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New obesity definition sidelines BMI to focus on health

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

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 29629 - Posted: 01.15.2025

Restricting calories may extend life. Can this molecule do it without the hunger pangs?

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.

To beat the heat, hypothalamus neurons in mice ramp up their firing

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

These neurons in the abdomen help form the gut-brain connection

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

Fasting can reduce weight — but also hair growth

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

Are Weight-Loss Drugs Contributing to a Fall in the Obesity Rate?

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.

Fish Have a Brain Microbiome. Could Humans Have One Too?

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

Novel neurons upend ‘yin-yang’ model of hunger, satiety in brain

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

Obesity Drugs Would Be Covered by Medicare and Medicaid Under Biden Proposal

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

Ozempic Could Crush the Junk Food Industry. But It Is Fighting Back.

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

Fat ‘remembering’ past obesity drives yo-yo diet effect

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

Limiting sugar in infancy reduces the risk of diabetes and hypertension

By Skyler Ware The occasional sweet treat likely won’t ruin your health. But too much added sugar at a young age could increase the risk of health complications later in life. Limiting added sugars during the first 1,000 days after conception — so during pregnancy and a baby’s first two years — reduces the risk of a child developing diabetes and hypertension in adulthood, researchers report October 31 in Science. “In the first 1,000 days of life, the brain and body are gearing up to finish developing,” says Sue-Ellen Anderson-Haynes, a registered dietician in Boston and a spokesperson for the Academy of Nutrition and Dietetics. Nutrition during that timeframe is particularly important, she says, because “everything the mother eats gets transformed into nutrients for the fetus.” Current nutritional guidelines recommend that adults consume less than 40 grams of added sugars per day and that children under age 2 consume no added sugars. But by age 2, the average American child consumes about 29 grams of added sugars a day; the average adult consumes nearly 80 grams per day. To study the effects of excess added sugars early in life, economist Tadeja Gracner of the University of Southern California in Los Angeles and colleagues took advantage of a natural experiment: the end of sugar rationing in the United Kingdom after World War II. While rationing was in effect, each person was allotted about 8 ounces (about 227 grams) of sugar per week. Once sugar rationing ended in September 1953, daily sugar consumption for adults jumped to around 80 grams per day. Even though other foods were rationed during and after WWII, sugar intake increased the most after rationing was lifted. Consumption of other rationed foods, such as cheese, milk and fresh fruits remained relatively constant once rationing ended. Similarly, the end of butter rationing caused many families to switch from margarine, with its unsaturated fats, back to butter, so overall fat consumption did not increase significantly. © Society for Science & the Public 2000–2024

‘Poo milkshake’ boosts the microbiome of c-section babies

By Mariana Lenharo Feeding a baby born by caesarean section milk containing a tiny bit of their mother’s poo introduces beneficial microbes to their gut, according to a clinical trial. The approach might one day help to prevent diseases during childhood and later in life. The study — which reported early results last week during IDWeek, a meeting of infectious-disease specialists and epidemiologists in Los Angeles, California — is the first randomized controlled trial to test the ‘poo milkshake’ concept. The preliminary findings confirm researchers’ hypothesis that a small faecal-matter transplant is enough to have a positive effect on the infant’s microbiome, says Otto Helve, director of the public-health department at the Finnish Institute for Health and Welfare in Helsinki, Finland, and the study’s primary investigator. Inherited microbes Some studies show that babies born by c-section, rather than vaginal birth, have a higher risk of asthma, inflammation of the digestive system and other diseases associated with a dysfunctional immune system1. Scientists think that these differences arise because babies born by c-section aren’t exposed to and rapidly colonized by the microbes in their mothers’ vaginas and guts. Studies have even shown that c-section babies are more vulnerable to pathogens in hospitals than are babies born by vaginal birth2. Experiments have attempted to compensate for that by swabbing babies born by c-section with microbes from their mother’s vagina or giving them these microbes orally, a practice known as ‘vaginal seeding’. But this technique has had limited success, because vaginal microbes, scientists have learnt, cannot effectively colonize infants’ guts, says Yan Shao, a microbiome scientist at the Wellcome Sanger Institute in Hinxton, UK. © 2024 Springer Nature Limited

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory and Learning
Link ID: 29525 - Posted: 10.26.2024

Eating less can lead to a longer life: massive study in mice shows why

By Elie Dolgin Cutting calorie intake can lead to a leaner body — and a longer life, an effect often chalked up to the weight loss and metabolic changes caused by consuming less food. Now, one of the biggest studies1 of dietary restrictions ever conducted in laboratory animals challenges the conventional wisdom about how dietary restriction boosts longevity. The study, involving nearly 1,000 mice fed low-calorie diets or subjected to regular bouts of fasting, found that such regimens do indeed cause weight loss and related metabolic changes. But other factors — including immune health, genetics and physiological indicators of resiliency — seem to better explain the link between cutting calories and increased lifespan. “The metabolic changes are important,” says Gary Churchill, a mouse geneticist at the Jackson Laboratory in Bar Harbor, Maine, who co-led the study. “But they don’t lead to lifespan extension.” To outside investigators, the results drive home the intricate and individualized nature of the body’s reaction to caloric restriction. “It’s revelatory about the complexity of this intervention,” says James Nelson, a biogerontologist at the University of Texas Health Science Center in San Antonio. The study was published today in Nature by Churchill and his co-authors, including scientists at Calico Life Sciences in South San Francisco, California, the anti-ageing focused biotech company that funded the study. Counting calories Scientists have long known that caloric restriction, a regimen of long-term limits on food intake, lengthens lifespan in laboratory animals2. Some studies3,4 have shown that intermittent fasting, which involves short bouts of food deprivation, can also increase longevity. © 2024 Springer Nature Limited

Should I stay (and eat) or should I go? How the brain balances hunger with competing drives

By Giorgia Guglielmi As the famed tale “Hansel and Gretel” makes clear, hunger can change behavior. The two lost and starving siblings give in to the temptation of a gingerbread cottage and ignore the danger lurking within—a wicked witch who has created the delicious house as a trap. Hunger is such a powerful driver that animals often pursue food at the expense of other survival needs, such as avoiding predators or recovering from injury. Hungry vicuñas, for example, will sometimes increase their risk of predation by pumas to get something to eat, behavioral ecologists have shown. Scientists know many of the key cells and circuits behind these competing drives—such as the hypothalamic “hunger neurons” that regulate food intake. But how the brain juggles the need to eat amidst other urges has remained mysterious, says Henning Fenselau, who leads the Synaptic Transmission in Energy Homeostasis group at the Max Planck Institute for Metabolism Research in Köln, Germany. “This is still a huge question [in neuroscience],” he says. In recent years, however, new clues about where and how hunger collides with rival motivations have come from technology to manipulate and monitor individual neurons across multiple brain regions at once. Those findings suggest that hunger neuron activity can override some brain signals, such as fear and pain. Exploring the brain’s ability to handle multiple needs simultaneously may offer insights into decision-making, anxiety and other neuropsychiatric conditions—helping to explain why people sometimes make maladaptive choices, says Nicholas Betley, associate professor of biology at the University of Pennsylvania. © 2024 Simons Foundation

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Higher Cognition
Link ID: 29515 - Posted: 10.12.2024

Why do obesity drugs seem to treat so many other ailments?

By Mariana Lenharo There’s a bar in Baltimore, Maryland, that very few people get to enter. It has a cocktail station, beer taps and shelves stacked with spirits. But only scientists or drug-trial volunteers ever visit, because this bar is actually a research laboratory. Here, in a small room at the US National Institutes of Health (NIH), scientists are harnessing the taproom ambience to study whether blockbuster anti-obesity drugs might also curb alcohol cravings. Evidence is mounting that they could. Animal studies and analyses of electronic health records suggest that the latest wave of weight-loss drugs — known as glucagon-like peptide 1 (GLP-1) receptor agonists — cut many kinds of craving or addiction, from alcohol to tobacco use. “We need randomized clinical trials as the next step,” says Lorenzo Leggio, an addiction researcher at the NIH in Baltimore. In the trial he is leading, volunteers sit at the bar and get to see, smell and hold their favourite drinks, while going through tests such as questions about their cravings; separately, participants will have their brains scanned while looking at pictures of alcohol. Some will be given the weight-loss drug semaglutide (marketed as Wegovy) and others will get a placebo. George Koob and Lorenzo Leggio pose for a photograph in a research laboratory designed as a bar inside the National Institutes of Health’s hospital. Curbing addiction isn’t the only potential extra benefit of GLP-1 drugs. Other studies have suggested they can reduce the risk of death, strokes and heart attacks for people with cardiovascular disease1 or chronic kidney ailments2, ease sleep apnoea symptoms3 and even slow the development of Parkinson’s disease4. There are now hundreds of clinical trials testing the drugs for these conditions and others as varied as fatty liver disease, Alzheimer’s disease, cognitive dysfunction and HIV complications (see ‘Diseases that obesity drugs might treat’ at the end of this article). © 2024 Springer Nature Limited

Brain goop that traps hunger neurons drives obesity

By Max Kozlov A build-up of sticky goo that traps neurons in an appetite-control centre in the brain has been implicated in worsening diabetes and obesity, according to research on mice1. The goo also prevents insulin from reaching brain neurons that control hunger. Inhibiting production of the goo led mice to lose weight, experiments found. These findings points to a new driver of metabolic disorders and could help scientists to identify targets for drugs to treat these conditions. These results were published today in Nature. Metabolic diseases such as type 2 diabetes and obesity can develop when the body’s cells become insensitive to insulin, a hormone that regulates blood-sugar levels. Scientists searching for the mechanism that causes this insulin resistance have homed in on a part of the brain called the arcuate nucleus of the hypothalamus, which senses insulin levels and, in response, adjusts energy expenditure and sensations of hunger. As the animals develop insulin resistance, a type of cellular scaffolding, called the extracellular matrix, that holds the hunger neurons in place becomes a disorganized goo. Previously, researchers had noticed that this scaffolding changes when mice are fed a high-fat diet2. The researchers wanted to see whether these brain changes might drive insulin resistance rather than merely developing alongside it. The authors fed mice a high-fat, high-sugar diet for 12 weeks and monitored the scaffolding around the hunger neurons by taking tissue samples and monitoring gene activity. © 2024 Springer Nature Limited

Research That Led to Obesity Drugs Wins Major Medical Prize

By Gina Kolata and Stephanie Nolen The Lasker Awards, a prestigious set of prizes given for advances in medicine and public health research, were given on Thursday to scientists whose research helped lead to the discovery of a new class of obesity drugs, infectious disease specialists who worked on the drivers of H.I.V. infection and how to stop it, and a scientist who discovered a way the body protects itself from infectious diseases and cancer. The Laskers are highly regarded in the fields of biomedicine and are sometimes seen as foretelling recipients of the Nobel Prizes in the sciences. This year’s Lasker-DeBakey Clinical Medical Research Award went to three scientists for their work on GLP-1, the hormone that led to drugs like Wegovy (the same compound is the basis for Ozempic), which have transformed the treatment of obesity. They are Dr. Joel Habener, Svetlana Mojsov and Lotte Bjerre Knudsen. Each of the three honorees played a role at a key moment: finding the new hormone; finding the biologically active shorter form of GLP-1; and, finally, showing that the shorter form elicits weight loss. Of course, as almost always happens in science, many others also played key roles, and the Lasker Foundation mentioned some as part of its citation. And one of the honorees, Dr. Mojsov, is receiving what many deem a long overdue recognition. The story of GLP-1 begins with Dr. Habener, an endocrinologist who arrived in the mid-1970s at Massachusetts General Hospital, where he decided to work on diabetes. Most of the focus had been on insulin, which lowers blood sugar levels. But there is another hormone, glucagon, that raises it. Dr. Habener decided to try to find the gene for glucagon, hoping it would lead to a way to squelch the hormone and so lower blood sugar. Working with anglerfish, he discovered a gene for another mysterious protein that resembles glucagon. © 2024 The New York Times Company

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 29488 - Posted: 09.21.2024

Inflammation May Be the Root of Our Maladies

By Daniela J. Lamas In the near future, the story of drugs like Ozempic may no longer be primarily about weight loss and diabetes. We now know that these drugs can reduce heart and kidney disease. They could very well slow the progression of dementia. They might help women struggling with infertility to get pregnant. They are even tied to lower mortality from Covid. It’s easy to attribute this to the dramatic weight loss provided by Ozempic and other drugs in its class, known as GLP-1 receptor agonists. But that isn’t the whole story. Rather, the drugs’ numerous benefits are pointing to an emerging cause of so much human disease: inflammation. As a critical care doctor, I have long considered inflammation a necessary evil, the mechanism through which our bodies sound an alarm and protect us from threat. But a growing body of research complicates that understanding. Inflammation is not just a marker of underlying disease but also a driver of it. The more medicine learns about inflammation, the more we are learning about heart disease and memory loss. This should serve as a reminder of the delicate balance that exists in our bodies, of the fact that the same system that protects us can also cause harm. Inflammation is the body’s response to infection or injury. Our innate immune system — the body’s first line of defense against bacterial or viral intruders — protects us by triggering an inflammatory response, a surge of proteins and hormones that fight infection and promote healing. Without that response, we would die of infectious disease in childhood. But by the time we make it to our 50s and beyond, our innate immune system can become more of a hindrance as inflammation begins to take a toll on the body. Acute inflammation, which happens in response to an illness, for instance, is often something we can see — an infected joint is swollen and red. But chronic inflammation is usually silent. Like high blood pressure, it’s an invisible foe. Sign up for the Opinion Today newsletter Get expert analysis of the news and a guide to the big ideas shaping the world every weekday morning. Get it sent to your inbox. © 2024 The New York Times Company

Should young kids take the new anti-obesity drugs? What the research says

By Julian Nowogrodzki Millions of adults around the world take potent drugs such as Wegovy to shed pounds. Should kids do the same? That question is growing more urgent in the face of mounting evidence that children and adolescents, as well as adults, slim down if they take the latest generation of obesity drugs. Clinical trials1,2 have shown that many adolescents with obesity lose substantial amounts of weight on these drugs, which work by mimicking a natural hormone called glucagon-like peptide 1 (GLP-1). The GLP-1 mimics semaglutide, commonly sold as Ozempic and Wegovy, and liraglutide, marketed as Saxenda and Victoza, are approved in the United States and Europe to treat obesity in children as young as 12. Now a trial has produced some of the first data on anti-obesity drugs in even younger children: those aged 6 to 11. The study3 reports that children who were treated with liraglutide showed a decrease in their body mass index (BMI), a measure of obesity. The results were published on 10 September in The New England Journal of Medicine. Nature asked specialists in obesity about the costs and benefits of giving the GLP-1 mimics to youngsters who are still growing and developing. Why test powerful weight-loss drugs on kids? Most kids with obesity become teens with obesity and then adults with obesity. Many young children with severe obesity have “already developed significant health issues”, says physician Sarah Ro, who directs the University of North Carolina Physicians Network Weight Management Program and has served as a consultant to Novo Nordisk, the manufacturer of semaglutide. Her clinic in Hillsborough treats children with severe obesity who have health issues such as high blood pressure, type 2 diabetes or an advanced form of liver disease linked to excess weight. © 2024 Springer Nature Limited

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