 

There is no cure for alpha-gal syndrome. Instead, people need to learn to avoid certain foods and mammal-based products. Symptoms are managed using antihistamines and corticosteroids.

Babesiosis

Babesiosis is a parasitic infection transmitted by the bite of deer ticks (also known as black-legged ticks). These ticks are about the size of a poppy seed and found on small mammals like the white-footed mice living in the Northeast and upper Midwest. Minnesota and Wisconsin are two Midwestern states with endemic transmission of babesiosis.

Once the Babesia parasite enters the human body, it targets red blood cells. The parasites infect and destroy red blood cells by forcing their cell membrane to break open. A tremendous loss of red blood cells can, over time, cause hemolytic anemia. “It’s actually the same way that malaria works, and is why it’s called ‘the malaria of the Northeast,’” says Handel.

Babesiosis is treatable. Your doctor would prescribe a seven- to 10-day course of antibiotics if you are severely ill. Some people are at a higher risk of complications from anemia—people who are immunocompromised, those without a spleen, and newborn babies—and may need to get blood transfusions or other supportive care.

Lyme disease

Lyme disease is also spread through deer ticks. “These ticks carry and spread multiple diseases,” explains Chad Cross, a researcher at the University of Nevada, Las Vegas who studies parasites and vector-borne diseases. “If you are bitten by one, there’s always the possibility of being infected by more than one disease agent at the same time.”

While the CDC estimate shows 476,000 Lyme disease cases in the US each year, Cross states there are “at least 10 times more cases of Lyme disease than are actually reported” to the department. One reason for the discrepancy is that most cases are asymptomatic. When people do show symptoms, the fatigue and chills they exhibit can be mistaken for another condition. If left untreated, there is a risk of developing neurological problems such as facial paralysis and nerve damage to the limbs. Chronic lyme can lead to a host of persistent issues, too, many of which are still less understood. 

[Related: Biologists successfully hatched gene-edited ticks for the first time]

Most early Lyme disease cases are curable with a two- to four-week regimen of oral antibiotics such as doxycycline and amoxicillin. However, some patients may continue to experience pain, fatigue, and concentration issues six months after treatment. 

Anaplasmosis

Anaplasmosis manifests as a flu-like illness in humans. The bacterium is present in deer ticks in the Northeast and Midwestern US. The Western blacklegged tick, most prevalent around the coast of California, Oregon, and Washington, can also spread the pathogen. There has been an upward trend of anaplasmosis cases from 348 cases in 2000 to 5,655 cases in 2019.

Similar to Lyme disease, people who develop anaplasmosis develop nonspecific symptoms such as fever and muscle aches. If left untreated, it may turn fatal with some developing severe bleeding problems and organ failure. Handel says doxycycline is the most effective treatment option.

Powassan virus infection

Three tick species carry the Powassan virus: the groundhog tick, the squirrel tick, and the deer tick. Of those, the deer tick is the one that often bites and infects humans. Nearly all cases of this rare virus have occurred in the Northeast and Great Lakes region.

The virus causes mild symptoms such as headache, vomiting, and fever. By the time a diagnosis is made, Handel says about half of the patients present some type of neurologic deficit. People may also continue to show neurological problems, such as chronic headaches and memory problems after recovery.

Because there are only about 20 to 30 cases a year, Handel says there’s not a lot of medical research on how to treat it. There is no cure or antivirals to treat Powassan virus. Instead, infected individuals are given fluids, over-the-counter medications, and other supportive care to ease symptoms while the immune system fights off the infection.

Rocky Mountain spotted fever

There are two main ticks responsible for spreading rocky mountain spotted fever: the Rocky Mountain wood tick and the American dog tick. Cross says the American dog tick is very common out East while the Rocky Mountain wood tick is found in the West. Despite its name, Cross says Rocky Mountain spotted fever is being found more in the East and South than in the actual Rocky Mountain region. The less-common brown dog tick has also caused several cases along the US-Mexico border. The disease is part of a larger class of illnesses that strike thousands of people in the states each year.

The most noticeable sign is a rash that looks like red splotches or pinpoint dots in the first three days after getting bit. If treated with either doxycycline or an antibacterial agent within the first one to four days, the symptoms won’t worsen. Otherwise, the disease can be fatal. After a week, Cross says that people can develop swelling in the brain, life-threatening respiratory problems, and a coma-like state. Those who recover from severe illness may be left with permanent disability, such as paralysis or amputation of limbs.

Reduce your chances of tick infections

These days, ticks are a threat across most of the US and in practically every season. Experts warn that cases will only continue to rise as ticks expand to previously uninhabitable areas. 

[Related: Climate change could introduce humans to thousands of new viruses]

Your best bet at avoiding tick-borne diseases is to keep the pests off your body. Rather than staying indoors for the rest of your life, both experts recommend spraying tick and mosquito repellant. “DEET is what we usually recommend at 20 to 30 percent,” says Handel. If you’re going to be hiking or spending a lot of time outside, learn how to handle an insecticide called permethrin. Handel advises leaving your clothes overnight in the solution to kill any insect on contact. The repellency lasts for up to 10 washes. But make sure to only use it on your clothes or gear—it’s not meant to be sprayed directly on human skin.

Remember, you can pick up ticks even if you’re not an avid hiker or camper. Ticks tend to live on tall grass, meaning they might climb on you at the park or even on your own property. Avoid rubbing up on any tall grass and keep to the middle when walking down a path. Wearing long sleeves and tucking your pants inside your socks further prevents any openings for the pests to crawl into if they latch on your clothes. 

Once you get home, immediately wash your clothes in high heat and perform a tick check for any stragglers. If you take your pet outdoors (even if it’s just the yard), you’ll want to check them daily for ticks as well. There are also topical medications that you or a vet can apply to your pet to control for any external parasites. If you or any members of your household are feeling unwell, always let your doctor know that you’ve been in wooded areas or places with high tick circulation.

“These tick-borne diseases have been around for a long time and they’re going to become more common over time,” says Handel. “But by following these steps you can keep yourself safe and still enjoying the outdoors without having to have too much anxiety about catching one of these infections.”

This post has been updated. It was originally published on March 27, 2023.

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The living relatives of Henrietta Lacks have reached a settlement with the biotechnology company that took her cervical cells without her knowledge over 70 years ago. Lacks’ descendants sued Massachusetts-based Thermo Fisher Scientific in 2021, accusing the leaders of profiting off of a racist medical system.

[Related: Five Reasons Henrietta Lacks is the Most Important Woman in Medical History.]

“The exploitation of Henrietta Lacks represents the unfortunately common struggle experienced by Black people throughout history,” the complaint from the family reads. “Too often, the history of medical experimentation in the United States has been the history of medical racism.”

In 1951, tissue was taken from a tumor on Lacks’ cervix when she sought treatment for cervical cancer at Johns Hopkins. Scientists quickly discovered that these “HeLa cells” had some incredibly special properties. They survived and thrived in laboratories, instead of quickly dying after being taken out of the body. The HeLa cell line has been reproduced numerous times ever since, and has become a cornerstone of modern medicine. Lacks’ cells have become a baseline for medicine and enabled numerous medical and scientific innovations including the development of genetic mapping, cancer treatments, HIV/AIDS treatments, and the polio and COVID-19 vaccines. 

Despite Lacks’ outsized impact, her family had never been compensated. Currently, the terms of the settlement are confidential. Prominent civil rights attorney Ben Crump represented the Lack family and said that both parties are “pleased” the matter was resolved outside of court, according to the Associated Press. The announcement also came on August 1, which would have been Lacks’ 103rd birthday.

“I can think of no better present… than to give her family some measure of respect for Henrietta Lacks, some measure of dignity for Henrietta Lacks, and most of all some measure of justice for Henrietta Lacks,” Crump said at a press conference on Tuesday morning, according to CBS News. The family present at the press conference included Lacks’ only living son and some of her grandchildren.

[Related: Racism is undeniably a public health issue.]

Lacks was a tobacco farmer from southern Virginia and was raising five children when the tumor on her cervix was discovered. She was only 31 when she died and was buried in an unmarked grave.

In a statement, Johns Hopkins Medicine officials said they reviewed all of the university’s interactions with Lacks and her family after the publication of Rebecca Skloot’s bestselling book, The Immortal Life of Henrietta Lacks in 2010. While acknowledging an ethical responsibility, Johns Hopkins said the medical system “has never sold or profited from the discovery or distribution of HeLa cells and does not own the rights to the HeLa cell line.”

On July 25, Senators Chris Van Hollen (D-Maryland) and Ben Cardin (D-Maryland) both introduced a bill to posthumously award Lacks the Congressional Gold Medal. “Henrietta Lacks changed the course of modern medicine,” Van Hollen said in a statement announcing the bill. “It is long past time that we recognize her life-saving contributions to the world.”

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More people in the United States are dying from causes related to excessive alcohol consumption since 1999. Surprisingly, this is particularly true for American women, according to a study published July 28 in the journal JAMA Network Open. While men are roughly three times more likely than women to die from alcohol use, the gap has narrowed and the risk to women has grown recently.  

[Related: COVID lockdown drinking habits led to a rise in deaths from alcoholic liver disease.]

The study looked at Centers for Disease Control and Prevention (CDC) data on more than 600,000 deaths linked to alcohol between 1999 and 2020. The data included deaths from alcoholic liver disease, alcohol poisoning, acute intoxication, alcoholic cardiomyopathy, and mental and behavioral disorders that can be linked to alcohol consumption, and other causes.

It found that alcohol-related deaths steadily increased in the United States in that period. However, from 2018 to 2020, the rate increased by 14.7 percent for women compared to 12.5 percent for men. The study also found rising rates among older women in particular. Alcohol-related deaths rose in women over 65 and older by 6.7 percent from 2012 to 2020, compared with a 5.2 percent increase per year in men 65 and older. 

According to the authors, this shift does not necessarily mean that women in this age group are drinking more, but could point to “the larger burden of accumulating harms of chronic alcohol use among female individuals.”

While this study did not point to the reasons behind this increase, co-author and assistant professor of population health at Hofstra University Ibraheem Karaye offered a few potential theories to The New York Times. Karaye said that alcohol consumption is likely increasing among women and that alcohol affects women’s bodies differently. Women’s bodies typically have less fluid to dilute alcohol, which can result in higher blood-alcohol concentrations, which may make women more vulnerable to health complications, according to Karaye.

Stress is also a major factor in alcohol misuse among both men and women. The narrowing gap could reflect an increase in both stress and stress-related disorders among women, according to the team. 

[Related: A powerful combo of psilocybin and therapy might help people overcome alcohol use disorder.]

Excessive drinking during the COVID-19 pandemic has also increased alcoholic liver disease deaths, with a recent report from KFF Health News finding that the condition killed more Californians than car accidents or breast cancer. The lockdowns made people feel isolated, depressed, stressed, and anxious, says KFF’s Philip Reese, which led to some increases in drinking and an increase in alcohol sales.

Additionally, shifting attitudes towards heavy drinking by women may be a factor.  Associate professor in the division of gastroenterology and liver disease at NYU Langone Health Lisa Ganjhu told NBC News that she regularly sees women who are not aware of how physically toxic it can be. 

“The article didn’t surprise me. Women are overusing alcohol with more frequency now. I’ve had to talk to a fair number of women about their alcohol use,” said Ganjhu, who was not affiliated with the new study. “I had one patient who developed pancreatitis from drinking ask me when she could start drinking again. She said it wasn’t acceptable to not drink with clients. It’s mind-boggling.”

Regardless of gender, Karaye agrees with most physicians that “reducing or eliminating exposure [to alcohol] at any point would be valuable.” The National Institute on Alcohol Abuse and Alcoholism’s Rethinking Drinking program can help people evaluate alcohol usage and create plans to scale down or quit drinking. 

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This article is republished from The Conversation.

As a veterinary science researcher, equine surgeon and sports medicine and rehabilitation specialist, I’ve seen firsthand the similarities between horses and humans.

Both horses and people with endocrine disorders like Type 2 diabetes can suffer multiple types of musculoskeletal disorders. For example, horses with pituitary pars intermedia dysfunction—similar to Cushing’s disease in people—suffer from tendon and ligament degeneration. Horses can also experience muscle loss, which can cause joint instability. That, and the chronic low-grade inflammation associated with endocrine disorders, can contribute to osteoarthritis.

There’s a principle in medicine called One Health, which says that animals, humans and the environment are inextricably connected—for one to be healthy, all must be healthy. It also means that we can learn a lot about our own health by studying the health of animals, and vice versa, including the many parallels in endocrine disorders between humans and horses.

Human and horse endocrine systems

Your endocrine system produces hormones that support many of your body’s basic functions, including growth and development, metabolism, sleep and more. Your hormones also play a role in the health of your bones, tendons and ligaments. Some endocrine disorders change how your body produces and releases hormones and can lead to osteoporosis, arthritis, ligament injury and other orthopedic diseases.

Humans aren’t the only species affected by this dynamic—horses are, too. In fact, approximately 20 percent of horses and over 34 percent of people in the U.S. are affected by endocrine disorders such as metabolic syndrome. These disorders are often accompanied by obesity.

For both species, the degree to which endocrine disorders are connected to obesity and its associated negative health effects is complex. As mammals, horses and people share similar anatomy and endocrine physiology, and researchers have noted their parallel genetic links between obesity and metabolic disease.

Like people, obese horses with endocrine disorders often develop low-grade inflammation. Inflammation is a normal response to injuries and sickness. But chronic, low-grade inflammation can have long-term negative effects on the body. For example, low-grade inflammation is associated with metabolic osteoarthritis in people, and my laboratory is studying this possible link in horses.

In people, childhood obesity, which is related to maternal obesity, is associated with a type of joint disease called osteochondrosis. Foals born from obese mares are also predisposed to this same type of joint disease.

Research to note

Because of the similarities between people and horses, research on diagnostics and treatments for metabolic conditions could provide health benefits to both species.

For example, a class of drug called glucagonlike peptide-1 agonists, which includes such brands as Trulicity (dulaglutide) and Ozempic (semaglutide), is commonly used to treat metabolic syndrome and Type II diabetes in people. This class of medication is also effective in treating these conditions in horses, similarly slowing down how quickly food empties the stomach and blunting glucose release into the bloodstream.

Another class of drugs called sodium-glucose cotransporter protein-2 inhibitors, which include such treatments as Jardiance (empagliflozin) and Farxiga (dapagliflozin), are used to treat Type 2 diabetes in people and a similar condition in horses. These drugs alter the kidneys’ ability to absorb sugar from urine such that the body eliminates some of the glucose it would normally absorb. This greatly reduces blood insulin spikes, which can help prevent obesity, metabolic syndrome and cardiovascular disease in both horses and people.

Some dietary supplements, such as resveratrol, especially when used in combination with an amino acid called leucine, also help with weight loss, mobility and insulin sensitivity in people and horses. Lowering blood insulin concentrations can also prevent horses from developing laminitis, a disease that inflames tissues in hooves that can necessitate euthanasia because of incurable pain.

Expanding precision medicine

I find one of the most exciting avenues of research in both animals and people to be the expansion of precision medicine. Instead of the standard one-size-fits-all protocol, precision medicine uses information from a person’s genes, environment and medical history to create a customized treatment plan. For example, precision medicine is often applied in oncology when doctors gather genetic information about the patient’s tumor to inform which treatments might work best for them.

In horses, precision medicine currently focuses on DNA-based diagnostic tests to inform exercise regimens, treatment and breeding decisions. Recent work with horses also suggests that measuring the heritability of certain metabolic traits could be used to screen for metabolic syndrome in the future.

Within precision medicine, doctors aim to get a full-picture view of an individual and their metabolic health by using multiomic analysis. Multiomics entails looking at multiple “omics”–or information from a range of biological disciplines, such as epigenomics, lipidomics, genomics and transcriptomics–to better treat an individual patient.

The more researchers learn from individual patients, including horses, the better doctors will be able to treat every patient. My lab and others use multiomic analysis to generate data that may one day help us identify more effective and safer therapies for horses and–likely–people with metabolic conditions.

Jane Manfredi is an associate professor of pathobiology and diagnostic investigation at Michigan State University. Manfredi receives funding from the Michigan Alliance for Animal Agriculture, USDA NIFA, AAVMC CIVME. Michigan State University provides funding as a founding partner of The Conversation US.

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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Every year, around 42,000 women and 500 men in the US die of breast cancer, a disease that when caught early before it spreads to the rest of the body has a 99-percent five-year survival rate. It’s when the cancer gets detected in later stages when things become more dire, with survival rates dropping below 30 percent if the cancer spreads to lungs, liver, bones, or elsewhere in the body.

The most common way to test for potential breast cancer is through a mammogram—an X-ray image of the breast. And while mammograms can typically find lumps in breast tissue much before a doctor or individual can feel them themselves, screening mammograms miss about one in eight breast cancers, according to the American Cancer Society. 

Mammograms are recommended for women above the age of 40 about every year or so, but for high-risk patients that might not be enough. “Interval cancers,” or cancers that develop in between routine scans, make up 20 to 30 percent of all breast cancer cases and can be more aggressive. 

However, scientists at Massachusetts Institute of Technology have come up with another possible solution—a flexible patch that can take ultrasound images comparable to those done by medical centers, but can fit into a bra. They published their recent development on July 28 in Scientific Advances. 

“We changed the form factor of the ultrasound technology so that it can be used in your home. It’s portable and easy to use, and provides real-time, user-friendly monitoring of breast tissue,” Canan Dagdeviren, an associate professor in MIT’s Media Lab and the senior author of the study, said in a release.

Inspired by her aunt who died at age 49 of breast cancer, Dagdeviren designed a tiny ultrasound scanner using piezoelectric material that could take images whenever a user wanted; the team also designed a flexible 3D-printed patch with “honeycomb-like” openings. Fitted up with a matching bra, the scanner can be moved around to six different spots to image the entire breast—no special training needed.

The researchers tested their device on a 71-year-old subject with a history of breast cysts, and were able to detect cysts as small as 0.3 centimeters in diameter up to 8 centimeters deep in the tissue, all while maintaining a resolution similar to traditional ultrasounds.

Right now, users need to plug in the device to an imaging center-style ultrasound device to see the images, but next steps for the team include building a mini, phone-sized imaging system. In the future, high-risk individuals could use the device at home over and over, and it could also come in handy for patients that don’t have access to regular screening.

“Access to quality and affordable health care is essential for early detection and diagnosis.” study author Catherine Ricciardi, nurse director at MIT’s Center for Clinical and Translational Research, said in the release. “As a nurse I have witnessed the negative outcomes of a delayed diagnosis. This technology holds the promise of breaking down the many barriers for early breast cancer detection by providing a more reliable, comfortable, and less intimidating diagnostic.” 

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New numbers from the Centers for Disease Control and Prevention (CDC) shows that weekly COVID-19 hospitalizations have jumped by over 10 percent across the United States. At least 7,109 admissions were reported for the week of July 15, up from 6,444 during the previous week. This is the largest increase of a key indicator of the virus since December 2022.

[Related: Your guide to COVID testing for the unforeseeable future.]

A second hospital metric is also trending upwards with summer’s temperatures. An average of 0.73 percent of emergency room visits in the past week were related to COVID-19 as of July 21, a jump from 0.49 percent through the same period in June. 

“US COVID-19 rates are still near historic lows after 7 months of steady declines.  Early indicators of COVID-19 activity (emergency department visits, test positivity and wastewater levels) preceded an increase in hospitalizations seen this past week,” CDC spokesperson Kathleen Conley said in a statement according to CBS News. “The U.S. has experienced increases in COVID-19 during the past three summers, so it’s not surprising to see an uptick.”

Hospitalizations do remain below the levels recorded at this time last year as of now. July 2022 peaked at over 44,000 weekly hospitalizations and five percent of emergency room visits in last year’s summer surge.

While this current uptick is small, it is a notable reversal after months of declining coronavirus numbers across the country.

In the Los Angeles area, cases increased by about 32 percent this week. Health officials suspect that this jump may be linked to celebrations from the Fourth of July, travel, and the region’s record breaking heat causing people to stay inside more frequently. Upticks in COVID-19 in wastewater samples from New York also showed a possible increase in cases in June. 

The Midwestern region of the country is the only part of the US that did not record more hospitalizations last week than the one before.

This rise in cases is not unique to the United States. Japan may have entered a ninth COVID-19 wave that continues to surge this month. Hospitalizations and emergency room visits in the Asian country have risen for nine straight weeks. 

[Related: The deadliest viruses in human history, from COVID to smallpox.]

Last week, the World Health Organization reported that “some countries continue to report high burdens of COVID-19, including increases in newly reported cases and, more importantly, increases in hospitalizations and deaths–the latter of which are considered more reliable indicators given the reductions in testing.”

The organization also stressed that COVID-19 “remains a major threat,” and urged governments to maintain and not dismantle their established COVID-19 infrastructure. The WHO ended their global health emergency for COVID-19 in May, citing a decrease in hospitalizations and death and an increase in population immunity. 

The arcturus variant (XBB.1.16) continues to be the most prevalent strain in the US, accounting for nearly 15 percent of all new infections. The WHO also added EG.5 to its list of “variants under monitoring.” This strain has been rising around the world since the end of may, but so far, the WHO says there is “no evidence of rising cases and deaths or a change in disease severity associated with EG.5.”

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This article was originally published on KFF Health News.

What do kidney and pancreas transplants have to do with airplane regulations?

Tucked into the hundreds of pages of legislative language to reauthorize the Federal Aviation Administration is a provision to change the life-or-death process by which human organs are flown commercially from donor to recipient.

But where on the plane organs are stowed during flights has been a long-standing issue for organ procurement organizations.

The sweeping measure, which is pending in Congress and faces a Sept. 30 deadline, aims to change regulations and move organs to the cabin from an aircraft’s cargo hold. Organizations managing organ transport consider it an opportunity to secure legislative relief from a system they say adds more hurdles to the task of shipping organs.

It used to be that a member of a transplant team could take a packaged organ to a plane’s gate and hand it off to the aircraft’s crew, who would stow it in the cockpit or on the flight deck. This access “allowed us to really expedite the process,” said Jeff Orlowski, president and CEO of LifeShare Oklahoma, a nonprofit organ procurement organization in the state. But the terrorist attacks of 9/11 led to tighter security protocols, including a rule that permitted only people with tickets to go through Transportation Security Administration checkpoints.

“In our case, we don’t have a ticket,” said Casey Humphries, logistics service line leader of the United Network for Organ Sharing, the nonprofit contracted by the federal government to manage the nation’s transplant system. “We’re not booked as a passenger on a plane,” she said. Instead, they’re part of the relay network bringing the organs to people in need. Airport employees who work behind security checkpoints have an airport badge and usually get in through a designated entrance.

Another consequence of the 2001 policy changes was that donor organs flown on commercial airplanes—which are mostly kidneys—were stashed in cargo spaces below the wing along with boxes and luggage, said Humphries.

But shipping organs as cargo requires they be at the airport for loading one to two hours before takeoff. “That’s a significant time before the wheels go up for the plane,” said Orlowski. And that variable—the “hours that the organ is going to just sit, going nowhere”—has to be factored into decisions about where it can be sent, he said. Donated organs can’t be treated like a golf bag or an Amazon box. They are delicate and have an imminent expiration date, which for kidneys is usually within 24 hours of surgical removal.

Since January 2022, around 80 percent of organs recovered in Oklahoma were sent to another state to be transplanted, Orlowski said. And of the organs LifeShare recovers, about 35 percent of them are flown commercially. Since kidneys can survive in a cooler longer than other organs, nearly all organs that travel on commercial flights are kidneys.

The first choice for transporting an organ, he said, is usually to drive it to its destination; it’s cheaper, and the transplant team can be more watchful.

But that’s not always an option, especially in rural areas. Orlowski said there are only two transplant centers within driving distance of LifeShare’s Oklahoma City base, in Dallas and Fort Worth, Texas. So his team relies on commercial airlines for transportation.

The current air travel security rules also cause geographic disparities, as fewer cargo-carrying planes fly in and out of smaller airports in rural areas, compared with airports in bigger cities.

“We need something that is available 24 hours a day because organs are available 24 hours a day,” Humphries said.

Charter planes can be a backup option, but one flight can cost organ procurement organizations thousands of dollars, whereas cargo shipping costs usually come in at less than $500 per flight, Orlowski said.

Although the security protocol has been in place for more than two decades, transplant advocates say this is the first time they have sought a legislative reversal, and they are optimistic about the outcome.

The provision to allow organs back in cabins is included in both the Senate and House versions of the reauthorization bill. Some hot-button parts of the bill, though, such as an increase in the mandatory retirement age for pilots, could stall progress. The House Transportation and Infrastructure Committee approved its version on June 14, and at press time it was being debated on the House floor. The Senate Committee on Commerce, Science and Transportation is expected to consider its version this month, according to Senate staffers.

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

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Whether you’re heading out to the beach or just taking a walk around the neighborhood, sunscreen is a must. The shelves are stocked with a broad spectrum of sprays and lotions that can be overwhelming. Fortunately, though, you can find UV protection for a range of situations and skin types. Whether you’re choosing sun protection for yourself or your family, the best sunscreens will keep you safer in the sun.

• Best mineral: Olita Mineral Sunscreen SPF 30 Lotion
• Best tinted: EltaMD UV Daily Tinted Face Sunscreen Moisturizer
• Best spray: Supergoop! PLAY Anti-Oxidant-Infused Body Mist
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• Best for tattoos: Makra Tattoo Care Sun Protection
• Best for babies: Blue Lizard Baby Mineral Sunscreen
• Best budget: Two Peas Organics Mineral Sunscreen Lotion

The best sunscreens: Reviews & Recommendations

First and foremost, a premium sunscreen should protect skin from harsh UV rays, but there are some other important factors to consider when making your selection. From tattoo-friendly lotion choices to a dermatologist-favorite best face sunscreen, these are the best sunscreens to keep your skin protected all summer long.

Best mineral: Olita Mineral Sunscreen SPF 30 Lotion

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Mineral sunscreens are a great pick for the impatient—as soon as you put it on, you’re good to head out the door, whereas chemical sunscreens need to seep into the skin for up to 30 minutes before becoming effective. Olita’s mineral sunscreen uses zinc oxide to protect your skin from UV rays, and its chemical-free ingredients are safe for marine life (so feel free to hop into the ocean as soon as you slather this on). It’s SPF 30 (double the FDA’s recommendation of SPF 15), and it absorbs quickly. Plus, the travel-sized tube will make it through TSA hassle-free so that you can protect yourself on any trip. 

Best tinted: EltaMD UV Daily Tinted Face Sunscreen Moisturizer

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EltaMD tinted sunscreen, with broad-spectrum SPF 40, protects your skin against harmful UVA and UVB rays from the sun. This best face sunscreen lotion contains hyaluronic acid, which helps to reduce fine lines and boosts moisture retention. The doctor-approved, mineral-based product is lightweight and non-greasy, which means it rubs into your skin easily and can be worn with or without makeup. This best tinted sunscreen keeps your skin tone even and protects your face from the elements whether you’ve planned an active day at the beach or you’re just relaxing by the pool.

Best spray: Supergoop! PLAY Antioxidant-Infused Body Mist

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This Supergoop! SPF 50 body mist tops the best spray sunscreen list for many reasons. Reef-friendly, broad-spectrum, and infused with natural ingredients like vitamin C, plus green tea and acai extracts, you can trust you’re protected from harsh UVA and UVB rays while the refreshing scent transports your mind to a tropical oasis (if you’re not already there). As an added bonus, the mist can be sprayed on wet skin, so you don’t have to wait to apply once you get out of the water. It’s also sweat-resistant for up to 80 minutes.

Best transparent: Supergoop! Unseen Sunscreen

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The Supergoop! Unseen Sunscreen is the stuff of legend for good reason (so great that Trader Joe’s introduced a comparable Daily Facial Sunscreen SPF 40 that sells out almost as quickly as it hits the shelves). On a safety level, its SPF 40 rating makes it ideal for everyday protection. But, it’s the sunscreen’s cosmetic benefits that really seal the deal—it’s sheer, so it won’t leave a white cast no matter how much you put on. It also works well as a makeup primer, and while it has a silky matte finish, it still catches some light for a healthy glow. If you’re looking for a mineral formula, you can also try the Supergoop! Mineral Sheerscreen (though some users say it leaves a white cast). 

Best for tattoos: Tattoo Care Sun Protection

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Tattoo sun protection is an increasing concern for people from all walks of life. This dermatologically tested choice, suitable for all skin types, contains natural ingredients, including calendula, cocoa butter, jojoba, and vitamins A and E—all proven to provide multiple skincare benefits. The lotion offers two layers of protection for both your skin and your body art—a 30 SPF with UVA and UVB broad-spectrum sun filter, plus a unique formula that moisturizes your tattoos to ensure they won’t dry out, crack, or fade.

Best for babies: Blue Lizard Baby Mineral Sunscreen

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Blue Lizard Baby Mineral Sunscreen is paraben- and fragrance-free, making it a great choice for your baby’s sensitive skin. Active minerals and ingredients such as zinc oxide and titanium dioxide offer broad-spectrum SPF 50+ protection against harmful UV rays for your little ones, while leaving out potential toxins like oxybenzone and octinoxate in order to protect the planet’s endangered coral reefs. Your kids will love the Elmo-themed bottle, while you appreciate the 80 minutes of water and sweat resistance!

Best budget: Two Peas Organics Mineral Sunscreen Lotion

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With Two Peas Organics Mineral Sunscreen, you’re getting a lot for an affordable price. The combination of all plant-derived, certified organic ingredients with SPF 50 broad-spectrum UVA and UVB protection makes this product a superior choice while remaining wallet-friendly for families on a budget. Two Peas is water- and sweat-resistant for up to 2 hours, plus it offers protection and peace of mind about what you’re applying to your child’s skin. Pro tip: This product contains zinc oxide, which helps to prevent sunburns, but it may require some extra time to rub in.

Things to consider when purchasing the best sunscreen

At baseline, a good sunscreen must protect your skin from harmful UV rays. The label should specifically indicate that the formula protects from both UVA (aging) and UVB (burning) rays—otherwise known as “full-spectrum” sunscreen. The best sunscreens not only have SPF levels of 30+, but they also moisturize your skin. Depending on how active you are during a day in the sun or how frequently you go in the water, look for a lotion that is also sweat- and water-resistant. Beyond that, different people will have different skincare and sun-protection needs, so let’s think about goals, health, and lifestyle values and highlight some options. 

Tinted vs. untinted

Dermatologists suggest wearing sunscreen every day, so look for a formula that fits into your daily skincare regimen and, if necessary, one that you can wear under makeup. Tinted sunscreens may be a good option for some people. The best tinted sunscreen will easily smooth into your skin and even out your complexion; no foundation or concealer needed.

Eco-friendliness

Many brands are now developing lotions without oxybenzone and octinoxate, which can be harmful to the beautiful coral reefs in our oceans. Eco-conscious consumers should look for the words “reef-safe” on sunscreen packaging. To further protect the environment, some spray bottles are now non-aerosol-free. And, if you find applying suntan lotion tedious, you might want to consider including spray sunscreen. You may have to work a bit harder to ensure you have full coverage, but it’s a good choice for speedy applications and for those who like to stay active.

Skin sensitivity

Individuals with tattoos will want the best sunscreen that works to keep their body art protected so it doesn’t fade over time. You definitely didn’t spend hours in the chair for that ink to last less than a lifetime.

Babies and toddlers will naturally have more sensitive skin than adults, so the best sunscreen for them has high coverage and is paraben- and fragrance-free. And if you have kids and don’t want to lug 10 different lotions in your beach bag for every family member, there are also options that will work for the majority of your crew.

Ingredients

If you want an organic option, seek out natural ingredients. Many brands, even ones on a budget, now contain vitamins A, C, and E, as well as cocoa butter, green tea extracts, and more beneficial additions. That is great news for your skin because you’re not only getting the UV protection you need from these products, but also boosting moisture and possibly reducing fine lines, too.

FAQs

Final thoughts on shopping for the best sunscreen

• Best mineral: Olita Mineral Sunscreen SPF 30 Lotion
• Best tinted: EltaMD UV Daily Tinted Face Sunscreen Moisturizer
• Best spray: Supergoop! PLAY Anti-Oxidant-Infused Body Mist
• Best transparent: Supergoop! Unseen Sunscreen
• Best for tattoos: Tattoo Care Sun Protection
• Best for babies: Blue Lizard Baby Mineral Sunscreen
• Best budget: Two Peas Organics Mineral Sunscreen Lotion

No matter your skin type—oily, acne-prone, or sensitive—there is a best face sunscreen lotion or best spray sunscreen, etc. out there created specifically for your needs. No matter how active you are and what ingredients appeal to your sense of health and wellness, the best sunscreen will offer maximum protection against UV rays and won’t irritate your skin, nor will it break the bank. Now get out there, get vitamin D, and don’t forget to reapply!

Why trust us

Popular Science started writing about technology more than 150 years ago. There was no such thing as “gadget writing” when we published our first issue in 1872, but if there was, our mission to demystify the world of innovation for everyday readers means we would have been all over it. Here in the present, PopSci is fully committed to helping readers navigate the increasingly intimidating array of devices on the market right now.

Our writers and editors have combined decades of experience covering and reviewing consumer electronics. We each have our own obsessive specialties—from high-end audio to video games to cameras and beyond—but when we’re reviewing devices outside of our immediate wheelhouses, we do our best to seek out trustworthy voices and opinions to help guide people to the very best recommendations. We know we don’t know everything, but we’re excited to live through the analysis paralysis that internet shopping can spur so readers don’t have to.

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Chronic constipation may be linked to cognitive decline, according to research presented at the  Alzheimer’s Association International Conference in the Netherlands on July 19. Roughly 16 percent of the world’s population struggles with constipation, with older adults particularly prone to have irregular bowel movements.

[Related: Why your poop gets weird on vacation—and what to do about it.]

In this ongoing study, chronic constipation was defined as only having a bowel movement every three or more days. Chronic constipation correlated with a 73 percent higher risk of subjective cognitive decline and showed changes in gut microbiome. Cognitive function is an umbrella term for individual mental capacity for thinking, reasoning, learning, decision-making, problem-solving, paying attention, and remembering.

While chronic constipation has been linked with anxiety, depression, and inflammation, the Alzheimer’s Association says that there are still several unanswered questions about the connections between digestive health and cognitive function. 

The team on this new study looked at over 112,000 adults who participated in the Nurses’ Health Study, Nurses’ Health Study II, and Health Professionals Follow-Up Study. The two Nurses’ studies are complete, and looked at the risk factors for major chronic diseases in North American women. The third study is ongoing and investigating this same topic in men.  

This latest research on constipation used data on the frequency of participants’ bowel movements from 2012 to 2013, their self-assessments of cognitive function between 2014 to 2017, and some of the participants’ objectively measured cognitive function between 2014 and 2018.

The researchers found that constipated participants had significantly worse cognition compared with those who pooped once a day. The impairment was equivalent to three years or more of chronological cognitive aging. The authors also found an increased risk among those who pooped more than twice per day, but the higher odds were small.

“These results stress the importance of clinicians discussing gut health, especially constipation, with their older patients,” senior investigator Dong Wang from Harvard Medical School, Brigham and Women’s Hospital, and Harvard T.H. Chan School of Public Health said in a statement. “Interventions for preventing constipation and improving gut health include adopting healthy diets enriched with high-fiber and high-polyphenol foods such as fruits, vegetables and whole grains; taking fiber supplementation; drinking plenty of water every day; and having regular physical activity.”

[Related: Baboon poop shows how chronic stress shortens lives.]

An unrelated study published in February in the journal Neurology found that those who regularly use laxatives may have an increased risk of developing dementia compared to those who don’t use laxatives. 

“Finding ways to reduce a person’s risk of dementia by identifying risk factors that can be modified is crucial,” co-author Feng Sha from the Shenzhen Institute of Advanced Technology at the Chinese Academy of Sciences said in a statement in February. “More research is needed to further investigate the link our research found between laxatives and dementia. If our findings are confirmed, medical professionals could encourage people to treat constipation by making lifestyle changes such as drinking more water, increasing dietary fiber and adding more activity into their daily lives.”

Eating enough fiber from vegetables, fruits, whole grains and nuts can prevent constipation. The Food and Drug Administration recommends that total fiber intake should be at least 25 grams per day. Proper hydration can also soften stools, and exercising a few times per week can also help.

It is also important to understand the challenges and individual nature of understanding gut bacteria and the microbiome at large, 

“Each person seems to have a unique microbiome, almost like a fingerprint,” gastroenterologist Monia Werlang from the University of South Carolina Greenville Medical School told NBC News. “Scientists are still learning how to manipulate it to promote health and to modify disease. Targeting the microbiome is promising, but there are many unknowns, especially considering the variability from person to person.”

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On Monday July 17, the Food and Drug Administration approved the first long-acting medication  to protect babies and toddlers against respiratory syncytial virus (RSV). The lung-attacking virus sends about 58,000 children under five to the hospital and kills 100 to 300 infants every year in the United States. 

[Related: Flu and RSV hybrid virus studied in a lab for the first time.]

Nirsevimab is a ready-made injectable antibody that can bind to RSV and block the virus from infecting healthy cells. It is not a vaccine, but instead, is a form of passive immunity. 

For most healthy people, RSV manifests as a cold, but the virus can be life-threatening for the elderly and the very young. Nirsevimab was approved for infants and children up to two years old who face increased risk of severe RSV. Babies can receive a single injection to protect against their first RSV season, which typically starts in the fall and peaks in the winter in the US. Children up to two can then receive a second dose during their next RSV season. 

“RSV can cause serious disease in infants and some children and results in a large number of emergency department and physician office visits each year,” director of the Office of Infectious Diseases in the FDA’s Center for Drug Evaluation and Research John Farley said in a statement. “Today’s approval addresses the great need for products to help reduce the impact of RSV disease on children, families and the health care system.” 

Nirsevimab will be sold under the brand name Beyfortus and is already approved for use in the United Kingdom, Europe, and Canada. Pharmaceutical company Sanofi, who developed the drug with AstraZeneca, did not immediately say that the price of the treatment would be in the US.  

According to an FDA analysis, nirsevimab was roughly 70 percent effective at reducing the risk that a baby would need to see a doctor for RSV and was about 78 percent effective at preventing hospitalizations compared with a placebo in the clinical trials that led to the drug’s approval. It was generally safe and well tolerated in the trials, with less than one percent of babies having skin reactions after the shots that went away with treatment. 

[Related: How our pandemic toolkit fought the many viruses of 2022.]

“We run this gauntlet every year — RSV season,” pediatric infectious disease specialist at the Cleveland Clinic in Ohio Frank Esper told CNN “We see a lot of these infants. They come in; they can’t breathe. That’s the problem. That’s what RSV does. It causes so much swelling and secretions in their breathing tubes, called the bronchioles, that they just can’t get enough oxygen.”

Advisers to the Centers for Disease Control and Prevention will meet in early August to recommend exactly who should receive the drug. recommend exactly who should get the drug.

The approval is welcome after multiple decades of setbacks in research for RSV. The FDA approved two RSV vaccines for older adults from GlaxoSmithKline and Pfizer in May and the agency is expected to make a decision on a vaccine for pregnant people next month.

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This article was published on KFF Health News.

Excessive drinking during the COVID-19 pandemic increased alcoholic liver disease deaths so much that the condition killed more Californians than car accidents or breast cancer, a KFF Health News analysis has found.

Lockdowns made people feel isolated, depressed, and anxious, leading some to increase their alcohol intake. Alcohol sales rose during the pandemic, with especially large jumps in the consumption of spirits.

While this led to a rise in all sorts of alcohol-related deaths, the number of Californians dying from alcoholic liver disease spiked dramatically, with 14,209 deaths between 2020 and 2022, according to provisional data from the Centers for Disease Control and Prevention.

Alcoholic liver disease is the most common cause of alcohol-induced deaths nationally. In California, the death rate from the disease during the last three years was 25 percent higher than in the three years before the pandemic. The rate peaked at 13.2 deaths per 100,000 residents in 2021, nearly double the rate from two decades ago.

The disease is usually caused by years of excessive drinking, though it can sometimes occur after a short period of heavy alcohol use. There are often no symptoms until late in the disease, when weakness, confusion, and jaundice can occur.

Many who increased their drinking during the pandemic were already on the verge of developing severe alcoholic liver disease, said Jovan Julien, a postdoctoral researcher at Harvard Medical School. The extra alcohol sped up the process, killing them earlier than they would have otherwise died, said Julien, who co-wrote a modeling study during the pandemic that predicted many of the trends that occurred.

Even before the pandemic, lifestyle and dietary changes were contributing to more deaths from alcoholic liver disease, despite little change in alcohol sales, said Brian Lee, a hepatologist and liver transplant specialist with Keck School of Medicine of the University of Southern California.

Lee and other researchers found a connection between alcoholic liver disease and metabolic syndrome, a condition often characterized by excess body fat around the waist. Metabolic syndrome — often caused by poor diet and an inactive lifestyle — has risen across the country.

“Having metabolic syndrome, which is associated with obesity, high blood pressure, and diabetes, more than doubles your risk of having advanced liver disease at the same level of drinking,” Lee said.

The Californians alcoholic liver disease most often kills are those between 55 and 74 years old. They make up about a quarter of the state’s adults but more than half the deaths from alcoholic liver disease.

However, death rates among Californians 25 to 44 roughly doubled during the last decade. About 2,650 Californians in that age group died of the disease during the last three years, compared with 1,270 deaths from 2010 through 2012.

“People are drinking at earlier levels,” Lee said. “People are developing obesity at younger ages.”

The highest death rates from alcoholic liver disease occur in rural eastern and Northern California. In Humboldt County, for instance, the death rate from alcoholic liver disease is more than double the statewide rate.

Jeremy Campbell, executive director of Waterfront Recovery Services in Eureka, said Humboldt County and other rural areas often don’t have the resources and facilities to address high rates of alcohol use disorder. His facility provides high-intensity residential services and uses medication to get people through detox.

“The two other inpatient treatment facilities in Eureka are also at capacity,” he said. “This is just a situation that there's just not enough treatment.”

Campbell also pointed to the demographics of Humboldt County, which has a much higher proportion of white and Native American residents than the rest of the state. Alcoholic liver disease death rates in California are highest among Native American and white residents.

Death rates rose more among Native American, Latino, Asian, and Black Californians during the last decade than among non-Latino white Californians, CDC data shows. Part of that is due to disparities in insurance coverage and access to care, said Lee. In addition, Lee said, rates of metabolic syndrome have increased more quickly among nonwhites than among whites. Racial health disparities also manifest in differing survival rates for Black and white patients after liver transplants, he added.

The trend is expected to continue. Julien projects a temporary dip in deaths because many people who would have died of the disease in 2022 or 2023 instead died sooner, after a boost in drinking during the pandemic, but that deaths will rise later as bad habits developed during the pandemic begin to take a long-term toll.

“As people increased their consumption during COVID-19, we have more folks who have now initiated alcohol use disorder,” Julien said.

Phillip Reese is a data reporting specialist and an assistant professor of journalism at California State University-Sacramento.

This article was produced by KFF Health News, which publishes California Healthline, an editorially independent service of the California Health Care Foundation. 

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

Subscribe to KFF Health News' free Morning Briefing.

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If you’ve ever stayed up at night wondering, “Who am I?” … you can quell that existential dread with this Prime Day deal on 23andMe’s DNA kit. The at-home kit requires you to spit into a test tube and send it to a lab. Within weeks, 23andMe will e-mail you your results, showing which region of the world your descendants came from. And you can get that glimpse into your heritage, and health, for less if you act now.

All of these Prime Day deals require an active Amazon Prime Membership. You can sign up here for a free 30-day trial.

23andMe Health + Ancestry Service: Personal Genetic DNA Test $98.99 (Was $199)

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As its name suggests, the 23andMe Health + Ancestry Service: Personal Genetic DNA Test can reveal more than your cultural heritage. By scanning your DNA, 23AndMe can offer insight into diseases you’re more likely to be susceptible to. The company—and us here at PopSci—recommend you take these insights with a grain of sale. While 23andMe’s process is solid, it’s not a replacement for regular visits to the doctor or intended to address immediate causes for concern.

That said, even a small heads-up to issues you may encounter down the road may be helpful. One of the most interesting things about 23andMe’s DNA kits is the company’s updated findings. As more people submit their DNA, the company can trace its samples more accurately. Your first results may show the historical region your family hails from, while an updated report a year later could offer the specific country they’re from. Heck, you may even be fortunate enough to learn you’re partially Croatian. If you’ve been considering finally getting your DNA tested, 23andMe’s Prime Day deal is the perfect time. With all this in mind, only one question remains: What about your dog?

Embark Breed & Health Kit $126.99 (Was $199)

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If you’re just as curious about your four-legged friend’s background, you can save $72 on a Dog DNA test from Embark. The company’s process is like 23andMe: Send in a test tube of your pup’s adorable drool, and wait for an e-mail with their results. You’ll not only know the breakdown of your dog’s breed but also its susceptibility to different illnesses. Again, you should still consult your veterinarian with any health concerns regarding your dog, but it doesn’t hurt to know a bit more about potential risks. Embark says it can test for 350 breeds, so you’ll get a surprising amount of specificity regarding its genealogical makeup. Dogs might be unable to talk to you about family folklore and whether glaucoma is prevalent on their dad’s side, but Embark’s Breed & Health Kit is the next best thing.

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This article originally appeared on MIT Press Reader. This article is excerpted from Richard Conniff’s book “Ending Epidemics: A History of Escape From Contagion.”

In 1918, epidemic disease and war once again embraced with all their old passion. The deadly pandemic that began that year became known as the Spanish flu because Spain was a neutral country, and its press was the first to report the devastating outbreak. The warring countries meanwhile suppressed the news, leaving their citizens unprepared. This flu was particularly terrifying because it spread so easily and because it concentrated its venom on the young. (Their elders may have acquired immunity from exposure to a previous flu outbreak.) It filled up its victims’ lungs with fluid, and the desperate hunger for air turned their skin blue as they suffocated.

The first of three waves hit soldiers in France early in 1918. But the flu soon spread from there, in two subsequent and far more virulent waves, to sicken soldiers and civilians almost everywhere. Over the course of two years, it infected an estimated 500 million people worldwide, a quarter to a third of the human population, and killed 50 million of them, with most of the dead between 20 and 40 years of age. (By comparison, the COVID-19 pandemic has infected about 750 million people at this writing — under 10 percent of the current human population.)

In most fatal cases, the immediate cause of death was pneumonia, marked by an abundance of Streptococcus, Staphylococcus, and other bacteria. But something else seemed to be preparing the way for these common microbes to proliferate. As a later physician put it, “The specific virus ploughs the land and the secondary bacteria germinate in the furrows.”

As one physician put it, “The specific virus ploughs the land and the secondary bacteria germinate in the furrows.”

A half century of germ theory and triumphant bacteriology led almost everyone to suspect a bacterial, not a viral, pathogen. In fact, they suspected one specific bacterial pathogen. Haemophilus influenzae was also known as Pfeiffer’s bacillus, for Richard Pfeiffer, a researcher at the Robert Koch Institute, who had identified it as the cause of an 1889–1890 influenza pandemic. Pfeiffer’s indictment of this bacillus went largely unquestioned for a quarter century, until the bodies started to pile up in 1918. Researchers around the world then searched desperately for H. influenzae in victims of the new pandemic, with little success. Pfeiffer himself admitted that he could find it in only about half of flu victims. Other scientists found it but couldn’t get it to produce flu even when sprayed as a pure culture into the respiratory tracts of monkeys and human test subjects.

Going viral

The failure of Pfeiffer’s bacillus—the failure of bacteriology—led some researchers to think back 20 years to a different and still relatively obscure line of microbial research. In 1898, Martinus Beijerinck (1851–1931), a microbiologist in Delft, The Netherlands, was studying a disease of tobacco plants. Beijerinck took an extract from plants infected with tobacco mosaic and put it through a Chamberland filter to screen out bacteria and other contaminants. With the filtered extract, he infected other plants, then took filtered extracts from those plants and infected still other plants, and so on in a series. Beijerinck thought the contagium consisted of nothing more than dissolved molecules. So how to explain its reproductive capabilities? He concluded that it “must be incorporated into the living protoplasm of the cell, into whose reproduction it is, in a manner of speaking, passively drawn.” This must have seemed to his contemporaries like a wildly improbable speculation. In fact, though, it fits remarkably well with the modern understanding of how a virus reproduces. What may also seem wildly improbable was that Beijerinck developed this first good description of a virus within a short walk of where Antoni van Leeuwenhoek had seen and described the first known bacteria. Thus Delft secured its place, over a distance of more than 200 years, as the cradle of microbiology.

That same year, a German team led by Friedrich Loeffler, who had previously discovered the bacterial agent of diphtheria, used filtration to identify the first animal virus, for foot-and-mouth disease. And in 1901 in Cuba, Americans James Carroll (1854–1907) and Walter Reed (1851–1902) demonstrated that the agent of yellow fever remained infectious after passing through a bacteria-proof filter, making it the first known human disease caused by a virus. (This was a footnote to their previous work demonstrating that yellow fever, like malaria, was a mosquito-borne disease.) By 1906, at least 18 such pathogens affecting plants, animals, or humans were known. Contemporaries called them filter-passing, or filterable, pathogens, or increasingly just viruses. But it would be years before anybody could see one or describe one morphologically or chemically. Virology meantime remained clouded in confusion and doubt.

The 1918 pandemic pushed researchers to look more closely and think much harder about this new science. Different research groups began to apply their Chamberland filters to samples from flu victims. Charles Nicolle and Charles Lebailly at the Pasteur Institute in Tunisia were the first to report success, in October 1918, after using filtered sputum from a flu victim to pass the disease to two volunteer test subjects. In Germany, two researchers tested a filtrate from a flu victim on themselves, with unknown results; and in Flanders, a British researcher died while experimenting with a filtrate. In Japan, researchers exposed 24 volunteers—“our friends, doctors and nurses”—to the flu, some with an emulsion of fluids straight from victims of the pandemic, others with a filtered extract. Six who had recovered from the flu showed no signs of a recurrence. The other 18, who were new to the disease, all came down with flu, in some cases with “very severe” symptoms. The filtered extract was equal to the emulsion as a source of contagion.

Skepticism persisted, however, with some critics still arguing well after the war that “the invisible virus concept” was little more than a ruse to absolve “the discoverers from the necessity of producing evidence of a characteristic microbe.” When a few researchers attempted to develop a flu vaccine in 1918, they worked instead with attenuated bacteria. Older defensive measures—quarantine and closures of schools, churches, movie theaters, and restaurants—proved more effective in bringing the pandemic to a close. That, and what may be the oldest measure: By 1920, almost all potential victims had acquired immunity by surviving the flu—or dying.

The pandemic launched medical thinking in a dramatically new direction over the next decade and, indeed, for the remainder of the 20th century. Having been routed by influenza, medical researchers now regrouped to address the puzzle of filter-passing viruses. “There could hardly be a set of problems whose solution has more potential importance for the community than this,” the secretary of the British Medical Research Council declared in 1922, noting that “in a few months in 1918–1919 [flu] killed more persons in India than had died from the plague there during the previous 20 years.” It was the beginning of a major initiative to apply “new technical methods of investigation” to viruses.

By 1920, almost all potential victims had acquired immunity by surviving the flu—or dying.

Other developed nations also pursued viral research, and by 1927, a Rockefeller Institute researcher could list close to 100 diseases thought to be viral, though he allowed plenty of room for subtractions from this list, on the reasonable assumption that some would later turn out to be caused by very small bacteria or protozoa. Among those affecting humans, the list correctly included smallpox, chicken pox, herpes, encephalitis, yellow fever, dengue, polio, rabies, mumps, measles, rubella, the common cold, and influenza.

The questions about viruses that were still outstanding seem like the ones we would ask on encountering a featureless but disturbingly forceful presence from some distant planet: What does it look like? Can it mutate? Is it alive? And always the one the pandemic had put in the front of peoples’ minds: Will it kill us? Getting the answers would be difficult. Viruses were obligate parasites — that is, totally dependent on living cells. Researchers trying to study them struggled with the challenge of keeping them alive outside a host species.

The British effort focused on canine distemper as an animal model for influenza, using dogs and later ferrets as experimental animals. By 1927, they were testing a distemper vaccine in a two-shot sequence, first with the killed virus, then with the live virus. By 1931 it was available commercially—for dogs. “Is it too much to ask,” the Times (London) wondered, peevishly, “that work on similar lines should be undertaken on the cause of influenza? … Has not the time arrived to launch a campaign and to come to grips with the enemy?”

In fact, researchers were already doing just that. In 1933, at Britain’s National Institute of Medical Research, workers filtered throat washings from flu patients, used the filtrate to infect ferrets, and identified the culprit as the influenza A virus. Soon after, a researcher at the Rockefeller Institute in New York used the same technique to identify a second potential culprit, influenza B. At Vanderbilt University, researchers devised a way to grow viruses apart from their normal host species, using fertilized chicken eggs. Max Theiler (1899–1972), a South African–born researcher at the Rockefeller Foundation in New York, soon put this technique to work developing an effective live attenuated vaccine against yellow fever. Other researchers used the new technique to develop and improve the first flu vaccines. Having risen up and become strong on the bones of the tens of millions lost to the 1918 pandemic, the science of viruses would go on to save hundreds of millions from premature death in the decades just ahead.

Richard Conniff is a National Magazine Award-winning science writer who has written for Smithsonian magazine, The Atlantic, National Geographic, and other publications. He is a past Guggenheim Fellow and the author of several books, including “The Species Seekers: Heroes, Fools, and the Mad Pursuit of Life on Earth,” “Swimming with Piranhas at Feeding Time: My Life Doing Dumb Stuff with Animals,” “The Natural History of the Rich: A Field Guide,” and “Ending Epidemics: A History of Escape From Contagion,” from which this article is excerpted.

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We all know how old we are. But the measure of years since when we were born, also called “chronological age,” is just one way to think about age. Epidemiologists, gerontologists, and geneticists also study “biological age” and the wide range of variables that affect it, as well as which populations are most at risk for accelerated aging, in an effort to better understand how to preserve our health for longer.

Intuitively, you might guess that biological age measures how old you are physically. That’s somewhat true—it’s a way to assess whether a person’s body, or even individual organs, are as healthy as those of others of the same age. For an individual in their 30s, a biological age of 50 means their biology more closely resembles someone 20 years their senior. 

In research, the term “biological age” can mean slightly different things depending on how it’s measured, says Andrea La Croix, a professor of epidemiology at the University of California San Diego. You could measure walking ability, and see how fast and agile or slow and stiff a person is compared to others their age. Or you could measure something much more granular, like whether the inflammation levels in their body are as expected for how old they are. Simply put, biological age is a way to gauge how people compare to others with different health metrics, La Croix says. 

[Related: Hydration seems to be the key to aging better and living longer]

Oftentimes when talking about biological age, researchers will also refer to “epigenetic age.” Epigenetics is the study of how genes turn on or off depending on an individual’s behaviors and environment. There are certain parts of our genome we want to keep off, and others we want to keep on, “but as we age, those distinctions become less pronounced,” says Steve Horvath. As a biogerontologist at Altos Labs, he developed the first epigenetic clock to look at which genes are active or not, and use that data to pretty accurately measure the age of specific organs and tissues in the human body. A higher-than-expected biological age means a person’s genes are activated in a way that deviates from what scientists would consider normal or expected for their chronological age.

What affects biological age?

The variables that determine biological aging overlap with the ones that influence health more generally. Smoking, obesity, and inflammation markers in your blood are all factors that causally increase your biological age, Horvath says; women who enter menopause earlier also have higher biological age. 

There are social and environmental factors to consider too, says Jamaji Nwanaji-Enwerem, a physician and environmental health scientist at Emory University. He has analyzed how exposure to air pollutants, metals, and life stressors are associated with higher biological age. In one 2021 study, he and his team found that mothers in California who had adverse childhood experiences (like experiencing violence, abuse, or neglect, for example) were more likely to give birth to babies with slightly higher epigenetic ages. Another US-based study published in June found that people living in neighborhoods with more access to green spaces had biological ages that were on average 2.5 years younger than those with limited access. The authors found further disparities when also looking at race, sex, and socioeconomic status.

There is one caveat to biological age to consider, Nwanaji-Enwerem notes. Assessing someone’s biological age, regardless of what variable you’re looking at, means jotting down their stats and comparing them to the rest of the population on a bell curve. But more research is needed to know exactly how biological age translates to good health, he says—if a 40-year-old person has a liver with a biological age of 40, does that automatically mean they’re healthy? We don’t have exact answers. 

Regardless, Nwanaji-Enwerem thinks biological age is a useful metric for researchers because it gives them a quick, quantitative explanation for the myriad variables that affect the health of individuals and populations. If experts look at a community and notice that “people who live in this certain region all have accelerated aging,” he adds, they can then ask “is there a larger factor that we need to be looking at to help explain that?”

Can you control biological age?

If biological aging is a proxy to assess health and mortality, is there a way to slow it down? The strategies to prevent accelerated aging are pretty much the same ones we always hear about, La Croix says: balanced nutrition, adequate physical activity, clean air and water, low stress, strong social support systems, and access to healthcare—“all of those things that we associate with good health will be important.”

That said, experts don’t think regular individuals need to be thinking about biological age in everyday life. It’s not realistic for most people to test or measure, say, epigenetics on their own, and even if they could, it’s not like we have a pill or some other easy intervention to reverse it, Horvath says. There have been reports that specific diets and marathon training can knock years off an aging body, but in reality, we don’t have an anatomical time machine.

[Related on PopSci+: Has the fountain of youth been in our blood all along?]

La Croix points out that many of us already “think about [biological age] without even knowing that we think about it.” We notice how our bodies, cells, and abilities change over the years, and feel the effects of biological age even if we don’t use those words. Unfortunately, as the science stands, “you can’t turn yourself back into a 25-year-old,” La Croix says. But by keeping healthy habits and reducing risk factors, “all we can do is kind of optimize and enjoy life.” 

The post Why you might feel older than you actually are appeared first on Popular Science.

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You’ve probably been told you should up your daily fiber intake by eating hearty foods like wheat bread and black beans. But despite a broad-spectrum recommendation for the roughage, researchers can’t say for certain why it’s so good for our microbiomes, what diseases it actually helps prevent, or how exactly we should consume it. Here’s what we do know.

First, what is fiber and how much of it do we need?

Broadly speaking, fiber is any carbohydrate that our bodies can’t digest. When we eat food, our digestive systems use various enzymes to break down the fat, carbohydrates, and protein therein. The resulting energy keeps our bodies running. Much of what’s left over consists of carbohydrates that we lack the enzymes necessary to digest. We divide that up into soluble and insoluble fibers, depending on which ones are dissolvable in water. Most unprocessed non-meat products like fresh fruits, mixed vegetables, and whole grains contain a combination of both forms.

The Dietary Guidelines for Americans recommends 22 to 34 grams of fiber per day for adults and 10 to 15 grams for kids, depending on age. This chart for standard portions of fiber will help you figure out what that means for different kinds of foods.

Cool, so what does fiber do for us?

That’s the big question. Why is something that we don’t even digest so important to our health?

[Related: 5 nutrition goals that are better than weight loss]

Some nutritionists used to think fiber was the catch-all good-for-you ingredient in food, but we now understand that it manages blood glucose levels and reduces the risk of heart disease. Most importantly, some studies have shown that it reduces our overall mortality risk. In other words, the people that eat more fiber and make other healthy life choices have a general lower risk of death from all causes.

So scientists are pretty dang confident that fiber is good for you, but aren’t entirely sure why. However, we now understand that the biggest benefit that fiber has for us is indirect: It feeds our microbes, which in turn keep us running smoothly.

We have microbes, and that’s a good thing?

It’s true. Our bodies are teeming with bacteria and other microbes that live mostly on our skin and in our guts. In fact, each person contains trillions of these microorganisms. All together, they make up anywhere between 1 and 3 percent of a human’s body weight. (For an average 175-pound person, that’s as much as 5 pounds of bacteria.)

[Related: Probiotics are more hype than science]

The more fiber we eat, the more food our microbes have, and the more food our microbes have, the more likely they are to thrive and reproduce. That’s why a low-fiber diet—one paltry in apples, citruses, leafy greens, and whole grains, and high in meat, starches, and processed foods—can lead to problems. While we may get the calories we need, our microbes don’t. They start to die off and become less diverse over time.

But how exactly does that translate into good health?

While we still don’t understand all the mechanisms through which our microbes work to prevent disease, a few standout studies are pointing us in the right direction.

First, we know that when our bacteria consume the fiber we eat, they produce nutrients for the body, including short chain fatty acids. Those molecules help our body thrive. In particular, scientists have found that butyrate helps to promote cell differentiation in the colon. This keeps the mucus in our colons healthy, which helps prevent colorectal cancer.

Two studies published in 2017 gave mice an extremely low-fiber diet. Researchers found that after just three days, diversity of the bacteria living in the gut had shrunk by ten-fold. That protective layer of lower-gut mucus had decreased, too. On the other end of the fiber intake spectrum, in a study out in 2017, researchers took poop samples from the Hadza people in Tanzania, who eat an impressive 100 grams of fiber a day. The hunter-gatherer community tends to live long and healthy lives, and many researchers believe their high intake of unprocessed foods, which results in a high intake of fiber, may have something to do with it.

But, let’s face it, eating a completely unprocessed diet isn’t exactly easy, fun, or feasible. So, there are a few tricks of the trade you can use to get more fiber. First, get out of the habit of peeling fruit. If there’s skin on there—apple or pear-type skin, not thick and inedible peels—you want to eat it. That’s where a lot of the fiber is hiding.

[Related: Feed a family for a week with a single bag of beans]

Next, add beans to your diet. Beans have sooooo much fiber. They are also low in fat and high in nutrients. Yes, beans do cause gas. That is very annoying and is, for many, a valid reason to skip the legumes. Unfortunately, it’s the fiber itself that’s partly to blame for all that farting. To alleviate this, try adding beans slowly into your diet, which has been shown to help get your body—and your microbes—used to that delicious increase in fiber.

While it might be hard at first, it won’t take very long to see an effect from these changes. As studies have shown, just three days of more or less fiber can influence the diversity of your gut microbes.

And while there is still more work to be done to understand the relationship and mechanisms through which our microbes work to keep us healthy, it’s clear that they’re important—and that they need our help getting plenty of fiber.

This story has been updated. It was originally published on April 4, 2018.

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On July 6, the Food and Drug Administration (FDA) fully approved the first drug shown to slow down Alzheimer’s disease. Sold under the brand name Leqembi (generic name lecanemab), this is the first time that a drug meant to slow the disease’s progression, and not only target its symptoms, has been granted full regulatory approval. 

[Related: One big reason why Alzheimer’s might be going undetected in the US.]

Leqembi is manufactured by Japanese drugmaker Eisai and the United States-based drugmaker Biogen. The drug targets beta-amyloid, a brain protein that has long been believed by scientists to be one of the underlying causes of Alzheimer’s. 

During a phase 3 clinical trial of the new drug, disease progression was slowed by 27 percent over an 18-month period in 1,795 patients with mild cognitive impairment or early-stage Alzheimer’s. The medication also reduced sticky beta-amyloid plaques that can accumulate in the brains of people with the disease.

“[This] action is the first verification that a drug targeting the underlying disease process of Alzheimer’s disease has shown clinical benefit in this devastating disease,” acting director of the Office of Neuroscience at the FDA’s Center for Drug Evaluation and Research Teresa Buracchio said in a press release. “This confirmatory study verified that it is a safe and effective treatment for patients with Alzheimer’s disease.”

The new approval means that Leqembi should be widely covered by Medicare, which primarily serves adults 65 and older. Until this approval, the federal insurance program has only covered the cost of Leqembi for patients in certain clinical trials. This expanded coverage means that an estimated one million Medicare patients are potential candidates for the treatment, and that people with Medicare who are in the early stages of Alzheimer’s could access the drug at an affordable price. Both companies have said the treatment will cost roughly $26,500 annually without insurance.

“It’s not something that’s going to stop the disease or reverse it,” Sanjeev Vaishnavi, director of clinical research at the Penn Memory Center, told NPR. “But it may slow down progression of the disease and may give people more meaningful time with their families. It’s very exciting that we’re targeting the actual pathology of the disease.”

In January, Leqembi received accelerated approval from the FDA due to its ability to remove beta-amyloid from the brain in those in early stages of the disease that affects more than 6.5 million Americans. Full or traditional approval reflects the FDA’s assessment that the drug also helps preserve thinking and memory. 

[Related: One secret to excellent memory in old age? Giant neurons.]

The Alzheimer’s Association has previously worked to accelerate the drug’s approval, and called it “an important development for people living with Alzheimer’s disease and their families.” However, some critics have mentioned the lack of diversity in the drug’s testing pool—specifically Black patients.

According to the FDA, Alzheimer’s disease is currently irreversible, progressive, and slowly destroys memory and thinking skills. Eventually, the ability to carry out simple tasks. Its specific cause is unknown, but it is generally characterized by changes in the brain. Some of these changes include the formation of amyloid beta plaques and neurofibrillary, or tau, tangles—that result in loss of neurons and their connections.

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This article was co-reported by The Markup and KFF Health News.

Looking for an at-home HIV test on CVS’ website is not as private an experience as one might think. An investigation by The Markup and KFF Health News found trackers on CVS.com telling some of the biggest social media and advertising platforms the products customers viewed.

And CVS is not the only pharmacy sharing this kind of sensitive data.

We found trackers collecting browsing- and purchase-related data on websites of 12 of the U.S.’ biggest drugstores, including grocery store chains with pharmacies, and sharing the sensitive information with companies like Meta (formerly Facebook); Google, through its advertising and analytics products; and Microsoft, through its search engine, Bing.

The tracking tools, popularly called “pixels,” collect information while a website runs. That information is often sent to social media firms and used to target ads, either to you personally or to groups of people that resemble you in demographics or habits. In previous investigations, The Markup found pixels transmitting information from the Department of Education, prominent hospitals, telehealth startups, and major tax preparation companies.

Pharmacy retailer websites’ pixels send a shopper’s IP address—a sort of mailing address for a person’s computer or household internet—to social media giants and other firms. They also send cookies, a way of storing information in a user’s browser that in this case helps track a user from page to page as the user browses a retailer’s site. Cookies can sometimes also associate individuals on a site with their account on a social media platform. In addition to the IP address and cookies, the pixels often send information about what you’ve clicked or bought, including sensitive items, such as HIV tests.

“HIV testing is the gateway to HIV prevention and treatment services,” said Oni Blackstock, the founder of Health Justice and a former assistant commissioner for the New York City Bureau of HIV/AIDS Prevention and Control, in an interview.

“People living with HIV should have control over whether someone knows their status,” she said.

Many retailers shared other detailed interaction data with advertising platforms as well. Ten of the retailers we examined alerted at least one tech platform when shoppers clicked “add to cart” as they shopped for retail goods, a capacious category that included sensitive products like prenatal vitamins, pregnancy tests, and Plan B emergency contraception.

Supermarket giant Kroger, for instance, informed Meta, Bing, Twitter, Snapchat, and Pinterest when a shopper added Plan B to the cart, and informed Google and Nextdoor, a social media platform on which people from the same neighborhood gather in forums, that a shopper had visited the page for the item. Walmart informed Google’s advertising service when a shopper browsed the page of an HIV test, and Pinterest when that shopper added it to the cart.

A previous investigation from The Markup found that Kroger used loyalty cards to track, analyze, and sell an array of data about customers to advertisers.

Using Chrome DevTools, a tool built into Google’s Chrome browser, The Markup and KFF Health News visited the websites of 12 of the U.S.’ biggest drugstores and examined their network traffic. This monitoring tool allowed us to see what information about shopping habits and, in some cases, prescriptions, were sent to third parties.

Over the course of the investigation, retailers frequently changed their trackers—sometimes activating them, sometimes removing them. Some retailers appeared to be taking steps to limit tracking on sensitive items.

For example, Walgreens’ website prevented some trackers from activating on the pages of some products, which included Plan B and HIV tests. This code didn’t prevent all tracking, though: Walgreens’ site continued sending Pinterest information about those sensitive items a user added to the cart.

Walgreens shared a new policy after learning of The Markup and KFF Health News’ findings. Spokesperson Fraser Engerman said that while the chain already had a “robust privacy program,” it would no longer share browsing data related to reproductive health and HIV testing. Engerman also told us that “Pinterest confirmed that the data will be deleted and that it has not been used for advertising purposes.” Crystal Espinosa, a spokesperson for Pinterest, said the company “can confirm that we will be deleting the data Walgreens requested.”

The pharmacy vs. the pharmacy aisle

In the U.S., drugstores and grocery stores with associated pharmacies are only partially covered by the Health Insurance Portability and Accountability Act, or HIPAA. The prescriptions picked up from the pharmacy counter do have this protection.

But in a separate section, sometimes confusingly called the pharmacy aisle, stores also often sell over-the-counter medications, tests, and other health-related products. Consumers might think such purchases have similar protections to their prescriptions, but HIPAA only covers the pharmacy counter’s clinical operations, such as dispensing prescriptions and answering patients’ questions about medication.

This distinction can be confusing enough inside the brick-and-mortar location of a retailer. But the line can become even harder to make out on a website, which lacks the clarifying delineations of physical space.

What’s more, descriptions about what will happen with retail data are generally in retailers’ privacy policies, which can usually be found in a link at the bottom of their webpages. The Markup and KFF Health News found them murky at best, and none of them were specific about the parts of the site that were covered by HIPAA and the parts that weren’t.

In the “Privacy Notice for California Residents” part of its privacy policy, Kroger says it processes “personal information collected and analyzed concerning a consumer’s health.” But, the policy continues, the company does not “sell or share” that information. Other information is sold: According to the policy, in the last 12 months, the company sold or shared “protected classification characteristics” to outside entities like data brokers.

Kroger spokesperson Erin Rolfes said the company strives to be transparent and that, “in many cases, we have provided more information to our customers in our privacy notices than our peers.”

Brokering of general retail data is widespread. Our investigation found, though, that some websites shared sensitive clinical data with third parties even when that information would be protected at a HIPAA-covered pharmacy counter. Users attempting to schedule a vaccine appointment at Rite Aid, for example, must answer a survey first to gauge eligibility.

This investigation found that Rite Aid has sent Facebook responses to questions such as:

• Do you have a neurological disorder such as seizures or other disorders that affect the brain or have had a disorder that resulted from a vaccine?
• Do you have cancer, leukemia, AIDS, or any other immune system problem?
• Are you pregnant or could you become pregnant in the next three months?

The Markup and KFF Health News documented Rite Aid sharing this data with Facebook in December 2022. In February of this year, a proposed class-action lawsuit based on similar findings was filed against the drugstore chain in California, alleging code on Rite Aid’s website sent Facebook the time of an appointment and an identifier for the appointment location, demographic information, and answers to questions about vaccination history and health conditions. Rite Aid has moved to dismiss the suit.

After the lawsuit was filed, The Markup and KFF Health News tested Rite Aid’s website again, and it was no longer sending answers to vaccination questions to Facebook.

Rite Aid isn’t the only company that sent answers to eligibility questionnaires to social media firms. Supermarkets Albertsons, Acme, and Safeway, which are owned by the same parent company, also sent answers to questions in their vaccination intake form—albeit in a format that requires cross-referencing the questionnaire’s source code to reveal the meaning of the data.

Using the Firefox web browser’s Network Monitor tool, and with the help of a patient with an active prescription at Rite Aid, KFF Health News and The Markup also found Rite Aid sending the names of patients’ specific prescriptions to Facebook. Rite Aid kept sharing prescription names even after the company stopped sharing answers to vaccination questions in response to the proposed class action (which did not mention the sharing of prescription information). Rite Aid did not respond to requests for comment, and as of June 23, the pixel was still present and sending the names of prescriptions to Facebook.

Other companies shared data about medications from other parts of their sites. Customers of Sam’s Club and Costco, for example, can search names of prescriptions on each retailer’s website to find the local pharmacy with the cheapest prices. But the two websites also sent the name of the medication the user searched for, along with the user’s IP address, to social media companies.

Many of the retailers The Markup and KFF Health News looked at did not respond to questions or declined to comment, including Costco and Sam’s Club. Albertsons said the company “continually” evaluates its privacy practices. CVS said it was compliant with “applicable laws.”

Kroger’s Rolfes wrote that the company’s “trackers disclose product information, which is not sensitive health information unless one or more inferences are made. Kroger does not make any inferences linking the product information collected or disclosed by trackers to an individual’s health condition.”

A huge regulatory challenge

Pharmacies are just one facet of a huge health care sector. But the industry as a whole has been roiled by disclosures of tracking pixels picking up sensitive clinical data.

After an investigation by The Markup in June 2022 found widespread use of trackers on hospital websites, regulatory and legal attention has homed in on the practice.

In December, the Department of Health and Human Services’ Office for Civil Rights published guidance advising health providers and insurers how pixel trackers’ use can be consistent with HIPAA. “Regulated entities are not permitted to use tracking technologies in a manner that would result in impermissible disclosures” of protected health information to tracking technology or other third-party vendors, according to the official bulletin. If implemented, the guidance would provide a path for the agency to regulate hospitals and other providers and fine those who don’t follow it. In an interview with an industry publication in late April, the director of the Office for Civil Rights said it would be bringing its first enforcement action for pixel use “hopefully soon.”

Lobbying groups are seeking to confine any regulatory fallout: The American Hospital Association, for example, sent a letter on May 22 to the Office for Civil Rights asking that the agency “suspend or amend” its guidance. The office, it claimed, was seeking to protect too much data.

This year the Federal Trade Commission has pursued action against companies like GoodRx, which offers prescription price comparisons, and BetterHelp, which offers online therapy, for alleged misuse of data from questionnaires and searches. The companies settled with the agency.

Health care providers have disclosed to the federal government the potential leakage of nearly 10 million patients’ data to various advertising partners, according to a review by The Markup and KFF Health News of breach notification letters and the Office for Civil Rights’ online database of breaches. That figure could be a low estimate: A new study in the journal Health Affairs found that, as of 2021, almost 99 percent of hospital websites contained tracking technologies.

One prominent law firm, BakerHostetler, is defending hospitals in 26 legal actions related to the use of tracking technologies, lawyer Paul Karlsgodt, a partner at the firm, said during a webinar this year. “We’ve seen an absolute eruption of cases,” he said.

Abortion- and pregnancy-related data is particularly sensitive and driving regulatory scrutiny. In the same webinar, Lynn Sessions, also with BakerHostetler, said the California attorney general’s office had made specific investigative requests to one of the firm’s clients about whether the client was sharing reproductive health data.

It’s unclear whether big tech companies have much interest in helping secure health data. Sessions said BakerHostetler had been trying to get Google and Meta to sign so-called business associate agreements. These agreements would bring the companies under the HIPAA regulatory umbrella, at least when handling data on behalf of hospital clients. “Both of them, at least at this juncture, have not been accommodating in doing that,” Sessions said. Google Analytics’ help page for HIPAA instructs customers to “refrain from using Google Analytics in any way that may create obligations under HIPAA for Google.”

Meta says it has tools that attempt to prevent the transfer of sensitive information like health data. In a November 2022 letter to Sen. Mark Warner (D-Va.) obtained by KFF Health News and The Markup, Meta wrote that “the filtering mechanism is designed to prevent that data from being ingested into our ads.” What’s more, the letter noted, the social media giant reaches out to companies transferring potentially sensitive data and asks them to “evaluate their implementation.”

“I remain concerned the company is too passive in allowing individual developers to determine what is considered sensitive health data that should remain private,” Warner told The Markup and KFF Health News.

Meta’s claims in its letter to Warner have been repeatedly questioned. In 2020, the company itself acknowledged to New York state regulators that the filtering system was “not yet operating with complete accuracy.”

To test the filtering system, Sven Carlsson and Sascha Granberg, reporters for SR Ekot in Sweden, set up a dummy pharmacy website in Swedish, which sent fake, but plausible, health data to Facebook to see whether the company’s filtering systems worked as stated. “We weren’t warned” by Facebook, Carlsson said in an interview with KFF Health News and The Markup.

Carlsson and Granberg’s work also found European pharmacies engaged in activities similar to what The Markup and KFF Health News have found. The reporters caught a Swedish state-owned pharmacy sending data to Facebook. And a recent investigation with The Guardian found the U.K.-based pharmacy chain LloydsPharmacy was sending sensitive data—including information about symptoms—to TikTok and Facebook.

In response to questions from KFF Health News and The Markup, Meta spokesperson Emil Vazquez said, “Advertisers should not send sensitive information about people through our Business Tools. Doing so is against our policies and we educate advertisers on properly setting up Business Tools to prevent this from occurring. Our system is designed to filter out potentially sensitive data it is able to detect.”

Meta did not respond to questions about whether it considered any of the information KFF Health News and The Markup found retailers sending to be “sensitive information,” whether any was actually filtered by the system, or whether Meta could provide metrics demonstrating the current accuracy of the system.

In response to our inquiries, Twitter sent a poop emoji, while TikTok and Pinterest said they had policies instructing advertisers not to pass on sensitive information. LinkedIn and Nextdoor did not respond.

Google spokesperson Jackie Berté said the company’s policies “prohibit businesses from using sensitive health information to target and serve ads” and that it worked to prevent such information from being used in advertising, using a “combination of algorithmic and human review” to remedy violations of its policy.

KFF Health News and The Markup presented Google with screenshots of its pixel sending the search company our browsing information when we landed on the retailers’ pages where we could purchase an HIV test and prenatal vitamins, and data showing when we added an HIV test to the cart. In response, Berté said the company had “not uncovered any evidence that the businesses in the screenshots are violating our policies.”

KFF Health News uses the Meta Pixel to collect information. The pixel may be used by third-party websites to measure web traffic and performance data and to target ads on social platforms. KFF Health News collects page usage data from news partners that opt to include our pixel tracker when they republish our articles. This data is not shared with third-party sites or social platforms and users’ personally identifiable information is not recorded or tracked, per KFF’s privacy policy. The Markup does not use a pixel tracker. You can read its full privacy policy here.

This article was co-published with The Markup, a nonprofit newsroom that investigates how powerful institutions are using technology to change our society. Sign up for The Markup’s newsletters.

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

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This article originally appeared in KFF Health News.

Federal regulators want most patients to see a health care provider in person before receiving prescriptions for potentially addictive medicines through telehealth—something that hasn’t been required in more than three years.

During the covid-19 public health emergency, the Drug Enforcement Administration allowed doctors and other health care providers to prescribe controlled medicine during telehealth appointments without examining the patient in person. The emergency declaration ended May 13, and in February, the agency proposed new rules that would require providers to see patients at least once in person before prescribing many of those drugs during telehealth visits.

Controlled medications include many stimulants, sedatives, opioid painkillers, and anabolic steroids.

Regulators said they decided to extend the current regulations—which don’t require an in-person appointment — until November 11 after receiving more than 38,000 comments on the proposed changes, a record amount of feedback. They also said patients who receive controlled medications from prescribers they’ve never met in person will have until November 11, 2024, to come into compliance with the agency’s future rules.

The public comments discuss the potential effects on a variety of patients, including people being treated for mental health disorders, opioid addiction, or attention-deficit/hyperactivity disorder. Thousands of commenters also mentioned possible impacts on rural patients.

Opponents wrote that health care providers, not a law enforcement agency, should decide which patients need in-person appointments. They said the rules would make it difficult for some patients to receive care.

Other commenters called for exemptions for specific medications and conditions.

Supporters wrote that the proposal would balance the goals of increasing access to health care and helping prevent medication misuse.

Zola Coogan, 85, lives in Washington, Maine, a town of about 1,600 residents northeast of Portland. Coogan has volunteered with hospice patients and said it’s important for very sick and terminally ill people in rural areas to have access to opioids to ease their pain. But she said it can be hard to see a doctor in person if they lack transportation or are too debilitated to travel.

Coogan said she supports the DEA’s proposed rules because of a provision that could help patients who can’t travel to meet their telehealth prescriber. Instead, they could visit a local health care provider, who then could write a special referral to the telehealth prescriber. But she said accessing controlled medications would still be difficult for some rural residents.

“It could end up being a very sticky wicket” for some patients to access care, she said. “It’s not going to be easy, but it sounds like it’s doable.”

Some health care providers may hesitate to offer those referrals, said Stefan Kertesz, a physician and professor at the University of Alabama at Birmingham whose expertise includes addiction treatment. Kertesz said the proposed referral process is confusing and would require burdensome record-keeping.

Ateev Mehrotra, a physician and Harvard professor who has studied telehealth in rural areas, said different controlled drugs come with different risks. But overall, he finds the proposed rules too restrictive. He’s worried people who started receiving telehealth prescriptions during the pandemic would be cut off from medicine that helps them.

Mehrotra said he hasn’t seen clear evidence that every patient needs an in-person appointment before receiving controlled medicine through telehealth. He said it’s also not clear whether providers are less likely to write inappropriate prescriptions after in-person appointments than after telehealth ones.

Mehrotra described the proposed rules as “a situation where there’s not a clear benefit, but there are substantial harms for at least some patients,” including many in rural areas.

Beverly Jordan, a family practice doctor in Alabama and a member of the state medical board, supports the proposed rule, as well as a new Alabama law that requires annual in-person appointments for patients who receive controlled medications. Jordan prescribes such medications, including to rural patients who travel to her clinic in the small city of Enterprise.

“I think that once-a-year hurdle is probably not too big for anybody to be able to overcome, and is really a good part of patient safety,” Jordan said.

Jordan said it’s important for health care practitioners to physically examine patients to see if the exam matches how the patients describe their symptoms and whether they need any other kind of treatment.

Jordan said that, at the beginning of the pandemic, she couldn’t even view most telehealth patients on her computer. Three-fourths of her appointments were over the phone, because many rural patients have poor internet service that doesn’t support online video.

The proposed federal rules also have a special allowance for buprenorphine, which is used to treat opioid use disorder, and for most categories of non-narcotic controlled substances, such as testosterone, ketamine, and Xanax.

Providers could prescribe 30 days’ worth of these medications after telehealth appointments before requiring patients to have an in-person appointment to extend the prescription. Tribal health care practitioners would be exempt from the proposed regulations, as would Department of Veterans Affairs providers in emergency situations.

Many people who work in health care were surprised by the proposed rules, Kertesz said. He said they expected the DEA to let prescribers apply for special permission to provide controlled medicine without in-person appointments. Congress ordered the agency to create such a program in 2008, but it has not done so.

Agency officials said they considered creating a version of that program for rural patients but decided against it.

Denise Holiman disagrees with the proposed regulations. Holiman, who lives on a farm outside Centralia, Missouri, used to experience postmenopausal symptoms, including forgetfulness and insomnia. The 50-year-old now feels back to normal after being prescribed estrogen and testosterone by a Florida-based telehealth provider. Holiman said she doesn’t think she should have to go see her telehealth provider in person to maintain her prescriptions.

“I would have to get on a plane to go to Florida. I’m not going to do that,” she said. “If the government forces me to do that, that’s wrong.”

Holiman said her primary care doctor doesn’t prescribe injectable hormones and that she shouldn’t have to find another in-person prescriber to make a referral to her Florida provider.

Holiman is one of thousands of patients who shared their opinions with the DEA. The agency also received comments from advocacy, health care, and professional groups, such as the American Medical Association.

The physicians’ organization said the in-person rule should be eliminated for most categories of controlled medication. Even telehealth prescriptions for drugs with a higher risk of misuse, such as Adderall and oxycodone, should be exempt when medically necessary, the group said.

Some states already have laws that are stricter than the DEA’s proposed rules. Amelia Burgess said Alabama’s annual exam requirement, which went into effect last summer, burdened some patients. The Minnesota doctor works at Bicycle Health, a telehealth company that prescribes buprenorphine.

Burgess said hundreds of the company’s patients in Alabama couldn’t switch to in-state prescribers because many weren’t taking new patients, were too far away, or were more expensive than the telehealth service. So Burgess and her co-workers flew to Alabama and set up a clinic at a hotel in Birmingham. About 250 patients showed up, with some rural patients driving from five hours away.

Critics of the federal proposal are lobbying for exemptions for medications that can be difficult to obtain due to a lack of specialists in rural areas.

Many of the public comments focus on the importance of telehealth-based buprenorphine treatment in rural areas, including in jails and prisons.

Rural areas also have shortages of mental health providers who can prescribe controlled substances for anxiety, depression, and ADHD. Patients across the country who use opioids for chronic pain have trouble finding prescribers.

It also can be difficult to find rural providers who prescribe testosterone, a controlled drug often taken by transgender men and people with various medical conditions, such as menopause. Controlled medications are also used to treat seizures, sleep disorders, and other conditions.

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

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For the first time in 20 years, malaria has been spread locally by mosquitoes in the United States. The Centers for Disease Control and Prevention (CDC) issued an alert on June 26 stating that at least four people in Florida and one in Texas have contracted the mosquito-borne illness in the past two months.

[Related: Ghana is the first country to approve Oxford’s malaria vaccine.]

“Malaria is a medical emergency and should be treated accordingly,” the CDC wrote in a Health Alert Network Health Advisory. “Patients suspected of having malaria should be urgently evaluated in a facility that is able to provide rapid diagnosis and treatment, within 24 hours of presentation.”

Malaria was once endemic in the US, but was eradicated by the 1970s. One of the CDC’s first tasks at its founding in 1946 was eliminating the disease as a public health threat.

It is caused by several species of parasites that are transmitted by Anopheles mosquitoes. Malaria usually causes flu-like symptoms, but it can also cause nausea, vomiting, and diarrhea in some cases. It can lead to severe disease if it is left untreated with medication. The World Health Organization estimates that it killed 619,000 people worldwide in 2021. Nearly half of the world’s population is at risk of the disease. 

Roughly 2,000 cases of malaria are diagnosed in the US annually, but those are typically contracted by people who have traveled outside the country. In 2003, there were eight cases of locally acquired mosquito-borne malaria identified in Palm Beach County, Florida. 

According to a Florida’s Department of Health statement announcing a statewide mosquito-borne illness advisory, the new cases were identified in Sarasota County. Texas has also issued a health advisory. The CDC recommends that hospitals around the country have malaria tests on hand, stock up on treatments, and that local public health officials have a plan to rapidly identify, prevent, and control the disease. 

The new cases were caused by the malaria parasite Plasmodium vivax, which is less likely to cause severe disease than some other species of malaria parasites. The CDC says that all five patients “have received treatment and are improving.” The agency also notes that the risk of locally acquired malaria still remains very low in the US.

[Related: Why did it take 35 years to get a malaria vaccine?]

“It’s not panic time,” Brian Grimberg, an associate professor of pathology and international health at Case Western Reserve University, told The Washington Post. “I think the message is to be aware. I mean, Americans never think about malaria unless they travel abroad.”

Malaria is most common in warm climates and some scientists worry that as the Earth warms, more regions will be affected by the disease. According to a 2022 study published in Nature, climate change can exacerbate a full 58 percent of the infectious diseases that humans come in contact with around the world. The authors of that study note that hepatitis can be spread by flooding, droughts can bring in rodents that are infected with hantavirus, and warmer temperatures can lengthen the life of mosquitoes carrying malaria. 

The CDC advises the public to take basic steps to prevent mosquito bites and control mosquitoes at home. Wearing insect repellent, long-sleeved shirts and pants when outdoors can help prevent bug bites, in addition to using good screens on windows and doors when inside. 

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This article was originally published on Undark.

In October 2021, 84-year-old Jim Yeldell was diagnosed with stage 3 lung cancer. The first drug he tried disrupted his balance and coordination, so his doctor halved the dose to minimize these side effects, Yeldell recalled. In addition, his physician recommended a course of treatment that included chemotherapy, radiation, and a drug targeting a specific genetic mutation. This combination can be extremely effective — at least in younger people — but it can also be “incredibly toxic” in older, frail people, said Elizabeth Kvale, a palliative care specialist at Baylor College of Medicine, and also Yeldell’s daughter-in-law.

Older patients are often under-represented in clinical trials of new cancer treatments, including the one offered to Yeldell. As a result, he only learned of the potential for toxicity because his daughter-in-law had witnessed the treatment’s severe side effects in the older adults at her clinic.

This dearth of age-specific data has profound implications for clinical care, as older adults are more likely than younger people to be diagnosed with cancer. In the U.S, approximately 42 percent of people with cancer are over the age of 70 — a number that’s poised to grow in the years to come — and yet they comprise less than a quarter of the people in clinical trials to test new cancer treatments. Those who do participate are often the healthiest of the aged, who may not have common age-related conditions such as diabetes or poor kidney or heart function, said Mina Sedrak, a medical oncologist and the director of the Cancer and Aging program and the University of California Los Angeles.

For decades, clinical trials have tended to exclude older participants for reasons that range from concerns about pre-existing conditions and other medications to participants’ ability to travel to trial locations. As a result, clinicians have little way of being certain that approved cancer drugs will work as predicted in clinical trials for the people most likely to have cancer. This dearth of data means that older cancer patients must decide if they want to pursue a treatment that might yield fewer benefits — and cause more side effects — than it did for younger people in the clinical trial.

This evidence gap extends across the spectrum of cancer treatments — from chemotherapy and radiation to immune checkpoint inhibitors — with sometimes dire results. Many forms of chemotherapy, for example, have proven to be more toxic in older adults, a discovery that came only after the drugs were approved for use in this population. “This is a huge problem,” Sedrak said. In an effort to minimize side effects, doctors will often tweak the dose or duration of medications that are given to older adults, but these physicians are doing this without any real guidance.

Despite recommendations from funders and regulators and extensive media coverage, not much has changed in the past three decades. “We’re in this space where everyone agrees this is a problem, but there’s very little guidance on how to do better for older adults,” Kvale said. “The consequences in the real world are stark.”

Post-approval studies of cancer drugs have helped shed light on the disconnect between how these drugs are used in clinical trials and how they are used in clinics around the country.

For example, when physician and cancer researcher Cary Gross of Yale University set out to study the use of a new kind of cancer drug known as an immune checkpoint inhibitor, he knew that most clinicians were well aware that clinical trials overlooked older patients. Gross’ research team suspected that some doctors might be wary of offering older adults the treatments, which work by preventing immune cells from switching off, thus allowing them to kill cancer cells. “Maybe they’re going to be more careful,” he said, and offer the intervention to younger patients first.

But in a 2018 analysis of more than 3,000 patients, Gross and his colleagues found that within four months of approval by the U.S. Food and Drug Administration, most patients eligible to receive a class of immune checkpoint inhibitors were being prescribed the drugs. And the patients receiving this treatment in clinics were significantly older than those in the clinical trials. “Oncologists were very ready to give these drugs to the older patients, even though they’re not as well represented,” Gross said.

In another analysis, published this year, Gross and his colleagues examined how these drugs helped people diagnosed with lung cancer. The team found that the drugs extended the life of patients under the age of 55 by a median of five months, but only by a month in those over the age of 75.

The evidence doesn’t suggest checkpoint inhibitors aren’t helpful for many patients, said Gross. But it’s important to identify which particular populations are helped the most by these drugs. “I thought that we would see a greater survival benefit than we did,” he said. “It really calls into question how we’re doing research, and we really have to double down on doing more research that includes older patients.”

People over the age of 65 don’t fare well with other types of cancer treatments either. About half of older patients with advanced cancer experience potentially life-threatening side effects with chemotherapy, which can lead oncologists to lower medication doses, as in Yeldell’s case.

There’s a strong connection between the lack of evidence from clinical trials and worse outcomes in the clinic, according to Kvale. “There’s a lot of enthusiasm for these medicines that don’t seem so toxic up front,” Kvale said, “but understanding where they do or don’t work well is key, not just because of the efficacy, but because those drugs are almost toxically expensive sometimes.”

This financial aspect is especially critical, said Gross, because Medicare benefits must cover new cancer treatments that are FDA-approved. “It’s a little bit crazy that Medicare is required to cover these drugs if we don’t know whether they work in the older population,” he said.

Since the earliest reports of this data gap, regulators and researchers have tried to fix the problem. Changes to clinical trials have, in principle, made it easier for older adults to sign up. For instance, most studies no longer have an upper age limit for participants. Last year, the FDA issued guidance to industry-funded trials recommending the inclusion of older adults, and relaxing other criteria, such as measures of kidney function, to allow for participants with natural age-related declines. Still, the problem persists.

When Sedrak and colleagues set out to understand why the needle had moved so little over the last few decades, their analysis found a number of explanations, beginning with eligibility criteria that may inadvertently disqualify older adults. Physicians may also be concerned about their older patients’ ability to tolerate unknown side effects of new drugs. Patients and caregivers shared these concerns. The logistics of participation can also prove problematic.

“But of all these, the main driving force, the upstream force, is that trials are not designed with older adults in mind,” Sedrak said. Clinical trials tend to focus on survival, and while older adults do care about this, they often have other motivations — and concerns — when considering treatment.

Most clinical trials are geared toward measuring improvements in health: They may track the size of tumors or months of life gained. These issues aren’t always top of mind for older adults, said Sedrak. He said he’s more likely to hear questions about how side effects may influence the patient’s cognitive function, ability to live independently, and more. “We don’t design trials that capture the endpoints that older adults want to know,” he said.

As a group, older adults do experience more side effects, sometimes so severe that the cure rivals the disease. In the absence of evidence from clinical trials, clinicians and patients have tried to find other ways to predict how a patient’s age might influence their response to treatment. In Yeldell’s case, discussions with Kvale and his care team led him to choose a less intensive course of treatment that has kept his cancer stable since October 2022. He continues to live in his own home and exercise with a trainer three times a week.

For others trying to weigh their choices, researchers are developing tools that can create a more complete picture by accounting for a person’s physiological age. In a 2021 clinical trial, geriatric oncologist Supriya Mohile of the University of Rochester and her colleagues tested the use of one such tool, known as a geriatric assessment, on the side effects and toxicity of cancer treatments. The tool assesses a person’s biological age based on various physiological tests.

The team recruited more than 700 people with an average age of 77 who were about to embark on a new cancer treatment regimen with a high risk of toxicity. Half the participants received guided treatment management recommendations based on a geriatric assessment, which their oncologists factored into their treatment decisions. Only half of this group of patients experienced serious side effects from chemotherapy, compared to 71 percent of those who didn’t receive specialized treatment recommendations.

This type of assessment can help avoid both under-treatment of people who might benefit from chemotherapy and over-treatment of those at risk of serious side effects, Mohile said. It doesn’t compensate for the data on older adults that’s missing from clinical trials. But in the absence of that evidence, tools such as geriatric assessment can help clinicians, patients, and families make better-informed choices. “We’re kind of going backwards around the problem,” Mohile said. Although geriatric oncologists recognize the need for better ways to make decisions, she said, “I think the geriatric assessment needs to be implemented until we have better clinical trial data.”

Since 2018, the American Society of Clinical Oncology has recommended the use of geriatric assessment to guide cancer care for older patients. But clinicians have been slow to follow through in their practice, in part because the assessment doesn’t show any cancer-specific benefits, such as tumors shrinking or people living longer. Instead, the tool’s main purpose is to improve quality of life. “We need more prospective therapeutic trials in older adults, but we also need all of these other mechanisms to be funded,” said Mohile. “So we actually know what to do for older adults who are in the real world.”

Jyoti Madhusoodanan is a science writer based in Portland, Oregon.

This article was originally published on Undark. Read the original article.

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Everyone’s immune system is unique. The way it responds to an incoming threat depends on your genetics, lifestyle, and other factors. But all healthy human immune systems have a first line of defenders: When a germ or infection appears, white blood cells called T cells spring into action against the menace. 

But what if your body’s natural defense system fails? For people with autoimmune disease, this question is their reality. For reasons scientists have not been able to figure out yet, the immune response mistakenly attacks its own healthy cells, struggling to distinguish between ally and enemy. There is no cure for autoimmune disease, because each situation may be different—making it vital to have a treatment tailored to a patient’s needs.

An experimental clinical trial introduces a new approach to managing autoimmune diseases. Published in The Lancet Neurology last week, the authors report the first results from a study of chimeric antigen receptor (CAR) T cell therapy on a rare form of autoimmune disease called myasthenia gravis. In CAR T therapy, doctors re-engineer a person’s immune system to identify, attack, and destroy certain proteins on cell surfaces. The modified treatment was safe to use and improved the symptoms of a 14 group of people living with the condition. 

“This is a remarkable new approach to treating autoimmune disorders with a newer safer, easier CAR T approach,” says Santosh Kesari, a neuro-oncologist and regional medical director of Providence Southern California, who was not involved in the study. While Kesari finds the study “exciting,” he cautions that understanding the true benefit of CAR T therapy depends on the results of randomized double-blind trials—this study was a proof-of-concept to test the safety of administering this treatment to this particular patient population. 

[Related: A ‘living’ cancer drug helped two patients stay disease-free for a decade]

Study participant Danny DeBerry, who had myasthenia gravis for 14 years, tells Popular Science in a statement that after multiple doses, the therapy restored his ability to work and travel. “Recently, I went on vacation with my lovely wife and was able to go on a 10-mile bike ride,” he says. “I’m now in full remission and feel like I gained 15 years of my life back.” 

The treatment has its origins as a cancer therapy, which helps stop the cells involved with the formation and spread of tumors. While effective, traditional CAR T therapy has some downsides. The process requires collecting T cells, removing them from the body, altering the cell’s DNA in a lab, and reinserting them back into the patient. The newly engineered T cells may ramp up the immune system too aggressively, releasing a large number of chemicals called cytokines into the blood. 

These cytokines create an inflammatory response to infection or cancer that, if prolonged, can damage healthy cells as well. CAR T cell therapy is also associated with substantial neurological complications. The current study used RNA instead of DNA to genetically engineer the cells to last for a finite life period. T cells engineered with DNA can instead live much longer, creating the negative effects. 

In the trial, using a CAR T therapy developed by Maryland-based biopharmaceutical company Cartesian Therapeutics, these white blood cells were altered to recognize a marker called B cell maturation antigen (BCMA). That marker signals cells to produce antibodies. In myasthenia gravis, these antibodies destroy healthy tissue that connect nerves and muscles. People with the condition show signs of droopy eyelids, have a weakness in their arms or legs, and, in the most severe cases, can struggle to breathe or swallow, explains lead author James Howard, a professor of neurology at the University of North Carolina at Chapel Hill. 

[Related: Doctors successfully treat two babies with leukemia using gene-edited immune cells]

The authors administered three different doses of CAR T therapy to figure out the highest dose that people could tolerate. Each person then received six doses of the maximum dose. A three to nine month follow-up showed only minor side effects with the maximum dose. The most mild after-effects involved headache, nausea, vomiting, and fever, which all went away 24 hours after the last infusion. More importantly, the authors did not notice any signs of neurotoxicity and an inflammatory condition called cytokine release syndrome—two severe side effects common with traditional CAR T therapy.

The small trial was a proof-of-concept only—assessing the side effects and clinical improvements would warrant a much larger study. The authors are currently in the midst of a phase 2 trial on the treatment’s effectiveness with a larger pool of participants. Howard says based on the data they collect, there may be plans to move forward with a regulatory trial for drug approval.

If additional trials show positive results, people with conditions other than cancer, such as those with dysfunctional immune systems, could benefit from regular CAR T therapy. One question that needs to be answered is how often patients need this treatment. Since this type of CAR T therapy uses cells that live for a limited amount of time, it won’t be a one-and-done infusion. Howard says longer and larger trials in the future will determine how often a person has to get retreated. However, he says, “if we can achieve results that will last years, that will be highly transformational to individuals with autoimmune disease who might only need to be treated once a year.”

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When urologic oncologist Dan Theodorescu thinks about his 25 years of research on bladder cancer, he remembers being in a flow. “When you hit something, you know in your gut that it’s really important and everything works out because you’re onto something.” His latest study, published on June 21 in the journal Nature, provides a clearer picture on why men have a greater risk for bladder cancer.

The trailblazing findings draw a clear connection between the disease and damage to the Y chromosome—the genetic structure that largely distinguishes male from female in mammals at birth. Bladder cancer is a sexually dimorphic disease with men making up a disproportionate amount of cases. In fact, men have a 1 in 28 chance of developing the cancer, compared to women, who have a 1 in 91 chance. Theodorescu, now the director of Cedars-Sinai Cancer, sought to understand why men are more prone to developing this type of cancer. Beyond risk factors like smoking cigarettes, he narrowed his decades-long search to changes in hormones and chromosomes. Previous work in the field had found that an increase in androgens, which are produced in the testes and ovaries, interferes with the body’s ability to fight off cancerous tumors. However, until this current study, few researchers focused on the role of chromosomes in bladder cancer.

As men get older, they naturally see the Y chromosome disappear in some cells. It’s a common phenomenon—at least 40 percent of men partially lose their Y chromosome by age 70. Previous research has linked that loss with several health problems, including an increase in heart failure, Alzheimer’s disease, and premature death. 

[Related: What is a pangenome?]

Theodorescu and his team started by studying several bladder cancer cell lines (a population of cells bred from a single common cell). They grew and isolated two sets of cells from male mice whose fathers had either kept or lost the Y chromosome. Tumor cells without a Y chromosome were more likely to exhibit aggressive growth than those with the Y chromosome. 

The next step involved pooling together 16 cancer cells from mice containing a normal Y chromosome with 16 cells missing a Y chromosome. Both cell lines had a similar growth rate. However, when they studied the same cell lines in animals, the authors noticed the tumor cells containing a Y chromosome did not grow as well as cells without a Y chromosome. 

While the cell models hint at the sex chromosome’s role in cancer development, they don’t explain why it makes bladder tumors grow more aggressively. One hypothesis is that tumor cells without a Y chromosome grow faster because they have an easier time evading a person’s immune system. To test this possibility, the researchers injected Y-positive and Y-negative cells into mice bred without an immune system. Both tumor cells grew at the same rate, unlike in the cell lines where natural defenses were intact. “This was the clue that Y-negative cells were messing with the immune system somehow,” Theodorescu says.

Another experiment used genetically engineered mice missing various pieces of their immune system and found that immune cells responsible for fighting infection, called T cells, were the ones most affected by the loss of the Y chromosome. “We compared T cells from Y-negative to Y-positive tumors and found Y-negative tumors are doing things to T cells to get them exhausted,” Theodorescu explains. “An exhausted T cell can no longer destroy the tumor.”

The study might provide some insights on biological processes like adaptive immunity that are affected by disappearing Y chromosomes, says Chris Lau, a professor of medicine at the University of California, San Francisco who studies the human Y chromosome in his own research. “This could very well be the mechanism contributing to the disadvantage that seems to doom men with a mosaic loss of the Y chromosome in many other diseases, in which the immune system could play a role.” 

Of course, the million-dollar question is whether doctors can use this knowledge to help patients with bladder cancer. One option includes immune checkpoint inhibitors. This common form of immunotherapy blocks the receptors that tumors use to send signals that confuse T cells. It also teaches T cells how to recognize cancer cells. When Theodorescu’s team administered immune checkpoint inhibitors to mice, they found those with Y-negative tumors responded better to treatment than Y-positive tumors.

[Related: A ‘living’ cancer drug helped two patients stay disease-free for a decade]

A new project Theodorescu and his colleagues are currently working on is seeing how many genes on the X chromosome are duplicates of genes found in the Y chromosome, also known as paralogs. Any mutations of these paralogs would cause a loss of gene function that could contribute to immune evasion in women, potentially adding to the risk of bladder cancer. Another issue the team is investigating is what happens to men who lose their Y chromosome and have mutations in Y-related genes on the X chromosome. “The loss may give you a worse cancer, but the response to immunotherapy could be even better,” Theodorescu notes. 

If all goes well, Theodorescu says he plans to use the data from his recent work to create a test that would predict a person’s response to immunotherapy for any cancer. Additionally, the findings could help enhance immunotherapy and make it more effective against Y-negative tumors. Theodorescu is also not discounting the possibility of boosting immune response against other types of cancer. “If this pans out,” he says, “we may be in a situation where we could use this platform to discover combination therapies that could potentially cure a significant number of patients than checkpoint inhibitor therapy alone.”

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The World Health Organization (WHO) has certified Belize as officially malaria-free. The Central American country with a population of just over 400,000 worked for more than 70 years to stop the deadly mosquito-borne disease.

[Related: Ghana is the first country to approve Oxford’s malaria vaccine.]

Belize joins 41 other countries and one territory that the WHO has certified as malaria-free, including 11 countries in the Americas. Belize is the second Central American nation to be certified malaria-free over the past five years. Paraguay, Argentina, and El Salvador have also been certified. Belize is also the third country in the world to be certified in 2023, following Azerbaijan and Tajikistan.

“WHO congratulates the people and government of Belize and their network of global and local partners for this achievement,”  WHO Director-General Tedros Adhanom Ghebreyesus said in a statement. “Belize is another example of how, with the right tools and the right approach, we can dream of a malaria-free future.”

Malaria is typically transmitted through bites by female Anopheles mosquitoes. According to the CDC, when a mosquito bites an infected person, it takes with it a small amount of blood containing microscopic malaria parasites. When a mosquito bites another person (usually about one week later), these parasites mix with the mosquito’s saliva and are injected into the person being bitten. The disease can also be transmitted through blood transfusions, organ transplants, shared needle use with contaminated blood, or from a mother to her unborn infant before or during delivery.

In 2021, the disease killed an estimated 619,000 people globally and infected 247 million others. Malaria symptoms include a fever and flu-like illness, including headache, muscle aches, chills, and fatigue. Vomiting, diarrhea, and nausea may also occur and malaria can cause anemia and jaundice due to a loss of red blood cells. Severe infection can cause mental confusion, seizures, and kidney failure. 

For the past 30 years, Belize has dramatically reduced its malaria burden. In 1994, the country saw a peak of about 10,000 cases in 1994, down to zero indigenous cases in 2019. The country has implemented strong surveillance for the disease, access to diagnostics, and vector control methods such as insecticide-treated mosquito nets, using insecticides indoors, and trained community health workers.

In 2015, Belize reorganized its malaria program to place more focus on enhanced surveillance in higher-risk populations. This allowed more strategic targeting of interventions and resources to priority areas. Malaria surveillance efforts were maintained throughout the COVID-19 pandemic and the country made efforts to integrate malaria and COVID-19 surveillance systems.

[Related: China becomes the largest country to officially eradicate malaria.]

“A dedicated network of trained community-based health workers and voluntary collaborators were the backbone of malaria elimination efforts in Belize. They helped ensure early detection of malaria cases within their respective communities and, for those with a confirmed malaria diagnosis, the provision of effective antimalarial treatment,” the WHO wrote in a statement.

A country can be certified by the WHO as malaria-free when it “has shown—with rigorous, credible evidence—that the chain of indigenous malaria transmission by Anopheles mosquitoes has been interrupted nationwide for at least the past three consecutive years.”

The world’s first malaria vaccine was approved in 2021 based on the results of an ongoing pilot program in Ghana, Kenya, and Malawi that has reached more than 800,000 children since 2019. In March, Ghana approved another malaria vaccine for young children. 

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The brain is the most complex part of the human body. To keep our heads running smoothly,  more than 100 types of neurotransmitters must shuttle messages across multiple regions of white and gray matter. It’s difficult for researchers to track the immense number of connections that these chemical messengers make—Google recently created one of the most detailed maps of neuronal connectivity patterns, but even the tech giant could only focus on a small section of the brain. 

While it may take decades until someone fully maps out the human brain, there are ways to trace different aspects of connectivity. A new study published today in Science Advances used mind-altering drugs, such as ketamine and the surgical anesthetic propofol, to follow which neurotransmitter systems those pharmaceuticals activate. The findings help identify associations between these drugs and unexpected neurotransmitters. They could also help identify new treatment options for certain conditions and diseases, as the authors found that brain regions commonly altered by different drugs were often similarly affected by various neurological disorders.

Pharmacological agents such as mind-altering drugs have powerful uses in medicine, says Andrea Luppi, a postdoctoral researcher of network neuroscience at the Alan Turing Institute in the United Kingdom. “Anesthetics are extremely useful for surgery. Modafinil and methylphenidate are used to treat certain conditions,” Luppi says. “So it’s important to know how they act on the brain to exert their effects.”

But these types of chemicals can be tricky to understand, because they activate more than one neurotransmitter receptor. Knowing how they work in the brain can improve how they are used in clinical practice in the future. But it’s not enough to predict a drug’s mechanism based purely  on its clinical effects. There is also a chance these drugs could influence other neurotransmitters beyond their main targets. 

[Related: If you grow a brain in a lab, will it have a mind of its own?]

To address these questions, Luppi and his coauthors analyzed two sets of neuroimaging data from past studies to map out the ways the human brain changes when taking 10 mind-altering drugs. These drugs fell under three categories: psychedelics (psilocybin, DMT, LSD, MDMA, ayahuasca, and ketamine), anesthetics (propofol and sevoflurane), and cognitive enhancers (modafinil and methylphenidate). The first data set, based on the PET scans of 1,200 people, helped the team sketch out 19 types of molecules in the brain: all neurotransmitter receptors and transporters.

The second dataset used the fMRI scans of 224 people who had acute exposure to one of the 10 drugs. According to the authors, this is the largest fMRI study to date that has plotted a detailed map of the neurotransmitter landscape when under the influence.

Brain mapping showed that mind-altering drugs work with multiple neurotransmitter systems. The mapping showed expected relationships, such as the link between MDMA and its well-known target, the serotonin 2A receptor. However, the team noticed some mind-altering drugs, like anesthetics and psychedelics, can affect other neurotransmitters beyonds their main molecular targets. For example, anesthetics at the lowest dose primarily target molecules in the brain called GABA_A receptors. But the molecules that the drugs bind to changes as doses increase, the authors found, activating a more diverse group of neurotransmitters. 

[Related: How your brain conjures dreams]

“We are used to thinking that many drugs have a single or few molecular targets. What we see suggests that even when a drug exerts its effect through a specific receptor, it can have downstream consequences on many neurotransmitter systems. This reinforces the idea that the brain is a complex system,” Luppi says. 

According to the study authors, their mapping provides new opportunities to explore how each of these mind-altering drugs affects the neurotransmitter landscape. It could also help vet certain drugs for neuropsychiatric treatments. The changes in activity caused by mind-altering drugs are similar to the changes seen in the brains of patients with conditions such as autism, depression, and schizophrenia, the authors say. Administering mind-altering drugs that rewire the connections in functionally impaired brain areas could be another treatment option for people who live with these conditions. 

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This week, the Federal Communications Commission issued a record-breaking fine against two operatives following their attempt to suppress Black voter turnout in the 2020 presidential election via a robocall scam.

According to the FCC’s official statement on Wednesday, Jacob Wohl and John Burkman previously pled guilty to telecommunications fraud in October 2022, in which they orchestrated over 1,100 of “unlawful robocalls” between August and September 2020. As Ars Technica explained on Thursday, Wohl and Burkman’s prerecorded message featured a Black voice actress identifying herself as “Tamika Taylor” who incorrectly stated that any personal information included in mail-in votes “will be part of a public database that will be used by police departments to track down old warrants and be used by credit card companies to collect outstanding debts.” The robocall additionally made the false claim that the CDC intended to use mail-in voting to “track people for mandatory vaccines.”

In a separate legal complaint against the two men, plaintiffs explained “Tamika Taylor” is the name previously misattributed to Breonna Taylor’s mother, Tamika Palmer. Taylor was shot and killed by Louisville, KY police in 2020, and subsequently became a figure within the racial justice and police reform movements.

[Related: You can stop bots and spammers from calling you so freaking much.]

“This penalty emphasizes the seriousness with which we take our obligations to protect American consumers, and in this instance American voters, from being targeted through the clear and illegal misuse of U.S. communications networks,” FCC Enforcement Chief Loyaan A. Egal said in Wednesday’s announcement. The FCC’s fines are only the latest in an ongoing crackdown on robocall scammers. In December 2022, the Commission fined two men nearly $300 million for their own auto warranty scam that sent out over 5 billion robocalls in just three months. 

A paper trail linked the two men to a coordinated, purposeful targeting of minority voters ahead of the 2020 election. In an email on August 25, 2020, Wohl sent Burkman an audiofile to be used in the robocalls, and suggested, “’We should send [the message] to black neighborhoods in Milwaukee, Detroit, Philadelphia, Charlotte, Richmond, Atlanta, and Cleveland.” Burkman replied soon after, suggesting they also target Chicago and Minneapolis voters.

In a separate Ohio court sentencing concerning the same scam, Wohl and Burkman were ordered to two years of probation, six months of GPS monitoring, $2,500 in fines each, and 500 hours of community service registering voters in Washington, DC.

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A once-daily pill cut the risk of death in half for a subset of patients with early-stage lung cancer who had undergone surgery. The results of a new clinical trial were presented on June 4 at the American Society of Clinical Oncology’s annual meeting and were published in the New England Journal of Medicine.

[Related: Poor lung cancer screening guidelines miss too many African American smokers.]

The pill named osimertinib and sold under the brand name Tagrisso is manufactured by drugmaker AstraZeneca, who funded the study. The pill is directed at a specific receptor that helps cancer cells grow. 

The study included a 682-patient trial that included patients diagnosed with non-small cell lung cancer, which is one of two main types of primary lung cancer that makes up 80 to 85 percent of all lung cancers. The participants in the study also had a mutation in the epidermal growth factor receptor (EGFR) gene. This gene codes for a protein that is found on the surface of cells. EGFR mutations can increase cancer’s ability to grow and spread throughout the body, which increases a patient’s risk of cancer recurrence after completing treatment. 

Roughly 10 to 15 percent of lung cancer cases in the United States have an EGFR mutation, however it is more common in Australia and Asia. The mutation is usually detected in those with little to no history of smoking. About two-thirds of the trial participants had no history of smoking, suggesting that it works for smokers and non-smokers diagnosed with lung cancer.

Osimertinib generally works by blocking the effects of these common EGFR mutations.

According to the results, five years after their diagnosis, 88 percent of those who took osimertinib were still alive, compared to 78 percent of the placebo group. The pill lowered the overall risk of death from lung cancer by 51 percent. This data is reportedly the first to show how targeted treatment for early-stage lung cancer can impact patient survival.

“Thirty years ago, there was nothing we could do for these patients,” study co-author and deputy director of Yale Cancer Center Roy Herbst said, according to The Guardian. “Now we have this potent drug. Fifty percent is a big deal in any disease, but certainly in a disease like lung cancer, which has typically been very resistant to therapies.”

[Related: 100 Years Of Smoking Studies In Popular Science.]

Over 100 countries have already approved osimertinib under the brand name Tagrisso, including the United States. The Food and Drug Administration (FDA) approved it in 2015 for those with more advanced lung cancer whose diseases worsened during or after other cancer treatments. In 2020, the FDA approved Tagrisso for early-stage versions of lung cancer.

Patrick Forde, an associate professor of oncology at Johns Hopkins Medicine who was not involved in the study told NBC News that before targeted treatments like Tagrisso were available, patients diagnosed with stage 1 to 3 lung cancer would typically receive chemotherapy after surgery. He estimated that the treatment would improve odds of survival by roughly five percent compared to those who did not receive chemo. 

“If you go back 15 years, for this patient population we would have expected maybe a survival of 50 percent at five years,” he said. “But because of the advances both for stage 4 cancer, and now this advance in earlier stage cancer, we’re up to 88 percent.”

Forde has consulted for AstraZeneca and obtained research funding from the drug company in the past.
Lung cancer accounts for about 1.8 million deaths per year and is the world’s leading cause of cancer death. More than 127,000 Americans die from lung cancer, according to data from the American Cancer Society.

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Although the World Health Organization only recently declared the end of the mpox global emergency, the virus is not gone. Chicago health authorities, for one, have identified up to 31 cases of the disease formerly known as monkeypox since the beginning of April, and the Centers for Disease Control and Prevention is raising awareness ahead of the summer. 

A full schedule of two doses of the Jynneos vaccine can be up to 89 percent effective, but the CDC urges high-risk communities to take extra precautions to avoid a health crisis like we had last summer. Understanding how the virus spreads and how to prevent infection is key to complementing the protection provided by vaccines.

It’s worth noting that mpox seldom requires hospitalization and is rarely lethal: The US reported 30,235 confirmed cases between May 2022 and March 2023, with 38 deaths, the majority of both among Black people. Last year, access to treatment was limited, but there’s no reason to believe that will be the case this year, especially in major cities, as the health system is currently better equipped to respond to new mpox surges. But prevention is still crucial as the skin lesions that are one of the most common symptoms of the virus can be extremely painful without proper medication. 

Matching last year’s domestic and international trends, the recent small surge in Chicago has mainly been concentrated within the community of gay, bisexual, and queer men who have sex with other men (GBMSM, in short), and their sexual network. Whether you identify as such or are currently at low risk of contracting the virus, you should know how mpox spreads and how to stay safe.  

“​​Let’s say you touch a lesion and the virus gets on your hand. Unless you have a break in the skin, you should be ok,” says Scott Roberts, assistant professor of infection prevention at Yale University’s School of Medicine. The problem is that we tend to touch our mouths, eyes, and faces throughout the day, which means you can infect yourself with viruses lingering on your digits, he explains. 

Because sex entails a lot of constant and persistent touching, involves the exchange of multiple bodily fluids, and the inherent friction can tear skin, it has become the main way mpox spreads. In 2022, sex was responsible for 82 percent of transmissions, and 84 percent of cases have been within the GBMSM community. This is why some experts believe mpox could be classified as a sexually transmitted infection or STI. But Roberts isn’t one of them.

[Related: A guide to preventing, spotting, and managing STIs]

“The reason that we’re seeing the spread through sexual contact is not that it’s a sexually transmitted infection, but rather the close, prolonged contact in an intimate encounter, where you’re touching parts of the skin, kissing, sharing bodily fluids,” Roberts says. “All of that is a good scenario for a virus to spread.”

Several studies have found traces of the mpox virus in semen, but only one of them, published by Italian researchers in The Lancet Infectious Diseases, showed the virus in the sample could replicate and actually infect another person. Unfortunately, there still isn’t enough evidence either way, so we still don’t know if mpox can spread directly through the exchange of semen, feces, or vaginal fluids.

Keep in mind that skin-to-skin contact doesn’t mean you’ll get infected by shaking hands with someone who has mpox—you’d need a high viral load for that to happen. 

“It definitely requires a much longer time of close and prolonged contact if you don’t touch somebody’s lesions,” says Roberts.

But mpox is not airborne, and it doesn’t behave like COVID-19, where microscopic droplets can infect you if enough of them get into your nose and mouth. Researchers including those who worked on the Lancet study have said that the viral load in a mpox patient’s airways is nowhere near as high as the one from lesion secretions. That means transmission from respiratory fluids may be possible, but a lot less likely.

How to prevent mpox

As mentioned above, because the current and 2022 outbreaks have been mostly contained within the GBMSM community, authorities have given its members priority access to vaccines and treatment options. But even with that and greater availability of inoculations compared to last year, the CDC says only one in four people eligible to get the Jynneos shots actually have received them. 

It’s because of this low vaccination rate, aggravated by the fact that vaccines are not 100 percent effective, that even if you’ve received your two doses, you should still strive to reduce your own risk of contracting mpox as much as possible.

You should also keep in mind that there are a lot of ways to have sex, and some don’t require touching or even being in the same room with your partner. Take this as an opportunity to be creative and explore these options as sexual alternatives.

Anonymity is another problem. We know the thrill of having sex with strangers is, well, the “strangers” part. But it’s better to stay in the know when it comes to stopping the spread of a virus. Anonymous sex rarely gives people the chance to have honest conversations about their levels of mpox exposure, potential symptoms, and vaccination status. Talking to someone before tearing off their clothes will allow everyone involved to stay safer, make informed decisions, and clearly establish how much risk you’re comfortable with. 

And since you’re already having a conversation, don’t forget to exchange real names and contact information with potential partners. These include people you kiss, have penetrative sex with, and do everything in between. This will make it easier to get in touch if you end up with mpox symptoms in the future. 

And if you don’t trust yourself to break the spell of anonymity, try to avoid contexts where anonymous sex is most likely to happen, like sex clubs, sex parties, and any other contexts where on-site casual sex is common.

“Mpox is actually a pretty easy virus to kill,” Roberts says. “Alcohol wipes, soap and water, disinfectant, all of that really easily kills the virus.”

In general, you should regularly disinfect surfaces like kitchen counters, door knobs, and light switches, the CDC says. You should also wash your hands frequently with an alcohol-based sanitizer, or soap and water. If you’re not sure whether your cleaning products will do the trick, the Environmental Protection Agency has a list of approved disinfectants. 

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But before you start, there are a few things you should keep in mind before you craft homemade hand sanitizer. First, it’s crucial that you understand that proper hand washing will always be better than simply rubbing your digits with hand sanitizer. Using the right amount of alcohol-based disinfectant (3 milliliters) for 25 to 30 seconds is fine in a pinch, but soap, water, and a good scrub are the absolute best way to protect yourself against contagious diseases.

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Knowing how to make hand sanitizer is useful if you ever find yourself in the middle of a health emergency like the COVID-19 pandemic. But these and other DIY recipes are only for extreme cases when hand washing is not an option and supplies are low. Professionals use these formulations in underserviced healthcare settings, and if at some point hand sanitizer is not available at local stores, you can use them too.

Lastly, your homemade hand sanitizer won’t last forever. The main active ingredient in the recipes below is isopropyl alcohol, a volatile compound that will evaporate over time and compromise the effectiveness of your hand sanitizer. When alcohol concentration drops below 60%, your hand sanitizer won’t be able to kill COVID-19 or influenza, for example. The shelf life of store-bought hand sanitizers can vary—the industry standard is three years, but it can go up to five. How long your DIY hand sanitizer lasts will depend on the type and size of the container you use and how often you open it, along with room temperature and humidity. Unfortunately, all of these factors make it hard to predict exactly how long your hand sanitizer will be good for, so proceed with caution. 

The WHO has a comprehensive guide on how to make hand sanitizer—the only problem is that if you follow their instructions, you’ll end up with a lot of it. Like, exactly 2.6 gallons of it. If you want to make enough to last you, your family, and all your friends through a zombie apocalypse, you definitely can. But if you want to keep things on a smaller scale, we’ve adapted the measurements for you.

5. Sanitize your spray bottles and pour in your hand sanitizer. Spray some of your leftover alcohol into your bottles and let them sit until the alcohol has evaporated. Then pour in your sanitizer.

6. Label your bottles. Hand sanitizers pose a real risk of involuntary alcohol poisoning, especially among children, who were largely affected by it during the first months of the COVID-19 pandemic. You don’t want anyone to accidentally ingest your newly made hand sanitizer. Take the time to label your bottles with their contents and the date, and keep them away from unsupervised kids.

6. Label your containers. Hand sanitizers pose a real risk of involuntary alcohol poisoning, especially among children, who were largely affected by it during the first months of the COVID-19 pandemic. You don’t want anyone to accidentally ingest your newly made hand sanitizer. Take the time to label your bottles with their contents and the date, and keep them away from unsupervised kids.

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Over the first two years of the COVID-19 pandemic, the coronavirus directly or indirectly killed about 15 million people worldwide, according to estimates from the World Health Organization. In the United States, more people died in 2020 and 2021 than during the 1918 influenza pandemic, which was widely called the most deadly in recorded history. 

The word “deadly” certainly applies to the virus that causes COVID-19. And yet, epidemiologists hesitate to give SARS-CoV-2 the superlative of deadliest virus in human history. To them, the raw number of mortalities caused by a given virus doesn’t always paint the full picture of a pathogen’s danger—especially when comparing viral outbreaks across time.

Raw mortality numbers have to be taken in the context of the world’s total population, says Jennifer Nuzzo, professor of epidemiology and director of the Pandemic Center at Brown University School of Public Health. “A lot of people talk about how COVID deaths eclipsed what we saw in 1918,” she says. “It’s really important to remember that the population of 1918 was a fraction of what it is today.” In that context, the flu of 1918 rises back up in the ranks in terms of deadliness.

Using the “case fatality rate” metric to determine what virus is the deadliest, rabies would likely come out on top. That’s because, if an infection becomes symptomatic, rabies is fatal to humans in more than 99 percent of cases. Globally, approximately 59,000 people die from rabies every year. Very few of those deaths—an average of two in the US—occur in the developed world because of rabies vaccines for household pets and swift medical interventions after bites.

But “a virus doesn’t have to have a very high case fatality ratio to cause a tremendous amount of death and disruption,” Nuzzo says. “It’s more about looking at the environments in which the viruses are spreading, and our social and human vulnerabilities to it.” 

A virus with a lower case fatality rate can kill more people if it’s highly transmissible, with a long period of time before severe or obvious symptoms set in. This allows an infected person to expose many others. That’s why SARS-CoV-2 caused such a rapid and devastating outbreak around the globe. It’s easily transmitted via airborne droplets, and doesn’t always or immediately cause severe illness. 

[Related: Can viruses be good for us?]

Globalization sped it along, too. “When a virus spreads at the pace of a human being walking, that’s very different than when you can hop on an airplane and be anywhere in the world in 36 hours,” Nuzzo says. 

During large outbreaks such as epidemics or pandemics, epidemiologists look at another metric, called excess deaths: how many more people died during a period of time than typically do over that same window. Excess deaths can account for other indirect ways that a virus causes death, Nuzzo says, such as patients who need critical care but can’t get it in overburdened hospitals.

Here’s how some of the most devastating viruses in human history tell different stories of how high a death toll can rise:

Influenza

The 1918 influenza pandemic still far and away ranks as the deadliest global outbreak of the 20th century. Thought to be caused by an H1N1 virus, it spread globally in 1918 and 1919. An estimated 500 million people were infected (approximately a third of the global population) and 50 million people died worldwide, about 675,000 of whom were in the United States, according to the Centers for Disease Control and Prevention. 

Without sophisticated testing and tracking, death toll estimates rely heavily on excess death calculations. Some suggest the true toll was closer to 17 million, while others set it much higher at 100 million. William Schaffner, professor of preventive medicine and professor of medicine in the division of infectious diseases at the Vanderbilt University School of Medicine, cautions against over-interpreting comparisons between the historic flu data and modern viral outbreaks.

[Related: Can you get diseases from bad bathroom smells?]

 “We are determining cases and even counting deaths with much more precision now than we did then,” he says. At the time, there were also no flu vaccines and no antibiotics to treat secondary bacterial infections, which likely drove the excess death toll higher.

Today, the youngest and oldest people are most likely to die from influenza. But during the pandemic over 100 years ago, Schaffner says, deaths bore a different signature: mortality peaked among young and middle-aged adults, too. Why that happened is still unclear, he says, but it contributed to the historic toll of that pandemic.

Influenza continues to hold its place as one of the deadliest viruses, despite the availability of vaccines. Variants of the influenza virus have led to other pandemic-level events, such as the 2009 outbreak colloquially called the swine flu pandemic. But the virus is also endemic in our society, and infects an estimated 1 billion people globally every year, according to the World Health Organization. Of those cases, the WHO reported in 2019, somewhere between 290,000 to 650,000 result directly or indirectly in deaths. 

An estimated 40.1 million people have died from AIDS-related illnesses since the start of the epidemic, according to the Joint United Nations Program on HIV and AIDS. That is nearly half of the number of people estimated to have become infected with HIV since the start of the epidemic, at an estimated 84.2 million. 

The case fatality rate of HIV/AIDS was historically quite high. Some estimates put it around 80 percent without treatment. But much has changed since the 1980s. Today, there are ways to manage HIV and mitigate the immunodeficiencies associated with an infection, and most patients are diagnosed sooner after an infection. In the United States, the rate of HIV-related deaths fell by nearly half from 2010 to 2017, according to the CDC. 

That excess deaths metric likely reached a much higher number by the time officials declared the public health emergency over in early May. The Omicron wave that swept around the globe in late 2021 and early 2022 saw one of the largest surges in cases of COVID-19 and, although the variant didn’t seem to be more deadly than previous variants, with millions of people infected, a high death toll in the hundreds of thousands was inevitable. 

Early in the pandemic, the case fatality rates calculated for SARS-Cov-2 varied considerably. Many estimates were likely higher than the true number, as researchers scrambled to devise tests for the virus and milder cases slipped through the cracks. In early 2020, estimates of the case fatality rate by country ranged as high as 25 percent or more. Since then, case fatality rates have dropped, and now, according to Johns Hopkins University, they are as high as 4.9 percent. In the US, the case fatality rate is 1.1 percent. 

Mortalities continued to stack up into the 20th century, with an average of three out of every 10 people infected dying. The disease, which is caused by variola virus, is estimated to have killed more than 300 million people from 1900, until a global vaccination campaign halted its path of devastation in 1977. It was the first disease ever to be eradicated. 

[Related: The first honeybee vaccine could protect the entire hive, starting with the queen]

But it was the very thing that made it particularly fearsome that was its downfall, Schaffner says. “It created such a distinctive rash that people could identify it and fear it. And that was one of its Achilles heels,” he says. Because it was so easily identifiable, and spread so slowly, vaccinating the local population near an outbreak swiftly curtailed transmission. Such an approach, he says, was part of the vaccination strategy that eradicated the great pestilence. 

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A phase 3 trial found that a new meningococcal disease vaccine is safe and effective and also induces a strong immune response across five strains of meningococcal bacteria. The results were published May 24 in the New England Journal of Medicine. The vaccine could be a useful tool in eliminating meningitis in African countries including parts of Senegal, Mali, and Ethiopia.

[Related: A once-forgotten antibiotic could be a new weapon against drug-resistant infections.]

Meningococcal disease is a cause of meningitis and blood poisoning. According to the World Health Organization, meningitis caused an estimated 25,000 deaths in 2019. While vaccines are readily available in wealthier countries, vaccinating the more vulnerable regions has been a challenge, largely due to cost. Developing affordable vaccines that provide broad coverage against meningococcal disease strains is a key part of the World Health Organization’s Defeating Meningitis by 2030 Global Roadmap.

The trial compared the immune response generated by a new pentavalent, or 5-in-1, vaccine  called NmCV-5 against that of the licensed quadrivalent, or 4-in-1, MenACWY-D vaccine. The participants included 1,800 healthy two to 29-year-olds in Mali and The Gambia in western Africa. The vaccinations occurred in June 2021, and the trial didn’t find any safety concerns with NmCV-5. 

After 28 days, the immune responses generated by one dose of NmCV-5 were generally higher than those generated by the 4-in-1 vaccine across all age groups. The 5-in-1 vaccine also induced a strong immune response across meningococcal bacteria strains A, C, W, and Y and the emerging X strain. Currently, there is no licensed vaccine against the X strain, which may be the cause of meningitis epidemics in sub-Saharan Africa.

“Meningitis is a deadly disease with the ability to spread like wildfire in the event of an outbreak, this affects all ages most especially within the meningitis belt region,” study co-author Ama Umesi said in a statement. Umesi is a clinical trial coordinator and clinician from the Medical Research Council’s Unit The Gambia at the London School of Hygiene & Tropical Medicine. 

“Epidemic preparedness is the way forward in providing available, affordable and accessible vaccines relevant to regions prone to meningitis outbreaks. Having meningitis vaccines should be a public health priority to prevent catastrophic outcomes during an outbreak and would be a game changer in the fight against meningitis,” Umensi said.

Issues with supply and affordability have limited the use of 4-in-1 meningococcal vaccines across a portion of sub-Saharan Africa called the meningitis belt. This region is at high-risk of epidemics of both meningococcal and pneumococcal meningitis. The NmCV-5 vaccine was developed by the Serum Institute of India and PATH, the global division of the Bill & Melinda Gates foundation. It follows the successful Meningitis Vaccine Project that developed an effective meningococcal A vaccine called MenAfriVac.

[Related: Ghana is the first country to approve Oxford’s malaria vaccine.]

According to the study, the new NmCV-5 vaccine can be made available at lower cost than existing 4-in-1 vaccines with more cost-effective production methods. The trial was designed to provide the World Health Organization with the evidence it needs to license the new vaccine for future epidemic control.

“As a researcher in the continent, I am hopeful that relevant vaccines for the common strains within the meningitis belt region will be readily available for timely interventions due to the collaboration and teamwork of multicentre trials like ours,” Umesi said. “Together we can defeat meningitis,” Umesi said. 

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This article originally published on The Conversation.

Intestinal infections take a heavy toll on impoverished Black communities that have out-of-date sewage systems. These infections often spread through contaminated soil and water and are among the most common diseases worldwide.

Approximately one-quarter of the global population is infected with soil-transmitted helminths, intestinal parasitic worms that can cause serious health problems.

Additionally, up to 50% of people around the world are infected with Helicobacter pylori, bacteria that live in the stomach and can cause ulcers and cancer.

I am a biological anthropologist, and it is clear to me that these two types of infections contribute to systemic health inequities, especially among communities of color in which limited access to medical care and inadequate sanitation systems may both increase exposure to pathogens and lead to worse outcomes.

Historically, intestinal infections have been prevalent in parts of the U.S. where high poverty rates and environmental factors – such as flooding and warm, humid summers – favor infection spread.

Although many Americans believe these diseases now exist only in lower-income countries, research that my colleague and I have conducted challenges this assumption.

Renewed interest in US intestinal infections

Launched in 2019, the Rural Embodiment and Community Health Study started with the goal of measuring current infection rates and determining which living conditions contribute to infection risk.

Though national infection rates remain unclear because of the absence of large-scale studies, our preliminary work in 2019 found that 38% of children sampled in a predominantly Black Mississippi Delta community had intestinal parasitic infections.

Moreover, 80% of those children exhibited high levels of intestinal inflammation. Those levels are much higher than those observed in other populations and may lead to several poor health outcomes, including impaired intestinal ability to absorb nutrients and stunted growth.

Our more recent analyses from 2022 focused on adults living in the Mississippi Delta and Southwestern Illinois, two areas that experience regular flooding.

Among those adults, 73% displayed elevated intestinal inflammation, while 45% were infected with H. pylori, the bacteria that can cause ulcers and cancer.

Taken together, those results demonstrate widespread intestinal infections and inflammation at all ages in these low-income, mostly Black communities.

Long-lasting intestinal infections and associated inflammation can lead to nutritional deficiencies, restricted growth, reduced educational attainment, decreased work productivity and increased risk for serious diseases later in life, including certain cancers).

A legal challenge in Alabama

The Rural Embodiment and Community Health Study is not alone in recognizing the impact of intestinal infections on Black communities. One of the most widely publicized recent research studies investigating intestinal infections focused on the health effects of poverty and crumbling sanitation infrastructure in Lowndes County, Alabama, a region characterized by a history of racial segregation and inequity.

Researchers found that more than 1 in 3 people tested in Lowndes County were infected with hookworm, an intestinal worm spread through sewage exposure that lives in soil and infects people by burrowing into bare feet.

This 2017 study has since led to legal action.

In a landmark May 2023 court ruling, the Biden administration found that Alabama’s public health department had discriminated against Black residents by denying access to adequate sanitation systems and imposed fines for resulting sewage issues.

This decision is being hailed by environmental justice advocates as a transformative environmental justice agreement that may increase public awareness of the ongoing health crisis that results from infrastructure neglect and associated pathogen exposure.

Community activists – such as Catherine Coleman Flowers, founder of the Center for Rural Enterprise and Environmental Justice – said they hope the federal government continues to intervene, leading to similar results in other affected communities.

“This country’s neglect of wastewater infrastructure in majority Black communities, both urban and rural, is resulting in a hygienic hell for far too many people, a hell that climate change is only making worse,” Flowers said in a March 2023 interview.

Why are there still parasites in the US?

The story of parasite infection in the U.S. is two-sided.

On one hand, the U.S. has successfully controlled many parasite infections. Malaria is one of them.

In addition, advancements in sanitation infrastructure and household construction mean that many Americans do not generally have to worry about parasite infections.

But this national success is not complete, as demonstrated by the recent findings in low-income Black communities across the country.

Limited awareness of the continued threat posed by neglected intestinal infections has made it more difficult to identify and treat these diseases in the U.S. than in lower-income nations.

For instance, in many countries the drugs needed to treat hookworm infections cost mere cents, but in the U.S., where drug prices are unregulated by the federal government, these same medications can cost hundreds of dollars.

The recent court decision in Alabama represents an important step toward increased national recognition of the role intestinal infections play in perpetuating racial health inequities.

Increased awareness will ideally result in improved access to testing and treatment in affected communities. But more work is needed to assess the full extent of these infections across the U.S.

Even if medical treatment is accessible and affordable, vulnerable individuals are often reinfected, as these pathogens continue to spread through the environment. Structural changes are needed to break the cycle of infection and poor health.

Current federal investment in community infrastructure – including water quality – is encouraging but does not go far enough. Ultimately, a concentrated nationwide effort to update and maintain sanitation systems is the best way to finally halt infection transmission and support health equity across the U.S.

Theresa E. Gildner, Assistant Professor of Biological Anthropology, Arts & Sciences at Washington University in St. Louis. This article is republished from The Conversation under a Creative Commons license. Read the original article.

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Humans are born with instincts for crying and smiling, but not for kissing. Sometime in the past, our ancestors had the idea to smack their mouths together and call it romantic. And though we may not know who gave the first smooch, ancient records of these steamy sessions are helping us piece together when people started locking lips. 

The generally accepted earliest evidence we have of making out is religious text written in India in 1500 BCE. And while there was no official word for kissing back then, sentences like “young lord of the house repeatedly licks the young woman” and lovers “setting mouth to mouth” implied more than platonic relationships. But whether this was when kissing all began is still up for debate. In fact, an overlooked collection of written texts from ancient Mesopotamia (modern-day Iraq and Syria) suggests people were kissing further in the past. 

Citing those texts, authors of a new perspective article published today in the journal Science argue romantic kissing occurred 1,000 years earlier than historians first predicted. And as kissing became more of the norm, old medical records reveal the widespread transmission of viruses that spread through lip-to-lip contact.

“Given what we know about the history of kissing in humans and the myriad of similar kissing-like behaviors observed around the animal kingdom, I’m not surprised by these findings,” says Sheril Kirshenbaum, the author of The Science of Kissing, who was not involved in the study. “Whether romantic or not, kissing influences our bodies and brains in so many meaningful ways by guiding our emotions and decisions.”

[Related: Scientists think they found a 2,000-year-old dildo in ancient Roman ruins]

Clay tablets left behind by ancient Mesopotamians in 2500 BCE describe two types of kissing. The first was the friendly-parental kiss. People kissed the feet of their elders or the ground as a sign of respect or submission. 

The second was the lip kiss with a more erotic and intimate overtone. However, there were a few cultural expectations when it came to this type of kissing. Romantic kissing was an action reserved for married couples, as people frowned upon any PDA in Mesopotamia. Kissing among unmarried folks was taboo, considered to be giving in to sexual temptation. People not meant to be sexually active, such as priestesses, were thought to lose their ability to speak if they kissed someone. “The need for such norms indicates that romantic kissing must have been practiced in society at large,” explains lead author Troels Pank Arbøll, an assyriologist (a person studying the language and civilization of ancient Mesopotamia) at the University of Copenhagen.

As more people adopted the practice of kissing on the lips, ancient medical texts described illnesses whose symptoms resemble viral infections spread through mouth-to-mouth contact. The authors note this aligns with DNA analysis from ancient human remains detecting viruses such as herpes simplex virus 1, Epstein-Barr virus, and human parvovirus. All three viruses transmit through saliva.

One example is a disease that the ancient Mesopotamians labeled bu’šānu. The infection involved boils in or around the mouth area. Its name also implies that the infected person might have stunk. While Arbøll says bu’šānu shares several symptoms with herpes, he warns people not to make any assumptions. “As with all ancient disease concepts, they do not match any modern diseases 1:1, and one should be very careful when applying these modern identifications. A disease concept like bu’šānu likely incorporated several modern diseases.”

Mesopotamians likely did not think infectious diseases were spread through kissing, since it is not listed anywhere in the medical texts. However, they had some religiously influenced ideas of contamination, which spurred some measures to avoid spreading the disease. For example, a letter from around 1775 BCE describes a woman in a palace harem with lesions all over her body. Assuming it was contagious, people avoided drinking from any cups she drank, sleeping in her bed, or sitting on her chair.

[Related: When you give octopus MDMA they hug it out]

The findings show that this form of kissing did not originate in a single place. Mesopotamia, India, and other societies separately learned to associate pecks on the lips as romantic. Arbøll says it’s possible other areas also learned about kissing but didn’t have the writing tools to record this behavior. This opens the question of how widely sexual kissing was practiced in the ancient world. 

Some experts are less convinced that kissing was a universal behavior. William Jankowiak, a professor of anthropology at the University of Nevada, Las Vegas, who was not involved in the study, points out that written records of kissing often occurred in complex societies and less so in people living in smaller foraging groups. It’s also difficult to know if romantic kissing was practiced in more than one class or reserved for elite groups in ancient civilizations. Additionally, other factors, such as living in tropical versus colder regions, could influence whether people wanted to lock lips. 

There’s still a long way to go in understanding the ancient history of kissing. But the study does clear up one thing—all the smooching our ancestors did is probably why oral herpes and other kiss-transmitted diseases are a global problem today.

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Doctors may have a new tool to protect patients against multi-drug resistant bacterial infections. But the new defense against increasingly difficult-to-treat bacteria isn’t a brand new development—it is an 80 year-old antibiotic. A study published May 16 in the open access journal PLOS Biology looked at a natural product made in soil called nourseothricin that was discovered in 1942.

[Related: Kids all over the US are getting strep, but antibiotics are hard to come by.]

The rise of antibiotic-resistant bacterial infections has encouraged a search for new antibiotics. Antibiotic resistance is a very serious and growing medical problem—according to the Centers for Disease Control and Prevention, antimicrobial resistance killed at least 1.27 million people worldwide and was associated with close to 5 million deaths in 2019. In the United States, more than 2.8 million antimicrobial-resistant infections occur each year, and over 35,000 people die as a result.

Nourseothricin contains multiple forms of a complex molecule called streptothricin. There were high hopes that the streptothricin inside would be a powerful agent against bacteria called gram-negative bacteria. These bacteria, such as E.coli., have a thick outer protective layer and are particularly hard for antibiotics to kill. 

Unfortunately, nourseothricin was toxic to kidneys according to the results of an unpublished limited human trial sometime in the 1940’s and its development was dropped. The team in this study decided to go back and take a second look at nourseothricin.

“We started searching around for drugs that we could use, and it turns out these super resistant bugs were highly susceptible to streptothricin, so we were able to use it as a selection agent to do these experiments,” study co-author and pathologist at Harvard Medical School James Kirby said in a statement. “What scientists were isolating in 1942 was not as pure as what we are working with today. In fact, what was then called streptothricin is actually a mixture of several streptothricin variants. The natural mixture of different types of streptothricins is now referred to as nourseothricin.”

Kirby is also the director of the Clinical Microbiology Laboratory at Beth Israel Deaconess Medical Center.

In the earlier studies on the antibiotic, nourseothricin suffered from incomplete purification of  streptothricin which was likely causing the toxicity. A study published in 2022 showed that multiple forms of streptothricin actually have different toxicities. 

One called streptothricin-F was significantly less toxic while also working against present day pathogens that are resistant to multiple drugs. 

[Related: Raw dog food can harbor antibiotic-resistant bacteria.]

In this study, the team looked closely at streptothricin-F and also streptothricin- D. Streptothricin-D strain was also highly selective for the gram-negative bacteria and was even more powerful than streptothricin-F against drug-resistant Enterobacterales and other bacterial species. However, it caused renal toxicity at a lower dose. 

The team used cryo-electron microscopy to show that streptothricin-F bound extensively to a subunit of the bacterial ribosome. This binding causes translation errors in the bacteria, which helps antibiotics inhibit the spread of a bacterial infection.  

“It works by inhibiting the ability of the organism to produce proteins in a very sneaky way. When a cell makes proteins, they make them off a blueprint or message that tells the cell what amino acids to link together to build the protein. Our studies help explain how this antibiotic confuses the machinery so that the message is read incorrectly, and it starts to put together gibberish. Essentially the cell gets poisoned because it’s producing all this junk,” said Kirby.

The team is still trying to figure out the mechanism behind how nourseothricin works, but found that it acts differently than other antibiotics. Kirby will continue studying nourseothricin with collaborators at Northwestern University and Case Western Reserve University Medical Center to dive deeper and understand how it actually works.

“We have great collaborators that have allowed us to pursue a project that crosses multiple fields. This work is an example of collaborative science really at its best,” said Kirby. 

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What use could health care have for someone who makes things up, can’t keep a secret, doesn’t really know anything, and, when speaking, simply fills in the next word based on what’s come before? Lots, if that individual is the newest form of artificial intelligence, according to some of the biggest companies out there.

Companies pushing the latest AI technology — known as “generative AI” — are piling on: Google and Microsoft want to bring types of so-called large language models to health care. Big firms that are familiar to folks in white coats — but maybe less so to your average Joe and Jane — are equally enthusiastic: Electronic medical records giants Epic and Oracle Cerner aren’t far behind. The space is crowded with startups, too.

The companies want their AI to take notes for physicians and give them second opinions — assuming they can keep the intelligence from “hallucinating” or, for that matter, divulging patients’ private information.

“There’s something afoot that’s pretty exciting,” said Eric Topol, director of the Scripps Research Translational Institute in San Diego. “Its capabilities will ultimately have a big impact.” Topol, like many other observers, wonders how many problems it might cause — like leaking patient data — and how often. “We’re going to find out.”

The specter of such problems inspired more than 1,000 technology leaders to sign an open letter in March urging that companies pause development on advanced AI systems until “we are confident that their effects will be positive and their risks will be manageable.” Even so, some of them are sinking more money into AI ventures.

The underlying technology relies on synthesizing huge chunks of text or other data — for example, some medical models rely on 2 million intensive care unit notes from Beth Israel Deaconess Medical Center in Boston — to predict text that would follow a given query. The idea has been around for years, but the gold rush, and the marketing and media mania surrounding it, are more recent.

The frenzy was kicked off in December 2022 by Microsoft-backed OpenAI and its flagship product, ChatGPT, which answers questions with authority and style. It can explain genetics in a sonnet, for example.

OpenAI, started as a research venture seeded by Silicon Valley elites like Sam Altman, Elon Musk, and Reid Hoffman, has ridden the enthusiasm to investors’ pockets. The venture has a complex, hybrid for- and nonprofit structure. But a new $10 billion round of funding from Microsoft has pushed the value of OpenAI to $29 billion, The Wall Street Journal reported. Right now, the company is licensing its technology to companies like Microsoft and selling subscriptions to consumers. Other startups are considering selling AI transcription or other products to hospital systems or directly to patients.

Hyperbolic quotes are everywhere. Former Treasury Secretary Larry Summers tweeted recently: “It’s going to replace what doctors do — hearing symptoms and making diagnoses — before it changes what nurses do — helping patients get up and handle themselves in the hospital.”

But just weeks after OpenAI took another huge cash infusion, even Altman, its CEO, is wary of the fanfare. “The hype over these systems — even if everything we hope for is right long term — is totally out of control for the short term,” he said for a March article in The New York Times.

Few in health care believe this latest form of AI is about to take their jobs (though some companies are experimenting — controversially — with chatbots that act as therapists or guides to care). Still, those who are bullish on the tech think it’ll make some parts of their work much easier.

Eric Arzubi, a psychiatrist in Billings, Montana, used to manage fellow psychiatrists for a hospital system. Time and again, he’d get a list of providers who hadn’t yet finished their notes — their summaries of a patient’s condition and a plan for treatment.

Writing these notes is one of the big stressors in the health system: In the aggregate, it’s an administrative burden. But it’s necessary to develop a record for future providers and, of course, insurers.

“When people are way behind in documentation, that creates problems,” Arzubi said. “What happens if the patient comes into the hospital and there’s a note that hasn’t been completed and we don’t know what’s been going on?”

The new technology might help lighten those burdens. Arzubi is testing a service, called Nabla Copilot, that sits in on his part of virtual patient visits and then automatically summarizes them, organizing into a standard note format the complaint, the history of illness, and a treatment plan.

Results are solid after about 50 patients, he said: “It’s 90% of the way there.” Copilot produces serviceable summaries that Arzubi typically edits. The summaries don’t necessarily pick up on nonverbal cues or thoughts Arzubi might not want to vocalize. Still, he said, the gains are significant: He doesn’t have to worry about taking notes and can instead focus on speaking with patients. And he saves time.

“If I have a full patient day, where I might see 15 patients, I would say this saves me a good hour at the end of the day,” he said. (If the technology is adopted widely, he hopes hospitals won’t take advantage of the saved time by simply scheduling more patients. “That’s not fair,” he said.)

Nabla Copilot isn’t the only such service; Microsoft is trying out the same concept. At April’s conference of the Healthcare Information and Management Systems Society — an industry confab where health techies swap ideas, make announcements, and sell their wares — investment analysts from Evercore highlighted reducing administrative burden as a top possibility for the new technologies.

But overall? They heard mixed reviews. And that view is common: Many technologists and doctors are ambivalent.

For example, if you’re stumped about a diagnosis, feeding patient data into one of these programs “can provide a second opinion, no question,” Topol said. “I’m sure clinicians are doing it.” However, that runs into the current limitations of the technology.

Joshua Tamayo-Sarver, a clinician and executive with the startup Inflect Health, fed fictionalized patient scenarios based on his own practice in an emergency department into one system to see how it would perform. It missed life-threatening conditions, he said. “That seems problematic.”

The technology also tends to “hallucinate” — that is, make up information that sounds convincing. Formal studies have found a wide range of performance. One preliminary research paper examining ChatGPT and Google products using open-ended board examination questions from neurosurgery found a hallucination rate of 2%. A study by Stanford researchers, examining the quality of AI responses to 64 clinical scenarios, found fabricated or hallucinated citations 6% of the time, co-author Nigam Shah told KFF Health News. Another preliminary paper found, in complex cardiology cases, ChatGPT agreed with expert opinion half the time.

Privacy is another concern. It’s unclear whether the information fed into this type of AI-based system will stay inside. Enterprising users of ChatGPT, for example, have managed to get the technology to tell them the recipe for napalm, which can be used to make chemical bombs.

In theory, the system has guardrails preventing private information from escaping. For example, when KFF Health News asked ChatGPT its email address, the system refused to divulge that private information. But when told to role-play as a character, and asked about the email address of the author of this article, it happily gave up the information. (It was indeed the author’s correct email address in 2021, when ChatGPT’s archive ends.)

“I would not put patient data in,” said Shah, chief data scientist at Stanford Health Care. “We don’t understand what happens with these data once they hit OpenAI servers.”

Tina Sui, a spokesperson for OpenAI, told KFF Health News that one “should never use our models to provide diagnostic or treatment services for serious medical conditions.” They are “not fine-tuned to provide medical information,” she said.

With the explosion of new research, Topol said, “I don’t think the medical community has a really good clue about what’s about to happen.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

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After spending 38 years in the Alabama prison system, one of the most violent and crowded in the nation, Larry Jordan felt lucky to live long enough to regain his freedom.

The decorated Vietnam War veteran had survived prostate cancer and hepatitis C behind bars when a judge granted him early release late last year.

“I never gave up hope,” said Jordan, 74, who lives in Alabama. “I know a lot of people in prison who did.”

At least 6,182 people died in state and federal prisons in 2020, a 46% jump from the previous year, according to data recently released by researchers from the UCLA Law Behind Bars Data Project.

“During the pandemic, a lot of prison sentences became death sentences,” said Wanda Bertram, a spokesperson for the Prison Policy Initiative, a nonprofit that conducts research and data analysis on the criminal justice system.

Now, Jordan worries about his longevity. He struggles with pain in his legs and feet caused by a potentially life-threatening vascular blockage, and research suggests prison accelerates the aging process.

Life expectancy fell in the United States in 2021 for the second year in a row, according to the Centers for Disease Control and Prevention. That decline is linked to the devastating effect of covid-19 and a spike in drug overdoses.

Some academic experts and activists said the trend also underscores the lasting health consequences of mass incarceration in a nation with roughly 2 million imprisoned or jailed people, one of the highest rates in the developed world.

A Senate report last year found the U.S. Department of Justice failed to identify more than 900 deaths in prisons and local jails in fiscal year 2021. The report said the DOJ’s poor data collection and reporting undermined transparency and congressional oversight of deaths in custody.

Thousands of people like Jordan are released from prisons and jails every year with conditions such as cancer, heart disease, and infectious diseases they developed while incarcerated. The issue hits hard in Alabama, Louisiana, and other Southeastern states, which have some of the highest incarceration rates in the nation.

A major reason the U.S. trails other developed countries in life expectancy is because it has more people behind bars and keeps them there far longer, said Chris Wildeman, a Duke University sociology professor who has researched the link between criminal justice and life expectancy.

“It’s a health strain on the population,” Wildeman said. “The worse the prison conditions, the more likely it is incarceration can be tied to excess mortality.”

Mass incarceration has a ripple effect across society.

Incarcerated people may be more susceptible than the general population to infectious diseases such as covid and HIV that can spread to loved ones and other community members once they are released. The federal government has also failed to collect or release enough information about deaths in custody that could be used to identify disease patterns and prevent fatalities and illness inside and outside of institutions, researchers said.

Over a 40-year span starting in the 1980s, the number of people in the nation’s prisons and jails more than quadrupled, fueled by tough-on-crime policies and the war on drugs.

Federal lawmakers and states such as Alabama have passed reforms in recent years amid bipartisan agreement that prison costs have grown too high and that some people could be released without posing a risk to public safety.

The changes have come too late and not gone far enough to curb the worst effects on health, some researchers and activists for reform said.

Still, no one has proven that incarceration alone shortens life expectancy. But research from the early 2000s did show the death rate for people leaving prison was 3.5 times higher than for the rest of the population in the first few years after release. Experts found deaths from drug use, violence, and lapses in access to health care were especially high in the first two weeks after release.

Another study found that currently or formerly incarcerated Black people suffered a 65% higher mortality rate than their non-Black peers. Black people also make up a disproportionately high percentage of state prison populations.

The enactment in 2000 of the Death in Custody Reporting Act, and its reauthorization in 2014, required the DOJ to collect information about deaths in state and local jails and prisons.

The information is supposed to include details on the time and location of a death, demographic data on the deceased, the agency involved, and the manner of death.

But a recent report from the Government Accountability Office found that 70% of the records the DOJ received were missing at least one required data point. Federal officials also lacked a plan to take corrective action against states that didn’t meet reporting requirements, the GAO found.

The deficiency in data means the federal government can’t definitively say how many people have died in prisons and jails since the covid-19 pandemic began, researchers said.

“Without data, we are operating in the dark,” said Andrea Armstrong, a professor at the Loyola University New Orleans College of Law, who has testified before Congress on the issue.

Armstrong said federal and state officials need the data to identify institutions failing to provide proper health care, nutritious food, or other services that can save lives.

The DOJ did not make officials available for interviews to answer questions about the GAO report.

In a written statement, agency officials said they were working with law enforcement and state officials to overcome barriers to full and accurate reporting.

“The Justice Department recognizes the profound importance of reducing deaths in custody,” the statement said. “Complete and accurate data are essential for drawing meaningful conclusions about factors that may contribute to unnecessary or premature deaths, and promising practices and policies that can reduce the number of deaths.”

Department officials said the agency is committed to enhancing its implementation of the Death in Custody Reporting Act and that it has ramped up its efforts to improve the quality and quantity of data that it collects.

The DOJ has accused Alabama, where Jordan was incarcerated, of failing to adequately protect incarcerated people from violence, sexual abuse, and excessive force by prison staff, and of holding prisoners in unsanitary and unsafe conditions.

Jordan served 38 years of a 40-year sentence for reckless murder stemming from a car accident, which his lawyer argued in his petition for early release was one of the longest sentences in Alabama history for the crime. A jury had found him guilty of being drunk while driving a vehicle that crashed with another, killing a man. If he were convicted today instead, he would be eligible to receive a sentence as short as 13 years behind bars, because he has no prior felony history, wrote Alabama Circuit Judge Stephen Wallace, who reviewed Jordan’s petition for early release.

With legal help from Redemption Earned, an Alabama nonprofit headed by a former state Supreme Court chief justice, Jordan petitioned the court for early release.

On Sept. 26, 2022, Wallace signed an order releasing Jordan from prison under a rule that allows Alabama courts to reconsider sentences.

A few months later, Jordan said, he had surgery to treat a vascular blockage that was reducing blood flow to his left leg and left foot. A picture shows a long surgical scar stretching from his thigh to near his ankle.

The Alabama Department of Corrections refused an interview request to answer questions about conditions in the state’s prisons.

Jordan said his vascular condition was excruciating. He said he did not receive adequate treatment for it in prison: “You could see my foot dying.”

KFF Health News is a national newsroom that produces in-depth journalism about health issues and is one of the core operating programs at KFF—an independent source of health policy research, polling, and journalism. Learn more about KFF.

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COVID-19 is no longer a public health emergency in the US. The Biden administration’s deadline follows the World Health Organization’s announcement last week that removed COVID’s status as a global health crisis.

Infectious disease experts tell Popular Science that it’s an encouraging step and a sign that we are in a very different place than where we were in 2020. And while the recent decisions in no way mean the virus is gone—it’s expected to be endemic like the flu—access to COVID testing, treatments such as Paxlovid, and the vaccines have put the US in a position to coexist with it.

That said, managing your safety will come at a higher cost now. In one of the biggest changes from ending the federal emergency response, insurances are no longer required to cover the costs of COVID testing or reimburse people if they bought an over-the-counter home COVID-19 test. The federal government is also ending its free COVID-test program over the mail. 

As the financial burden of testing shifts to families and individuals, knowing where and when to get tested will keep you protected as the country transitions into this new stage of the pandemic. “We’re still seeing up to 1,000 deaths a week in the US from COVID for people that are older and at risk,” warns Del DeHart, a medical director of the infectious diseases department at the University of Michigan Health-West. “For those people, COVID is still not over and so testing for early treatment is going to be critical.”

Where to get COVID tests

There are still options for getting free COVID tests around the US The last day to order four free at-home COVID tests from the government is May 31, but local community clinics can give away free COVID tests or at a lower cost until supplies run out. 

Access to free testing might also depend on where you live. David Souleles, the director of the COVID-Response Team at the University of California, Irvine, says some state governments are taking measures to avoid financial barriers with COVID testing. California, for example, issued a mandate for health insurances to continue providing reimbursement for eight monthly at-home tests. Check your state government’s website to see what policies are in place following the end of the public health emergency.

If you are uninsured, the US government will continue to provide access to swabs through the Increasing Community Access to Testing Program. This government program partners with specific healthcare sites such as Walgreens and Quest Diagnostics to provide no-cost COVID tests with priority for people with a known exposure to the virus or who are showing symptoms.

[Related: An at-home test for both COVID-19 and the flu gains approval]

At-home rapid tests and PCR laboratory testing will still be available at your local pharmacies and doctor’s office, but it’s up to your insurance company if they want to bear the cost or require a copayment. What’s more, insurance companies may charge different prices for COVID tests; if they cover the cost, they may set limits on how many tests they will cover per individual. 

Prices for COVID test kits in stores like CVS range from $9.99 to $28.99, meaning testing can quickly get expensive. DeHart is concerned that the prices will create a financial barrier that will deter people from getting tested. If affordability becomes a question, it’s important to make every COVID test you take count.

When it’s still important to get tested for COVID

While most COVID mandates have lifted around the country, some employers and places might require you to get tested. For instance, healthcare workers employed in facilities like nursing homes will likely continue routine COVID testing. And as of now, many hospitals still require routine COVID testing for admitted patients, though it remains unclear whether the hospitals will cover the cost or if the test will be added to a person’s medical bill.

For voluntary testing, it’s important to evaluate your risk of having a severe COVID infection. DeHart says individuals above the age of 65 and those with immunosuppressive conditions should get tested regularly, along with loved ones in close contact with those that fall under this category. Souleles also recommends taking a test before visiting a relative in assisted living or anyone who is considered at high-risk of exposure. 

Other scenarios may apply, too, Souleles adds. “We would still encourage people to test before and after travel and before and after gatherings if they have the ability to do so. Anytime that you have the ability to test before you’re going to be around lots of people is great, and anytime you have the ability to test three to five days after being around a lot of people, that’s also a good thing.”

[Related: Long COVID recovery is finally getting the attention it deserves in the US]

If you have COVID-like symptoms, get tested before going out in public, even if the side effects seem mild. Testing early will give you more chances to get Paxlovid, which is most effective when taken within the first five days of seeing symptoms, and potentially avoid life-threatening complications. 

If you need to purchase a COVID test, treat it like you would any other over-the-counter goods. This includes checking the expiration dates to avoid a false positive or false negative result. You will also want to throw out any recalled COVID tests. If purchased for a later date, keep COVID tests at room temperature and away from the hands of pets and young children.

What to do if you test positive for COVID

If the test comes out positive, follow the Centers for Disease Control and Prevention’s (CDC) guidelines. Stay home and isolate yourself from others in the household for five days. People experiencing moderate symptoms like difficulty breathing should isolate for 10 days. Monitor your condition and go to the hospital if there are any severe or life-threatening complications. 

If you must go outside, wear a high-quality mask and avoid going to places where you would have to take it off. Also contact your doctor to see if you are eligible for any COVID-19 treatments and start those as soon as possible.

You can stop isolating after five days if you have no symptoms. If you continue to show symptoms, the CDC says you should stay put until your symptoms improve or you are fever-free for 24 hours without using medication.

[Related: Getting COVID more than once might be even worse than we thought]

Keep in mind that COVID tests are only one of the many tools available to reduce your risk of severe infection and death. Both DeHart and Souleles strongly urge people to get vaccinated and get their booster shot when eligible. Insurers will still be expected to cover the bivalent COVID vaccine as a routine immunization, and the Biden administration’s Bridge Access Program for COVID-19 Vaccines and Treatments will continue to provide vaccines free-of-charge to the uninsured.

“Stay up to date with your vaccines,” says Souleles. “It’s still the most important tool that we have right now.”

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Scientists in Australia have just begun vaccinating wild koalas against chlamydia. This field trial in the state of New South Wales is an effort to protect one of Australia’s most beloved animals against the disease that can cause blindness, infertility, and death. The chlamydia epidemic in koalas has been ravaging populations of the marsupial since the 1990s. 

[Related: A new vaccine may curb the koala chlamydia epidemic.]

Koalas along the east and southeast Australian coasts have been particularly affected, with some populations having infection rates of up to 100 percent. In 2021, Australia Zoo Wildlife Hospital veterinarian and research coordinator Amber Gillett called chlamydia one of the most significant threats to koalas and treatment after infection is not enough to save them. “Although many koalas with chlamydia can be treated using traditional antibiotics, some animals cannot be saved due to the severity of their infection. Having a vaccine that can help prevent both infection and the severity of the disease is a critical element in the species’ conservation management.”

While origins of the disease is koalas aren’t fully confirmed, but scientists believe that marsupials possibly caught the disease from exposure to the feces from infected cattle and sheep. Chlamydia then spread via sexual contact or was passed from mother to offspring.  

This single-shot vaccine has been designed just for koalas and was tested in a few hundred fluffy specimens in wildlife rescue centers. For this new field trial, the team hopes to catch, vaccinate, and subsequently monitor about half of the koala population living in the Northern Rivers region of New South Wales–about 50 koalas. 

“It’s killing koalas because they become so sick they can’t climb trees to get food, or escape predators, and females can become infertile,” Samuel Phillips, a microbiologist at the University of the Sunshine Coast who helped to develop the new vaccine, told the Associated Press.

The first koalas were caught and vaccinated in March, and the effort is expected to last for three months. To find them, the team spots koalas in eucalyptus trees to then build circular enclosures around the base of the trees with doors that lead into cages. Eventually, the koalas climb down from one tree to get more eucalyptus leaves from another tree and wander into the traps.

They are then given a check-up to assess their health and given anesthesia before getting the vaccine. They are kept under observation for 24 hours after waking up to check for unexpected side effects, according to Jodie Wakeman, the veterinary care and clinical director at Friends of the Koala. The nonprofit organization runs a wildlife hospital where the koalas are getting vaccinated.

[Related: How to handle a koala-chlamydia epidemic.]

The koalas are marked with a pink dye on their backs so that the same animals are not caught twice before being released back into the wild. 

Australia’s federal government declared that the koalas in the eastern regions of New South Wales, Queensland, and the Australian Capital Territory were endangered. A 2020 report from the New South Wales government found that the unique creatures could become extinct by 2050 due to disease, road collisions, and habitat loss. Climate change is only exacerbating the problem.

The trial was approved by multiple Australian governing bodies balancing the risk of disturbing the marsupials against the danger of allowing chlamydia to continue to spread unchecked. It is one of only a few worldwide examples of scientists attempting to inoculate endangered wildlife for the purposes of conservation. In 2016, a team began to vaccinate Hawaiian monk seals morbillivirus and in 2020, biologists in Brazil started vaccinating golden lion tamarins against yellow fever.

“Vaccination for wildlife is certainly not routine yet,” Jacob Negrey, a biologist at Wake Forest University School of Medicine told the AP. “But whether it should be used more often is a fundamental question that conservation biologists are really wrangling with right now.”

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On May 5, the The World Health Organization (WHO) announced that we are no longer in a global COVID-19 emergency. The emergency was first declared over three years ago in the early days of the pandemic. During the 15th meeting of the International Health Regulations Emergency Committee regarding COVID-19, the members highlighted a decreasing trend in deaths, decline of COVID-19 related hospitalizations and intensive care unit admissions, and higher levels of population immunity to the virus as the basis of their decision. 

“With great hope, I declare COVID-19 over as a global health emergency,” WHO director general, Tedros Adhanom Ghebreyesus announced during a media briefing. 

[Related: Biden will end COVID-19 national emergencies in May. Here’s what that means.]

However, Tedros stressed that just because the global emergency declaration is ending, it does not mean that COVID-19 is not still a threat to public health. “As we speak, thousands of people around the world are fighting for their lives in intensive care units. And millions more continue to live with the debilitating effects of post-COVID19 condition,” Tedros said. 

The WHO first made the emergency declaration on January 30, 2020, when only 213 people were known to have died from the novel virus. The declaration was a signal to the international community that COVID-19 posed a threat to the whole world and that they should begin to prepare. 

The WHO will continue to list COVID-19 as a pandemic, similar to how they designate HIV. While it acts as a symbolic milestone, this decision does not change much, but it is a significant moment in the evolving human relationship with the novel virus that brought life to a screeching halt in 2020 after it first emerged in China in December 2019.

Many countries, including the European Union, have already ended their COVID-19 states of emergency and have moved away from mitigation efforts. The United States is scheduled to lift its COVID-10 emergency on May 11.

The WHO decision was not welcomed by all public health experts. Respiratory physician and member of Brazil’s National Academy of Medicine Margareth Dalcolmo told The New York Times that it was too soon to lift the emergency, due to the urgent tasks such as research into COVID variants and development of better vaccines. She added that the designation of a global public health emergency also creates leverage for lower-income nations to access needed treatments and support.

Around the world, 765,222,932 confirmed COVID cases, including 6,921,614 deaths, have been reported to the WHO as of May 3. However, these figures are likely a vast undercount of the pandemic’s true toll on human life. In 2022, the WHO said 15 million more people had died in the first two years of the pandemic than they would have in normal times, with developing and indigenous nations experiencing the worst of the devastation. Close to eight million more people than expected died in lower-middle-income nations by the end of 2021.

[Related: White House invests $5 billion in new COVID vaccines and treatments as national emergency ends.]

“One of the greatest tragedies of COVID-19 is that it didn’t have to be this way. We have the tools and the technologies to prepare for pandemics better, to detect them earlier, to respond to them faster, and to mitigate their impact But globally, a lack of coordination, a lack of equity, and lack of solidarity meant that those tools were not used as effectively as they could have been,” Tedros said.

Additionally, on May 4, the United States Centers for Disease Control and Prevention released provisional data that COVID-19 dropped to the fourth leading cause of death in the US in 2022, falling behind heart disease, cancer, and unintended injuries like shootings, car accidents, and drug overdoses. In 2020 and 2021, only heart disease and cancer were ahead of COVID-19 as leading causes of death.

Death rates due to COVID-19 fell for nearly all Americans and the virus was the underlying cause of roughly 187,000 deaths in the US in 2022.  According to the CDC, the highest COVID-19 death rates were in the South and in the adjacent region that stretches west to Texas, Oklahoma, and New Mexico.

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After 60 years of trial and error, the Food and Drug Administration (FDA) approved the first vaccine to prevent respiratory syncytial virus (RSV) on May 3. More preventative shots for the respiratory virus are on the way.

[Related: How our pandemic toolkit fought the many viruses of 2022.]

The FDA approved Arexvy from pharmaceutical company GSK. The vaccine is designed to protect those over 60 in a single dose. A vaccine from Pfizer is currently under consideration for older adults and pregnant people as a maternal vaccination to protect newborn babies. Sanofi and AstraZeneca’s monoclonal antibody treatment for babies that offers vaccine-like protection during RSV season is also under consideration by the FDA. Additionally, a late-stage trial of an RSV vaccine that uses mRNA technology from Moderna showed promise in late-stage trials. 

The vaccine could be available as soon as this fall, pending a recommendation for its use from the Centers for Disease Control and Prevention’s Advisory Committee on Immunization Practices, which will meet in June. GSK says it has “millions of doses ready to be shipped,” according to a recent earnings presentation.

“Older adults, in particular those with underlying health conditions, such as heart or lung disease or weakened immune systems, are at high risk for severe disease caused by RSV,” said Peter Marks, director of the FDA’s Center for Biologics Evaluation and Research, in a statement. “Today’s approval of the first RSV vaccine is an important public health achievement to prevent a disease which can be life-threatening and reflects the FDA’s continued commitment to facilitating the development of safe and effective vaccines for use in the United States.”

RSV can affect all age groups, but it is particularly worrisome in babies and older adults. It is a highly contagious virus that causes infections of the lungs and breathing passages. According to the Centers for Disease Control and Prevention (CDC), RSV leads to approximately 60,000 to 120,000 hospitalizations and 6,000 to 10,000 deaths among adults 65 years of age and older every year. It is also a common cause of lower respiratory tract disease in older adults. This disease affects the lungs and can cause life-threatening pneumonia and bronchiolitis.

The virus circulates seasonally, usually beginning in the fall and peaking in the winter. The 2022-2023 RSV season started particularly early and flooded hospitals and pediatric wards across the United States, leading pharmacies to limit the sales of children’s medicines.

According to the results of a clinical trial of close to 25,000 older adults, the GSK vaccine was 83 percent effective at preventing lower respiratory tract disease by the virus. It was 94 percent effective at preventing severe disease in seniors. In the trial, severe disease was defined as the need for supplemental oxygen or a mechanical help to breathe. The results were published in the New England Journal of Medicine in February. 

[Related: Fighting RSV in babies starts with a mother’s antibodies.]

The vaccine works by using a small piece of the virus called a fusion protein, or F-protein. The F-protein sticks out on the virus’ surface and helps it latch onto cells in the upper airway and infect them. The F-proteins were made in a lab with specially programmed cells. 

In 2013, researchers at the National Institutes of Health discovered how to freeze the normally wiggly and shape-shifting F-protein in the shape that it takes before it fuses onto a cell. When it’s in this shape, the body can produce antibodies against it. The GSK vaccine uses this pre-fusion form of the F-protein and an ingredient called an adjuvant that can boost immune activity.

The search for a vaccine to RSV began in the 1960s, but has been mired by tragedy. Two toddlers died after receiving an experimental shot in the 60’s after it unexpectedly caused them to contract a very serious version of the virus. Many of the safety measures currently in place during vaccine trials were put in place after the failures of the RSV vaccine.

Barney Graham, a vaccine scientist at Morehouse School of Medicine worked alongside Jason McLellan, a structural biologist at the University of Texas at Austin, and Peter Kwong, a vaccine scientist at the National Institutes of Health, to jump-start the RSV vaccine field after decades of failure.

“This is my life’s work, so it’s kind of amazing to see it come to this point,” Graham told The Washington Post.  “It’s exciting for me to see this happening because of all the other people who’ve come before me working on RSV, some of whom are no longer with us. I wish they could see this is happening. It’s been a long struggle.”

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Deep beneath the Pacific Ocean, the edge of one tectonic plate was being jammed beneath the tectonic plate that held Japan. This wasn’t news. It had been happening at a rate of three inches a year since long before humans had invented the concept of news. But that March, it became news in the biggest possible way, when a chunk of the underlying plate suddenly gave way, causing the seafloor to pop up by about 15 feet and the plate holding parts of Japan to suddenly drop by about three feet. The magnitude 9 Tohoku earthquake was so big it shunted Japan eight feet to the east. It was so big it shifted the Earth six inches on its axis. It was so big it sped up the rotation of the planet
(only by 1.8 microseconds a day, but still—your days are now just a tiny bit shorter. Thanks Obama!). The earthquake and resultant tsunami also wreaked havoc on human systems—transportation systems, energy systems, water systems, telecommunication systems, and that most important of all human systems, the biological system that allows us to slobber, reproduce, and contemplate the irrationality of high baby-formula prices (usually in that order).

The tsunami killed more than twenty thousand people and caused multiple nuclear meltdowns, a disastrous toll for everyone except sellers of supplements, who pivoted to prey on the baseless fears of Americans living thousands of miles away from the radiation. Toby McAdam, still selling his RisingSun products, told the local newspaper that he doubted the radiation would drift to Montana—“but it could.” He recommended that his “Lugol’s Iodine solution” be applied to the skin daily as “an ounce of prevention.” Though public health officials said people self-treating with iodide supplements were more likely to harm than help themselves, orders spiked so sharply that Toby’s website crashed.

The multifaceted nature of the tsunami-caused chaos makes it perhaps appropriate that the event also marked the beginning of the United States’ descent into a full-blown zombie apocalypse.

The June following the earthquake, the CDC began a conversation about emergency preparedness on Twitter that led to a handful of people jokingly tweeting that they would like the CDC to weigh in on a catastrophic zombie attack.

This led to the predictable wave of lols, rofls, and laughy-face emoticons, but it also sparked an idea for Dave Daigle (a CDC communications administrator) and Dr. Ali S. Khan (a CDC expert in disaster preparedness).

With Daigle’s input, Khan wrote a piece for the CDC website explaining how to prepare for a zombie apocalypse. This neatly demonstrated the humanity of the person on the other side of the icy-cold stethoscope even as it leveraged the innate appeal of zombies to teach real-life strategies to cope with actual disasters.

It turned out people were hungry for messaging about people hungry for brains. The CDC zombie apocalypse preparedness plan was an instant hit, racking up so many views that the CDC server froze up, overwhelmed by all the traffic.

This bit of fun was so successful that a team of researchers from the University of California, Irvine, published a congratulatory paper in the journal Emerging Infectious Diseases urging other public health officials to follow suit. It argued that zombies were an opportunity “to capitalize on the benefits of spreading public health awareness through the use of relatable popular culture tools and scientific explanations for fictional phenomena.” They proposed that the medical establishment build o those efforts to stimulate the conversation and do better public education on a variety of health topics.

Suddenly, zombies were everywhere in public health and safety. The CDC, the Department of Homeland Security, and the Federal Emergency Management Agency all published in-depth zombie-related literature. Finally, public officials were seizing the initiative and taking back the cul tural space they had inadvertently ceded to promoters of One True Cures.

Also in 2011, a Harvard Medical School physician and aspiring nov elist named Steven Schlozman appeared on the radio show Coast to Coast AM, which spun tales of conspiracy and paranormal phenomena to a large and credulous national audience from 2 a.m. to 4 a.m., seven days a week. Because Coast to Coast AM was the most popular late-night radio show in the country, with ten million listeners, it was a great opportunity for Schlozman, who was there to promote his latest work, The Zombie Autopsies: Secret Notebooks from the Apocalypse. In the book, Schlozman drew on his medical knowledge to describe “Ataxic Neurodegenerative Satiety Deficiency syndrome” as the medical cause
of zombies (it was of course a fictional work of fictitious fiction). The format of the show required that Schlozman spend the opening stretch talking about the events of his novel as if they were real, before shifting to an acknowledgment that it was all pure fantasy.

Daigle, Khan, and Schlozman were helping people learn a bit of science in a fun way.

But their efforts quickly ran up against a problem: there is more than one way to view a zombie apocalypse.

One fact that the CDC and its fellow agencies failed to fully appreciate was that, in zombie properties like 2009’s feature film Zombieland and 2010’s hit television series The Walking Dead, very little
screen time is given to public health concepts like water sanitation. The action takes place after most health authorities have had their faces eaten, leaving individual survivors to run around attacking infected people with baseball bats, crossbows, and shotguns as a means of self-preservation.

That’s why other groups were quickly lining up to enlist the hot new cultural craze into their own, very different agendas. Zombies became the centerpiece in gun advertisements and were a major part of the NRA’s annual conventions, where shooting at the undead carried none of the moral baggage that came with shooting at human targets.

“Because the zombie canon focuses so squarely on the apocalypse, its spread into popular culture can erode faith in the resiliency of civilization,” wrote Daniel Drezner, the Tufts University professor and zombie expert. “The zombie narrative, as it is traditionally presented, socially constructs the very narrative that agencies like the CDC and FEMA are trying to prevent.”

Drezner documented the way that zombie references became a sort of dog whistle for gun rights—those on the outside glossed over a quirky head-scratcher while targeted audiences became fired up, even though they would clearly never need to shoot a zombie in real life.

Until some Americans began to ask, Will I need to shoot a zombie in real life?

Toby McAdam had told me about the 2012 Miami incident in which a man bit the face off a homeless man and then was himself described by authorities as slow to die after being shot. But Toby was not the only person fascinated by that attack. It let the undead cat out of the bag.

Soon after the news broke, a self-described Bitcoin evangelist and promoter of alternative-health supplements doctored a Huffington Post article about the incident so that it attributed the cause of the face eating to “LQP-79,” a virus that destroys internal organs and makes the host hungry for human flesh.

The fake article went viral, blitzing digital media feeds so thoroughly that LQP-79 was soon the third-most-searched term on the CDC website, forcing the agency to officially deny the existence of a zombie virus.

Around then, communities of zombie-themed survivalists and militias sprang up all across America. One was an offshoot of the well-established Michigan Militia, while others had names like the Kansas Anti Zombie Militia, the Anti Zombie Unified Resistance Effort (AZURE), Zombie-Fighting Rednecks, the Zombie Eradication and Survival Team, Postmortem Assault Squadron, and the US Department of Zombie Defense.

One, a loosely affiliated national group called the US Zombie Outbreak Response Team (ZORT), popularized a strange mishmash of survivalism and cosplay. Its website features pictures of preppers in tactical gear and tinted sunglasses using stickers and goofy accessories to trick out their trucks as zombie-fighting vehicles that would be equally at home in Ghostbusters or Mad Max universes. It was in some ways good fun. But they also carried real firearms. And engaged in real postapocalyptic survival exercises.

“A Zombie could be anything from a person infected by a pandemic outbreak to a crazy nut job, criminal or gangster who wants to hurt your family and steal your food and preps,” reads ZORT’s promotional material.

Though ZORT purports to be simply providing tongue-in-cheek cover for legit training that would be helpful in a natural disaster, of course the real difference between zombies and hurricane survivors is that one must be shot in the head and the other should be given a hot toddy and a shower.

Did any of these folks actually believe in zombies?

Probably not. But there was potential.

Drezner cited research showing that when considering paranormal ideas, people look less to the logical evidence and more to whether other people believe in the ideas. This means that even if no one believes in zombies, if some people believe that other people believe in zombies, then some people will believe in zombies. The gaslighting became so effective that the gaslit then gaslighted others, until fear of actual zombies took on an undead life of its own—call it masslighting.

And really, the online picture was becoming quite blurry. At the CDC, Daigle and Khan began getting inquiries about their Zombie Preparedness Plan from concerned citizens who wanted to know what sort of firearm was recommended to repel undead invaders. Meanwhile, after his Coast to Coast AM appearance, Schlozman got emails from listeners who wanted to know what medicines could stave off a zombie infection, and whether he had recommendations for how to protect one’s home. China’s state media had to formally debunk a robust rumor that Ebola victims were rising from the dead as zombies. And in 2014 in the Florida statehouse, a representative formally proposed “An Act Relating to the Zombie Apocalypse” as the name of a bill that would allow citizens to carry firearms without a permit in an emergency.

Shockingly, a 2015 survey showed that 2 percent of American adults thought the most likely apocalyptic scenario would be one caused by zombies.

And zombie references kept popping up in unexpected places. People downloaded audio fitness tracks in which joggers were kept motivated by imaginary zombie antagonists that pursued them as they ran.

A man named Vermin Supreme, who sought the 2016 Libertarian Party nomination for president, added a platform plank on “zombie apocalypse awareness.” He also advocated using zombies for renewable energy. Even Big Tech was in on it. Buried in Amazon’s user agreement for a game-development engine, clause 57.10—a gag, probably?—read that the software should not be used in life-and-death situations, such as in medical equipment, nuclear facilities, spacecraft, or military combat operations. “However, this restriction will not apply in the event of the occurrence (certified by the United States Centers for Disease Control or successor body) of a widespread viral infection transmitted via bites or contact with bodily fluids that causes human corpses to reanimate and seek to consume living human flesh, blood, brain or nerve tissue and is likely to result in the fall of organized civilization.”

With zombie stories saturating popular culture, the lore in TV and film began to expand beyond the simple trope of shambling brain eaters. There were zombie rom-coms and zombie mockumentaries. On the CW Television Network, a show called iZombie tells the story of a Seattle morgue worker infected by a zombie virus. In this world, zombies retain their personality and capacity for reason, as long as they are well fed (on brains). During the third season, which aired in 2017, a militant group of zombies releases a deadly flu virus in Seattle; local public health officials announce a mandatory flu vaccination, only to find that the zombies have tainted the vaccines with a substance that will turn the vaccinated into zombies.

Vaccines that zombified ordinary citizens?

Luckily for public health, no one would believe that in real life.

Buy If It Sounds Like a Quack by Matthew Hongoltz-Hetling here.

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A new sound wave technique can help treat a deadly brain cancer called glioblastoma in only four minutes. The breakthrough report was published May 2 in the journal The Lancet Oncology and demonstrates the results of a phase 1 in-human clinical trial with 17 patients.

In the trial, the patients underwent surgery for resection, or removal, of their tumors and had an ultrasound device implanted. The device inside the skull opens the blood-brain barrier, repeatedly using sound waves to permeate the barrier and reach the brain tumor. IV chemotherapy is then able to reach the neurological tissues where the cancer can grow.

Treating this type of brain tumor, which has a 6.8 percent survival rate within the first five years of diagnosis, with the most potent types of chemotherapy is difficult. The strongest cancer medicines are typically unable to permeate the blood-brain barrier. The blood-brain barrier acts as a line of defense, making an extra wall around the brain to keep toxins and pathogens from getting into such a crucial area of the body. However, the repertoire of drugs that can be used to treat brain diseases is very limited. In 2014, scientists first found that sound waves could be used to permeate the blood-brain barrier and this study builds on that discovery.

[Related: Understanding glioblastoma, the most common—and lethal—form of brain cancer.]

“This is potentially a huge advance for glioblastoma patients,” co-author and Northwestern University neurosurgeon Adam Sonabend said in a statement. 

The study reports that using a novel skull-implantable grid of nine ultrasound emitters made by French biotech company Carthera can open the blood-brain barrier in a volume of the brain nine times larger than the small single-ultrasound emitter implants originally used. This importantly helps treat a large region of the brain next to the cavity that remains after glioblastoma tumors are removed.  

This is also the first study that shows how quickly the blood-brain barrier closes after being opened by the ultrasound. It closes in the first 30 to 60 minutes after the communication. and this will help scientists optimize what order to deliver the drugs to allow for better penetration of the brain. The procedure to open the blood-brain barrier only takes four minutes and is performed while the patient is awake. The new results show that the treatment is safe, well-tolerated, and some patients received up to six cycles of treatment. 

[Related: Scientists used Zika to kill aggressive brain cancer cells in mice.]

Opening up the blood-brain barrier led to a roughly four- to six-fold increase in the drug concentrations in the human brain. The team observed this increase with two chemotherapy drugs called paclitaxel and carboplatin. These drugs are typically not used to treat glioblastoma patients, because they typically do not cross the blood brain barrier in normal circumstances. 

According to Sonobend, the current chemotherapy used for glioblastoma (Temozolomide) does cross the blood-brain barrier, but is weak. Sonabend also said that previous studies that injected paclitaxel directly into the brains of patients with these tumors had promising signs of efficacy, but the direct injection was associated with toxicity such as brain irritation and meningitis.

A phase 2 clinical trial is already underway. “While we have focused on brain cancer (for which there are approximately 30,000 gliomas in the U.S.), this opens the door to investigate novel drug-based treatments for millions of patients who suffer from various brain diseases,” said Sonabend.

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Archaeologists in Rome have unearthed a treasure trove of Renaissance-era medical supplies inside the Forum of Caesar. Among the “golden” finds are 500 year-old medicine bottles and urine flasks. In a study published April 11 in the journal Antiquity, the authors believe that the containers were used to collect pee for medical analysis and diagnosis. 

According to the researchers, the pathogens that could have been present in these bottles helps uncover how urban waste was managed.

[Related: Pee makes for great fertilizer. But is it safe?]

The current excavation initially began in 2021 and is part of an international collaboration called the Caesar’s Forum Excavation Project. The 16th century medical dump was found inside Caesar’s Forum, which was built centuries prior in 46 BCE. About 1,500 years later, a guild of bakers used this space to build the Ospedale dei Fornari or Bakers’ Hospital. According to the authors, the waste dump was then created by the hospital’s workers. 

The archaeologists also found rosary beads, broken glass jars, coins, a ceramic camel, and a Renaissance-era cistern full of ceramic vessels. The team of researchers from institutions in Italy and Denmark believes that the objects were likely related to patient care in the hospital. Each patient at the hospital may have been given a basket with a bowl, drinking glass, jug, and a plate for hygiene purposes. 

The glass urine flasks are called “matula” in medieval Latin medical texts and were likely used for the practice of uroscopy. This was a diagnostic tool for physicians during the Middle Ages and Renaissance. Urine was also once believed to be a cure for motion sickness. 

The authors believe that doctors would use the flasks to observe urine’s sedimentation, smell, color, and even taste. This would help the physicians diagnose ailments like kidney disease, jaundice, and diabetes. The excess glucose in diabetic urine gives it a saccharine quality. English physician Thomas Willis was credited with discovering this during the 17th Century and described the pee as “wonderfully sweet as if it were imbued with honey or sugar.”

[Related from PopSci+: What’s in a packrat’s petrified pee? Just a few thousand years of secrets.]

Also included in the cistern were lead clamps that were associated with wood treated with fire. According to the study, this may be evidence of burning objects brought into the hospital from houses with known plague cases. Italian physician Quinto Tiberio Angelerio wrote this in a series of rules for preventing the spread of the contagious disease in 1588, which included burning objects touched by plague patients. Plague killed roughly 25 million people throughout the 14th century alone as it spread across Eurasia, North Africa, and eventually the Americas for 500 years.

Once the cistern was full, it was likely capped with clay While landfills existed at this time outside the city walls of Rome, “the deposition of waste in cellars, courtyards, and cisterns, although prohibited, was a common practice,” study lead author Cristina Boschetti told Live Science. 

The unique find sheds more light on how hygiene practices and controls in European medical settings progressed during the early modern era. 

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BUMS. HEINIES. FANNIES. DERRIERES. Few muscles in the human body carry as much cultural clout as the gluteus maximus. “Butts are a bellwether,” writes journalist Heather Radke in her 2022 book Butts: A Backstory. Radke goes on to explain that our feelings about our hindquarters often have more to do with race, gender, and sex than with the actual meat of them. Unlike with a knee or an elbow, Radke argues, when it comes to the tuchus, we’re far more likely to think about form than function—even though it features the largest muscle in the human body. 

For all the scrutiny we spare them (outside of when we’re trying on new jeans) our butts aren’t mere aesthetic flourishes. A booty is, in fact, a unique feat of evolution: Out of any species, humans have the most junk in their trunks. Many other creatures have muscle and fat padding their backsides, and some even have butt cheeks. But none pack anything close to the same proportions as us.

So why did our ancestors develop such a unique cushion? Evolutionary biologists’ best guess is that our shapely rears help us walk upright. The curved pelvic bone that gives the butt its prominence likely developed as our weight moved upward and our muscular needs shifted. Research increasingly suggests that more massive muscles in the vicinity of the buttocks make for faster sprinting and better running endurance too. “The butt is an essential adaptation for the human ability to run steadily, for long distances, and without injury,” Radke writes. 

That said, the gluteus maximus does more than just keep us on our feet. The fat that sits atop it affects how we feel whenever we sit or lie down. The organs nestled behind those cheeks also have a massive influence on our health and wellbeing. Here are a few of the ways our bums factor into scientific understanding, lifesaving medicine, and the future of engineering. 

Digging deep for ancient backsides 

For as long as humans have been making art, they’ve been thinking about bodacious butts. The 30,000-year-old Venus of Willendorf is a famous pocket-size figurine carved by a Western European civilization during the Upper Paleolithic. The statuette, which some archaeologists suspect served as a fertility charm, immortalizes a body too thick to quit.

Scientists also love peeping at the actual posteriors of our early ancestors, which hold a broader archaeological significance in telling the stories of ancient people and their lifestyles. Differences in the pelvis and other sat-upon bones have long been used to determine the sex of unearthed skeletal remains, though we know now there isn’t as clear-cut a binary as researchers long assumed. In 1972, anthropologist Kenneth Weiss flagged that experts were 12 percent more likely to classify skeletons found at dig sites as men versus women, which he blamed on a bias for marking indeterminate skeletons as male. Recent research bears that out, with anthropologists now designating many more remains as having a mix of pelvic characteristics (or simply being inconclusive) than they did historically. Still, while the distinction isn’t completely black and white, the signs of a body primed for or changed by childbirth are useful in figuring out the age and sex of ancient remains. Butt bones can also tell us about how people lived: This March, archaeologists published the oldest known evidence for human horseback riding in the journal Science Advances. They identified their 5,000-year-old equestrians—members of the Yamnaya culture, which spread from Eurasia throughout much of Europe around that same time—with the help of signs of wear and tear to hip sockets, thigh bones, and pelvises. 

Supporting heinies of all shapes and sizes

As Sharon Sonenblum, a principal research scientist at the School of Mechanical Engineering at Georgia Tech, puts it, “What could be better than studying butts?” The Rehabilitation Engineering and Applied Research Lab that she’s part of is perhaps more aptly referred to by its acronym: REAR. 

Stephen Sprigle, a Georgia Tech professor in industrial design, bioengineering, and physiology, started REARLab with better solutions for wheelchair users in mind. A decade ago, he and Sonenblum saw the potential for an engineering-minded solution to the serious clinical problem of injuries from sitting or lying down for extended periods. Pressure sores and ulcers are a risk whenever soft tissue presses against a surface for a prolonged time, and they become more dangerous in hospital settings—where antibiotic-resistant bacteria often lurk—and in people with conditions that hinder wound healing, like diabetes. 

Sonenblum recalls that they set out to answer a deceptively simple question: What makes one backside different from another? To answer it, they had to put a whole lot of booties into an MRI scanner. Those imaging studies and others (including some done on supine patients) have provided an unprecedented amount of data about butt cheeks and the stuff inside them. 

The big headline, Sprigle says, is that “we’re big bags of water. What the skeleton does in that big bag of goo is totally fascinating.” 

The work proved particularly humbling for Sonenblum, who’d intended to spend her career studying how the gluteus maximus affects seating. Instead, she and her colleagues figured out that humans don’t rest on muscle at all—the fat is what really counts. Sonenblum and the rest of the REARLab team are investigating how the natural padding in our rears changes over time, particularly in people who spend a lot of time sitting or supine.

Today, REARLab creates more precise computer models and “phantoms” to help cushion testing—mainly for wheelchair seats, but also for ergonomic chairs of all stripes—better account for real-world bums. Phantoms aren’t quite faux butts; they’re simple and scalable geometric shapes, almost like the convex version of a seat cushion designed for your tuchus to nestle into. They don’t account for bodies’ individual differences either. 

“Phantoms are always a tricky balance between time and representation,” Sonenblum says. “You want to represent the population well, but you can’t have too many or you’ll spend your entire life running tests.”

REARLab’s current approach is to use two shapes—elliptical and trigonometric—to represent a fuller backside and one more likely to pose biomechanical problems when seated, respectively. It would be reasonable to assume the trigonometric butt is the bonier of the two, Sonenblum says, but the reality isn’t so simple. Large individuals with lots of adipose tissue can still lose the round cushioning when they sit. 

“I’ve seen scans of butts that look like this, and when I do, I think, Wow, that’s a high-risk butt,” Sonenblum explains. It comes down to the quality of the tissue, she adds. “If you touch a lot of butts, you’ll find that the tissue changes for people who are at risk [of pressure injuries]. It feels different.”

Sonenblum and Sprigle hope that continued work on backside modeling, cushion-testing standards, and adipose analysis will help wheelchair users and patients confined to their beds for long stretches stay safer and more comfortable. But their work has implications for absolutely anyone who sits down. When asked what folks should take away from their studies, they’re both quick to answer: Move. People with limited mobility may not be able to avoid the loss of structural integrity in their butt tissue, but anyone with the ability to get up often and flex their muscles can keep that natural padding in prime health. 

Finding better bellwethers for bowel cancer

When it comes to protecting your posterior, it’s not just the bodacious bits of the outside that count. One of the biggest backside-related issues scientists are tackling today is the sharp rise in colorectal cancer, which starts with abnormal cell growth in the colon or rectum. It’s already the third most common cancer and second leading cause of cancer death, but it represents a mounting threat, especially for millennials. New cases of young-onset colorectal cancer (yoCRC)—defined as a diagnosis before age 50—have gone up by around 50 percent since the mid-1990s. 

Blake Buchalter, a postdoctoral fellow at Cleveland Clinic Lerner Research Institute focused on cancer epidemiology, says that the most troubling thing about this recent uptick in cases is how little we know about what’s causing it. He and his colleagues suspect that 35- to 49-year-olds who die from colorectal cancer may share many of the same demographics and risk factors—higher body weight, lower activity levels, smoking, alcohol use, and diets high in processed and red meats—seen in patients aged 50 and older. But those under the age of 35 don’t follow those patterns as closely as expected. 

“This indicated to us that mortality among the youngest colorectal cancer patients may have different drivers than among older populations,” Buchalter says. “Our future work in this space aims to identify underlying factors that might be driving higher incidence and mortality among certain age groups in particular geographic regions.” 

Buchalter hopes that more granular data will encourage more granular screening guidelines too. While he was heartened to see the US Preventative Services Task Force shift the recommended colon cancer screening age down from 50 to 45 in 2021, it’s clear that some populations are at risk for the disease earlier, he says. Buchalter and his colleagues hope to zero in on who should be getting screened in their 20s and 30s. 

But colonoscopies, the most commonly recommended form of detection, present a major hurdle in themselves. A 2019 study found that only 60 percent of age-eligible US adults were up to date on their colorectal cancer screenings, with others citing fear, embarrassment, and logistical challenges such as transportation to explain their delayed colonoscopies. At-home fecal tests offer a less invasive alternative, but research shows that fear of a bad diagnosis and disgust with the idea of collecting and mailing samples still keep many folks from using them. Blood tests and colon capsule endoscopy (CCE), in which patients swallow a pill-size camera to allow doctors to examine the gastrointestinal tract, both show promise in supplementing, and perhaps someday replacing, the oft-dreaded colonoscopy.

For now, it’s worth going in for the physical screening if you can manage it. While blood and stool tests can accurately detect signs of the cancer, colonoscopies can actually help prevent it. During a standard colonoscopy, gastro­enterologists are able to identify and remove potentially precancerous polyps known as adenomas on the spot. No DIY kit can manage that.  

Tracking microbiomes with futuristic commodes

Meanwhile, other researchers are uncovering health secrets from long-ago water closets. In 2022, archaeologists uncovered what they believe to be the oldest flush toilet ever found, in Xi’an, China. The 2,400-year-old lavatory features a pipe leading to an outdoor pit. Researchers believe the commode, which was located inside a palace, allowed servants to wash waste out of sight with buckets of water. Flush toilets wouldn’t appear in Europe until the 1500s, and wouldn’t become commonplace until the late 19th century. Up until that point, major US cities employed fleets of “night soil men” to dig up and dispose of the contents of household privies and public loos.

As far as we’ve come from the days of night soil, the future of the humble toilet looks even brighter. Sonia Grego, an associate research professor in the Duke University Department of Electrical and Computer Engineering, says she’s “super-excited” to see commodes enter the 21st century. 

“Smart” toilets boast everything from app-controlled heated seats to detailed water-usage trackers, and could grow into a $13.5 billion industry by the end of the decade. But Grego’s team—the Duke Smart Toilet Lab at the Pratt School of Engineering—is focused on turning waste flushed down porcelain bowls into a noninvasive health tool. She envisions a future in which your toilet can warn you of impending flare-ups of gut conditions like irritable bowel syndrome, flag dietary deficiencies, and even screen for signs of cancer. 

“When we first started to work on the smart toilet for stool analysis, laboratory scientists were skeptical that accurate analytical results could be obtained from specimens that had been dropped in a toilet instead of a sterile collection container,” Grego recalls. “The perspective is very different now.”

Drawing inspiration from wild butts 

Humans may be unusually blessed in the butt-cheek department, but that doesn’t mean other animals’ rears hold less scientific appeal. From modeling the evolution of the anus to cracking the code on climate-friendly gut microbes, scientists are keeping close tabs on all sorts of animal bottoms. Some researchers are even hoping to harness the power of butt breathing—yes, actually breathing through your butt—for future applications in human medicine. 

We’ll circle back to backside breathing in a moment. First, let’s consider the wombat. While it’s true enough that everybody poops, these marsupials are the only animals known to drop cubes. For years, no one was quite sure how they managed to get a square peg out of a round hole. Some even assumed the wombat must have an anus designed for squeezing out blocks instead of cylinders. In 2020, mechanical engineers and wildlife ecologists at Georgia Tech teamed up to publish a surprising new explanation for the shape in the aptly named journal Soft Matter. They’d borrowed roadkill from Australia to do the first-ever close examination of a wombat’s intestines. By inflating the digestive tract and comparing it to more familiar pig intestines, they were able to show that the marsupial’s innards have more variation in elasticity: Instead of being fairly uniform throughout, the organs have some inflexible zones. The team’s findings suggest that a few nooks within the digestive system—some stretchy, others stiff—provide a means to shape the refuse into a square. 

Wombat butts themselves, by the by, are veritable buns of steel. Their rumps contain four fused bony plates surrounded by cartilage and fat and can be used to effectively plug up the entrance to a burrow when potential predators come sniffing around. While this has yet to be caught happening live, some scientists think wombats can even use their powerful bums to crush the skulls of intruders like foxes and dingoes who manage to make it inside. 

So now we have more clarity on how wombats poop cubes, but the question of why remains unanswered. Experts have posited that wombats communicate with one another by sniffing out the location of poop cubes, making it advantageous to produce turds less likely to roll out of place. Others argue that the unusual shape is a happy accident: Wombats can spend as long as a week digesting a single meal, with their intestines painstakingly squeezing out every possible drop of moisture to help them survive the arid conditions Down Under. Their entrails, when unwound, stretch some 33 feet—10 feet more than typical human guts—to help facilitate the frugal squeezing. When the species is raised in captivity with loads of food and water, their poops come out moister and rounder. 

Elsewhere in the world of scat science, folks are working to understand the secrets of nonhuman gut microbiomes. Earlier this year, biotechnologists at Washington State University showed that baby kangaroo feces could help make beef more eco-friendly. Joey guts contain microbes that produce acetic acid instead of methane, which cows burp out in such abundance that it significantly worsens climate change. By reseeding a simulated cow stomach with poop from a newborn kangaroo, researchers say they successfully converted the gut to a factory of acetic acid, which doesn’t trap heat in the atmosphere. They hope to try the transfer out in a real bovine sometime soon. 

Going back to the butt breathing, scientists are hoping to suss out how to give humans a superpower already exhibited by catfish and sea cucumbers. In 2021, Japanese researchers reported in the journal Med that they’d been able to keep rodents alive in oxygen-poor conditions by ventilating them through their anuses. Inspired by loaches—freshwater fish that can take in oxygen through their intestines—the scientists are trying to find new ways to help patients who can’t get enough air on their own. They’ve moved on to study pigs, which they say do wonderfully with a shot of perfluorodecalin (a liquid chemical that can carry large amounts of oxygen) up the bum. 

From an evolutionary standpoint, it’s not all that surprising that our outbox can handle the same duties as our inbox. Though it’s still not clear which came first, it’s well established that the anus and the mouth develop out of the same rudimentary cell structures wherever they appear. Some of the most basic animals still use a single opening for all their digestive needs. And one creature—just one, as far as we know—has a “transient anus.”

In 2019, Sidney Tamm of the Marine Biological Laboratory in Woods Hole, Massachusetts, demonstrated that the warty comb jelly creates new anuses as needed. Whenever sufficient waste builds up—which happens as often as every 10 minutes in young jellies—the gut bulges out enough to fuse with the creature’s epidermis, creating an opening for defecation. Then it closes right back up. It’s possible that the world’s first anuses followed the same on-demand model, proving yet again that the butt and its contents are worthy of our awe, curiosity, and respect.  

Read more PopSci+ stories.

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Three years ago, Nancy Klimas sat in an auditorium waiting to discuss her latest research progress. The audience was made up of the usual suspects at a scientific conference: doctors, scientists, and other academic colleagues. But this group was a bit different. The room was also packed to the brim with retired US veterans, all waiting to hear about any new developments over a “moonshot” idea that could be the closest attempt to a cure for Gulf War illness. 

Klimas, who serves as the director for the Institute for Neuro-Immune Medicine at Nova Southeastern University in Florida, has been studying this debilitating condition for three decades. The strange sickness affects 175,000 to 250,000 soldiers who were deployed in the 1990-1991 Persian Gulf War. For those veterans, nearly half of who are pushing 50 or above, life has been an uphill battle. There is currently no cure for Gulf War illness, and because it involves a cluster of symptoms—fatigue, joint pain, diarrhea, memory loss—attempts to treat it have come up short. “These people served our country and put themselves in harm’s way,” says Klimas. “Now they’re sick with a chronic illness that ruined their quality of life and ability to work for more than 30 years.” Exhausting her options, Klimas came up with a rather unconventional idea: use a well-established abortion drug to reset the body’s overwhelming response to chronic illness.

[Related: The PACT Act will take the burden of proof off US veterans exposed to burn pits]

Mifepristone, more widely known as the abortion pill, is capable of treating multiple illnesses. At low doses and when paired with another pill, misoprostol, the synthetic steroid binds to a protein in the uterus and stops the release of progesterone and other hormones needed to sustain pregnancy. But the drug has another effect, which Klimas is looking to tap. When taken at higher doses, mifepristone also blocks hormone receptors in the adrenal gland, which regulates the body’s stress response. The drug has already proven capable of doing this, and is currently approved as a treatment for the metabolic disorder Cushing’s syndrome. 

Based on that evidence, Klimas wondered if the medication could temporarily block the adrenal gland and rebalance the hormone signals that are blunted with Gulf War illness. Repurposing the FDA-approved drug would also save the 10 to 15 years it would take to develop and test a brand-new drug. Klimas is halfway through her phase 1 trial testing the safety of the drug at different dosages on veterans, and is making plans for the second phase of the study. 

The recent legal mess surrounding mifepristone access threw a wrench in Klimas’s plans, along with those of other researchers using mifepristone in their work. In early April, a federal circuit judge in Texas overturned the FDA’s 23-year-long approval of mifepristone, citing claims that the drug is unsafe for public use because abortion is now illegal in some states. And while the Supreme Court blocked the ruling that would have suspended mifepristone access across clinics, pharmacies, and mail orders, the future of the treatment remains uncertain in the US. “Obviously, we’re very concerned,” says Klimas, adding that mifepristone was already hard to get for research purposes. “Attempts to limit access to this drug has already had a splashback on the veteran population in these trials, as we’re delayed in rolling things out. How long will they have to wait for an effective therapy?”

Further constraints on mifepristone could impact medical progress on many other diseases and conditions as well. The medication is being studied as a potential treatment for diabetes in people without Cushing’s syndrome. It has also shown some potential in preventing weight gain caused by antipsychotic medication. Some ongoing clinical trials have found that mifepristone can be effective in slowing down the spread of breast cancer: The drug blocks progesterone receptors from releasing the hormone, which would normally stimulate tumor cell growth. And at different dosages, the pill can improve the quality of life of people dealing with painful uterine growths.

[Related: Abortion bans are impeding access to ulcer, arthritis, and cancer medications]

Banning mifepristone goes beyond stalling research—it puts any FDA-approved treatment at risk of being recalled. “You have a medication with an excellent track record of safety, efficacy, and high patient satisfaction,” says Carrie Cwiak, an OB-GYN at Emory Healthcare in Georgia. “The idea that the entire process for approving medication can be overturned [in court] is earth-shattering.” She says that restricting mifepristone opens a dangerous door to having people with legal power make treatment decisions based on their opinion and ideology rather than medical evidence. 

If the courts decide to bar or limit mifepristone use down the line, it would discourage pharmaceutical companies from spending money on producing new drugs that appear controversial. That could include contraceptives, hormone blockers, or treatments completely unrelated to reproductive issues. “If you were a pharmaceutical company and it was going to cost you $20 million to move a pipeline drug all the way up through phase three [clinical trials], would you want to invest the money for it if it’s possible the bench could reverse the authority of the FDA?” Klimas asks. 

Despite the setbacks on mifepristone access and potential legal battles, Klimas is optimistic that the research she is doing will help give veterans their long and overdue treatment. Her team is hoping to start their phase 2 trial soon and get as many results before politics interferes in science again. 

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On April 26, the Food and Drug Administration approved the first pill for fecal transplants. The pill is made from healthy bacteria found in human waste which can help fight dangerous infections in the gut.

[Related: The FDA approved a fecal transplant treatment for the first time.]

According to the FDA, the pill from Massachusetts-based Seres Therapeutics provides doctors and patients with a simpler, and rigorously tested version of the procedure that has been used for just over a decade. Previously, when a patient experienced a Clostridium difficile infection or CDI, doctors would perform a fecal transplant using the stool from a healthy donor. Donor bacteria can help restore the balance of bacteria in the gut and prevent reinfections.  

The new treatment will be sold under the brand name Vowst as four daily capsules for three consecutive days. Vowst was cleared for adults 18 and older who face risks from repeat infections from C. diff, and have already received antibiotic treatment. A CDI can cause severe nausea, cramping, and diarrhea, and is dangerous when it reoccurs. CDI’s lead to roughly 15,000 to 30,000 deaths per year. 

While C. diff can be killed with antibiotics, the drugs can also destroy the beneficial bacteria that live inside the gut, leaving  it more susceptible to infections in the future. People over age 65 are at an increased risk for contracting an infection, but other risk factors include hospitalization, a weakened immune system, and a previous history of infection. Some patients may get the infection again following recovery, and the risk of additional recurrences increases with each infection. 

The FDA approved Vowst based on a study of 180 patients wherein nearly 88 percent of the patients taking the capsules did not experience a reinfection after eight weeks. About 60 percent of those who received dummy pills did see a reinfection. Some of the common side effects included abdominal swelling, constipation and diarrhea.

According to Seres, via reporting from the Associated Press, manufacturing the pills relies on the same techniques and equipment that is used to purify both blood products and other biologic therapies. It starts with stool from a screened group of donors that is tested for potential infections, viruses, and parasites. The samples are then processed to remove the waste and isolate the healthy bacteria,killing any lingering organisms. 

In the approval announcement, the FDA warned that the drug “may carry a risk of transmitting infectious agents. It is also possible for Vowst to contain food allergens.”

[Related: What to know about fecal transplants in the wake of the first death.]

In late 2022, the FDA approved Rebyota, the first pharmaceutical-grade version of a fecal transplant treatment from Ferring Pharmaceuticals. This product must be delivered via the rectum. 

The approvals of both Rebyota and Vowst are the product of years of pharmaceutical research into the bustling community of fungi, bacteria, and viruses that lives in the gut called the microbiome.

A network of stool banks from hospitals and medical institutions across the US have provided most fecal transplants. However, that growing number of fecal transplant practitioners and stool banks around the US has created a regulatory mess for the FDA, since the agency doesn’t traditionally regulate medical procedures performed by doctors. As long as stool donors are carefully screened for any potential infectious diseases, the FDA has rarely intervened in using the procedure.

In response to these new FDA-approved options, the largest stool bank in the US called OpenBiome said it will keep serving the patients like children and adults with treatment-resistant cases who are not eligible for the new treatments. Since 2013, OpenBiome has supplied more than 65,000 stool samples for CDI patients.

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A common diabetes drug has become trendy because of its use as an off-label weight loss drug. From tech moguls to influencers, this drug has become the latest “celebrity secret” for shedding the pounds. 

Ozempic, and a similar medication called Wegovy, are brand names for an injectable medicine called semaglutide. This drug is the synthetic version of a hormone called glucagon-like peptide-1 (GLP-1), which belongs to a class of medications known as GLP-1 agonists. 

The chemistry explains how Ozempic works and what its main side effects are. GLP-1 is a compound that increases insulin production and lowers blood sugar. After we eat, GLP-1 also signals to the brain a feeling of fullness. Meanwhile, GLP-1 agonists slow down the rate at which food empties out of the stomach, further promoting a feeling of satiety. This prevents cravings and overeating, which can result in weight loss. 

While Ozempic and Wegovy are now lumped together with weight loss fads, these medications are not diet hacks. Instead, they are medications proven to lower weight in certain patient populations. 

Despite this, there is a growing concern that these drugs are misused and overprescribed in individuals who casually use them for aesthetic reasons. There’s concern this type of use is resulting in repercussions like unmanaged side effects and drug shortages. Here are some proven facts and common misconceptions surrounding Ozempic. 

Fact: Ozempic’s side effects include weight loss, but it’s not a weight loss drug

This distinction is important. Ozempic is only approved by the Food and Drug Administration (FDA) for Type 2 diabetes. It is intended to help diabetes patients control their blood sugar. While it is not a weight loss drug, diabetes patients on Ozempic may lose weight as a side effect because of the way the medication works. Losing weight can improve insulin production and, in turn, benefit some individuals. Meanwhile, Wegovy is FDA-approved for chronic weight management in adults with obesity.

[Related: There’s still a lot we don’t know about the new generation of weight loss pills.]

Swetha Bhat, a primary care physician in the California Bay Area, prescribes Ozempic and Wegovy to patients who meet the criteria. She tells PopSci she has denied requests for semaglutide for weight loss because patients don’t qualify. 

“I can’t prescribe medications to someone who doesn’t meet the FDA indication,” Bhat says. “There are med spa clinics run by dermatologists or plastic surgeons who prescribe semaglutide and that is simply out of scope for their practice.”

Fact: Ozempic and Wegovy are the same medication

Ozempic and Wegovy are two names for the same injectable drug manufactured by Novo Nordisk: semaglutide. But they are approved for different conditions and administered at different dosages.

Ozempic first received FDA approval as a treatment for type 2 diabetes in 2017 at a maximum dosage of 1 milligram once weekly, and was approved again in 2022 for a larger maximum dose of 2.0 milligrams. 

Wegovy received FDA approval in 2021 for adults who are obese or overweight with at least one weight-related condition (high blood pressure, type 2 diabetes, or high cholesterol). People taking Wegovy start at a dose of 0.25 milligrams once a week and increase the dose every four weeks until they reach the full dose of 2.4 milligrams.

Despite the recent Wegovy approval, there’s already a new drug on the block, which seemingly packs even more punch. In 2022, Eli Lilly launched its first in-class diabetes drug called Mounjaro (generic name tirzepatide), which activates both GLP-1 and GIP receptors for increased blood glucose control. According to the FDA, the average weight loss on Mounjaro at the maximum dose is 12 pounds more than with semaglutide. 

Fact: Ozempic has other side effects, but they’re not the same for everyone

There are some reports that Ozempic use results in a side effect called “Ozempic face,” in which the face becomes noticeably more gaunt and sunken due to the drastic weight loss. 

[Related: Experts rank the raw food diet as the worst of 2023.]

However, the term “Ozempic face” is misleading. It’s not necessarily a side effect of Ozempic, but a general possible side effect of weight loss. Sometimes a large weight reduction can result in excess skin in the face among other places. But not everyone who uses Ozempic will experience this, and it’s not a clinically proven side effect.

The most common side effects of taking GLP-1 agonists are nausea and diarrhea. Another common side effect is lack of appetite, to the point where some patients need to remind themselves to eat.

Fact: The Ozempic shortage was caused by the weight loss fad—and many other reasons 

There are several reasons for the Ozempic shortage. Novo Nordisk stated the shortage was due to issues with manufacturers coupled with the increase in demand for both on-label and off-label use. Pharmacies also tend to not stock Ozempic as it is expensive with poor cost-benefit. 

Meanwhile, social media increased interest in semaglutide among people who wouldn’t qualify for the drug for FDA-approved reasons. For example, a TikTok of Chelsea Handler went viral after she was unknowingly given Ozempic by her “anti-aging doctor.” This is referred to as “off-label” prescribing—when a doctor uses their best judgment to prescribe a medication for which the drug isn’t FDA approved.

[Related: Weight might not be the best way to detect diabetes early.]

Digital health companies, meanwhile, have made it easy for people who want the drug to access it. This has contributed to drug shortages.

A retail pharmacist in Central California, who did not want their name published, spoke about the opposite end of the experience with PopSci. “At first we were getting an influx of patients who were diabetic and we saw how much it helped. Then all of a sudden there was a surge of non-diabetic patients and we could not get semaglutide for our diabetic patients.”

Now, most practitioners have to provide a diabetes diagnosis when prescribing Ozempic for insurance reasons, they explain. “At the same time, the supply chain was also a major contributor to the shortage. For a while, we couldn’t get the drug at all through McKesson [a drug distributor] and our diabetes patients suffered. We had to switch them to Trulicity [the brand name for the drug dulaglutide] and even that went out of stock for a while.”

Fact: Ozempic is made from lizard lips (kind of)

In a recent episode of the pop culture podcast “Psychobabble,” hosted by Tyler Oakley and Korey Kuhl, the duo giggled in wonderment after reading on Twitter that Ozempic was made from “Gila monster spit.” 

GLP-1 agonists are derived from the venomous saliva of the Gila monster, a giant lizard that lives in US and Mexican deserts. In 1990, an endocrinologist named John Eng researched both the toxic and nontoxic chemicals produced by the species for medicinal use. He discovered that Gila monsters went long periods without eating and slowed down their metabolism while maintaining constant blood sugar levels. 

The peptide that allows them to do this is called Exendin-4 and is strikingly similar in both structure and function to human GLP-1. So Exendin-4 was derived to make the first synthetic GLP-1 drug, called Exenatide.

Fact: Ozempic can be a life-changing medication for the right patients

GLP-1 agonists, including Ozempic, continuously prove to be powerful blood glucose and weight-lowering medicines. They are also one of the few classes of diabetes drugs that have a significant clinical benefit in patients with a cardiovascular disease history and chronic kidney disease, which are risk factors for diabetes. 

With so many headlines and news outlets, the amount of information the average individual has to filter through can be overwhelming, especially when it comes to health. The Ozempic craze is a fantastic example of pop culture amplifying potentially misleading information. It is important to weed out the fact from fodder to avoid an unwarranted bias against a possible life-saving medication for the right candidate.

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This article originally appeared in Knowable Magazine.

The seizures started when Samantha Gundel was just four months old. By her first birthday, she was taking a cocktail of three different anticonvulsant medicines. A vicious cycle of recurrent pneumonia, spurred on by seizure-induced inhalation of regurgitated food, landed the young toddler in and out of the hospital near her Westchester County home in New York State.

Genetic testing soon confirmed her doctors’ suspicions: Samantha, now age 4, has Dravet syndrome, an incurable form of epilepsy. Her brain was misfiring because of a mutation that is unlike those responsible for most genetic diseases; it’s a type that has long eluded the possibility of correction. Available drugs could help alleviate symptoms, but there was nothing that could address the root cause of her disease.

That’s because the mutation at the heart of Dravet creates a phenomenon known as haploinsufficiency, in which a person falls ill if they have only a single working copy of a gene. That lone gene simply can’t produce enough protein to serve its molecular purpose. In the case of Dravet, that means that electrical signaling between nerve cells gets thrown out of whack, leading to the kinds of neuronal shock waves that trigger seizures.

Most genes are not like this. Though the human genome contains two copies of almost every gene, one inherited from each parent, the body can generally do fine with just one.

Not so for genes such as SCN1A, the main culprit behind Dravet. For SCN1A and hundreds of other known genes like it, there’s a delicate balance of molecular activity that is needed to ensure proper function. Too little activity is a problem — and oftentimes, so is too much.

This Goldilocks paradigm partially explains why conventional gene therapy strategies are ill-suited to the task of haploinsufficiency correction. With therapies of this kind — several of which are now available to treat “recessive” genetic diseases such as the blood disorder beta thalassemia and a form of inherited vision loss — the amount of protein made by an introduced gene just needs to cross a minimum threshold to undo the disease process.

In those contexts, it’s not a problem if the added gene is overactive — there’s a floor, but no ceiling, to therapeutic protein levels. That is simply not the case with many dosage-sensitive diseases like Dravet, especially for brain disorders in which too much protein can overexcite neuronal activity, says Gopi Shanker, who served as chief scientific officer of Tevard Biosciences in Cambridge, Massachusetts, until earlier this year. “That’s what makes it more challenging,” he says.

Adding to the challenge: The special types of modified viruses that are used to ferry therapeutic genes into human cells can handle only so much extra DNA — and the genes at the heart of Dravet and many related haploinsufficiency disorders are much too big to fit inside of these delivery vehicles.

Overlooked no more

Faced with these technical and molecular hurdles, the biotechnology industry long ignored haploinsufficiencies. For more than 30 years, companies jostled to get a piece of the drug development action in other areas of rare genetic disease — for cystic fibrosis, say, or for hemophilia — but conditions like Dravet got short shrift. “It’s one of the most neglected classes of disorder,” says Navneet Matharu, cofounder and chief scientific officer of Regel Therapeutics, based in Berkeley, California, and Boston.

Not anymore. Thanks to new therapeutic ideas and a better understanding of disease processes, Regel, Tevard and a group of other biotech startups are taking aim at Dravet, with experimental treatments and technologies that they say should serve as testing grounds for going after haploinsufficiency diseases more broadly.

Currently, there’s little to offer patients with these maladies other than drugs to aid with symptom control, says Kenneth Myers, a pediatric neurologist at Montreal Children’s Hospital who cowrote an article about emerging therapies for Dravet and similar genetic epilepsies in the 2022 issue of the Annual Review of Pharmacology and Toxicology. But thanks to new advances, he says, “there’s a huge reason for optimism.”

Samantha, for one, now seems to have her disease under control because of a drug called STK-001; it is the first ever to be evaluated clinically that addresses the root cause of Dravet.

Between February and April 2022, doctors thrice inserted a long needle into the young girl’s lower spine and injected the investigational therapy, which is designed to bump up levels of the sodium-shuttling protein whose deficiency is responsible for Dravet. It seemed to work. For a time, Samantha lived nearly seizure-free — presumably because the increased protein levels helped correct electrical imbalances in her brain.

She went from epileptic attacks every 7 to 10 days, on average, to nothing for months on end. Her verbal skills improved, as did her physical capabilities. Her gait improved and her tremors disappeared.

Eventually, as the therapy wore off, Samantha began to backslide, with seizures returning every couple of weeks or so. But she started receiving additional doses of STK-001 under a new trial protocol in October 2022, and since then has experienced only two epileptic episodes over the span of six months. “It’s really pretty amazing,” says her mother, Jenni Barnao.

“Is it a cure? No.… But this is absolutely our best shot,” Barnao says. “There’s definitely something with this drug that’s very good. Her brain is just working better.”

Give a boost

The STK-001 treatment relies on the fact that the normal activity of genes is somewhat inefficient and wasteful. When genes get decoded into mRNA, the resulting sequences require further cutting and splicing before they’re mature and ready to serve as guides for making protein. But often, this process is sloppy and doesn’t result in usable product.

Which is where STK-001 comes in.

A kind of “antisense” therapy, STK-001 consists of short, synthetic pieces of RNA that are tailor-made to stick to part of the SCN1A gene transcript and, as a result, make productive cutting and splicing more efficient. The synthetic pieces glom on to mRNA from the one working version of the gene that people with Dravet have and help to ensure that unwanted bits of the mRNA sequence are spliced out, just as a movie editor might cut scenes that detract from a film’s story. As a result, more functional ion channel protein gets made than would otherwise happen.

Protein levels don’t get completely back to normal. According to mouse studies, there’s a 50 percent to 60 percent boost, not a full doubling of the relevant protein in the brain. But that bump seems to be enough to make a real impact on patients’ lives.

Stoke Therapeutics, the company in Bedford, Massachusetts, that is behind STK-001, reported at the American Epilepsy Society’s 2022 Annual Meeting that 20 of the first 27 Dravet patients to receive multiple doses of the therapy in early trials experienced reductions in seizure frequency. The greatest benefits were observed among young children like Samantha whose brains have accumulated less damage from years of debilitating seizures and abnormal cell function. Larger confirmatory trials that could lead to marketing approval are scheduled to begin next year.

Stoke is hardly alone in its quest to fix Dravet and haploinsufficiency disorders more generally. Several other biotech startups are nearing clinical trials with their own technological approaches to enhancing what working gene activity remains. Encoded Therapeutics, for example, will soon begin enrolling participants for a trial of its experimental Dravet therapy, ETX-001; it uses an engineered virus to deliver a protein that ramps up SCN1A gene activity so that many more mRNA copies are made of the single, functional gene.

And if any of these companies succeed in reversing the course of Dravet, their technologies could then be adapted to take on any comparable disease, says Orrin Devinsky, a neurologist at NYU Langone Health who works with several of the firms and is involved in Samantha’s care. “An effective therapy would provide a potential platform to address other haploinsufficiencies,” he says.

New targets, new tactics

Stoke will soon put that idea to the test.

Buoyed by the early promise of its Dravet therapeutic, the company developed a second drug candidate, STK-002, that similarly targets splicing to turn nonproductive gene transcripts into constructive ones. But in this case, it’s designed to tackle an inherited vision disorder known as autosomal dominant optic atrophy, caused by haploinsufficiency of a gene called OPA1. In this disease, a single working copy of OPA1 is not enough to sustain proper nerve signaling from the eyes to the brain.

Clinical evaluation of STK-002 is expected to start next year. Meanwhile, in partnership with Acadia Pharmaceuticals of San Diego, Stoke is also exploring treatments for Rett syndrome and SYNGAP1-related intellectual disability, both severe brain disorders caused by insufficient protein levels.

Stoke’s splice-modulating approach flows naturally from the success of another antisense drug, Spinraza. Developed by Ionis Pharmaceuticals in collaboration with Biogen, Spinraza also works on splicing of mRNA transcripts to promote production of a missing protein. In 2016, it became the first therapy approved for treating a rare neuromuscular disorder called spinal muscular atrophy (SMA).

SMA is somewhat different, though. It isn’t a haploinsufficiency — it occurs when both gene copies are defective, not just one — but it’s an unusual disease from a genetics standpoint. Because of a quirk in the human genome, it turns out that people have a kind of backup gene that doesn’t normally function because its mRNA undergoes faulty splicing. With Spinraza acting as a guide to help the mRNA splice correctly, that backup gene can be made operational and do the job that the damaged gene copies can’t do.

Few diseases are like this. But Stoke’s scientific cofounders, molecular geneticist Adrian Krainer of Cold Spring Harbor Laboratory in New York (who helped to develop Spinraza) and his former postdoctoral researcher Isabel Aznarez, realized that there was a whole world of other ailments — haploinsufficiencies — for which this type of splice modulation could be beneficial.

Spinraza was the prototype. Stoke’s portfolio is full of the next-generation editions. “We brought it to the next level,” says Aznarez, who now serves as head of discovery research at Stoke.

Striking a balance

There was a time when Dravet researchers were more focused on traditional gene replacement therapies. They aimed to insert a working version of the SCN1A gene into the genome of a virus and then introduce the engineered virus into brain cells. The problems proved manifold, though.

For starters, the virus vehicles generally used in gene therapy strategies — adeno-associated viruses (AAVs) — are too small to hold all 6,030 of the DNA letters that constitute the SCN1A gene sequence.

Researchers tried a few potential workarounds. At University College London, for example, gene therapist Rajvinder Karda and her colleagues split the SCN1A gene in half and delivered both parts into mice in different virus carriers. And at the University of Toronto, neuroscientist David Hampson and his group tried introducing a smaller gene that would fit in a single AAV vector and compensate for the SCN1A deficiency in an indirect way.

But none of those efforts advanced past mouse experiments. And while it is technically feasible to deliver the entire SCN1A gene into cells if you use other kinds of viral vectors, as researchers at the University of Navarra in Spain showed in mice, those viruses are generally considered unsafe for use in people.

What is more, even if gene replacement could be made to work, there are many reasons to think it would not be ideal for diseases like Dravet in which the underlying defect is mediated by an imbalance of protein levels. The amount of protein produced by those kinds of gene therapies can be unpredictable, and so are the types of cells that end up manufacturing the proteins.

To get protein levels just right, scientists say, it is best to follow the cell’s own lead, tapping into the ways that it naturally produces the protein of interest only in certain tissues of the body, and then providing a therapeutic nudge to aid the process along.

CAMP4 Therapeutics, for example, is using antisense therapies, like Stoke. But instead of targeting the splicing of gene transcripts, CAMP4’s drugs are directed at regulatory molecules that act like rheostats to control how much of those transcripts are made in the first place. By blocking or stabilizing different regulatory molecules, the company claims it can ramp up the activity of target genes in a precise and tunable way.

“It’s basically teaching the body to do it a little bit better,” says Josh Mandel-Brehm, president and CEO of CAMP4, which is based in Cambridge, Massachusetts.

In theory, the gene-editing technology known as CRISPR could obviate the need for all of these therapeutic approaches. Gene editing allows you to perfectly correct a mistake in a gene — so one could edit a faulty DNA sequence to correct it and render kids with Dravet or some other haploinsufficiency disease as good as new.

But the technology is nowhere near ready for prime time. (Some of the first CRISPR therapies to be tested in children have failed to demonstrate much benefit.) Plus, any gene-correction therapy would have to be tailored to the unique nature of a given patient’s mutations — and there are more than 1,200 Dravet-causing mutations in the SCN1A gene alone.

That’s why Jeff Coller, an RNA biologist at Johns Hopkins University and a scientific cofounder of Tevard, prefers therapeutic strategies that can address all manner of disease-causing alterations in a gene of interest, as most companies are doing now. “Having a mutation-agnostic technology is a way of going after the entire cohort of patients,” he says.

Tevard, whose mission is to “reverse” Dravet syndrome (the company’s name is Dravet spelled backward), is approaching this challenge in various ways. Some involve engineered versions of other RNAs that are key for protein production; known as “transfer” RNAs, they help to ferry amino acid building blocks to the growing protein strands. Others are intended to help bring beneficial regulatory molecules to sites of SCN1A gene activity.

But all of Tevard’s therapeutic candidates remain at least a year away from clinical testing, whereas STK-001 is in human trials today. So the company’s chief executive, Daniel Fischer — who, along with board chair and cofounder Warren Lammert, has a daughter affected by Dravet — is considering enrolling his child, now 13, in the Stoke trial rather than waiting for his own company’s efforts to bear fruit.

“We’re open to any approach that would help our daughters,” Fischer said over lunch last November at the company’s headquarters.

“And help people with Dravet generally,” added Lammert. “We’d love to see many of these things succeed.”

Editor’s note: This article was amended on April 14, 2023, to correct Gopi Shanker’s relationship with Tevard Biosciences. Shanker is Tevard’s former chief scientific officer; he is now chief scientific officer with Beam Therapeutics.

This article originally appeared in Knowable Magazine, an independent journalistic endeavor from Annual Reviews. Sign up for the newsletter.

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This article originally appeared in Grist.

A new report by the American Lung Association found that more than one in three Americans were exposed to unhealthy levels of air pollution between 2019 to 2021. Released on Wednesday, the 24th annual State of the Air report grades Americans’ exposure to two of the nation’s most pervasive air pollutants: ground-level ozone, an air pollutant that forms smog, and particle pollution, also known as soot. 

The report found that while overall smog and soot pollution continues to decrease across the U.S., racial and geographic disparities are rising. As climate-fueled wildfires and drought increase and intensify, more people living in the West face potentially deadly particle and ozone pollution compared to their Eastern counterparts.

People of color were found to be 64 percent more likely than white people to breathe unhealthy air, compared to 61 percent in last year’s report. They are also 3.7 times more likely than white people to live in a county that received the American Lung Association’s lowest rating for all three pollution metrics that the group examined: ozone pollution, annual particle pollution, and short-term particle pollution. The report’s ratings were informed by national air quality standards set by the U.S. Environmental Protection Agency. Last year, people of color were 3.6 times more likely to live in a county that received a failing grade on all three measures.

Paul Billings, national senior vice president of public policy for the American Lung Association, said that those findings reflect the continued impact of systemic racism. Pollution sources ranging from refineries to highways are disproportionately sited in communities of color — a persistent legacy of racist housing policies such as redlining. “The benefits of clean air have not been equally shared, and in fact, we’re seeing in this report an even wider disparity than we saw last year,” he said. 

Ozone causes what experts describe as a “sunburn of the lungs,” causing shortness of breath and wheezing and increasing the risk for asthma and respiratory infections. And particulate matter pollution bypasses the human body’s natural defenses to enter the deepest part of the lungs. Even short-term exposure to fine particles — those smaller than 2.5 microns across, also known as PM 2.5 — can lead to a host of health harms, including asthma attacks and heart attacks. 

The number of people experiencing 24-hour spikes in particle pollution rose to the highest levels reported in the last decade. Close to 64 million people lived in counties with failing grades for those daily spikes, according to the report. “That’s nearly a half a million more than we saw in last year’s report,” said Billings.

One major contributor is more frequent and intense wildfires linked to climate change, which spew smoke and fine particles.

Billings said that when the American Lung Association started issuing its State of the Air reports 24 years ago, the organization noticed a much broader spread of communities across the U.S. experiencing high levels of pollution. Now, because of wildfires and increasingly hotter and drier weather, Western states are dominating the lists of top 25 cities most impacted by pollution. 

California cities make up four out of the top five in the lists of cities most impacted by annual particle pollution and ozone pollution. 

“We really see this marked shift, and a lot of that we think is due to climate change, not only for the wildfires but also the hot conditions that create the opportunity for ozone formation,” said Billings. 

Ozone forms when nitrogen oxides and other pollutants “cook” in the sun through a series of chemical reactions. According to the EPA, ozone is more likely to form “on warm, sunny days when the air is stagnant.” 

Those hotter days have become more frequent as a result of climate change, leading to “the number of unhealthy ozone days being higher than it would otherwise be,” the report says. “Simply, climate change is undercutting the progress we would have made.”

In response to these challenges, the American Lung Association and other public health groups are calling on the EPA to further limit ozone and particle pollution by significantly strengthening national ambient air quality standards under the federal Clean Air Act passed in 1970. The agency is currently reviewing both the particulate matter and ozone standards. 

Billings said tightening those limits would fulfill the central promise of the Clean Air Act to provide everyone with clean, healthy air. “While we’ve made progress — no question about it — here we are more than 50 years later looking in the rearview mirror, and we still have more than 1 in 3 living in this country, living in a county that has unhealthy air,” Billings said. “No child born in 2023 should have to breathe air pollution that can make them sick.” 

This article originally appeared in Grist at https://grist.org/health/pollution-smog-wildfires-1-in-3-americans-breathe-unhealthy-air-new-report-says-strong/. Grist is a nonprofit, independent media organization dedicated to telling stories of climate solutions and a just future. Learn more at Grist.org

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Ozone is like Earth’s natural sunscreen, protecting living things from the sun’s harsh UV rays. But this sunscreen is running out. Greenhouse gases are thinning out the ozone layer, and our skin is starting to pay the price. According to the World Health Organization, losing an extra 10 percent of ozone levels will cause an additional 300,000 non-melanoma and 4,500 skin cancer cases.

With skin cancer as the most diagnosed cancer in America, the US Preventative Services Task Force (USPSTF) updated their screening recommendations earlier this month, emphasizing the need for people to get moles and other spots checked early for potential tumors. 

The quicker skin cancer is caught, the better your chances of recovering from it. And recent technological advances in skin cancer research is transforming the way doctors and patients approach this deadly disease. Here are five tech tools to keep an eye on.

Therapeutic skin cancer vaccine

As multiple companies experiment with cancer vaccines, Merck and Moderna are focusing theirs on melanoma. Their phase II clinical trial results, shared last week, showed a 44 percent decrease in risk of death or a melanoma relapse when pairing the vaccine with the immunotherapy Keytruda. Additionally, about 79 percent of people who took the vaccine plus immunotherapy stayed cancer-free for 18 months compared to the 62 percent who just took immunotherapy. The data shows enough promise for the companies to start a Phase 3 trial in adjuvant melanoma this year, and could compel them to rapidly expand the vaccine to other tumor types, including non-small cell lung cancer, Eric Rubin, a senior vice president at Merck, wrote in an email.

[Related: A vaccine trial targeting the most lethal breast cancer just took its next step]

The vaccine isn’t a preventative treatment, but is instead given to melanoma patients early in recovery. The researchers take tumor samples from biopsies and identify which proteins are most likely to be recognized by the human immune system. They then make a personalized mRNA vaccine (adapted from the technology behind Moderna’s COVID jab) using a certain number of these abnormal genes to boost an individual’s adaptive immunity. If the rest of the trials go as planned, the vaccine could be available as soon as 2025 or early 2026, says Eric Whitman, the medical director of Atlantic Health System’s oncology service line.

Genetic tests and personal risk scores

Precision prevention is when doctors use multiple tools to map out a person’s risk of cancer and use that assessment to tailor their treatment and risk-reduction strategy. Instead of following a standard guideline like an annual dermal exam, a person who is considered high-risk (like someone with a history of skin cancer) may need more frequent screenings and extra body imaging, says Meredith McKean, the director of melanoma & skin cancer research at the Sarah Cannon Research Institute in Tennessee. People with very low risk, on the other hand, may be encouraged to learn how to do their own self-checks at home. McKean adds that it’s really helpful “to stratify patients and really help them do the best that we can to prevent another melanoma or skin cancer [case].”

Genetic tests can also be used to identify people with a predisposition to skin cancer. A 2022 study in the journal Cancer Research Communications found that people who were told they had a MC1R mutation, which carries a higher risk for melanoma, made more of an effort to protect themselves against the sun and get regular skin checks. Some doctors even use AI technology to a personalized risk score for individuals based on photos of skin lesions and moles.

Melanoma sticker

The Dermtech SmartSticker is an easy precursor for checking suspicious moles for melanoma. A dermatologist places four skin patches on the potential tumor for less than five seconds, and ships the sample to a Dermtech lab in San Diego, California. The lab then tests for DNA from cancerous cells. If the results come back positive, the dermatologist would follow up with a biopsy. If not, this painful step can be avoided and the doctor would just continue clinically monitoring the patient. 

“It’s a very good test. If it comes up negative, there is a greater than 99-percent reliability that the mole is not melanoma,” says Emily Wood, a dermatologist at Westlake Dermatology & Cosmetic Surgery in Texas. She adds that patients in her clinic favor the stickers over biopsies because they’re painless, cost-effective, and quick. “We’re going to save lives in catching melanoma earlier. I think this will make a dramatic impact for patients long-term.” While the studies are ongoing, there is research suggesting the tool could extend to detecting non-melanoma skin cancer. 

Artificial intelligence apps

Medical researchers are now training computers to recognize patterns and atypical features associated with skin cancer. “AI picks up a lot more subtle changes than the naked eye,” says Trevan Fischer, a surgical oncologist at Providence Saint John’s Health Center. The high accuracy in AI deep learning can help doctors determine whether a mole is malignant and worth biopsying—saving patients from some unneeded discomfort.

The beauty of AI is that you can do a full home skin exam with a press of a few buttons. Popular smartphone apps like MoleMapper lets users upload a picture and have it analyzed for potential skin lesions. They also let you store photos to show your doctor and keep track of any changes to your mole. (Wood warns that a smartphone app is not meant to substitute in-person skin check-ups with your doctor.)

While these apps are useful, there’s always room for improvement. For example, the AI’s accuracy goes down when the view of the mole has shadowing, blurriness, hair, or if the image is rotated. There’s also been research showing that AI databases lack images of darker skin types that would teach the system to better detect skin cancer from people of color. If anything, Wood says the apps can encourage people to submit photos of suspicious moles and start the conversation early with their doctor. 

Millimeter wave imaging 

The same technology used in airport security scanners is getting revamped and used to detect skin tumors. Millimeter wave imaging is a non-invasive method and a low-cost alternative to biopsies that works by scanning a person’s skin for any biochemical and molecular changes related to a disease or disorder. The radio waves reflect differently when looking at benign versus cancerous moles. 

[Related: Everything you need to know about UPF sun protection]

While the approach is not yet available for clinical practice, there is evidence backing up the proof of concept. A 2017 study in IEEE Transactions on Biomedical Engineering found considerable differences when looking back at the scans of healthy skin and those for two common skin cancer types: squamous cell carcinoma and basal cell carcinoma. The study authors could see detailed changes in water molecules, glucose concentrations, and protein levels. A 2018 study in the same journal used ultra-high resolution millimeter wave imaging to identify early-stage skin cancer. Most recently, the diagnostic tool was studied on 136 people suspected of skin cancer. Ultimately, it found malignant tumors from various types of skin cancer on 71 patients, giving the tech a “high diagnostic accuracy.” 

“We’re really trying to leverage all the different ways that advanced technology can help us diagnose and treat skin cancer like melanoma,” Whitman from Atlantic Health Systems says. He emphasizes that most of these strategies weren’t imaginable 10 years ago. Using data to improve on existing AI technology and create new models for personalized medicine, he notes, “can really make a difference for people and their lives.”

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Approximately 300 miles south of New Zealand, the Auckland Islands lie in a belt of winds known as the Roaring Forties. In the late 19th century, sailing ships departing Australasia would catch a ride back to Europe by plunging deep into the Southern Ocean to ride the westerlies home.

But these seas were poorly charted, and weather conditions frequently horrendous.

Sometimes, navigators miscalculated the islands’ position and, too late, found their vessels thrown upon the islands’ rocky ramparts. Ships were torn to pieces and survivors cast ashore on one of the most remote and inhospitable places on the planet. These castaways soon found out they were not alone.

The main land mass in the Auckland archipelago, Auckland Island, was — and still is — home to pigs, initially introduced in the first half of the 19th century by European hunters and explorers, as well as a group of Indigenous New Zealanders fleeing conflict.

The pigs have no natural predators, and over time, they have wrought destruction upon Auckland Island’s flora and fauna. Government conservationists now want them gone — but there’s a twist: These once domesticated farm animals have evolved into ultra-resilient, disease-free pigs that have caught the eye of scientists who study xenotransplantation, a type of medical procedure in which cells, tissues, or organs from one species are transferred into another species.

Last year, for the first time, surgeons transplanted pig hearts and pig kidneys into humans. Such procedures have not yet been tested in clinical trials, and they are not approved by the U.S. Food and Drug Administration or regulatory agencies in New Zealand. But researchers say that xenotransplantation could eventually prove effective at treating a range of conditions and may alleviate the huge global need for donor organs. The Auckland Island pigs, with their unique genetics, may be especially well-suited for this purpose.

Some of the hardy quadrupeds are now housed in a research facility on the New Zealand mainland. Meanwhile, conservation authorities are preparing a massive effort to eradicate those left in the wild.

The first European ship to reach the Auckland Islands (known as Maukahuka or Motu Maha in the Māori language) was the whaler Ocean, in 1806. The ship’s captain returned the following year to drop off a team of seal hunters. During this visit, pigs were first released as a food source. Subsequent introductions continued, and in the late 1800s, with the tales of shipwreck and survival piling up, the New Zealand and Australian governments got involved, releasing additional pigs for the castaways.

The pigs, which were of mostly European and Asian origin, had to learn to live with the persistent cold, rain, and wind — far from ideal conditions for animals bred for sheltered barnyards. But because pigs produce up to two litters each year, they can adapt relatively quickly, said Michael Willis, of the Rare Breeds Conservation Society of New Zealand. Soon, Auckland Island’s pigs formed one unique strain.

In the winter, they survived by eating the island’s endemic plants and scavenging carrion. In the summer, their fortunes changed, and they gorged on plump albatross chicks and protein-filled penguin eggs. Twenty-five species of seabird breed on the Auckland Islands, but after two centuries of pig predation, their numbers have fallen. New Zealand conservationists are increasingly wary of the porcine prowlers.

The archipelago is “an immensely special place,” said Stephen Horn, a project manager at New Zealand’s Department of Conservation. It’s the biggest remaining stronghold of the yellow-eyed penguin, the world’s rarest penguin species, and the Gibson’s wandering albatross, which breeds there exclusively. (Currently, said Horn, seabirds on Auckland Island nest only on the precipitous edges of the land, where even the most tenacious pig won’t venture.)

The pigs have also taken a toll on the spectacular flowering plants known as megaherbs, which are now “almost non-existent” on Auckland Island, Horn said. “They’re absent until you get to the extremely steep cliff areas. Then you can see patches of green that are out of reach” of the pigs.

Horn believes there are between 700 and 1,500 pigs on the island, with the population fluctuating widely. Survival to breeding age, he said, is low. Those that do make it have to be tough and adaptable. “On one hand, super admirable,” he said, “the way they’re able to adapt and survive in those conditions.” And on the other hand, incredibly damaging. “They use the coastline pretty heavily,” he said. “They’ll eat anything that turns up, scavenging things like dead whales and seals or even krill and squid.”

Mindful of the Department of Conservation’s long-held wish to eradicate the pigs, the Rare Breeds Conservation Society sent a team to retrieve some in 1999. Using dogs, they managed to catch 17. “Hunger appeared to be the pigs’ constant companion,” wrote team member Peter Jackson for New Zealand Geographic. “The suckling sows had only two or three teats producing milk, which told how few piglets survived.”

The team loaded the pigs on a boat and brought them back to the southern New Zealand town of Invercargill. There, the animals were put into a quarantine facility, intended to protect the country’s domestic pig herd from potential diseases.

Keeping the pigs in quarantine required money the Society didn’t have, so they prevailed upon Invercargill’s then-mayor, Tim Shadbolt, a colorful former left-wing activist, who dipped into his contingency fund for the approximately 2,300 in today’s New Zealand dollars, or $1,400, needed to feed them.

During the first year of quarantine, the pig population ballooned. “They dined on porridge and swedes and they became raging sexual beasts, producing larger litters than they did on the Auckland Islands,” Shadbolt recalled in a 2008 article in the Otago Daily Times. The pig’s food bill increased tenfold — an expenditure that whipped up a political storm in Invercargill, with councilors and constituents railing against what they characterized as a scandalous waste of public money. Shadbolt was unceremoniously stripped of his contingency fund.

The mayor, though, would be vindicated. These pigs from a previous century soon found an unlikely home in the futuristic world of xenotransplantation.

Globally, the demand for transplant organs is overwhelming. Every year, thousands of people die waiting for a new heart, liver, kidney, or lung that never arrives. In the United States alone, around 17 people on the organ waiting list die every day. For decades, xenotransplantation has been seen as a possibility to bridge this shortfall.

Since the 1960s, surgeons have transplanted chimpanzee and baboon parts into a small number of humans with life-threatening conditions, but these efforts have had little success. The biggest challenge is getting the human body’s immune system to accept the new organ.

The use of non-human primates for biomedical research is controversial, so over time, researchers looked to pigs. “Their organs, their tissues, and their physiology are sufficiently close to humans,” said Paul Tan, founder and CEO of New Zealand xenotransplantation research company NZeno. “Their cells function in a manner that is very close to humans. So their blood sugar levels and our blood sugar levels are pretty close.”

In the late 1980s, New Zealand pediatrician Bob Elliott and colleague David Collinson started a company called Diatranz to investigate whether pig islet cells could be used to treat Type-1 diabetes. For Collinson, the quest was personal. His son suffered from the disease.

Islet cells are found in the pancreas and produce insulin, but in Type-1 diabetes patients, are destroyed by the immune system. Trial transplants of human islet cells had met with mixed results, and in any case, with millions of Type-1 diabetes sufferers globally, there were nowhere near enough human donors to meet demand.

Diatranz aimed to surgically implant pig islet cells, encapsulated in a seaweed-derived polymer that shielded them from the human immune system, into the pancreases of diabetes patients. In the 1990s, though, the work stalled amid fears of disease.

Xenotransplantation, of both cells or organs, carries the risk of bacterial or viral infections crossing from the donor animal into humans. Pigs are not as closely related to humans as apes and baboons, a circumstance that makes transplanted pig parts less likely to spread disease to humans. Still, the risk persists.

While common diseases might be eliminated with medicines, a more serious risk was thought to come from viruses that essentially gatecrash the genetic material of the host animal. These are called retroviruses; they include HIV as well as viruses that cause certain cancers.

Some retroviruses, called endogenous retroviruses, have, in the deep past, even insinuated themselves into the DNA of sperm and egg cells — they are therefore part of the animal’s genetic makeup, replicated in every cell in the body and passed down through generations. There is currently no medication to eliminate retroviruses.

The concern was that pig tissues could secrete infectious particles of a porcine endogenous retrovirus, or PERV, which could then infect human cells to create a new, transmissible human disease. In the worst-case scenario, it was feared, such an event could trigger a global pandemic.

In the late 1990s, a London-based research team confirmed that, in a laboratory setting at least, PERVs could infect human cells.

The discovery, for a time, “killed xenotransplantation,” said Björn Petersen, a xenotransplantation researcher with the Friedrich Loeffler Institute, the German government’s animal-disease research center. “Pharmaceutical companies withdrew their money from the research.”

Around the world, the hunt was on for pigs that were as disease-free as possible.

In 1998, Diatranz partner Olga Garkavenko turned on her radio and got wind of Invercargill’s new arrivals. She decided to investigate.

The company obtained tissue samples from the quarantined pigs for analysis. The islands’ harsh conditions, it seemed, had been tough on disease.

“They remained isolated and therefore they remained free of a lot of common infections that you have in pigs,” said Tan. “The pigs that were weak were probably wiped out. Only the fittest survived.”

The pigs also have an unusually low number of retrovirus copies in their genome. Petersen noted that the population is also completely free of a type of PERV called PERV-C, which may pose the biggest risk to human transplant recipients. This was possible “because they were isolated for a long time and they never had contact with other pigs.”

Joachim Denner, a xenotransplantation researcher from the Free University of Berlin, said the Auckland Island pigs had another major advantage over other pig breeds — their small stature. At around 90 pounds in weight, he said, “they are the right size for transplantation.” A domestic pig weighs 300 to 700 pounds, and its organs, he added, are too large.

In 2004, Elliott, Tan, and others set up a company called Living Cell Technologies, or LCT, which absorbed Diatranz and took over the pigs’ care, building an expensive facility near Invercargill to keep them in medical-grade isolation while they were selectively bred for xenotransplantation.

The animals housed in quarantine were suddenly reputed to be worth hundreds of thousands of dollars each, much to then-Mayor Shadbolt’s barely-concealed glee.

The project brought jobs and millions of dollars of investment to Invercargill. “It has all come to fruition,” Shadbolt said in the 2008 Otago Daily Times article. “I rub it into those people who didn’t support me at every opportunity.”

By the 2010s, concerns around PERVs were lessening, as multiple clinical trials of cell transplants suggested not only that pig cells could be effective in treating diabetes, but also that PERVs weren’t passing to humans. New gene-editing technology also meant that retrovirus genes could be rendered non-functional before an animal was born.

With these advancements, the race to successfully implant pig organs in humans has gathered pace. Groups around the world now breed pigs for this purpose. It’s big business — a recent report estimated the global xenotransplantation market could be worth $24.5 billion by 2029.

In January 2022, a University of Maryland group, using a pig organ from the U.S. company Revivicor, conducted the first successful transplant of a pig heart into a living patient. The patient survived for two months. While the cause of his death is still being examined, evidence of a disease called porcine cytomegalovirus was found during the autopsy. The pig used in the transplant, said Tan, would have been rigorously screened for the virus, which, he added, shows the importance of breeding pigs that are genuinely free from such diseases.

Paul Tan now runs NZeno, which has taken over the breeding and keeping of the Auckland Island pigs. LCT, meanwhile, has switched its focus to Parkinson’s disease and recently began clinical trials of a treatment that involves inserting capsules containing pig brain cells into the human brain to repair nerve damage.

NZeno supplies pig cells to LCT and is also trying to establish itself as a major player in the organ game. “We like to think that our strain of pigs, derived from the Auckland Islands, further developed at Nzeno, would be the ideal pig strain for human organ xenotransplantation,” said Tan. Their cells, he noted, have already been used in humans for years, and have a very good track record of safety. The small number of retrovirus copies in the pigs’ genomes, he said, also require less gene editing compared to other breeds.

NZeno recently provided its pig cells to a team at Ludwig Maximilian University in Munich, which aims to have a genetically-modified pig ready for a pig-human heart transplant by 2025. NZeno is also working with another xenotransplantation group in China that aims to develop kidneys for transplant.

Petersen agreed that there is a solid rationale for minimizing gene editing. “The more genetic modifications you do,” he said, “the more side effects you can maybe expect.” But, he added, there may be cases in which it doesn’t make sense to prioritize the minimization of gene editing. For example, “if you want to have a universal donor” — an animal that can supply a variety of suitable organs or cells for human transplant — “then you need to have a pig with more genetic modifications right from the beginning.”

Denner said the Auckland Island pigs, which he describes as the most disease-free pigs in the world, may yet prove their true worth. But he cautioned against viewing them — or any pig — as a silver bullet. “All these studies have limitations,” he said. “The real effect of PERVs on humans, we will see when we perform the first transplants of organs.”

For now, wild Auckland Island pigs continue to run free in their storm-battered home, but the clock is ticking. Over the last five years, New Zealand’s Department of Conservation has been preparing for eradication.

Stephen Horn leads the team charged with this enormous task. Previous work attached GPS trackers to pigs, trying to learn their movements, and Horn’s team has trialed various methods of killing them. The plan is to wipe out the pigs using a combination of traps, poisoning, and hunters shooting from helicopters and on foot.

“The approach is really high intensity, as quickly as possible,” said Horn, “and try to keep the population as naive as possible.

“You need a suite of tools,” he continued, “because pigs are smart. Not every pig is going to be vulnerable to the same technique.”

Compounding the difficulty is the island’s size and isolation. It is several days’ dangerous sail from the mainland and, aside from a few uninhabitable hut shelters, the islands have no infrastructure to support human life. Once ashore, movement through the dense undergrowth and shoulder-high grasses is extraordinarily difficult.

“It’s rugged, remote, and massive,” said Horn. “It’s pretty overwhelming when you’re looking at it through a lens of animal pest control.”

Not everyone is thrilled at the prospect of the pigs’ demise. The animals are “very much part of our heritage,” said Willis of the Rare Breeds Conservation Society. The organization argues more effort should be made to preserve at least some of them. Perhaps the pigs could be fenced off, so as not to disrupt the entire island, said Willis. Or some could be relocated to another island, where they might not pose as much of a problem. As far as he is aware, however, these options are not being considered.

Paul Tan said he would also jump at the chance to retrieve more pigs.

The Department of Conservation, said Horn, has fielded inquiries about recovering pigs, but the logistics of retrieving them from the Auckland Islands, as well as the enormous costs involved in quarantine, are major hurdles to overcome.

Horn said that while staff are actively discussing options for retrieving pigs, their focus is eradication. With a plan in place, the department just needs to secure enough funding to make it happen, he said, “to undo some of the damage that was done by people, on what is an extremely fragile, but important place.”

Bill Morris is a documentary filmmaker, wildlife cameraman, and science journalist based in Dunedin, New Zealand. He is a regular contributor to New Zealand Geographic magazine and his work has also appeared on the BBC and Animal Planet.

This article was originally published on Undark. Read the original article.

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Ghana is the first country to approve a malaria vaccine for young children, who have the highest risk of death from the disease. Some scientists have called the new vaccine a potential “game-changer” in the fight against the disease that is the leading cause of child death in Africa.

This new vaccine, called R21, has an efficacy rate of 77 percent, according to a September review in the journal The Lancet. One approved Malaria vaccine already exists, called Mosquirix, which has a 30 to 60 percent efficacy rate. 

Late stage testing is still underway in Burkina Faso, Kenya, Mali, and Tanzania. It’s unusual for a country to approve a vaccine before clinical trials are completed, according to WHO guidelines, and the World Health Organization has yet to approve it. 

Oxford researchers shared the mid-stage data with regulatory authorities in Ghana over the past six months and their new data suggests similar performance as in earlier trials, according to Oxford Professor and Chief investigator of the R21/Matrix-M programme, Adrian Hill. The results of R21’s final trials are expected to be published in the coming months. 

[Related: New four-dose malaria vaccine is up to 80 percent effective]

Oxford researchers shared the mid-stage data with regulatory authorities in Ghana over the past six months and their new data suggests similar performance as in earlier trials, according to Oxford Professor and Chief investigator of the R21/Matrix-M programme, Adrian Hill. The results of R21’s final trials are expected to be published in the coming months.

The R21 vaccine is designed to stop disease and death, not prevent transmission, although vaccines that prevent transmission between people are currently in the works at Oxford, Hill said in a press interview.

“The main idea now is to get R21 out there as soon as possible, and then add a transmission blocking vaccine,” Hill said. “That will allow us to use vaccination, not just for disease control, but for initial disease elimination, and then eventually global eradication.”

Ghana’s Food and Drug authority approved its use for children aged five months to three years, but rollout will be delayed until the WHO approves it. Once it is approved, Ghana’s drug regulator has a deal with the Serum Institute of India to produce up to 200 million doses of R21 a year. Each dose is expected to cost a couple dollars, per the BBC.

The mosquito-borne disease kills about 620,000 people globally each year, and 77 percent of those deaths are children. That translates to a death toll of over one thousand children each day, nearly one child lost per minute, according to UNICEF.

Malaria is a parasitic disease transmitted by mosquitoes, most often seen in tropical and subtropical climates. It is preventable and curable. Symptoms range from mild to life-threatening, including tissue inflammation in the brain, kidneys, and lungs. In extreme cases, leading to cerebral malaria, kidney failure, and acute respiratory distress syndrome. Children, pregnant women, and immunocompromised individuals are most at risk.

The parasite responsible for Malaria is the unicellular plasmodium. There are multiple plasmodium species known to cause the disease, each with its own unique characteristics. Unfortunately, the most common species in sub-saharan Africa, Plasmodium falciparum, is also the most deadly. 

Vaccinations are a relatively recent method of treatment for malaria. Since Mosquirix was introduced in 2019, 1.4 million children across Ghana, Kenya, and Malawi were vaccinated, resulting in a 10 percent drop in child mortality. A lack of funding and commercial potential has prevented drugmakers from producing adequate amounts of Mosquirix.

The release of the R21 vaccine “marks a culmination of 30 years of malaria vaccine research at Oxford with the design and provision of a high efficacy vaccine that can be supplied at adequate scale to the countries who need it most,” Hill said in a statement.

There are multiple reasons why a Malaria vaccine is hard to develop—including the complex life cycles of the parasite and its ability to evade immune responses. 

However, the biggest barrier is not biological, it’s financial. Malaria is most prevalent in sub-saharan Africa, making up 95 percent of all malaria cases and 96 percent of malaria deaths. This region is also home to low-income countries, which have limited resources for research funding and vaccine development. 

[Related: White House invests $5 billion in new COVID vaccines and treatments as national emergency ends]

“Malaria is a life-threatening disease that disproportionately affects the most vulnerable populations in our society and remains a leading cause of death in childhood,” Adar Poonawalla, CEO of the Serum Institute of India, said in a press release statement. 

“We remain steadfast in our commitment to scaling up production of the vaccine to meet the needs of countries with high malaria burden and to support global efforts towards saving lives,” he said.

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Sitting for too long is harmful to your health—even if you don’t feel it at the moment, your body will remember. Staying motionless for at least four hours has been linked to an increased risk of blood clotting in humans. 

But there are some exceptions. People with permanent paralysis don’t show an elevated risk for blood clotting while those who are temporarily immobile—like being stuck in a hospital bed or in a cramped airplane seat—are more susceptible to clot formation. 

A new study published today in the journal Science probes this blood-circulation question in brown bears, a species known to withdraw in their dens for five to eight months out of the year and emerge clot-free. Hibernating bears avoided blood clots by reducing a protein in their body that triggers the blood clotting process. Humans also have this protein, it turns out, and can regulate it under certain circumstances.

[Related: Scientists stuck grizzly bears on treadmills and confirmed they hate hills as much as we do]

“I would have never thought to go to bears, but it’s an excellent idea to turn to nature for studying human biology,” says Mirta Schattner, the director of the Instituto de Medicina Experimental del CONICET in Argentina who wrote an accompanying perspective piece on the study, but wasn’t involved in the research. 

An international team led by scientists from Ludwig-Maximilians-University of Munich ran tests on brown bears and people who have long-term mobility issues to compare anti-clotting strategies. They collected blood samples from 13 free-ranging brown bears during hibernation and again when they were awake during spring. When analyzing the contents of the blood samples, the authors noticed hibernating bears showed more signs of an anti-clotting mechanism. It worked by lowering several protein levels, including heat shock protein 47 (HSP47), which regulates immune responses. Reducing HSP47 tamps down inflammation that would have otherwise started the process of blood clotting.

To see if chronically immobilized humans have a similarly helpful reaction, the authors extracted blood from 23 people with spinal cord injuries and compared it to the blood of 23 able-bodied adults. Just like with the hibernating bears, people with spinal cord injuries showed a decrease in HSP47 levels and fewer clumped platelets that form clots. 

The similar process in bears and humans suggests prolonged immobility is the trigger that switches on the anti-clotting strategy. In situations where you might be bedridden for only a couple of days, Schattner says the inflammatory proteins are more powerful than this protective mechanism. “It would be interesting to know if it’s worth blocking the clotting mechanism in patients with acute immobilization,” she theorizes. “It’s a new pharmacological target to access.”

[Related: Heart disease-related deaths rise in extreme heat and extreme cold]

Anti-clotting mechanisms are one of many adaptations biologists can study from bear hibernation. The ursine body has developed different tactics to remain dormant throughout the winter without waking up to a horde of health problems. For example, bears use their fat to break down energy without reducing their muscle mass. They also limited the renewal of damaged bone cells to prevent osteoporosis in their sleep. Another feature includes changing biological processes like heart rate when entering hibernation. Studying how bears lower their heart rate for months at a time could help doctors better understand the mechanisms that drive cardiac diseases in humans.

But the opportunity to look at these body-regulating strategies might be short-lived. Warmer temperatures and shorter winters from climate change are affecting bear hibernation patterns, says Heather Johnson, a wildlife biologist for the United States Geological Survey Alaska Science Center who was not involved in the study. “We’re seeing that bears are hibernating for a shorter period and having longer active periods.” The warmer winters signal to bears that there is less of a need to sleep when the conditions are fine to go foraging for food. 

There have also been a few anecdotal observations of bears not needing to hibernate at all, for example, because they have access to human food all winter. Johnson says that while it’s too soon to predict how climate change will affect bear survival, we are already seeing indirect effects by having more bears awake during open hunting season and getting into more conflicts with humans. As bears adjust to the changing climate, there’s no telling how their bodies will adapt. The anti-blood-clotting mechanisms they have today may be gone tomorrow—a disadvantage for the animals and a loss for potential thrombosis treatments.

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The national COVID-19 emergency is drawing to a close, which means certain treatments and tests that have previously been available without cost is soon to change. However, working on effective vaccines and therapies for COVID-19 is far from over. The federal government recently announced plans to spend over $5 billion in order to speed up new vaccines and treatments, according to a Department of Health and Human Services (HHS) spokesperson and a Biden administration official.

The plan, called Project NextGen, was first announced in the Washington Post on April 10 and aims to provide better protection from future coronaviruses that could become public health threats. It is the follow-up to the Trump Administration’s Operation Warp Speed, which sped up the production of COVID-19 vaccines in 2020. Project NextGen would take a similar approach by partnering public and private-sector organizations to accelerate development of different vaccines and therapies in an ever changing virus. 

[Related: Biden will end COVID-19 national emergencies in May. Here’s what that means.]

“It’s been very clear to us that the market on this is moving very slowly,” White House coronavirus coordinator Ashish Jha, the White House coronavirus coordinator, told the Post on April 10. “There’s a lot that the government can do, the administration can do, to speed up those tools … for the American people.”

According to Jha, Operation Next Gen will have three main goals: creating long-lasting monoclonal antibodies, speeding up the development of mucosal vaccines to possibly reduce transmission and infection risks, and speeding efforts to develop a universal coronavirus vaccine that protects against COVID-19 and other coronaviruses. 

Medical treatments for COVID-19 have lost effectiveness as the virus has continued to evolve. Even once-hailed “miracle” monoclonal antibodies are no longer effective in the face of the Omicron variant. 

“Our ability to develop … vaccines that generate mucosal immunity will have very large benefits for other respiratory pathogens we deal with all the time, like flu and RSV,” Jha said.

Mucosal vaccinations given in the nose can provide patients “sterilizing immunity” against the virus. Some of these types of vaccines are already in development around the world, with China and India rolling out the nasal vaccines, but it is not clear how well they are working. The ChAdOx1 vaccine failed to induce nasal immunity in a phase 1 trial late last year, but a nasal vaccine in Germany has shown some promise after experiments with hamsters. 

[Related: China approves world’s first nasal COVID-19 vaccine booster.]

Michael Osterholm, an epidemiologist who worked with the administration to develop the new program, told USA Today that the rapidly developed current vaccines are “really good, but they’re not great. There is a substantial amount of work [to be done] to take these good vaccines and hopefully achieve better vaccines,” he added.

Jha did not announce a timeline for when the new products will be available to the general public, but did note that it would be based on factors including drug manufacturer production plans and Food and Drug Administration (FDA) reviews. 

Previous vaccine funding requests have been repeatedly denied by Congress, with Republicans insisting that the Biden Administration use funds left over from previous pandemic aid packages. The White House directed HHS to free up $5 billion for Operation Next Gen and the agency responded by shifting funds from testing and other priorities. 

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A new report from the Centers for Disease Control and Prevention (CDC) reports that cases of infections from A Streptococcus (commonly called strep-a or strep throat) have surged this past winter. During the time period while most COVID-19 mitigations were still in place, cases dropped by about 25 percent, but now cases are above pre-pandemic levels. 

Across the US, the CDC report found that the most severe cases of invasive group A strep infections have been seen in children. Caitlin Rivers, an epidemiologist at the Johns Hopkins Center for Health Security, told NPR that in an invasive strep infection, the bacteria has spread to other parts of the body instead of just staying in the throat. It can spread to the bloodstream, cause rashes on the skin, and even infect the body’s organs. 

[Related: Strep throat is figuring out how to beat our go-to antibiotics.]

The recent spike in strep throat cases coincides with a shortage of amoxicillin, an antibiotic commonly used to treat strep throat, especially in children. Rivers also recounted the difficulty her own family and patients have had finding the antibiotics needed to treat strep cases. “We had to visit several pharmacies to find the medication that we needed,” she tells NPR. “It just adds another burden on what’s already been a really difficult winter respiratory season for families.”

Health officials in Illinois warned parents in March to be vigilant, as five pediatric deaths were reported in the state. Illinois Department of Public Health Director Sameer Vohra warned that cases of strep throat infections that lead to severe complications were on the rise in the state “with more cases reported in 2023 than in any of the past five years.”

In October 2022, the Food and Drug Administration (FDA) added amoxicillin products to its list of drug shortages.  Some amoxicillin medications are still not widely available. The shortage is linked to the lack of liquid versions of products  that are easier for children to consume The shortage is affecting multiple generic brands, including Teva and Sandoz.

The current shortage appears to be a demand issue and not a quality issue. “Companies typically look to see what their sales were the prior year. They might make a little bit of an adjustment,” Erin Fox, a national expert on drug shortages at the University of Utah, told NPR. “But with the really severe respiratory season we’ve had this year, it just simply was a mismatch between what people manufactured and what was available.”

[Related: Tik Tokers are taking a diabetes drug to lose weight. Now it’s in short supply.]

Fox also added that while a popular strength of amoxicillin – 400 mg/5mL – isn’t always available, pharmacists have other options, like giving a lower dose at a greater volume. Shortages of many commonly used prescription medications, including adderall and some diabetes drugs, have been common throughout the United States over the past year. Increases in demand and supply chain issues being partially to blame. 

Strep throat cases are typically most common from December through April, however the pandemic has thrown seasonal infection cycles off their usual track. RSV surged especially early and severely in late summer and fall 2022 along with norovirus.

Some of the most common strep throat symptoms include pain, fever, swollen tonsils, and tiny spots at the roof of the mouth called petechiae. Infected patients should see a healthcare provider if the symptoms become serious, get worse, or if they do not go away after two weeks of initial treatment.

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