Links for Keyword: Obesity

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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

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.

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: 23093 - Posted: 01.13.2017

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.

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: 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

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: 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

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: 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

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: 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 23039 - 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

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: 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

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: 23026 - Posted: 12.27.2016