Chapter 13. Homeostasis: Active Regulation of the Internal Environment
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By Melissa Banigan Twenty years ago, I started experiencing what turned into a long list of seemingly unrelated health issues. Headaches, depression, insomnia, peripheral neuropathy, fatigue, joint pain, chest pain, shortness of breath, a lesion on my spine and a variety of uncomfortable gastrointestinal ailments. Over the past five years, things went from bad to worse as I also became lactose-intolerant, developed mild vitiligo (a condition that leads to loss of skin pigmentation) and major vertigo, experienced a series of low-grade fevers and started to have some memory loss that I referred to as brain fogs. Doctors told me that as an overworked single mother of 40, I might just need to figure out ways to get more sleep and relax. Some of what was happening, they said, might be attributed to the normal processes of aging. What was happening, however, didn’t feel normal. Always a voracious reader and a writer by profession, I could no longer focus on work, read even a page of a book or grip a pen long enough to write a grocery list. I often felt too exhausted to keep plans with friends. When I did pull myself off my couch to see them, I couldn’t concentrate on conversations, so I sequestered myself in my apartment and let my friendships fade. I had been a runner, a swimmer and a hiker, but just walking up a flight of stairs made me lose my breath so completely that I succumbed to inactivity. I did everything the doctors asked me to do. I changed my diet and sleep schedule, went to a physical therapist and saw specialists in neurology and rheumatology and even a mental-health therapist. I then also turned to massage therapists, herbalists and an acupuncturist. © 1996-2017 The Washington Post
Obese people who get surgery to lose weight have half the risk of developing heart failure as do patients who make lifestyle changes to shed excess pounds, a recent study suggests. “We were surprised by the large difference in heart failure incidence between the two groups,” said lead study author Johan Sundstrom of Uppsala University in Sweden. It’s possible that gastric bypass patients had a lower risk of heart failure because they lost more weight than the group trying to do so without surgery. Researchers also found that losing 22 pounds by any means was tied to a 23 percent drop in heart failure risk. The study team examined data on 25,805 obese people who had gastric bypass surgery, which reduces the stomach to a small pouch, and 13,701 patients who were put on low-calorie diets. After following half of the patients for at least four years, people who had gastric bypass were found to be 46 percent less likely to have developed heart failure. After one year, surgery patients had an average weight loss 41.4 pounds greater than that of those who relied on diet and exercise, the study found. After two years, surgery was associated with an average weight loss that was 49.8 pounds more than those who undertook lifestyle changes. Some previous research has linked obesity to heart failure, and a growing body of evidence suggests that obesity might directly cause the heart condition, Sundstrom said. While the new study wasn’t designed to prove a causal relationship, it adds more evidence in support of this possibility. © 1996-2017 The Washington Post
Link ID: 23372 - Posted: 03.19.2017
By Mitch Leslie It sounds like a crazy way to improve your health—spend some time on a platform that vibrates at about the same frequency as the lowest string on a double bass. But recent research indicates that the procedure, known as whole-body vibration, may be helpful in illnesses from cerebral palsy to chronic obstructive pulmonary disease. Now, a new study of obese mice reveals that whole-body vibration provides similar metabolic benefits as walking on a treadmill, suggesting it may be useful for treating obesity and type II diabetes. “I think it’s very promising,” says exercise physiologist Lee Brown of the California State University in Fullerton, who wasn’t connected to the study. Although the effects are small, he says, researchers should follow-up to determine whether they can duplicate them in humans. Plenty of gyms feature whole-body vibration machines, and many athletes swear the activity improves their performance. The jiggling does seem to spur muscles to work harder, possibly triggering some of the same effects as exercise. But researchers still don’t know how the two compare, especially when it comes to people who are ill. So biomedical engineer Meghan McGee-Lawrence of the Medical College of Georgia in Augusta and colleagues decided to perform a head-to-head comparison of exercise and whole-body vibration. The researchers tested mutant mice resistant to the appetite-controlling hormone leptin, resulting in obesity and diabetes. © 2017 American Association for the Advancement of Science.
Link ID: 23362 - Posted: 03.16.2017
An international team of researchers has conducted the first study of its kind to look at the genomic underpinnings of obesity in continental Africans and African-Americans. They discovered that approximately 1 percent of West Africans, African-Americans and others of African ancestry carry a genomic variant that increases their risk of obesity, a finding that provides insight into why obesity clusters in families. Researchers at the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, and their African collaborators published their findings March 13, 2017, in the journal Obesity. People with genomic differences in the semaphorin-4D (SEMA4D) gene were about six pounds heavier than those without the genomic variant, according to the study. Most of the genomic studies conducted on obesity to date have been in people of European ancestry, despite an increased risk of obesity in people of African ancestry. Obesity is a global health problem, contributing to premature death and morbidity by increasing a person’s risk of developing diabetes, hypertension, heart disease and some cancers. While obesity mostly results from lifestyle and cultural factors, including excess calorie intake and inadequate levels of physical activity, it has a strong genomic component. The burden of obesity is, however, not the same across U.S. ethnic groups, with African-Americans having the highest age-adjusted rates of obesity, said Charles N. Rotimi, Ph.D., chief of NHGRI’s Metabolic, Cardiovascular and Inflammatory Disease Genomics Branch and director of the Center for Research on Genomics and Global Health (CRGGH) at NIH. CRGGH examines the socio-cultural and genomic factors at work in health disparities — the negative health outcomes that impact certain groups of people — so they can be translated into policies that reduce or eliminate healthcare inequalities in the United States and globally.
By Abby Olena Researchers have shown that a hormone secreted by bone, called lipocalin 2 (LCN2), suppresses appetite in mice. The results, published today (March 8) in Nature, suggest that LCN2 crosses the rodents’ blood-brain barrier and binds a receptor in the hypothalamus. The team also found a link between body weight and LCN2 levels in people with type 2 diabetes. The authors “have identified a protein that’s secreted from bone that has a pretty significant impact on feeding behavior,” Lora Heisler of the University of Aberdeen in Scotland, who did not participate in the work, told The Scientist. “And the fact that they found that some supporting evidence in humans is really exciting.” “We have found a new role for bone as an endocrine organ, and that is its ability to regulate appetite,” said study coauthor Stavroula Kousteni of Columbia University in New York City. Scientists had previously identified LCN2 as a protein expressed in fat cells, but Kousteni and colleagues showed that it is enriched 10-fold in osteoblasts. When they generated mice without LCN2 in their osteoblasts, levels of the circulating hormone dropped 67 percent. These mice ate more than control animals and showed increases in fat mass and body weight. When the authors injected LCN2 into wild-type or obese mice, the rodents ate less food. The treated animals showed decreases in body weight, fat mass, and weight gain. LCN2 injections also led to increases in insulin levels and glucose tolerance, the scientists showed. © 1986-2017 The Scientist
Ian Sample Science editor Selling high calorie foods in plain packaging could help in the battle against obesity according to a leading researcher who has won a share of the most lucrative prize in neuroscience for his work on the brain’s reward system. The colourful wrapping and attractive advertising of calorie-rich foods encourage people to buy items that put them at risk of overeating and becoming obese in the future, said Wolfram Schultz, a professor of neuroscience at the University of Cambridge. “We should not advertise, propagate or encourage the unnecessary ingestion of calories,” Schultz said at a press conference held on Monday to announce the winners of the 2017 Brain Prize. “There should be some way of regulating the desire to get more calories. We don’t need these calories.” “Colourful wrapping of high energy foods of course makes you buy more of that stuff and once you have it in your fridge, it’s in front of you every time you open the fridge and ultimately you’re going to eat it and eat too much,” he added. Schultz shares the €1m prize from the Lundbeck Foundation in Denmark with professors Peter Dayan, director of the Gatsby Computational Neuroscience Unit at UCL, and Ray Dolan, director of the Max Planck UCL Centre for Computational Psychiatry and Ageing. Together, the scientists unravelled how the brain uses rewards to learn and shape behaviour.
Aaron E. Carroll While we have long known about the existence of microbes — the tiny bacteria, fungi and archaea that live all around, on and in us — our full relationship has become one of the hottest topics for research only in recent years. Scientists believe that every person contains as many independent microbial cells as human cells. This collection of life, known as the microbiome, provides useful functions for us. Indeed, some of the things we think our bodies do are actually the abilities and enzymes of life-forms living within us. They can help with digestion, vitamin synthesis and even immunological responses. But, as with many new breakthroughs and advances, the hype of the microbiome often outweighs the reality. This seems especially likely in the field of nutrition. Doing research on the microbiome is not easy, and there are many opportunities to foul things up. To accomplish human studies, large samples of people and microbiomes are needed to account for potential confounding variables. Specimens have to be collected and stored carefully because contamination has been a big problem. DNA has to be extracted, amplified and sequenced. Finally, powerful bioinformatics tools are necessary to assemble and analyze the huge amount of data contained in a sequence of nucleotides — all of which has resulted in a wide range of new “omics,” including genomics, proteomics, transcriptomics and metabolomics. Of course, if we think that microbes play a large role in health, we have to rethink the role that antimicrobials play in our lives. In this thinking, antibiotics and antifungals could be life-changing or life-threatening. But that’s not the case. There are many reasons to avoid unnecessary use of these medications, but the microbiome appears able to withstand most treatment. © 2017 The New York Times Company
Link ID: 23318 - Posted: 03.06.2017
By NICHOLAS BAKALAR There is some evidence that stress prompts people to turn to sweet, high-calorie “comfort foods.” Now scientists have confirmed a link between long-term stress and obesity. The study, published in Obesity, tested 2,527 men and women over 50 years old, quantifying stress by measuring levels of cortisol, the stress hormone, in 2-centimeter hair clippings, or about two months’ growth. After controlling for age, sex, ethnicity, smoking, diabetes and other factors that might be linked to obesity, they found that the higher the level of cortisol, the greater the body weight, B.M.I. and waist circumference. Higher cortisol levels were also associated with persistence of obesity over time. Other studies have relied on measures of cortisol in blood, urine or saliva, which can vary by time of day and be affected by temporary stressors and other factors. But this study was able to measure general stress levels over two months to get a picture of the long-term effect. The researchers acknowledge that they were unable to determine whether chronically high cortisol levels are a cause or a consequence of obesity (feeling “fat,” for example, could raise your stress levels). The lead author, Sarah E. Jackson, an epidemiologist at University College London, said that while it may not be possible to eliminate stress, “you may be able to find ways to control it. Even just being aware that stress might make you eat more may help.” © 2017 The New York Times Company
By Emma Hiolski There’s more to those love handles than meets the eye. Fat tissue can communicate with other organs from afar, sending out tiny molecules that control gene activity in other parts of the body, according to a new study. This novel route of cell-to-cell communication could indicate fat plays a much bigger role in regulating metabolism than previously thought. It could also mean new treatment options for diseases such as obesity and diabetes. “I found this very interesting and, frankly, very exciting,” says Robert Freishtat of Children’s National Health System in Washington, D.C., a pediatrician and researcher who has worked with metabolic conditions like obesity and diabetes. Scientists have long known that fat is associated with all sorts of disease processes, he says, but they don’t fully understand how the much-reviled tissue affects distant organs and their functions. Scientists have identified hormones made by fat that signal the brain to regulate eating, but this new study—in which Freishtat was not involved—takes a fresh look at another possible messenger: small snippets of genetic material called microRNAs, or miRNAs. MiRNAs, tiny pieces of RNA made inside cells, help control the expression of genes and, consequently, protein production throughout the body. But some tumble freely through the bloodstream, bundled into tiny packets called exomes. There, high levels of some miRNAs have been associated with obesity, diabetes, cancer, and cardiovascular disease. © 2017 American Association for the Advancement of Science.
Link ID: 23247 - Posted: 02.17.2017
By Alice Callahan Once fat cells are formed, can you ever get rid of them? The number of fat cells in a person’s body seems to be able to change in only one direction: up. Fat cell number increases through childhood and adolescence and generally stabilizes in adulthood. But this doesn’t mean that fat cells, or adipocytes, are stagnant. The size of individual fat cells is remarkably variable, expanding and contracting with weight gain or weight loss. And as with most cell types in the body, adipocytes die eventually. “Usually when old ones die, they are replaced by new fat cells,” said Dr. Michael Jensen, an endocrinologist and obesity researcher at the Mayo Clinic. Cell death and production appear to be tightly coupled, so although about 10 percent of adipocytes die each year, they’re replaced at the same rate. Even among bariatric surgery patients, who can lose massive amounts of weight, the number of fat cells tends to remain the same, although the cells shrink in size, studies show. Liposuction reduces the number of fat cells in a person’s body, but studies show the weight lost is typically regained within a year. It isn’t known whether this regain occurs through the production of new fat cells or expansion of existing ones. People who are obese tend to have more fat cells than those who are not, and several studies have found an increase in fat cell number with weight regain following weight loss. The fact that fat cell number can be increased but not decreased most likely contributes to the body’s drive to regain weight after weight loss, said Dr. Kirsty L. Spalding, a cell biologist at the Karolinska Institute in Sweden and the lead author of a 2008 study showing that fat cells die and are replaced. Beyond their role in storing fat, adipocytes secrete proteins and hormones that affect energy metabolism. © 2017 The New York Times Company
Link ID: 23246 - Posted: 02.17.2017
By Mitch Leslie Fasting is all the rage. Self-help books promise it will incinerate excess fat, spruce up your DNA, and prolong your life. A new scientific study has backed up some health claims about eating less. The clinical trial reveals that cutting back on food for just 5 days a month could help prevent or treat age-related illnesses like diabetes and cardiovascular disease. “It’s not trivial to do this kind of study,” says circadian biologist Satchidananda Panda of the Salk Institute for Biological Studies in San Diego, California, who wasn’t connected to the research. “What they have done is commendable.” Previous studies in rodents and humans have suggested that periodic fasting can reduce body fat, cut insulin levels, and provide other benefits. But there are many ways to fast. One of the best known programs, the 5:2 diet, allows you to eat normally for 5 days a week. On each of the other 2 days, you restrict yourself to 500 to 600 calories, about one-fourth of what the average American consumes. An alternative is the so-called fasting-mimicking diet, devised by biochemist Valter Longo of the University of Southern California in Los Angeles and colleagues. For most of the month, participants eat as much of whatever they want. Then for five consecutive days they stick to a menu that includes chips, energy bars, and soups, consuming about 700 to 1100 calories a day. © 2017 American Association for the Advancement of Science
Link ID: 23236 - Posted: 02.16.2017
Laura Beil People who undergo gastric bypass surgery are more likely to experience a remission of their diabetes than patients who receive a gastric sleeve or intensive management of diet and exercise, according to a new study. Bypass surgery had already shown better results for diabetes than other weight-loss methods in the short term, but the new research followed patients for five years. “We knew that surgery had a powerful effect on diabetes,” says Philip Schauer of the Bariatric & Metabolic Institute at the Cleveland Clinic. “What this study says is that the effect of surgery is durable.” The results were published online February 15 in the New England Journal of Medicine. The study followed 134 people with type 2 diabetes for five years in a head-to-head comparison of weight-loss methods. At the end of that time, two of 38 patients who only followed intensive diet and exercise plans were no longer in need of insulin to manage blood sugar levels. For comparison, 11 of 47 patients who had a gastric sleeve, which reduces the size of the stomach, and 14 of 49 who underwent gastric bypass, a procedure that both makes the stomach smaller and shortens digestion time, did not need the insulin anymore. In general, patients who had been diabetic for fewer than eight years were more likely to be cured, Schauer says. Even those surgical patients who still needed to take insulin had greater weight loss and lower median glucose levels than others in the study. This study was also one of the few to show that bariatric surgery could help those with only mild obesity, defined as a body mass index between 27 and 34. How bariatric surgery might improve diabetes is still unknown, but scientists have pointed to effects on the body’s metabolism (SN: 8/24/13, p. 14) and gut microbes (SN: 9/5/15, p. 16). |© Society for Science & the Public 2000 - 2016.
Link ID: 23235 - Posted: 02.16.2017
By Andy Coghlan It’s as if a switch has been flicked. Evidence is mounting that chronic fatigue syndrome (CFS) is caused by the body swapping to less efficient ways of generating energy. Also known as ME or myalgic encephalomyelitis, CFS affects some 250,000 people in the UK. The main symptom is persistent physical and mental exhaustion that doesn’t improve with sleep or rest. It often begins after a mild infection, but its causes are unknown. Some have argued that CFS is a psychological condition, and that it is best treated through strategies like cognitive behavioural therapy. But several lines of investigation are now suggesting that the profound and painful lack of energy seen in the condition could in many cases be due to people losing their ability to burn carbohydrate sugars in the normal way to generate cellular energy. Instead, the cells of people with CFS stop making as much energy from sugar as usual, and start relying more on lower-yielding fuels, such as amino acids and fats. This kind of metabolic switch produces lactate, which can cause pain when it accumulates in muscles. Together, this would explain both the shortness of energy, and why even mild exercise can be exhausting and painful. © Copyright Reed Business Information Ltd.
Link ID: 23226 - Posted: 02.14.2017
Moises Velasquez-Manoff This Valentine’s Day, as you bask in the beauty of your beloved, don’t just thank his or her genes and your good fortune; thank microbes. Research on the microbes that inhabit our bodies has progressed rapidly in recent years. Scientists think that these communities, most of which live in the gut, shape our health in myriad ways, affecting our vulnerability to allergic diseases like hay fever, how much weight we put on, our susceptibility to infection and maybe even our moods. They can also, it seems, make us sexy. Susan Erdman, a microbiologist at M.I.T., calls it the “glow of health.” The microbes you harbor, she argues, can make your skin smooth and your hair shiny; they may even put a spring in your step. She stumbled on the possibility some years ago when, after feeding mice a probiotic microbe originally isolated from human breast milk, a technician in her lab noticed that the animals grew unusually lustrous fur. Further observation of males revealed thick skin bristling with active follicles, elevated testosterone levels and oversize testicles, which the animals liked showing off. Microbes had transformed these animals into rodent heartthrobs. When given to females, the probiotic also prompted deeper changes. Levels of a protein called interleukin 10, which helps to prevent inflammatory disease and ensure successful pregnancy, went up, as did an important hormone called oxytocin. Oxytocin, often called the love hormone, helps mammals bond with one another. Our bodies may release it when we kiss (and mean it), when women breast-feed, even when people hang out with good friends. And the elevated oxytocin Dr. Erdman saw had important effects during motherhood. Some of the mice in her studies were eating a high-fat, high-sugar diet — junk-foody fare that’s known to shift the microbiome into an unhealthy state. Not surprisingly perhaps, mothers that didn’t imbibe the probiotics were less caring and tended to neglect their pups. But mothers that had high oxytocin thanks to the probiotic were nurturing and reared their pups more successfully. © 2017 The New York Times Company
By JANE E. BRODY “Bariatric surgery is probably the most effective intervention we have in health care,” says Laurie K. Twells, a clinical epidemiologist at Memorial University of Newfoundland. She bases this bold claim on her experience with seriously obese patients and a detailed analysis of the best studies yet done showing weight-loss surgery’s ability to reverse the often devastating effects of being extremely overweight on health and quality of life. “I haven’t come across a patient yet who wouldn’t recommend it,” Dr. Twells said in an interview. “Most say they wish they’d done it 10 years sooner.” She explained that the overwhelming majority of patients who undergo bariatric surgery have spent many years trying — and failing — to lose weight and keep it off. And the reason is not a lack of willpower. “These patients have lost hundreds of pounds over and over again,” Dr. Twells said. “The weight that it takes them one year to lose is typically back in two months,” often because a body with longstanding obesity defends itself against weight loss by drastically reducing its metabolic rate, an effect not seen after bariatric surgery, which permanently changes the contours of the digestive tract. In reviewing studies that followed patients for five to 25 years after weight-loss surgery, Dr. Twells and colleagues found major long-lasting benefits to the patients’ health and quality of life. Matched with comparable patients who did not have surgery, those who did fared much better physically, emotionally and socially. They rated themselves as healthier and were less likely to report problems with mobility, pain, daily activities, social interactions and feelings of depression and anxiety, among other factors that can compromise well-being. © 2017 The New York Times Company
Link ID: 23219 - Posted: 02.13.2017
By Tamar Haspel In his new book “The Case Against Sugar,” journalist Gary Taubes makes, as you might easily guess, a spirited case against sugar. His argument is based on the straightforward idea that sugar contributes to obesity and disease well beyond its calorie content, because it affects human metabolism in a way that encourages fat storage. In his new book, the science journalist Gary Taubes takes a hard-nosed look at sugar — and further advances the idea that not all calories are created equal. But there are competing theories of obesity. Who’s right? The debate is often framed as being over the nature of calories themselves, with scientists holding that calories are units of energy — each one no different than the other. Sugar is a carbohydrate, and the body converts carbs to glucose which is then absorbed into the bloodstream. This, in turn, triggers the pancreas to release insulin, the hormone that enables the body to use energy or store it as fat. If a person doesn’t eat many carbohydrates, the pancreas doesn’t release as much insulin, and less fat is stored, forcing the body’s metabolism to increase and burn off that energy. In practical terms, the theory goes, such a person will have an easier time losing weight — or avoiding gaining it. This hypothesis is called, appropriately, the carbohydrate/insulin, or C/I, model, and it is the basis for any number of popular low-carb diets, including Atkins, the Paleo diet, and others. It is also a “minority position” among food scientists, Taubes concedes, and many mainstream nutrition authorities reject it. Copyright 2017 Undark
Link ID: 23208 - Posted: 02.09.2017
By Simon Oxenham Ever felt hungry and angry at the same time? There’s evidence that “hanger” is a real phenomenon, one that can affect your work and relationships. The main reason we become more irritable when hungry is because our blood glucose level drops. This can make it difficult for us to concentrate, and more likely to snap at those around us. Low blood sugar also triggers the release of stress-related hormones like cortisol and adrenaline, as well as a chemical called neuropeptide Y, which has been found to make people behave more aggressively towards those around them. This can all have an alarming effect on how you feel about other people – even those you love. A classic study of married couples asked them to stick pins into “voodoo dolls” that represented their loved ones, to reflect how angry they felt towards them. The volunteers then competed against their spouse in a game, in which the winner could blast loud noise through the loser’s headphones. The researchers tracked the participants’ blood glucose levels throughout. They found that when people had lower sugar levels, the longer the blasts of unpleasant noise they subjected their spouse to, and the more pins they stuck into their dolls. But while being hungry really does change your behaviour, the effects of hanger have sometimes been overstated. One study that attracted attention a few years ago found that judges are less likely to set lenient sentences the closer it gets to lunch. © Copyright Reed Business Information Ltd.
Link ID: 23172 - Posted: 02.01.2017
By Mitch Leslie When we have food poisoning, the last thing we want to do is eat. But in mice, a microbe that causes this ailment actually increases appetite, a new study reveals. Researchers say they might be able to use the same trick to increase eating in cancer patients and old folks, who often lose their desire for food. “I think it’s a fantastic paper,” says immunophysiologist Keith Kelley of the University of Illinois in Urbana, who wasn’t connected to the study. The researchers deserve praise for combining approaches from several disciplines such as microbiology, neurobiology, and immunology to draw a surprising conclusion, he says. “It’s the way disease responses should be investigated.” Some of the symptoms you endure when you are ill, such as lethargy and fever, are actually good for you. Lolling on the couch all day, for instance, saves energy for your immune cells. But the picture is more complex for another of these so-called sickness behaviors—reduced appetite. Animal studies have found that eating less seems to improve the odds of surviving some infections, perhaps because it robs the invading microbes of key nutrients, but in other cases the loss of appetite often proves fatal. © 2017 American Association for the Advancement of Science
Eating disorders, including anorexia and bulimia, affect a small but substantial number of women in their 40s and 50s, UK research suggests. The study, involving more than 5,000 women, found just over 3% reported having an eating disorder. Some said they had experienced it since their teens, others developed it for the first time in their middle age. Julie Spinks, from Beaconsfield, is 48. She was not involved in the study, but can relate first-hand to its findings. She developed anorexia for the first time when she was 44. "It was a complete shock at the time," she recalls. "I knew that I was restricting my food but I didn't ever think I had anorexia. "I'd been really unhappy at work and had very low self-esteem. To begin with I just thought I had lost my appetite. "I felt depressed, like I was not worth feeding or existing. I wanted to disappear and fade away." Julie started to lose weight quite quickly and began to exercise as well. She realised something was very wrong one day after she had been to the gym. Mind struggle "I'd run for about an hour and burnt off about 500 calories. I remember thinking that's about the same as a chocolate bar. That's when I started to link food and exercise." Julie still did not recognise she had anorexia though. "I thought anorexia was something that happened to other people. It didn't occur to me that I might have it." After a breakdown at work she went for a mental health assessment. Her doctors then diagnosed her with anorexia and depression. Julie was given antidepressants and began therapy sessions to help with her eating disorder. © 2017 BBC.
Keyword: Anorexia & Bulimia
Link ID: 23112 - Posted: 01.17.2017
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
Link ID: 23105 - Posted: 01.14.2017