Links for Keyword: Obesity

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By GINA KOLATA For many obese adults, the die was cast by the time they were 5 years old. A major new study of more than 7,000 children has found that a third of children who were overweight in kindergarten were obese by eighth grade. And almost every child who was very obese remained that way. Some obese or overweight kindergartners lost their excess weight, and some children of normal weight got fat over the years. But every year, the chances that a child would slide into or out of being overweight or obese diminished. By age 11, there were few additional changes: Those who were obese or overweight stayed that way, and those whose weight was normal did not become fat. “The main message is that obesity is established very early in life, and that it basically tracks through adolescence to adulthood,” said Ruth Loos, a professor of preventive medicine at the Icahn School of Medicine at Mount Sinai in New York, who was not involved in the study. These results, surprising to many experts, arose from a rare study that tracked children’s body weight for years, from kindergarten through eighth grade. Experts say they may reshape approaches to combating the nation’s obesity epidemic, suggesting that efforts must start much earlier and focus more on the children at greatest risk. The findings, to be published Thursday in The New England Journal of Medicine, do not explain why the effect occurs. Researchers say it may be a combination of genetic predispositions to being heavy and environments that encourage overeating in those prone to it. But the results do provide a possible explanation for why efforts to help children lose weight have often had disappointing results. The steps may have aimed too broadly at all schoolchildren, rather than starting before children enrolled in kindergarten and concentrating on those who were already fat at very young ages. © 2014 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: 19187 - Posted: 01.30.2014

By Eric Niiler, It may come as a surprise that Finland — one of the least polluted, wealthiest countries, where average life expectancy is among the world’s highest — has the highest rate of Type 1 diabetes. Each year, there are about 58 cases diagnosed per 100,000 children; in the United States there are 24 cases per 100,000, according to the International Diabetes Federation. Some researchers suspect there may be a connection between Finland’s cleanliness and the incidence of the disease there. They are investigating whether the lack of exposure to a specific group of bacteria found in the intestine may be causing weaker immune systems in Finnish children, making them more susceptible to Type 1 diabetes. This so-called hygiene hypothesis — that cleaner living can result in a weaker immune system — has also been linked to ailments such as asthma, allergies and other autoimmune diseases. “We are working along the idea that we have a trigger which most likely is an infectious agent,” said Mikael Knip, a professor of pediatrics at the University of Helsinki who has been studying diabetes for 30 years. “There is an association between such infections and appearance of antibodies.” Just as there are microbes that trigger the disease, Knip says there are also some bacterial or viral infections that, if they occur at an early age, can protect a young child from developing Type 1 diabetes. Type 1 diabetes, which affects approximately 37 million people worldwide, is an autoimmune disease in which the body does not produce sufficient insulin, a hormone needed to break down sugars. Typically diagnosed in children, teens and young adults, the disease can eventually damage the eyes and organs such as the kidneys, and it increases the likelihood of stroke and heart failure. © 1996-2014 The Washington Post

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19160 - Posted: 01.22.2014

Overweight and obese adults who drink diet pop also tend to eat more calories each day from food, a finding that hints at how relying on diet beverages for weight loss could be a mistake. In this week’s issue of the American Journal of Public Health, researchers from Johns Hopkins Bloomberg School of Public Health in Baltimore analyzed U.S. survey data for 24,000 people from 1999 to 2010. They looked for patterns in beverage consumption and calories. The sweet taste of beverages, whether from sugar or artificial sweeteners, seems to enhance our appetite and encourage cravings for sugar. (Rob Carr/Associated Press) Overweight consumers of diet beverages took in 1,965 in food calories a day compared with 1,874 calories among those in the same weight class who drank beverages sweetened with sugar, such as non-diet soda, sports drinks, fruit drinks and sweetened tea. As people increasingly switch to diet beverages, the focus on reducing sugar from drinks might not be enough to lose weight in the long term, the researchers concluded. "The switch from a sugary beverage to a diet beverage should be coupled with other changes in the diet, particularly reducing snacks," suggested lead author Sara Bleich. In the study, snacking patterns were generally the same between diet and sugary beverage drinkers. The researchers said the finding is consistent with evidence that the sweet taste of beverages, whether from sugar or artificial sweeteners, enhances our appetite and encourage cravings for sugar. © CBC 2014

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: 19148 - Posted: 01.18.2014

By ANAHAD O'CONNOR Scientists call it the obesity paradox, the notion that being overweight or moderately obese lowers the risk of an early death. They have documented the phenomenon in large population studies and in groups of patients with chronic diseases like hypertension and Type 2 diabetes. But now a new report, published on Wednesday in The New England Journal of Medicine, is calling the obesity paradox into question, at least for patients with Type 2 diabetes. The study, of nearly 12,000 people with the disease, found that there was no survival advantage for those who had a body mass index that put them in the overweight or obese categories. Instead, the researchers found that the diabetics with the lowest mortality rate were those who were considered normal weight. The study is among the largest to examine the obesity paradox among people with Type 2 diabetes, an illness that afflicts more than 25 million Americans. The authors argue that previous studies showing a protective effect of a high B.M.I. among diabetics were flawed because they were too small or failed to account for factors like smoking or undiagnosed illnesses that can contribute to low body weight but a shorter life span as well. The new study found that when smoking and other factors that can contribute to weight loss were accounted for, people in the highest B.M.I. groups had higher mortality rates. “I think the case is not necessarily closed,” said Deirdre K. Tobias, the lead author of the paper and a research fellow at the Harvard School of Public Health. “But at this point, there is no reason to believe that being overweight or obese would be protective for people with diabetes.” © 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: 19138 - Posted: 01.16.2014

By ANDREW POLLACK Launch media viewer Kristin Tremblay helps make dinner at home in Gainesville, Fla. She has a disorder that makes her uncontrollably hungry. Rob C. Witzel for The New York Times Lisa Tremblay still recalls in horror the time her daughter Kristin pulled a hot dog crawling with ants from the garbage at a cookout and prepared to swallow it. Kristin has a rare genetic abnormality that gives her an incessant, uncontrollable hunger. Some people with the condition, called Prader-Willi syndrome, will eat until their stomach ruptures and they die. And, not surprisingly, many are obese. “She’s eaten dog food. She’s eaten cat food,” said Ms. Tremblay, who lives in Nokomis, Fla. When Kristin, now 28, was a child, neighbors once called social welfare authorities, thinking Kristin was not being fed because she complained of being hungry so much. Once an obscure and neglected disease, Prader-Willi is starting to attract more attention from scientists and pharmaceutical companies for a simple reason: It may shed some light on the much broader public health problems of overeating and obesity. “These are remarkable human models of severe obesity,” said Dr. Steven B. Heymsfield, a professor and former executive director of the Pennington Biomedical Research Center in Baton Rouge, La. “When we discover the underlying mechanism of these very rare disorders, they will shed light on garden-variety obesity.” One drug being developed to help obese people lose weight has shown some preliminary signs of success in patients with Prader-Willi. The drug, beloranib, is believed to work by reducing fat synthesis and increasing fat use. In a small trial, it reduced weight and body fat and lowered the food-seeking urge, according to the drug’s developer, Zafgen. © 2014 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: 19136 - Posted: 01.15.2014

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