Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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By NICHOLAS BAKALAR A handful of walnuts may be an effective weight loss tool. Walnuts are rich in omega-3 fatty acids and other substances and, in moderation, have been linked to reduced risk of obesity and diabetes. They may also efficiently reduce appetite. Researchers now may have found out why. They had nine hospitalized obese patients drink, on five consecutive days, either a smoothie containing 48 grams of walnuts (1.7 ounces, or about 14 walnut halves and 315 calories) or a placebo smoothie identical in taste and calorie content. Then, after a month on their regular diet, the patients returned for a second five-day trial, with placebo drinkers on the first trial receiving a walnut smoothie, and vice versa. The participants underwent M.R.I. brain exams while looking at pictures of high-fat food (cake, for example), low-fat food (vegetables) or neutral pictures of rocks and trees. The study, published in Diabetes, Obesity and Metabolism, found that when people looked at pictures of high-fat food, activation in the insula, a part of the brain involved in appetite and impulse control, increased among those who drank the walnut smoothie, but not among placebo drinkers. The study was funded in part by the California Walnut Commission. “Walnuts can alter the way our brains view food and impact our appetites,” said the lead author, Olivia M. Farr, of Beth Israel Deaconess Medical Center in Boston. “Our results confirm the current recommendations to include walnuts as part of a healthy diet.” © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23975 - Posted: 08.19.2017

By Kate Kyle, CBC News Widespread, prolonged hunger that existed in residential schools is a contributing factor in the disproportionate health issues facing many Indigenous people, such as diabetes and obesity, according to an article published Monday in the Canadian Medical Association Journal. "Hunger is really central to the experiences of residential school survivors," says Ian Mosby who co-authored the article with Tracy Galloway, both with the University of Toronto. They say childhood malnutrition experienced in many government-funded schools is contributing to the higher risk for obesity, diabetes and heart disease among Indigenous people in adulthood. "While this wasn't every single residential school," says Mosby, "it's common enough through survivor testimony that we need to start looking at hunger in residential schools as a real predictor of long-term health problems." Residential school kitchen 1920s Residential schools across Canada faced significant underfunding, along with inadequate cooking facilities and untrained staff. Historians and former students have described children getting "one or two pieces of stale bread for lunch. Rarely getting meat, rarely getting milk and butter, and few fruits and vegetables," says Mosby. ©2017 CBC/Radio-Canada.

Keyword: Obesity; Development of the Brain
Link ID: 23958 - Posted: 08.15.2017

By NICHOLAS BAKALAR Children who sleep less may be at increased risk for Type 2 diabetes, researchers report. Earlier studies found a link between shorter sleep and diabetes in adults, but the connection has been little studied in children. British researchers studied 4,525 9- and 10-year olds from varying ethnic backgrounds. On average, their parents reported they slept 10 hours a night, with 95 percent sleeping between eight and 12 hours. The study, in Pediatrics, found that the less sleep, the more likely the children were to have higher body mass indexes, higher insulin resistance and higher glucose readings. All three are risk factors for Type 2 diabetes. Over all, increasing weekday sleep duration by an hour was associated with a 0.2 lower B.M.I. and a 3 percent reduction in insulin resistance. The reasons for the link remain unclear, but the researchers suggest that poor sleep may affect appetite regulation, leading to overeating and obesity. This observational study could not establish cause and effect. Still, the senior author, Christopher G. Owen, a professor of epidemiology at St. George’s University of London, said that for children, the more sleep the better — there is no threshold. “Increasing sleep is a very simple, low-cost intervention,” he said. “We should be doing our utmost to make sure that children sleep for an adequate amount of time.” © 2017 The New York Times Company

Keyword: Sleep; Obesity
Link ID: 23957 - Posted: 08.15.2017

By Kristine Phillips The Food and Drug Administration is investigating the sudden deaths of five people who had undergone an obesity treatment that places an inflated silicone balloon in their stomach. All deaths happened within a month of the procedure, the FDA said in a letter earlier this week to health-care providers. Three people died just one to three days later. The agency, however, cautioned that it has yet to determine whether the devices or the way in which they were placed in the stomachs directly caused those deaths. “At this time, we do not know the root cause or incidence per rate of patient death,” the FDA said, adding that it is working with the companies that manufacture the devices. The devices are manufactured by two California companies. Four of the cases involved the Orbera Intragastric Balloon System by Apollo Endosurgery. One involved the ReShape Integrated Dual Balloon System by ReShape Medical. The deaths happened from 2016 to present, according to the FDA. The agency said two more death reports it received happened within the same time frame and are potentially related to complications from the balloon treatment. The procedure lasts for up to 30 minutes. One or two balloons are placed inside the stomach through the mouth using an endoscope while a patient is mildly sedated. Once inside, it's inflated with liquid, usually with saline solution. The idea is for the balloon, which is about the size of a grapefruit once inflated, to leave less room for food. It stays in the stomach for up to six months, while the patient also follows a diet and exercises regularly. © 1996-2017 The Washington Post

Keyword: Obesity
Link ID: 23955 - Posted: 08.14.2017

By Megan Scudellari Neuropharmacology postdoc Nick DiPatrizio was stumped. His advisor, University of California, Irvine, researcher Daniele Piomelli, had discovered eight years earlier that hungry rats have high levels of endocannabinoids, endogenous molecules that bind to the same receptors as the active ingredient in marijuana. Now, in 2009, DiPatrizio was trying to identify exactly where and how those molecules were controlling food intake in rats. But under specific feeding conditions, he couldn’t locate any changes in endocannabinoid levels in the brain, which is flush with endocannabinoid receptors and the obvious place to look for behavioral signals. Piomelli gently chastised his mentee. “He said, ‘You’re being neurocentric. Remember, there’s a body attached to the head. Look in the other organs of the body,’ ” recalls DiPatrizio. So the young scientist persisted, and eventually discovered that hunger—and the taste of fat—leads to increased endocannabinoid levels in the jejunum, a part of the small intestine. Endocannabinoid signaling in the gut, not the brain, was controlling food intake in the rodents in response to tasting fats.1 The evolution of endocannabinoid research has mirrored DiPatrizio’s early thinking: ever since the first endocannabinoid receptor was identified in the late 1980s, the field has been overwhelmingly focused on the central nervous system. The main endocannabinoid receptor, CB1, was first discovered in a rat brain and is now known to be among the most abundant G protein–coupled receptors in neurons there. Plus, cannabis is well-known for its psychotropic effects. “That has led the research field to be very CNS-oriented,” says Saoirse O’Sullivan, who studies endocannabinoids at the University of Nottingham in the U.K. © 1986-2017 The Scientist

Keyword: Drug Abuse
Link ID: 23954 - Posted: 08.14.2017

By GRETCHEN REYNOLDS Some types of exercise may be better than others at blunting appetite and potentially aiding in weight management, according to an interesting new study of workouts and hunger. It finds that pushing yourself during exercise affects appetite, sometimes in surprising ways. As anyone who has begun an exercise program knows, the relationships between exercise, appetite, weight control and hunger are complex and often counterintuitive. The arithmetic involved seems straightforward. You burn calories during exercise and, over time, should drop pounds. But the reality is more vexing. In both scientific studies and the world inhabited by the rest of us, most people who start exercising lose fewer pounds than would be expected, given the number of calories they are burning during workouts. Many people even gain weight. The problem with exercise as a weight-loss strategy seems to be in large part that it can make you hungry, and many of us wind up consuming more calories after a workout than we torched during it, a biological response that has led some experts and frustrated exercisers to conclude that exercise by itself — without strict calorie reduction — is useless for shedding pounds. But much of the past research into exercise and appetite has concentrated on walking or other types of relatively short or light activities. Some scientists have begun to wonder whether exercise that was physically taxing, either because it was prolonged or intense, might affect appetite differently than more easeful exercise. So for the new study, which was published recently in the Journal of Endocrinology, scientists from Loughborough University in Britain and other institutions who have been studying exercise and appetite for years recruited 16 healthy, fit young men. (They did not include women because this was a small, pilot study, the authors say, and controlling for the effects of women’s menstrual cycles would have been difficult.) © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23934 - Posted: 08.09.2017

By TAFFY BRODESSER-AKNER James Chambers was watching membership sign-ups on Jan. 4, 2015, like a stock ticker — it was that first Sunday of the year, the day we all decide that this is it, we’re not going to stay fat for one more day. At the time, he was Weight Watchers’ chief executive, and he sat watching, waiting for the line on the graph to begin its skyward trajectory. Chambers knew consumer sentiment had been changing — the company was in its fourth year of member-recruitment decline. But they also had a new marketing campaign to help reverse the generally dismal trend. But the weekend came and went, and the people never showed up. More than two-thirds of Americans were what public-health officials called overweight or obese, and this was the oldest and most trusted diet company in the world. Where were the people? Weight Watchers was at a loss. Chambers called Deb Benovitz, the company’s senior vice president and global head of consumer insights. ‘‘We’re having one of the worst Januaries that anyone could have imagined,’’ she remembers him telling her. In the dieting business, January will tell you everything you need to know about the rest of the year. ‘‘Nothing like we had anticipated.’’ Chambers and Benovitz knew that people had developed a kind of diet fatigue. Weight Watchers had recently tried the new marketing campaign, called ‘‘Help With the Hard Part,’’ an attempt at radical honesty. No one wanted radical honesty. Chambers told Benovitz that they needed to figure out what was going on and how to fix it before the February board meeting. Benovitz got to work. She traveled the country, interviewing members, former members and people they thought should be members about their attitudes toward dieting. She heard that they no longer wanted to talk about ‘‘dieting’’ and ‘‘weight loss.’’ They wanted to become ‘‘healthy’’ so they could be ‘‘fit.’’ They wanted to ‘‘eat clean’’ so they could be ‘‘strong.’’ © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23930 - Posted: 08.08.2017

By GINA KOLATA For middle-aged women struggling with their weight, a recent spate of scientific findings sounds too good to be true. And they may be, researchers caution. Studies in mice indicate that a single hormone whose levels rise at menopause could be responsible for a characteristic redistribution of weight in middle age to the abdomen, turning many women from “pears” to “apples.” At the same time, the hormone may spur the loss of bone. In mouse studies, blocking the hormone solves those problems, increasing the calories burned, reducing abdominal fat, slowing bone loss and even encouraging physical activity. The notion that such a simple intervention could solve two big problems of menopause has received the attention of researchers and has prompted commentaries in prestigious journals like The New England Journal of Medicine and Cell Metabolism. “It’s a super interesting idea,” said Dr. Daniel Bessesen, an obesity expert and professor of medicine at the University of Colorado School of Medicine. With obesity rising, “we definitely need some new ideas.” The work began when Dr. Mone Zaidi, a professor of medicine at the Icahn School of Medicine at Mount Sinai in New York City, became curious about whether a reproductive hormone — F.S.H., or follicle-stimulating hormone — affects bone density. It had long been assumed that the hormone’s role was limited to reproduction. F.S.H. stimulates the production of eggs in women and sperm in men. Researchers knew that blood levels of F.S.H. soar as women’s ovaries start to fail before menopause. At the same time, women rapidly lose bone — even when blood levels of estrogen, which can preserve bone, remain steady. © 2017 The New York Times Company

Keyword: Obesity; Hormones & Behavior
Link ID: 23929 - Posted: 08.08.2017

Nicola Davis A drug commonly used to treat diabetes could help those living with Parkinson’s disease, research has revealed. By 2020 it is predicted that 162,000 individuals in the UK will be living with the condition. While existing drugs help to control its symptoms, there are currently none available which slow or halt its progression. But now scientists say they have found that a drug commonly used to treat type 2 diabetes appears to improve movement-related issues. The benefit persisted even when the drug had not been taken for 12 weeks, suggesting it might be helping to slow the progression of the disease. “It is not ready for us to say ‘well, everyone needs to start this drug’,” said Thomas Foltynie, professor of neurology at University College London and co-author of the study. “[But] if we can replicate these findings in a multicentre trial, especially with longer follow-up, then this can change the face of our approach to treating Parkinson’s.” Writing in the Lancet, Foltynie and colleagues in the UK and US describe how they tested the impact of the drug, known as exenatide. With recent studies suggesting problems with insulin signalling in the brain could be linked to neurodegenerative disorders, hopes have been raised that diabetes drugs could also be used to tackle Parkinson’s, with previous research – including in cell cultures and animals, as well as a recent pilot study on humans by Foltynie and colleagues – backing up the notion.. But the latest study is the first robust clinical trial of the drug, randomly allocating 60 people with Parkinson’s to one of two treatments – either receiving injections of exenatide or a placebo once a week. © 2017 Guardian News and Media Limited

Keyword: Parkinsons
Link ID: 23918 - Posted: 08.05.2017

By Mitch Leslie Prions are insidious proteins that spread like infectious agents and trigger fatal conditions such as mad cow disease. A protein implicated in diabetes, a new study suggests, shares some similarities with these villains. Researchers transmitted diabetes from one mouse to another just by injecting the animals with this protein. The results don’t indicate that diabetes is contagious like a cold, but blood transfusions, or even food, may spread the disease. The work is “very exciting” and “well-documented” for showing that the protein has some prionlike behavior, says prion biologist Witold Surewicz of Case Western Reserve University in Cleveland, Ohio, who wasn’t connected to the research. However, he cautions against jumping to the conclusion that diabetes spreads from person to person. The study raises that possibility, he says, but “it remains to be determined.” Prions are misfolded proteins that can cause normally folded versions of the same protein to misfold themselves. When this conversion occurs in the brain, the distorted proteins bunch up inside cells and kill them. Although prion diseases are rare in people, they share some similarities with more common illnesses. In Alzheimer’s disease, for instance, globs of a misshapen protein known as β amyloid build up in the brain. Parkinson’s disease and Huntington disease, two other brain maladies, also feature aggregates, or lumps of misfolded proteins. © 2017 American Association for the Advancement of Science.

Keyword: Obesity; Prions
Link ID: 23910 - Posted: 08.02.2017

Obese people aren’t able to regulate the way body fat is stored or burned because a “switch” in their brain stays on all the time, a new study by Australian researchers has shown. Specialised fat cells called adipocytes are switched back and forth from brown cells, which are energy burning, to white, which store energy. The study, published on Wednesday in Cell Metabolism, showed that after a meal the brain responds to insulin when sugars spike by sending signals to promote the browning of fat to expend energy. Then, after a fast, the brain instructs these browned cells to convert back to white adipocytes, again storing energy. The brain’s ability to sense insulin and coordinate feeding with burning energy is controlled by a switch-like mechanism, researchers from the metabolic disease and obesity program at Monash University say. “What happens in the context of obesity is that the switch stays on all the time – it doesn’t turn on off during feeding,” said the lead researcher, Prof Tony Tiganis. “As a consequence, browning is turned off all the time and energy expenditure is decreased all the time, so when you eat, you don’t see a commensurate increase in energy expenditure – and that promotes weight gain.” Researchers are exploring the possibility of inhibiting the switch to aid weight loss but they say any therapy is “a long way off”. © 2017 Guardian News and Media Limited

Keyword: Obesity
Link ID: 23909 - Posted: 08.02.2017

By Ariana Eunjung Cha By now, the connection between sleep and weight gain has been well established. Numerous studies have provided evidence that sleeping too little — less than five hours — messes with your hormones, slows down your metabolism and reprograms your body to eat more. But just how serious are the consequences in terms of numbers? A new study published in PLOS One takes a stab at this question by studying the relationship between sleep duration and a number of quantifiable factors: waist circumference, blood pressure, lipids, glucose, thyroid hormones and other important measures of a person's metabolic profile. The research, led by the Leeds Institute of Cardiovascular and Metabolic Medicine and the School of Food Science and Nutrition, involved 1,615 people ages 19 to 65 in Great Britain. The most striking suggestion was that getting insufficient sleep may make you go up a clothing size. People in the study who were sleeping an average of six hours each night had waist measurements about 1.2 inches (or 3 centimeters) more than those getting nine hours of sleep a night. Those with less sleep also weighed more. The relationship between more sleep and smaller waists and a lower body mass index (BMI) appeared to be almost linear, as shown below. The findings appear to contradict other studies that show that too much sleep — nine hours or more — might have a similar impact on the body as too little sleep. This new study appears to show that waist circumference and BMI are lowest for those with 12 hours of sleep. The theory of why this relationship exists has to do with two hormones that help tell you when to eat and when to stop. Less sleep upsets the balance, making you eat more. Combine that with the slower metabolism that people with lack of sleep appear to have it's no wonder that people are prone to becoming larger and gaining weight. © 1996-2017 The Washington Post

Keyword: Sleep; Obesity
Link ID: 23903 - Posted: 08.01.2017

People who drink three to four times a week are less likely to develop type 2 diabetes than those who never drink, Danish researchers suggest. Wine appears to be particularly beneficial, probably as it plays a role in helping to manage blood sugar, the study, published in Diabetologia, says. They surveyed more than 70,000 people on their alcohol intake - how much and how often they drank. But experts said this wasn't a "green light" to drink more than recommended. And Public Health England warned that consuming alcohol contributed to a vast number of other serious diseases, including some cancers, heart and liver disease. "People should keep this in mind when thinking about how much they drink," a spokeswoman said. Prof Janne Tolstrup, from the National Institute of Public Health of the University of Southern Denmark, who led the research, said: "We found that drinking frequency has an independent effect from the amount of alcohol taken. "We can see it's a better effect to drink the alcohol in four portions rather than all at once." After around five years, study participants were followed up and a total of 859 men and 887 women group had developed diabetes - either type 1 or the more common type 2. The researchers concluded that drinking moderately three to four times a week reduced a woman's risk of diabetes by 32% while it lowered a man's by 27%, compared with people drinking on less than one day a week. Findings also suggest that not all types of alcohol had the same effect. Wine appeared to be particularly beneficial because polyphenols, particularly in red wine, play a role in helping to manage blood sugar. © 2017 BBC.

Keyword: Drug Abuse
Link ID: 23892 - Posted: 07.29.2017

Sarah Boseley Health editor Men who consume a lot of added sugar in drinks, cakes and confectionery run an increased risk of depression, according to a new study. Researchers from University College London (UCL) looked at sugar in the diet and common mental health problems in a very large cohort of 5,000 men and 2,000 women recruited for the Whitehall II study in the 1980s. Sugar tax must apply to sweets as well as drinks, say campaigners Read more They found a strong association between consuming higher levels of sugar and depression in men. Men with the highest intake – more than 67g a day – had a 23% increased chance of suffering a common mental disorder after five years than those who consumed the lowest levels of sugar – less than 39.5g. The researchers investigated whether men might be eating more sugary foods because they were depressed, but found that was not the case. Lead author Anika Knüppel, of the UCL Institute of Epidemiology and Health, said: “High sugar diets have a number of influences on our health but our study shows that there might also be a link between sugar and mood disorders, particularly among men. There are numerous factors that influence chances for mood disorders, but having a diet high in sugary foods and drinks might be the straw that breaks the camel’s back. © 2017 Guardian News and Media Limited

Keyword: Depression; Obesity
Link ID: 23890 - Posted: 07.28.2017

By Mitch Leslie If these sweltering summer days prompt you to reach for a cold drink, you can thank your hypothalamus, a region of the brain that helps us regulate body temperature and other internal conditions. But the region may fail us when we get older. A new study in mice suggests that the hypothalamus promotes aging, hastening physical and mental decline as its stem cells die off. “It’s a pretty stunning paper,” says Charles Mobbs, a neuroendocrinologist at the Icahn School of Medicine at Mount Sinai in New York City. The new aging mechanism “is totally novel and quite unexpected,” adds neuroendocrinologist Marianna Sadagurski of Wayne State University in Detroit, Michigan. Tucked away deep in the brain, the hypothalamus monitors and maintains our blood concentration, our body temperature, and other physiological variables. Researchers have also suspected that it plays a role in aging. The hypothalamus becomes inflamed as we get older, and 4 years ago a team led by neurodendocrinologist Dongsheng Cai of Albert Einstein College of Medicine in New York City showed that quelling this inflammation delays physical deterioration and boosts life span in mice. In the new study, the team turned its attention to the hypothalamus’s stem cells, which in young animals divide to produce replacements for dead and damaged cells. As mice get older, the scientists found, the number of stem cells in the hypothalamus plunges. By later ages they are “basically all gone,” Cai says. © 2017 American Association for the Advancement of Science

Keyword: Development of the Brain; Stem Cells
Link ID: 23886 - Posted: 07.27.2017

Sara Reardon Mice aged more slowly when injected with stem cells from the brains of newborns. Stem cells in the brain could be the key to extending life and slowing ageing. These cells — which are located in the hypothalamus, a region that produces hormones and other signalling molecules — can re­invigorate declining brain function and muscle strength in middle-aged mice, according to a study published on 26 July in Nature1. Previous studies have suggested that the hypothalamus is involved in ageing, but the latest research shows that stem cells in this region can slow the process. That makes sense, because the hypothalamus is involved in many bodily functions, including inflammation and appetite, says Dongsheng Cai, a neuroendocrinologist at Albert Einstein College of Medicine in New York City. In their study, Cai and his colleagues found that stem cells in the hypothalamus disappear as mice grow older. When the researchers injected their mice with viruses that destroy these cells, the animals seemed to grow older faster, experiencing declines in memory, muscle strength, endurance and coordination. They also died sooner than untreated mice of the same age. Next, the team injected stem cells taken from the hypothalami of newborn mice into the brains of middle-aged mice. After four months, these animals had better cognitive and muscular function than untreated mice of the same age. They also lived about 10% longer, on average. © 2017 Macmillan Publishers Limited

Keyword: Development of the Brain; Stem Cells
Link ID: 23885 - Posted: 07.27.2017

By Megan Scudellari Neuropharmacology postdoc Nick DiPatrizio was stumped. His advisor, University of California, Irvine, researcher Daniele Piomelli, had discovered eight years earlier that hungry rats have high levels of endocannabinoids, endogenous molecules that bind to the same receptors as the active ingredient in marijuana. Now, in 2009, DiPatrizio was trying to identify exactly where and how those molecules were controlling food intake in rats. But under specific feeding conditions, he couldn’t locate any changes in endocannabinoid levels in the brain, which is flush with endocannabinoid receptors and the obvious place to look for behavioral signals. Piomelli gently chastised his mentee. “He said, ‘You’re being neurocentric. Remember, there’s a body attached to the head. Look in the other organs of the body,’ ” recalls DiPatrizio. So the young scientist persisted, and eventually discovered that hunger—and the taste of fat—leads to increased endocannabinoid levels in the jejunum, a part of the small intestine. Endocannabinoid signaling in the gut, not the brain, was controlling food intake in the rodents in response to tasting fats.1 The evolution of endocannabinoid research has mirrored DiPatrizio’s early thinking: ever since the first endocannabinoid receptor was identified in the late 1980s, the field has been overwhelmingly focused on the central nervous system. The main endocannabinoid receptor, CB1, was first discovered in a rat brain and is now known to be among the most abundant G protein–coupled receptors in neurons there. Plus, cannabis is well-known for its psychotropic effects. “That has led the research field to be very CNS-oriented,” says Saoirse O’Sullivan, who studies endocannabinoids at the University of Nottingham in the U.K. © 1986-2017 The Scientist

Keyword: Drug Abuse; Obesity
Link ID: 23870 - Posted: 07.25.2017

Katherine Hobson The theory behind artificial sweeteners is simple: If you use them instead of sugar, you get the joy of sweet-tasting beverages and foods without the downer of extra calories, potential weight gain and related health issues. In practice, it's not so simple, as a review of the scientific evidence on non-nutritive sweeteners published Monday shows. After looking at two types of scientific research, the authors conclude that there is no solid evidence that sweeteners like aspartame and sucralose help people manage their weight. And observational data suggest that the people who regularly consume these sweeteners are also more likely to develop future health problems, though those studies can't say those problems are caused by the sweeteners. The health effects of artificial sweeteners are important to study, because so many people use them. Another study published earlier this year found that a quarter of U.S. children and 41 percent of adults reported consuming them, most of them once per day. Even more people may be consuming them unwittingly in products such as granola bars or yogurt. "We were really interested in the everyday person who is consuming these products not to lose weight, but because they think it's the healthier choice, for many years on end," says Meghan Azad, lead author of the review and a research scientist at the University of Manitoba. While more research needs to be done, from what we know now, "there is no clear benefit for weight loss, and there's a potential association with increased weight gain, diabetes and other negative cardiovascular outcomes," says Azad. © 2017 npr

Keyword: Obesity
Link ID: 23845 - Posted: 07.18.2017

By TALYA MINSBERG When Marti Noxon set out to make “To the Bone,” a film about a 20-year-old battling an eating disorder, she initially faced the question: Was the topic too niche? The answer came in the form of a rousing premiere in January at the Sundance Film Festival, Netflix’s reported $8 million purchase of the film, a trailer that went viral with 54 million views in the first week and arguments over whether it glamorized excessive thinness. The film debuted on Netflix on Friday. The film is loosely based on Ms. Noxon’s experience with an eating disorder. She and its star, Lily Collins, are among the 30 million Americans — a third of them men — who have struggled with one. Ms. Collins plays Ellen, an anorexia patient who enters her fifth eating disorder treatment center, an unorthodox group home run by a doctor played by Keanu Reeves. Many of those reacting to the film’s trailer worried that watching it could trigger unhealthy thoughts in viewers who may be prone to eating disorders or already struggling with them. Indeed, some experts said that people who have had eating disorders should consider the state of their health before watching the film. “If you don’t feel solid in your recovery, don’t watch it right now. It could be triggering at any part of your life if you aren’t feeling strong and solid in your recovery,” Dr. Dena Cabera, executive clinical director at Rosewood Centers for Eating Disorders said. “It will always be there; you can look it up later.” Others say the film may help spur action. Eating disorders have the highest mortality rate of any psychiatric disorder, and can affect individuals across every demographic. “If the film helps raise awareness and more people seek treatment, that would be a success that we can be pleased with,” Dr. S. Bryn Austin, a professor at Boston Children’s Hospital and Harvard T.H. Chan School of Public Health, said. “Eating disorders can be successfully treated, they just need to take the first step in reaching out for care.” © 2017 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 23843 - Posted: 07.17.2017

Carina Storrs In the late 1960s, a team of researchers began doling out a nutritional supplement to families with young children in rural Guatemala. They were testing the assumption that providing enough protein in the first few years of life would reduce the incidence of stunted growth. It did. Children who got supplements grew 1 to 2 centimetres taller than those in a control group. But the benefits didn't stop there. The children who received added nutrition went on to score higher on reading and knowledge tests as adolescents, and when researchers returned in the early 2000s, women who had received the supplements in the first three years of life completed more years of schooling and men had higher incomes1. “Had there not been these follow-ups, this study probably would have been largely forgotten,” says Reynaldo Martorell, a specialist in maternal and child nutrition at Emory University in Atlanta, Georgia, who led the follow-up studies. Instead, he says, the findings made financial institutions such as the World Bank think of early nutritional interventions as long-term investments in human health. Since the Guatemalan research, studies around the world — in Brazil, Peru, Jamaica, the Philippines, Kenya and Zimbabwe — have all associated poor or stunted growth in young children with lower cognitive test scores and worse school achievement2. A picture slowly emerged that being too short early in life is a sign of adverse conditions — such as poor diet and regular bouts of diarrhoeal disease — and a predictor for intellectual deficits and mortality. But not all stunted growth, which affects an estimated 160 million children worldwide, is connected with these bad outcomes. Now, researchers are trying to untangle the links between growth and neurological development. Is bad nutrition alone the culprit? What about emotional neglect, infectious disease or other challenges? © 2017 Macmillan Publishers Limited

Keyword: Development of the Brain
Link ID: 23831 - Posted: 07.13.2017