By Gina Kolata People with obesity now have a choice between two powerful drugs to help them lose weight. One is semaglutide, sold by Novo Nordisk as Wegovy for obesity treatment and as Ozempic for diabetes. The second, tirzepatide, is sold by Eli Lilly as Zepbound for obesity and as Mounjaro for diabetes. Many with neither obesity or diabetes take the drugs to get thinner. A recent study suggested that people lost more weight taking Mounjaro than they did taking Ozempic, and it may leave you wondering: Which should I take? And if I’m already taking one of them, should I switch? The answers, obesity medicine experts say, are not so simple. Here are some factors that can help sort out hype from realistic hope. Is one weight loss drug really better than the other? For now, it’s hard to say. All of the information available comes from “highly flawed studies,” said Dr. Diana Thiara, medical director of the weight loss clinic at the University of California, San Francisco. That includes the recent study comparing Mounjaro and Ozempic. Using electronic health records, the researchers reported that those taking Mounjaro lost an average of 15.3 percent of their weight after a year. Those taking Ozempic lost an average of 8.3 percent. While that sounds impressive, Dr. Susan Z. Yanovski, co-director of the Office of Obesity Research at the National Institute of Diabetes and Digestive and Kidney Diseases, said, “I wouldn’t make any decisions on my medical care based solely on a study like this.” There’s an inherent difficulty in using electronic health records, she noted, because it is not known why the patients were taking the drugs — the study was underway before Zepbound was approved for treating obesity. The investigators looked at prescriptions for Ozempic and Mounjaro, which were approved to treat diabetes. Yet many in the study did not have diabetes. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29402 - Posted: 07.23.2024

By Mitch Leslie Millions of people have taken glucagon-like peptide-1 (GLP-1) agonist drugs such as Ozempic to lose weight, despite the fact that the drugs can cause severe nausea and vomiting. But a new mouse study shows distinct groups of neurons in the brain diminish appetite and trigger nausea, a finding that could lead to less stomach-turning treatments that activate one set of cells and not the other. “It’s a very solid paper,” says neuroscientist Chuchu Zhang of the University of California, Los Angeles, who wasn’t connected to the study. “It shows us something new” about the activity of GLP-1 agonists. Scientists haven’t pinned down exactly how GLP-1 agonist drugs work, and previous studies have produced conflicting results on where they exert their effects. Some research suggests the drugs curb appetite by targeting the hypothalamus, a control center for physiological functions such as thirst and hunger that is located in the center of the brain. Other findings point to the rear portion of the brain, known as the hindbrain, and still others implicate the vagus nerve, which carries messages to and from organs such as the stomach and heart. All of these locations contain cells bearing GLP-1 receptors, to which the drugs bind. Another key question is whether the drugs cause weight loss primarily because people feel full or because they feel nauseated—a side effect suffered by more than half of individuals who take the drugs. “Do we need the nausea and aversion [to food] to see the appetite suppression and weight loss?” asks neuroscientist Amber Alhadeff of the Monell Chemical Senses Center. To answer that question, she and her colleagues first tried to pinpoint where GLP-1 agonists act. Using a genetically modified virus containing genes for either of two cell-killing molecules, they selectively eliminated cells bearing GLP-1 receptors in the hypothalamus, the hindbrain, or the vagus nerve. Only destroying the hindbrain cells prevented weight loss when mice received a GLP-1 agonist, suggesting this region curtails appetite. In a follow-up experiment, the researchers stimulated cells in the hindbrain and found that even slender mice lost weight. © 2024 American Association for the Advancement of Science.

Keyword: Obesity
Link ID: 29390 - Posted: 07.11.2024

By Teddy Rosenbluth The process for diagnosing a child with autism heavily relies on a parent's description of their child’s behavior and a professional’s observations. It leaves plenty of room for human error. Parents’ concerns may skew how they answer questionnaires. Providers may hold biases, leading them to underdiagnose certain groups. Children may show widely varying symptoms, depending on factors like culture and gender. A study published Monday in Nature Microbiology bolsters a growing body of research that suggests an unlikely path to more objective autism diagnoses: the gut microbiome. After analyzing more than 1,600 stool samples from children ages 1 to 13, researchers found several distinct biological “markers” in the samples of autistic children. Unique traces of gut bacteria, fungi, viruses and more could one day be the basis of a diagnostic tool, said Qi Su, a researcher at the Chinese University of Hong Kong and a lead author of the study. A tool based on biomarkers could help professionals diagnose autism sooner, giving children access to treatments that are more effective at a younger age, he said. “Too much is left to questionnaires,” said Sarkis Mazmanian, a microbiome researcher at the California Institute of Technology. “If we can get to something we can measure — whatever it is — that’s a huge improvement.” For decades, researchers have scoured the human genome, medical histories and brain scans for a reliable indicator of A.S.D., with limited success. The Food and Drug Administration has approved two diagnostic tests based on eye-tracking software, which Dr. Su said required significant involvement from a psychiatrist. © 2024 The New York Times Company

Keyword: Autism
Link ID: 29386 - Posted: 07.09.2024

By Lauren J. Young Kimberly Chauche, a corporate secretary in Lincoln, Neb., says she’s always been overweight. When she was as young as five years old, her doctors started trying to figure out why. Since then her life has involved nutritionists and personal trainers, and eventually she sought therapists to treat her compulsive eating and weight-related anxiety. Yet answers never arrived, and solutions never lasted. At 43, Chauche was prescribed a weight-loss medi­cation called Wegovy—one of a new class of drugs that mimic a hormone responsible for insulin pro­duction. She took her first dose in March 2024, in­jecting it into herself with a needle. Within a couple of months she had lost almost 20 pounds, and that felt great. But the weight loss seemed like a bonus com­pared with a startling change in how she reacted to food. She noticed the shift almost immediately: One day her son was eating popcorn, a snack she could never resist, and she walked right past the bowl. “All of a sudden it was like some part of my brain that was always there just went quiet,” she says. Her eating habits improved, and her anxiety eased. “It felt almost surreal to put an injector against my leg and have happen in 48 hours what decades of intervention could not ac­complish,” she says. “If I had lost almost no weight, just to have my brain working the way it’s working, I would stay on this medication forever.” Chauche is hardly alone in her effusive descriptions of how Wegovy vanquished her intrusive thoughts about food—an experience increasingly referred to as the “quieting of food noise.” Researchers—some of whom ushered in the development of these blockbuster drugs—want to understand why. Among them is biochemist Svetlana Mojsov of the Rockefeller University, who has spent about 50 years investigating gut hormones that could be key to regulating blood glucose levels. In seeking potential treatments for type 2 diabetes, Mojsov ultimately focused on one hormone: glucagonlike peptide 1, or GLP-1. Her sequence of the protein in the 1980s became the initial template for drugs like Wegovy. The medications, called GLP-1 receptor agonists, use a synthetic version of the natural substance to activate the hormone’s receptors. The first ones arrived in 2005. In 2017 the U.S. Food and Drug Administration approved semaglutide—now widely known as Ozempic. © 2024 SCIENTIFIC AMERICAN,

Keyword: Obesity; Hormones & Behavior
Link ID: 29373 - Posted: 06.26.2024

By Dana G. Smith In July 2016, a heat wave hit Boston, with daytime temperatures averaging 92 degrees for five days in a row. Some local university students who were staying in town for the summer got lucky and were living in dorms with central air-conditioning. Other students, not so much — they were stuck in older dorms without A.C. Jose Guillermo Cedeño Laurent, a Harvard researcher at the time, decided to take advantage of this natural experiment to see how heat, and especially heat at night, affected the young adults’ cognitive performance. He had 44 students perform math and self-control tests five days before the temperature rose, every day during the heat wave, and two days after. “Many of us think that we are immune to heat,” said Dr. Cedeño, now an assistant professor of environmental and occupational health and justice at Rutgers University. “So something that I wanted to test was whether that was really true.” It turns out even young, healthy college students are affected by high temperatures. During the hottest days, the students in the un-air-conditioned dorms, where nighttime temperatures averaged 79 degrees, performed significantly worse on the tests they took every morning than the students with A.C., whose rooms stayed a pleasant 71 degrees. A heat wave is once again blanketing the Northeast, South and Midwest. High temperatures can have an alarming effect on our bodies, raising the risk for heart attacks, heatstroke and death, particularly among older adults and people with chronic diseases. But heat also takes a toll on our brains, impairing cognition and making us irritable, impulsive and aggressive. Numerous studies in lab settings have produced similar results to Dr. Cedeño’s research, with scores on cognitive tests falling as scientists raised the temperature in the room. One investigation found that just a four-degree increase — which participants described as still feeling comfortable — led to a 10 percent average drop in performance across tests of memory, reaction time and executive functioning. © 2024 The New York Times Company

Keyword: Aggression
Link ID: 29370 - Posted: 06.26.2024

By Esther Landhuis Last month, researchers discovered cells in the brainstem that regulate inflammation throughout the body. In response to an injury, these nerve cells not only sense inflammatory molecules, but also dial their circulating levels up and down to keep infections from harming healthy tissues. The discovery adds control of the immune system to the brainstem’s core functions — a list that also includes monitoring heart rate, breathing and aspects of taste — and suggests new potential targets for treating inflammatory disorders like arthritis and inflammatory bowel disease. During an intense workout or high-stakes exam, your brain can sense the spike in your heart rate and help restore a normal rhythm. Likewise, the brain can help stabilize your blood pressure by triggering chemical signals that widen or constrict blood vessels. Such feats often go unnoticed, but they illustrate a fundamental concept of physiology known as homeostasis — the capacity of organisms to keep their internal systems working smoothly and stably amid shifting circumstances. Now, in a paper published on May 1 in Nature, researchers describe how homeostatic control extends even to the sprawl of cells and tissues that comprise our immune system. The team applied a clever genetic approach in mice to identify cells in the brainstem that adjust immune reactions to pathogens and other outside triggers. These neurons operate like a “volume controller” that keeps the animals’ inflammatory responses within a physiological range, said paper author Hao Jin, a neuroimmunologist at the National Institute of Allergy and Infectious Diseases. © 2024 Simons Foundation.

Keyword: Miscellaneous
Link ID: 29361 - Posted: 06.15.2024

By Emily Underwood You’re driving somewhere, eyes on the road, when you start to feel a tingling sensation in your lower abdomen. That extra-large Coke you drank an hour ago has made its way through your kidneys into your bladder. “Time to pull over,” you think, scanning for an exit ramp. To most people, pulling into a highway rest stop is a profoundly mundane experience. But not to neuroscientist Rita Valentino, who has studied how the brain senses, interprets and acts on the bladder’s signals. She’s fascinated by the brain’s ability to take in sensations from the bladder, combine them with signals from outside of the body, like the sights and sounds of the road, then use that information to act — in this scenario, to find a safe, socially appropriate place to pee. “To me, it’s really an example of one of the beautiful things that the brain does,” she says. Scientists used to think that our bladders were ruled by a relatively straightforward reflex — an “on-off” switch between storing urine and letting it go. “Now we realize it’s much more complex than that,” says Valentino, now director of the division of neuroscience and behavior at the National Institute of Drug Abuse. An intricate network of brain regions that contribute to functions like decision-making, social interactions and awareness of our body’s internal state, also called interoception, participates in making the call. In addition to being mind-bogglingly complex, the system is also delicate. Scientists estimate, for example, that more than 1 in 10 adults have overactive bladder syndrome — a common constellation of symptoms that includes urinary urgency (the sensation of needing to pee even when the bladder isn’t full), nocturia (the need for frequent nightly bathroom visits) and incontinence. Although existing treatments can improve symptoms for some, they don’t work for many people, says Martin Michel, a pharmacologist at Johannes Gutenberg University in Mainz, Germany, who researches therapies for bladder disorders. Developing better drugs has proven so challenging that all major pharmaceutical companies have abandoned the effort, he adds.

Keyword: Miscellaneous
Link ID: 29337 - Posted: 06.02.2024

By Meghan Rosen An experimental weight loss procedure cranks up the heat to dial down hunger. Blasting a patch of patients’ stomach lining with thermal energy curbed hunger and cut pounds, researchers reported in a small pilot study to be presented at the annual Digestive Disease Week meeting on May 19 in Washington, D.C. Called gastric fundus mucosal ablation, the procedure relies on an endoscope, a thin tube that can be threaded down the throat. It takes less than an hour and doesn’t require hospitalization. “The advantage of this is that it’s a relatively straightforward procedure,” says Cleveland Clinic surgical endoscopist Matthew Kroh, who was not involved with the work. Side effects, which included mild nausea and cramping, are minimal, one study author said in a news conference on May 8. That’s a big difference from bariatric surgery, considered the gold standard treatment for obesity, which includes many techniques to restrict stomach size or affect food absorption. Patients can be hospitalized for days and take weeks to recover. Obese people often avoid these treatments because they don’t want to endure surgery, Kroh says. The new procedure could one day offer an easier option — if the results hold up in larger groups of patients. “There’s potential,” Kroh says, “but I think we have to be cautious.” The trial included 10 women, so the method is still at the proof-of-concept stage. On average, the women lost nearly 8 percent of their body weight, some 19 pounds, over six months. That’s less than patients typically see from bariatric surgery or pharmaceutical treatments like the anti-obesity drug Wegovy (SN 12/13/23). © Society for Science & the Public 2000–2024.

Keyword: Obesity; Hormones & Behavior
Link ID: 29311 - Posted: 05.18.2024

By Asher Mullard With obesity drugs now helping people to slim down, researchers are working to capitalize on their popularity by bulking up the weight-loss drug pipeline. The latest contender takes a Trojan horse approach — hiding a small molecule in a gut-hormone-mimicking peptide already used in obesity drugs — to strike a double blow to the brain cells that control appetite. The new work, which demonstrated the effects of this drug candidate in mice and rats, was published today in Nature1. “It’s a strong paper,” says Daniel Drucker, an endocrinologist at Mount Sinai Hospital in Toronto, Canada, who helped to unravel the role of gut hormones such as GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide) in obesity. The blockbuster weight-loss drugs semaglutide (Wegovy) and tirzepatide (Zepbound) act by mimicking these hormones, binding to their receptors on neurons in the brain that control hunger pangs. These drugs can help people to lose 15–20% of their body weight. And it could be possible to eke even more activity from these hormone mimics by fusing them to other drugs, the new study suggests. “Very high marks for the novelty” of the research, says Drucker, who was not involved and consults for the pharmaceutical industry. “Let’s hope that we’ll see some proof of concept in the clinic”, when the approach is tested in humans. Trojan therapeutics The drug contender takes aim at both the GLP-1 receptor and the NMDA receptor, an ion channel found on cells in the brain that was linked to obesity in 20152. At the time, small molecules that blocked the NMDA receptor seemed like a non-starter for obesity-drug developers, because this type of compound, which includes the party drug and antidepressant ketamine, is riddled with harmful side effects. But Christoffer Clemmensen, a metabolism specialist at the University of Copenhagen, saw a path forwards. He speculated that it might be possible to sidestep the safety risks by fusing an NMDA-receptor blocker to a gut-hormone mimic that acts only on the neurons that regulate appetite. © 2024 Springer Nature Limited

Keyword: Obesity
Link ID: 29307 - Posted: 05.16.2024

By Johann Hari Ever since I was a teenager, I have dreamed of shedding a lot of weight. So when I shrank from 203 pounds to 161 in a year, I was baffled by my feelings. I was taking Ozempic, and I was haunted by the sense that I was cheating and doing something immoral. I’m not the only one. In the United States (where I now split my time), over 70 percent of people are overweight or obese, and according to one poll, 47 percent of respondents said they were willing to pay to take the new weight-loss drugs. It’s not hard to see why. They cause users to lose an average of 10 to 20 percent of their body weight, and clinical trials suggest that the next generation of drugs (probably available soon) leads to a 24 percent loss, on average. Yet as more and more people take drugs like Ozempic, Wegovy and Mounjaro, we get more confused as a culture, bombarding anyone in the public eye who takes them with brutal shaming. This is happening because we are trapped in a set of old stories about what obesity is and the morally acceptable ways to overcome it. But the fact that so many of us are turning to the new weight-loss drugs can be an opportunity to find a way out of that trap of shame and stigma — and to a more truthful story. In my lifetime, obesity has exploded, from being rare to almost being the norm. I was born in 1979, and by the time I was 21, obesity rates in the United States had more than doubled. They have skyrocketed since. The obvious question is, why? And how do these new weight-loss drugs work? The answer to both lies in one word: satiety. It’s a concept that we don’t use much in everyday life but that we’ve all experienced at some point. It describes the sensation of having had enough and not wanting any more. The primary reason we have gained weight at a pace unprecedented in human history is that our diets have radically changed in ways that have deeply undermined our ability to feel sated. My father grew up in a village in the Swiss mountains, where he ate fresh, whole foods that had been cooked from scratch and prepared on the day they were eaten. But in the 30 years between his childhood and mine, in the suburbs of London, the nature of food transformed across the Western world. He was horrified to see that almost everything I ate was reheated and heavily processed. The evidence is clear that the kind of food my father grew up eating quickly makes you feel full. But the kind of food I grew up eating, much of which is made in factories, often with artificial chemicals, left me feeling empty and as if I had a hole in my stomach. In a recent study of what American children eat, ultraprocessed food was found to make up 67 percent of their daily diet. This kind of food makes you want to eat more and more. Satiety comes late, if at all. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29296 - Posted: 05.07.2024

By Gillian Dohrn No one wants to eat when they have an upset stomach. To pinpoint exactly where in the brain this distaste for eating originates, scientists studied nauseated mice. The work, published in Cell Reports on 27 March1, describes a previously uncharacterized cluster of brain cells that fire when a mouse is made to feel nauseous, but don’t fire when the mouse is simply full. This suggests that responses to satiety and nausea are governed by separate brain circuits. “With artificial activation of this neuron, the mouse just doesn’t eat, even if it is super hungry,” says Wenyu Ding at the Max Planck Institute for Biological Intelligence in Martinsried, Germany, who led the study. Ding and colleagues suspected that this group of neurons was involved in processing negative experiences, such as feeling queasy, so they injected the mice with a chemical that induces nausea and then scanned the animals’ brains. This confirmed that the neurons are active when mice feel nauseous. Using a light-based technique called optogenetics, the team artificially activated the neurons of mice that had been deprived of food in the hours before the experiment. When the neurons were ‘off’, the mice ate. When the researchers turned them on, the mice walked away mid-chow. These brain cells could influence how fast you eat — and when you stop Researchers also blocked the activity of these neurons in nauseated mice that were hungry and found that the mice overcame their nausea to eat. © 2024 Springer Nature Limited

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 29263 - Posted: 04.20.2024

By McKenzie Prillaman Wegovy, Ozempic and similar weight-loss drugs have become some of the most popular medications in the world. But legions of people are also quitting them. About two-thirds of those in the United States who started taking a drug of this class, known as GLP-1 agonists, in 2021 had stopped using them within a year, according to an industry analysis. Researchers and clinicians often view GLP-1 agonists as lifelong treatments. But myriad factors can force individuals off the medications. People might lose the means to pay for the costly drugs, experience brutal side effects, be affected by continuing shortages or be offered limited-term prescriptions. The UK National Health Service (NHS), for instance, provides only two years of coverage for people taking the drugs for weight loss. As the number of people with obesity continues to rise — the World Health Organization estimates that more than one billion people, or one-eighth of the global population, now have obesity — researchers have been answering a few key questions about what happens when people stop taking these medications for weight management. What happens to weight and health when people quit? Ozempic and Wegovy are both brand names for the drug semaglutide, which has been prescribed for several years to treat type 2 diabetes (Ozempic) and, since 2021, to those who are overweight or have obesity (Wegovy). The treatment’s aim is to reduce the risk of health complications posed by a large amount of excess body fat, such as heart and liver disease and certain cancers. The drug curbs hunger and food intake by mimicking a hormone, released by the gut after eating, that affects brain regions involved in appetite and reward. Research has shown what happens when people stop taking GLP-1 agonists. Many regain a substantial amount of what they lost with the help of the medications. The body naturally tries to stay around its own weight point, a pull that obesity specialist Arya Sharma likens to a taut rubber band. © 2024 Springer Nature Limited

Keyword: Obesity
Link ID: 29260 - Posted: 04.16.2024

By David Adam A diabetes drug related to the latest generation of obesity drugs can slow the development of the symptoms of Parkinson’s disease, a clinical trial suggests1. Participants who took the drug, called lixisenatide, for 12 months showed no worsening of their symptoms — a gain in a condition marked by progressive loss of motor control. Further work is needed to control side effects and determine the best dose, but researchers say that the trial marks another promising step in the decades-long effort to tackle the common and debilitating disorder. “This is the first large-scale, multicentre clinical trial to provide the signs of efficacy that have been sought for so many years,” says Olivier Rascol, a Parkinson’s researcher at Toulouse University Hospital in France, who led the study. The diabetes connection Lixisenatide is a glucagon-like peptide-1 (GLP-1) receptor agonist, making it part of a large family of similar compounds used to treat diabetes and, more recently, obesity. (The weight-loss drug semaglutide, sold under the brand name Wegovy, is a GLP-1 compound.) Many studies have shown a link between diabetes and Parkinson’s2. People with diabetes are around 40% more likely to develop Parkinson’s. And people who have both Parkinson’s and diabetes often see more rapid progression of symptoms than do those who have only Parkinson’s. Animal studies3 have suggested that some GLP-1 drugs, which influence levels of insulin and glucose, can slow the symptoms of Parkinson’s. Smaller trials, published in 20134 and 20175, suggested that the GLP-1 molecule exenatide, another diabetes drug, could do the same in people.

Keyword: Parkinsons
Link ID: 29240 - Posted: 04.04.2024

By Angie Voyles Askham For Christopher Zimmerman, it was oysters: After a bout of nausea on a beach vacation, he could hardly touch the mollusks for months. For others, that gut-lurching trigger is white chocolate, margaritas or spicy cinnamon candy. Whatever the taste, most people know the feeling of not being able to stomach a food after it has caused—or seemed to cause—illness. That response helps us learn which foods are safe, making it essential for survival. But how the brain links an unpleasant gastric event to food consumed hours prior has long posed a mystery, says Zimmerman, who is a postdoctoral fellow in Ilana Witten’s lab at Princeton University. The time scale for this sort of conditioned food aversion is an order of magnitude different from other types of learning, which involve delays of only a few seconds, says Peter Dayan, director of computational neuroscience at the Max Planck Institute for Biological Cybernetics, who was not involved in the work. “You need to have something that bridges that gap in time” between eating and feeling ill, he says. A newly identified neuronal circuit can do just that. Neurons in the mouse brainstem that respond to drug-induced nausea reactivate a specific subset of cells in the animals’ central amygdala that encode information about a recently tasted food. And that reactivation happens with novel—but not familiar—flavors, according to work that Zimmerman presented at the annual COSYNE meeting in Lisbon last month. With new flavors, animals seem primed to recall a recent meal if they get sick, Zimmerman says. As he put it in his talk, “it suggests that the common phrase we associate with unexpected nausea, that ‘it must be something I ate,’ is literally built into the brain in the form of this evolutionarily hard-wired prior.” © 2024 Simons Foundation

Keyword: Learning & Memory; Evolution
Link ID: 29226 - Posted: 03.30.2024

Andrew Gregory Health editor Previous evidence has suggested a link between high body mass index (BMI) in adolescence and an increased risk of MS. But most of these studies were retrospective in design and used self-reported data. Researchers involved with the new study sought to prospectively evaluate the risk of developing MS in a large cohort of obese children compared with the general population. Academics analysed data from the Swedish Childhood Obesity Treatment Register. The database, known as Boris, is one of the world’s largest registries for treatment of childhood obesity. The research team looked at data on children aged two to 19 who joined the registry between 1995 and 2020, and compared their information with that of children in the general population. The study included data on more than 21,600 children with obesity, who started treatment for obesity when they were an average age of 11, and more than 100,000 children without obesity. Children involved in the study were tracked for an average of six years. During the follow-up period, MS was diagnosed in 28 of those with obesity (0.13% of the group) and 58 in the group without obesity (0.06%). © 2024 Guardian News & Media Limite

Keyword: Multiple Sclerosis; Obesity
Link ID: 29224 - Posted: 03.30.2024

By Daniel Gilbert and David Ovalle The U.S. Food and Drug Administration approved the weight-loss drug Wegovy as a treatment to reduce cardiovascular risk in adults who are overweight, the first approval of its kind that could dramatically expand the already huge market for the drug. Wegovy, which has the same active ingredient as diabetes drug Ozempic, already had FDA approval to treat patients who are obese or overweight. It has become a cultural sensation and a blockbuster, bringing in billions of dollars in revenue for its manufacturer, Novo Nordisk. “Wegovy is now the first weight loss medication to also be approved to help prevent life-threatening cardiovascular events in adults with cardiovascular disease and either obesity or overweight,” John Sharretts, a director in the FDA’s Center for Drug Evaluation and Research, said in a statement Friday. “We recognize how important this moment is for the millions of people who live with excess weight or obesity and known heart disease, and we will continue to advance options that put their needs first,” Doug Langa, head of Novo Nordisk’s North American operations, said in a statement. The FDA’s expansion of Wegovy’s regulatory label comes after a closely watched clinical trial last year found that the drug dramatically reduced the risk of heart problems for overweight people. In a five-year study of more than 17,600 patients, Wegovy cut the risk of strokes, heart attacks and other cardiovascular problems by 20 percent among overweight adults with a history of heart disease. Expanding Wegovy’s regulatory label could also entice more insurers to cover the pricey drug, according to researchers and Wall Street analysts. “The result will pressure insurers and the federal government to cover this medication,” said Harlan Krumholz, a cardiologist at the Yale School of Medicine. “It will be increasingly difficult to deny people access to these medications, as this is not about appearance but concerns health.”

Keyword: Obesity
Link ID: 29185 - Posted: 03.09.2024

By McKenzie Prillaman It’s no secret that global obesity rates have been rising over the past few decades. But a new analysis quantifies the upsurge. More than 1 billion people worldwide were living with obesity as of 2022, researchers report February 29 in the Lancet. That’s about one-eighth of the global population (SN: 11/15/22). For comparison, nearly 800 million people had obesity in 2016, according to the World Health Organization, or WHO. Obesity is “defined by the presence of excess body fat that impairs health,” says obesity expert Arya Sharma of the University of Alberta in Edmonton, Canada, who was not involved in the study. The chronic disease can raise the risk for conditions like heart disease and type 2 diabetes, vulnerability to diseases like COVID-19, and can also limit mobility and negatively affect mental health (SN: 4/22/20). Global health researcher Majid Ezzati and colleagues examined more than 3,600 population-based studies published over the last several decades encompassing 222 million participants across nearly 200 countries and territories. The researchers divided each participant’s reported weight by their height squared to find their body mass index, or BMI. Analyzing the trends suggested that in 2022, almost 900 million adults worldwide had a BMI of 30 or above, classifying them as having obesity. In children and adolescents ages 5 to 19, nearly 160 million were estimated to have the chronic disease, defined as BMI above a certain point on the WHO’s growth reference curves, which account for age and sex. From 1990 to 2022, the prevalence of obesity roughly doubled in women, tripled in men and quadrupled in children and adolescents. At the same time, global rates of those who were underweight fell. “We shouldn’t be thinking about [underweight and obesity] as two separate things, because the transition from one to the other has been very rapid,” says Ezzati, of Imperial College London. © Society for Science & the Public 2000–202

Keyword: Obesity
Link ID: 29174 - Posted: 03.02.2024

By Saima Sidik Eye diseases long thought to be purely genetic might be caused in part by bacteria that escape the gut and travel to the retina, research suggests1. Eyes are typically thought to be protected by a layer of tissue that bacteria can’t penetrate, so the results are “unexpected”, says Martin Kriegel, a microbiome researcher at the University of Münster in Germany, who was not involved in the work. “It’s going to be a big paradigm shift,” he adds. The study was published on 26 February in Cell. Inherited retinal diseases, such as retinitis pigmentosa, affect about 5.5 million people worldwide. Mutations in the gene Crumbs homolog 1 (CRB1) are a leading cause of these conditions, some of which cause blindness. Previous work2 suggested that bacteria are not as rare in the eyes as ophthalmologists had previously thought, leading the study’s authors to wonder whether bacteria cause retinal disease, says co-author Richard Lee, an ophthalmologist then at the University College London. CRB1 mutations weaken linkages between cells lining the colon in addition to their long-observed role in weakening the protective barrier around the eye, Lee and his colleagues found. This motivated study co-author Lai Wei, an ophthalmologist at Guangzhou Medical University in China, to produce Crb1-mutant mice with depleted levels of bacteria. These mice did not show evidence of distorted cell layers in the retina, unlike their counterparts with typical gut flora. Furthermore, treating the mutant mice with antibiotics reduced the damage to their eyes, suggesting that people with CRB1 mutations could benefit from antibiotics or from anti-inflammatory drugs that reduce the effects of bacteria. “If this is a novel mechanism that is treatable, it will transform the lives of many families,” Lee says. © 2024 Springer Nature Limited

Keyword: Vision
Link ID: 29167 - Posted: 02.27.2024

By Erin Garcia de Jesús DENVER — A weight-loss drug used to treat obesity and diabetes has shown promise to treat another disorder: opioid addiction. Early results from a small clinical trial, presented February 17 at the annual meeting of the American Association for the Advancement of Science, suggest that a close relative of the weight-loss drugs Wegovy and Ozempic significantly lessened cravings for opioids in people with opioid use disorder. “For them to have any time when they might be free of that craving seems to be very hopeful,” Patricia “Sue” Grigson, a behavioral neuroscientist at Penn State College of Medicine in Hershey said at the conference. The vast majority of drug overdose deaths in the United States are due to opioids (SN: 2/14/24). The drug, called liraglutide, mimics a hormone called GLP-1 that the body releases after people eat. Wegovy and Ozempic — brand names for semaglutide, a molecule that induces weight loss more effectively than liraglutide — also imitate the hormone. It’s unclear exactly how the drugs work when it comes to weight loss, but researchers think such GLP-1 dupes prompt the body and brain to make people feel full (SN: 12/13/23). There are hints that such drugs could work for addiction, too. People taking Wegovy or Ozempic have reported lessened desire for not just food but also alcohol and nicotine. What’s more, Grigson and colleagues showed in a previous study in rats that liraglutide can cut down on heroin-seeking behavior, perhaps by changing the animals’ brain activity (SN: 8/30/23). © Society for Science & the Public 2000–2024.

Keyword: Drug Abuse; Obesity
Link ID: 29150 - Posted: 02.20.2024

By Kristin Kiesel and Richard J. Sexton Many public health advocates and scholars see sugar-sweetened-beverage taxes (often simply called soda taxes) as key to reducing obesity and its adverse health effects. But a careful look at the data challenges this view. We reviewed close to 100 studies that have analyzed current taxes in more than 50 countries and conducted our own research on the effectiveness of soda taxes in the US. There is no conclusive evidence that soda taxes have reduced how much sugar or calories people consume in any meaningful way. Soda taxes alone simply cannot nudge consumers toward healthier food choices. The World Health Organization estimates that more than 17 million people die prematurely each year from chronic noncommunicable diseases. Being overweight or obese is a major risk factor for many of these conditions, including type 2 diabetes, cardiovascular diseases, asthma and several types of cancer. A widely publicized 2019 Lancet Commission report pegged annual obesity-related health-care costs and economic productivity losses at $2 trillion, about 3 percent of the global gross domestic product. Consuming large amounts of added sugars is a key part of this problem. A single 12-ounce can of soda can have more than 10 teaspoons of sugar; drinking just one exceeds the American Heart Association’s recommended daily limits on added sugars. It is easy to see why reducing soda consumption has been a popular target in the war against obesity. One would think that taxing sodas would raise their prices and discourage consumers from purchasing them. With this idea in mind, a wave of taxes has been slapped on sugar-sweetened beverages across the world. For example, cities in California’s Bay Area have imposed a tax of 1 cent per ounce on sugary beverages (a seemingly large price increase given soda’s cost of about 5 cents per ounce in the western US).

Keyword: Obesity
Link ID: 29143 - Posted: 02.10.2024