By Nathan Seppa The link between obesity and vitamin D deficiency appears to be a one-way street. A large study of the genetics underpinning both conditions finds that obesity may drive down vitamin D levels, but a predisposition to the vitamin deficiency doesn’t lead to obesity. The findings also suggest that boosting vitamin D levels won’t reverse obesity. An association between the two has been observed for years, but determining cause and effect has been difficult. “I find this very plausible and a correct interpretation of the data,” says Robert Heaney, an endocrinologist at Creighton University in Omaha, Neb. “I think it’s worth reporting.” In the new study, researchers tapped into a huge international database, accessing the genetic profiles of more than 42,000 people. The scientists noted whether a person harbored any of 12 genetic variants associated with being overweight. Not surprisingly, people with these variants were more likely to be obese than those without them. People with these obesity-associated gene variants were also apt to have low vitamin D levels, Elina Hyppönen, an epidemiologist and nutritionist at University College London, and colleagues report online February 5 in PLOS Medicine. When the researchers tested for four genetic variants linked to low vitamin D levels, they found that people with the variants were not necessarily prone to obesity. The researchers checked both findings against a separate database of people and got similar results. © Society for Science & the Public 2000 - 2013

Keyword: Obesity
Link ID: 17767 - Posted: 02.06.2013

by Virginia Morell The male Eurasian jay is an accommodating fellow. When his mate has been feasting steadily on mealworm larvae, he realizes that she'd now prefer to dine on wax moth larvae, which he feeds her himself. The finding adds to a small but growing number of studies that show that some animals have something like the human ability to understand what others are thinking. "It's great for a first test of this ability in birds," says Thomas Bugnyar, a cognitive biologist at the University of Vienna in Austria who was not involved in the work. Scientists still debate about whether even our closest ape relatives can attribute an unseen, mental desire to another; some continue to argue that this is a peculiarly human talent. "But some of us think that some aspects of this ability should be found here and there in different species," Bugnyar says, "and so it is good to have this jay study to compare" with the other studies on primates, humans, and human children. Male Eurasian jays feed their mates during courtship displays, says Ljerka Ostojić, a comparative psychologist and postdoc at the University of Cambridge in the United Kingdom who led the study. Because of that behavior, Ostojić and her colleagues thought that the jays might be good subjects for testing whether these birds understand their mates' desires. The group's previous research had shown that Eurasian jays and scrub jays can plan for the future. "It is commonly thought that any action animals take is determined solely by whatever they want at that moment," Ostojić says, "but the jays also plan for needs in the future." © 2010 American Association for the Advancement of Science

Keyword: Intelligence; Evolution
Link ID: 17766 - Posted: 02.05.2013

By DOUGLAS QUENQUA Why are some people able to use cocaine without becoming addicted? A new study suggests the answer may lie in the shape of their brains. Sporadic cocaine users tend to have a larger frontal lobe, a region associated with self-control, while cocaine addicts are more likely to have small frontal lobes, according to the study, which was published in the journal Biological Psychiatry. The scientists, at the University of Cambridge, collected brain scans and personality tests from people who had used cocaine over several years — some addicted, some not. While the nonaddicts shared a penchant for risk-taking behavior, the increased gray matter seemed to help them resist addiction by exerting more self-control and making more advantageous decisions. “They could take it or leave it,” said Karen Ersche, the lead author. The researchers believe the differences in brain shape predated the drug use rather than occurring as a result of it. Dr. Ersche said the findings reinforced the idea, now popular among addiction experts, that addiction depends less on character and more on biological makeup. “It’s not the Nancy Reagan approach, just say no or one day or another you will get addicted,” she said. “How the drugs work and how much you are at risk depends on what type of person you are and what type of brain you have.” © 2013 The New York Times Company

Keyword: Drug Abuse
Link ID: 17765 - Posted: 02.05.2013

By melody Yesterday, Alan Schwarz, reporting for the Sunday edition of The New York Times, published an alarmist piece on Adderall abuse. The story chronicles the short life of Richard Fee, a popular young pre-med who, after dabbling in fast-acting stimulants in college, faked his way into an ADHD diagnosis and, within months of filling his first prescription, began heavily abusing the drug, leading to severe addiction and psychosis, and ultimately to his suicide, two years ago, at the age of twenty-four. The story of Richard Fee is a tragic one, and one that highlights both the dangers of prescribing ADHD drugs to neurotypical adults and some of the problems endemic in psychiatric diagnosis. Regrettably, the reporter seems to believe that these problems are somehow specific to amphetamines, signaling “widespread failings in the system through which five million Americans take medication for ADHD”, and that Richard’s harrowing case, while undoubtedly rare, “underscores aspects of ADHD treatment that are mishandled every day with countless patients”. Schwarz is a Pulitzer-prize nominated journalist, renowned for exposing the danger of concussive head injuries in football. More recently, he has cast that same critical eye on how attention-deficit disorder is diagnosed. The question is – to what end? Presumably – in the case of this story – to tighten the restrictions on how amphetamines are prescribed to adults, and to ward against the kind of negligence and lack of oversight that characterized Richard’s case. But there is a delicate balance to be struck here between serving the needs of the ADHD population, many of whom benefit tremendously from the regulated use of stimulants, and potential drug addicts, like Richard. It is also far from clear, given the nature of psychiatric nosology, that there are any surefire ways of stopping con-artists and addicts from gaming the system. © 2013 Scientific American

Keyword: ADHD; Drug Abuse
Link ID: 17764 - Posted: 02.05.2013

By Laura Hambleton, Winter often brings the flu, coughs, ski injuries and shoveling strains. Add to these ailments a more deadly one: heart attacks. A recent study has found that more fatal heart attacks and strokes occur during the winter than at other times of the year. And it doesn’t seem to matter if the winter is occurring in the warmer climes of Southern California or the frostier ones of Boston. After sifting through about 1.7 million death certificates filed between 2005 and 2008, cardiologists Bryan Schwartz of the University of New Mexico and Robert A. Kloner of the Heart Institute at the Good Samaritan Hospital in Los Angeles found a 26 to 36 percent greater death rate for heart attacks in winter than summer “despite different locations and climates,” Kloner says. The worst months are December, January, February and the beginning of March. The doctors analyzed the cause of death for people in Texas, Arizona, Georgia, Los Angeles, Washington state, Pennsylvania and Massachusetts. Of those who died of heart disease, the winter weather pattern was clear. In Los Angeles, for example, there were about 70 deaths per day from cardiac disease, Schwartz said. “In the summer, L.A. had an average circulatory death rate of about . . . 55 deaths per day.” The research uncovered patterns in cardiac deaths from “seven different climate patterns,” according to the study, and “death rates at all sites clustered closely together and no one site was statistically different from any other site.” An abstract of the study was published in the American Heart Association journal Circulation. © 1996-2013 The Washington Post

Keyword: Biological Rhythms; Stroke
Link ID: 17763 - Posted: 02.05.2013

By Ian Chant Stress and neglect at home take an obvious toll on kids as they grow up. Many decades of research have documented the psychological consequences in adulthood, including struggles with depression and difficulties maintaining relationships. Now studies are finding that a troubled home life has profound effects on neural development. Kids' brains are exquisitely sensitive. Even sleeping infants are affected by family arguments, a new study concludes. Researchers at the University of Oregon showed with functional MRI scans that infants from families who reported more than the usual levels of conflict in the home were more sensitive to aggressive or angry voices. While asleep, these babies had an uptick in brain activity in response to sentences read in an angry tone of voice, with most of the activity clustered in the parts of the brain responsible for regulating emotions and stress. “Infants are constantly absorbing and learning things, not just when we think we're teaching them,” says Alice Graham, a doctoral student who led the study, forthcoming in the journal Psychological Science. “We should expect that what's going on in the environment is literally shaping the physical connections in their brains.” As with family fighting, neglect leaves no external marks but powerfully affects the architecture of the brain. A Yale University study of teenagers found evidence using MRI scans that neglect and emotional abuse during childhood reduces the density of cells in emotion-regulating regions of the brain later on. The teens in the study did not meet the criteria for full-blown psychiatric disorders, according to the paper published in 2011 in the Journal of the American Medical Association, yet many experienced emotional problems such as impulsive behavior and risk taking. © 2013 Scientific American,

Keyword: Stress; Development of the Brain
Link ID: 17762 - Posted: 02.05.2013

Marissa Fessenden U.S. business and policy leaders have made it a priority to increase the number of students pursuing degrees in science, technology, engineering and math, collectively known as STEM. But one source of STEM talent is often overlooked: young people with autism spectrum disorders. A study published late last year in the Journal of Autism and Developmental Disorders found that students with autism choose majors in science, technology, engineering and math at higher rates than students in the general population. Yet students with autism enter college at far lower rates. The authors say the results highlight the need to encourage students with autism to pursue a post-secondary education and that doing so may strengthen participation in the STEM fields. The only previous study to directly examine the connection between autism spectrum disorders and STEM majors was limited to a single university in the U.K. That paper, co-authored by Simon Baron-Cohen, director of the Autism Research Center at the University of Cambridge, found a link between autism and mathematical talent. The new study, led by researchers at the independent research institute SRI International, based in Menlo Park, CA, examined 11,000 students across the country and found that more young adults with an autism spectrum disorder choose STEM majors than their peers in the general population (34.31 vs. 22.8 percent) as well as their peers in 10 other disability groups (which included visual disabilities, intellectual disabilities, speech and language impairment and others). Students with autism, however, were unlikely to enroll in college at all—their rate of enrollment was the third lowest of all disability categories. © 2013 Nature Publishing Group

Keyword: Autism
Link ID: 17761 - Posted: 02.05.2013

By C. CLAIBORNE RAY Q. Nearing 70, I have increasing difficulty hearing conversations, yet music in restaurants is too loud. Why? A. Age-related hearing loss, called presbycusis, is characterized by loss of hair cells in the base of the cochlea, or inner ear, that are attuned to capture and transmit high-frequency sounds, said Dr. Anil K. Lalwani, director of otology, neurotology and skull-base surgery at NewYork-Presbyterian Hospital/Columbia University Medical Center. Loss of high-frequency hearing leads to deterioration in the ability to distinguish words in conversation. Additionally, any noise in the environment leads to even greater loss in clarity of hearing. “Contrary to expectation, presbycusis is also associated with sensitivity to loud noises,” Dr. Lalwani said. “This is due to a poorly understood phenomenon called recruitment.” Normally, a specific sound frequency activates a specific population of hair cells located at a specific position within the cochlea. With hearing loss, this specificity is lost, and a much larger population of hair cells in the adjacent areas is “recruited” and also activated, producing sensitivity to noise. “Patients with presbycusis perceive an incremental increase in loudness to be much greater than those with normal hearing,” he said. “This explains why the elderly parent complains that ‘I am not deaf!’ ” when a son or daughter repeats a misheard sentence. © 2013 The New York Times Company

Keyword: Hearing; Development of the Brain
Link ID: 17760 - Posted: 02.05.2013

By James Gallagher Health and science reporter, BBC News A tiny "genetic patch" can be used to prevent a form of deafness which runs in families, according to animal tests. Patients with Usher syndrome have defective sections of their genetic code which cause problems with hearing, sight and balance. A study, published in the journal Nature Medicine, showed the same defects could be corrected in mice to restore some hearing. Experts said it was an "encouraging" start. There are many types of Usher syndrome tied to different errors in a patient's DNA - the blueprint for building every component of the body. One of those mutations runs in families descended from French settlers in North America. When they try to build a protein called hormonin, which is needed to form the tiny hairs in the ear that detect sound, they do not finish the job. It results in hearing loss at birth and has a similar effect in the eye where it causes a gradual loss of vision. Scientists at the Rosalind Franklin University of Medicine and Science, in Chicago in the US, designed a small strip of genetic material which attaches to the mutation and keeps the body's factories building the protein. There has been something of a flurry of developments in restoring hearing in the past year. BBC © 2013

Keyword: Hearing; Genes & Behavior
Link ID: 17759 - Posted: 02.05.2013

By Erin Wayman The story of the Neandertals may need a new ending, a controversial study suggests. Using improved radiocarbon methods, scientists redated two of the youngest known Neandertal cave sites and concluded that they are at least 10,000 years older than previous studies have found. The findings cast doubt on the reliability of radiocarbon dates from other recent Neandertal sites, the researchers suggest online February 4 in the Proceedings of the National Academy of Sciences. This means the last Neandertals might have died out much earlier than previously thought, which could cause anthropologists to rethink how and why these hominids vanished. Researchers have long debated whether the harsh Ice Age climate, the appearance of modern humans migrating out of Africa, or some other factor drove Neandertals to extinction. “The paper is simply excellent,” says archaeologist Olaf Jöris of the Romano-Germanic Central Museum in Mainz, Germany. The new research supports Jöris’ own review of Neandertal dates, in which he concluded that the most-recent Neandertals probably lived around 42,000 years ago. The standard view suggests that the last of these hominids occupied Europe as recently as about 28,000 years ago. But other archaeologists are not convinced by the new work. “We shouldn’t get too carried away over results that amount to a few radiocarbon dates from two sites,” says Paul Pettitt, an archaeologist at Durham University in England. © Society for Science & the Public 2000 - 2013

Keyword: Evolution
Link ID: 17758 - Posted: 02.05.2013

By Melissa Dahl, NBC News Scarlet fever plays the villain in some of the best children's books: It got "Little Women's" Beth March. It got the child in "The Velveteen Rabbit" (although the kid survives, so, really, the fever got the stuffed rabbit). And it robbed Mary Ingalls, sweet sister of "Little House" series author Laura Ingalls Wilder, of her sight. Or so we were told. But today, the journal Pediatrics asserts that it wasn't scarlet fever that caused Mary's blindness -- it was viral meningoencephalitis, an inflammatory disease that attacks the brain. This is the sort of thing that is extremely interesting if you are interested in this sort of thing. And we'd wager many people are: The "Little House" books have remained in print ever since the initial publication of "Little House in the Big Woods" in 1932, and they're still popular today, with three titles landing on the School Library Journal's 2012 list of best children's chapter books. Even if you never read the books, you probably remember the TV series, which aired from 1974 to 1983. Dr. Beth Tarini, assistant professor of pediatrics at the University of Michigan, and her co-authors make their claim after scouring epidemiological data on blindness and infectious disease around the time of Mary's illness, plus analyzing local newspapers and Laura's unpublished memoir, "Pioneer Girl." For Tarini, it's the culmination of a project she began in medical school 10 years ago, after a confusing conversation with a professor. © 2013 NBCNews.com

Keyword: Vision
Link ID: 17757 - Posted: 02.05.2013

By Tia Ghose The identity of a mysterious patient who helped scientists pinpoint the brain region responsible for language has been discovered, researchers report. The finding, detailed in the January issue of the Journal of the History of the Neurosciences, identifies the patient as Louis Leborgne, a French craftsman who battled epilepsy his entire life. In 1840, a wordless patient was admitted to the Bicetre Hospital outside Paris for aphasia, or an inability to speak. He was essentially just kept there, slowly deteriorating. It wasn’t until 1861 that the man, who was known only as “Monsieur Leborgne” and who was nicknamed “Tan” for the only word he could say, came to physician Paul Broca’s ward at the hospital. Leborgne died shortly after the meeting, and Broca performed his autopsy, during which Broca found a lesion in a region of the brain tucked back and up behind the eyes. After doing a detailed examination, Broca concluded that Tan’s aphasia was caused by damage to this region and that the particular brain region controlled speech. That part of the brain was later renamed Broca’s area. At the time, scientists were debating whether different areas of the brain performed separate functions or whether it was an undifferentiated lump that did one task, like the liver, said Marjorie Lorch, a neurolinguist in London who was not involved in the study. © 1996-2013 The Washington Post

Keyword: Language; Stroke
Link ID: 17756 - Posted: 02.05.2013

by Elizabeth Pennisi Though often associated with dirty environments, cockroaches are actually quite fastidious, especially when it comes to their antennae. They clean them often by grabbing one in with a front leg and drawing it through their mouth. Researchers have long observed that many insects groom themselves, and now they know why. When scientists restrained American cockroaches or prevented grooming by gluing mouthparts for 24 hours, they noticed a shiny, waxy buildup on the antennae that clogs the tiny pores that lead to odor-sensing cells. Measurements of the electrical activity in those cells in response to sex-attractant and food odors showed that the gunk interfered with the roach's sense of smell, they report online today in the Proceedings of the National Academy of Sciences. The insects appear to produce wax continuously, likely to keep from drying out, and grooming helps remove the excess as well as dust and other foreign chemicals that land on the antennae and get trapped in the gunk. Carpenter ants, houseflies, and German cockroaches also suffered from gunk overload when prohibited from grooming, suggesting that fastidiousness is widespread. © 2010 American Association for the Advancement of Science

Keyword: Chemical Senses (Smell & Taste)
Link ID: 17755 - Posted: 02.05.2013

A telltale boost of activity at the back of the brain while processing emotional information predicted whether depressed patients would respond to an experimental rapid-acting antidepressant, a National Institutes of Health study has found. “We have discovered a potential neuroimaging biomarker that may eventually help to personalize treatment selection by revealing brain-based differences between patients,” explained Maura Furey, Ph.D., of NIH’s National Institute of Mental Health (NIMH). Furey, NIMH’s Carlos Zarate, M.D., and colleagues, reported on their functional magnetic resonance imaging (fMRI) study of a pre-treatment biomarker for the antidepressant response to scopolamine, Jan. 30, 2013, online in JAMA Psychiatry. Scopolamine, better known as a treatment for motion sickness, has been under study since Furey and colleagues discovered its fast-acting antidepressant properties in 2006. Unlike ketamine, scopolamine works through the brain’s acetylcholine chemical messenger system. The NIMH team’s research has demonstrated that by blocking receptors for acetylcholine on neurons, scopolamine can lift depression in many patients within a few days; conventional antidepressants typically take weeks to work. But not all patients respond, spurring interest in a predictive biomarker. The acetylcholine system plays a pivotal role in working memory, holding information in mind temporarily, but appears to act by influencing the processing of information rather than through memory. Imaging studies suggest that visual working memory performance can be enhanced by modulating acetylcholine-induced activity in the brain’s visual processing area, called the visual cortex, when processing information that is important to the task.

Keyword: Depression; Brain imaging
Link ID: 17754 - Posted: 02.05.2013

By Laura Sanders Not all fear is the same. A woman who laughs at horror movies, grabs dangerous snakes and calmly deals with knife-wielding men nonetheless surrenders to terror at a single puff of suffocating carbon dioxide. This woman, known as SM, has a disease that damaged her amygdala, a brain structure implicated in fear. But the new results involving her and two others with the same disease, published online February 3 in Nature Neuroscience, show that a certain kind of danger signal can bypass the amygdala, hitting the panic button in other parts of the brain. The need to breathe is one of the most fundamental requirements for survival. Clinical neuropsychologist Justin Feinstein of the University of Iowa in Iowa City believes that the instinct to get air might tap into a brain system that’s more primal than the amygdala. Feinstein and colleagues work with SM and other patients who suffer from a rare genetic disorder called Urbach-Wiethe disease. In late childhood, this disease destroys the amygdala, a pair of almond-shaped structures deep in the brain. SM shows no fear when confronted with haunted houses, ominous spiders and scary movies (SN: 1/15/11, p/ 14). Now, the scientists have found something that does scare her. A breath of gas that is 35 percent carbon dioxide can immediately provoke a strong, panicky fear. (By contrast, normal air is less than one percent carbon dioxide.) When the gas hits the body, specialized proteins sense that something is amiss and send an urgent “must have air, now” message to the brain. © Society for Science & the Public 2000 - 2013

Keyword: Emotions
Link ID: 17753 - Posted: 02.04.2013

By ALAN SCHWARZ VIRGINIA BEACH — Every morning on her way to work, Kathy Fee holds her breath as she drives past the squat brick building that houses Dominion Psychiatric Associates. It was there that her son, Richard, visited a doctor and received prescriptions for Adderall, an amphetamine-based medication for attention deficit hyperactivity disorder. It was in the parking lot that she insisted to Richard that he did not have A.D.H.D., not as a child and not now as a 24-year-old college graduate, and that he was getting dangerously addicted to the medication. It was inside the building that her husband, Rick, implored Richard’s doctor to stop prescribing him Adderall, warning, “You’re going to kill him.” It was where, after becoming violently delusional and spending a week in a psychiatric hospital in 2011, Richard met with his doctor and received prescriptions for 90 more days of Adderall. He hanged himself in his bedroom closet two weeks after they expired. The story of Richard Fee, an athletic, personable college class president and aspiring medical student, highlights widespread failings in the system through which five million Americans take medication for A.D.H.D., doctors and other experts said. Medications like Adderall can markedly improve the lives of children and others with the disorder. But the tunnel-like focus the medicines provide has led growing numbers of teenagers and young adults to fake symptoms to obtain steady prescriptions for highly addictive medications that carry serious psychological dangers. These efforts are facilitated by a segment of doctors who skip established diagnostic procedures, renew prescriptions reflexively and spend too little time with patients to accurately monitor side effects. © 2013 The New York Times Company

Keyword: ADHD; Drug Abuse
Link ID: 17752 - Posted: 02.04.2013

The number of children being diagnosed with epilepsy has dropped dramatically in the UK over the past decade, figures show. A study of GP-recorded diagnoses show the incidence has fallen by as much as half. Researchers said fewer children were being misdiagnosed, but there had also been a real decrease in some causes of the condition. Other European countries and the US had reported similar declines, they added. Epilepsy is caused when the brain's normal electrical activity result in seizures. Data from more than 344,000 children showed that the annual incidence of epilepsy has fallen by 4-9% year on year between 1994 and 2008. Overall the number of children born between 2003-2005 with epilepsy was 33% lower then those born in 1994-96. When researchers looked in more detail and included a wider range of possible indicators of an epilepsy diagnosis the incidence dropped by 47%. Correct diagnosis Better use of specialist services and increased caution over diagnosing the condition explains some, but not all, of the decline in the condition, the researchers reported in Archives of Diseases in Childhood. Introduction of vaccines against meningitis and a drop in the number of children with traumatic brain injuries, both of which can cause epilepsy, has probably also contributed to falling cases, they added. BBC © 2013

Keyword: Epilepsy; Development of the Brain
Link ID: 17751 - Posted: 02.04.2013

By JUDY BATTISTA NEW ORLEANS — The N.F.L., faced with increasing concern about the toll of concussions and confronted with litigation involving thousands of former players, is planning to form a partnership with General Electric to jump-start development of imaging technology that would detect concussions and encourage the creation of materials to better protect the brain. The four-year initiative, which is expected to begin in March with at least $50 million from the league and G.E., is the result of a late October conversation between Commissioner Roger Goodell and G.E.’s chief executive, Jeffrey Immelt, a former offensive tackle at Dartmouth. When Goodell explained his idea of getting leading companies in innovation to join the N.F.L. to accelerate research, Immelt said he wanted to help. After years of insisting there was no link between head injuries sustained on the field and long-term cognitive impairment, the N.F.L. has altered rules, fined and suspended players who hit opponents in the head and contributed millions of dollars for the study of head injuries. “Is this their way of defending themselves with this cloud over the sport? I’d be lying if I told you it had nothing to do with it,” Kevin Guskiewicz, the founding director of the Matthew Gfeller Sport-Related Traumatic Brain Injury Research Center at the University of North Carolina, said of the initiative. Guskiewicz is a member of the league’s Head, Neck and Spine Committee and the chairman of a subcommittee focused on safety equipment and playing rules. He will work with the N.F.L. and G.E. to identify areas of focus. © 2013 The New York Times Company

Keyword: Brain imaging; Brain Injury/Concussion
Link ID: 17750 - Posted: 02.04.2013

IF TWO animals have identical brain cells, how different can they really be? Extremely. Two worm species have exactly the same set of neurons, but extensive rewiring allows them to lead completely different lives. Ralf Sommer of the Max Planck Institute for Developmental Biology in Tübingen, Germany, and colleagues compared Caenorhabditis elegans, which eats bacteria, with Pristionchus pacificus, which hunts other worms. Both have a cluster of 20 neurons to control their foregut. Sommer found that the clusters were identical. "These species are separated by 200 to 300 million years, but have the same cells," he says. P. pacificus, however, has denser connections than C. elegans, with neural signals passing through many more cells before reaching the muscles (Cell, doi.org/kbh). This suggests that P. pacificus is performing more complex motor functions, says Detlev Arendt of the European Molecular Biology Laboratory in Heidelberg, Germany. Arendt thinks predators were the first animals to evolve complex brains, to find and catch moving prey. He suggests their brains had flexible wiring, enabling them to swap from plant-eating to hunting. © Copyright Reed Business Information Ltd.

Keyword: Genes & Behavior; Evolution
Link ID: 17749 - Posted: 02.04.2013

By Morgen Peck Co-sleeping, the practice of sharing a bed with your baby, has a controversial place in modern society. Proponents argue that it increases the parent-child bond, whereas detractors worry about safety. Now an anthropological study adds a new finding to the debate: fathers who sleep next to their babies tend to have significantly lower levels of testosterone than those who sleep in a different room. Lee Gettler, an anthropologist at the University of Notre Dame, compared Filipino men's testosterone levels before having a child and again four years later. Men who reported sleeping on the same surface as their child experienced a steep decline in nighttime testosterone levels not seen in men who slept in another room, according to the paper published in September 2012 in PLOS One. Studies on women have shown that mothers who sleep with their children pass in and out of sleep. The same disruptions in men could possibly decrease testosterone production, Gettler and his co-authors write. Previous work in the same population showed that fathers who fully throw themselves into caring for their children are more likely to have low testosterone, suggesting that hormonal fluctuations may support men in being good fathers. “Lower testosterone might orient men more toward the needs of the partner and children and away from risky behavior and competition with other males—which could conflict with investments in parenting,” Gettler says. © 2013 Scientific American

Keyword: Sexual Behavior; Sleep
Link ID: 17748 - Posted: 02.04.2013