Chapter 9. Homeostasis: Active Regulation of the Internal Environment
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
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
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
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
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
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
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.
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
Link ID: 19046 - Posted: 12.18.2013
by Bethany Brookshire “You are what you eat.” We’ve all heard that one. What we eat can affect our growth, life span and whether we develop disease. These days, we know that we also are what our mother eats. Or rather, what our mothers ate while we were in the womb. But are we also what our father eats? A new study shows that in mice, a dietary deficiency in dad can be a big downer for baby. The dietary staple in the study was folic acid, or folate. Folate is one of the B vitamins and is found in dark leafy greens (eat your kale!) and has even been added to some foods like cereals. It is particularly essential to get in the diet because we cannot synthesize it on our own. And it plays roles in DNA repair and DNA synthesis, as well as methylation of DNA. It’s particularly important during development. Without adequate folate, developing fetuses are prone to neural tube disorders, such as spina bifida. Some of the neural tube disorders caused by folate deficiency could result from breaks in the DNA itself. But folic acid is also important in the epigenome. Epigenetics is a mechanism that allows cells to change how genes are used without changing the genes themselves. Instead of altering the DNA itself, epigenetic alterations put chemical “marks” or “notes” —methyl or acetyl groups — on the DNA and the proteins associated with it. The marks can either make a gene more accessible (acetylation) or less accessible (methylation), making it more or less likely to be made into a protein. This means that each cell type can have a different epigenome, allowing a neuron to function differently than a muscle cell, even though they contain the same DNA. Folate affects DNA synthesis, but it can also affect DNA methylation. In fact, DNA methylation requires the presence of folate. So low folate could affect whether genes are turned off or on and by how much. In a developing fetus, that could contribute to developmental problems. © Society for Science & the Public 2000 - 2013.
Many physicians and parents report that their autistic children have unusually severe gastrointestinal problems, such as chronic constipation or diarrhea. These observations have led some researchers to speculate that an ailing gut contributes to the disorder in some cases, but scientific data has been lacking. Now, a provocative study claims that a probiotic treatment for gastrointestinal issues can reduce autismlike symptoms in mice and suggests that this treatment could work for humans, too. The reported incidence of gut maladies in people with autism varies wildly between published studies—from zero to more than 80%—making it difficult to establish just how commonly the two conditions go together, says principal investigator Sarkis Mazmanian, a microbiologist at the California Institute of Technology (Caltech) in Pasadena. Overall, however, the evidence seems to point toward a connection. Last year, for example, a Centers for Disease Control and Prevention study of thousands of children with developmental disabilities found that kids with autism were twice as likely as children with other types of disorders to have frequent diarrhea or colitis, an inflammation of the large intestine. For many years, Mazmanian and his and colleagues have been studying the effects of a nontoxic strain of the bacterium Bacteroides fragilis on diseases such as Crohn's disease, which causes intestinal inflammation and allows potentially harmful substances that should pass out of the body to leak through junctions between cells that are normally tight. Although the researchers don’t understand the mechanism, the bacterium appears to restore the damaged gut, possibly by helping close these gaps. © 2013 American Association for the Advancement of Science.
Link ID: 19009 - Posted: 12.06.2013
By NICHOLAS BAKALAR A high body mass and a large waist are both associated with self-reported hearing loss, a new study has found. Researchers used data from a 20-year prospective study of 68,421 women who were25 to 42 years old at the start. After controlling for age, smoking, diabetes, hypertension and other factors, they found that the higher the body mass index, the greater the risk for hearing loss. Compared with women with a B.M.I. under 25, those with an index of 25 to 29 had an 8 percent increased risk. The numbers kept going up in tandem: 11 percent for 30 to 34, 16 percent for 35 to 39 and 19 percent for those above 40. The increasing risk associated with larger waist circumference followed a similar pattern. The study, published in the December issue of The American Journal of Medicine, found that moderate physical activity — as little as four hours of walking a week — also reduced the risk for hearing loss. Researchers found no further advantage in more vigorous exercise. The lead author, Dr. Sharon G. Curhan, a clinical researcher at Brigham and Women’s Hospital in Boston, suggested that obesity might compromise blood flow to the inner ear, and that exercise might improve it, which could explain the associations. “Hearing loss may not be an inevitable part of growing older,” she said. “There may be things we can do to prevent it.” Copyright 2013 The New York Times Company
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
by Jessica Griggs HAVING type 2 diabetes may mean you are already on the path to Alzheimer's. This startling claim comes from a study linking the two diseases more intimately than ever before. There is some good news: the same research also offers a way to reverse memory problems associated with diabetes – albeit in rats – which may hint at a new treatment for Alzheimer's. "Perhaps you should use Alzheimer's drugs at the diabetes stage to prevent cognitive impairment in the first place," says Ewan McNay from the University at Albany in New York. Alzheimer's cost the US $130 billion in 2011 alone. One of the biggest risk factors is having type 2 diabetes. This kind of diabetes occurs when liver, muscle and fat cells stop responding efficiently to insulin, the hormone that tells them to absorb glucose from the blood. The illness is usually triggered by eating too many sugary and high-fat foods that cause insulin to spike, desensitising cells to its presence. As well as causing obesity, insulin resistance can also lead to cognitive problems such as memory loss and confusion. In 2005, a study by Susanne de la Monte's group at Brown University in Providence, Rhode Island, identified a reason why people with type 2 diabetes had a higher risk of developing Alzheimer's. In this kind of dementia, the hippocampus, a part of the brain involved in learning and memory, seemed to be insensitive to insulin. Not only could your liver, muscle and fat cells be "diabetic" but so it seemed, could your brain. © Copyright Reed Business Information Ltd.
By Sandra G. Boodman, Dorsey Davidge felt her thrumming anxiety burst into barely controlled panic as she watched her 14-year-old daughter Cate Chapin struggle to get from her bedroom to the bathroom. During the last week of January, the eighth-grader contracted what appeared to be a bad case of the flu. After a week, a doctor decided she had pneumonia, a diagnosis that was later changed to a possible infectious disease. Davidge, a single mother who lives in McLean, had maintained her equanimity during the early days of Cate’s illness. But when she saw that her older daughter was unable to walk 10 feet without stopping midway to rest, she was shocked by how cadaverous-looking Cate had become in a matter of weeks. “I was really scared for the first time,” Davidge said. “She was incredibly weak, and I thought, “ ‘Oh, my God, my child is just wasting away.’ ” By then, the 5-foot-2 Cate, a skinny 95 pounds before she got sick, had shriveled to a little over 80 pounds. She had no appetite, was barely drinking anything and seemed unable to consume more than a quarter of a bagel at a sitting. “That day was the last straw,” Davidge recalled. She telephoned Cate’s pediatrician, who agreed that the girl needed to be admitted immediately to a Northern Virginia hospital. It would take another harrowing month — which included the insertion of a feeding tube to help restore Cate’s weight, consultations with a bevy of specialists and numerous tests — before doctors figured out what was actually wrong, a diagnosis made possible after Cate developed a seemingly unrelated condition that sent her to an ophthalmologist. © 1996-2013 The Washington Post
Keyword: Anorexia & Bulimia
Link ID: 18943 - Posted: 11.19.2013
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.
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
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
Guest post by Bruce Bower Among 16- to 22-year-old U.S. males, 7.6 percent report taking various potentially dangerous substances at least monthly to counteract what they regard as an alarming lack of muscularity. Young men whose insecurities inspire them to use growth hormones, steroids and other body-altering chemicals represent the male counterpart of females whose idealization of thinness prompts them to induce vomiting and otherwise purge their bodies of food, proposes a team led by epidemiologist Alison Field of Boston Children’s Hospital. Purging and other eating disorders occur mainly in girls and women. Boys and men so obsessed with muscles that they take substances prohibited in competitive sports are more numerous than researchers and clinicians realized, and have been overlooked, Field and her colleagues conclude November 4 in JAMA Pediatrics. The researchers examined questionnaires that each of 5,527 males completed eight times between 1999 — at ages 12 to 18 — and 2010. Most participants were white and from middle-class families. No information on sports team participation was available. © Society for Science & the Public 2000 - 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.
by Tina Hesman Saey BOSTON— Siberians may use genes to stay warm, a new study shows. As part of an effort to catalog genetic diversity in Siberia, Alexia Cardona of the University of Cambridge and collaborators sampled DNA from 200 Siberians representing 10 native groups. The team looked for genes that have more changes in Siberians than would be expected by chance — a sign that the genes evolved rapidly in the 24,000 years since people settled the frigid land. Rapid changes suggest that a gene is important for adapting to an environment. Several of the Siberians’ genes have variants that may help keep Arctic dwellers warm during the long winters, Cardona reported October 24 at the annual meeting of the American Society of Human Genetics. Among the candidates for genetic heaters are genes involved in metabolizing fats. Some Siberian groups eat mostly meat, so genes that help convert animal fat to energy are important for creating heat. Another gene with variants unique to Siberians is called PRKG1; it helps regulate body heat by controlling muscle contraction and the constriction and dilation of blood vessels. Muscle contractions are an important part of shivering, which can raise body temperature. The researchers also identified variants in genes involved in thyroid function, which plays a role in temperature regulation. A. Cardona et al. Genome-wide analysis of cold adaption in indigenous Siberian populations. American Society of Human Genetics annual meeting, Boston, October 24, 2013. © Society for Science & the Public 2000 - 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