Chapter 9. Homeostasis: Active Regulation of the Internal Environment

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Infants who sleep longer through the night and with fewer interruptions may be less likely to become overweight during their first six months of life, according to a study published in the journal SLEEP(link is external). While the research only showed a link – not a cause-effect relationship – between infants’ sleep and weight, the findings suggest that newborns can reap some of the same health benefits that others get from consistent, quality shut-eye. The research emerged from the Rise and SHINE (Sleep Health in Infancy & Early Childhood) study, which analyzes ways sleep may influence a newborn’s growth and development. The five-year study is being supported in part by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health. “What is particularly interesting about this research is that the sleep-obesity association we see across the lifespan appears in infancy and may be predictive of future health outcomes,” said Marishka K. Brown, Ph.D., director of the National Center on Sleep Disorders Research, located within the NHLBI. Brown noted that multiple studies have shown links between good sleep and improved health. For children, this includes a reduced risk of developing obesity and diabetes, while supporting development, learning, and behavior. In the current study, researchers observed 298 newborns and found that for every hourly increase in nighttime sleep, measured between 7 p.m. and 8 a.m., the infants were 26% less likely to become overweight. Likewise, for each reduction in nighttime awakening, they were 16% less likely to become overweight.

Keyword: Sleep; Obesity
Link ID: 28047 - Posted: 10.23.2021

For years, Theresa Babb blamed herself for her obesity. "It was always my fault," she told The Current. "Who else's fault would it be?" She says she spent thousands of dollars trying to lose weight, even going so far as to try commercial weight-loss programs like Weight Watchers and Jenny Craig. She also sought medical help from health-care providers, but she found some of them weren't willing to discuss her weight with her aside beyond uttering clichés about eating less or working out more. "I don't understand why a health-care professional would be afraid of talking to somebody or be uncomfortable about talking with a patient about health," she said. Nothing seemed to work for Babb, and she said she felt like a "failure" for not succeeding. That was until she met obesity specialist Dr. Laura Reardon two years ago. "One of the very first things that Dr. Reardon said to me … was 'It's not your fault,'" she said. "And it was hearing those words for the first time in my life that changed everything for me." According to Statistics Canada data from 2018, 7.3 million Canadian adults reported heights and weights classified as obese. Another 9.9 million Canadian adults were classified as overweight. Combined, these numbers represent 63.1 per cent of the Canadian adult population. Reardon said Babb's journey is one shared with millions of Canadians. "A lot of patients who come to see me probably have experiences like lots of the people out there, which is they've tried everything," she said. "They've gone to all these commercial weight loss programs. They've hired personal trainers. They've gone to the gym." ©2021 CBC/Radio-Canada.

Keyword: Obesity
Link ID: 28045 - Posted: 10.23.2021

by Angie Voyles Askham The gut microbiome is having a moment. An explosion of research over the past decade has delved into a possible connection between the microbiome and brain conditions, including autism. Once-fringe microbial treatments for autism, such as fecal transplants and probiotic pills, are receiving serious scientific attention and funding. It’s still an open question, however, whether the microbiome has a direct effect on autism traits. The most promising data supporting this idea involve altering a mouse’s gut flora, but it is not clear exactly what the mechanism is or if this work translates to people. And the evidence from human studies linking microbes to autism is thin, if a 2021 review of the literature is any guide. Adding to the uncertainty, new unpublished data from one of the largest human studies yet suggests that the link between an atypical gut microbiome and autism is driven solely by a difference in diet. At least four small firms are spearheading early-stage trials of ‘bug as drug’ treatments for autism-associated traits. But until those trials play out, the role of the microbiome in autism is far from clear, says Gaspar Taroncher-Oldenburg, a consultant on microbiome research for the Simons Foundation, Spectrum’s parent organization. “There’s no denying that the microbiome is part of the [autism] conversation,” Taroncher-Oldenburg says. “But it’s a very complex conversation, and we’re only starting to scratch the surface.” A potential connection between the gut microbiome and autism first surfaced in the 1990s, after parents reported changes in their autistic children’s behavior when the children took antibiotics, which kill some gut bacteria. A 2000 study following up on this idea showed that 8 of 10 autistic children taking an antibiotic had temporary improvements in their speech and sociability. Later work associated an atypical gut microbiome with unusual social behaviors in mice. © 2021 Simons Foundation

Keyword: Autism
Link ID: 28043 - Posted: 10.20.2021

Allison Aubrey The "diet" in diet drinks may be a false promise for some soda lovers. True, they deliver the fizz and taste of a soda experience, without the calories. Yet, new research shows they also can leave people with increased food cravings. A study published recently in JAMA Network Open adds to the evidence that drinks made with sucralose may stimulate the appetite, at least among some people, and the study gives some clues as to why. "We found that females and people with obesity had greater brain reward activity" after consuming the artificial sweetener, says study author Katie Page, a physician specializing in obesity at the University of Southern California. Both groups also had a reduction in the hormone that inhibits appetite, and they ate more food after they consumed drinks with sucralose, compared with after regular sugar-sweetened drinks. In contrast, the study found males and people of healthy weight did not have an increase in either brain reward activity or hunger response, suggesting they're not affected in the same way. The study notes that most earlier research focused on males and people of normal weight. But this finding suggests that diet drinks sweetened with sucralose could be disadvantageous to the people who could benefit most from an effective diet strategy. © 2021 npr

Keyword: Obesity; Sexual Behavior
Link ID: 28027 - Posted: 10.09.2021

By Gretchen Reynolds For better health and a longer life span, exercise is more important than weight loss, especially if you are overweight or obese, according to an interesting new review of the relationships between fitness, weight, heart health and longevity. The study, which analyzed the results of hundreds of previous studies of weight loss and workouts in men and women, found that obese people typically lower their risks of heart disease and premature death far more by gaining fitness than by dropping weight or dieting. The review adds to mounting evidence that most of us can be healthy at any weight, if we are also active enough. I have written frequently in this column about the science of exercise and weight loss, much of which is, frankly, dispiriting, if your goal is to be thinner. This past research overwhelmingly shows that people who start to exercise rarely lose much, if any, weight, unless they also cut back substantially on food intake. Exercise simply burns too few calories, in general, to aid in weight reduction. We also tend to compensate for some portion of the meager caloric outlay from exercise by eating more afterward or moving less or unconsciously dialing back on our bodies’ metabolic operations to reduce overall daily energy expenditure, as I wrote about in last week’s column. Glenn Gaesser, a professor of exercise physiology at Arizona State University in Phoenix, is well versed in the inadequacies of workouts for fat loss. For decades, he has been studying the effects of physical activity on people’s body compositions and metabolisms, as well as their endurance, with a particular focus on people who are obese. Much of his past research has underscored the futility of workouts for weight loss. In a 2015 experiment he oversaw, for instance, 81 sedentary, overweight women began a new routine of walking three times a week for 30 minutes. After 12 weeks, a few of them had shed some body fat, but 55 of them had gained weight. In other studies from Dr. Gaesser’s lab, though, overweight and obese people with significant health problems, including high blood pressure, poor cholesterol profiles or insulin resistance, a marker for Type 2 diabetes, showed considerable improvements in those conditions after they started exercising, whether they dropped any weight or not. Seeing these results, Dr. Gaesser began to wonder if fitness might enable overweight people to enjoy sound metabolic health, whatever their body mass numbers, and potentially live just as long as thinner people — or even longer, if the slender people happened to be out of shape. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 28024 - Posted: 10.06.2021

By Kim Tingley It’s simple, we are often told: All you have to do to maintain a healthy weight is ensure that the number of calories you ingest stays the same as the number of calories you expend. If you take in more calories, or energy, than you use, you gain weight; if the output is greater than the input, you lose it. But while we’re often conscious of burning calories when we’re working out, 55 to 70 percent of what we eat and drink actually goes toward fueling all the invisible chemical reactions that take place in our body to keep us alive. “We think about metabolism as just being about exercise, but it’s so much more than that,” says Herman Pontzer, an associate professor of evolutionary anthropology at Duke University. “It’s literally the running total of how busy your cells are throughout the day.” Figuring out your total energy expenditure tells you how many calories you need to stay alive. But it also tells you “how the body is functioning,” Pontzer says. “There is no more direct measure of that than energy expenditure.” Though scientists have been studying metabolism for at least a century, they have not been able to measure it precisely enough — in real-world conditions, in enough people, across a broad-enough age range — to see how it changes throughout the human life span. It is clear that the bigger someone is, the more cells they have, and thus the more total calories they burn per day. But it has been much harder to assess whether variables like age, sex, lifestyle and illness influence our rate of energy expenditure. This lack of data led to assumptions rooted in personal experience: for instance, that significant hormonal changes like those that take place during puberty and menopause cause our metabolism to speed up or slow down, prompting us to burn more or fewer calories per day; or that men have inherently faster metabolisms than women, because they seem able to shed pounds more easily; or that our energy expenditure slows in midlife, initiating gradual and inevitable weight gain. “I’m in my 40s; I feel different than I did in my 20s — I buy it, too,” Pontzer says. “All that intuition was never backed up by data. It just seemed so sure.” © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27994 - Posted: 09.15.2021

Natalie Grover Losing weight through exercise appears to be more difficult for obese people, research suggests. Initially, researchers thought that the total energy we spend in a day is the sum of energy expended due to activity (ranging from light gardening to running a marathon) and energy used for basic functioning (what keeps us ticking even when we are doing nothing, such as immune function and wound healing). But preliminary lab research indicates that that simple addition could be misleading – estimates of total daily expenditure tend to be less than the sum of baseline and activity expenditure in individuals. To explore this further, a group of international scientists analysed measurements of energy expenditure from 1,754 adults from a dataset collected over decades and supplied by the International Atomic Energy Agency. They found that increasing levels of activity by exercising more, for instance, led to each person’s body compensating by limiting the energy expended on basic metabolic functions over a longer period, according to the study published in the journal Current Biology. For instance, if you go for a run and your activity tracker says you burned 300 calories (and you didn’t eat any differently) – you may assume that your total daily energy expenditure went up by 300 calories. That may be the case in the short term, but over the long term the body starts to compensate for this extra energy exertion by reducing the energy spent on other processes, said lead author Prof Lewis Halsey from the University of Roehampton. “It’s like the government trying to balance the budget – if it’s spending more on education for instance, then it might need to spend less on roads,” he said. © 2021 Guardian News & Media Limited

Keyword: Obesity
Link ID: 27971 - Posted: 09.01.2021

By Gina Kolata Everyone knows conventional wisdom about metabolism: People put pounds on year after year from their 20s onward because their metabolisms slow down, especially around middle age. Women have slower metabolisms than men. That’s why they have a harder time controlling their weight. Menopause only makes things worse, slowing women’s metabolisms even more. All wrong, according to a paper published Thursday in Science. Using data from nearly 6,500 people, ranging in age from 8 days to 95 years, researchers discovered that there are four distinct periods of life, as far as metabolism goes. They also found that there are no real differences between the metabolic rates of men and women after controlling for other factors. The findings from the research are likely to reshape the science of human physiology and could also have implications for some medical practices, like determining appropriate drug doses for children and older people. “It will be in textbooks,” predicted Leanne Redman, an energy balance physiologist at Pennington Biomedical Research Institute in Baton Rouge, La., who also called it “a pivotal paper.” Rozalyn Anderson, a professor of medicine at the University of Wisconsin-Madison, who studies aging, wrote a perspective accompanying the paper. In an interview, she said she was “blown away” by its findings. “We will have to revise some of our ideas,” she added. But the findings’ implications for public health, diet and nutrition are limited for the moment because the study gives “a 30,000-foot view of energy metabolism,” said Dr. Samuel Klein, who was not involved in the study and is director of the Center for Human Nutrition at the Washington University School of Medicine in St. Louis. He added, “I don’t think you can make any new clinical statements” for an individual. When it comes to weight gain, he says, the issue is the same as it has always been: People are eating more calories than they are burning. Metabolic research is expensive, and so most published studies have had very few participants. But the new study’s principal investigator, Herman Pontzer, an evolutionary anthropologist at Duke University, said that the project’s participating researchers agreed to share their data. There are more than 80 co-authors on the study. By combining efforts from a half dozen labs collected over 40 years, they had sufficient information to ask general questions about changes in metabolism over a lifetime. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27949 - Posted: 08.14.2021

By Rachel Fritts As you age, your brain slows down. You may forget where you left your glasses or have trouble picking up a new skill. Now there’s hope from rodent experiments that some of these declines could be reversed—but it takes guts. New research shows a transplant of gut microbes, in the form of feces, from young mice to old ones can turn back the clock on the aging brain. The study is “a tour de force” for the scope of data it collected, says Sean Gibbons, a gut microbe researcher at the Institute for Systems Biology. Still, he says, more work must be done before anyone considers doing anything similar with humans. The bacteria in our intestines influence everything from our daily moods to our overall health. This “gut microbiome” also changes over the course of our lives. But whereas some studies have shown young blood can have rejuvenating effects on old mice, the microbiome’s impact on age-related declines hasn’t been clear. To test whether a young microbiome could reverse signs of aging, researchers took fecal samples from 3- to 4-month-old mice, the equivalent of young adults, and transplanted them into 20-month-old animals—ancient by mouse standards. The scientists fed a slurry of feces to the old mice using a feeding tube twice a week for 8 weeks. As controls, old mice received transplants from fellow old mice, and young from young. The first thing the team noticed was that the gut microbiomes of the old mice given young mouse microbes began to resemble those of the younger ones. The common gut microbe Enterococcus became much more abundant in old mice, just as it is in young mice, for example. © 2021 American Association for the Advancement of Science

Keyword: Obesity; Development of the Brain
Link ID: 27939 - Posted: 08.11.2021

By Jane E. Brody No one with debilitating symptoms likes to be told “it’s all in your head.” Yet, this is often what distressed patients with irritable bowel syndrome hear, implicitly or explicitly, when a medical work-up reveals no apparent explanation for their repeated bouts of abdominal pain, bloating, diarrhea or constipation. In fact, irritable bowel syndrome, or I.B.S., is a real problem causing real symptoms, no matter how hard its sufferers may wish it gone. But unlike an infection or tumor, I.B.S. is what medicine calls a functional disorder: a condition with no identifiable cause. Patients have no visible signs of damage or disease in their digestive tracts. Rather, the prevailing theory holds that overly sensitive nerves in the patient’s gastrointestinal tract send distress signals to the brain that result in pain and malfunction. However, as medical science progresses, experts are beginning to find physical explanations for disorders that previously had no known biological cause. For example, conditions like epilepsy, Alzheimer’s disease and migraine were once considered functional disorders, but are now known to have measurable physical or biochemical underpinnings. And recent research has revealed at least one likely explanation for the symptoms of I.B.S.: an infection in the digestive tract that triggers a localized allergic reaction in the gut. As Dr. Marc E. Rothenberg wrote in The New England Journal of Medicine in June, “Patients with I.B.S. often report that their symptoms started at the time of a gastrointestinal infection.” Dr. Rothenberg, who is the director of the division of allergy and immunology at Cincinnati Children’s Hospital Medical Center, explained in an interview that the infection can temporarily disrupt the layer of cells that normally lines the bowel. These cells form a barrier that prevents allergy-inducing proteins in foods from being absorbed. When that barrier is penetrated, people can become intolerant to foods that previously caused them no issue. Sign up for the Well Newsletter Get the best of Well, with the latest on health, fitness and nutrition. Get it sent to your inbox. © 2021 The New York Times Company

Keyword: Stress
Link ID: 27935 - Posted: 08.07.2021

By Jennifer Couzin-Frankel They rose to fame as the world’s fattest mice. At about 130 grams, the rodents were “the equivalent of 600 pounds in humans,” says diabetes researcher Philipp Scherer. They were born to genetically engineered mouse parents in his lab at the University of Texas Southwestern Medical Center. One set of parents lacked the hormone leptin, an appetite suppressant that signals when it’s time to stop eating. The other parents overproduced the hormone adiponectin, churned out by fat cells, which is thought to support metabolic health, protecting against obesity-linked diseases such as type 2 diabetes. Scherer’s mouse pups melded their parents’ traits. They ate constantly and became obese. But unlike other leptin-deficient mice (and people), the animals had healthy cholesterol and blood glucose levels and didn’t develop metabolic illnesses such as type 2 diabetes. “ They were exceptionally quote-unquote healthy,” Scherer says, though he wonders whether it’s possible to be truly well while carrying such a considerable fat burden. Despite their metabolic health, the mice didn’t live a normal life span: Their weight left them so off balance that they often flipped over and got stuck, causing dehydration and death. Still, to Scherer, who described the animals in 2007 and continues to study them, the rodents sharpened an emerging message for people as well as mice: Weight and health can be uncoupled. Many researchers and doctors—and broader societies—take it as a given that obesity means ill health. In fact, says Ruth Loos, who studies the genetics of obesity at the University of Copenhagen, “We can be obese but remain healthy.” Scherer, Loos, and other researchers worldwide are examining genes, animal models, and humans to understand how factors such as the distribution of fat in the body and the nature of fat itself can blunt or compound any health impacts of extra weight. The researchers are also working to define metabolically healthy obesity (MHO) and examine how common it is and how long it persists. © 2021 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 27930 - Posted: 08.04.2021

By Jonathan Lambert Winter on the Qinghai-Tibetan Plateau is unfriendly to pikas. Temperatures across the barren, windy highlands routinely dip below –30° Celsius, and the grass that typically sustains the rabbitlike mammals becomes dry and brittle. It would seem the perfect time for these critters to hibernate, or subsist on stores of grass in burrows to stay warm, like the North American pika. Instead, plateau pika (Ochotona curzoniae) continue foraging in winter, but reduce their metabolism by about 30 percent to conserve energy, researchers report July 19 in the Proceedings of the National Academy of Sciences. Some pikas also resort to unusual rations: yak poop. Camera data from four sites confirmed that pikas regularly brave the cold to forage. “Clearly they’re doing something fancy with their metabolism that’s not hibernation,” says John Speakman, an ecophysiologist at the University of Aberdeen in Scotland. Speakman and colleagues measured daily energy expenditure of 156 plateau pikas in summer and winter, and implanted 27 animals with temperature sensors. While many nonhibernating animals keep warm in winter by using more energy, these pikas did the opposite (SN: 1/22/14). On average, pikas reduced their metabolism by 29.7 percent, in part by cooling their bodies a couple degrees overnight. The animals were also less active, relative to summertime levels. © Society for Science & the Public 2000–2021.

Keyword: Obesity
Link ID: 27916 - Posted: 07.21.2021

By Gretchen Reynolds We all know that lifting weights can build up our muscles. But by changing the inner workings of cells, weight training may also shrink fat, according to an enlightening new study of the molecular underpinnings of resistance exercise. The study, which involved mice and people, found that after weight training, muscles create and release little bubbles of genetic material that can flow to fat cells, jump-starting processes there related to fat burning. The results add to mounting scientific evidence that resistance exercise has unique benefits for fat loss. They also underscore how extensive and interconnected the internal effects of exercise can be. Many of us pigeonhole resistance training as muscle building, and with good reason. Lifting weights — or working against our body weight as we bob through push-ups, squats or chair dips — will noticeably boost our muscles’ size and strength. But a growing number of studies suggest weight training also reshapes our metabolisms and waistlines. In recent experiments, weight workouts goosed energy expenditure and fat burning for at least 24 hours afterward in young women, overweight men and athletes. Likewise, in a study I covered earlier this month, people who occasionally lifted weights were far less likely to become obese than those who never lifted. But how weight training revamps body fat remains murky. Part of the effect occurs because muscle is metabolically active and burns calories, so adding muscle mass by lifting should increase energy expenditure and resting metabolic rates. After six months of heavy lifting, for example, muscles will burn more calories just because they are larger. But that doesn’t fully explain the effect, because adding muscle mass requires time and repetition, while some of the metabolic effects of weight training on fat stores seem to occur immediately after exercise. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27915 - Posted: 07.21.2021

Yuki Noguchi Health conditions exacerbated by obesity include heart disease, stroke, Type 2 diabetes and certain types of cancer, according to the CDC. Researchers say the newly approved drug Wegovy could help many who struggle with obesity lose weight. adamkaz/Getty Images When a promising new drug to treat obesity was approved by the Food and Drug Administration for sale in the U.S. last month, it was the first such treatment to gain approval since 2014. In clinical trials, weekly injections of semaglutide — or Wegovy, as it's been branded — helped people drop an average of 15% of their body weight. That's an average of about 34 pounds over 16 months, before their weight plateaued — roughly triple what's achieved with other drugs on the market. At least as important, Wegovy raised none of the alarm bells with the FDA or obesity doctors that it might trigger serious side effects of the sort some people experienced by taking fen-phen or other previous medical treatments for obesity. But with a price tag for Wegovy of $1,000 to $1,500 a month, a big question remains: Will insurers cover its significant cost for the millions such as Marleen Greenleaf who might benefit? Greenleaf grew up on the island of Trinidad, where her family paid little heed to what they ate and paid a high medical price, she says: "My husband has diabetes, my sister has diabetes, my brother has diabetes." Since then, she's tried — and failed — at numerous diets, says Greenleaf, now 58 and an administrator at a charter school in Washington, D.C. Then, in 2018, she signed up for the clinical trial of a new drug — a once-weekly shot that changes the way her brain signals hunger. © 2021 npr

Keyword: Obesity
Link ID: 27896 - Posted: 07.08.2021

By Rodrigo Pérez Ortega For some people, no amount of exercise and dieting keeps the kilograms off. For others, leanness comes naturally. Now, scientists might know one reason why. In one of the most comprehensive studies of the genetics of obesity to date, a research team has identified rare gene variants that protect lucky carriers from putting on weight. The work is “a tour de force of genetics,” says Sadaf Farooqi, an obesity researcher at the University of Cambridge who was not involved with the study. Geneticists generally look for mutations that cause disease, but people can also carry subtly different versions of a gene that promote good health. Finding rare variants that offer protection against a disease is very hard because sequencing studies are usually small, Farooqi notes. Yet such variants can lead to new drug targets, she adds. At least 2.8 million people die every year from being overweight or clinically obese. Obesity increases the risk of developing type 2 diabetes, heart disease, some cancers, and even severe COVID-19. Diet and exercise can help people with obesity lose weight, but genetics also strongly influence whether a person develops the disease. Studies that focused on people with extreme obesity have identified common gene variants—like a “broken” copy of the MC4R gene, linked to appetite regulation—that make people more likely to be overweight. Other work has found thousands of genetic variants, each of which has a tiny impact on body weight; together, they can significantly increase the likelihood of obesity. In the new study, researchers sequenced the genomes of more than 640,000 people from Mexico, the United States, and the United Kingdom, homing in on only the exome—the part of the genome that codes for proteins. © 2021 American Association for the Advancement of Science.

Keyword: Obesity; Genes & Behavior
Link ID: 27887 - Posted: 07.03.2021

By Kim Tingley Childhood obesity has increased significantly in the United States during the past four decades. In 1980, about 5 percent of the country’s children between 2 and 19 were experiencing obesity, according to the C.D.C.; as of 2018, more than 19 percent were — and an additional 16 percent were considered overweight. Because children are far more likely to gain an unhealthful amount of weight while out of school over the summer, experts were worried last spring when in-person schooling was suspended indefinitely because of the pandemic. They feared extended closures might “exacerbate the epidemic of childhood obesity and increase disparities in obesity risk,” as researchers from the Mailman School of Public Health at Columbia University and colleagues put it in a paper in the journal Obesity in June 2020. That, in turn, would mean more children living with related conditions such as Type 2 diabetes, hypertension and fatty-liver disease. Those concerns were warranted, according to a May study in Pediatrics. Based on measurements of body mass index taken for more than 500,000 children between the ages of 2 and 17 during visits to the Children’s Hospital of Philadelphia Care Network, researchers found that, on average, between January 2019 and December 2020 the prevalence of obesity increased by almost 2 percentage points overall, from 13.7 percent to 15.4 percent. (In the most recent years for which national data is available, the increase has been 1 percentage point or less.) Black and Latino children, as well as those from families with lower incomes, displayed sharper increases than children from other groups did. Such gains early in life make it more likely that children will have higher B.M.I.s when they grow up. (Obesity already affects more than 40 percent of American adults.) “This isn’t just baby fat that’s going to go away,” says Brian Jenssen, the study’s lead author and a pediatrician at Children’s. “That’s why I think this is so alarming.” © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27875 - Posted: 06.26.2021

By Emily Underwood In the 1930s, neurosurgeon Wilder Penfield pioneered a daring new kind of cartography. As a stenographer took notes, he delicately touched an electrode to the exposed brains of his awake, consenting patients and asked what they felt as electrical current hit different areas. Penfield wanted to better predict which brain functions would be threatened when surgeons had to remove tumors or chunks of tissue that were triggering epileptic seizures. Stimulating adjacent brain regions, he found, produced sensations in corresponding body parts: hand, forearm, elbow. The result of his mapping was the iconic “homunculus”: a map on the brain’s wrinkled outer layer representing the surface of the body. Penfield then ventured into more mysterious territory. When he probed the insula, a deep fold of cortex, some patients felt nauseated or gassy; others belched or vomited. “My stomach is upset and I smell something like medicine,” one said. Penfield found those visceral signals harder to decipher than the brain’s map of the body’s surface. Brain regions responsible for different internal sensations seemed to overlap. Sensory regions were hard to distinguish from those that sent motor instructions such as telling the intestines to contract. Penfield once asked participants to swallow an electrode to detect changes in gut contractions while he stimulated their brains. But his map of the inner organs was blurry and ambiguous—and stayed that way for most of the next century. Decades later, scientists are starting to unravel how our wet, spongy, slippery organs talk to the brain and how the brain talks back. That two-way communication, known as interoception, encompasses a complex, bodywide system of nerves and hormones. Much recent exploration has focused on the vagus nerve: a massive, meandering network of more than 100,000 fibers that travel from nearly every internal organ to the base of the brain and back again. © 2021 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 27850 - Posted: 06.11.2021

By Mitch Leslie For the past 3 years, about 6000 middle-aged and elderly Australians have pumped iron, loaded up on greens and whole grains, strived to quell stress, and challenged their wits with computer exercises, all in an effort to preserve their cognition. They’re part of a clinical trial called Maintain Your Brain, one of about 30 current or planned studies that eschew pharmaceutical interventions and test whether altering multiple aspects of participants’ lives improves brain health. Such multidomain studies may finally reveal whether modifying diet, exercise, and other factors can slow cognitive decline as people age—or even prevent dementia. “There’s a lot of hope for multidomain trials,” says psychologist Kaarin Anstey of the University of New South Wales, Sydney, one of the principal investigators of the Maintain Your Brain trial, which will finish by the end of this year. Although people can’t escape some mental decline as they get older, lifestyle exerts a powerful influence over the risk of developing dementia—the type of severe cognitive impairment seen in conditions such as Alzheimer’s disease. Last year, an international committee of scientists and psychiatrists known as the Lancet Commission on dementia prevention, intervention, and care estimated that so-called modifiable factors account for 40% of dementia risk. Their report highlighted a dozen factors, including many familiar villains—diabetes, high blood pressure, smoking, obesity, and lack of exercise. Researchers are still probing exactly how these risk factors steal people’s faculties, but they’ve identified some likely mechanisms. Lack of physical activity may impair cognition, for instance, because exercise stimulates formation of new neurons and soothes brain inflammation. © 2021 American Association for the Advancement of Science.

Keyword: Alzheimers; Obesity
Link ID: 27834 - Posted: 05.29.2021

By Gina Kolata Obesity has stalked Marleen Greenleaf, 58, all of her life. Like most people with obesity, she tried diet after diet. But the weight always came back. With that, she has suffered a lifetime of scorn and stigma. Jeering comments from strangers when she walked down the street. Family members who told her, when she trained for a half-marathon, “I don’t think it’s good for you.” Then, in 2018, Ms. Greenleaf, an administrator at a charter school in Washington, D.C., participated in a clinical trial for semaglutide, which is a new type of obesity drug, known as incretins. Over the course of the 68-week study, Ms. Greenleaf slowly lost 40 pounds. Until then, she had always believed that she could control her weight if she really tried. “I thought I just needed more motivation,” she said. But when she took semaglutide, she said that “immediately, the urge to eat just dissipated.” Incretins appear to elicit significant weight loss in most patients, enough to make a real medical and aesthetic difference. But experts hope that the drugs also do something else: change how society feels about people with obesity, and how people with obesity feel about themselves. If these new drugs allow obesity to be treated like a chronic disease — with medications that must be taken for a lifetime — the thought is that doctors, patients and the public might understand that obesity is truly a medical condition. © 2021 The New York Times Company

Keyword: Obesity; Hormones & Behavior
Link ID: 27821 - Posted: 05.15.2021

By Nicholas Bakalar Type 2 diabetes is a chronic, progressive illness that can have devastating complications, including hearing loss, blindness, heart disease, stroke, kidney failure and vascular damage so severe as to require limb amputation. Now a new study underscores the toll that diabetes may take on the brain. It found that Type 2 diabetes is linked to an increased risk for Alzheimer’s disease and other forms of dementia later in life, and the younger the age at which diabetes is diagnosed, the greater the risk. The findings are especially concerning given the prevalence of diabetes among American adults and rising rates of diabetes in younger people. Once referred to as “adult-onset diabetes” to distinguish it from the immune-related “juvenile-onset” Type 1 disease that begins in childhood, Type 2 diabetes is seen in younger and younger people, largely tied to rising rates of obesity. The Centers for Disease Control and Prevention estimates that more than 34 million American adults have Type 2 diabetes, including more than a quarter of those 65 and over. About 17.5 percent of those aged 45 to 64 have Type 2 disease, as do 4 percent of 18- to 44-year-olds. “This is an important study from a public health perspective,” said the director of the Yale Diabetes Center, Dr. Silvio Inzucchi, who was not involved in the research. “The complications of diabetes are numerous, but the brain effects are not well studied. Type 2 diabetes is now being diagnosed in children, and at the same time there’s an aging population.” © 2021 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 27803 - Posted: 05.05.2021