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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

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 27994 - Posted: 09.15.2021

Weight loss via exercise harder for obese people, data suggests

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

What We Think We Know About Metabolism May Be Wrong

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

New poo, new you? Fecal transplants reverse signs of brain aging in mice

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

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory and Learning
Link ID: 27939 - Posted: 08.11.2021

Obesity doesn’t always mean ill health. Here’s what scientists are learning

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

Pikas survive winter using a slower metabolism and, at times, yak poop

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.

Lifting Weights? Your Fat Cells Would Like to Have a Word

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

Obesity Drug's Promise Now Hinges On Insurance Coverage

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

Massive DNA study finds rare gene variants that protect against obesity

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.

The Pandemic Seems to Have Made Childhood Obesity Worse, but There’s Hope

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

New Role for Leptin: Promoting Synapse Formation in Rat Neurons

Abby Olena Leptin is a hormone released by fat cells in adult organisms, and researchers have largely focused on how it controls appetite. In a study published May 18 in Science Signaling, the authors show that leptin promotes synapse formation, or synaptogenesis, in developing rodent neurons in culture. “This paper does a really wonderful job [breaking] down the mechanisms” of leptin signaling, and the authors look at changes in synaptic function, not just at the protein level, but also on a physiological level, says Laura Cocas, a neuroscientist at Santa Clara University who was not involved in the study. “Because all of the work on the paper is done in vitro, they can do very careful analysis . . . to break down each step in the signaling pathway.” When Washington State University neuroscientist Gary Wayman and his group started working on leptin about 10 years ago, most of the research had examined the hormone’s function in regulating satiety. But “we and others knew that leptin surged during a critical period of neuronal—and in particular synaptic—development in the brain,” he says. In people, this surge happens during the third trimester of fetal development and, in rodents, over the first few weeks of life. “This surge in leptin is independent of the amount of adipose tissue that’s present. And it does not control feeding during this period because feeding circuits have not developed, so we really wanted to understand what the developmental role was.” Wayman and colleagues focused on the hippocampus because, despite being one of the best-characterized regions in the brain, there wasn’t a lot of information out there about what the leptin receptors present were doing—particularly during development. Multiple groups had also shown that leptin injected in this brain region can improve cognition and act as an antidepressant. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 13: Memory and Learning
Link ID: 27837 - Posted: 05.29.2021

New Drugs Could Help Treat Obesity. Could They End the Stigma, Too?

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

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 27821 - Posted: 05.15.2021

Intermittent fasting and why when you eat makes a difference

By Andreas von Bubnoff The world is getting fatter. More than 40 percent of U.S. adults are obese — almost three times more than in 1980. One reason for this weight gain is Americans are consuming more: National figures suggest an increase of about 200 daily calories between the early 1970s and 2010. Another is more snacking. In 2010, U.S. adults ate about 20 percent more of their daily calories as snacks than they did 50 years ago. But there is more to rising obesity rates than endless grazing. What also matters is timing, some experts believe. We eat when we shouldn’t, and don’t give our bodies a long enough break in between. We didn’t evolve to eat day and night, says neuroscientist Dominic D’Agostino of the University of South Florida. Until the dawn of agriculture about 12,000 years ago, we subsisted on hunting and gathering and often had to perform those activities with empty bellies. “We are hard-wired,” D’Agostino says, “to undergo periodic intermittent fasting.” What’s more, people are now eating at times of the day when historically they would have been asleep, says Satchin Panda, a circadian biologist at the Salk Institute for Biological Studies in La Jolla, Calif., who co-wrote an overview on the timing of eating in the 2019 Annual Review of Nutrition. For thousands of years, he says, our nightly fast probably started much earlier than in these times of late-night television. Although the research is still mixed, the timing of eating seems to matter for body weight and health. Studies suggest significant potential benefits from fasting every other day or so — or, on a daily basis, eating only when we would normally be awake, within a window of 12 hours or fewer — a practice known as time-restricted eating. © 1996-2021 The Washington Post

Unhealthy Foods Aren’t Just Bad For You, They May Also Be Addictive

By Anahad O’Connor Five years ago, a group of nutrition scientists studied what Americans eat and reached a striking conclusion: More than half of all the calories that the average American consumes comes from ultra-processed foods, which they defined as “industrial formulations” that combine large amounts of sugar, salt, oils, fats and other additives. Highly processed foods continue to dominate the American diet, despite being linked to obesity, heart disease, Type 2 diabetes and other health problems. They are cheap and convenient, and engineered to taste good. They are aggressively marketed by the food industry. But a growing number of scientists say another reason these foods are so heavily consumed is that for many people they are not just tempting but addictive, a notion that has sparked controversy among researchers. Recently, the American Journal of Clinical Nutrition explored the science behind food addiction and whether ultra-processed foods might be contributing to overeating and obesity. It featured a debate between two of the leading experts on the subject, Ashley Gearhardt, associate professor in the psychology department at the University of Michigan, and Dr. Johannes Hebebrand, head of the department of child and adolescent psychiatry, psychosomatics and psychotherapy at the University of Duisburg-Essen in Germany. Dr. Gearhardt, a clinical psychologist, helped develop the Yale Food Addiction Scale, a survey that is used to determine whether a person shows signs of addictive behavior toward food. In one study involving more than 500 people, she and her colleagues found that certain foods were especially likely to elicit “addictive-like” eating behaviors, such as intense cravings, a loss of control, and an inability to cut back despite experiencing harmful consequences and a strong desire to stop eating them. At the top of the list were pizza, chocolate, potato chips, cookies, ice cream, French fries and cheeseburgers. © 2021 The New York Times Company

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: Development of the Brain
Link ID: 27706 - Posted: 02.23.2021

‘A Game Changer’: Drug Brings Weight Loss in Patients With Obesity

By Gina Kolata For the first time, a drug has been shown so effective against obesity that patients may dodge many of its worst consequences, including diabetes, researchers reported on Wednesday. The drug, semaglutide, made by Novo Nordisk, already is marketed as a treatment for Type 2 diabetes. In a clinical trial published in the New England Journal of Medicine, researchers at Northwestern University in Chicago tested semaglutide at a much higher dose as an anti-obesity medication. Nearly 2,000 participants, at 129 centers in 16 countries, injected themselves weekly with semaglutide or a placebo for 68 weeks. Those who got the drug lost close to 15 percent of their body weight, on average, compared with 2.4 percent among those receiving the placebo. More than a third of the participants receiving the drug lost more than 20 percent of their weight. Symptoms of diabetes and pre-diabetes improved in many patients. Those results far exceed the amount of weight loss observed in clinical trials of other obesity medications, experts said. The drug is a “game-changer,” said Dr. Robert F. Kushner, an obesity researcher at Northwestern University Feinberg School of Medicine, who led the study. “This is the start of a new era of effective treatments for obesity.” Dr. Clifford Rosen of Maine Medical Center Research Institute, who was not involved in the trial, said, “I think it has a huge potential for weight loss.” Gastrointestinal symptoms among the participants were “really marginal — nothing like with weight loss drugs in the past,” added Dr. Rosen, an editor at the New England Journal of Medicine and a co-author of an editorial accompanying the study. For decades, scientists have searched for ways to help growing numbers of people struggling with obesity. Five currently available anti-obesity drugs have side effects that limit their use. The most effective, phentermine, brings about a 7.5 percent weight loss, on average, and can be taken only for a short time. After it is stopped, even that amount of weight is regained. © 2021 The New York Times Company

How gut microbes could drive brain disorders

Cassandra Willyard In 2006, soon after she launched her own laboratory, neuroscientist Jane Foster discovered something she felt sure would set her field abuzz. She and her team were working with two groups of mice: one with a healthy selection of microorganisms in their guts, and one that lacked a microbiome. They noticed that the mice without gut bacteria seemed less anxious than their healthy equivalents. When placed in a maze with some open paths and some walled-in ones, they preferred the exposed paths. The bacteria in the gut seemed to be influencing their brain and behaviour. Foster, at McMaster University in Toronto, Canada, wrote up the study and submitted it for publication. It was rejected. She rewrote it and sent it out again. Rejected. “People didn’t buy it. They thought it was an artefact,” she says. Finally, after three years and seven submissions, she got an acceptance letter1. John Cryan, a neuroscientist at University College Cork in Ireland, joined the field about the same time as Foster did, and knows exactly how she felt. When he began talking about the connections between bacteria living in the gut and the brain, “I felt very evangelical”, he says. He recalls one Alzheimer’s disease conference at which he presented in 2014. “I’ve never given a talk in a room where there was less interest.” Today, however, the gut–brain axis is a feature at major neuroscience meetings, and Cryan says he is no longer “this crazy guy from Ireland”. Thousands of publications over the past decade have revealed that the trillions of bacteria in the gut could have profound effects on the brain, and might be tied to a whole host of disorders. Funders such as the US National Institutes of Health are investing millions of dollars in exploring the connection. © 2021 Springer Nature Limited

To Lose Weight With Exercise, Aim for 300 Minutes a Week

By Gretchen Reynolds Can exercise help us shed pounds? An interesting new study involving overweight men and women found that working out can help us lose weight, in part by remodeling appetite hormones. But to benefit, the study suggests, we most likely have to exercise a lot — burning at least 3,000 calories a week. In the study, that meant working out six days a week for up to an hour, or around 300 minutes a week. The relationship between working out and our waistlines is famously snarled. The process seems as if it should straightforward: We exercise, expend calories and, if life and metabolisms were just, develop an energy deficit. At that point, we would start to use stored fat to fuel our bodies’ continuing operations, leaving us leaner. But our bodies are not always cooperative. Primed by evolution to maintain energy stores in case of famine, our bodies tend to undermine our attempts to drop pounds. Start working out and your appetite rises, so you consume more calories, compensating for those lost. The upshot, according to many past studies of exercise and weight loss, is that most people who start a new exercise program without also strictly monitoring what they eat do not lose as much weight as they expect — and some pack on pounds. But Kyle Flack, an assistant professor of nutrition at the University of Kentucky, began to wonder a few years ago if this outcome was inevitable. Maybe, he speculated, there was a ceiling to people’s caloric compensations after exercise, meaning that if they upped their exercise hours, they would compensate for fewer of the lost calories and lose weight. © 2020 The New York Times Company

Where You Carry Body Fat May Affect How Long You Live

By Nicholas Bakalar Being overweight is linked to an increased risk for premature death, but which part of the body carries the added fat could make a big difference. Extra weight in some places may actually lower the risk. Researchers, writing in BMJ, reviewed 72 prospective studies that included more than two and a half million participants with data on body fat and mortality. They found that central adiposity — a large waist — was consistently associated with a higher risk of all-cause mortality. In pooled data from 50 studies, each four-inch increase in waist size was associated with an 11 percent increased relative risk for premature death. The association was significant after adjusting for smoking, physical activity and alcohol consumption. Waist size is an indicator of the amount of visceral fat, or fat stored in the abdomen around the internal organs. This kind of fat is associated with an increased risk for heart disease, Type 2 diabetes, cancer and Alzheimer’s disease. But increased fat in two places appears to be associated with a lower risk of death. Three studies showed that each two-inch increase in thigh circumference was associated with an 18 percent lower risk of all-cause mortality. In nine studies involving almost 300,000 participants, a four-inch increase in a woman’s hip circumference was associated with a 10 percent lower risk of death. “Thigh size is an indicator of the amount of muscle, which is protective,” said a co-author of the review, Tauseef Ahmad Khan, a postdoctoral fellow at the University of Toronto. “And hip fat is not visceral fat, but subcutaneous fat, which is considered beneficial.” © 2020 The New York Times Company

The Underused Weight Loss Option: Bariatric Surgery

By Jane E. Brody Growing rates of obesity among Americans are clear evidence that even the best intentions and strongest motivations are often not enough to help seriously overweight people lose a significant amount of weight and, more important, keep it off. But for those who can overcome fears of surgery and perhaps do battle with recalcitrant insurers, there remains another very successful option that experts say is currently vastly underused. That option is bariatric surgery, an approach that is now simpler, safer and more effective than in its early days in the 1990s. “Only one-half of 1 percent of people eligible for bariatric surgery currently undergo it,” Dr. Anne P. Ehlers, a bariatric surgeon at the University of Michigan, told me. Bariatric surgery is generally considered a treatment option for people with a body mass index (B.M.I.) of 40 or more who failed to lose weight with diet and exercise alone. It is also recommended for those with lesser degrees of obesity — a B.M.I. of 30 to 35 — who have obesity-related medical conditions. The underuse of weight-loss surgery has been largely attributed to “the reluctance of the medical community and patients to accept surgery as a safe, effective and durable treatment of obesity,” other experts at the University of Michigan wrote in JAMA in 2018. They added that patients “may be reluctant to pursue surgical treatment because they may be judged by others for taking the easy way out and not having the willpower to diet and exercise.” © 2020 The New York Times Company

Losing 13 percent of your weight could lead to big improvements in your health

By Linda Searing If you’re obese, losing just 5 percent of your weight starts you on the path to better health, but new research finds that losing 13 percent of your weight may make a good-size dent in your chances of developing several unhealthy conditions. For instance, the odds of developing Type 2 diabetes were at least 42 percent lower among obese people who lost that much weight than for those who did not lose weight, according to a report from the European and International Congress on Obesity. The research was based on eight years of data on 552,953 middle-aged adults who were obese and intentionally lost weight (meaning their weight loss did not occur because of an illness). Besides the diabetes effect, losing 13 percent of their weight also made people 25 percent less likely to develop high blood pressure or sleep apnea, and it correlated to a 22 percent risk reduction for high cholesterol and a 20 percent lower risk for osteoarthritis. Obesity, defined as excessive fat accumulation that presents a risk to health, is often determined by a person’s body mass index (BMI), a calculation of body fatness based on weight and height. The simplest way to figure your BMI is to plug your height and weight into an online calculator. A BMI of 30 or above is considered obese. Treatment for obesity usually starts with a modest weight-loss goal of 5 to 10 percent (10 to 20 pounds for someone weighing 200) and includes a change in eating habits and an increase in physical activity.

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