Links for Keyword: Obesity

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By Stephen L. Macknik Hypoglycemia occurs when your blood sugar gets dangerously low, resulting in sweating, the feeling of weakness and dysphoria (the “don’t touch me” feeling you have when you’re sick and nauseous, possibly unconscious, as with the flu), and a variety of other symptoms. You basically go into a state similar to shock. The principal problem, however, arises from low blood sugar supply to the brain, resulting in impairment of function. It’s a common problem in diabetic non-compliance (not eating low-carbohydrate foods while diabetic), which is especially prevalent in the poor. SABRINA TAVERNISE, of The New York Times reported on a new study in the journal Health Affairs, by Seligman and colleagues of the University of California, San Francisco, in which they analyzed the prevalence of hypoglycemia in low income populations at risk for hypoglycemia, as a function of time since the patients’ households’ last pay day. They found that hypoglycemia increases at the end of a pay cycle in low-income diabetics. They thus concluded that low-income diabetic patients have low access to food at the end of the month, resulting in frank starvation and thus low blood sugar. I find this to be an unlikely scenario. It’s not that I don’t believe that low-income is tied to diabetes and hypoglycemia at the end of the pay cycle. I do believe it, and the Centers for Disease Control have determined that 8% of the population has diabetes, and that the burden is carried by low-income families. So I think the main effect, increased hypoglycemia in the poor at the end of their pay cycle, is correct (and Ms. Tavernise reports that experts in the field are happy with the methods, so I’m happy with them too as a non-expert in this field). © 2014 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: 19114 - Posted: 01.09.2014

Just in time for all those New Year’s resolutions to exercise more, scientists have a better idea of how the body turns pain into gain. Exertion stimulates muscles to release a molecule that modifies fat cells, turning them into calorie-burning machines, a research team has found. Exercise works the muscles but affects cells throughout the body, even in the brain. An important player in this process is a protein called PGC-1α. In exercising muscles, it activates genes that ramp up energy use. But its impact extends beyond these tissues. The protein somehow indirectly prompts, for example, white fat—the energy-storing variety that pads our hips and stomachs—to switch on genes that are characteristic of brown fat, a form that burns calories. PGC-1α doesn’t travel outside muscle cells, so researchers aren’t sure how its influence spreads, however. By sifting through the secretions of PGC-1α-making muscle cells, Robert Gerszten of Harvard Medical School in Boston and colleagues have nabbed one molecule that might be doing the protein’s bidding: β-aminoisobutyric acid (BAIBA). They found that BAIBA induces white fat cells to become more like brown fat cells, altering their gene activity patterns. And it stimulates other cell types, stoking fat metabolism in the liver, the team also reveals today in Cell Metabolism. These effects may translate into a healthier metabolism. When mice lapped up water laced with the molecule, the rodents lost weight and were better at absorbing glucose. © 2014 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: The Sensorimotor System
Link ID: 19110 - Posted: 01.08.2014

By SABRINA TAVERNISE Poor people with diabetes are significantly more likely to go to the hospital for dangerously low blood sugar at the end of the month when food budgets are tight than at the beginning of the month, a new study has found. Researchers found no increase in such hospitalizations among higher-income people for the condition known as hypoglycemia, suggesting that poverty and exhausted food budgets may be a reason for the increased health risk. Hypoglycemia occurs when people with diabetes have not had enough to eat, but continue taking medications for the disease. To control diabetes, patients need to keep their blood sugar within a narrow band. Levels that are too low or too high (known as hyperglycemia) can be dangerous. Researchers found a clear pattern among low-income people: Hospital admissions for hypoglycemia were 27 percent higher at the end of the month than at the beginning. Researchers said they could not prove that the patients’ economic circumstances were the reason for the admission, but the two things were highly correlated. The study, published online Monday in the journal Health Affairs, comes as Congress continues to debate legislation that includes the food stamp program for poor Americans. House Republicans are advocating $40 billion in cuts to the program, a step that Democrats oppose. About 25 million Americans, or 8 percent of the population, have diabetes, according to the Centers for Disease Control and Prevention. The poor are disproportionately affected. The United States spends more than $100 billion a year treating people with the disease, the agency estimates. © 2014 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: 19103 - Posted: 01.07.2014

By NICHOLAS BAKALAR Are there good scientific studies that show that drinking sugar-sweetened soda increases the risk for obesity? The answer may vary depending on who is paying for the study. Researchers examined 17 large reviews of the subject (one review assessed results for adults and children separately, so there were 18 sets of study conclusions). Six of the studies reported receiving funds from industry groups, including Coca-Cola, PepsiCo, the American Beverage Association and others. The other 12 reviews claimed no conflicts of interest. The analysis appears in the December issue of PLOS Medicine. Among the reviews with no conflicts of interest, 10 of 12, or 83.3 percent, reported that sugary drinks were directly associated with weight gain or obesity. The conclusions of studies supported by industry were a mirror image: five of six — the same 83.3 percent — reported that there was insufficient evidence to draw a conclusion. “I wouldn’t say that industry participation alone is enough to dismiss the study’s results in the whole of nutrition research,” said the lead author, Maira Bes-Rastrollo, a professor of preventive medicine at the University of Navarra in Spain. “But I think that the general public and the scientific community should be aware that the food industry has vested interests that may influence their conclusions.” Copyright 2014 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: 19099 - Posted: 01.06.2014

JoNel Aleccia NBC News Surgery to remove a brain tumor two years ago has left a 12-year-old Texas girl with a heartbreaking condition that makes her gain massive amounts of weight — even though her body thinks it’s starving. Doctors say a gastric bypass operation is the only thing that can help Alexis Shapiro, who is 4-foot-7 and weighs 198 pounds. But the U.S. military, which provides her family’s health insurance, says it won’t pay for the $50,000 weight-loss procedure because she’s too young. “Our reviewers have denied your request for Roux-En-Y Gastric Bypass,” reads the rejection notice sent this month. Alexis’ parents — and her doctor — are protesting the decision from insurer TRICARE, which they say sentences the child to a fate of dangerous health problems and social isolation caused by hypothalamic obesity, which is packing on at least 2 pounds every week. “It just keeps going up and up,” said her mother, Jenny Shapiro, 34, of Cibolo, Texas. “She desperately needs this. I feel like she will die if she does not get this surgery.” In just the past three months, Alexis was hospitalized for a kidney infection and developed Type 2 diabetes that requires nightly insulin injections, both related to her growing girth. Dr. Thomas H. Inge, a Cincinnati expert in pediatric obesity who is treating Alexis, acknowledged that there have been few cases like hers. But he said surgery may be the only way to stop weight gain that could top out at 400 pounds — and to cut the brain cravings that make Alexis want to eat an entire jar of peanut butter at one sitting.

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: 19076 - Posted: 12.28.2013

By MICHAEL MOSS WEST LAFAYETTE, Ind. — “Here are the nuts,” said Drew Sayer, a graduate student in nutrition science, before shoving me into the M.R.I. machine, flat on my back. “Chew them. Swallow them. And don’t move your head.” I moved my head, which blurred the resulting images. But if all goes well in the coming weeks, researchers here at Purdue University will have stacks of brain scans with crystal-clear views inside the minds of their test subjects — while they were eating nuts. These images could help answer a timely question: Do nuts really merit the hype they’ve been getting as a guilt-free indulgence? The reports about their many benefits have come thick and fast: studies finding that people who eat nuts (tree nuts like cashews, almonds and pistachios, along with their legume pal, the peanut) live longer and healthier lives, with less risk of chronic ailments like heart disease, respiratory problems and Type 2 diabetes. But perhaps the most startling news is that nuts may help in maintaining a healthy weight. Research has found that people can snack on modest amounts of them without gaining pounds, and that nuts can even help in slimming down. This dieting power is particularly hard to fathom when you consider that nuts pack 160 to 200 calories in each tiny ounce, not even a handful. And most of those calories come from fat. Ounce for ounce, cashews and pecans and walnuts are loaded with more calories than many of the processed foods being blamed for the surge in obesity. In the conventional wisdom, a dieter’s best friends are watery foods like celery and carrot sticks. One of the country’s leading nutrition scientists, Richard Mattes of Purdue, has been exploring this seeming paradox and has some intriguing, if still uncertain, findings. His current work on nuts is being funded by a marketing group, the Almond Board of California, which would normally raise concerns about bias. But Dr. Mattes has a record of biting the hands that feed science, and challenging presumptions about nutrition. © 2013 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: 19046 - Posted: 12.18.2013

By KRISTIN WARTMAN THE solution to one of America’s most vexing problems — our soaring rates of obesity and diet-related diseases — may have its roots in early childhood, and even in utero. Researchers at the Monell Chemical Senses Center, a nonprofit research organization in Philadelphia, have found that babies born to mothers who eat a diverse and varied diet while pregnant and breast-feeding are more open to a wide range of flavors. They’ve also found that babies who follow that diet after weaning carry those preferences into childhood and adulthood. Researchers believe that the taste preferences that develop at crucial periods in infancy have lasting effects for life. In fact, changing food preferences beyond toddlerhood appears to be extremely difficult. “What’s really interesting about children is, the preferences they form during the first years of life actually predict what they’ll eat later,” said Julie Mennella, a biopsychologist and researcher at the Monell Center. “Dietary patterns track from early to later childhood but once they are formed, once they get older, it’s really difficult to change — witness how hard it is to change the adult. You can, but it’s just harder. Where you start, is where you end up.” This may have profound implications for the future health of Americans. With some 70 percent of the United States population now overweight or obese and chronic diseases skyrocketing, many parents who are eating a diet high in processed, refined foods are feeding their babies as they feed themselves, and could be setting their children up for a lifetime of preferences for a narrow range of flavors. The Monell researchers have identified several sensitive periods for taste preference development. One is before three and a half months of age, which makes what the mother eats while pregnant and breast-feeding so important. “It’s our fundamental belief that during evolution, we as humans are exposed to flavors both in utero and via mother’s milk that are signals of things that will be in our diets as we grow up and learn about what flavors are acceptable based on those experiences,” said Gary Beauchamp, the director of the Monell Center. © 2013 The New York Times Company

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: 18991 - Posted: 12.02.2013

by Jessica Griggs, San Diego Glugging lots of sugary drinks won't just make you fat, it might also lead to changes in the brain that have been linked to cancer and Alzheimer's – at least in rats. This finding comes from the first analysis of how sugary drinks affect proteins in the brain. It showed that 20 per cent of the proteins produced in a brain region related to decision-making were altered in rats that drank sugary drinks compared with those given water. It is well established that drinking sugar-sweetened drinks is linked to obesity and diabetes, as well as increasing the risk of cardiovascular problems. A recent estimate put the number of deaths associated with soft drinks at 184,000 a year globally. But the effects of sugar-rich drinks on the brain have received much less attention. "For many people around the world, soft drinks are their sole source of liquid, or at least they provide a very high proportion of their daily calories", says Jane Franklin at the behavioural neuropharmacology lab at Macquarie University in Sydney, Australia, who carried out the study. "We know that soft drinks are bad for the body, so it's reasonable to assume that they aren't doing anything good for your brain either". To find out, Franklin and her colleague Jennifer Cornish gave 24 adult rats either water or a solution of water containing 10 per cent sugar – about the proportion you would find in an average can of soft drink – for 26 days. © 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: 18932 - Posted: 11.16.2013

By SENDHIL MULLAINATHAN Why is obesity soaring? The answer seems pretty clear. In 1955, a standard soda at McDonald’s was only seven ounces. Today, a medium is three times as large, and even a child’s-size version is 12 ounces. It’s a widely held view that obesity is a consequence of our behaviors, and that behavioral economics thus plays a central role in understanding it — with markets, preferences and choices taking center stage. As a behavioral economist, I subscribed to that view — until recently, when I began to question my thinking. For many health problems, of course, behavior plays some role but biology is often a major villain. “Biology” here is my catchall term for the myriad bodily mechanics that are only weakly connected to our choices. A few studies have led me to wonder whether the same is true with obesity. Have I been the proverbial owner of a (behavioral) hammer, looking for (behavioral) nails everywhere? Have I failed to appreciate the role of biology? A first warning sign comes from looking at other animals. Our pets have been getting fatter along with us. In 2012, some 58.3 percent of cats were, literally, fat cats. That is taken from a survey by the Association for Pet Obesity Prevention. (The very existence of this organization is telling.) Pet obesity, however, can easily be tied to human behavior: a culture that eats more probably feeds its animals more, too. And yet, a study by a group of biostatisticians in the Proceedings of the Royal Society challenges this interpretation. They collected data from animals raised in captivity: macaques, marmosets, chimpanzees, vervets, lab rats and mice. The data came from labs and centers and spanned several decades. These captive animals are also becoming fatter: weight gain for female lab mice, for example, came out to 11.8 percent a decade from 1982 to 2003. But this weight gain is harder to explain. Captive animals are fed carefully controlled diets, which the researchers argue have not changed for decades. Animal obesity cannot be explained through eating behavior alone. We must look to some other — biological — driver. © 2013 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: 18905 - Posted: 11.10.2013

By NICHOLAS BAKALAR Children who do not sleep enough may be increasing their risk for obesity, according to a new study. Researchers randomly divided 37 children aged 8 to 11 into two groups. Each group increased their habitual time in bed by an hour and a half per night for one week, then decreased their time by the same amount the next week. They wore electronic devices to measure sleep time, were assessed for daily food intake three times a week, and had blood tests to measure leptin, a hormone that affects hunger, and high levels of which correlate with fat tissue accumulations. Children consumed 134 calories fewer each day during the increased sleep week than the during the week with less sleep. Fasting leptin levels were lower when the children slept more and, over all, the children’s weight averaged about a half pound less at the end of long sleep weeks than short ones. The study was published online in Pediatrics. The lead author, Chantelle N. Hart, an associate professor of public health at Temple University who was at Brown University when she did the study, cautioned that it was small, and looked only at acute changes in sleep and their effect on eating behaviors. Still, she said, “I think these findings suggest that getting a good night’s sleep in childhood could have important benefits for weight regulation through decreased food intake.” Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 10: Biological Rhythms and Sleep
Link ID: 18884 - Posted: 11.07.2013

JoNel Aleccia NBC News Obesity may be a factor in early puberty in U.S. girls, a new study finds. About 17 percent of American kids ages 2 to 17 are obese, according to the CDC. There’s yet another reason to worry about the obesity epidemic among America’s kids: Extra weight may be sending U.S. girls into puberty earlier than ever. Researchers have found that girls with higher body mass index, a ratio of height and weight, may start developing breasts more than a year before their thinner friends — perhaps as early as second grade. The change is spawning a whole new market of child-sized sanitary pads — decorated with hearts and stars — and deodorants aimed at 8- to 10-year-olds, according to a new study and an editorial published Monday in the journal Pediatrics. “The girls who are obese are clearly maturing earlier,” said Dr. Frank Biro, a pediatrics professor at Cincinnati Children’s Hospital Medical Center. “BMI is, we found, the biggest single factor for the onset of puberty.” In addition, white girls are maturing about four months earlier than in a landmark 1997 study that shocked parents with the news that their daughters who played with My Little Pony could be entering puberty. Biro’s team followed more than 1,200 girls ages 6 to 8 in three cities — San Francisco, Cincinnati and New York — from 2004 to 2011, carefully documenting their BMI and their maturation process.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 18867 - Posted: 11.04.2013

By James Gallagher Health and science reporter, BBC News The mocked "obesity excuse" of being born with a slow metabolism is actually true for some people, say researchers. A team at the University of Cambridge has found the first proof that mutated DNA does indeed slow metabolism. The researchers say fewer than one in 100 people are affected and are often severely obese by early childhood. The findings, published in the journal Cell, may lead to new obesity treatments even for people without the mutation. Scientists at the Institute of Metabolic Science, in Cambridge, knew that mice born without a section of DNA, a gene called KSR2, gained weight more easily. But they did not know what effect it may be having in people, so they analysed the DNA of 2,101 severely obese patients. Some had mutated versions of KSR2. It had a twin effect of increasing their appetite while their slowing metabolism. "You would be hungry and wanting to eat a lot, you would not want to move because of a slower metabolism and would probably also develop type 2 diabetes at a young age," lead researcher Prof Sadaf Farooqi told the BBC. She added: "It slows the ability to burn calories and that's important as it's a new explanation for obesity." BBC © 2013

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: 18834 - Posted: 10.26.2013

By Tori Rodriguez The digestive tract and the brain are crucially linked, according to mounting evidence showing that diet and gut bacteria are able to influence our behavior, thoughts and mood. Now researchers have found evidence of bacterial translocation, or “leaky gut,” among people with depression. Normally the digestive system is surrounded by an impermeable wall of cells. Certain behaviors and medical conditions can compromise this wall, allowing toxic substances and bacteria to enter the bloodstream. In a study published in the May issue of Acta Psychiatrica Scandinavica, approximately 35 percent of depressed participants showed signs of leaky gut, based on blood tests. The scientists do not yet know how leaky gut relates to depression, although earlier work offers some hints. Displaced bacteria can activate autoimmune responses and inflammation, which are known to be associated with the onset of depression, lower mood and fatigue. “Leaky gut may maintain increased inflammation in depressed patients,” which could exacerbate the symptoms of depression if not treated, says Michael Maes, a research psychiatrist with affiliations in Australia and Thailand and an author of the paper. Currently leaky gut is treated with a combination of glutamine, N-acetylcysteine and zinc—believed to have anti-inflammatory or antioxidant properties—when behavioral and dietary modifications fail. © 2013 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: 18830 - Posted: 10.24.2013

By GINA KOLATA William Howard Taft, the only massively obese man ever to be president of the United States, struggled mightily to control his weight a century ago, worrying about his health and image, and endured humiliation from cartoonists who delighted in his corpulent figure. But new research has found that his weight-loss program was startlingly contemporary, and his difficulties keeping the pounds off would be familiar to many Americans today. On the advice of his doctor, a famed weight-loss guru and author of popular diet books, he went on a low-fat, low-calorie diet. He avoided snacks. He kept a careful diary of what he ate and weighed himself daily. He hired a personal trainer and rode a horse for exercise. And he wrote his doctor, Nathaniel E. Yorke-Davies, with updates on his progress, often twice a week. In a way, he was ahead of his time. Obesity became a medical issue by the middle of the 20th century, around the time the term “obesity” rather than “corpulence” came into vogue, said Abigail C. Saguy, a sociologist at the University of California, Los Angeles, who specializes in the study of obesity. Taft’s story shows that “at least in some cases, corpulence was already treated as a medical problem early in the century,” she added. Like many dieters today, Taft, 6 feet 2 inches tall, lost weight and regained it, fluctuating from more than 350 to 255 pounds. He was 48 when he first contacted Dr. Yorke-Davies, and spent the remaining 25 years of his life corresponding with the doctor and consulting other physicians in a quest to control his weight. Taft’s struggles are recounted by Deborah Levine, a medical historian at Providence College in Rhode Island. She discovered the extensive correspondence between Taft and the diet doctor, including Taft’s diet program, his food diary, and a log of his weight. Her findings were published Monday in The Annals of Internal Medicine. His story, Dr. Levine said, “sheds a lot of light on what we are going through now.” © 2013 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: 18788 - Posted: 10.15.2013

By ANAHAD O'CONNOR They are a mystery to researchers: people who are significantly overweight and yet show none of the usual metabolic red flags. Despite their obesity, they have normal cholesterol levels, healthy blood pressure levels and no apparent signs of impending diabetes. Researchers call them the metabolically healthy obese, and by some estimates they represent as many as a third of all obese adults. Scientists have known very little about them, but new research may shed some light on the cause of their unusual metabolic profile. A study in the journal Diabetologia has found that compared with their healthier counterparts, people who are obese but metabolically unhealthy have impaired mitochondria, the cellular powerhouses that harvest energy from food, as well as a reduced ability to generate new fat cells. Unlike fat tissue in healthy obese people, which generates new cells to help store fat as it accumulates, the fat cells of the unhealthy obese swell to their breaking point, straining the cellular machinery and ultimately dying off. This is accompanied by inflammation, and it leads to ectopic fat accumulation — the shuttling of fat into organs where it does not belong, like the liver, heart and skeletal muscle. A fatty liver frequently coincides with metabolic abnormalities, and studies suggest that it may be one of the causes of insulin resistance, the fundamental defect in Type 2 diabetes. In the healthy obese, however, the fat tends to remain in the subcutaneous padding just beneath the skin, where it appears to be fairly innocuous. “The group that doesn’t gain fat in the liver as they get obese seems to avoid inflammation and maintain their metabolic health,” said Dr. Jussi Naukkarinen, a research scientist specializing in internal medicine at the University of Helsinki. “There is a complete difference in how they react to obesity.” Copyright 2013 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: 18771 - Posted: 10.10.2013

by Linda Geddes They are identical in almost every way, except one twin is fat and the other is thin. Now a study of this rare group is shedding light on a medical mystery: how some people can be obese and perfectly healthy. Obesity usually goes hand in hand with metabolic syndrome – high blood pressure, high cholesterol and type 2 diabetes – but a minority of obese people escape this fate. To probe the fit fat phenomenon, Jussi Naukkarinen at the University of Helsinki in Finland and his colleagues turned to a registry of identical twins, picking 16 pairs whose body weight differed by 17 kilograms on average. They are a perfect model for studying such differences because they are genetically identical and have usually been raised in very similar environments. Naukkarinen's team started by looking at the siblings' body fat distribution and quickly saw that the fat twins fell into two groups: those that tended to accumulate fat within their livers, and those whose liver fat resembled that of their thin twin. Suppressed activity Next, they looked at other markers of ill-health, including insulin resistance, cholesterol, inflammation and blood pressure. These measures also divided the group. "Basically all the hallmarks of the metabolic syndrome were lacking in the group where there was no liver fat," Naukkarinen says. Researchers also compared samples of the twins' abdominal fat, or adipose tissue. In unhealthy obese twins, genes involved in inflammation were activated – genes that were not activated in their thin twin. The activity of cellular powerhouses called mitochondria seemed to be suppressed as well. But in healthy obese twins, gene expression was similar to that of the thin twin. © 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: 18754 - Posted: 10.07.2013

By Shelly Fan Disclaimer: First things first. Please note that I am in no way endorsing nutritional ketosis as a supplement to, or a replacement for medication. As you’ll see below, data exploring the potential neuroprotective effects of ketosis are still scarce, and we don’t yet know the side effects of a long-term ketogenic diet. This post talks about the SCIENCE behind ketosis, and is not meant in any way as medical advice. The ketogenic diet is a nutritionist’s nightmare. High in saturated fat and VERY low in carbohydrates, “keto” is adopted by a growing population to paradoxically promote weight loss and mental well-being. Drinking coffee with butter? Eating a block of cream cheese? Little to no fruit? To the uninitiated, keto defies all common sense, inviting skeptics to wave it off as an unnatural “bacon-and-steak” fad diet. Yet versions of the ketogenic diet have been used to successfully treat drug-resistant epilepsy in children since the 1920s – potentially even back in the biblical ages. Emerging evidence from animal models and clinical trials suggest keto may be therapeutically used in many other neurological disorders, including head ache, neurodegenerative diseases, sleep disorders, bipolar disorder, autism and brain cancer. With no apparent side effects. Sound too good to be true? I feel ya! Where are these neuroprotective effects coming from? What’s going on in the brain on a ketogenic diet? In essence, a ketogenic diet mimics starvation, allowing the body to go into a metabolic state called ketosis (key-tow-sis). © 2013 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: 18732 - Posted: 10.02.2013

By Julianne Wyrick Some people are drawn to the thick smell of bacon, sizzling and crackling in the skillet on a Saturday morning. For others, it’s the aroma of freshly baked cookies on a Friday night or the smell of McDonald’s fries creeping in through the car window. At this time of year, I find the scent of freshly baked pumpkin muffins irresistible. Of course, I’d like to think I’m not a slave to my nose, at least not when I’m nice and full from dinner. If I were a fruit fly, my outlook might not be so good. Already-fed fruit fly larvae exposed to certain food-related odors ate more food than larvae that didn’t experience the smells, according to research published by scientists at the University of Georgia last spring. “They’re not hungry, but they will get an extra kick in terms of appetite, so they will eat, for example, 30 percent extra,” said Ping Shen, lead author on the study. The scents, which included the sweet odor of bananas or the sharper smell of balsamic vinegar, served as “cues” or triggers that the flies associated with food. The triggers motivated the fly larvae to eat, even when they’d already had dinner. That doesn’t bode so well for flies trying to watch their weight. For the fly to feel this urge to eat, the smell has to be transported from sensory receptors in the nose to the part of the brain that regulates appetite—the brain’s “feeding center”—via a series of neurons. Part of this signal transfer involves dopamine, a neurotransmitter associated with behavior motivated by a cue or hint of something to come, like smells associated with food. © 2013 Scientific American

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 18730 - Posted: 10.01.2013

By Laura Sanders By hijacking connections between neurons deep within the brain, scientists forced full mice to keep eating and hungry mice to shun food. By identifying precise groups of cells that cause eating and others that curb it, the results begin to clarify the intricate web of checks and balances in the brain that control feeding. “This is a really important missing piece of the puzzle,” says neuroscientist Seth Blackshaw of Johns Hopkins University in Baltimore. “These are cell types that weren’t even predicted to exist.” A deeper understanding of how the brain orchestrates eating behavior could lead to better treatments for disorders such as anorexia and obesity, he says. Scientists led by Joshua Jennings and Garret Stuber of the University of North Carolina at Chapel Hill genetically tweaked mice so that a small group of neurons would respond to light. When a laser shone into the brain, these cells would either fire or, in a different experiment, stay quiet. These neurons reside in a brain locale called the bed nucleus of the stria terminalis, or BNST. Some of the message-sending arms of these neurons reach into the lateral hypothalamus, a brain region known to play a big role in feeding. When a laser activated these BNST neurons, the mice became ravenous, voraciously eating their food, the researchers report in the Sept. 27 Science. “As soon as you turn it on, they start eating and they don’t stop until you turn it off,” Stuber says. The opposite behavior happened when a laser silenced BNST neurons’ messages to the lateral hypothalamus: The mice would not eat, even when hungry. © Society for Science & the Public 2000 - 2013

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: 18717 - Posted: 09.28.2013

Declan Butler Ghost writing is taking on an altogether different meaning in a mysterious case of alleged scientific fraud. The authors of a paper published in July (A. Vezyraki et al. Biochem. Biophys. Res. Commun. http://doi.org/nxb; 2013), which reported significant findings in obesity research, seem to be phantoms. They are not only unknown at the institution listed on the paper, but no trace of them as researchers can be found. The paper, published in the Elsevier journal Biochemical and Biophysical Research Communications (BBRC), is not the kind of prank that journals have encountered before, in which hoaxsters have submitted dummy papers to highlight weaknesses in the peer-review process. The paper’s reported findings — that overexpression of two novel proteins in fat cells leads to improvements in metabolic processes related to diabetes and obesity in mice — are, in fact, true. Too true, in the opinion of Bruce Spiegelman, a cell biologist at Harvard Medical School’s Dana-Farber Cancer Institute in Boston, Massachusetts. He says that he has presented similar findings at about six research meetings, and is preparing to submit them to a journal. He suspects that the BBRC paper was intended as a spoiler of his own lab’s work. Now withdrawn, the article lists five authors who are all supposedly from the School of Health Sciences at the University of Thessaly in Trikala, Greece, and is entitled ‘Identification of meteorin and metrnl as two novel pro-differentiative adipokines: Possible roles in controlling adipogenesis and insulin sensitivity’. Adipokines are proteins secreted by fat tissue that play an active part in such processes as sugar and fat metabolism, inflammation and obesity-related metabolic disorders, including insulin resistance and diabetes. © 2013 Nature Publishing Group

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: 18701 - Posted: 09.25.2013