By Gordy Slack, MindSite News Lauren Kennedy West was still a teenager when she began to smell and hear things that weren’t there. Then to see things, too, that were invisible to others. Meanwhile, her moods began to intensify, sometimes turning very, very dark. “It was confusing, disturbing, and depressing,” she recalls. She had periods of elation, too. But when she came down from these, she’d keep descending until she hit emotional bottom. It got so bad that in her early 20s, at college, Kennedy West tried to end her life twice. Finally, when she was 25, she was diagnosed with schizoaffective disorder, a form of schizophrenia with powerful mood swings. The medications she was prescribed eased her worst symptoms, she said, but they also had troubling side effects that ranged from extreme weight gain and “dry mouth” to feeling lethargic and an episodic condition called oculogyric crisis which causes people to continually, involuntarily, gaze upward. Worst of all, she said, was the feeling of being “emotionally blunted.” Learning that she’d likely be taking those medications for the rest of her life was a blow, but the diagnosis gave Kennedy West a meaningful framework for her struggle. To be as stable, happy, and engaged as possible she would have to cultivate acceptance of her condition and the limitations it imposed, she was told. Driven by a hope that others might be spared the disabling confusion and depression she suffered before her diagnosis, Kennedy West and her partner started a YouTube Channel, which they called “Living Well with Mental Illness” (now “Living Well with Schizophrenia“) In frequent posts, Kennedy West recounted her own struggles and triumphs and interviewed experts on mental illness and related subjects. In early 2023, Christopher Palmer was a guest on the channel.

Keyword: Schizophrenia
Link ID: 29842 - Posted: 06.28.2025

Diana Kwon There might be a paradox in the biology of ageing. As humans grow older, their metabolisms tend to slow, they lose muscle mass and they burn many fewer calories. But certain cells in older people appear to do the exact opposite — they consume more energy than when they were young. These potential energy hogs are senescent cells, older cells that have stopped dividing and no longer perform the essential functions that they used to. Because they seem idle, biologists had assumed that zombie-like senescent cells use less energy than their younger, actively replicating counterparts, says Martin Picard, a psychobiologist at Columbia University in New York City. But in 2022, Gabriel Sturm, a former graduate student of Picard’s, painstakingly observed the life course of human skin cells cultured in a dish1 and, in findings that have not yet been published in full, found that cells that had stopped dividing had a metabolic rate about double that of younger cells. For Picard and his colleagues, the energetic mismatch wasn’t a paradox at all: ageing cells accumulate energetically costly forms of damage, such as alterations in DNA, and they initiate pro-inflammatory signalling. How that corresponds with the relatively low energy expenditure for ageing organisms is still unclear, but the researchers hypothesize that this tension might be an important driver of many of the negative effects of growing old, and that the brain might be playing a key part as mediator2. As some cells get older and require more energy, the brain reacts by stripping resources from other biological processes, which ultimately results in outward signs of ageing, such as greying hair or a reduction in muscle mass (see ‘Energy management and ageing’). Picard and his colleagues call this concept the ‘brain–body energy-conservation model’. And although many parts of the hypothesis are still untested, scientists are working to decipher the precise mechanisms that connect the brain to processes associated with ageing, such as senescence, inflammation and the shortening of telomeres — the stretches of repetitive DNA that cap the ends of chromosomes and protect them. © 2025 Springer Nature Limited

Keyword: Obesity; Stress
Link ID: 29836 - Posted: 06.18.2025

By Tina Hesman Saey People trying to lose weight often count calories, carbs, steps and reps and watch the scales. Soon, they may have another number to consider: a genetic score indicating how many calories a person needs to feel full during a meal. This score may help predict whether someone will lose more weight on the drugs liraglutide or phentermine-topiramate, researchers report June 6 in Cell Metabolism. A separate study, posted to medRXiv.org in November, suggests that individuals with a higher genetic propensity for obesity benefit less from semaglutide compared to those with a lower genetic predisposition. Such genetic tests may one day help doctors and patients select personalized weight-loss treatments, some researchers say. But the genetic scores “are not perfect predictors of drug response,” says Paul Franks, a genetic epidemiologist at Queen Mary University of London who was not involved in either study. “They show a tendency.” For the Cell Metabolism study, Mayo Clinic researchers measured how many calories it took for about 700 adults with obesity to feel full when given an all-you-can-eat meal of lasagna, pudding and milk. The calorie intake varied widely, ranging from about 140 to 2,200 calories, with men generally needing more than women. The team used machine learning to compile a genetic score based on variants of 10 genes associated with obesity. That score is designed to reflect the calories people required to feel full. Then, the Mayo team and colleagues from Phenomix Sciences Inc, headquartered in Menlo Park, Calif., conducted two clinical trials. In one 16-week trial, people with obesity received either a placebo or liraglutide­ — a GLP-1 drug branded as Saxenda. GLP-1s are a class of diabetes drugs that have shown promise with weight loss. People with a lower genetic score lost more weight on liraglutide than those with higher genetic scores. © Society for Science & the Public 2000–2025.

Keyword: Obesity; Genes & Behavior
Link ID: 29830 - Posted: 06.14.2025

Elie Dolgin Sheree had maintained a healthy weight for 15 years, thanks to a surgery that wrapped a silicone ring around the top of her stomach. But when the gastric band repeatedly slipped and had to be removed, the weight came back — fast. She gained nearly 20 kilograms in just 2 months. Frustrated, she turned to the latest generation of anti-obesity medications, hoping to slow the rapid weight gain. She cycled through various formulations of the blockbuster therapies semaglutide (sold under the brand names Ozempic and Wegovy) and tirzepatide (sold as Zepbound for weight loss), finding some success with higher doses of these drugs, which mimic the effects of the appetite-suppressing hormone GLP-1. But each time, drug shortages disrupted her treatment, forcing her to start again with a new formulation or to go without the drugs for weeks. Tired of the uncertainty around the therapies, she decided to try something different. Sheree, who asked that her middle name be used to protect her privacy, underwent two minimally invasive procedures designed to reduce the size of her stomach and to blunt hunger cues. Developed over the past two decades, these ‘endoscopic’ procedures — performed using flexible tubes inserted through the mouth, and no scalpels — are just one part of a growing toolkit to help people who want to move away from GLP-1 therapy. More-conventional bariatric surgeries, used routinely since the 1980s to reroute the flow of food through the gut or to restrict the stomach’s size, might also gain wider appeal. And the search is picking up for other drugs that could offer lasting alternatives for a post-GLP-1 population. That momentum is driven by a convergence of factors: chronic shortages of GLP-1 therapies, high costs, insurance barriers and debilitating side effects. As a result, many people who start the drugs ultimately stop — with discontinuation rates in clinical trials ranging from 37% to 81% in the first year1. And once treatment ends, the weight lost often piles back on. © 2025 Springer Nature Limited

Keyword: Obesity
Link ID: 29829 - Posted: 06.14.2025

By Amber Dance The experiment was a striking attempt to investigate weight control. For six weeks, a group of mice gorged on lard-enriched mouse chow, then scientists infected the mice with worms. The worms wriggled beneath the animals’ skin, migrated to blood vessels that surround the intestines, and started laying eggs. Bruno Guigas, a molecular biologist at the Leiden University Center for Infectious Diseases in the Netherlands, led this study some years back and the results, he says, were “quite spectacular.” The mice lost fat and gained less weight overall than mice not exposed to worms. Within a month or so, he recalls, the scientists barely needed their scale to see that the worm-infested mice were leaner than their worm-free counterparts. Infection with worms, it seems, reversed obesity, the researchers reported in 2015. While it’s true that worms gobble up food their hosts might otherwise digest, that doesn’t seem to be the only mechanism at work here. There’s also some intricate biology within the emerging scientific field of immunometabolism. Over the past couple of decades, researchers have recognized that the immune system doesn’t just fight infection. It’s also intertwined with organs like the liver, the pancreas and fat tissue, and implicated in the progression of obesity and type 2 diabetes. These and other metabolic disorders generate a troublesome immune response — inflammation — that worsens metabolism still further. Metabolic disease, in other words, is inflammatory disease. Scientists have also observed a metabolic influence of worms in people who became naturally infected with the parasites or were purposely seeded with worms in clinical trials. While the physiology isn’t fully understood, the worms seem to dampen inflammation, as discussed in the 2024 Annual Review of Nutrition.

Keyword: Obesity; Neuroimmunology
Link ID: 29828 - Posted: 06.14.2025

Myrian Wares for Quanta Magazine You’ve just gotten home from an exhausting day. All you want to do is put your feet up and zone out to whatever is on television. Though the inactivity may feel like a well-earned rest, your brain is not just chilling. In fact, it is using nearly as much energy as it did during your stressful activity, according to recent research. Sharna Jamadar (opens a new tab), a neuroscientist at Monash University in Australia, and her colleagues reviewed research from her lab and others around the world to estimate the metabolic cost of cognition (opens a new tab) — that is, how much energy it takes to power the human brain. Surprisingly, they concluded that effortful, goal-directed tasks use only 5% more energy than restful brain activity. In other words, we use our brain just a small fraction more when engaging in focused cognition than when the engine is idling. It often feels as though we allocate our mental energy through strenuous attention and focus. But the new research builds on a growing understanding that the majority of the brain’s function goes to maintenance. While many neuroscientists have historically focused on active, outward cognition, such as attention, problem-solving, working memory and decision-making, it’s becoming clear that beneath the surface, our background processing is a hidden hive of activity. Our brains regulate our bodies’ key physiological systems, allocating resources where they’re needed as we consciously and subconsciously react to the demands of our ever-changing environments. “There is this sentiment that the brain is for thinking,” said Jordan Theriault (opens a new tab), a neuroscientist at Northeastern University who was not involved in the new analysis. “Where, metabolically, [the brain’s function is] mostly spent on managing your body, regulating and coordinating between organs, managing this expensive system which it’s attached to, and navigating a complicated external environment.” © 2025 Simons Foundation.

Keyword: Attention; Brain imaging
Link ID: 29825 - Posted: 06.07.2025

Anna Bawden Health and social affairs correspondent Weight loss drugs could at least double the risk of diabetic patients developing age-related macular degeneration, a large-scale study has found. Originally developed for diabetes patients, glucagon-like peptide-1 receptor agonist (GLP-1 RA) medicines have transformed how obesity is treated and there is growing evidence of wider health benefits. They help reduce blood sugar levels, slow digestion and reduce appetite. But a study by Canadian scientists published in Jama Ophthalmology has found that after six months of use GLP-1 RAs are associated with double the risk of older people with diabetes developing neovascular age-related macular degeneration compared with similar patients not taking the drugs. Academics at the University of Toronto examined medical data for more than 1 million Ontario residents with a diagnosis of diabetes and identified 46,334 patients with an average age of 66 who were prescribed GLP-1 RAs. Nearly all (97.5%) were taking semaglutide, while 2.5% were on lixisenatide. The study did not exclude any specific brand of drugs, but since Wegovy was only approved in Canada in November 2021, primarily for weight loss, it is likely the bulk of semaglutide users in the study were taking Ozempic, which is prescribed for diabetes. Each patient on semaglutide or lixisenatide was matched with two patients who also had diabetes but were not taking the drugs, who shared similar characteristics such as age, gender and health conditions. The researchers then compared how many patients developed neovascular age-related macular degeneration over three years. © 2025 Guardian News & Media Limited

Keyword: Vision; Obesity
Link ID: 29822 - Posted: 06.07.2025

By Abby Ellin Sally Odenheimer starved herself because she was an athlete and thought she’d run faster on an empty stomach. Karla Wagner starved herself because she wanted to be in charge of at least one aspect of her life. Janice Bremis simply felt too fat. They all sought perfection and control. Not eating helped. They are women in their 60s and 70s who have struggled with anorexia nervosa since childhood or adolescence. Years later, their lives are still governed by calories consumed, miles run, laps swum, pounds lost. “It’s an addiction I can’t get rid of,” said Ms. Odenheimer, 73, a retired teacher who lives outside Denver. For decades, few people connected eating disorders with older people; they were seen as an affliction of teenage girls and young women. But research suggests that an increasing number of older women have been seeking treatment for eating disorders, including bulimia, binge eating disorder (known as BED) and anorexia, which has the highest mortality rate of any psychiatric disorder, and brings with it an elevated risk of suicide. In a 2017 paper in the journal BMC Medicine, researchers reported that more than 15 percent of 5,658 women surveyed met the criteria for a lifetime eating disorder while in their 30s and 40s. A 2023 review of recent research reported that the prevalence rates among women 40 and older with full diagnoses of eating disorders were between 2.1 and 7.7 percent. (For men, they were less than 1 percent.) © 2025 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 29816 - Posted: 06.04.2025

Anna Bawden in Málaga and agency Giving obese children weight loss jabs works and could help avoid arguments over mealtimes, according to research. Clinicians treating very obese children at a hospital in Sweden analysed whether liraglutide injections could be used as well as diet and lifestyle changes to increase weight loss. In real-life analysis of 1,000 children under 16 with severe obesity over a number of years, about a quarter of patients in 2023 were given the weight loss drug liraglutide in addition to receiving intensive health behaviour and lifestyle treatment at the National Childhood Obesity Centre in Stockholm. The clinicians found that nearly a third of these children dropped enough weight to improve their health, compared with about 27% in earlier treated groups with no access to the drugs. Patients starting the programme in 2024 have been given semaglutide but results from these children are not yet available. Semaglutide, better known as Wegovy, and liraglutide, sold as Saxenda, are both GLP-1 receptor agonists, which help curb appetite. In the UK they are available on the NHS only for adults with a BMI above 35 with a weight-related condition, although in certain circumstances specialist paediatric clinics can prescribe them. Dr Annika Janson, of Karolinska university hospital in Sweden, the lead author of the study, whose findings were presented at the European Congress on Obesity, said the beneficial impact of weight loss jabs on children’s weight could accelerate in future years. © 2025 Guardian News & Media Limited

Keyword: Obesity
Link ID: 29786 - Posted: 05.14.2025

By Gina Kolata Do we really have free will when it comes to eating? It’s a vexing question that is at the heart of why so many people find it so difficult to stick to a diet. To get answers, one neuroscientist, Harvey J. Grill of the University of Pennsylvania, turned to rats and asked what would happen if he removed all of their brains except their brainstems. The brainstem controls basic functions like heart rate and breathing. But the animals could not smell, could not see, could not remember. Would they know when they had consumed enough calories? To find out, Dr. Grill dripped liquid food into their mouths. “When they reached a stopping point, they allowed the food to drain out of their mouths,” he said. Those studies, initiated decades ago, were a starting point for a body of research that has continually surprised scientists and driven home that how full animals feel has nothing to do with consciousness. The work has gained more relevance as scientists puzzle out how exactly the new drugs that cause weight loss, commonly called GLP-1s and including Ozempic, affect the brain’s eating-control systems. The story that is emerging does not explain why some people get obese and others do not. Instead, it offers clues about what makes us start eating, and when we stop. While most of the studies were in rodents, it defies belief to think that humans are somehow different, said Dr. Jeffrey Friedman, an obesity researcher at Rockefeller University in New York. Humans, he said, are subject to billions of years of evolution leading to elaborate neural pathways that control when to eat and when to stop eating. © 2025 The New York Times Company

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 29762 - Posted: 04.26.2025

Humberto Basilio What Rina Green calls her “living hell” began with an innocuous backache. By late 2022, two years later, pain flooded her entire body daily and could be so intense that she couldn’t get out of bed. Painkillers and physical therapy offered little relief. She began using a wheelchair. Green has fibromyalgia, a mysterious condition with symptoms of widespread and chronic muscle pain and fatigue. No one knows why people get fibromyalgia, and it is difficult to treat. But eight months ago, Green received an experimental therapy: pills containing living microorganisms of the kind that populate the healthy human gut. Her pain decreased substantially, and Green, who lives in Haifa, Israel, and is now 38, can go on walks — something she hadn’t done since her fibromyalgia diagnosis. Green was one of 14 participants in a trial of microbial supplements for the condition. All but two reported an improvement in their symptoms. The trial is so small that “we should take the results with a grain of salt”, says co-organizer Amir Minerbi, a pain scientist at the Technion — Israel Institute of Technology in Haifa. “But it is encouraging [enough] to move forward.” The trial results and data from other experiments linking fibromyalgia to gut microbes are published today in Neuron1. Fibromyalgia affects up to 4% of the global population and occurs in the absence of tissue damage. In 2019, Minerbi and his colleagues discovered that the gut microbiomes — the collection of microbes living in the intestines — of women with fibromyalgia differed significantly from those of healthy women2. This led the scientists to wonder whether a dose of microbes from healthy people would ease the pain and fatigue caused by the condition. After all, previous research3 had shown that gut microbes might indirectly influence an array of chemical signals tied to pain perception. The team transplanted minuscule samples of microbe-laden faeces from both women with fibromyalgia and healthy women into mice without any microbes in their bodies. The researchers found that mice that received microbes from women with fibromyalgia showed signs of greater sensitivity to pain in response to pressure, heat and cold than did mice that got microbes from healthy women. The first group also showed more evidence of spontaneous pain. © 2025 Springer Nature Limited

Keyword: Pain & Touch; Obesity
Link ID: 29760 - Posted: 04.26.2025

By Elise Cutts Food poisoning isn’t an experience you’re likely to forget — and now, scientists know why. A study published April 2 in Nature has unraveled neural circuitry in mice that makes food poisoning so memorable. “We’ve all experienced food poisoning at some point … And not only is it terrible in the moment, but it leads us to not eat those foods again,” says Christopher Zimmerman of Princeton University. Luckily, developing a distaste for foul food doesn’t take much practice — one ill-fated encounter with an undercooked enchilada or contaminated hamburger is enough, even if it takes hours or days for symptoms to set in. The same is true for other animals, making food poisoning one of the best ways to study how our brains connect events separated in time, says neuroscientist Richard Palmiter of the University of Washington in Seattle. Mice usually need an immediate reward or punishment to learn something, Palmiter says; even just a minute’s delay between cause (say, pulling a lever) and effect (getting a treat) is enough to prevent mice from learning. Not so for food poisoning. Despite substantial delays, their brains have no trouble associating an unfamiliar food in the past with tummy torment in the present. Researchers knew that a brain region called the amygdala represents flavors and decides whether or not they’re gross. Palmiter’s group had also shown that the gut tells the brain it’s feeling icky by activating specific “alarm” neurons, called CGRP neurons. “They respond to everything that’s bad,” Palmiter says. © Society for Science & the Public 2000–2025.

Keyword: Learning & Memory; Emotions
Link ID: 29756 - Posted: 04.23.2025

By Rachel Brazil Drugs that mimic glucagonlike peptide-1 (GLP-1), such as semaglutide—marketed as Ozempic or Wegovy—have revolutionized the treatment of obesity and type 2 diabetes, but they have major drawbacks. “[They] are expensive to manufacture, they have to be refrigerated, and they often have to be injected because they cannot go through the gastrointestinal tract without being degraded,” explains Alejandra Tomas, a cell biologist at Imperial College London who studies the cellular receptor GLP-1 drugs target. That’s all because they consist of peptides, or long chains of amino acids. A small-molecule version of the therapy, on the other hand, could be given as a daily pill and would be much cheaper to produce. Companies including Eli Lilly, Pfizer, and Roche have launched clinical trials of such compounds. Results from Lilly’s first phase 3 trial of its oral drug are expected later this year. But Pfizer announced this week it was halting development of its candidate after signs of liver injury in a trial participant. The candidates furthest along in development activate the same receptors as peptide drugs do, in much the same way. But several firms are exploring more innovative small molecules that target different sites on those receptors—and could lead to even more effective treatments with fewer side effects. “In the next 4 or 5 years, this field will mature and more patients ultimately should be able to get these medicines,” says Kyle Sloop, a molecular biologist at Lilly Research Laboratories. By mimicking a natural hormone, semaglutide and other drugs in its class help regulate blood sugar by increasing insulin secretion from the pancreas in response to glucose, and suppress appetite by slowing down digestion. The first generation of peptide drugs were essentially copies of GLP-1, with modifications to prevent the peptide from quickly degrading once in the body. Novo Nordisk first won U.S. approval for semaglutide to treat type 2 diabetes in 2017. It needed to be injected, but in 2019 the company added a pill form, which includes an absorption-enhancing ingredient that allows the peptide to penetrate the stomach wall. However, it requires a high dose and has to be taken while fasting, with minimal liquid.

Keyword: Obesity
Link ID: 29746 - Posted: 04.16.2025

Nora Bradford Scientists have created the first map of the crucial structures called mitochondria throughout the entire brain ― a feat that could help to unravel age-related brain disorders1. The results show that mitochondria, which generate the energy that powers cells, differ in type and density in different parts of the brain. For example, the evolutionarily oldest brain regions have a lower density of mitochondria than newer regions. The map, which the study’s authors call the MitoBrainMap, is “both technically impressive and conceptually groundbreaking”, says Valentin Riedl, a neurobiologist at Friedrich-Alexander University in Erlangen, Germany, who was not involved in the project. The brain’s mitochondria are not just bit-part players. “The biology of the brain, we know now, is deeply intertwined with the energetics of the brain,” says Martin Picard, a psychobiologist at Columbia University in New York City, and a co-author of the study. And the brain accounts for 20% of the human body’s energy usage2. Wielding a tool typically used for woodworking, the study’s authors divided a slice of frozen human brain ― from a 54-year-old donor who died of a heart attack ― into 703 tiny cubes. Each cube measured 3 × 3 × 3 millimetres, which is comparable to the size of the units that make up standard 3D images of the brain. “The most challenging part was having so many samples,” says Picard. The team used biochemical and molecular techniques to determine the density of mitochondria in each of the 703 samples. In some samples, the researchers also estimated the mitochondria’s efficiency at producing energy. To extend their findings beyond a single brain slab, the authors developed a model to predict the numbers and types of mitochondria across the entire brain. They fed it brain-imaging data and the brain-cube data. To check their model, they applied it to other samples of the frozen brain slice and found that it accurately predicted the samples’ mitochondrial make-up. © 2025 Springer Nature

Keyword: Brain imaging
Link ID: 29721 - Posted: 03.27.2025

By Emily Kwong You probably know the feeling of having a hearty meal at a restaurant, and feeling full and satisfied … only to take a peek at the dessert menu and decide the cheesecake looks just irresistible. So why is it that you just absolutely couldn't have another bite, but you somehow make an exception for a sweet treat? Or as Jerry Sienfeld might put it back in the day "Whhaaaat's the deal with dessert?!" Scientists now have a better understanding of the neural origins of this urge thanks to a recent study published in the journal Science. Sponsor Message Working with mice, researchers tried to set up a scenario similar to the human experience described above. They started by offering a standard chow diet to mice who hadn't eaten since the previous day. That "meal" period lasted for 90 minutes, and the mice ate until they couldn't eat any more. Then it was time for a 30-minute "dessert" period. The first round of the experiment, researchers offered mice more chow for dessert, and the mice ate just a little bit more. The second time around, during the "dessert" period, they offered a high sugar feed to the mice for 30 minutes. The mice really went for the sugary feed, consuming six times more calories than when they had regular chow for dessert. In the mice, researchers monitored the activity of neurons that are associated with feelings of fullness, called POMC neurons. They're located in a part of the brain called the hypothalamus, which is "very important for promoting satiety," says Henning Fenselau, one of the study authors and a researcher at the Max Planck Institute for Metabolism Research in Cologne, Germany. © 2025 npr

Keyword: Obesity
Link ID: 29706 - Posted: 03.15.2025

By Elie Dolgin For Kristian Cook, every pizza box he opened was another door closed on the path to overcoming obesity. “I had massive cravings for pizza,” he says. “That was my biggest downfall.” At 114 kilograms and juggling a daily regimen of medications for high cholesterol, hypertension and gout, the New Zealander resolved to take action. In late 2022, at the age of 46, Cook joined a clinical trial that set out to test a combination of the weight-loss drug semaglutide — better known by its brand names, Ozempic or Wegovy — and an experimental drug designed to preserve muscle while shedding fat. Muscle loss is a big concern for people on anti-obesity medications such as semaglutide. These ‘GLP-1 agonists’ mimic a natural gut hormone — glucagon-like peptide 1 — to suppress appetite and regulate metabolism. But reducing calories leads to an energy deficit, which the body often makes up for by burning muscle. The experimental drug that Cook received, called bimagrumab, seems to counteract this muscle loss. It’s one of more than 100 anti-obesity drug candidates that are in various stages of development. The next wave of medications, which are likely to hit pharmacy shelves in the next few years, resemble drugs that are already on the market. But close behind are numerous therapies being developed specifically for their muscle-sparing weight-loss potential. Dozens more are aimed at different biological pathways and could redefine obesity treatment in decades to come. “We’re working to create the next generation of healthy weight-loss solutions,” says Philip Larsen, who played a key part in the early development of GLP-1 drugs and is now chief executive of SixPeaks Bio, an obesity-focused start-up company in Basel, Switzerland. The surge in anti-obesity drug development has been made possible by the blockbuster success of semaglutide and its rival drug tirzepatide — sold as Zepbound or Mounjaro. These drugs have unlocked the potential for a global market that is projected to surpass US$100 billion by the end of the decade. © 2025 Springer Nature Limited

Keyword: Obesity
Link ID: 29674 - Posted: 02.15.2025

By Giorgia Guglielmi Amid the rising buzz around Ozempic and similar weight-loss drugs, a group of 58 researchers is challenging the way obesity is defined and diagnosed, arguing that current methods fail to capture the complexity of the condition. They offer a more nuanced approach. The group’s revised definition, published in The Lancet Diabetes & Endocrinology1 on 14 January, focuses on how excess body fat, a measure called adiposity, affects the body, rather than relying only on body mass index (BMI), which links a person’s weight to their height. They propose two categories: preclinical obesity, when a person has extra body fat but their organs work normally, and clinical obesity, when excess fat harms the body’s organs and tissues. This shift could improve clinical care, public-health policies and societal attitudes toward obesity, says Elisabeth van Rossum, an endocrinologist at the Erasmus University Medical Center Rotterdam in the Netherlands. “Now the idea is, eat less, move more, and you’ll lose weight,” says van Rossum, who wasn’t involved in the work. Although a healthy lifestyle is important, she adds, “if it would be so simple, we wouldn’t have an epidemic, and this paper is an excellent contribution to the discussion about the complexity of obesity”. Global problem More than 1 billion people worldwide live with obesity, and the condition is linked to about 5 million deaths every year2 from disorders such as diabetes and cardiovascular disease. Because it is easy to measure and compare, BMI has long been used as a tool to diagnose obesity. But it doesn’t offer a full picture of a person’s health, because it doesn’t account for differences in body composition, such as muscle versus fat. © 2025 Springer Nature Limited

Keyword: Obesity
Link ID: 29629 - Posted: 01.15.2025

By Mitch Leslie It’s a dismaying thought during a holiday season full of cookies and big meals, but severely restricting calories consumed is one of the best supported strategies for a healthier, longer life. Slicing food consumption stretches the lives of animals in lab experiments, and similar deprivation seems to improve health in people, although almost no one can sustain such a calorie-depleted diet for long. Now, researchers in China studying animals on lean rations have identified a molecule made by gut bacteria that delivers some of the same benefits. When given on its own, the molecule makes flies and worms live longer and refurbishes age-weakened muscles in mice, all without leaving the animals hungry. Although the molecule’s effects in people remain unclear, the discovery is “a really important step forward,” says gerontologist Richard Miller of the University of Michigan, who wasn’t connected to the research. The work, reported in two studies today in Nature, “is very thorough.” Research over the past 90 years has shown that calorie restriction—which to scientists typically means a diet with between 10% and 50% fewer calories than normal—can extend longevity in organisms as diverse as yeast, nematodes, and mice. One experiment also found an effect in monkeys. Trials to test whether calorie restriction increases human life span would take too long, but participants in the 2-year CALERIE trial, which ran from 2007 to 2010 and aimed to cut calorie intake by 25%, enjoyed a slew of improvements, including lower levels of low-density lipoprotein cholesterol, increased sensitivity to insulin, and a 10% reduction in weight. However, the trial also illustrates what makes calorie restriction so challenging: Participants on average cut their caloric intake by only half the experiment’s goal. So, scientists have been hunting for molecules that trigger health-promoting, longevity-stretching effects without privation. To identify new candidates, molecular biologist and biochemist Sheng-Cai Lin of Xiamen University and colleagues took a systematic approach, analyzing the levels of more than 1200 metabolic molecules in blood samples from calorically restricted mice and from counterparts with no dietary limits. They discovered that just over 200 molecules became more abundant when food was in short supply.

Keyword: Obesity
Link ID: 29607 - Posted: 12.21.2024

By Calli McMurray A strong, long-lasting sensory stimulus—be it visual, auditory, olfactory or tactile—triggers plasticity in the neurons that respond to it. But as a scientist long interested in temperature, Jan Siemens wondered: Does the same principle apply to prolonged heat? In mammals, the body changes when temperatures soar—blood vessels dilate, heat-generating brown adipose tissue shuts off, the heart rate lowers, locomotion slows—but it wasn’t clear if the brain played a role in these changes, or even changed itself, says Siemens, professor of pharmacology at the University of Heidelberg. Siemens and his team started a search for heat-induced neuronal plasticity in the ventromedial preoptic area of the hypothalamus (VMPO) in mice. They chose the region because of its involvement in regulating body temperature and generating fever; neurons there receive temperature information downstream from cells innervating the skin, whereas others are themselves warm-sensitive. They identified cells to target by measuring the expression of c-FOS, a gene that is activated by neuronal activity, after housing the mice at 36 degrees Celsius for up to eight hours. At first, however, their investigative trail went cold. In brain slices, those warm-responding cells showed only slight and inconsistent changes in synaptic plasticity. “That was actually quite humbling and disappointing,” Siemens says. But then they made a “serendipitous observation,” he says: A subgroup of neurons expressing the leptin receptor became almost constantly active after four weeks of heat acclimation. The firing was so synchronized and regular that Wojciech Ambroziak, a postdoctoral scholar in the lab at the time, described it as “soldiers marching in a line,” Siemens recalls. © 2024 Simons Foundation

Keyword: Obesity
Link ID: 29602 - Posted: 12.14.2024

Jon Hamilton Not all brain cells are found in the brain. For example, a team at Caltech has identified two distinct types of neurons in the abdomens of mice that appear to control different aspects of digestion. The finding, reported in the journal Nature, helps explain how clusters of neurons in the body play a key role in the gut-brain connection, a complex two-way communication system between the brain and digestive system. It also adds to the evidence that neurons in the body can take on specialized functions, "just like in the brain," says Yuki Oka, an author of the study. "The peripheral nervous system is smart," says Frank Duca of the University of Arizona, who was not involved in the study. "You have specific neurons within this system that are performing a wide variety of functions, either with the brain's help or sometimes even without the brain's input," he says. The study focused on a subset of the peripheral nervous system called the sympathetic nervous system, which becomes active when the brain detects danger. "Your adrenaline goes up and your glucose level in the blood is really high because you need to fight or flight," Oka says. At the same time, the sympathetic nervous system dials back functions that are less urgent, like digestion and moving food through the gut. © 2024 npr

Keyword: Obesity
Link ID: 29601 - Posted: 12.14.2024