Chapter 13. Homeostasis: Active Regulation of the Internal Environment

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 21 - 40 of 1507

By GARY TAUBES The first time the sugar industry felt compelled to “knock down reports that sugar is fattening,” as this newspaper put it, it was 1956. Papers had run a photograph of President Dwight D. Eisenhower sweetening his coffee with saccharin, with the news that his doctor had advised him to avoid sugar if he wanted to remain thin. The industry responded with a national advertising campaign based on what it believed to be solid science. The ads explained that there was no such thing as a “fattening food”: “All foods supply calories and there is no difference between the calories that come from sugar or steak or grapefruit or ice cream.” More than 60 years later, the sugar industry is still making the same argument, or at least paying researchers to do it for them. The stakes have changed, however, with a near tripling of the prevalence of obesity in the intervening decades and what the Centers for Disease Control and Prevention figures reveal to be an almost unimaginable 655 percent increase in the percentage of Americans with diabetes diagnoses. When it comes to weight gain, the sugar industry and purveyors of sugary beverages still insist, a calorie is a calorie, regardless of its source, so guidelines that single out sugar as a dietary evil are not evidence-based. Surprisingly, the scientific consensus is technically in agreement. It holds that obesity is caused “by a lack of energy balance,” as the National Institutes of Health website explains — in other words, by our taking in more calories than we expend. Hence, the primary, if not the only, way that foods can influence our body weight is through their caloric content. Another way to say this is that what we eat doesn’t matter; it’s only how much — just as the sugar industry would have us believe. A 2014 article in an American Diabetes Association journal phrased the situation this way: “There is no clear or convincing evidence that any dietary or added sugar has a unique or detrimental impact relative to any other source of calories on the development of obesity or diabetes.” © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23105 - Posted: 01.14.2017

By Anthony Warner Other things being equal, you’d think the strongest influence on expanding midriffs might be fizzy drinks or fried food. But a study out yesterday reinforces the growing idea that poverty is a bigger factor. It found socio-economic status offered the best explanation for greater weight gain when comparing people in the UK with the same genetic vulnerability to obesity (International Journal of Epidemiology, DOI: 10.1093/ije/dyw337). Mounting evidence of poverty’s role in this health crisis makes even more repulsive the rise in vile and deeply offensive prejudice based solely on a failure to fit with the physical ideals of privileged society. This is no longer just about random acts of unkindness. It is everywhere. These views were aired without challenge at a large food and health conference recently. I heard open expression of the idea that obese people should be banned from working in the public sector or that food prices should be increased to force poorer people to eat less. This is the respectable face of prejudice and it has crept into just about every walk of life, stoked by extreme media commentators. It risks creating bigger divides within already fragmented societies. In countries battling obesity, such vitriol extends to repeated talk of denying access to healthcare. It seems this prejudice is OK if its intention is to help people lose weight and often portrays them as slovenly, lazy, lacking self-control, a drain on our health system and morally weak. © Copyright Reed Business Information Ltd.

Keyword: Obesity
Link ID: 23093 - Posted: 01.13.2017

By Catherine Caruso If you give a mouse a beer, he’s going to ask for a cookie—and another, and another. If you give a person enough beer, she might find herself wolfing down a plate of greasy nachos. But why does binge drinking make us binge eat as well? The reason may lie not in the stomach but in the brain, recent research suggests. A study published today in Nature Communications found alcohol activated brain cells that control hunger, sending drunk mice scampering for snacks even when they were not really hungry. Researchers from The Francis Crick Institute Mill Hill Laboratory in London got mice drunk, then tagged and recorded the electrical activity in brain cells linked to hunger, uncovering a neural mechanism that could explain why the animals ate significantly more after binge-drinking sessions even though their bodies did not need the calories. Although hunger pangs in our stomach usually alert us that it is time to eat, the impulse to consume food originates in our brains, and brain cells located in the hypothalamus called agouti-related protein (AgRP) neurons play a key role in controlling hunger. A previous study showed that when AgRP neurons are activated, mice almost immediately seek out food and start eating, even if their stomachs are full. By contrast, when AgRP neurons are deactivated, hungry mice will not eat. AgRP neurons play a similar role in human hunger: Under natural conditions they are activated when our bodies need calories, signaling to us that we should find food. Something different happens, however, when alcohol is involved. Although alcohol is second only to fat in caloric density, previous studies have shown drinking causes humans to eat more, a paradox that made lead authors Craig Blomeley and Sarah Cains and colleagues wonder whether the brain could be to blame. © 2017 Scientific American,

Keyword: Drug Abuse; Obesity
Link ID: 23083 - Posted: 01.11.2017

Brandie Jefferson When I told my coworker that I was participating in a study that involved fasting, she laughed until she nearly cried. My boyfriend, ever supportive, asked hesitantly, "Are you sure you want to try this?" Note the use of "try" instead of "do." When I told my father over the phone, the line went silent for a moment. Then he let out a long, "Welllllll," wished me luck, and chuckled. Turns out, luck might not be enough. I like to eat. Often and a lot. Now, however, my eating habits have become more than a source of amusement for friends and coworkers. Now they are data in a study focusing on people with multiple sclerosis, like me. The pilot study, led by Dr. Ellen Mowry at the Johns Hopkins University in Baltimore, is looking at the impact of intermittent fasting on our microbiomes — the universe of trillions of microbes, mainly bacteria, that live in our guts. Intermittent fasting is pretty much what it sounds like. For six months, participants are allowed to eat during an 8-hour period each day. The remaining 16 hours we are limited to water, tea and coffee. No added sugar, cream, honey or sweetener. Several studies have suggested that the predominant bacteria in the guts of people with MS tend to be different than those in the guts of those without the chronic autoimmune inflammatory disease, according to Samantha Roman, the study's research coordinator. Depending on their makeup, bacteria have the ability to soothe or trigger inflammation, potentially affecting the symptoms of MS and other diseases. Exactly how gut bacteria and inflammation are related, though, is not well understood. © 2017 npr

Keyword: Multiple Sclerosis
Link ID: 23070 - Posted: 01.09.2017

Eating a Mediterranean diet has been linked to less brain shrinkage in older adults. Human brains naturally shrink with age. But a study that followed 401 people in their 70s found that the brains of those who adhered more closely to a Mediterranean-style diet shrank significantly less over a period of three years. A typical Mediterranean diet contains a high amount of vegetables, fruits, olive oil, beans and cereal grains, moderate amounts of fish, dairy products, and wine, and only a small amount of red meat and poultry. “As we age, the brain shrinks and we lose brain cells, which can affect learning and memory,” says Michelle Luciano, at the University of Edinburgh, UK, who led the study. “This study adds to the body of evidence that suggests the Mediterranean diet has a positive impact on brain health.” The differences in brain shrinkage were measured using brain scans. Statistical analysis of diet data found that simply eating more fish and less meat were not associated with reduced shrinking. “While the study points to diet having a small effect on changes in brain size, it didn’t look at the effect on risk of dementia,” says David Reynolds, at the charity Alzheimer’s Research UK. “We would need to see follow-up studies in order to investigate any potential protective effects against problems with memory and thinking.” Other studies have found that being overweight seems to accelerate shrinking of the brain’s white matter. © Copyright Reed Business Information Ltd.

Keyword: Obesity; Alzheimers
Link ID: 23057 - Posted: 01.05.2017

By Joshua A. Krisch Experiments in mice find that obesity reinforces a sedentary lifestyle. According to a December 29 study in Cell, obese mice were less active due to changes in their dopamine receptors—specifically, a drop in activity in DR2 receptors in the brain’s striatum, which plays a role in motor control. “There’s a common belief that obese animals don’t move as much because carrying extra body weight is physically disabling,” coauthor Alexxai Kravitz of the National Institute of Diabetes and Digestive and Kidney Diseases said in a press release. “But our findings suggest that assumption doesn't explain the whole story.” Kravitz and colleagues fed mice either a standard diet or a high-fat diet for 18 weeks, and then examined their dopamine signaling pathways. They found that the least active mice had less-active DR2 dopamine receptors in the striatum. Then they genetically engineered mice to have the same DR2 deficiency, and found that even those that remained lean engaged in less physical activity than other mice. Together, the findings suggest that the DR2 deficiency may account for a lack of movement in obese mice. “Other studies have connected dopamine signaling defects to obesity, but most of them have looked at reward processing—how animals feel when they eat different foods,” Kravitz said in the press release. “We looked at something simpler: dopamine is critical for movement, and obesity is associated with a lack of movement. Can problems with dopamine signaling alone explain the inactivity?” © 1986-2017 The Scientist

Keyword: Obesity; Genes & Behavior
Link ID: 23050 - Posted: 01.03.2017

Michael Byrne Hunger is complicated. It's not merely a single drive, though this is mostly how may experience it consciously: a single dimension of hunger magnitude. We are more or less hungry, sometimes not at all. But there's something else lurking in the brain: anti-hunger. We can be hungry and not hungry simultaneously, in a sense. In more concrete terms, we can imagine that there is in the brain a certain subset of "hunger neurons." When we feel hungry—as during periods of fasting—it means that these neurons are active. Otherwise, the hunger neurons are silent. Hunger neurons are quite real: neuroscientists have demonstrated their function by stimulating hunger neurons artificially, causing mice to eat at weird times and gain weight. But something interesting happens as we start cranking hunger neurons (agouti-related protein, or AgRP, neurons) up. There's a limit. Mice won't just eat themselves to death. This indicates that there's something else to hunger, a moderating factor. This factor is described for the first time this week in Nature Neuroscience by researchers at Harvard Medical School: a new population of neurons that intermingle with AgRP neurons and basically have the opposite effect. Anti-hunger. Anti-hunger is in itself not a brand new idea. For a long time, neuroscientists looked to pro-opiomelanocortin (POMC) neurons, which are likewise intermingled with the AgRP hunger neurons, for filling this role. This is reasonable: genetic mutations and manipulations to the POMC neurons have been observed to lead to obesity in mice. © 2017 Vice Media LLC

Keyword: Obesity
Link ID: 23044 - Posted: 01.02.2017

By JANE E. BRODY The adornments in the office of Eric L. Adams, the Brooklyn borough president, are hardly typical: a full-size refrigerator stocked with fresh fruits and vegetables; a work station where he prepares and blends these plant-based ingredients for his meals and snacks; and a convection oven and hot plate where he cooks them. In an adjacent anteroom, there’s a stationary bike, 15-pound weights, a multipurpose fitness tower and a TRX suspension trainer hanging on the door. His laptop is mounted on a music stand so he can use it while working out on a mini-stepper. Eight months ago, Mr. Adams learned during a health checkup for abdominal pain that he had Type 2 diabetes. He said his average blood sugar level was so high that the doctor was surprised he had not already lapsed into a coma. His hemoglobin A1C level — a lab test that shows the average level of blood glucose over the previous three months — was 17 percent, about three times normal. He wasted no time in tackling his disease with fervor. Spurning the American tendency to treat every ailment with medication, he instead explored the body’s ability to heal itself. Mr. Adams, a 56-year-old former police captain, now needs a new publicity photo. He no longer resembles the roly-poly image on official posters. By adopting a vegan diet, preparing his own meals and working exercise into his everyday routines, he’s shed 30 pounds and completely reversed his diabetes, a pancreatic disorder that can lead to heart attacks, stroke, nerve damage, kidney disease, visual loss and cognitive impairment. Within three months, his A1C level was down to a normal 5.7. He now strives to inform his millions of constituents about how to counter this health- and life-robbing disease, which has reached epidemic proportions in this country, even among children. Starting on the home front, he stripped the Brooklyn Borough Hall drink machine of sugary beverages and the snack machine of everything cooked in oil or unnaturally sweetened. Those searching for a pick-me-up can indulge in plain or sparkling water, diet soda, nuts, dried fruit, protein bars and whole-grain baked chips. © 2017 The New York Times Company

Keyword: Obesity
Link ID: 23043 - Posted: 01.02.2017

Alan Yu Being overweight can raise your blood pressure, cholesterol and risk for developing diabetes. It could be bad for your brain, too. A diet high in saturated fats and sugars, the so-called Western diet, actually affects the parts of the brain that are important to memory and make people more likely to crave the unhealthful food, says psychologist Terry Davidson, director of the Center for Behavioral Neuroscience at American University in Washington, D.C. He didn't start out studying what people ate. Instead, he was interested in learning more about the hippocampus, a part of the brain that's heavily involved in memory. He was trying to figure out which parts of the hippocampus do what. He did that by studying rats that had very specific types of hippocampal damage and seeing what happened to them. In the process, Davidson noticed something strange. The rats with the hippocampal damage would go to pick up food more often than the other rats, but they would eat a little bit, then drop it. Davidson realized these rats didn't know they were full. He says something similar may happen in human brains when people eat a diet high in fat and sugar. Davidson says there's a vicious cycle of bad diets and brain changes. He points to a 2015 study in the Journal of Pediatrics that found obese children performed more poorly on memory tasks that test the hippocampus compared with kids who weren't overweight. He says if our brain system is impaired by that kind of diet, "that makes it more difficult for us to stop eating that diet. ... I think the evidence is fairly substantial that you have an effect of these diets and obesity on brain function and cognitive function." © 2016 npr

Keyword: Obesity; Learning & Memory
Link ID: 23039 - Posted: 12.31.2016

By Laura Beil, Justin Shamoun began to hate his body a few weeks into seventh grade. He was a year younger than his suburban Detroit classmates, having skipped a grade. Many of his peers were entering puberty, their bodies solidifying into sleek young men. Justin still had the doughy build of a boy. After gym class one day, someone told Justin he could probably run faster if he weren’t so fat. The remark crushed him. Ashamed, he started hiding his body under ever-baggier clothes and making excuses to skip P.E., the pool, anywhere required to expose bare skin. Finally, he decided to fix himself. He dove headlong into sports and cut back on food. Before long, he was tossing his lunch into the garbage and picking at his dinner. He ate just enough to blunt his hunger, until the time came when he ate barely at all. The thought that he had an eating disorder never occurred to him. Long considered an affliction of women, eating disorders — the most deadly of all mental illnesses — are increasingly affecting men. The National Eating Disorders Association predicts that 10 million American men alive today will be affected, but that number is only an estimate based on the limited research available. The official criteria for diagnosing eating disorders were updated to be more inclusive of men only in 2013. And last year, Australian researchers writing in the Journal of Eating Disorders noted that “the prevalence of extreme weight control behaviors, such as extreme dietary restriction and purging” may be increasing at a faster rate in men than women. © 2016 Scientific American

Keyword: Anorexia & Bulimia; Sexual Behavior
Link ID: 23036 - Posted: 12.31.2016

By GINA KOLATA It was Oct. 11, 2015, and a middle-aged man and a young woman, both severely obese, were struggling with the same lump-in-the-throat feeling. The next day they were going to have an irreversible operation. Were they on the threshold of a new beginning or a terrible mistake? They were strangers, scheduled for back-to-back bariatric surgery at the University of Michigan with the same doctor. He would cut away most of their stomachs and reroute their small intestines. They were almost certain to lose much of their excess weight. But despite the drastic surgery, their doctor told them it was unlikely that they would ever be thin. Nearly 200,000 Americans have bariatric surgery each year. Yet far more — an estimated 24 million — are heavy enough to qualify for the operation, and many of them are struggling with whether to have such a radical treatment, the only one that leads to profound and lasting weight loss for virtually everyone who has it. Most people believe that the operation simply forces people to eat less by making their stomachs smaller, but scientists have discovered that it actually causes profound changes in patients’ physiology, altering the activity of thousands of genes in the human body as well as the complex hormonal signaling from the gut to the brain. It often leads to astonishing changes in the way things taste, making cravings for a rich slice of chocolate cake or a bag of White Castle hamburgers simply vanish. Those who have the surgery naturally settle at a lower weight. © 2016 The New York Times Company

Keyword: Obesity
Link ID: 23027 - Posted: 12.27.2016

By GINA KOLATA Bariatric surgery is an option that obesity medicine specialists say is too often ignored or dismissed. Yet it is the only option that almost always works to help very heavy people lose a lot of weight and that also can mysteriously make some chronic conditions vanish. Here are some answers about bariatric surgery and what it does. HOW MANY AMERICANS ARE ELIGIBLE FOR BARIATRIC SURGERY? Twenty-four million, according to the American Society for Metabolic and Bariatric Surgery. The criteria are a body mass index above 40, or a B.M.I. of at least 35 along with other medical conditions like diabetes, hypertension, sleep apnea or acid reflux. HOW MANY HAVE THE SURGERY EACH YEAR? Fewer than 200,000. WHAT ARE THE OPERATIONS? There are four in use today. The two most popular procedures are the Roux-en-Y gastric bypass and the gastric sleeve. Both make the stomach smaller. The bypass also reroutes the small intestine. A simpler procedure, the gastric band, is less effective and has fallen out of favor. And a much more drastic operation, the biliopancreatic diversion with duodenal switch, which bypasses a large part of the small intestine, is rarely used because it has higher mortality and complication rates. HOW MUCH DO THE OPERATIONS COST? The average cost of a sleeve gastrectomy is $16,000 to $19,000, and the average cost of a gastric bypass is $20,000 to $25,000. Most insurance plans cover the cost for patients who qualify, though some plans require that patients try dieting for a certain amount of time first. DOES THE SURGERY SAVE MONEY ON OTHER HEALTH CARE COSTS IN THE END? © 2016 The New York Times Company

Keyword: Obesity
Link ID: 23026 - Posted: 12.27.2016

By NICHOLAS BAKALAR Using a sauna may be more than just relaxing and refreshing. It may also reduce the risk for Alzheimer’s disease and other forms of dementia, a new study suggests. Researchers in Finland analyzed medical records of 2,315 healthy men ages 42 to 60, tracking their health over an average of about 20 years. During that time, they diagnosed 204 cases of dementia and 123 cases of Alzheimer’s disease. The study, in Age and Ageing, controlled for alcohol intake, smoking, blood pressure, diabetes and other health and behavioral factors. It found that compared with men who used a sauna once a week, those who used a sauna four to seven times a week had a 66 percent lower risk for dementia and a 65 percent lower risk for Alzheimer’s disease. The senior author, Jari Antero Laukkanen, a professor of clinical medicine at the University of Eastern Finland, said that various physiological mechanisms may be involved. Sauna bathing may, for example, lead to reduced inflammation, better vascular function or lowered blood pressure. “Overall relaxation and well-being can be another reason,” he added, though the findings were only an association. “We need more studies to clarify mechanisms and confirm our findings.” © 2016 The New York Times Company

Keyword: Miscellaneous
Link ID: 23018 - Posted: 12.26.2016

By STEPH YIN Inuit who live in Greenland experience average temperatures below freezing for at least half of the year. For those who live in the north, subzero temperatures are normal during the coldest months. Given these frigid conditions, anthropologists have wondered for decades whether the Inuit in Greenland and other parts of the Arctic have unique biological adaptations that help them tolerate the extreme cold. A new study, published on Wednesday in Molecular Biology and Evolution, identifies gene variants in Inuit who live in Greenland, which may help them adapt to the cold by promoting heat-generating body fat. These variants possibly originated in the Denisovans, a group of archaic humans who, along with Neanderthals, diverged from modern humans about half a million years ago. “As modern humans spread around the world, they interbred with Denisovans and Neanderthals, who had already been living in these different environments for hundreds of thousands of years,” said Rasmus Nielsen, a professor of integrative biology at the University of California, Berkeley and an author of the paper. “This gene exchange may have helped some modern humans adapt to and conquer new environments.” The new study follows earlier research by Dr. Nielsen and colleagues, which found genetic mutations that might help the Inuit metabolize unsaturated fatty acids common in their diet of whales, seals and fish. In this study, Dr. Nielsen’s team focused on another distinct region in the Inuit genome, which seems to affect body fat distribution and other aspects of development. The researchers compared the genomes of nearly 200 Inuit with genomes of Neanderthals, Denisovans and modern populations around the world. © 2016 The New York Times Company

Keyword: Evolution
Link ID: 23011 - Posted: 12.23.2016

Hannah Devlin Science Correspondent Scientists have offered a genetic explanation for why some people are obese and healthy while others develop diabetes and heart disease as a result of their weight. The study identified three genes, which appear to influence whether fat is compartmentalised and stored around the outside of the body or whether it spills into the circulatory system. Higher levels of fat in the blood supply increase the risk of type 2 diabetes and can lead to fatty deposits around the heart and liver. Professor Haja Kadarmideen, a geneticist who led the work at the University of Copenhagen, said: “People who have the ability to store large amounts of fat are able to be fat, but not unhealthy.” Yo-yo weight gain driven by gut bacteria's 'memory' of obesity, says study Read more Previous studies have found that while being overweight or obese is a risk factor for diabetes, liver disease and heart disease, about 15-20% of those who are obese appear to suffer no health consequences. Other research, involving more than 100,000 adults in Denmark, found that those with an “overweight” body mass index (or BMI) were more likely to live longer than those in the “healthy”, “underweight”, and “obese” categories, suggesting that the relationship between weight, health and lifespan is not straightforward. “We wanted to ask what is it that allows some people to be overweight and remain healthy,” said Kadarmideen. © 2016 Guardian News and Media Limited

Keyword: Obesity; Genes & Behavior
Link ID: 23005 - Posted: 12.22.2016

By PHIL BARBER SAN FRANCISCO — Paraag Marathe’s structured, analytical mind has served him well in the offices of Silicon Valley and the National Football League. He figured that he could lean on those traits the first time he spoke publicly about his sister, Shilpa, and how anorexia had taken her life. But composure failed Marathe in 2011, six years after Shilpa’s death, while he spoke to survivors and grieving family members at an event for Andrea’s Voice, a nonprofit foundation that tries to promote education about eating disorders and their treatments. “Not only did I break down a little bit during that speech,” said Marathe, 39, the San Francisco 49ers’ chief strategy officer and executive vice president for football operations. “It was also one of those weird moments afterwards. I emotionally collapsed in the arms of somebody there who had lost her daughter.” The memories were back. Marathe had watched his brilliant sister succumb to self-destructive thoughts and starve herself. He had seen Shilpa wither to less than 50 pounds in the last years of her life, had felt the shame and puzzlement that her condition brought to his family. Fueled by regret — why had he not noticed sooner, and why wasn’t he more assertive in trying to help Shilpa? — Marathe has found his voice. He will patiently tell you that 30 million Americans are believed to suffer from eating disorders, and that medical insurance plans rarely cover treatment of the condition. He will remind you that anorexia has the highest fatality rate among mental illnesses — about 10 percent, according to a 2011 meta-analysis published in Archives of General Psychiatry and cited by the National Institute of Mental Health. Eating-disorder caregivers and advocates welcome Marathe’s help in shattering the myth that anorexia afflicts only well-to-do white girls and women. The illness claims men, too, and frequently remains a taboo subject in less affluent or nonwhite families, said Kristina Saffran of Project HEAL, an organization that raises money to cover care from diagnosis to recovery. © 2016 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 22992 - Posted: 12.15.2016

By GINA KOLATA Dr. Frank Sacks, a professor of nutrition at Harvard, likes to challenge his audience when he gives lectures on obesity. “If you want to make a great discovery,” he tells them, figure out this: Why do some people lose 50 pounds on a diet while others on the same diet gain a few pounds? Then he shows them data from a study he did that found exactly that effect. Dr. Sack’s challenge is a question at the center of obesity research today. Two people can have the same amount of excess weight, they can be the same age, the same socioeconomic class, the same race, the same gender. And yet a treatment that works for one will do nothing for the other. The problem, researchers say, is that obesity and its precursor — being overweight — are not one disease but instead, like cancer, they are many. “You can look at two people with the same amount of excess body weight and they put on the weight for very different reasons,” said Dr. Arya Sharma, medical director of the obesity program at the University of Alberta. Not only can that explain why treatment is so difficult and results so wildly variable, but it can explain why prevention efforts often fail. After trial and error, here are six stories from people who finally found diets, drugs and other methods that helped them keep the weight off. If obesity is many diseases, said Dr. Lee Kaplan, director of the obesity, metabolism and nutrition institute at Massachusetts General Hospital, there can be many paths to the same outcome. It makes as much sense to insist there is one way to prevent all types of obesity — get rid of sugary sodas, clear the stores of junk foods, shun carbohydrates, eat breakfast, get more sleep — as it does to say you can avoid lung cancer by staying out of the sun, a strategy specific to skin cancer. One focus of research is to figure out how many types of obesity there are — Dr. Kaplan counts 59 so far — and how many genes can contribute. So far, investigators have found more than 25 genes with such powerful effects that if one is mutated, a person is pretty much guaranteed to become obese, said Dr. Stephen O’Rahilly, head of the department of clinical biochemistry and medicine at Cambridge University. © 2016 The New York Times Company

Keyword: Obesity
Link ID: 22976 - Posted: 12.12.2016

By Karinna Hurley Autonomy, peer relationships, and parental conflict — these are the universal themes that made the popular 1990s comic Zits identifiable for anyone who has, or has been, a teenager. In one strip, hands in pockets and making a sullen sideways glance, Jeremy slouches next to his father. His t-shirt reads, “question authority.” Next to him, his equally chagrined father sports the t-shirt: “do not question my authority.” While his parents work to steer the 16-year-old in the right direction on his path to adulthood, Jeremy is equally determined to forge his own way. For the most part, their suggestions, pleas, and cajoles, don’t make it past his headphones. Figuring out how to effectively appeal to adolescents was the first challenge facing researchers in a fascinating new study published in the Proceedings of the National Academy of Sciences. Their goal was to induce teens to change one critically important behavior — food choice — in a completely novel way. The researchers set-up a scenario where healthy eating itself became an avenue for fighting authority. While such a unique value-based intervention also has the potential to be applicable to other groups and values, it’s hard to find a better place to start in today’s society than healthy eating. One of the major initiatives developed and championed by outgoing First Lady Michelle Obama was aimed at reducing childhood obesity. Because, despite the consequences — heart disease, stroke, diabetes — about one in three American adults and nearly one in five children are obese. Carrying extra weight is harmful to individuals and also costly to society. But changing eating habits, one factor in being overweight, is just plain hard. It is not enough to know the consequences of eating junk food: In movie theaters, on best-seller lists and billboards, the warnings are all around us. Yet, even widespread public health messages and access to kitchen gardens, like on the South Lawn of the White House, have not yet curbed rising obesity levels. © 2016 Scientific American

Keyword: Obesity
Link ID: 22961 - Posted: 12.07.2016

By PAGAN KENNEDY Abby Solomon suffers from a one-in-a-billion genetic syndrome: After just about an hour without food, she begins to starve. She sleeps in snatches. In her dreams she gorges on French fries. But as soon as she wakes up and nibbles a few bites, she feels full, so she ends up consuming very few calories. At 5 feet 10 inches tall, she weighs 99 pounds. Now 21 years old, she is one of the few people in the world to survive into adulthood with neonatal progeroid syndrome, a condition that results from damage to the FBN1 gene. This mutation mangles noses and eyes and destroys the layer of fat under the skin so that even teenagers look middle-aged. It also interferes with the body’s ability to make a hormone called asprosin, which regulates blood sugar. Atul Chopra, a medical geneticist at Baylor College of Medicine, told me that people with the disorder don’t experience ordinary hunger — instead they waver on the edge of hypoglycemia and must constantly snack to keep from passing out. And yet when I asked Ms. Solomon if she wished she could magically repair her damaged gene, she answered without hesitation: “I wouldn’t change it for anything.” This is because her painful body may hold the clues to a lifesaving treatment for millions of people with obesity and diabetes. Dr. Chopra told me that, as far as medical science is concerned, Abby Solomon is worth thousands of the rest of us. By observing her, scientists can see how a hormone deficiency affects a living person, from her thoughts to her liver function. Several years ago, she spent a day inside a metabolic chamber in a lab so that Dr. Chopra could measure everything she breathed and ate. The results showed that Ms. Solomon takes in about half the calories of a typical woman her age, and also expends half as much energy. “Nothing comes close to starting with people who are naturally different,” he said. This is why he searches out patients at the extreme ends of the spectrum — those who are wired to weigh 80 pounds or 380 pounds. He said, “We have the opportunity to help a bigger swath of humanity when we learn from these outliers.” © 2016 The New York Times Company

Keyword: Obesity; Genes & Behavior
Link ID: 22919 - Posted: 11.28.2016

By Tracy Vence Lose weight, gain it back. That’s the frustrating routine for many individuals who have experienced only short-term success with diets. To examine the microbial and metabolic factors underlying this weight loss-regain cycle, researchers at the Weizmann Institute of Science in Rehovot, Israel, ran a series of experiments using a mouse model of recurrent obesity. The composition of a mouse’s microbiome is predictive of post-diet weight regain, which is in part modulated by metabolites released by the bugs, the researchers found. Their results were published today (November 24) in Nature. “This work adds some insight on how the microbiome acts as a buffer to changes in our diet,” study coauthor Eran Segal of the Weizmann Institute said during a press briefing this week (November 22). In particular, the researchers found evidence to suggest that mice that were once obese tend to experience alterations in microbiome composition that persist during and after weight loss. They also linked the metabolic health of mice to levels of the dietary flavonoids apigenin and naringenin, among other metabolites exchanged between the host and microbiome. See “How Diet Influences Host-Microbiome Communication in Mice” There is hope, however. Segal and colleagues also reported that microbiome- and metabolite-mediating therapies—such as antibiotic treatment, fecal transplant, or postbiotic supplementation—can ameliorate the rate of weight regain in mice predisposed to recurrent obesity. © 1986-2016 The Scientist

Keyword: Obesity
Link ID: 22916 - Posted: 11.26.2016