By Amber Dance Maybe it starts with a low-energy feeling, or maybe you’re getting a little cranky. You might have a headache or difficulty concentrating. Your brain is sending you a message: You’re hungry. Find food. Studies in mice have pinpointed a cluster of cells called AgRP neurons near the underside of the brain that may create this unpleasant hungry, even “hangry,” feeling. They sit near the brain’s blood supply, giving them access to hormones arriving from the stomach and fat tissue that indicate energy levels. When energy is low, they act on a variety of other brain areas to promote feeding. By eavesdropping on AgRP neurons in mice, scientists have begun to untangle how these cells switch on and encourage animals to seek food when they’re low on nutrients, and how they sense food landing in the gut to turn back off. Researchers have also found that the activity of AgRP neurons goes awry in mice with symptoms akin to those of anorexia, and that activating these neurons can help to restore normal eating patterns in those animals. Understanding and manipulating AgRP neurons might lead to new treatments for both anorexia and overeating. “If we could control this hangry feeling, we might be better able to control our diets,” says Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center in Philadelphia. AgRP neurons appear to be key players in appetite: Deactivating them in adult mice causes the animals to stop eating — they may even die of starvation. Conversely, if researchers activate the neurons, mice hop into their food dishes and gorge themselves. © 2023 Annual Reviews

Keyword: Obesity
Link ID: 28799 - Posted: 05.27.2023

By Leo Sands Just under half of obese adolescents administered the latest in a new generation of recently approved weight-loss drugs were no longer considered to be clinically obese by the end of a 16-month trial, a study found. The findings support a small but growing body of evidence that the drug semaglutide, which goes by the brand names of Ozempic and Wegovy, can be an effective treatment option for chronic weight management for a range of ages. Obesity rates for children and adolescents are now alarmingly high in many countries, with such significant implications for young lives that the World Health Organization considers childhood obesity “one of the most serious public health challenges of the 21st century.” The authors of the new peer-reviewed study, published Wednesday in the journal Obesity, found that semaglutide was “highly effective” in reducing body mass index among teens. The weights of 134 clinically obese adolescents were monitored for 68 weeks, with participants given a 2.4 milligram injection of semaglutide weekly. By the end of the study, 45 percent of the group recorded a drop in BMI to below the clinical threshold for obesity. Just 12 percent of participants in a separate group who received a placebo were no longer considered to be obese at the end of the trial. Both groups also got lifestyle counseling and had a daily goal of 60 minutes of moderate- to high-intensity physical activity.

Keyword: Obesity
Link ID: 28784 - Posted: 05.18.2023

By Erin Blakemore Newly published research suggests that the sons of women with polycystic ovary syndrome (PCOS) are up to twice as likely to develop obesity as their peers. The study in Cell Reports Medicine used data from cohort research following 467,275 male infants born in Sweden between July 2006 and December 2015. Of those, 9,828 were born to a mother with PCOS — and 147 of those boys were eventually diagnosed with obesity. About 2 in 100 Swedish boys who were born to mothers with PCOS became obese during childhood, compared with about 1 in 100 for boys whose mothers did not have PCOS. The risk was higher among the sons of women who had PCOS and a body mass index (BMI) greater than 25 and highest among the sons of women who both had PCOS and did not take metformin during pregnancy. Researchers followed up the analysis with an RNA sequencing study that found higher cholesterol in sons of Chilean women with PCOS than controls. In another analysis, researchers fed a group of mice a fatty, sugary diet and exposed them to high levels of dihydrotestosterone, a hormone that mimics that of pregnant women with PCOS. Their sons were born with metabolic problems that persisted into adulthood, even when they ate a healthy diet throughout their lives. “We could see that these male mice had more fat tissue, larger fat cells, and a disordered basal metabolism, despite eating a healthy diet,” says Elisabet Stener-Victorin, a reproductive endocrinology and metabolism investigator at the Karolinska Institute in Sweden and the study’s lead author, in a news release.

Keyword: Obesity; Hormones & Behavior
Link ID: 28776 - Posted: 05.10.2023

By Tim Vernimmen This story starts in an unusual place for an article about human nutrition: a cramped, humid and hot room somewhere in the Zoology building of the University of Oxford in England, filled with a couple hundred migratory locusts, each in its own plastic box. It was there, in the late 1980s, that entomologists Stephen Simpson and David Raubenheimer began working together on a curious job: rearing these notoriously voracious insects, to try and find out whether they were picky eaters. Every day, Simpson and Raubenheimer would weigh each locust and feed it precise amounts of powdered foods containing varying proportions of proteins and carbohydrates. To their surprise, the young scientists found that whatever food the insects were fed, they ended up eating almost exactly the same amount of protein. In fact, locusts feeding on food that was low in protein ate so much extra in order to reach their protein target that they ended up overweight — not chubby on the outside, since their exoskeleton doesn’t allow for bulges, but chock-full of fat on the inside. Inevitably, this made Simpson and Raubenheimer wonder whether something similar might be causing the documented rise in obesity among humans. Many studies had reported that even as our consumption of fats and carbohydrates increased, our consumption of protein did not. Might it be that, like locusts, we are tricked into overeating, in our case by the irresistible, low-protein, ultraprocessed foods on the shelves of the stores where we do most of our foraging? That’s what Raubenheimer and Simpson, both now at the University of Sydney, argue in their recent book “Eat Like the Animals” and in an overview in the Annual Review of Nutrition. © 2023 Annual Reviews

Keyword: Obesity; Attention
Link ID: 28764 - Posted: 05.03.2023

By Darius Tahir & Hannah Norman, KHN Suzette Zuena is her own best advertisement for weight loss. Zuena, the “founder/visionary” of LH Spa & Rejuvenation in Livingston and Madison, New Jersey, has dropped 30 pounds. Her husband has lost 42 pounds. “We go out a lot,” Zuena said of the pair’s social routine. “People saw us basically shrinking.” They would ask how the couple did it. Her response: point people to her spa and a relatively new type of medication — GLP-1 agonists, a class of drug that’s become a weight loss phenomenon. But she’s not just spreading her message in person. She’s also doing it on Instagram. And she’s not alone. A chorus of voices is singing these drugs’ praises. Last summer, investment bank Morgan Stanley found mentions of one of these drugs on TikTok had tripled. People are streaming into doctors’ office to inquire about what they’ve heard are miracle drugs. What these patients have heard, doctors said, is nonstop hype, even misinformation, from social media influencers. “I’ll catch people asking for the skinny pen, the weight loss shot, or Ozempic,” said Priya Jaisinghani, an endocrinologist and clinical assistant professor at New York University’s Grossman School of Medicine. Competition to claim a market that could be worth $100 billion a year for drugmakers alone has triggered a wave of advertising that has provoked the concern of regulators and doctors worldwide. But their tools for curbing the ads that go too far are limited — especially when it comes to social media. Regulatory systems are most interested in pharma’s claims, not necessarily those of doctors or their enthused patients.

Keyword: Obesity
Link ID: 28754 - Posted: 04.26.2023

by Sarah DeWeerdt Many papers about autism-linked genes note that the genes are expressed throughout both the central and the peripheral nervous systems. The proportion of such prolific genes may be as high as two-thirds, according to one 2020 analysis. Yet few studies delve into what those genes are actually doing outside the brain. That’s starting to change. Although autism is typically thought of as a brain condition, a critical mass of researchers has started to investigate how the condition alters neurons elsewhere in the body. Their work — part of a broader trend in neuroscience to look beyond the brain — hints that the role of the peripheral nervous system in autism is, well, anything but peripheral: Neuronal alterations outside the brain may help to explain a host of the condition’s characteristic traits. Much of the research so far focuses on touch and the workings of the gut, but there is increasing interest in other sensory and motor neurons, as well as the autonomic nervous system, which orchestrates basic body functions such as heartbeat, blood pressure, breathing and digestion. It’s difficult to pinpoint whether some autism traits arise in the peripheral nervous system or the central nervous system; in many cases, complex feedback loops link the two. “Your nervous system doesn’t know that we’ve divided it that way,” says Carissa Cascio, associate professor of psychiatry and behavioral sciences at Vanderbilt University in Nashville, Tennessee. But at least some peripheral changes may offer novel treatment targets. And drugs that act in the peripheral nervous system could also prove more effective and have fewer side effects than brain-based therapies, says Julia Dallman, associate professor of biology at the University of Miami in Coral Gables, Florida. © 2023 Simons Foundation

Keyword: Autism
Link ID: 28739 - Posted: 04.15.2023

Heidi Ledford Under the right circumstances, even moderately hungry mice prefer to socialize with the opposite sex than to eat, researchers have found1. In research published on 23 February in Cell Metabolism, scientists treated male mice with a technique that mimics the effects of leptin, a hormone that acts on the brain to suppress appetite. Treated mice were more likely to approach female mice than their food bowls — even if the test rodents had been deprived of food for almost an entire day. The findings reveal a surprising role for leptin in social behaviour. They are also a step towards understanding how animals prioritize different behavioural options in response to ongoing needs — an enduring question in neuroscience, says Gina Leinninger, who studies the neural regulation of feeding at Michigan State University in East Lansing. The paper “addresses a huge gap in the field”, she says. “When you no longer need to eat urgently, it should free you up to do other things.” The new work, Leinninger says, illuminates how the brain juggles these various demands. Food versus friends Neuroscientists Anne Petzold and Tatiana Korotkova at the University of Cologne in Germany, and their colleagues, sought to understand how such decision-making is affected by leptin, which activates a subset of cells in the brain and promotes a feeling of fullness. The researchers injected male mice with leptin and saw that it suppressed feeding, as expected — but also promoted interactions with female mice. The team examined neurons in the brain’s ‘hunger center’, the lateral hypothalamus, that are activated by leptin. The authors’ experiments showed that neurons that can sense leptin were activated when mice interacted with members of the opposite sex. Artificially activating those neurons using a technique called optogenetics raised the likelihood that a mouse would approach a member of the opposite sex. Both results suggest that leptin plays a part in promoting social behaviour. © 2023 Springer Nature Limited

Keyword: Obesity; Sexual Behavior
Link ID: 28682 - Posted: 02.25.2023

By Kelsey Herbers The comments started the day I became engaged in December 2018: “You’re going to be such a beautiful bride.” “I can’t wait to see you in your dress.” “Everything is going to be perfect.” Before my fiancé and I even booked our wedding date, originally April 25, 2020, or saved a color scheme on Pinterest, I felt an intensifying pressure to live up to the high expectations that I thought my friends and family already had for my wedding day. I was determined to meet those expectations. But the innocent, wedding-driven diet that commenced shortly after my engagement ultimately spiraled into a full-fledged eating disorder. I was shocked by how quickly I fell ill and how deep that illness was. There was nothing about my journey, however, that surprised Robyn L. Goldberg, a registered dietitian and author of “The Eating Disorder Trap.” “The research shows one out of three people who diet develop an eating disorder — it’s very, very common,” said Ms. Goldberg, who has worked in private practice for the last 25 years with clients who have eating disorders, including many future brides. Some have ended up in residential treatment, she said. “You get so consumed that to pull yourself out of that dark hole seems impossible.” In the early days of wedding planning, my lifestyle changes were subtle. I bought an elliptical machine, took note of my calorie intake and found healthier meal options. But when the pandemic hit and kept me at home with my gym equipment, measuring cups and extra time on my hands, the opportunities to try new weight loss methods and obsess over my progress grew. It also forced us to postpone our wedding date. In just a few months, I was severely limiting my calorie intake, weighing myself several times a day and adhering to strict, self-proclaimed exercise rules. This included 45 minutes of running on a treadmill and 120 minutes of walking (180 minutes on weekends) daily. Before my engagement, I had never heard of intermittent fasting, but it didn’t take long for me to master it. These behavioral changes happened so gradually that I didn’t even recognize something was wrong until nearly two years later. By then I had lost 50 pounds, though initially I had wanted to shed only 25. © 2023 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 28650 - Posted: 02.01.2023

McKenzie Prillaman The hotel ballroom was packed to near capacity with scientists when Susan Yanovski arrived. Despite being 10 minutes early, she had to manoeuvre her way to one of the few empty seats near the back. The audience at the ObesityWeek conference in San Diego, California, in November 2022, was waiting to hear the results of a hotly anticipated drug trial. The presenters — researchers affiliated with pharmaceutical company Novo Nordisk, based in Bagsværd, Denmark — did not disappoint. They described the details of an investigation of a promising anti-obesity medication in teenagers, a group that is notoriously resistant to such treatment. The results astonished researchers: a weekly injection for almost 16 months, along with some lifestyle changes, reduced body weight by at least 20% in more than one-third of the participants1. Previous studies2,3 had shown that the drug, semaglutide, was just as impressive in adults. The presentation concluded like no other at the conference, says Yanovski, co-director of the Office of Obesity Research at the US National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland. Sustained applause echoed through the room “like you were at a Broadway show”, she says. This energy has pervaded the field of obesity medicine for the past few years. After decades of work, researchers are finally seeing signs of success: a new generation of anti-obesity medications that drastically diminish weight without the serious side effects that have plagued previous efforts. These drugs are arriving in an era in which obesity is growing exponentially. Worldwide obesity has tripled since 1975; in 2016, about 40% of adults were considered overweight and 13% had obesity, according to the World Health Organization (WHO). With extra weight often comes heightened risk of health conditions such as type 2 diabetes, heart disease and certain cancers. The WHO recommends healthier diets and physical activity to reduce obesity, but medication might help when lifestyle changes aren’t enough. The new drugs mimic hormones known as incretins, which lower blood sugar and curb appetite. Some have already been approved for treating type 2 diabetes, and they are starting to win approval for inducing weight loss. © 2023 Springer Nature Limited

Keyword: Obesity
Link ID: 28621 - Posted: 01.04.2023

By Laurie McGinley and  Lenny Bernstein Rachel Graham has battled excess weight for years, cycling through trendy diets, various drugs, even bariatric surgery. Nothing worked for long. But last summer, she started a new medication, and today is 40 pounds lighter — and still shedding weight. “It used to be that if I saw food, I would want to eat it,” said the 54-year-old Graham, who is 5-foot-7 and 190 pounds. “Now, if I have three or four bites of food, I don’t want to eat more.” The drug she’s taking, Mounjaro by Eli Lilly, is part of a new crop of therapies that experts are hailing as a medical milestone — a long-sought way to transform the treatment of obesity, one of the nation’s most serious health threats. Designed for diabetes but used for obesity at higher doses, the medications induce loss of 15 to 22 percent of body weight on average — more than enough to significantly reduce cardiovascular and other health risks. That makes them far superior to old-style diet pills that delivered smaller benefits along with nasty side effects such as high blood pressure and loose stools. But during the past year, soaring demand for the drugs has ignited a mad scramble, exposing some of the most persistent problems in the nation’s health-care system, including supply shortages, high costs and health-care inequities. Tensions are surging as patients with diabetes and those with weight problems sometimes compete for the same medications, which are self-administered in weekly injections. Some doctors worry that the drugs, which might have to be taken for life, will overshadow the need for lifestyle changes involving diet and exercise.

Keyword: Obesity
Link ID: 28606 - Posted: 12.21.2022

ByElizabeth Pennisi Willpower might be key to getting off the couch to exercise, but bacteria may lend a helping hand. Studies in mice reported today in Nature suggest microbes in the gut may be behind differences in the desire to work out. A research team has homed in on specific microbial molecules that stimulate a rodent’s desire to run—and keep running. By revealing exactly how these molecules talk to the brain, this group has set the stage for finding out whether similar signals help keep humans active. The work “establishes just how critical the microbiome is for exercise and goes incredibly deep in providing a new gut-brain [connection],” says Aleksandar Kostic, a microbiologist at Harvard Medical School who is co-founder of FitBiomics, a company developing probiotics to improve fitness. Kostic, who wasn’t involved in the research, and others speculate that exercise-inducing commands from the microbes might one day be packaged into pills people could take. To explore why some people like to exercise and others don’t, University of Pennsylvania microbiologist Christoph Thaiss studied mice bred to have a lot of genetic and behavioral variation. His team found more than a fivefold difference in how far the mice ran on wheels in their cages—some covered more than 30 kilometers in 48 hours, whereas others rarely moved in their wheels. The active and lazy mice didn’t show any significant differences in their genetics or biochemistry. But the researchers did notice one clue: When treated with antibiotics, mice that were normally highly energetic tended to exercise less. Follow-up studies showed the antibiotic treatment affected the brains of the formerly active mice. The activity of certain brain genes declined, along with levels of dopamine, a neurotransmitter that has been linked to “runner’s high”—that sense of wellbeing that comes with prolonged exercise.

Keyword: Obesity
Link ID: 28596 - Posted: 12.15.2022

By Allison Gasparini Are you drinking enough water? The question seems like it should have a straightforward answer — a specific amount of water you need to drink daily to combat dehydration.      But the rate and way in which the human body takes in and excretes water is not as universal as you might expect. By studying more than 5,000 people living in 23 countries and ranging in age from 8 days to 96 years, researchers have found that the turnover of water in a person’s body varies widely depending on the individual’s physical and environmental factors. The results, published in the Nov. 24 Science, suggest that the idea that a person should ideally consume eight 8-ounce glasses of water a day is not a one-size-fits-all solution to peak hydration.     Even within the calculations, “individual variabilities could be huge,” says biomedical engineer Kong Chen, director of the metabolic research program at the National Institutes of Health’s Clinical Center. Yosuke Yamada, a physiologist at the National Institute of Biomedical Innovation, Health and Nutrition in Japan, and colleagues used a stable isotope of hydrogen known as deuterium to track the movement of water through people’s bodies. Drinking water accounts for only half of the total water intake by humans, with the rest coming from food. Simply measuring the amount of water that a person drinks in a day is not enough to accurately gauge water turnover or the amount of water used by the body daily. © Society for Science & the Public 2000–2022.

Keyword: Obesity
Link ID: 28592 - Posted: 12.13.2022

By Joanna Thompson Two recent papers have shown that during a critical early period of brain development, the gut’s microbiome — the assortment of bacteria that grow within in it — helps to mold a brain system that’s important for social skills later in life. Scientists found this influence in fish, but molecular and neurological evidence plausibly suggests that some form of it could also occur in mammals, including humans. In a paper published in early November in PLOS Biology, researchers found that zebra fish who grew up lacking a gut microbiome were far less social than their peers with colonized colons, and the structure of their brains reflected the difference. In a related article in BMC Genomics in late September, they described molecular characteristics of the neurons affected by the gut bacteria. Equivalents of those neurons appear in rodents, and scientists can now look for them in other species, including humans. In recent decades, scientists have come to understand that the gut and the brain have powerful mutual influences. Certain types of intestinal ulcers, for example, have been linked to worsening symptoms in people with Parkinson’s disease. And clinicians have long known that gastrointestinal disorders are more common in people who also have neurodevelopmental disorders, such as ADHD and autism spectrum disorder. “Not only does the brain have an impact on the gut, but the gut can also profoundly affect the brain,” said Kara Margolis, a pediatric gastroenterologist at New York University’s Langone Health, who was not involved in the new research. How these anatomically separate organs exert their effects, however, is far less clear. Philip Washbourne, a molecular biologist at the University of Oregon and one of the principal co-authors of the new studies, has been studying genes implicated in autism and the development of social behaviors for over two decades. But he and his lab were looking for a new model organism, one that displayed social behavior but was quicker and easier to breed than their go-to, mice. “Can we do this in fish?” he recalls thinking, and then: “Let’s get really quantitative about it and see if we can measure how friendly the fish get.” All Rights Reserved © 2022

Keyword: Sexual Behavior; Obesity
Link ID: 28557 - Posted: 11.16.2022

By Gina Kolata What if an uncontrollable urge to rapidly eat large amounts of food is rooted in an impaired brain circuit? If that were the case, people who live with binge eating disorder — a psychiatric diagnosis — might be no more at fault for overeating than a patient with Parkinson’s disease is for their tremors. That question led doctors to try a new treatment different from anything ever attempted to help people with this common but underreported eating disorder. At least 3 percent of the population has it, said Dr. Casey Halpern, a neurosurgeon at the University of Pennsylvania. He and his colleagues decided to try deep brain stimulation, a method routinely used to quell tremors in patients with Parkinson’s. It involves placing electrodes in the brain to regulate aberrant signals. The wires, connected to the electrodes, are placed under the scalp, where they are invisible and unobtrusive. For the binge eating treatment, the device only stimulates neurons when the device detects a signal to start a binge. The pilot study, funded by the National Institutes of Health and published earlier this year in the journal Nature Medicine, involves two women and will be expanded in a few months to include four more people living with binge eating disorder who regained the weight they lost after bariatric surgery. Before the treatment can be approved by the Food and Drug Administration, researchers will need to rigorously test the method in at least 100 people in multiple medical centers. Such a study would take several years to complete. The two women whose devices were implanted a year ago will be followed for up to three years. They had the option to have their devices removed after 12 months, but both wanted to keep them because they no longer felt irresistible urges to binge. One of them, Robyn Baldwin, 58, of Citrus Heights, Calif., described herself as a “chunko child” who had “always been big.” She tried a wide range of diets. Once, she consumed only protein shakes for a month. In 2003 she had bariatric surgery, which usually involves altering the digestive system so that the stomach is smaller and food is more difficult to digest. It has enabled many people to lose weight when other methods failed. But for Ms. Baldwin, the weight she lost came back. © 2022 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 28545 - Posted: 11.09.2022

By Veronique Greenwood Anyone who’s had a shady oyster or a mushroom soup that didn’t sit well remembers the ominous queasiness heralding impending bad times. Bacteria release toxins that start the body’s process of speedily evacuating the contents of the stomach. It’s a protective mechanism of sorts — getting rid of the invaders en masse is probably helpful in the long term, even if it’s unpleasant in the short. But it has remained something of a mystery how the brain gets the alarm signal, then sends another one to tell the stomach to initiate a technicolor yawn. Your next bout of food poisoning isn’t the only reason to understand this particular neural pathway. Figuring out how to counter it could be helpful for people who develop nausea caused by chemotherapy medication and other drugs. As if fighting cancer isn’t painful and scary enough, patients are often so turned off by food that keeping their weight up becomes a major struggle. In a new study, researchers report that both bacteria and chemotherapy drugs appear to trigger the same molecular pathways in the gut. The findings, which were based on experiments with mice and published Tuesday in the journal Cell, showed that a bacterial toxin and a chemo medication both set in motion a cascade of similar neural messages that cause queasiness. Choosing mice for the study was unusual. Mice, it turns out, can’t puke — a little foible that typically makes it difficult to use them to study nausea. Researchers have used cats and dogs in the past, but the biology of mice in general is so much better understood, with much better tools available to scientists to do so. Cao Peng, a professor at Tsinghua University in Beijing, and his colleagues wondered whether mice might still be capable of feeling ill in the way people do after ingesting a chemo drug or a bad salad — or close enough, anyway, that researchers could use the creatures to understand the origins of the sensation. © 2022 The New York Times Company

Keyword: Obesity; Stress
Link ID: 28537 - Posted: 11.02.2022

Kate Siber Sharon Maxwell spent much of her life trying to make herself small. Her family put her on her first diet when she was 10. Early on Saturday mornings, she and her mother would drive through the empty suburban streets of Hammond, Ind., to attend Weight Watchers meetings. Maxwell did her best at that age to track her meals and log her points, but the scale wasn’t going down fast enough. So she decided to barely eat anything on Fridays and take laxatives that she found in the medicine cabinet. Food had long been a fraught subject in the Maxwell household. Her parents were also bigger-bodied and dieted frequently. They belonged to a fundamentalist Baptist megachurch where gluttony was seen as a sin. To eat at home was to navigate a labyrinth of rules and restrictions. Maxwell watched one time as her mother lost 74 pounds in six months by consuming little more than carrot juice (her skin temporarily turned orange). Sometimes her father, seized with a new diet idea, abruptly ransacked shelves in the kitchen, sweeping newly forbidden foods into the trash. Maxwell was constantly worried about eating too much. She started to eat alone and in secret. She took to chewing morsels and spitting them out. She hid food behind books, in her pockets, under mattresses and between clothes folded neatly in drawers. Through Maxwell’s teenage years and early 20s, eating became even more stressful. Her thoughts constantly orbited around food: what she was eating or not eating, the calories she was burning or not burning, the size of her body and, especially, what people thought of it. Her appearance was often a topic of public interest. When she went grocery shopping for her family, other customers commented on the items in her cart. “Honey, are you sure you want to eat that?” one person said. Other shoppers offered unsolicited advice about diets. Strangers congratulated her when her cart was filled with vegetables. As she grew older, people at the gym clapped and cheered for her while she worked out. “People would say: ‘Go! You can lose the weight!’” she says. While eating in public, other diners offered feedback — and still do to this day — on her choices, a few even asking if she wanted to join their gym. Some would call her names: Pig, Fatty. Sometimes people told her she was brave for wearing shorts, while others said she should cover up. She was always aware, whether she wanted to be or not, of how others viewed her body. © 2022 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 28519 - Posted: 10.19.2022

By Greg Miller If you’re lucky enough to live to 80, you’ll take up to a billion breaths in the course of your life, inhaling and exhaling enough air to fill about 50 Goodyear blimps or more. We take about 20,000 breaths a day, sucking in oxygen to fuel our cells and tissues, and ridding the body of carbon dioxide that builds up as a result of cellular metabolism. Breathing is so essential to life that people generally die within minutes if it stops. It’s a behavior so automatic that we tend to take it for granted. But breathing is a physiological marvel — both extremely reliable and incredibly flexible. Our breathing rate can change almost instantaneously in response to stress or arousal and even before an increase in physical activity. And breathing is so seamlessly coordinated with other behaviors like eating, talking, laughing and sighing that you may have never even noticed how your breathing changes to accommodate them. Breathing can also influence your state of mind, as evidenced by the controlled breathing practices of yoga and other ancient meditative traditions. In recent years, researchers have begun to unravel some of the underlying neural mechanisms of breathing and its many influences on body and mind. In the late 1980s, neuroscientists identified a network of neurons in the brainstem that sets the rhythm for respiration. That discovery has been a springboard for investigations into how the brain integrates breathing with other behaviors. At the same time, researchers have been finding evidence that breathing may influence activity across wide swaths of the brain, including ones with important roles in emotion and cognition. “Breathing has a lot of jobs,” says Jack L. Feldman, a neuroscientist at the University of California, Los Angeles, and coauthor of a recent article on the interplay of breathing and emotion in the Annual Review of Neuroscience. “It’s very complicated because we’re constantly changing our posture and our metabolism, and it has to be coordinated with all these other behaviors.” © 2022 Annual Reviews

Keyword: ADHD
Link ID: 28508 - Posted: 10.08.2022

By Claudia Lopez Lloreda If you look at parts of the circulatory system of whales and dolphins, you might think that you are looking at a Jackson Pollock painting, not blood vessels. These cetaceans have especially dense, complex networks of blood vessels mainly associated with the brain and spine, but scientists didn’t know why. A new analysis suggests that the networks protect cetaceans’ brains from the pulses of blood pressure that the animals endure while diving deep in the ocean, researchers report in the Sept. 23 Science. Whales and dolphins “have gone through these really amazing vascular adaptations to support their brain,” says Ashley Blawas, a marine scientist at the Duke University Marine Lab in Beaufort, N.C., who was not involved with the research. Called retia mirabilia, which means “wonderful nets,” the blood vessel networks are present in some other animals besides cetaceans, including giraffes and horses. But the networks aren’t found in other aquatic vertebrates that move differently from whales, such as seals. So scientists had suspected that the cetaceans’ retia mirabilia play a role in controlling blood pressure surges. When whales and dolphins dive, they move their tail up and down in an undulating manner, which creates surges in blood pressure. Land animals that experience similar surges, like galloping horses, are able to release some of this pressure by exhaling. But some cetaceans hold their breath to dive for long periods of time (SN: 9/23/20). Without a way to relieve that pressure, those blasts could tear blood vessels and harm other organs, including the brain. In the new study, biomechanics researcher Margo Lillie of the University of British Columbia in Vancouver and colleagues used data on the morphology of 11 cetacean species to create a computational model that can simulate the animals’ retia mirabilia. It revealed that the arteries and veins in this tangle of blood vessels are really close and may even sometimes be joined. As a result, the retia mirabilia could equalize the differences in blood pressure generated by diving, perhaps by redistributing the blood pulses from arteries to veins and vice versa. This way, the networks get rid of, or at least weaken, huge blood pressure surges that might otherwise reach and devastate the brain. © Society for Science & the Public 2000–2022.

Keyword: Brain imaging
Link ID: 28499 - Posted: 10.05.2022

By Alice Callahan Katherine Flegal wanted to be an archaeologist. But it was the 1960s, and Flegal, an anthropology major at the University of California, Berkeley, couldn’t see a clear path to this profession at a time when nearly all the summer archaeology field schools admitted only men. “The accepted wisdom among female archaeology students was that there was just one sure way for a woman to become an archaeologist: marry one,” Flegal wrote in a career retrospective published in the 2022 Annual Review of Nutrition. And so Flegal set her archaeology aspirations aside and paved her own path, ultimately serving nearly 30 years as an epidemiologist at the National Center for Health Statistics (NCHS), part of the US Centers for Disease Control and Prevention. There, she spent decades crunching numbers to describe the health of the nation’s people, especially as it related to body size, until she retired from the agency in 2016. At the time of her retirement, her work had been cited in 143,000 books and articles. In the 1990s, Flegal and her CDC colleagues published some of the first reports of a national increase in the proportion of people categorized as overweight based on body mass index (BMI), a ratio of weight and height. The upward trend in BMI alarmed public health officials and eventually came to be called the “obesity epidemic.” But when Flegal, along with other senior government scientists, published estimates on how BMI related to mortality — reporting that being overweight was associated with a lower death rate than having a “normal” BMI — she became the subject of intense criticism and attacks. Flegal and her coauthors were not the first to publish this seemingly counterintuitive observation, but they were among the most prominent. Some researchers in the field, particularly from the Harvard School of Public Health, argued that the findings would detract from the public health message that excess body fat was hazardous, and they took issue with some of the study’s methods. Flegal’s group responded with several subsequent publications reporting that the suggested methodological adjustments didn’t change their findings. © 2022 Annual Reviews

Keyword: Obesity
Link ID: 28469 - Posted: 09.10.2022

Short ribs glazed in a sweet sticky sauce and slow-cooked to perfection, potato chips hand-fried and tossed with a generous coating of sour cream, chicken wings battered and double-fried so that they stay crispy for hours. What is it about these, and other, mouth-watering — but incredibly fatty — foods that makes us reach out, and keep coming back for more? How they taste on the tongue is one part of the story, but to really understand what drives “our insatiable appetite for fat,” we have to examine what happens after fat is consumed, says Columbia University’s Charles Zuker, a neuroscientist and molecular geneticist who has been a Howard Hughes Medical Institute (HHMI) Investigator since 1989. Two years ago, Zuker and his team reported how sugar, upon reaching the gut, triggers signals that are sent to the brain, thus fueling cravings for sweet treats. Now, in an article published in Nature on September 7, 2022, they describe a similar gut-to-brain circuit that underlies a preference for fat. “The gut is the source of our great desire for fat and sugar,” says Zuker. The topic in question is an incredibly timely one, given the current global obesity epidemic. An estimated 13 percent of adults worldwide are obese — thrice that in 1975. In the US, that figure is even higher — at a staggering 42 percent. “It’s a very significant and important health problem,” says Zuker. Having a high body-mass index is a risk factor for stroke, diabetes, and several other diseases. “It’s clear that if we want to help make a difference here, we need to understand the biological basis for our strong appetite for fat and sugar,” he says. Doing so will help us design interventions in the future to “suppress this strong drive to consume” and combat obesity.

Keyword: Obesity; Hormones & Behavior
Link ID: 28468 - Posted: 09.10.2022