By Jeneen Interlandi In the mid-2010s, when they were still postdoctoral fellows at the Massachusetts Institute of Technology, Mathilde Poyet and Mathieu Groussin kept bumping into different sides of the same obstacle. Poyet, an ecologist and a microbiologist, was trying to study rare bacterial species, the kind that had never been grown in a lab before. Groussin, a computational biologist in the same lab, wanted to understand how humans and microbes evolved together over millenniums. Each was focused on microbes that make their homes in and on the human body, what scientists collectively refer to as the human microbiome. But the only samples they could find to work with came from the same small sliver of humanity, namely populations that were wealthy, Western and white. “About 90 percent of all human diversity has been completely left out of the picture,” Groussin told me recently. It was as if someone had shone a bright flashlight on one small segment of a giant canvas and left the rest shrouded in darkness. The bright spot was well defined (imagine the face of a man). But they couldn’t really tell what they were looking at (whether that man was a monk, for example, or a matador) without seeing the rest of the canvas. Scientists refer to this vast, unexplored terrain as biology’s dark matter. Our bodies are home to more bacteria — on our skin, up our noses, in our guts and mouths and around our genitals — than there are stars in the Milky Way. These microbes have evolved not only with us but inside us, and scientists who study them closely say that hardly a biological process or system exists in which they do not play a role. They helped create our digestive systems and our immune systems. They influence the size and shape of our bodies. At least some research suggests that they also affect our brains, moods, personalities and behaviors. And yet, most of them have still not been identified, let alone studied. It was tantalizing to think about what a fuller picture might reveal. In recent years, scientists had linked the gut microbiome to a long list of conditions, including Crohn’s and irritable bowel syndrome, Parkinson’s, dementia and autism, and they were hopeful that a better understanding of those links would lead to treatments, if not cures. They were also sifting through the nearly unfathomable array of molecules that microbes produce, in search of biological treasures: not only potential medications but also compounds capable of breaking down pollutants or repairing damaged ecosystems. © 2026 The New York Times Company

Keyword: Obesity
Link ID: 30312 - Posted: 07.08.2026

By Giorgia Guglielmi Neuroscience textbooks have long cast mitochondria as pure neuronal powerhouses: These bean-shaped organelles just crank out a cell’s energy. That picture, however, is starting to look incomplete. Mitochondria do far more than fuel neurons, a growing body of research suggests. They also appear to help synapses communicate, regulate neurotransmitter release and shape social behavior. Mitochondrial function has also been tied to autism and related neurodevelopmental conditions, though that link remains debated. Even memory formation may lean on these tiny, double-membraned structures, according to a study published in Nature Metabolism in February. Increasing mitochondrial metabolism boosted long-term memory in both fruit flies and mice. Mitochondria are “not just permissive but also instructive,” says Ezgi Hacisuleyman, assistant professor of molecular medicine at the Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, who was not involved in the February study. Her unpublished results show that mitochondrial proteins are translated near active synapses, for example. Over the past decade, work from Hacisuleyman and others has fast expanded the repertoire of mitochondria in the brain. Taken together, she adds, the findings put mitochondria “more in the center of how we think about brain function and memory.” Mitochondria may be central to brain function, but they are not central inside neurons. Many synapses sit hundreds of micrometers away from a cell’s soma, so small, mobile mitochondria must travel there to deliver fuel in the form of ATP. In dendrites, mitochondria often linger near spines, and activity recruits them to presynaptic boutons, where they help stabilize neurotransmitter release. © 2026 Simons Foundation

Keyword: Development of the Brain; Obesity
Link ID: 30310 - Posted: 07.04.2026

By Sarah Thau Hunger pangs build with activity in Agouti-related protein (AgRP) neurons, and when we eat, these cells fall silent, signaling to the body that it’s full. Until recently, researchers thought these neurons responded to calorie intake alone, but a new study shows fructose quiets them less effectively than glucose does, even though both simple monomeric sugars carry the same number of calories. “We were really surprised when we tested these different sugars and found that fructose looks much different than glucose,” says study investigator Amber Alhadeff, a member of the Monell Chemical Senses Center and adjunct assistant professor of neuroscience at the University of Pennsylvania. Fiber photometry recordings of individual AgRP neurons in mice consuming fructose or glucose solutions first tipped the lab off to the fact that fructose is the weaker inhibitor. The same difference surfaced when the team infused the solutions directly into the animals’ guts, controlling for the fact that the mice tended to take more licks of the glucose than fructose. Glucose does not require the vagus nerve to inhibit AgRP neurons, according to previous work from Alhadeff’s group, but fructose does, the new study demonstrates. This study is the first to show “that the brain is responding to these things in different ways, and with a real mechanistic underpinning,” says Martin Myers, professor of diabetes research at the University of Michigan Medical School, who was not involved in the research. “This is an absolutely fabulous lab that is doing things that few, if any, other people in the world can do.” Once the team discovered that fructose acts through the vagus nerve, Alhadeff’s graduate student Aaron McKnight hit the mechanistic ground running. He worked for five years, according to Alhadeff, to show that fructose activates the vagus nerve, releasing a hormone called PYY that signals Y2 receptor-expressing vagal afferent neurons and then inhibits AgRP neurons. Glucose does not lead to increased PYY levels, acting through gut-spinal afferent signaling—a separate peripheral pathway. © 2026 Simons Foundation

Keyword: Obesity
Link ID: 30306 - Posted: 07.01.2026

By Bethany Brookshire Once people understood glucagonlike peptide 1 (GLP-1) drugs’ potential for weight loss, the race among pharmaceutical companies was on. Among the current options, Wegovy can help people lose an average of 10 percent of their body weight in a year, while people taking Zepbound have had about a 15 percent loss, on average, in the same period. Soon the most powerful GLP-1 treatment to date could hit the market: retatrutide. Already popular on the online peptide gray market, the new drug, originally developed by Eli Lilly, caused participants in a recent clinical study to lose more than a quarter of their body weight over 80 weeks at the highest dose—results comparable to bariatric surgery. U.S. Food and Drug Administration approval could soon follow. But bodies don’t just drop weight with no potential adverse effects. Weight loss on its own can change muscle, bone and more. As new-generation GLP-1 drugs promote higher rates of loss, clinicians want to ensure that the desire to shed pounds and see improvements such as better cardiovascular health are balanced with the very real risks that may come with the treatment. Fat, Muscle or Bone? People typically lose weight when they eat fewer calories than their body expends. A common way to cut calories is to diet, while bariatric surgery removes or changes part of the gastrointestinal tract to reduce food—and therefore calorie—absorption. GLP-1 is a gut hormone released in response to a meal that helps people feel full. It also increases insulin release and reduces glucose in the blood. Semaglutide (sold as Ozempic and Wegovy by Novo Nordisk) binds to the hormone’s receptor for longer periods of time, making people feel fuller for longer and eat less. Newer versions of GLP-1 drugs, such as tirzepatide (sold as Zepbound and Mounjaro by Eli Lilly) and Novo Nordisk’s upcoming drug CagriSema target more than one type of gut hormone receptor, while retatrutide hits three. © 2026 SCIENTIFIC AMERICAN

Keyword: Obesity
Link ID: 30261 - Posted: 05.30.2026

By Marta Zaraska 05.19.2026 On a blazing hot day in South Africa, female southern pied babblers can’t think straight. The medium-sized black-and-white birds are trying to get at tasty mealworms behind a see-through barrier. On cooler days, the birds can quickly figure out that all they have to do is go around the small wall of plastic. But when the mercury goes up, the birds just keep stubbornly pecking at the barrier. That experiment is part of a growing body of research showing that animals get their minds muddled during heat waves. When it’s hot outside, birds struggle to learn, dogs bite more often, goat-like chamois pick fights. This is bad news not just for those who get on Fido’s toasted nerves. If the animals can’t stay alert enough to find food or avoid predators, their chances of survival go downhill, says Amanda Ridley, a behavioral ecologist at the University of Western Australia who coauthored the pied babbler study. With climate change making heat waves more common, such cognitive impairments across the animal kingdom could ripple through entire ecosystems, putting already fragile species at greater risk. If pollinators forget which flowers to visit, crops and wild plants may fail. If birds can’t find food as easily, their young may not survive. And on a warming planet, a sharp mind is particularly vital. “A changing climate means that your ability to behaviorally adapt is even more important,” Ridley says.

Keyword: Intelligence; Learning & Memory
Link ID: 30250 - Posted: 05.20.2026

By Christina Caron Dr. Kyle Staller is a gastroenterologist, so it may be surprising that many of his patients come to him complaining not only about stomach trouble but about their brains, too. Irritable bowel syndrome and other digestive dysfunction can be accompanied by a mental haze. People experiencing constipation and bloating, for example, may describe “a sense of heaviness or being weighed down both physically and mentally,” said Dr. Staller, who works at Massachusetts General Hospital in Boston. “So many of my patients talk about problems like fatigue, brain fog and feeling sluggish,” he added. Scientists are making progress in understanding how the pathway between the brain and the digestive system influences our overall health. They call it the gut-brain axis, and it has been shown to play a big role in immune system support, anxiety, depression, metabolism and disease prevention. It can also affect mental clarity. We asked scientists and clinicians what to know about the gut and brain fog. How does the gut-brain axis work? There are thousands of fibers running from the brain to the abdomen that are known as the vagus nerve. It is a primary conduit of the gut-brain axis. And as the main nerve of the parasympathetic nervous system, it helps the body rest, digest and deter inflammation. Signals also travel back and forth between the gut and brain via stress hormones and immune cells. Crucially, gut bacteria produce chemical messengers (called neurotransmitters) like serotonin, dopamine and GABA that affect the nervous system. When they enter the bloodstream or stimulate the vagus nerve, they can help improve mood, drive motivation, and calm the nervous system. © 2026 The New York Times Company

Keyword: Attention
Link ID: 30243 - Posted: 05.16.2026

By Kate Golembiewski By watching their peers, dolphins learn to capture fish in empty conch shells, then ferry the shells up to the water’s surface in order to eat. Octopuses can master experimental tasks by watching their tankmates in the laboratory. Crows follow the cues of others in their flock to attack specific humans who have harassed fellow crows in the past. Scientists call it “social learning,” and it essentially means monkey see, monkey do, an adage that turns out to apply to many animals beyond just primates. Now, a study of Australia’s sulfur-crested cockatoos shows that the birds employ social learning to understand whether unfamiliar foods are safe to eat. In more forested areas of the cockatoos’ native range in Australia, New Guinea, and Indonesia, these mohawked parrots eat plant roots, seeds, fruits and insect larvae. But the birds have learned to thrive in urban environments. “They’re everywhere in Sydney,” said Julia Penndorf, a behavioral ecologist and lead author of the study in PLOS Biology, who encountered the birds as a postdoctoral researcher at the Australian National University in Canberra. In urban areas, the birds have expanded their diets to include nonnative plants and nuts, including almonds and sunflower seeds people offer to them, and they can be seen prying the lids off garbage bins in order to forage. “The big issue with urban birds is, they kind of eat everything,” Dr. Penndorf, who now works at the University of Exeter, said. This expanded diet is high-risk, high-reward: the birds have more options for food, but there’s always a chance that strange new snacks might be poisonous. © 2026 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 30229 - Posted: 05.02.2026

By Gina Kolata Before the new obesity drugs came on the market, almost no one used the term food noise. Researchers studying and developing drugs like Ozempic, Wegovy, Mounjaro and Zepbound analyzed doses, side effects, weight loss and improvements in conditions such as diabetes, heart disease and sleep apnea. Incessant thoughts about food and internal dialogues about what to eat, what not to eat, when to eat, how to resist eating — these were not on the research agenda. But if the obesity-drug researchers weren’t talking about food noise, people taking GLP-1s had a lot to say about it. For as long as they could remember, users of the drugs said, they had been plagued by food noise. But they thought it was just a normal part of life. They thought everyone had it. Until they took one of the new drugs. Suddenly, food noise was silenced. And that effect is leading to new questions about the drugs. If researchers can clarify the source of this inner buzz and what makes it go away, that could lead to a clearer understanding of what causes obesity in the first place. ‘You Don’t Want the Salad’ People who struggle with their weight describe relentless thoughts of food. Lena Smith Parker, 53, of Hamden, Conn., spent decades dieting and regaining weight. All the while, she said, she was plagued by internal voices urging her to eat and shaming her for eating. © 2026 The New York Times Company

Keyword: Obesity
Link ID: 30221 - Posted: 04.29.2026

Ian Sample Science editor Changes to microbes that live in the gut can identify people at greater risk of Parkinson’s disease long before symptoms develop, according to work that also raises hopes for new therapies. Researchers discovered signature changes in the gut microbiome that are more pronounced in people with a genetic risk for Parkinson’s and even more stark in those diagnosed with the disease. The signature could help doctors spot patients at risk of Parkinson’s years before they display clear symptoms and suggests that healthier diets and treatments that reshape the microbiome might prevent or delay the disease. Prof Anthony Schapira, the head of clinical and movement neurosciences at University College London and lead investigator on the study, said it was the first time a microbial signature in Parkinson’s patients had been seen in people with a genetic susceptibility but had yet to develop symptoms. The signature appears to become stronger as the disease progresses. “These same changes can be found in a small proportion of the general population that may put them at increased risk,” Schapira said. Cases of Parkinson’s have doubled in the past 25 years, with more than 8.5 million people globally now living with the condition. The disease causes progressive brain damage, leading to tremors, slow movement and stiff and inflexible muscles. Patients often experience depression, anxiety, sleep and memory problems, and difficulty with balance. © 2026 Guardian News & Media Limited

Keyword: Parkinsons
Link ID: 30209 - Posted: 04.22.2026

By Jamie Ducharme More than 10 percent of U.S. adults take GLP-1 drugs. But not all of them are taking full doses. Around one in seven users has “microdosed” injections, a recent survey by the health tracking app Evidation found. Some take tiny portions for practical reasons, such as cutting costs. Others have loftier ambitions: They hope to harness the drugs’ powerful effects to achieve better health and longer lives without losing a lot of weight or experiencing side effects such as GI issues and muscle loss. Medications such as Ozempic and Wegovy mimic the body’s GLP-1 hormone, which helps regulate appetite, metabolism and blood sugar. That has made the drugs blockbuster treatments for type 2 diabetes and obesity. But to date, “there is no rigorous scientific data to support microdosing,” says bariatric medicine specialist Katy Williams of the University of Missouri Health Care in Jefferson City. That hasn’t stopped some intrepid biohackers from trying it, though. Companies like AgelessRx, a longevity-focused telehealth clinic, explicitly sell GLP-1 microdoses for this purpose, advertising them as “a powerful new path to promoting long-term wellness.” There is some research to suggest GLP-1s can promote healthy aging by improving overall health. The drugs have been found to reduce inflammation and oxidative stress, lower risks of major cardiovascular problems, lower cancer risk and more. Such findings have prompted scientists to study the drugs as potential treatments for illnesses as diverse as Alzheimer’s disease and arthritis. Some experts have even wondered whether the drugs’ systemic effects might slow cellular aging and prevent age-related chronic conditions, potentially making them the first true longevity drugs to hit the market. © Society for Science & the Public 2000–2026.

Keyword: Obesity
Link ID: 30167 - Posted: 03.21.2026

Mariana Lenharo The weight-loss drugs that took the world by storm a few years ago have a drawback for anyone afraid of needles: they must be injected weekly. But scientists have been racing to perfect anti-obesity pills — which are now coming to market. An oral anti-obesity drug called orforglipron is likely to be approved by US regulators by the end of April, pharmaceutical analysts say. In December, a pill version of the obesity drug semaglutide won US regulatory approval. Both drugs belong to the class of therapies called glucagon-like peptide-1 (GLP-1) receptor agonists. Semaglutide, sold as Wegovy, is made by Novo Nordisk in Bagsværd, Denmark; orforglipron is made by Eli Lilly and Company in Indianapolis, Indiana. Clinical-trial results have been positive. After around one year of treatment at the highest dosage, people taking orforglipron lost, on average, about 11% of their body weight1, and those taking semaglutide pills lost almost 14%2. But it’s uncertain whether pills could one day replace the GLP-1 pens that have become a weight-loss staple. Oral drugs face formidable developmental challenges, and several injected drugs cause greater weight loss than does either orforglipron or oral semaglutide: the approved injectable drug Zepbound, for example, leads to weight loss of up to 21% of body weight3. “It’s encouraging, and it’s fantastic to have double-digit weight loss with a pill,” says Daniel Drucker, an endocrinologist at the University of Toronto in Canada. “But so far, rather than replace, I would say they’re going to complement the options that we have.” There’s a good reason why the original GLP-1 receptor agonists, which mimic the natural hormone glucagon-like peptide-1, were sold in injectable form. The drugs are composed of peptides, which are relatively large molecules. Because of their size, digestive enzymes quickly break them down, and the intestinal lining limits their entry into the bloodstream. © 2026 Springer Nature Limited

Keyword: Obesity
Link ID: 30163 - Posted: 03.19.2026

By Catherine Offord Scientists have plenty of ideas about why aging impairs memory. Reductions in blood flow in the brain, shrinking brain volume, and malfunctioning neural repair systems have all been blamed. Now, new research in mice points to another possible culprit: microbes in the gut. In a study published today in Nature, scientists show how a bacterium that is particularly common in older animals can drive memory loss. This microbe makes compounds that impair signaling along neurons connecting the gut with the brain, dampening activity in brain regions associated with learning and memory, the team found. “This is a tour de force,” says Haijiang Cai, a neuroscientist at the University of Arizona who studies gut-brain communication and was not involved in the work. “They define the pathway all the way from aging and bacteria … to cognitive function—it’s really impressive.” However, he and others emphasize it remains to be seen whether a similar mechanism exists in humans—and if so, how important it is compared with other drivers of cognitive decline. Research on the so-called gut-brain axis has exploded in recent decades. Multiple studies have identified differences in microbiome composition between healthy people and those with cognitive disorders such as Alzheimer’s disease. This kind of research can’t establish cause and effect, though, and the literature is rife with conflicting results. Some groups have used animal experiments to probe the microbe-memory link. In the new study, Stanford University researchers Christoph Thaiss and Maayan Levy tinkered with the microbiomes of young mice—either by housing them with older animals or feeding them these animals’ poop—and then gave them memory tests. For example, one such test rates animals higher if they spend more time exploring new objects than those they’ve seen before. © 2026 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 30162 - Posted: 03.14.2026

By Catherine Offord Scientists have plenty of ideas about why aging impairs memory. Reductions in blood flow in the brain, shrinking brain volume, and malfunctioning neural repair systems have all been blamed. Now, new research in mice points to another possible culprit: microbes in the gut. In a study published today in Nature, scientists show how a bacterium that is particularly common in older animals can drive memory loss. This microbe makes compounds that impair signaling along neurons connecting the gut with the brain, dampening activity in brain regions associated with learning and memory, the team found. “This is a tour de force,” says Haijiang Cai, a neuroscientist at the University of Arizona who studies gut-brain communication and was not involved in the work. “They define the pathway all the way from aging and bacteria … to cognitive function—it’s really impressive.” However, he and others emphasize it remains to be seen whether a similar mechanism exists in humans—and if so, how important it is compared with other drivers of cognitive decline. Research on the so-called gut-brain axis has exploded in recent decades. Multiple studies have identified differences in microbiome composition between healthy people and those with cognitive disorders such as Alzheimer’s disease. This kind of research can’t establish cause and effect, though, and the literature is rife with conflicting results. Some groups have used animal experiments to probe the microbe-memory link. In the new study, Stanford University researchers Christoph Thaiss and Maayan Levy tinkered with the microbiomes of young mice—either by housing them with older animals or feeding them these animals’ poop—and then gave them memory tests. For example, one such test rates animals higher if they spend more time exploring new objects than those they’ve seen before. © 2026 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 30161 - Posted: 03.14.2026

Denis Campbell Weight loss drugs could help people avoid getting addicted to alcohol, tobacco and drugs such as cannabis and cocaine, a study has found. They could also reduce the risk of people already addicted to illicit substances having an overdose, ending up in hospital or dying, according to research published in the British Medical Journal. Glucagon-like peptide-1 receptor agonists used to treat type 2 diabetes and obesity, such as Mounjaro and Ozempic, are thought to work by influencing the brain’s reward pathways in order to cut cravings. They help people feel fuller by mimicking the natural substance released after eating. The US study analysed 606,434 US veterans with type 2 diabetes, who were monitored for up to three years. It found that GLP-1s reduced the risk of alcohol-related disorders in those with no history of substance use by 18% and of using cannabis (14%), cocaine (20%), nicotine (20%) and opioids (25%), compared with those on other sodium-glucose cotransporter-2 drugs also used to treat diabetes. Weight loss drugs also reduce the risk of people already using substances from overdosing (39%), needing emergency help in A&E (31%) or dying (50%). “This study adds to emerging research exploring whether GLP-1 medicines may influence brain pathways involved in reward and addiction”, said Prof Claire Anderson, the president of the Royal Pharmaceutical Society, which represents 35,500 UK pharmacists. She added: “As this was an observational study, it is important to be clear that it does not show these medicines prevent or treat addiction. Further research, including clinical trials, will be needed to understand whether GLP-1 medicines have a direct effect.” © 2026 Guardian News & Media Limited

Keyword: Drug Abuse; Obesity
Link ID: 30150 - Posted: 03.07.2026

By Hannah Thomasy In 1774, British physician-scientist Charles Blagden received an unusual invitation from a fellow physician: to spend time in a small room that was hotter, he wrote, “than it was formerly thought any living creature could bear.” Many people may have been appalled by this offer, but Blagden was delighted by the opportunity for self-experimentation. He marveled as his own temperature remained at 98 degrees Fahrenheit (approximately 37 degrees Celsius), even as the temperature of the room approached 200°F (about 93°C). Today, this ability to maintain a stable body temperature — called homeothermy — is known to exist among myriad species of mammals and birds. But there are also some notable exceptions. The body temperature of the fat-tailed dwarf lemur, for example, can fluctuate by nearly 45°F (25°C) over a single day. In fact, a growing body of research suggests that many more animals than scientists once appreciated employ this flexible approach — heterothermy — varying their body temperature for minutes, hours or weeks at a time. This may help the animals to persist through all sorts of dangers. “Because we’re homeotherms, we assume all mammals work the way we do,” says Danielle Levesque, a mammalian ecophysiologist at the University of Maine. But in recent years, as improvements in technology allowed researchers to more easily track small animals and their metabolisms in the wild, “we’re starting to find a lot more weirdness,” she says. The most extreme — and well-known — form of heterothermy is classic hibernation, which has been most extensively studied in critters who use it to save energy and so survive the long, cold winters of the Northern Hemisphere. These animals enter long periods of what scientists call deep torpor, when metabolism slows to a crawl and body temperature can drop to just above freezing.

Keyword: Evolution
Link ID: 30137 - Posted: 02.25.2026

By Emma Gometz Caribou, large deer that are native to the northernmost parts of the world (and sometimes called reindeer), are the only deer whose females grow antlers. In a study published today, researchers observed behavior that might explain why: female caribou appear to gnaw on shed antlers as a kind of postbirthing supplement. Caribou migrate huge distances every year between the places where they graze during the winter and the grounds where they calve in the spring. They can walk thousands of miles per year and likely have the longest terrestrial migration of any animal. Caribou mothers complete these extremely long migrations with antlers on their head and a calf in their womb. The period is very nutritionally demanding for them but culminates with a reserve stock of supplements when they need it the most. The researchers behind the new study figured this out when they observed bite marks in more than 80 percent of the 1,500 caribou antlers that littered the part of the Arctic National Wildlife Refuge in northeastern Alaska where the deer give birth. “[Caribou] are just really going after the antlers. They are highly selective,” says study co-author Joshua Miller, a paleoecologist at the University of Cincinnati. Female caribou shed their antlers just days before giving birth. Miller and co-author Madison Gaetano, a conservation paleobiologist, say that the findings suggest that female caribou are essentially banking nutrients in the form of antlers before they give birth and then gnawing on their freshly shed antlers to get a boost of protein, calcium and phosphorus they need to make up for having less time to graze as they nurse their calves. © 2025 SCIENTIFIC AMERICAN,

Keyword: Sexual Behavior
Link ID: 30136 - Posted: 02.25.2026

By Delthia Ricks Susan E. Leeman, who helped reshape scientific understanding of how the brain sends chemical signals throughout the body, did not hesitate to leave the laboratory when her research demanded it — even if it meant visiting slaughterhouses. In the late 1960s, while running a small lab at Brandeis University, she was trying to isolate a stress hormone and needed large quantities of the bovine hypothalamus, a cow’s version of the structure found deep in all mammalian brains. When supplies ran short at a local meatpacker in Boston, Dr. Leeman traveled to Chicago, home at the time to the sprawling Union Stock Yards, to secure fresh tissue. What ultimately emerged was not the hormone that she sought but an elusive chemical called Substance P. Discovered decades earlier but never fully understood, it was finally identified by Dr. Leeman in 1970 as a neuropeptide, released by cells in the brain or spinal cord in response to pain. Three years later, she identified another neuropeptide. The two discoveries established her as a leading figure in neuroendocrinology. Dr. Leeman died on Jan. 20 in Manhattan, at the home of her daughter Eve Leeman, where she had been living. She was 95. Her death was confirmed by another daughter, Jennifer Leeman. Although Substance P was identified in 1931 by Ulf von Euler and John Gaddum, researchers working in London, it was Dr. Leeman who discovered that it was a neuropeptide — a tiny, protein-like molecule released by neurons, or nerve cells in the brain and spinal cord, that transmits signals to target tissues. It was the first neuropeptide discovered in what would become a large class known as tachykinins. Dr. Leeman found that Substance P relays pain signals and amplifies the sensation of pain by triggering inflammation. It has since been linked to chronic pain syndromes, arthritis pain and migraines. © 2026 The New York Times Company

Keyword: Pain & Touch
Link ID: 30135 - Posted: 02.25.2026

By Meghan Rosen Ozempic’s key ingredient may act directly on cartilage to repair creaky joints. In mice and people, semaglutide can ease symptoms of the joint disease osteoarthritis and thicken the cartilage pillowed between bones, researchers report February 9 in Cell Metabolism. Thicker cartilage suggests the tissue is being rebuilt, says Di Chen, a physician and biologist at Shenzhen University of Advanced Technology in China. “That’s a good thing,” he says. “That’s the key thing.” More cartilage means more cushion, which means less bone-on-bone grinding and less pain. Osteoarthritis is the most common form of arthritis, affecting more than 500 million people worldwide. The disease can affect the hands, knees, hips and other joints, causing severe pain as cartilage wears away and tissues inflame. There’s no cure, and no medications that prevent it from becoming worse. Doctors can only help patients try to manage pain, Chen says. Scientists think weight loss can help alleviate symptoms by reducing the load on joints. That’s why semaglutide, the smash weight loss drug in Ozempic and Wegovy, is considered a contender for osteoarthritis treatment. And indeed, in 2024, a clinical trial in people with obesity reported that the drug improved joint pain and function. Doctors assumed those benefits were due to weight loss, Chen says. His team wasn’t so sure. The researchers conducted a similar study in mice with a form of osteoarthritis. One group received semaglutide, the other did not. In the drug-free mice, Chen’s team restricted food intake to match that of the semaglutide group. Both groups shed weight, but only the treated mice saw joint-based benefits. These mice had less pain, less broken-down cartilage and more cartilage growth, the team found. The results suggest that weight loss isn’t driving semaglutide’s benefits. © Society for Science & the Public 2000–2026.

Keyword: Neuroimmunology; Obesity
Link ID: 30129 - Posted: 02.21.2026

Mariana Lenharo Exercise pumps up your muscles — but it might also be pumping up your neurons. According to a study published today in Neuron1, repeated exercise sessions on a treadmill strengthen the wiring in a mouse’s brain, making certain neurons quicker to activate. This ‘rewiring’ was essential for mice in the study to gradually improve their running endurance. The work reveals that the brain — in mice and, presumably, in humans — is actively involved in the development of endurance, the ability to get better at a physical activity with repeated practice, says Nicholas Betley, a neuroscientist at the University of Pennsylvania in Philadelphia, and a co-author of the paper. “You go for a run, and your lungs expand, your heart gets pumping better, your muscles break down and rebuild. All this great stuff happens, and the next time, it gets easier,” Betley says. “I didn’t expect that the brain was coordinating all of that.” Betley and his colleagues were curious about what happens in the brain as people get stronger through exercise. They decided to focus on the ventromedial hypothalamus, a brain region that regulates appetite and blood sugar. The team then zeroed in on a group of neurons in that region that produce a protein called steroidogenic factor 1 (SF1), which is known to play a part in regulating metabolism2. A previous study3 found that the deletion of the gene that codes for SF1 impairs endurance in mice. © 2026 Springer Nature Limited

Keyword: Obesity; Learning & Memory
Link ID: 30120 - Posted: 02.14.2026

Yuki Noguchi At just over 5 foot, 5 inches, Christie Woodard weighs a lean 125 pounds. She's also open about relying on a low-dose GLP-1 to keep her weight there. She says sometimes people question why she's on the drug, "because they look at me and think I'm at healthy weight, or maybe they even think I'm thin." What people don't see is Woodard's previous struggles with obesity, which began in her 30s, and landed her at 260 pounds. She took up running half-marathons, but at that weight, it was painful. "I was not fast," she says. "I had massive issues; I was in physical therapy constantly. I tore my meniscus." Woodard, now 53 and living in Easton, Md., got gastric bypass surgery four years ago and cut her weight in half. Elated, she set a goal of completing half-marathons in all 50 states. Her weight remained stable until last year, when pounds began creeping back, despite adhering to a strict diet and lots of exercise. "I feel it in my knees, and mainly I feel it in my soul," she says. "I feel it in my confidence. It's messing with my head in a big way. I was terrified that I was going to go back to what I was." So her bariatric surgeon, Dr. Betsy Dovec, prescribed a low dose of the drug Zepbound, even though Woodard's body mass index didn't technically classify her as overweight. Dovec says Woodard isn't her only normal-weight patient on GLP-1s. "I prescribe medications for all types of people," she says. Though, she clarifies, she does not give the drugs to people for purely aesthetic reasons, like someone trying to shed a few pounds before an event, for example. © 2026 npr

Keyword: Obesity
Link ID: 30118 - Posted: 02.14.2026