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

By Molly Glick Not long after upending federal diet guidelines in order to prioritize “real food” on our plates, United States Health and Human Services Secretary Robert F. Kennedy Jr. has offered a new piece of questionable advice. During a tour to promote these dietary recommendations, Kennedy recently claimed that a keto diet can cure schizophrenia—an assertion that experts have quickly thrown cold water on. The ketogenic diet promotes fat-rich meals and low amounts of carbohydrates. While keto eating has skyrocketed in popularity in recent years—it ranked the most Googled diet in the U.S. in 2020—it was initially designed in the early 20th century for patients with epilepsy. More recent studies have confirmed that the diet is effective for certain types of epilepsy because it can control seizures. Meanwhile, we have much less evidence for its impacts on symptoms of schizophrenia. So far, small studies have offered some early evidence that ketogenic diets may help people with the condition. “There is currently no credible evidence that ketogenic diets cure schizophrenia,” Mark Olfson, a psychiatrist at Columbia University, told The New York Times. Kennedy also proclaimed that the diet can essentially cure bipolar disorder, according to studies he recently read. But as with schizophrenia, keto’s impacts on bipolar disorder have only been examined in limited numbers of patients so far. Preliminary findings have also hinted that a keto diet could ease symptoms of depression. It may offer “small antidepressant benefits” for people who don’t respond to medication, according to a recently published JAMA Psychiatry paper. But this work is in the early stages as well and remains far from conclusive. © 2026 NautilusNext Inc.

Keyword: Schizophrenia; Depression
Link ID: 30109 - Posted: 02.07.2026

By Jake Buehler Though fearsome predators, snakes can go weeks or even months without eating. Now, scientists think they may know how they do it. Snakes have lost the genes to produce ghrelin, a key hormone that regulates appetite, digestion, and fat storage, researchers report today in Royal Society Open Biology. Chameleons and a group of desert lizards called toadhead agamas that also have huge spaces between meals have also lost the same genes, hinting that cutting off ghrelin is a key way to excel at fasting, possibly by suppressing appetite and holding onto fat stores. “I give [the researchers] a lot of credit for looking more deeply into the data that was staring us all in the face—myself included,” says Todd Castoe, a genomicist at the University of Texas at Arlington not involved with the study. The hormone is ubiquitous across vertebrates, from fish to mammals. So finding that reptiles have repeatedly ditched it is “pretty remarkable,” he says. When scientists first discovered ghrelin nearly 30 years ago, they thought this “hunger hormone” could be key to fighting obesity in humans. But it hasn’t been that simple. Since then, researchers have found that ghrelin has a complicated role within a network of hormones constantly tweaking hunger and energy stores. And even though ghrelin is commonly found in vertebrates, it’s been unclear how it has evolved across various groups of vertebrates. So in the new study, Rui Resende Pinto, an evolutionary biologist at the University of Porto, and his colleagues focused on reptiles, many of which can go long periods without food. The researchers scanned the genomes of 112 species. In snakes, chameleons, and toadhead agamas, ghrelin genes were either missing or so warped by mutations they could no longer encode the hormone, the team found. The degree of the genes’ erosion also varied considerably between snake families: Some snakes such as boas and pythons had malformed ghrelin genes, but others, such as vipers, cobras, and their relatives, barely had anything left.

Keyword: Obesity; Evolution
Link ID: 30104 - Posted: 02.04.2026

By Diana Kwon edited by Jeanna Bryner By the time Maggie May, an Arkansas resident in her 30s, was admitted to a psychiatric clinic in 2024, she had been struggling for years with atypical anorexia nervosa, an eating disorder that leads to severe food restriction and profound disturbances in body image. (Her name has been changed for privacy.) She had already tried traditional interventions with a psychotherapist and a dietitian, but they had failed to improve her condition. So when May heard about a trial of a new and unconventional therapy, she jumped at the opportunity. The treatment was unusual in that alongside talk therapy, May underwent several sessions in a sensory-deprivation chamber: a dark, soundproof room where she floated in a shallow pool of water heated to match the temperature of her skin and saturated with Epsom salts to make her more buoyant. The goal was to blunt May’s external senses, enabling her to feel from within—focusing on the steady thudding of her heart, the gentle flow of air in and out of her lungs, and other internal bodily signals. The ability to connect with the body’s inner signals is called interoception. Some people are better at it than others, and one’s aptitude for it may change. Life events can also bolster or damage a person’s interoceptive skills. Sahib Khalsa, a psychiatrist and neuroscientist at the University of California, Los Angeles, and his colleagues think a disrupted interoception system might be one of the driving forces behind anorexia nervosa. So they decided to repurpose a decades-old therapy called flotation-REST (for “reduced environmental stimulation therapy”) and launched a trial with it in 2018. They hypothesized that in people with anorexia and some other disorders, an underreliance on internal signals may lead to an overreliance on external ones, such as how one looks in the mirror, that ultimately causes distorted body image, one of the key factors underlying these conditions. “When they’re in the float environment, they experience internal signals more strongly,” Khalsa says. “And having that experience may then confer a different understanding of the brain-body relationship that they have.” © 2025 SCIENTIFIC AMERICAN,

Keyword: Schizophrenia; Anorexia & Bulimia
Link ID: 30067 - Posted: 01.03.2026

By Emily Anthes In just a few short years, new diabetes and weight loss drugs like Ozempic, Wegovy and Mounjaro have taken the world by storm. In the United States, one in eight adults say they’ve tried one of these medications, which are known as GLP-1 drugs, and that number seems sure to rise as prices fall and new oral formulations hit the market. Fluffy and Fido could be next. On Tuesday, Okava Pharmaceuticals, a biopharmaceutical company based in San Francisco, is set to announce that it has officially begun a pilot study of a GLP-1 drug for cats with obesity. The company is testing a novel approach: Instead of receiving weekly injections of the drugs, as has been common in human patients, the cats will get small, injectable implants, slightly larger than a microchip, that will slowly release the drug for as long as six months. “You insert that capsule under the skin, and then you come back six months later, and the cat has lost the weight,” said Dr. Chen Gilor, a veterinarian at the University of Florida, who is leading the study. “It’s like magic.” Results are expected next summer. If they are promising, they could represent the next frontier for a class of drugs that has upended human medicine, and a potentially transformative treatment option for millions of pets. Some veterinarians have already begun administering human GLP-1 drugs, off label, to diabetic cats, and Okava is not the only company developing a product specifically for companion animals. “I think this is going to be the next big thing,” said Dr. Ernie Ward, a veterinarian and the founder of the Association for Pet Obesity Prevention. Veterinarians, he added, are “on the precipice of a complete new era in obesity medicine.” © 2025 The New York Times Company

Keyword: Obesity
Link ID: 30041 - Posted: 12.06.2025

Elie Dolgin Last April, neuroscientist Sue Grigson received an e-mail from a man detailing his years-long struggle to kick addiction — first to opioids, and then to the very medication meant to help him quit. The man had stumbled on research by Grigson, suggesting that certain anti-obesity medications could help to reduce rats’ addiction to drugs such as heroin and fentanyl. He decided to try quitting again, this time while taking semaglutide, the blockbuster GLP-1 drug better known as Ozempic. “That’s when he wrote to me,” says Grigson, who works at Pennsylvania State University College of Medicine in Hershey. “He said that he was drug- and alcohol-free for the first time in his adult life.” Stories like this have been spreading fast in the past few years, through online forums, weight-loss clinics and news headlines. They describe people taking diabetes and weight-loss drugs such as semaglutide (also marketed as Wegovy) and tirzepatide (sold as Mounjaro or Zepbound) who find themselves suddenly able to shake long-standing addictions to cigarettes, alcohol and other drugs. And now, clinical data are starting to back them up. Earlier this year, a team led by Christian Hendershot, a psychologist now at the University of Southern California in Los Angeles, reported in a landmark randomized trial that weekly injections of semaglutide cut alcohol consumption1 — a key demonstration that GLP-1 drugs can alter addictive behaviour in people with a substance-use disorder. More than a dozen randomized clinical studies testing GLP-1 drugs for addiction are now under way worldwide, with some results expected in the next few months. © 2025 Springer Nature Limited

Keyword: Drug Abuse; Obesity
Link ID: 30036 - Posted: 12.03.2025

Jonathan Lambert For centuries, the nature of a fever — and whether it's good or bad — has been hotly contested. In ancient Greece, the physician Hippocrates thought that fever had useful qualities, and could cook an illness out of a patient. Later on, around the 18th century, many physicians regarded fever as a distinct illness, one that could actually cook the patient, and so should be treated. These days, researchers understand that fever is part of the immune system's response to a pathogen, one that's shared by many animal species. And while there's accumulating evidence that fevers can help kick an infection, precisely how they can help remains mysterious. Sponsor Message "There's a cultural knowledge that there's this relationship between temperature and viruses, but at a molecular level, we're quite unsure how temperature might be impacting viruses," says Sam Wilson, a microbiologist at the University of Cambridge. There are two main ideas, he says. The heat of a fever itself could be harming the virus, akin to Hippocrates' hypotheses. Alternatively, the heat is a means to an end, either stoking our immune system to work better, or simply a regrettable, but unavoidable byproduct of fighting off an infection. "The fact that there weren't definitive answers to these questions piqued my interest," says Wilson. That interest led to a study, published Thursday in Science, that suggests — at least in mice — that elevated temperature alone is enough to fight off some viruses. © 2025 npr

Keyword: Neuroimmunology
Link ID: 30035 - Posted: 12.03.2025

By Carl Zimmer Last year, Ardem Patapoutian got a tattoo. An artist drew a tangled ribbon on his right arm, the diagram of a protein called Piezo. Dr. Patapoutian, a neuroscientist at Scripps Research in San Diego discovered Piezo in 2010, and in 2021 he won a Nobel Prize for the work. Three years later, he decided to memorialize the protein in ink. Piezo, Dr. Patapoutian had found, allows nerve endings in the skin to sense pressure, helping to create the sense of touch. “It was surreal to feel the needle as it was etching the Piezo protein that I was using to feel it,” he recalled. Dr. Patapoutian is no longer studying how Piezo informs us about the outside world. Instead, he has turned inward, to examine the flow of signals that travel from within the body to the brain. His research is part of a major new effort to map this sixth, internal sense, which is known as interoception. Scientists are discovering that interoception supplies the brain with a remarkably rich picture of what is happening throughout the body — a picture that is mostly hidden from our consciousness. This inner sense shapes our emotions, our behavior, our decisions, and even the way we feel sick with a cold. And a growing amount of research suggests that many psychiatric conditions, ranging from anxiety disorders to depression, might be caused in part by errors in our perception of our internal environment. Someday it may become possible to treat those conditions by retuning a person’s internal sense. But first, Dr. Patapoutian said, scientists need a firm understanding of how interoception works. “We’ve taken our body for granted,” he said. Everyone has a basic awareness of interoception, whether it’s a feeling of your heart racing, your bladder filling or a flock of butterflies fluttering in your stomach. And neuroscientists have long recognized interoception as one function of the nervous system. Dr. Charles Sherrington, a Nobel Prize-winning neuroscientist, first proposed the existence of “intero-ceptors,” in 1906. © 2025 The New York Times Company

Keyword: Obesity; Stress
Link ID: 30030 - Posted: 11.26.2025

By Gina Kolata Hopes were high. In retrospect, perhaps too high. On Monday, Novo Nordisk announced that two large studies failed to find any effect of the drug semaglutide on cognition and functioning in people with mild cognitive impairment — an early stage of Alzheimer’s — or with dementia. The participants were randomly assigned to take a pill of semaglutide, the compound at the heart of the weight-loss injections Ozempic and Wegovy, or a placebo for two years. “Today we announced that our efforts to slow down the progression of Alzheimer’s disease has come to an end,” said Maziar Mike Doustdar, chief executive at Novo Nordisk, in a video posted on LinkedIn. He added, “Based on the indicative data points we had, this is not the outcome we had hoped for.” The studies, involving 1,855 people in one trial and 1,953 in the other, seemed to stem an initial phase of optimism. The drugs appeared miraculous in their treatment of obesity, diabetes, heart disease and kidney disease. Alzheimer’s and other brain illnesses looked like the next frontier. But there had been other recent warnings, in two smaller studies of brain diseases. One, done by researchers in Britain, asked if a similar drug could help with Parkinson’s disease. That drug had no effect. Another study found that semaglutide did not help with cognitive impairment in people with major depression, a severe form of the disease. The company will present more detailed results from its Alzheimer’s study at a conference on Dec. 3, and another in March of 2026. Novo Nordisk’s stock was down nearly 6 percent on Monday, deepening a monthslong slump for the once-surging company. “We always knew there would be a low likelihood of success, but it was important to determine if semaglutide could take on one of medicine’s most challenging frontiers,” Mr. Doustdar said. © 2025 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 30026 - Posted: 11.26.2025

Mariana Lenharo The obesity drug tirzepatide, sold as Mounjaro or Zepbound, can suppress patterns of brain activity associated with food cravings, a study suggests. Researchers measured the changing electrical signals in the brain of a person with severe obesity who had experienced persistent ‘food noise’ — intrusive, compulsive thoughts about eating — shortly after the individual began taking the medication. The study is the first to use electrodes to directly measure how blockbuster obesity drugs that mimic the hormone GLP-1 affect brain activity in people, and to hint at how they curb extreme food cravings. “It’s a great strategy to try and find a neural signature of food noise, and then try to understand how drugs can manipulate it,” says Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center in Philadelphia, Pennsylvania. The findings were published today in Nature Medicine1. Casey Halpern, a neurosurgeon-scientist at the University of Pennsylvania in Philadelphia, and his colleagues did not set out to investigate the effects of obesity drugs on the brain. The team’s goal was to test whether a type of deep brain stimulation — a therapy that involves delivering a weak electrical current directly into the brain — can help to reduce compulsive eating in people with obesity for whom treatments such as bariatric surgery haven’t worked. The scientists set up a study in which participants had an electrode implanted into their nucleus accumbens, a region of the brain that is involved in feelings of reward. It also expresses the GLP-1 receptor, notes Christian Hölscher, a neuroscientist at the Henan Academy of Innovations in Medical Science in Zhengzhou, China, “so we know that GLP-1 plays a role in modulating reward here”. This type of electrode, which can both record electrical activity and deliver an electrical current when needed, is already used in people to treat some forms of epilepsy. © 2025 Springer Nature Limited

Keyword: Obesity; Attention
Link ID: 30016 - Posted: 11.19.2025

By Lauren Schenkman The purported autism-microbiome connection is having a moment. It’s the focus of a new $50-million call for proposals from Wellcome Leap—a research initiative of the Wellcome Trust—and a 2024 Netflix documentary portrays fecal microbiota transplants as a promising treatment for autism-related traits. “It seems to have captured the public’s imagination,” says Kevin Mitchell, associate professor of genetics and neuroscience at Trinity College in Dublin. But Mitchell says he has long been skeptical. Eventually, he and some colleagues “collectively got exasperated enough by this that we felt that we had to say something about it,” Mitchell says. Today, they published a comprehensive review in Neuron of more than 30 studies on the autism-microbiome connection, including preclinical experiments in mice, human observational studies and clinical trials. After accounting for statistical, technical and conceptual flaws, the team reached a clear conclusion: “There’s nothing there,” Mitchell says. Research projects that include the keywords “autism” and “microbiome” have netted about $20 million to $25 million in U.S. federal funding annually since 2018, Mitchell’s team found using the funding database NIH RePORTER. It’s worrying that funders assume “there’s a solid foundation of work,” Mitchell says. “It’s just this huge amount of scientific effort and funding going into exploring these ideas.” Mitchell spoke with The Transmitter about the problems he sees with studies that claim to show a microbiome-autism link, and how neuroscientists can read them with an analytical eye. © 2025 Simons Foundation

Keyword: Autism
Link ID: 30015 - Posted: 11.19.2025

By Alex Marshall When a Swiss theater invited people with eating disorders to be involved in a play about Joan of Arc this fall, it caused a furor. Some therapists and parents of girls with anorexia criticized the move as “ethnically reprehensible” and said it could jeopardize performers’ health. So when Janine Rickenbach, who has had anorexia for decades, took the Theater Basel stage last week in the premiere, she knew that some audience members were judging her appearance as much as her performance. Yet during the two-hour show, Rickenbach, 44, appeared unfazed. At one point, wearing a camisole top that revealed her arms and neck, she stared impassively at the audience while delivering a monologue that seemed to address the outcry. “What are you thinking right now?” she said: “Are you thinking, ‘Oh my God…’” Was that “because I look the way I look?” she asked, “Or because I’m standing here on this stage? Because my struggle is visible?” Theater makers have long depicted health struggles onstage, including the realities of living with H.I.V. and cancer, but the debate around this production, titled “Jeanne Dark” and running through May 22, has shown that ethical questions remain about how various conditions are portrayed theatrically — and who gets to shape those depictions. Ulrike Schmidt, a specialist in eating disorders at King’s College, London, said in an email that anybody depicting mental health onstage needed to consider the potential for stigmatization, perpetuating stereotypes or “inappropriate glamorization” © 2025 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 30014 - Posted: 11.19.2025

By Meghan Rosen Maybe you’ve seen an influencer make French fries out of almond flour. Or a sandwich recipe that swaps bread for fried cheese. They’re called keto meals, and they’re largely shared for one reason: to help people lose weight. In the ketogenic diet, fat is king, and carbs are public enemy number one. Going keto means restricting carbs to the bare minimum and replacing those lost calories with fat. It’s the antithesis of the low-fat diet craze of the 1990s. Losing fat on keto diets typically means eating fat — and lots of it. The idea may sound paradoxical. But without our typical go-to energy source (sugar), our bodies learn to rely on a different type of fuel. In keto dieters, the liver converts fat into molecules called ketone bodies, which the body can burn instead of sugar. That can lead to weight loss, despite an unusually high intake of fat. Such results may explain why so many Americans have tried the keto diet on for size. “I think a lot of people look at a ketogenic diet and think, ‘I’ll lose weight, I’ll be healthier,’” says Molly Gallop, a physiologist at Earlham College in Richmond, Ind. On the surface, they may be right. But staying on the diet long-term could carry some risks, a new study in mice suggests. Mice fed a ketogenic diet for up to about a year — decades in human time — experienced health problems including glucose intolerance and signs of liver and cardiovascular disease, Gallop and her colleagues report September 19 in Science Advances. The work uncovers some potential hidden costs to going keto, says physiologist Amandine Chaix, at the University of Utah in Salt Lake City. “It’s a cautionary tale,” she says. People sticking to this high-fat plan need to be careful, she says, “because this is not a magical dietary approach.” © Society for Science & the Public 2000–2025.

Keyword: Obesity
Link ID: 29933 - Posted: 09.20.2025

Andrew Gregory Health editor A daily pill for weight loss can help people reduce their body weight by as much as a fifth, according to a trial that could pave the way for millions more people to shed pounds. The drug, called orforglipron, is manufactured by Eli Lilly and targets the same GLP-1 receptors as weight loss injections such as Mounjaro and Wegovy. In a trial of 3,127 adults, one in five people who took the once-a-day tablet for 72 weeks lost 20% or more of their body weight. Weight loss jabs have been transformative but pill versions are seen as a holy grail because they are easier to store, distribute and administer and are also expected to be cheaper, offering fresh hope for the millions of people trying to lose weight. Orforglipron is a GLP-1 agonist, a type of medication that helps lower blood sugar levels, slows the digestion of food and can reduce appetite. The weight loss seen among people taking the tablet is not as stark as that among patients taking tirzepatide (Mounjaro), which is also made by Eli Lilly, but experts believe the tablet will be more accessible and convenient compared with injections. Orforglipron is not yet approved by the US Food and Drug Administration (FDA) or regulators in other countries. Eli Lilly has said it expects substantial demand when the new pill is launched. The company published a snapshot of the results in August and the full paper detailing the findings has now been published in the New England Journal of Medicine and presented to the annual meeting of the European Association for the Study of Diabetes in Vienna, Austria. © 2025 Guardian News & Media Limited

Keyword: Obesity
Link ID: 29930 - Posted: 09.17.2025

Nic Fleming In the early 2000s, Brazilian nutrition researcher Carlos Monteiro made a puzzling discovery that led to an epiphany. While trawling survey data on household spending to try to understand why rates of obesity and type 2 diabetes were rising so rapidly in his home country, he was surprised to note that people were buying smaller quantities of sugar, salt and other ingredients generally associated with these conditions than they had in previous decades. Only when Monteiro and his colleagues dug deeper did they find the culprit. People were buying less sugar to prepare cakes and desserts, but eating more of it in pre-made pastries and breakfast cereal. They were buying less salt, but consuming more of it in frozen pizzas, chicken nuggets and dehydrated packet soups. “We realized the problem was our traditional dietary patterns were being replaced by foods that are processed so many times that they can no longer be recognized in the final products. We called them ultra-processed foods.” Monteiro, a nutrition and public-health researcher at the University of São Paulo, first used the term ultra-processed food (UPF) in a paper in 2009, arguing that people interested in promoting healthy diets should focus more on the degree, extent and purpose of processing than on nutrient profiles1. It was a radical idea that caught the attention of other researchers, who, over the next decade or so, published dozens of papers linking UPFs with obesity and a range of other health problems. Governments took notice, too. In 2014, Brazil began advising people to avoid UPFs. Other countries, including France, Belgium and Israel, followed suit. Robert F. Kennedy Jr, secretary of the US Department of Health and Human Services (HHS), has been a critic of UPFs, saying in January that they are “poisoning the American people”. In May, the US government announced plans for a research agenda to support nutrition policy and improve people’s diets, in part by improving understanding of the impacts of UPFs on health. © 2025 Springer Nature Limited

Keyword: Obesity
Link ID: 29929 - Posted: 09.17.2025

By Ute Eberle Before weight coach Bella Barnes consults with new clients, she already knows what they’ll say. The women struggle with their weight, naturally. But they don’t want to lose pounds. They want to gain them. Her clients find themselves too thin, and they’re suffering. “Last week, I signed up a client who wears leggings that have bum pads in them,” says Barnes, who lives in Great Britain. “I’ve had another client recently that, in summer, wears three pairs of leggings just to try and make herself look a bit bigger.” These women belong to a demographic group that has been widely overlooked. As the world focuses on its billion-plus obese citizens, there remain people at the other end of the spectrum who are skinny, often painfully so, but don’t want to be. Researchers estimate that around 1.9 percent of the population are “constitutionally thin,” with 6.5 million of these people in the United States alone. YOU MAY ALSO LIKE Conceptual illustration shows three dinner plates, two at night with crescent moons are empty, representing a nightly fast, and a third with a sun theme, full of food and representing the benefits of eating during a limited time during the day. Constitutionally thin individuals often eat as much as their peers and don’t exercise hard. Yet their body mass index is below 18.5 — and sometimes as low as 14, which translates to 72 pounds on a five-foot frame — and they don’t easily gain weight. The condition is “a real enigma,” write the authors of a recent paper in the Annual Review of Nutrition. Constitutional thinness, they say, challenges “basic dogmatic knowledge about energy balance and metabolism.” It is also understudied: Fewer than 50 clinical studies have looked at constitutionally thin people, compared with thousands on unwanted weight gain. © 2025 Annual Reviews

Keyword: Obesity
Link ID: 29916 - Posted: 09.06.2025

By Joshua Cohen Roughly 40 percent of adult Americans are considered obese, and weight-loss drugs have come to play a central role in medical treatment over the past few years. As of the spring of 2024, one in eight U.S. adults had taken drugs including Wegovy, Zepbound, or Ozempic, among others, for weight loss. These products belong to a class of drugs known as glucagon-like peptide-1 agonists, or GLP-1s, which can be remarkably effective, but when patients go off GLP-1s, weight rebound occurs. And as it turns out, a relatively large portion of patients discontinue these medications within one year. Prime Therapeutics, a company that manages prescription drug coverage benefits for insurers, employers, and government programs, has been documenting this phenomenon. In 2023, the company published research indicating that merely 32 percent of patients remained on their GLP-1 at the end of one year. A follow-up analysis found that by year two, only 15 percent remained on the drug. And in a new review, the company found that only 8 percent of patients remained on the drugs after three years. The main reason for discontinuation — cited by almost half of patients in a large-scale survey — is concern about the medications’ side effects. People may quit their medication after experiencing common side effects, such as uncomfortable gastrointestinal issues. They may also quit out of fear of more serious ones, like certain cancers — although research suggests GLP-1s are associated with a lower risk for many types of cancer. Additionally, some GLP-1 users may also be at risk of nutrient deficiency and muscle or bone loss without a proper diet and exercise regimen. Health and nutrition experts suggest that optimizing the benefits conferred by GLP-1s requires lifestyle interventions aimed at modifying patient behavior. GLP-1 medicines work for weight loss by curbing hunger and slowing digestion, but they don’t replace the need for improved diet and increased physical activity. Rather, these prescription pharmaceuticals and other non-GLP-1 obesity drugs work together with nutrition and exercise to promote optimal health. In an email to Undark, Jody Dushay, an assistant professor at Harvard Medical School, wrote that “nutrition and exercise hugely benefit overall health” and increase the positive effects of the medications.

Keyword: Obesity
Link ID: 29910 - Posted: 09.03.2025