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

By Max Kozlov A popular weight-loss regimen stunts hair growth, data collected from mice and humans suggest1. The study’s findings show that intermittent fasting, which involves short bouts of food deprivation, triggers a stress response that can inhibit or even kill hair-follicle stem cells, which give rise to hair. The results, published in today in Cell, suggest that although short-term fasting can provide health benefits, such as increased lifespan in mice, not all tissue and cell types benefit. “I was shocked to hear these results,” says Ömer Yilmaz, a stem-cell biologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the study. “We’ve come to expect that fasting is going to be beneficial for most, if not all cell types and good for stem cells. This is the inverse of what we expected, and the finding seems to hold true in humans.” Deliberate deprivation During the past decade, intermittent fasting has become one of the most popular dieting regimens; by one count, about 12% of adults in the United States practised it in 2023. One of the most common forms is time-restricted eating, which involves eating only within a limited time frame each day. Stem cells seem to be particularly vulnerable to changes in diet. For example, Yilmaz and his colleagues reported2 in August that stem cells in the guts of mice showed a burst of activity during post-fast feasting. This activity helped to repair damage in the animals’ intestines. To learn whether dieting affects hair regrowth, which can be affected by stress, Bing Zhang, a regenerative biologist at Westlake University in Zhejiang, China, and his colleagues shaved mice and subjected them to one of two intermittent-fasting regimens: time-restricted eating and alternate-day fasting, in which animals fasted for 24 hours and then ate their normal diet for the following 24 hours. By the end of the three-month study, the dieting mice had not regrown as much hair as control animals that ate a similar number of calories, the authors found. © 2024 Springer Nature Limited

Keyword: Obesity
Link ID: 29600 - Posted: 12.14.2024

By Joshua Cohen Earlier this fall, the Centers for Disease Control and Prevention reported data showing that adult obesity rates — long trending upwards — had fallen modestly over the past few years, from 41.9 to 40.3 percent. The decline sparked discussion on social media and in major news outlets about whether the U.S. has passed so-called “peak obesity” — and whether the growing use of certain weight-loss drugs might account for the shift. An opinion piece in the Financial Times suggested that the public health world might look back on the current moment in much the same way that it now reflects on 1963, when cigarette sales hit their high point and then dropped dramatically over the following decades. The article’s author, John Burn-Murdoch, speculated that the dip is “highly likely” to be caused by the use of glucagon-like peptide-1 receptor agonists, or GLP-1s, for weight loss. It’s easy to see why one might make that connection. Although GLP-1s have been used for nearly two decades in the treatment of type 2 diabetes, their use for obesity only took off more recently. In 2014, the Food and Drug Administration approved a GLP-1 agonist named Saxenda specifically for this purpose. Then in the late 2010s, a GLP-1 drug named Ozempic, made from the active ingredient semaglutide, began to be used off-label. The FDA also authorized Wegovy, another semaglutide-based GLP-1 medication, explicitly for weight loss in 2021. Still, it is premature to declare that GLP-1s have caused overall declining obesity rates in the U.S. There are a number of ways to interpret the CDC data, and not all of them suggest that obesity rates have actually fallen. Further, recent evidence indicates that GLP-1s might not be as effective for weight loss as initially thought. And there are reasons to question the comparison to cigarette sales. Taken together, all of this suggests that we may need to wait to understand how this new class of drugs affects weight loss at the population level.

Keyword: Obesity
Link ID: 29594 - Posted: 12.11.2024

By Shane O’Neill In 2018, Matt Christensen kicked heroin by replacing drugs with drinking. When he stopped drinking in 2022, he turned to food. He put on 95 pounds. His doctor recommended he try Wegovy, part of a class of drugs known as GLP-1 receptor agonists, to help him lose weight. Eventually he switched to a different drug called Zepbound, which targets both GLP-1 and GIP agonists. The drugs worked. Get concise answers to your questions. Try Ask The Post AI. But a funny thing happened on his weight-loss journey: His cravings for food had diminished but so had his cravings for drugs and alcohol. Christensen, 42, started drinking at age 9 and using heroin at 17. For decades, catching a cold meant reaching for a hot toddy. Work stress meant numbing out with Xanax. Even passing through certain neighborhoods in Chicago where he used to buy drugs would lead to cravings. But after he started taking GLP-1 agonists, those triggers became, well, less triggering. “It was the weirdest thing,” he said. “It was just quiet. I just found it really easy all of a sudden.” More than that, Christensen noticed that an unease he had always felt in his body — a discomfort he perpetually tried to quell with fidgeting, food or drugs — was diminishing. “That’s a feeling that I’ve had my entire life,” he said. “Taking these drugs has toned that down. “There’s no silver bullet for addiction or mental illness, but for me, in concert with the other treatments, it has been an absolute game changer,” he said. Matt Christensen says weight-loss drugs like Ozempic and Zepbound have been “an absolute game changer” when it comes to his addiction struggles.

Keyword: Drug Abuse; Obesity
Link ID: 29589 - Posted: 12.07.2024

By Yasemin Saplakoglu Bacteria are in, around and all over us. They thrive in almost every corner of the planet, from deep-sea hydrothermal vents to high up in the clouds, to the crevices of your ears, mouth, nose and gut. But scientists have long assumed that bacteria can’t survive in the human brain. The powerful blood-brain barrier, the thinking goes, keeps the organ mostly free from outside invaders. But are we sure that a healthy human brain doesn’t have a microbiome of its own? Over the last decade, initial studies have presented conflicting evidence. The idea has remained controversial, given the difficulty of obtaining healthy, uncontaminated human brain tissue that could be used to study possible microbial inhabitants. Recently, a study published in Science Advances provided the strongest evidence yet (opens a new tab) that a brain microbiome can and does exist in healthy vertebrates — fish, specifically. Researchers at the University of New Mexico discovered communities of bacteria thriving in salmon and trout brains. Many of the microbial species have special adaptations that allow them to survive in brain tissue, as well as techniques to cross the protective blood-brain barrier. Matthew Olm (opens a new tab), a physiologist who studies the human microbiome at the University of Colorado, Boulder and was not involved with the study, is “inherently skeptical” of the idea that populations of microbes could live in the brain, he said. But he found the new research convincing. “This is concrete evidence that brain microbiomes do exist in vertebrates,” he said. “And so the idea that humans have a brain microbiome is not outlandish.” While fish physiology is, in many ways, similar to humans’, there are some key differences. Still, “it certainly puts another weight on the scale to think about whether this is relevant to mammals and us,” said Christopher Link (opens a new tab), who studies the molecular basis of neurodegenerative disease at the University of Colorado, Boulder and was also not involved in the work. © 2024 Simons Foundation

Keyword: Obesity; Brain imaging
Link ID: 29588 - Posted: 12.04.2024

Amy Fleming Nine years ago, Nikki Schultek, an active and healthy woman in her early 30s, experienced a sudden cascade of debilitating and agonising symptoms – including cognitive and breathing problems and heart arrhythmia – and was investigated for multiple sclerosis. But three brain scans and numerous X-rays later, there was still no diagnosis or treatment plan. “It was like living in a nightmare, imagining not watching my children – three and five years old – grow up,” says Schultek. Now, speaking on a video call from North Carolina, she is as bright as a button and shows no signs of degenerative brain disease. It turned out she had multiple chronic infections, including Borrelia burgdorferi bacteria, which causes Lyme disease and which had stealthily reached her brain. Antibiotics restored her health, but B burgdorferi is hard to eradicate once in the brain. She may need maintenance treatment to keep the disease at bay. Schultek is not the only person whose neurological disorder turned out to be caused by microbes in the brain. A recent paper she jointly lead-authored, published in Alzheimer’s and Dementia, compiled a long list of case reports where infectious disease was discovered to be the primary cause of dementia, meaning that, in many cases, the dementia was reversible. A few of the patients died, but most survived and saw significant improvements in cognitive function, including a man in his 70s who had been diagnosed with Alzheimer’s disease after his swift cognitive decline saw him unable to drive or, eventually, leave the house alone. A sample of his cerebrospinal fluid was taken and revealed a fungal infection caused by Cryptococcus neoformans. Within two years of taking antifungal medication, he was driving again and back at work as a gardener. Richard Lathe, a professor of infectious medicine at the University of Edinburgh and another lead author of the paper, says these patients “were by accident found to be suffering from various fungal, bacterial or viral infections, and when they treated the patient with antifungals, antivirals or antibiotics, the dementia went away”. He, among others, has been investigating the possibility that, like the gut, the brain hosts a community of microbes – an area of largely scientifically uncharted waters, but with huge life-saving potential. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Obesity
Link ID: 29587 - Posted: 12.04.2024

By Giorgia Guglielmi For years, scientists have thought of hunger regulation as a tug-of-war between two types of neurons in the hypothalamus: those that express the AGRP gene and increase hunger, and those that express the POMC gene and act as a brake. Now a new study challenges this long-standing model, revealing a third player in the hunger-satiety network—a neuron type that expresses the BNC2 gene and suppresses hunger faster than those that express POMC. These BNC2 neurons are activated by leptin—a hormone that helps suppress appetite and boost metabolism. Their discovery “reshapes our understanding of feeding behavior,” says lead investigator Han Tan, “and how leptin regulates body weight.” Tan is a research associate in Jeffrey Friedman’s lab at Rockefeller University. “We’ve known for a long time there must be [other] neurons in the brain that are sensing leptin and decreasing appetite, but we didn’t know who they were until now,” says John Campbell, assistant professor of biology at the University of Virginia, who wasn’t involved in the study. The results jibe with two other recent reports of leptin-sensitive neurons in the arcuate nucleus—a region in the hypothalamus that processes signals related to hunger and satiety. The neurons generate feelings of fullness, an independent team reported in Science in June, and they dampen appetite by inhibiting AGRP-expressing “hunger neurons,” according to a preprint Campbell and his colleagues posted on bioRxiv in July. The studies all point to a unique group of neurons that inhibit hunger, says Martin Myers, professor of internal medicine and molecular and integrative physiology at the University of Michigan, who was not involved in the work. “The three groups essentially found [these neurons] simultaneously.” © 2024 Simons Foundation

Keyword: Obesity
Link ID: 29584 - Posted: 12.04.2024

By Margot Sanger-Katz The Biden administration, in one of its last major policy directives, proposed on Tuesday that Medicare and Medicaid cover obesity medications, a costly and probably popular move that the Trump administration would need to endorse to become official. The proposal would extend access of the drugs to millions of Americans who aren’t covered now. The new obesity drugs, including Wegovy from Novo Nordisk and Zepbound from Eli Lilly, have been shown to improve health in numerous ways, but legislation passed 20 years ago prevents Medicare from covering drugs for “weight loss.” The new proposal sidesteps that restriction, specifying that the drugs would be covered to treat the disease of obesity and prevent its related conditions. “We don’t want to see people having to wait until they have these additional diseases before they get treatment,” said Chiquita Brooks-LaSure, the administrator of the Centers for Medicare and Medicaid Services, or C.M.S., noting the growing medical consensus that obesity is a chronic health condition. The classification would also mean that every state Medicaid program would be required to cover the drugs. Currently, only a handful do. C.M.S. estimates that around 3.4 million more patients in Medicare would become eligible for obesity drugs, and around four million patients in Medicaid would gain coverage, costing the programs billions of dollars. Medicare mostly covers Americans 65 and older; Medicaid mostly covers poor and disabled Americans. The proposal is part of an annual policy update for all Medicare drug plans and private Medicare Advantage plans starting in 2026. In a conference call with reporters Tuesday, Daniel Tsai, the top Medicaid official, said Medicaid coverage could start sooner than 2026. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29580 - Posted: 11.30.2024

By Tomas Weber Trinian Taylor, a 52-year-old car dealer, pushed his cart through the aisles of a supermarket as I pretended not to follow him. It was a bright August day in Northern California, and I had come to the store to meet Emily Auerbach, a relationship manager at Mattson, a food-innovation firm that creates products for the country’s largest food and beverage companies: McDonald’s and White Castle, PepsiCo and Hostess. Auerbach was trying to understand the shopping behavior of Ozempic users, and Taylor was one of her case studies. She instructed me to stay as close as I could without influencing his route around the store. In her experience of shop-alongs, too much space, or taking photos, would be a red flag for the supermarket higher-ups, who might figure out we were not here to shop. “They’d be like, ‘You need to exit,’” she said. Auerbach watched in silence as Taylor, who was earning $150 in exchange for being tailed, propelled his cart through snack aisles scattered with products from Mattson’s clients. He took us straight past the Doritos and the Hostess HoHos, without a side glance at the Oreos or the Cheetos. We rushed past the Pop-Tarts and the Hershey’s Kisses, the Lucky Charms and the Lay’s — they all barely registered. Clumsily, close on his heels, Auerbach and I stumbled right into what has become, under the influence of the revolutionary new diet drug, Taylor’s happy place: the produce section. He inspected the goods. “I’m on all of these,” he told us. “I eat a lot of pineapple. A lot of pineapple, cucumber, ginger. Oh, a lot of ginger.” Taylor, who lives in Hayward, Calif., used to nurse a sugar addiction, he said, but he can no longer stomach Hostess treats. A few days earlier, his daughter fed him some candy. “I just couldn’t,” he said. “It was so sweet it choked me.” His midnight snack used to be cereal, but now he stirs at night with strange urges. Salads. Chicken. He has sworn off canned sodas and fruit juices and infuses his water with lemon and cucumber. He dropped a heavy bag of lemons into the cart and sauntered over to the leafy vegetables. “I love Swiss chard,” he said. “I eat a lot of kale.” For decades, Big Food has been marketing products to people who can’t stop eating, and now, suddenly, they can. The active ingredient in Ozempic, as in Wegovy, Zepbound and several other similar new drugs, mimics a natural hormone, called glucagon-like peptide-1 (GLP-1), that slows digestion and signals fullness to the brain. Around seven million Americans now take a GLP-1 drug, and Morgan Stanley estimates that by 2035 the number of U.S. users could expand to 24 million. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29569 - Posted: 11.20.2024

Ian Sample Science editor Losing weight can be a frustrating game: after months of successful slimming, the kilos may soon pile on again, leaving people back where they started. No one factor drives the yo-yo effect, but new research points to fatty tissue as a leading culprit. Fat “remembers” past obesity and resists attempts to lose weight, scientists found. Researchers identified the biological memory after examining fat tissue from people with obesity before and after they lost weight after bariatric surgery. The tissues were further compared with fat from healthy individuals who had never been obese. The analysis showed that fat cells were affected by obesity in a way that altered how they responded to food, potentially for years. In tests, the cells grew faster than others by absorbing nutrients more swiftly. Prof Ferdinand von Meyenn, a senior author on the study at the Federal Institute of Technology in Zurich, said: “Our study indicates that one reason maintaining body weight after initial weight loss is difficult is that the fat cells remember their prior obese state and likely aim to return to this state. “The memory seems to prepare cells to respond quicker, and maybe also in unhealthy ways, to sugars or fatty acids.” Further work on mouse cells traced the biological memory to chemical modifications on DNA or the proteins DNA is wrapped around. These epigenetic changes alter gene activity and metabolism. Writing in Nature, the scientists describe how formerly obese mice gained weight faster than others when put on a high-fat diet, suggesting a shift in metabolism that made it easier for them to gain weight. The memory of obesity in fat cells was not solely to blame, however. The scientists suspect a similar memory exists in brain cells that affects how much food animals consume and how much energy they expend. © 2024 Guardian News & Media Limited

Keyword: Obesity
Link ID: 29568 - Posted: 11.20.2024