Sarah Berg Here is something we have never quite said out loud: for a significant portion of the world’s women, hunger is not a temporary state. It is a cognitive condition. It flows beneath everything: the meeting, the conversation, the stream of thought that almost ran its course before something more insistent pulled it back. For many of us, the state of hunger was present since we were old enough to understand that our bodies were under review. I was 11. I was sitting beside a swimming pool that summer, the one before middle school started, trying to follow a conversation I kept losing. I had decided, with the particular certainty children sometimes develop about the rules of the world they are entering, that I would eat as little as possible before sixth grade. The plan involved a sleeve of SnackWell’s cookies per day: fat-free, engineered to taste like cardboard, manufactured specifically for women and girls who had been told that fat was the enemy and desire was something to be managed rather than answered. The SnackWell’s cookie was itself a cultural artefact, a product designed to help women comply with an instruction they had already internalised. It did not quiet the hunger, because hunger is not a preference. It is biology doing what biology does when a body is not fed, sending signals that push everything else aside. During the day, we swam, lay on the concrete, and talked about the coming year. My attention kept sliding away from the conversation. A thought would begin and dissolve into the same insistent loop: how long until dinner, how little I could manage when it arrived, whether anyone had noticed what my body was doing without my permission. I remember listening to a teammate tell a long story and realising I had not heard most of it. Something louder had taken the space the story needed. © Aeon Media Group Ltd. 2012-2026.

Keyword: Anorexia & Bulimia
Link ID: 30381 - Posted: 08.22.2026

By Sara Reardon The protein tau is best known for its potential to clog the brain. In neurodegenerative conditions including Alzheimer’s disease, chains of the molecule twist into tangles inside neurons and choke out the cells. But a new study suggests tau may play an earlier and more fundamental role in neurodegeneration: sneaking into the cell’s power-generating mitochondria—the cell’s power generators—and interfering with aging neurons’ energy production. If this process gets out of control, it creates tangle-prone forms of tau and other toxic byproducts that damage neurons, long before a person’s cognitive symptoms start. The research, published today in Neuron, also showed interrupting this process can prevent brain damage and disease symptoms in mice. “It really is opening up something we’ve needed for a while, which is some really new ideas and fresh directions” for understanding neurodegenerative diseases, says Kenneth Kosik, a neuroscientist at the University of California, Santa Barbara who was not involved in the research. “I think this paper will reinvigorate the idea that [modifying tau] is going to be a possible therapeutic approach.” Researchers and companies developing treatments for Alzheimer’s have long seen tau as a potential drug target. One recent clinical trial, for instance, showed lowering the levels of tau in the brains of people with Alzheimer’s reduced their rate of cognitive decline by as much as 26%. Other approaches have tried to prevent enzymes from adding chemical tags called phosphate groups to tau proteins. These phosphorylated forms of tau (p-tau) are especially prone to misfolding and clumping into tangles. But tau therapies have seen limited success so far, leading researchers to wonder whether the protein actually drives neurodegeneration or is merely a sign of it. So geneticist Bingwei Lu of Stanford University and his colleagues set out to find specific ways in which p-tau affects cells. Previous research has suggested Alzheimer’s and other so-called tauopathies, including frontotemporal dementia and Parkinson’s disease, all involve problems with energy production in the brain’s mitochondria © 2026 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 30365 - Posted: 08.08.2026

By Jake Buehler A craving for sweets may have helped set the stage for the evolution of the human brain. Over 4 million years, our lineage’s brains grew from about 300 grams to 1,500 grams. Much of the brain growth occurred before early humans had mastered both fire and cooking, which would have unlocked access to the energy of starches. A new analysis of existing data from human ancestors, as well as chimps, suggests that a large proportion of that energy probably came from sugary foods like fruits and honey. These simple carbohydrates may have played an important, overlooked role in humankind’s evolutionary story, researchers argue August 6 in Science. A major part of the story of diet and human evolution revolves around meat-eating: Around 2.5 million years ago, our hominid ancestors began increasing their intake of animal food. This influx of protein and fat is seen as instrumental in fueling our ancestors’ ever-expanding brains. But Jennie Brand-Miller, a human nutrition scientist at the University of Sydney, was interested in how dietary sugars factored into the lives and overall evolution of our early ancestors. A 2017 study suggested that fruit-eating primates had bigger brains than leaf-eating species. Other researchers had hypothesized in the 1990s that the cognitive demands of fruit eating may have kick-started the evolution of big brains in humans. “You need to remember when various species of ripe fruit begin to ripen, then you need to remember where it is in the forest,” Brand-Miller says. “Your memory is associated with a bigger brain.” © Society for Science & the Public 2000–2026.

Keyword: Obesity; Evolution
Link ID: 30361 - Posted: 08.08.2026

BY Christie Wilcox The vagus nerve snakes through the human body like an elaborate highway system, transmitting signals from the brain to the heart, lungs, and gastrointestinal system and back. But despite its critical role in regulating breathing, heart rate, and digestion, researchers have long struggled to map its anatomical structure—until now. Scientists have created the first comprehensive map of the human vagus nerve, tracing thousands of individual nerve fibers stretching from the lower brain stem to all major organs. The map—announced last week and detailed in a data set released earlier this year—might help scientists and doctors more precisely stimulate the nerve as a potential treatment for conditions such as epilepsy, stroke, and inflammatory diseases. Some existing therapies stimulate the vagus nerve with electrodes implanted in the chest or neck sending signals that can suppress seizure activity in the brain, for example, or blunt pain. But the vagus nerve is a staggeringly intricate network: After forking into a main left and right branch, it shoots out finer branches made up of fascicles—small bundles of nerve fibers—that project to organs throughout the body. That complexity makes it hard to isolate and target specific nerve fibers or to understand the effects of stimulating at a given point. “We place an electrode on the vagus nerve, and things happen. But why do these things happen in this certain way?” asks Stavros Zanos, the physician-scientist at the Feinstein Institutes for Medical Research who led the mapping project. “We just had no idea, and we looked at the literature, and it just wasn’t there.” To build a comprehensive map of the nerve structures, Zanos and his colleagues analyzed 30 sets of left and right vagus nerves dissected from 30 human cadavers. © 2026 American Association for the Advancement of Science.

Keyword: Brain imaging; Stress
Link ID: 30358 - Posted: 08.05.2026

By Alexandra Pattillo It was 2022, and Christina was running out of options. The Londoner, then age 34, was desperate to fix her anorexia nervosa, even as the disease consumed her. After six years of battling the disease, she’d tried various forms of behavioral therapy and months of in-patient care, but nothing stuck. At its worst, the disease was preventing her from sleeping and zapping so much energy that she was unable to climb her stairs or brush her teeth. She needed a radical fix. “You become your anorexia,” says Christina (a pseudonym to protect her privacy). “You have no life around it. You don’t laugh. You don’t smile. You don’t find joy in anything,” she recalls. Her relationships suffered, and she almost lost her job and house. Eventually, a frantic Google search for “cures for anorexia” alerted her to a clinical trial for the psychedelic psilocybin—an active ingredient in magic mushrooms—as a treatment for the disease. She signed up. “I genuinely believe, had I not done that trial, I would either be stuck in a hospital loop, or I wouldn't be here today,” she says. “It saved my life.” Life with an eating disorder can turn the mind and body into a prison. Intrusive, never-ending thought spirals drive compulsive behaviors such as binging, overexercising, purging and restrictive eating. Conventional psychiatric treatments, such as cognitive-behavioral therapy or antidepressants, work in only about half of patients. People with anorexia are more than 18 times more likely to die by suicide than the general population—the highest mortality rate of any psychiatric disorder. © 2026 SCIENTIFIC AMERICAN INC.

Keyword: Anorexia & Bulimia; Drug Abuse
Link ID: 30357 - Posted: 08.05.2026

By Liz Seegert More than one in 10 Americans takes a GLP-1 medication for weight loss. As more people take a GLP-1, or glucagonlike peptide 1, receptor agonist, such as Wegovy, so, too, do more older adults—and those numbers are set to skyrocket. Last week the Trump administration launched the Medicare GLP-1 Bridge program, a new initiative that would set the cost of three weight-loss medications— Wegovy, the KwikPen version of Zepbound (tirzepatide) and Foundayo (orforglipron)—at $50 a month. That may be welcome news for the estimated 38.9 percent of adults aged 60 and up in the U.S. who are living with obesity. But it could also supercharge an ongoing and risky experiment in growing old on weight-loss drugs. For years, clinicians have had few good options to safely treat obesity in older adults. But while GLP-1s, long used to treat diabetes, are now approved for weight loss, the evidence supporting their use in the age-60-and-older population is limited. Someone in their 70s may benefit as much from weight loss as a person in their 30s but may respond very differently to these drugs’ side effects; we simply don’t have enough evidence yet to make informed conclusions, experts advise. “Eligibility doesn’t mean benefit automatically,” says Ruchi Gaba, an associate professor of endocrinology at Baylor College of Medicine. “We have to individualize.” And within the 60-and-older group, there is huge variety: a healthy, active 68-year-old with obesity and sleep apnea is a very different patient than an 88-year-old who’s frail, has poor appetite and is at risk of falls, Gaba says. Older adults are underrepresented in the clinical trials for GLP-1 drugs. Despite the high prevalence of obesity among this age group, only about one in 10 participants in early GLP-1 trials was age 65 or older, says Alissa Chen, a primary care physician and a researcher at the Yale School of Medicine, who specializes in obesity. Older adults are more heterogeneous than people in younger age groups in terms of chronic conditions and multiple medications, Chen says, which can pose challenges with both prescriptions and side effects. © 2026 SCIENTIFIC AMERICAN

Keyword: Obesity; Development of the Brain
Link ID: 30334 - Posted: 07.22.2026

By Dana G. Smith In theory, taking an omega-3, or fish oil, supplement makes a lot of sense. Omega-3 fatty acids are vital for brain health: They are used to build brain cells, keeping the cell walls flexible and enabling the neurons to sprout new connections and communicate with other cells. Numerous studies have shown that people with higher levels of omega-3s in their blood have better cognition and healthier looking brains, as well as a lower risk of developing dementia. In contrast, people with Alzheimer’s disease have been shown to have lower omega-3 levels. But there’s a catch: The vast majority of clinical trials have found that taking omega-3 supplements offers virtually no benefit for cognition or dementia symptoms. “It kind of intuitively makes sense” that neurons need fatty acids for their health, so you should take a fatty acid supplement, said Dr. Kristine Yaffe, a professor of psychiatry, neurology and epidemiology at the University of California, San Francisco. “The problem is that most of the evidence, particularly the trial evidence, just doesn’t support it at all,” she said. A study published last month offers a prime example. The scientists who ran the clinical trial tried to cover all their bases: The participants were older adults who didn’t eat a lot of fish (which is rich in omega-3s), suggesting they might benefit the most from a supplement. Roughly half of the participants had an increased genetic risk for Alzheimer’s, which is another group that experts think might need more omega-3s. The researchers even did lumbar punctures on some of the participants to confirm that the supplement caused omega-3 levels in the brain to go up. But compared with a placebo, the supplement didn’t result in any benefit when it came to people’s cognition or brain structure. So what’s behind the disconnect? Scientists have a few hypotheses, and most are connected to diet and lifestyle. © 2026 The New York Times Company

Keyword: Development of the Brain; Alzheimers
Link ID: 30322 - Posted: 07.15.2026

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