Chapter 9. Homeostasis: Active Regulation of the Internal Environment

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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

By Matt Richtel For decades, eating disorders were thought to afflict mostly, if not exclusively, women and girls. In fact, until 2013, the loss of menstruation had long been considered an official symptom of anorexia nervosa. Over the last decade, however, health experts have increasingly recognized that boys and men also suffer from eating disorders, and they have gained a better understanding of how differently the illness presents in that group. A small but growing body of scientists and physicians have dedicated themselves to identifying the problem, assessing its scope and developing treatments. Recently, two of these experts spoke to The New York Times about how the disease is affecting adolescent boys, what symptoms and behaviors parents should look for, and which treatments to consider. Dr. Jason Nagata is a pediatrician at the University of California, San Francisco, who specializes in eating disorders; he is senior editor of the Journal of Eating Disorders and editor of the book “Eating Disorders in Boys and Men.” Dr. Sarah Smith is a child and adolescent psychiatrist at the University of Toronto who specializes in eating disorders; she was the lead author on a study published in JAMA Open Network in December that showed sharp increases in the rates of hospitalizations for boys with eating disorders. The medical and scientific understanding of eating disorders is changing and expanding. What happened? Dr. Smith: Historically, eating disorders have been conceptualized mostly as anorexia, which has been portrayed as an illness of adolescent females who want to lose weight for aesthetic reasons. Dr. Nagata: There’s increasing recognition, particularly in the last decade or so, that some people with body image dissatisfaction are not trying to lose weight at all. Some men and boys are trying to become large and muscular. In fact, one-third of teenage boys across the United States report that they’re trying to bulk up and get more muscular. And a subset of those may develop eating disorders or muscle dysmorphia that can lead to significant psychological distress and physical health complications. © 2024 The New York Times Company

Keyword: Anorexia & Bulimia; Sexual Behavior
Link ID: 29140 - Posted: 02.08.2024

By Harriet Brown The minute I saw the headline — “Should Patients Be Allowed to Die From Anorexia?” — in The New York Times Magazine last month, my heart sank. Over the last two years, more and more psychiatrists have floated the idea that it’s OK to stop trying to cure some people with anorexia nervosa. People with anorexia develop a deep fear of food and eating, often losing so much weight that they die of starvation or complications. About 20 percent die by suicide. Anorexia is a terrible disease, one that inflicts maximum pain on the person diagnosed and their families and friends. The suffering is continuous and intense, and it gets even worse during recovery. Our family experienced this for eight years. Having to watch my daughter suffer made me realize that anorexia is not a choice or a question of vanity but a tsunami of fear and anxiety that makes one of the most basic human acts, the act of eating, as terrifying as jumping out of a plane without a parachute. It usually takes years of steady, consistent, calorie-dense eating to fully heal the body and brain of a person with anorexia. Without the right kind of support and treatment, it’s nearly impossible. So when psychiatrists suggest that maybe some people can’t recover and should be allowed to stop trying, they’re sidestepping their own responsibility. What they should be saying instead is that current views on and treatments of anorexia are abysmal, and medicine needs to do better. If you’ve never experienced anorexia firsthand, consider yourself blessed. Anorexia has one of the highest mortality rates of any psychiatric illness. People with anorexia are 18 times as likely to die from suicide as their peers. Fewer than half of those with anorexia make a full recovery.

Keyword: Anorexia & Bulimia
Link ID: 29139 - Posted: 02.08.2024

April Smith Did you know that anorexia is the most lethal mental health condition? One person dies from an eating disorder every hour in the U.S. Many of these deaths are not from health consequences related to starvation, but from suicide. Up to 1 in 5 women and 1 in 7 men in the U.S. will develop an eating disorder by age 40, and 1 in 2 people with an eating disorder will think about ending their life. About 1 in 4 people with anorexia nervosa or bulimia nervosa will attempt to kill themselves, and those with anorexia have a risk of death by suicide 31 times higher than peers without the disorder. In fact, nonsuicidal self-injury, suicidal ideation, suicide attempts and suicide deaths are all more prevalent among those with any type of eating disorder compared to those without an eating disorder. Why might that be? I am a clinical psychologist who studies eating disorders and self-harm, and I have spent the past 15 years researching this question. We still don’t have the answer. But new work on perception of the internal state of the body points to some promising possibilities for treatment. And what we’re learning could help anyone improve their relationship with their body. To understand why people with eating disorders are at risk of dying by suicide, I first want to ask you to do a little thought exercise. I’d like you to really think about your body: Think about your hair, face, arms, stomach, chest and legs. What words and feelings come to mind? Are there any things you wish you could change? Feel free to close your eyes and try this out. © 2010–2024, The Conversation US, Inc.

Keyword: Anorexia & Bulimia
Link ID: 29127 - Posted: 02.03.2024

By David Levin It can start small: a peculiar numbness; a subtle facial tic; an inexplicably stiff muscle. But then time goes by — and eventually, the tremors set in. Roughly a million people in the United States (and roughly 10 million people worldwide) live with Parkinson’s disease, a potent neurological disorder that progressively kills neurons in the brain. As it does so, it can trigger a host of crippling symptoms, from violent tremors to excruciating muscle cramps, terrifying nightmares and constant brain fog. While medical treatments can alleviate some of these effects, researchers still don’t know exactly what causes the disease to occur in the first place. A growing number of studies, however, are suggesting that it may be tied to an unlikely culprit: bacteria living inside our guts. Every one of us has hundreds or thousands of microbial species in our stomach, small intestine and colon. These bacteria, collectively called our gut microbiome, are usually considerate guests: Although they survive largely on food that passes through our insides, they also give back, cranking out essential nutrients like niacin (which helps our body convert food into energy) and breaking down otherwise indigestible plant fiber into substances our bodies can use. As Parkinson’s advances in the brain, researchers have reported that the species of bacteria present in the gut also shift dramatically, hinting at a possible cause for the disease. A 2022 paper published in the journal Nature Communications recorded those differences in detail. After sequencing the mixed-together genomes of fecal bacteria from 724 people — a group with Parkinson’s and another without — the authors saw a number of distinct changes in the guts of people who suffered from the disease. The Parkinson’s group had dramatically lower amounts of certain species of Prevotella, a type of bacterium that helps the body break down plant-based fiber (changes like this in gut flora could explain why people with Parkinson’s disease often experience constipation). At the same time, the study found, two harmful species of Enterobacteriaceae, a family of microbes that includes Salmonella, E. coli and other bugs, proliferated. Those bacteria may be involved in a chain of biochemical events that eventually kill brain cells in Parkinson’s patients, says Tim Sampson, a biologist at Emory University School of Medicine and coauthor of the study.

Keyword: Parkinsons
Link ID: 29098 - Posted: 01.13.2024

By Tim Vernimmen It is increasingly well understood that the countless microbes in our guts help us to digest our food, to absorb and produce essential nutrients, and to prevent harmful organisms from settling in. Less intuitive — perhaps even outlandish — is the idea that those microbes may also affect our mood, our mental health and how we perform on cognitive tests. But there is mounting evidence that they do. For nearly two decades, neuroscientist John Cryan of University College Cork in Ireland has been uncovering ways in which intestinal microbes affect the brain and behavior of humans and other animals. To his surprise, many of the effects he’s seen in rodents appear to be mirrored in our own species. Most remarkably, research by Cryan and others has shown that transplanting microbes from the guts of people with psychiatric disorders like depression to the guts of rodents can cause comparable symptoms in the animals. These effects may occur in several ways — through the vagus nerve connecting the gut to the brain, through the influence of gut bacteria on our immune systems, or by microbes synthesizing molecules that our nerve cells use to communicate. Cryan and coauthors summarize the science in a set of articles including “Man and the Microbiome: A New Theory of Everything?,” published in the Annual Review of Clinical Psychology. Cryan told Knowable Magazine that even though it will take much more research to pin down the mechanisms and figure out how to apply the insights, there are some things we can do already. This conversation has been edited for length and clarity.

Keyword: Depression; Stress
Link ID: 29091 - Posted: 01.11.2024

By Gina Kolata People taking the wildly popular drugs Ozempic, to treat diabetes, and Wegovy, to combat obesity, are slightly less likely to have suicidal thoughts than people who are not taking them, researchers reported on Friday. Millions of people take Ozempic and Wegovy, which are considered to be among the biggest blockbusters in medical history. But last year a European drug safety agency said it was investigating whether the drugs cause suicidal thoughts. The new study, published in the journal Nature Medicine, was funded by the National Institutes of Health and used a huge population. The findings provide data that may potentially reassure people who take the drugs. Novo Nordisk, maker of the drugs, had no role in the study, and the study’s investigators had no conflicts of interest. The investigators used anonymized electronic health records from a database of 100.8 million people. That allowed them to look at two groups: 240,618 who were prescribed Wegovy or other weight loss drugs, and 1,589,855 who were prescribed Ozempic or other medicines to lower their blood sugar. Suicidal thoughts were included in patients’ records as part of routine monitoring of their health. The investigators compared the incidence of suicidal thoughts in people who were taking the drugs with the incidence among similar people who were not taking them but were taking other weight loss and anti-diabetes medications. They also asked if there was an increase in the recurrence of suicidal thoughts among those taking the drugs who had previously reported thoughts of suicide. The database’s size allowed the researchers to look at subgroups such as sex, race and age groups. “No matter how hard we tried we did not see any increased risk,” said Rong Xu, director of the Center for Artificial Intelligence in Drug Discovery at Case Western Reserve University in Cleveland. Dr. Xu conceived the study and interpreted the data with Dr. Nora D. Volkow, director of the National Institute on Drug Abuse. But it was an observational study, so it is impossible to draw conclusions about cause and effect. Such studies can only show associations. “More studies are absolutely needed,” Dr. Volkow said. © 2024 The New York Times Company

Keyword: Obesity; Depression
Link ID: 29078 - Posted: 01.06.2024

By Katie Engelhart The doctors told Naomi that she could not leave the hospital. She was lying in a narrow bed at Denver Health Medical Center. Someone said something about a judge and a court order. Someone used the phrase “gravely disabled.” Naomi did not think she was gravely disabled. Still, she decided not to fight it. She could deny that she was mentally incompetent — but this would probably just be taken as proof of her mental incompetence. Of her lack of insight. She would, instead, “succumb to it.” It was early 2018. She had come to the hospital voluntarily, because she was getting so thin. In the days before, she had felt her electrolyte levels dip toward the danger zone — and she had decided that, even after everything, she did not want to be dead. By then, Naomi was 37 and had been starving herself for 26 years, and she was exquisitely attuned to her body’s corrupted chemistry. At the hospital, she was admitted to the ACUTE Center for Eating Disorders & Severe Malnutrition for medical stabilization. There, doctors began what was once called refeeding but is now more commonly called nutritional rehabilitation, using an intravenous line that fed into her neck. Reintroducing food to an emaciated body can be dangerous and even lethal if done too quickly. Physicians identified this phenomenon in the aftermath of World War II, when they observed skeletal concentration-camp survivors and longtime prisoners of war eat high-caloric foods and then drop dead of cardiac failure. “Well, here I am,” Naomi said in a video message that she recorded for her parents. “I am alive, but am I happy? I don’t know. … It’s pretty pathetic. I don’t know how I feel about the fact that I would have died had I not come.” In the video, she was wearing a hot pink tank top, even though it was cool in the hospital room, because she wanted to shiver, because shivering burned calories. A few days later, when she was not imminently dying anymore, Naomi announced that she was going home — and the hospital responded by placing her on a 72-hour mental-health hold. Clinicians then obtained what Colorado calls a short-term certification, which required, by judicial order, that Naomi be detained and treated, in her case until she reached what physicians determined to be 80 percent of her “ideal body weight.” In Colorado, as in most states, a patient can be treated against her will if she is mentally ill and found incapable of making informed decisions. That day, Naomi was transferred to a residential program at Denver’s Eating Recovery Center (E.R.C.) © 2024 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 29075 - Posted: 01.03.2024