Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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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
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.
Link ID: 23093 - Posted: 01.13.2017
By Catherine Caruso If you give a mouse a beer, he’s going to ask for a cookie—and another, and another. If you give a person enough beer, she might find herself wolfing down a plate of greasy nachos. But why does binge drinking make us binge eat as well? The reason may lie not in the stomach but in the brain, recent research suggests. A study published today in Nature Communications found alcohol activated brain cells that control hunger, sending drunk mice scampering for snacks even when they were not really hungry. Researchers from The Francis Crick Institute Mill Hill Laboratory in London got mice drunk, then tagged and recorded the electrical activity in brain cells linked to hunger, uncovering a neural mechanism that could explain why the animals ate significantly more after binge-drinking sessions even though their bodies did not need the calories. Although hunger pangs in our stomach usually alert us that it is time to eat, the impulse to consume food originates in our brains, and brain cells located in the hypothalamus called agouti-related protein (AgRP) neurons play a key role in controlling hunger. A previous study showed that when AgRP neurons are activated, mice almost immediately seek out food and start eating, even if their stomachs are full. By contrast, when AgRP neurons are deactivated, hungry mice will not eat. AgRP neurons play a similar role in human hunger: Under natural conditions they are activated when our bodies need calories, signaling to us that we should find food. Something different happens, however, when alcohol is involved. Although alcohol is second only to fat in caloric density, previous studies have shown drinking causes humans to eat more, a paradox that made lead authors Craig Blomeley and Sarah Cains and colleagues wonder whether the brain could be to blame. © 2017 Scientific American,
Brandie Jefferson When I told my coworker that I was participating in a study that involved fasting, she laughed until she nearly cried. My boyfriend, ever supportive, asked hesitantly, "Are you sure you want to try this?" Note the use of "try" instead of "do." When I told my father over the phone, the line went silent for a moment. Then he let out a long, "Welllllll," wished me luck, and chuckled. Turns out, luck might not be enough. I like to eat. Often and a lot. Now, however, my eating habits have become more than a source of amusement for friends and coworkers. Now they are data in a study focusing on people with multiple sclerosis, like me. The pilot study, led by Dr. Ellen Mowry at the Johns Hopkins University in Baltimore, is looking at the impact of intermittent fasting on our microbiomes — the universe of trillions of microbes, mainly bacteria, that live in our guts. Intermittent fasting is pretty much what it sounds like. For six months, participants are allowed to eat during an 8-hour period each day. The remaining 16 hours we are limited to water, tea and coffee. No added sugar, cream, honey or sweetener. Several studies have suggested that the predominant bacteria in the guts of people with MS tend to be different than those in the guts of those without the chronic autoimmune inflammatory disease, according to Samantha Roman, the study's research coordinator. Depending on their makeup, bacteria have the ability to soothe or trigger inflammation, potentially affecting the symptoms of MS and other diseases. Exactly how gut bacteria and inflammation are related, though, is not well understood. © 2017 npr
Keyword: Multiple Sclerosis
Link ID: 23070 - Posted: 01.09.2017
Eating a Mediterranean diet has been linked to less brain shrinkage in older adults. Human brains naturally shrink with age. But a study that followed 401 people in their 70s found that the brains of those who adhered more closely to a Mediterranean-style diet shrank significantly less over a period of three years. A typical Mediterranean diet contains a high amount of vegetables, fruits, olive oil, beans and cereal grains, moderate amounts of fish, dairy products, and wine, and only a small amount of red meat and poultry. “As we age, the brain shrinks and we lose brain cells, which can affect learning and memory,” says Michelle Luciano, at the University of Edinburgh, UK, who led the study. “This study adds to the body of evidence that suggests the Mediterranean diet has a positive impact on brain health.” The differences in brain shrinkage were measured using brain scans. Statistical analysis of diet data found that simply eating more fish and less meat were not associated with reduced shrinking. “While the study points to diet having a small effect on changes in brain size, it didn’t look at the effect on risk of dementia,” says David Reynolds, at the charity Alzheimer’s Research UK. “We would need to see follow-up studies in order to investigate any potential protective effects against problems with memory and thinking.” Other studies have found that being overweight seems to accelerate shrinking of the brain’s white matter. © Copyright Reed Business Information Ltd.
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
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
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
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