Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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By Gina Kolata The study subjects had been thin all their lives, and not because they had unusual metabolisms. They just did not care much about food. They never ate enormous amounts, never obsessed on the next meal. Now, a group of researchers in Britain may have found the reason. The people carry a genetic alteration that mutes appetite. It also greatly reduces their chances of getting diabetes or heart disease. The scientists’ study, published on Thursday in the journal Cell, relied on data from the U.K. Biobank, which includes a half million people aged 40 to 69. Participants have provided DNA samples and medical records, and have allowed researchers to track their health over years. A second study in the same journal also used data from this population to develop a genetic risk score for obesity. It can help predict, as early as childhood, who is at high risk for a lifetime of obesity and who is not. Together, the studies confirm a truth that researchers wish more people understood. There are biological reasons that some struggle mightily with their weight and others do not, and the biological impacts often are seen on appetite, not metabolism. People who gain too much weight or fight to stay thin feel hungrier than naturally thin people. The study of the appetite-dulling mutation was led by Dr. Sadaf Farooqi, professor of metabolism and medicine at the University of Cambridge, and Nick Wareham, an epidemiologist at the university. The study drew on Dr. Farooqi’s research into a gene, MC4R. She has probed it for 20 years, but for the opposite reason: to understand why some people are overweight, not why some are thin. © 2019 The New York Times Company

Keyword: Obesity; Genes & Behavior
Link ID: 26156 - Posted: 04.19.2019

Tina Hesman Saey There’s a new way to predict whether a baby will grow into an obese adult. Combining the effect of more than 2.1 million genetic variants, researchers have created a genetic predisposition score that they say predicts severe obesity. People with scores in the highest 10 percent weighed, on average, 13 kilograms (about 29 pounds) more than those with the lowest 10 percent of scores, the team reports April 18 in Cell. The finding may better quantify genes’ roles in obesity than previous prediction scores, but still fails to account for lifestyle, which may be more important in determining body weight, other researchers say. Still, the study shows that “your genetics really start to take hold very early in life,” says coauthor Amit Khera, a cardiologist at Massachusetts General Hospital and the Broad Institute of MIT and Harvard. Weight differences showed up as early as age 3, and by age 18, those with the highest scores weighed 12.3 kilograms more on average than those with the lowest scores, Khera and his colleagues found. Some people with high genetic scores had normal body weights, but those people may have to work harder to maintain a healthy weight than others, he says. People with the highest scores were 25 times more likely to have severe obesity — a body mass index (BMI) greater than 40 — than those with the lowest scores. BMI is a measurement of body fat based on height and weight. A BMI of 18.5 (calculated as kilograms per meters squared of height) to 24.9 is considered healthy. BMIs 30 and above are considered obese. |© Society for Science & the Public 2000 - 2019

Keyword: Obesity; Genes & Behavior
Link ID: 26155 - Posted: 04.19.2019

/ By Richard Kemeny Northern Ethiopia was once home to a vast, ancient lake. Saber-toothed cats prowled around it, giant crocodiles swam within. The streams and rivers that fed it — over 3 million years ago, during the Pliocene — left behind trails of sediment that have now hardened into sandstone. Deposited within these layers are fossils: some of early hominins, along with the bones of hippos, antelope, and elephants. Anthropologist Jessica Thompson encountered two of these specimens, from an area named Dikika, in 2010. At the time, she was a visiting researcher at the Institute of Human Origins at Arizona State University. Given no explanation as to their history, she analyzed the bones and found signs of butchery. Percussion marks suggested someone may have accessed the marrow; cut marks hinted that flesh was stripped from bone. To her surprise, the specimens were 3.4 million years old, putting the butcher’s behaviors back 800,000 years earlier than conventional estimates would suggest. That fact got Thompson, now an assistant professor in the Department of Anthropology at Yale University, thinking there might be more traces of tool use from those early times. In a wide-ranging review published in February’s issue of Current Anthropology, Thompson joins a team of researchers to weave together several strands of recent evidence and propose a new theory about the transition to large animal consumption by our ancestors. The prevailing view, supported by a confluence of fossil evidence from sites in Ethiopia, is that the emergence of flaked tool use and meat consumption led to the cerebral expansion that kickstarted human evolution more than 2 million years ago. Thompson and her colleagues disagree: Rather than using sharpened stones to hunt and scrape meat from animals, they suggest, earlier hominins may have first bashed bones to harvest fatty nutrients from marrow and brains. Copyright 2019 Undark

Keyword: Evolution
Link ID: 26107 - Posted: 04.03.2019

By Jane E. Brody Attention all consumers seeking to protect brain health: You can save hundreds of dollars a year and enhance the health of your brain and body by ignoring the myriad unproven claims for anti-dementia supplements and instead focusing on a lifestyle long linked to better mental and physical well-being. How many of these purported brain boosters have you already tried — Ginkgo biloba, coenzyme Q10, huperzine A, caprylic acid and coconut oil, coral calcium, among others? The Alzheimer’s Association says that, with the possible exception of omega-3 fatty acids, all that were properly tested thus far have been found wanting. I admit it’s very appealing to think you can maintain your cognitive powers by swallowing a few pills a day instead of adopting a brain-healthy diet, getting regular exercise and adequate sleep, among other health-preserving measures like not smoking. But you’d only be fooling yourself and wasting precious dollars that could be better spent on nutritious foods and a good pair of walking shoes. “No known dietary supplement prevents cognitive decline or dementia,” Dr. Joanna Hellmuth stated emphatically in JAMA in January. “Yet,” she added, “supplements advertised as such are widely available and appear to gain legitimacy when sold by major U.S. retailers.” Dr. Hellmuth, a neurologist at the University of California, San Francisco, Memory and Aging Center, reminds consumers that supplement manufacturers do not have to test their products for effectiveness or safety. Lacking sound scientific backing, most are promoted by testimonials that appeal to people worried about developing dementia. © 2019 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 26101 - Posted: 04.01.2019

By Richard Schiffman The patient, a 48-year-old real estate professional in treatment for anxiety and mild depression, revealed that he had eaten three dozen oysters over the weekend. His psychiatrist, Dr. Drew Ramsey, an assistant clinical professor of psychiatry at Columbia University, was impressed: “You’re the only person I’ve prescribed them to who came back and said he ate 36!” Dr. Ramsey, the author of several books that address food and mental health, is a big fan of oysters. They are rich in vitamin B12, he said, which studies suggest may help to reduce brain shrinkage. They are also well stocked with long chain omega-3 fatty acids, deficiencies of which have been linked to higher risk for suicide and depression. But shellfish are not the only food he is enthusiastic about. Dr. Ramsey is a pioneer in the field of nutritional psychiatry, which attempts to apply what science is learning about the impact of nutrition on the brain and mental health. Dr. Ramsey argues that a poor diet is a major factor contributing to the epidemic of depression, which is the top driver of disability for Americans aged 15 to 44, according to a report by the World Health Organization. Together with Samantha Elkrief, a chef and food coach who sits in on many of his patient sessions, he often counsels patients on how better eating may lead to better mental health. The irony, he says, is that most Americans are overfed in calories yet starved of the vital array of micronutrients that our brains need, many of which are found in common plant foods. A survey published in 2017 by the Centers for Disease Control and Prevention reported that only one in 10 adults meets the minimal daily federal recommendations for fruit and vegetables — at least one-and-a-half to two cups per day of fruit and two to three cups per day of vegetables. © 2019 The New York Times Company

Keyword: Depression
Link ID: 26087 - Posted: 03.28.2019

Jon Hamilton When you're thirsty, a swig of fresh water brings instant relief. But gulp down some salty sea water and you'll still feel parched. That's because your brain is trying to keep the concentration of salt in your body within a very narrow range, says Zachary Knight, an associate professor in physiology at the University of California, San Francisco and an investigator with the Howard Hughes Medical Institute. "If you experience, for example, a 10 percent change, you would be very sick," he says. "A 20 percent change and you could die." Knight and a team of researchers wanted to know how the brain keeps that from happening. They report the results of their search in an article published Wednesday in the journal Nature. "There has to be a mechanism for the brain to track how salty the solutions that you drink are and use that to fine-tune thirst," Knight says. "But the mechanism was unknown." So Knight's team began studying brain cells known as thirst neurons. First, the team piped fresh water directly into the stomachs of some thirsty mice. "Within a minute or two, infusing water into the stomach rapidly turns off these thirst neurons in the brain," says Chris Zimmerman, a graduate student in Knight's lab who conducted the experiment. "And not only that," Zimmerman says, "if we give [the mouse] access to water it doesn't drink at all." © 2019 npr

Keyword: Miscellaneous
Link ID: 26086 - Posted: 03.28.2019

By Andrew Jacobs What do these ads featuring Joe Camel, Kool-Aid Man and the maniacal mascot for Hawaiian Punch have in common? All three were created by Big Tobacco in the decades when cigarette makers, seeking to diversify their holdings, acquired some of America’s iconic beverage brands. They used their expertise in artificial flavor, coloring and marketing to heighten the products’ appeal to children. That tobacco companies once sold sugar-sweetened drinks like Tang, Capri Sun and Kool-Aid is not exactly news. But researchers combing through a vast archive of cigarette company documents at the University of California, San Francisco stumbled on something revealing: Internal correspondence showed how tobacco executives, barred from targeting children for cigarette sales, focused their marketing prowess on young people to sell sugary beverages in ways that had not been done before. The archive, known as the Truth Tobacco Industry Documents, was created as part of a settlement between major cigarette companies and states that were seeking to recoup smoking-related health care costs. The researchers published their findings on Thursday in the medical publication BMJ. Using child-tested flavors, cartoon characters, branded toys and millions of dollars in advertising, the companies cultivated loyalty to sugar-laden products that health experts said had greatly contributed to the nation’s obesity crisis. At a time of mounting childhood obesity, with nearly a third of children in the United States overweight or obese and rates of type 2 diabetes soaring among adolescents, the study’s authors said it was important to chart how companies created and marketed junk food and sugary drinks to youngsters. © 2019 The New York Times Company

Keyword: Drug Abuse; Obesity
Link ID: 26036 - Posted: 03.15.2019

By JoAnna Novak “U guys I had this awesome thing for dinner,” my little sister texts our family. “ICE CREAM HEHE.” After 20 years of dealing with an eating disorder, recovered-me has a response and sick-me has a response, but neither seems right. My siblings, my mom and I chat all day in our “Fam” text thread. Morning roll call? Check. Terrier on kitchen table? Yep. Food talk? A feast of food talk. Actually, not just talk. And not just food. “Did 74 min on tread,” my sister texts. “Exhausted.” I know. She started 2018 with a goal to lose 20 lingering college pounds, and she’s been in lifestyle-overhaul ever since. Often she calls me post-workout, breathless, gushing endorphins. Other times she sends sports bra selfies. (“Get it,” my mom responds.) She shares meal pics, too, plates of sheet-pan chicken or “healthy” comfort food (turkey hot dogs, cauli-mac and cheese), a latte pink with beet juice, a splurge. (That ice cream she had was Halo Top, which is low in calories and high in protein.) I was buying blue cheese for burgers last week when she said she was 10 pounds from her target. I picked up the Roquefort and blinked off memories of closing in on a number, those hazy promises that, soon, everything might change. “That’s amazing,” I said. “I’m proud of you.” She’d gained so much confidence over the last year; she was already feeling more comfortable in her skin, she said. “You know what I mean.” In a way, I did. It’s a conversation I’d never thought we’d be having, one where my sister trusts me enough to share anxieties about her body and I’m recovered enough to listen. I went on my first diet when she was 5 and I was 12. A few months later she was crying, begging newly anorexic me to eat a canned peach. © 2019 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 26031 - Posted: 03.14.2019

By Nicholas Bakalar Eating a heart-healthy diet beginning in your 20s may provide brain benefits in middle age, new research suggests. The study, in Neurology, ranked 2,621 people on their degree of adherence to three different diets considered to be good for the heart. All emphasize vegetables, fruits and whole grains and minimize saturated fat consumption: the Mediterranean diet, which involves mainly plant-based foods and moderate alcohol intake; a research-based diet plan that rates food groups as favorable or not; and the DASH diet, which stresses low-sodium foods. Researchers tracked their diet compliance at ages 25, 32 and 45, and tested mental acuity at 50 and then again at 55. Those who adhered most strictly to the Mediterranean or the food group diet scored higher than those who did not, especially on tests of executive function, which involves organizing and planning. After adjusting for many health and behavioral factors, people with the strictest adherence to these diets had a 46 to 52 percent lower risk of poor cognitive function. But adherence to the DASH diet, which does not consider alcohol consumption, was not associated with cognitive test scores. Which diet is best? “We can say at this point that a heart-healthy diet like the Mediterranean diet is a good option,” said the lead author, Claire T. McEvoy, a dietitian and epidemiologist at Queen’s University Belfast. “It’s palatable and adaptable, and in that respect it’s a pretty good dietary pattern.” © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26018 - Posted: 03.09.2019

By Andrew Jacobs CAMBRIDGE, Mass. — There’s a new war raging in health care, with hundreds of millions of dollars at stake and thousands of lives in the balance. The battle, pitting drug companies against doctors and patient advocates, is being fought over the unlikeliest of substances: human excrement. The clash is over the future of fecal microbiota transplants, or F.M.T., a revolutionary treatment that has proved remarkably effective in treating Clostridioides difficile, a debilitating bacterial infection that strikes 500,000 Americans a year and kills 30,000. The therapy transfers fecal matter from healthy donors into the bowels of ailing patients, restoring the beneficial works of the community of gut microbes that have been decimated by antibiotics. Scientists see potential for using these organisms to treat diseases from diabetes to cancer. At the heart of the controversy is a question of classification: Are the fecal microbiota that cure C. diff a drug, or are they more akin to organs, tissues and blood products that are transferred from the healthy to treat the sick? The answer will determine how the Food and Drug Administration regulates the procedure, how much it costs and who gets to profit. In 2013, the F.D.A. announced a draft decision to regulate the therapy as a new drug but said it would continue to study the matter before reaching a final decision — which is expected to happen soon. Critics say that approach is based on outdated science and could lead to increased costs for patients, most of whom currently rely on a nonprofit stool bank in Cambridge. At stake, some researchers say, is the future of pioneering therapies that harness the human microbiome — the trillions of organisms that colonize the body and are increasingly seen as critical for healthy brain development and immune function. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26006 - Posted: 03.05.2019

By Gretchen Reynolds A few minutes of brief, intense exercise may be as effective as much lengthier walks or other moderate workouts for incinerating body fat, according to a helpful new review of the effects of exercise on fat loss. The review finds that super-short intervals could even, in some cases, burn more fat than a long walk or jog, but the effort involved needs to be arduous. I have written many times about the health, fitness and brevity benefits of high-intensity interval training, which typically involves a few minutes — or even seconds — of strenuous exertion followed by a period of rest, with the sequence repeated multiple times. Most H.I.I.T. workouts require less than half an hour, from beginning to end (including a warm-up and cool-down), and the strenuous portions of the workout are even briefer. But despite this concision, studies show that interval workouts can improve aerobic fitness, blood sugar control, blood pressure and other measures of health and fitness to the same or a greater extent than standard endurance training, such as brisk walking or jogging, even if it lasts two or three times as long. People being people, though, the most common question I hear about quickie intervals and have asked, on my own behalf, is whether they also will aid in weight control and fat loss. Only a few past studies have directly compared the fat-burning effects of endurance training to those of short interval workouts, however, and their results have been inconsistent. Some indicate that intervals prompt significant fat loss and others that any losses are negligible when compared to the effects of endurance training.

Keyword: Obesity
Link ID: 25994 - Posted: 02.28.2019

By Achim Peters Although our brain accounts for just 2 percent of our body weight, the organ consumes half of our daily carbohydrate requirements—and glucose is its most important fuel. Under acute stress the brain requires some 12 percent more energy, leading many to reach for sugary snacks. Carbohydrates provide the body with the quickest source of energy. In fact, in cognitive tests subjects who were stressed performed poorly prior to eating. Their performance, however, went back to normal after consuming food. When we are hungry, a whole network of brain regions activates. At the center are the ventromedial hypothalamus (VMH) and the lateral hypothalamus. These two regions in the upper brain stem are involved in regulating metabolism, feeding behavior and digestive functions. There is, however, an upstream gatekeeper, the nucleus arcuatus (ARH) in the hypothalamus. If it registers that the brain itself lacks glucose, this gatekeeper blocks information from the rest of the body. That’s why we resort to carbohydrates as soon as the brain indicates a need for energy, even if the rest of the body is well supplied. To further understand the relationship between the brain and carbohydrates, we examined 40 subjects over two sessions. In one, we asked study participants to give a 10-minute speech in front of strangers. In the other session they were not required to give a speech. At the end of each session, we measured the concentrations of stress hormones cortisol and adrenaline in participants’ blood. We also provided them with a food buffet for an hour. When the participants gave a speech before the buffet, they were more stressed, and on average consumed an additional 34 grams of carbohydrates, than when they did not give a speech. © 2019 Scientific American

Keyword: Stress; Obesity
Link ID: 25987 - Posted: 02.27.2019

By C. Claiborne Ray Q. What keeps squirrels from gaining huge amounts of weight as they gorge on acorns and nuts each fall? A. In fact, many squirrels do achieve huge weight gain ahead of the privations of winter. Common gray squirrels may increase their weight by 25 percent in the harvest season. But not because they hibernate — they don’t. Winter foraging is hard, and gray squirrels tend to spend the winter months mostly in their nests. But they must make forays every few days to seek squirreled-away food and other nourishment. Among hibernating squirrels, much of the stored nourishment is needed to survive the cold season without foraging. A study of the Arctic ground squirrel found extreme weight gains during the active season: 42 percent among males and 63 percent among females. They slow their activity drastically before hibernating in order to maintain peak mass. While some do emerge from winter lighter, a significant share of their fat stores may remain. © 2019 The New York Times Company

Keyword: Obesity; Biological Rhythms
Link ID: 25952 - Posted: 02.12.2019

By Elizabeth Pennisi Of all the many ways the teeming ecosystem of microbes in a person’s gut and other tissues might affect health, its potential influences on the brain may be the most provocative. Now, a study of two large groups of Europeans has found several species of gut bacteria are missing in people with depression. The researchers can’t say whether the absence is a cause or an effect of the illness, but they showed that many gut bacteria could make substances that affect nerve cell function—and maybe mood. “It’s the first real stab at tracking how” a microbe’s chemicals might affect mood in humans, says John Cryan, a neuroscientist at University College Cork in Ireland who has been one of the most vocal proponents of a microbiome-brain connection. The study “really pushes the field from where it’s been” with small studies of depressed people or animal experiments. Interventions based on the gut microbiome are now under investigation: The University of Basel in Switzerland, for example, is planning a trial of fecal transplants, which can restore or alter the gut microbiome, in depressed people. Several studies in mice had indicated that gut microbes can affect behavior, and small studies of people suggested this microbial repertoire is altered in depression. To test the link in a larger group, Jeroen Raes, a microbiologist at the Catholic University of Leuven in Belgium, and his colleagues took a closer look at 1054 Belgians they had recruited to assess a “normal” microbiome. Some in the group—173 in total—had been diagnosed with depression or had done poorly on a quality of life survey, and the team compared their microbiomes with those other participants. Two kinds of microbes, Coprococcus and Dialister, were missing from the microbiomes of the depressed subjects, but not from those with a high quality of life. The finding held up when the researchers allowed for factors such as age, sex, or antidepressant use, all of which influence the microbiome, the team reports today in Nature Microbiology. They also found the depressed people had an increase in bacteria implicated in Crohn disease, suggesting inflammation may be at fault. © 2018 American Association for the Advancement of Science

Keyword: Depression
Link ID: 25932 - Posted: 02.05.2019

By Carl Zimmer In 2014 John Cryan, a professor at University College Cork in Ireland, attended a meeting in California about Alzheimer’s disease. He wasn’t an expert on dementia. Instead, he studied the microbiome, the trillions of microbes inside the healthy human body. Dr. Cryan and other scientists were beginning to find hints that these microbes could influence the brain and behavior. Perhaps, he told the scientific gathering, the microbiome has a role in the development of Alzheimer’s disease. The idea was not well received. “I’ve never given a talk to so many people who didn’t believe what I was saying,” Dr. Cryan recalled. A lot has changed since then: Research continues to turn up remarkable links between the microbiome and the brain. Scientists are finding evidence that microbiome may play a role not just in Alzheimer’s disease, but Parkinson’s disease, depression, schizophrenia, autism and other conditions. For some neuroscientists, new studies have changed the way they think about the brain. One of the skeptics at that Alzheimer’s meeting was Sangram Sisodia, a neurobiologist at the University of Chicago. He wasn’t swayed by Dr. Cryan’s talk, but later he decided to put the idea to a simple test. “It was just on a lark,” said Dr. Sisodia. “We had no idea how it would turn out.” He and his colleagues gave antibiotics to mice prone to develop a version of Alzheimer’s disease, in order to kill off much of the gut bacteria in the mice. Later, when the scientists inspected the animals’ brains, they found far fewer of the protein clumps linked to dementia. Just a little disruption of the microbiome was enough to produce this effect. Young mice given antibiotics for a week had fewer clumps in their brains when they grew old, too. © 2019 The New York Times Company

Keyword: Obesity; Depression
Link ID: 25915 - Posted: 01.29.2019

Amy Lewis Cynthia Bulik began her scientific career studying childhood depression. But while she was working as a research assistant at the University of Pittsburgh in the 1980s, psychiatrist David Kupfer asked her to help write a book chapter comparing electroencephalography studies in depression and anorexia. As preparation, she shadowed a psychiatrist at a hospital inpatient unit for people with eating disorders. Bulik was intrigued by what she witnessed there. “These people were my age, my sex, and weighed half as much as I did,” she says. “They seemed very eloquent and interactive, but at the same time, in this one area of their psychology and biology, they occupied a completely different space.” Now the founding director of the Center of Excellence for Eating Disorders at the University of North Carolina at Chapel Hill, Bulik has been unraveling the biology behind eating disorders such as anorexia nervosa (AN) ever since. Characterized by extreme caloric restriction resulting in weight loss, an intense fear of gaining weight, and a distorted body image, anorexia has the highest mortality rate of any psychiatric disorder. Death can be a result of various risks associated with the condition, from suicide to heart failure. While many AN sufferers go undiagnosed, making incidence rates hard to pin down, some researchers estimate that up to 2 percent of women and 0.3 percent of men are affected globally. © 1986 - 2019 The Scientist

Keyword: Anorexia & Bulimia; Genes & Behavior
Link ID: 25914 - Posted: 01.29.2019

By Gretchen Reynolds Exercise and eating have a fraught, unsettled relationship with each other. Workouts can blunt or boost appetites. People who start an exercise program often overeat and gain weight — and yet studies and lived experience demonstrate that regular exercise is needed to avoid regaining the weight lost during a successful diet. Intrigued by these contradictory outcomes, researchers at the University of Texas Southwestern Medical Center, along with colleagues from other institutions, ran an experiment on the melanocortin circuit, a brain network in the hypothalamus known to be involved in metabolism. The resulting study, published in December in Molecular Metabolism, suggests that intense exercise might change the workings of certain neurons in ways that could have beneficial effects on appetite and metabolism. The melanocortin circuit consists mainly of two types of neurons. The neuropeptide Y (NPY) cells relay signals encouraging the body to seek food, while the pro-opiomelanocortin (POMC) neurons countermand those orders, reducing interest in food. Animals, including humans, that lack healthy POMC neurons usually become morbidly obese. The researchers focused on what exercise would do to these cells in mice, whose melanocortin circuits resemble ours. Healthy adult male mice either ran on small treadmills or, in a control group, were placed on unmoving treadmills. The exercise routine consisted of 60 minutes of fast, intense running, broken into three 20-minute blocks. Afterward, the mice were free to eat or not, as they chose. The researchers then checked neuronal activity in some of their brains by microscopically probing individual cells in living tissue to measure their electrical and biochemical signals. The tests were repeated throughout the study, which ran for as many as 10 days for some mice. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 25911 - Posted: 01.29.2019

By Jane E. Brody I had hoped to avoid ushering in the new year with yet another weight/diet column, but three circumstances prompted me to reconsider: 1) The latest data released by the Centers for Disease Control and Prevention showed that the weight of American men and women has continued its upward climb, with the average B.M.I. now almost at the cutoff for obesity; 2) The Food and Drug Administration is rolling out changes in serving sizes on packaged foods that could very well make matters worse, especially for consumers of ice cream and soda, and 3) Some good news for a change: the publication of an eminently sensible approach to weight loss, “Finally Full, Finally Slim,” written by a leading expert on portion control, Lisa R. Young, a registered dietitian and adjunct professor of nutrition at New York University. Unlike the myriad diet fads that have yet to stem the ever-increasing girth of American men and women, what Dr. Young describes is not a diet but a practical approach to food and eating that can be adapted to almost any way of life, even if most meals are eaten out or taken out. It is not prescriptive or even proscriptive. It does not cut out any category of food, like carbohydrates or fats, nor does it deprive people of their favorite foods, including sweet treats. And it works. I know, because more than half a century ago I lost 40 pounds in two years following Dr. Young’s approach, and I’ve kept the weight off ever since without dieting or deprivation. It fills me up with delicious, nutritious foods and allows me to enjoy a frequent nightcap of ice cream — half a cup (measured) at 150 calories or less. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 25907 - Posted: 01.28.2019

By Smitha Mundasad Global Health Correspondent, BBC News Scientists say they have discovered the secret behind why some people are skinny while others pile on the pounds easily. Their work reveals newly discovered genetic regions linked to being very slim. The international team say this supports the idea that, for some people, being thin has more to do with inheriting a "lucky" set of genes than having a perfect diet or lifestyle. The study appears in PLOS Genetics. In the past few decades, researchers have found hundreds of genetic changes that increase the chance of a person being overweight - but there has been much less focus on the genes of people who are thin. In this investigation, scientists compared DNA samples from 1,600 healthy thin people in the UK - with a body mass index (BMI) of less than 18 - with those of 2,000 severely obese people and 10,400 people of normal weight. They also looked closely at lifestyle questionnaires - to rule out eating disorders, for example. Researchers found people who were obese were more likely to have a set of genes linked to being overweight. Meanwhile, people who were skinny not only had fewer genes linked to obesity but also had changes in gene regions newly associated with healthy thinness. Lead researcher Prof Sadaf Farooqi, from the University of Cambridge, called on people to be less judgemental about others' weight. "This research shows for the first time that healthy thin people are generally thin because they have a lower burden of genes that increase a person's chances of being overweight and not because they are morally superior, as some people like to suggest," she said. © 2019 BBC.

Keyword: Obesity; Genes & Behavior
Link ID: 25905 - Posted: 01.26.2019

Marise Parent Of course you know that eating is vital to your survival, but have you ever thought about how your brain controls how much you eat, when you eat and what you eat? This is not a trivial question, because two-thirds of Americans are either overweight or obese and overeating is a major cause of this epidemic. To date, the scientific effort to understand how the brain controls eating has focused primarily on brain areas involved in hunger, fullness and pleasure. To be better armed in the fight against obesity, neuroscientists, including me, are starting to expand our investigation to other parts of the brain associated with different functions. My lab’s recent research focuses on one that’s been relatively overlooked: memory. For many people, decisions about whether to eat now, what to eat and how much to eat are often influenced by memories of what they ate recently. For instance, in addition to my scale and tight clothes, my memory of overeating pizza yesterday played a pivotal role in my decision to eat salad for lunch today. Memories of recently eaten foods can serve as a powerful mechanism for controlling eating behavior because they provide you with a record of your recent intake that likely outlasts most of the hormonal and brain signals generated by your meal. But surprisingly, the brain regions that allow memory to control future eating behavior are largely unknown. Studies done in people support the idea that meal-related memory can control future eating behavior. © 2010–2019, The Conversation US, Inc.

Keyword: Obesity; Learning & Memory
Link ID: 25866 - Posted: 01.15.2019