Links for Keyword: Obesity

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By Knvul Sheikh Scientists have known for decades that what we eat can change the balance of microbes in our digestive tracts. Choosing between a BLT sandwich or a yogurt parfait for lunch can increase the populations of some types of bacteria and diminish others—and as their relative numbers change they secrete different substances, activate different genes and absorb different nutrients. And those food choices are probably a two-way street. Gut microbes have also been shown to influence diet and behavior as well as anxiety, depression, hypertension and a variety of other conditions. But exactly how these trillions of tiny guests—collectively called the microbiome—influence our decisions on which foods to stuff into our mouths has been a mystery. Now neuroscientists have found specific types of gut flora help a host animal detect which nutrients are missing in food, and then finely titrate how much of those nutrients the host really needs to eat. “What the bacteria do for appetite is kind of like optimizing how long a car can run without needing to add more petrol to the tank,” says senior author Carlos Ribeiro, who studies the eating behaviors of Drosophila melanogaster, a type of fruit fly, at Champalimaud Center for the Unknown in Lisbon. In a paper published Tuesday in PLoS Biology Ribeiro and his team demonstrated how the microbiome influences drosophila’s nutritional decisions. First, they fed one group of flies a sucrose solution containing all the necessary amino acids. Another group got a mix that had some of the amino acids needed to make protein but lacked essential amino acids that the host cannot synthesize by itself. For a third group of flies, the scientists removed essential amino acids from the food one by one to determine which was being detected by the microbiome. © 2017 Scientific American,

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23538 - Posted: 04.26.2017

By NICHOLAS BAKALAR Drinking sugary beverages is associated with markers of accelerated aging and early signs of Alzheimer’s disease, a new study reports. Researchers used data on more than 4,000 people over 30, examining their brains with M.R.I. and measuring memory with psychological tests. All completed well-validated food frequency questionnaires. Sugary beverage intake is an indirect measure of how much sugar we get in our diets, which is difficult to measure precisely. The authors defined “sugary beverage” to include sodas as well as fruit juices, which may contain added sugars. The study, in Alzheimer’s & Dementia, found that on average, the more sugary drinks consumed, the lower the total brain volume and the lower the scores on memory tests. Brain shrinkage is tied to an increased risk of Alzheimer’s disease. Compared with those who drank no sugary drinks, those who drank one or two a day had a reduced brain volume equivalent to 1.6 years of normal aging, and lower memory scores equivalent to 5.8 years of aging. Those who drank more than two had decreased brain volume equivalent to two years of normal aging and lower memory scores by the equivalent of 11 years. The researchers controlled for diabetes, blood pressure, cholesterol, smoking and many other health and behavioral characteristics. “Although we can’t prove cause and effect, these data suggest that we should be cautious about drinking sugary beverages,” said the lead author, Matthew P. Pase, a senior research fellow at Boston University. “They’re empty calories that contribute to weight gain and metabolic disease.” © 2017 The New York Times Company

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23535 - Posted: 04.26.2017

By Clare Wilson Could fasting boost your brainpower? A stomach hormone that stimulates appetite seems to promote the growth of new brain cells and protect them from the effects of ageing – and may explain why some people say that fasting makes them feel mentally sharper. When ghrelin was first discovered, it became known as the hunger hormone. It is made by the stomach when it gets empty, and whenever we go a few hours without food its levels rise in our blood. But there is also evidence that ghrelin can enhance cognition. Animals that have reduced-calorie diets have better mental abilities, and ghrelin might be part of the reason why. Injecting the hormone into mice improves their performance in learning and memory tests, and seems to boost the number of neuron connections in their brains. Now Jeffrey Davies at Swansea University, UK, and his team have found further evidence that ghrelin can stimulate brain cells to divide and multiply, a process called neurogenesis. When they added the hormone to mouse brain cells grown in a dish, it switched on a gene known to trigger neurogenesis, called fibroblast growth factor. If the same effect happens in animals, this could be how ghrelin exerts its effects on memory, says Davies, whose work was presented at the British Neuroscience Association conference this month. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 23530 - Posted: 04.25.2017

By Meredith Knight A complex cascade of biochemical signals determines what we eat, when we eat and how much we eat. Our digestive tracts and fat cells are known to secrete hormones that drive our hunger levels and our sense of satisfaction after eating. Now a new player has come to the table, our bones. A paper published this March in Nature shows bone cells secrete a hormone called lipocalin 2—and it has a surprising effect in mouse experiments of reducing appetite and stabilizing blood sugar independently of other hormones Stavroula Kousteni, a physiologist at Columbia University College of Physicians and Surgeons, and her colleagues showed 90 percent of the hormone lipocalin 2 was produced by osteoblasts, bone cells that create the chemicals necessary to build new bone. Because of its chemical structure scientists previously thought fat cells made the hormone. Lipocalin 2 is released after eating and reaches peak levels about an hour after a meal. When researchers genetically designed mice with defective lipocalin 2 genes in bone, the mice had 20 percent more body fat than mice that had the defective gene inserted into fatty tissue. The animals also ate 16 percent more chow. When mice with the broken gene were injected with lipocalin 2, their feeding behavior returned to normal. Injections of the hormone even reduced eating and improved blood sugar and insulin regulation in healthy mice. “In general, we found we could improve their metabolic phenotype,” Kousteni says. © 2017 Scientific American

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23523 - Posted: 04.22.2017

Hannah Devlin Science correspondent They feel no pain, don’t get cancer and look like baggy-skinned sausages with teeth: the naked mole rat is already famously weird. Now scientists have discovered what could be the subterranean rodents’ strangest trait yet: they can survive without oxygen by switching to a metabolic strategy normally used by plants. By switching from a glucose-based metabolic system, which depends on oxygen, to one that uses fructose instead, mole rats can cope with nearly twenty minutes in air with 0% oxygen. Under the same conditions, a human would die within minutes. “The naked mole rat has simply rearranged some basic building-blocks of metabolism to make it super-tolerant to low oxygen conditions,” said Thomas Park, professor of biological sciences at the University of Illinois at Chicago, who made the discovery after studying the species for 18 years. The apparently unique metabolic strategy probably evolved along with the mole rats’ niche life-style, he said. The animals live in stuffy, hyper-crowded burrows, with chambers in which a hundred-odd colony mates sleep together in a heap of hairless bodies. Scientists were aware that oxygen supplies in the mole rats’ tunnels drop to levels that would be unsurvivable for other land mammals, but until now had not tested the limits of their ability to cope with oxygen deprivation, or how this works biologically. In the latest study, published in the journal Science, the team found that mole rats showed no ill effects after five hours breathing air with 5% oxygen – slightly lower that oxygen levels at the summit of Everest. Laboratory mice, by contrast, died within ten minutes. © 2017 Guardian News and Media Limited

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23519 - Posted: 04.21.2017

Sarah Boseley in Amsterdam The city of Amsterdam is leading the world in ending the obesity epidemic, thanks to a radical and wide-reaching programme which is getting results even among the poorest communities that are hardest to reach. Better known for tulips and bicycles, Amsterdam has the highest rate of obesity in the Netherlands, with a fifth of its children overweight and at risk of future health problems. The programme appears to be succeeding by hitting multiple targets at the same time – from promoting tap water to after-school activities to the city refusing sponsorship to events that take money from Coca Cola or McDonalds. It is led by a dynamic deputy mayor with the unanimous backing of the city’s politicians. From 2012 to 2015, the number of overweight and obese children has dropped by 12%. Even more impressive, Amsterdam has done what nobody else has managed, because the biggest fall has been amongst the lowest socio-economic groups. It is in neighbourhoods like the Bijlmer in the south-east that the programme is changing lives. The Bijlmer is notorious, says Wilbert Sawat, coordinator and PE teacher at De Achtsprong primary school, and that’s why he wanted to work there. Other teachers do too, he says. “Here we can make a difference.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23493 - Posted: 04.15.2017

By ANAHAD O’CONNOR About a year and a half ago, Robin Collier and her husband, Wayne, were like millions of other Americans: overweight and living with Type 2 diabetes. Despite multiple diets, the couple could not seem to lose much weight. Then Ms. Collier’s doctor told her she was going to need daily insulin shots to control her diabetes. That was the motivation she needed. “I made up my mind right then and there,” said Ms. Collier, 62, an administrator at an accounting firm in Lafayette, Ind. “I said to myself, ‘I’m not going on insulin. I’m too young to have this disease.’” Instead, Ms. Collier and her husband entered a study sponsored by a company called Virta Health, one of a new crop of high-tech companies that have designed programs aimed at helping people prevent or even reverse their diabetes. On the program, patients video-chat with a remote Virta doctor, who consults with their primary care doctor, reviews their blood tests and medical history, and makes diet and drug recommendations. While studies show that a variety of different diets can benefit people with Type 2 diabetes, Virta, based in San Francisco, takes a low-carbohydrate approach, training patients to swap foods like pastries, pasta and sugary snacks for veggie omelets, almonds and salads with grilled chicken and beef. Every day, patients use an app to upload their blood sugar levels, blood pressure, body weight and other measurements. A health coach, usually a registered dietitian, monitors their data and checks in by phone, text or email to discuss any problems or just to provide daily encouragement. Today, Ms. Collier has lost 75 pounds and has avoided taking insulin. Her husband has lost 45 pounds and was able to stop two diabetes medications. Both are still in the program, which she called “life changing,” as part of an ongoing clinical trial. © 2017 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23481 - Posted: 04.12.2017

Ewen Callaway It may not be the most appetizing way to extend life but researchers have shown for the first time that older fish live longer after they consumed microbes from the poo of younger fish. The findings were posted to the bioRxiv.org preprint server on 27 March1by Dario Valenzano, a geneticist at the Max Planck Institute for Biology of Ageing in Cologne, Germany, and colleagues. So-called ‘young blood’ experiments that join the circulatory systems of two rats — one young and the other old — have found that factors coursing through the veins of young rodents can improve the health and longevity of older animals. But the new first-of-its-kind study examined the effects of 'transplanting' gut microbiomes on longevity. “The paper is quite stunning. It’s very well done,” says Heinrich Jasper, a developmental biologist and geneticist at the Buck Institute for Research on Aging in Novato, California, who anticipates that scientists will test whether such microbiome transplants can extend lifespan in other animals. Life is fleeting for killifish, one of the shortest-lived vertebrates on Earth: the fish hits sexual maturity at three weeks old and dies within a few months.The turquoise killifish (Nothobranchius furzeri) that Valenzano and colleagues studied in the lab inhabits ephemeral ponds that form during rainy seasons in Mozambique and Zimbabwe. © 2017 Macmillan Publishers Limited

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23448 - Posted: 04.05.2017

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23351 - Posted: 03.14.2017

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 23340 - Posted: 03.10.2017

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23318 - Posted: 03.06.2017

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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23235 - Posted: 02.16.2017

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23208 - Posted: 02.09.2017

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23105 - Posted: 01.14.2017