By ANAHAD O'CONNOR Losing sleep tends to make people eat more and gain weight, and now a new study suggests that one reason may be the impact that sleep deprivation has on the brain. The research showed that depriving people of sleep for one night created pronounced changes in the way their brains responded to high-calorie junk foods. On days when the subjects had not had proper sleep, fattening foods like potato chips and sweets stimulated stronger responses in a part of the brain that helps govern the motivation to eat. But at the same time, the subjects experienced a sharp reduction in activity in the frontal cortex, a higher-level part of the brain where consequences are weighed and rational decisions are made. The findings suggested that one unfortunate result of sleep loss is this “double hit” in brain activity, said Matthew P. Walker, an author of the study and a professor of psychology and neuroscience at the University of California, Berkeley. A sleepy brain appears to not only respond more strongly to junk food, but also has less ability to rein that impulse in. Some experts have theorized that in a sleep-deprived state, people eat more food simply to make up for all the calories they expend as they burn the midnight oil. But the new study showed that the changes in brain activity were evident even when the subjects were fed extra food and not experiencing any increased sensations in hunger. “Their hunger was no different when they were sleep deprived and when they had a normal night of sleep,” Dr. Walker said. “That’s important because it suggests that the changes we’re seeing are caused by sleep deprivation itself, rather than simply being perhaps more metabolically impaired when you’re sleep deprived.” Copyright 2013 The New York Times Company

Keyword: Sleep; Obesity
Link ID: 18471 - Posted: 08.07.2013

// by Jennifer Viegas Single parenting takes on new extremes for certain starfish that are hermaphrodites -- male and female at the same time and, in some cases, self-fertilizing. The species faces high risk of extinction, according to new research. The dire situation faced by the non-mating starfish, Parvulastra parvivipara and Parvulastra vivipara, helps to explain why so many organisms, including humans, have sex. Genetic diversity and the dispersal of youngsters support population growth. The plight of the starfish, documented in the latest issue of the journal Biology Letters, reveals how a life without sex but with self-fertilization could result in eventual oblivion. “There are quite a few reasons why these species are vulnerable,” senior author Michael Hart of Simon Fraser University’s Department of Biological Sciences told Discovery News. “The whole species could be wiped out.” Hart and his team studied the starfish, which are restricted to high intertidal pools of South Australia and Tasmania. These starfish also go by the nickname "sea cushions," since they look a bit more like a cushion than a star when viewed from the side. Most adult starfish of other species do reproduce via a separate male and female. Females usually produce eggs that males fertilize in the seawater. At that point, the fertilized eggs develop and grow before becoming little starfish that will attach themselves to the substrate and start the whole process over again. © 2013 Discovery Communications, LLC.

Keyword: Sexual Behavior; Evolution
Link ID: 18470 - Posted: 08.07.2013

Daniel Cressey Killing research animals is one of the most unpleasant tasks in science, and it is imperative to do it as humanely as possible. But researchers who study animal welfare and euthanasia are growing increasingly concerned that widely used techniques are not the least painful and least stressful available. This week, experts from across the world will gather in Newcastle upon Tyne, UK, to debate the evidence and try to reach a consensus. “There are lots of assumptions made about the humaneness of various techniques for euthanizing animals,” says Penny Hawkins, deputy head of the research animals department at the Royal Society for the Prevention of Cruelty to Animals, a charity based in Southwater, UK. “Sometimes an animal might not appear to be suffering, but might be conscious and suffering.” Much of the debate centres on rodents, which make up the vast majority of research animals. Current techniques for killing them include inhalation methods — such as chambers that fill with carbon dioxide or anaesthetic gases — and injecting barbiturates. Physical methods include cervical dislocation (breaking of the neck), or decapitation with specialist rodent guillotines (see ‘Methods used to kill lab rats’). Experts hotly debate which method is preferable. The most-discussed question at the meeting is likely to be about the use of CO2. © 2013 Nature Publishing Group

Keyword: Animal Rights
Link ID: 18469 - Posted: 08.07.2013

A gene that affects the brain's dopamine system appears to have influenced mothers' behavior during a recent economic downturn, researchers say. At the beginning of the recession that began in 2007, mothers with the "sensitive" version of a gene called DRD2 became more likely to strike or scream at their children, the researchers say. Mothers with the other "insensitive" version of the gene didn't change their behavior. But once it appeared that the recession would not become a full-fledged depression, the "sensitive" mothers became less likely than "insensitive" mothers to engage in harsh parenting. "You have the same genes, and with a different environment it's a completely different story," says , a professor of contemporary urban problems at Columbia University. "I think that's the most amazing part of what we found." Garfinkel and four other researchers in the Proceedings of the National Academy of Sciences. The surprising finding came about because Garfinkel and the other researchers happened to be studying "fragile" families in 20 large cities when the 2007 recession began. One of the things they were tracking was reports of harsh parenting, including spanking, hitting or screaming at a child, he says. Previous research had found that harsh parenting is more common during economic hard times, so Garfinkel says that's what researchers expected to see during the 2007-2009 period, often called the Great Recession. ©2013 NPR

Keyword: Stress; Genes & Behavior
Link ID: 18468 - Posted: 08.07.2013

Women living in urban centres in Canada with more than 500,000 inhabitants are at higher risk of postpartum depression than women in other areas, suggests a new study in the Canadian Medical Association Journal. Looking at the experiences of over 6,000 women who lived in rural, semi-rural, semi-urban or urban areas from the 2006 Canadian Maternity Experiences Survey, the study suggests that women in urban areas were at higher risk, with almost 10 per cent reporting postpartum depression compared with six per cent of women in rural areas, almost seven per cent of women in semirural areas and about five per cent in semiurban areas. Urban areas were found to have higher numbers of immigrant populations, and more women in these areas reported lower levels of social support during and after pregnancy. "We found that Canadian women who lived in large urban areas … were at higher risk of postpartum depression than women living in other areas," said Dr. Simone Vigod, psychiatrist at Women's College Hospital and scientist at Women's College Research Institute in Toronto. "The risk factors for postpartum depression [including history of depression, social support and immigration status] that were unequally distributed across geographic regions accounted for most of the variance in the rates of postpartum depression." The reason why immigrant woman appear to be at higher risk is not really known, she said. "Some theories are that it's related to social support or being away from their family." They could also have cultural barriers or needs that are not being met, she added. © CBC 2013

Keyword: Depression; Stress
Link ID: 18467 - Posted: 08.07.2013

Lying in bed, unable to move a muscle, so-called locked-in patients have few ways to communicate with the outside world. But researchers have now found a way to use the widening and narrowing of the pupils to send a message, potentially helping these patients break the silence. Doctors use the constriction of pupils under bright light to test whether a patient’s brain stem is intact. But our pupils also show the opposite response—dilation—based on our thoughts and emotions, says Wolfgang Einhäuser, a neurophysicist at Philipps University of Marburg in Germany. Einhäuser had been struggling to interpret changes in pupil size during decision-making when he began to wonder about a different application. He contacted Steven Laureys, a member of the Coma Science Group at the University Hospital of Liège in Belgium, to explore how the pupil could be used to communicate a choice. Laureys works with locked-in patients, who have normal mental acuity but are paralyzed and unable to express thoughts to those around them. Many can control only the muscles that move their eyes; some, not even that. They can learn to communicate using EEG technology, in which electrodes on the scalp detect changes in brain activity. But applying the electrode cap is time-consuming, and the equipment is expensive, Einhäuser says. “If you imagine doing that every day, basically to communicate, that’s troublesome.” To find a different technique, Einhäuser, Laureys, and colleagues reached back in time. “The pieces have been there since the early ’60s,” Einhäuser says. A 1964 study showed that our pupils dilate when we perform mental arithmetic, like attempting to multiply 27 and 15 with no pencil and paper, and that harder tasks led to more dramatic dilation. The team set up a camera and a laptop to explore this automatic response. © 2012 American Association for the Advancement of Science.

Keyword: Movement Disorders; Vision
Link ID: 18466 - Posted: 08.06.2013

Researchers have achieved dynamic, atomic-scale views of a protein needed to maintain the transparency of the lens in the human eye. The work, funded in part by the National Institutes of Health, could lead to new insights and drugs for treating cataract and a variety of other health conditions. Aquaporin proteins form water channels between cells and are found in many tissues, but aquaporin zero (AQP0) is found only in the mammalian lens, which focuses light onto the retina, at the back of the eye. The lens is primarily made up of unique cells called lens fibers that contain little else besides water and proteins called crystallins. Tight packing of these fibers and of the crystallin proteins within them helps create a uniform medium that allows light to pass through the lens, almost as if it were glass. Abnormal development or age-related changes in the lens can lead to cataract — a clouding of the lens that causes vision loss. Besides age, other risk factors for cataract include smoking, diabetes, and genetic factors. Mutations in the AQP0 gene can cause congenital cataract and may increase the risk of age-related cataract. “The AQP0 channel is believed to play a vital role in maintaining the transparency of the lens and in regulating water volume in the lens fibers, so understanding the molecular details of how water flows through the channel could lead to a better understanding of cataract,” said Dr. Houmam Araj, who oversees programs on lens, cataract and oculomotor systems at NIH’s National Eye Institute (NEI), which helped fund the research.

Keyword: Vision
Link ID: 18465 - Posted: 08.06.2013

By Meeri Kim, Dizziness, vertigo and nausea are common symptoms of an inner-ear infection. But they can also be signs of a stroke. For doctors, especially those working in emergency rooms, quickly and accurately making the distinction is vital. But basic diagnostic tools, including the otoscope and simple eye-movement tests, are far from definitive. As a result, many doctors resort to a pricey imaging test such as a CT scan or an MRI. Nearly half of the 4 million people who visit U.S. emergency rooms each year with dizziness are given an MRI or CT scan, according to a study issued last month. Only about 3 percent of those 4 million people are actually having strokes. Why did the physical therapist’s staff push him to make more visits? Hefty insurance payments, perhaps. For the 25 percent of strokes that restrict blood flow to the back portions of the brain, CT scans are a poor diagnostic tool, according to the study’s leader, David Newman-Toker, an associate professor of neurology and otolaryngology at the Johns Hopkins University School of Medicine. “CT scans are so bad at detecting [these strokes] that they miss about 85 percent of them” in the first day after symptoms begin, he said. “That’s pretty close to useless.” Even MRIs miss almost 20 percent of strokes if the test is done within the first 24 hours. A new device offers a promising option for rooting out the cause of dizziness: eye-tracking goggles. © 1996-2013 The Washington Post

Keyword: Stroke; Hearing
Link ID: 18464 - Posted: 08.06.2013

By Scicurious Most current treatments for depression target the serotonin system, a chemical messenger that plays a role in mood (though it also plays a role in many, many other things). Most of the antidepressant drugs on the market (such as Prozac, Celexa, and Zoloft) that target serotonin do it by blocking the recycling of serotonin, keeping it in the spaces between neurons and allowing it to be active for far longer than it might otherwise. The problem is, these drugs take a long time to work. Often many weeks. In that time, patients may grow frustrated as side effects happen and the needed effects don’t. Patients may be in very desperate straights when they first go on medication, and any extra time before the drugs work becomes that much more dangerous. The drugs may not work at all, causing doctors and patients to have to go through the entire, weeks long process over and over again. Scientists are looking for new antidepressant mechanisms, and trying to create more effective drugs. But there are various ways to go about it. You can go looking for an entirely new way of working, but you can also look at ways to make the current drugs work faster. One target that might help antidepressant drugs work faster is one of the many receptors for serotonin, the 5-HT1A receptor. Receptors are proteins that sit on cell surfaces, and bind chemicals. When they bind a chemical, they cause change, maybe by opening a channel, or starting a signal to make a neuron fire more, or less. What a receptor does depends on its type, but also where in the brain it is located and on what type of cell. © 2013 Scientific American

Keyword: Depression
Link ID: 18463 - Posted: 08.06.2013

Rachel Seifert Over 40 years ago President Richard Nixon declared war on "public enemy No 1" in the US – drug abuse. Since then, aggressive US anti-drug policies have continued unabated, with over $1 trillion spent on law enforcement and over 45 million people arrested on drugs charges. However, the numbers remain relatively unchanged, with over 20 million users of illegal drugs in the US today. Many voices on the international stage are starting to speak out against not only the failure of these policies but the harm they are causing. Yet the PR machine created around the war on drugs still exerts a huge influence over public opinion. In High Price, Dr Carl Hart joins the growing number of professionals breaking with conventional thinking as he debunks myths and misconceptions associated with illegal drugs. Hart brings two very different but complementary perspectives to the debate: his experience of growing up in a poor African-American community in Miami, and his scientific learning as a neuroscientist studying the effects of drugs. Although the two are not always joined seamlessly, they give him a rare insight into the often deep misunderstanding of illegal drugs, with which he attempts to turn sensationalist, stereotypical views on their head. By telling his own life story, Hart gives us a fascinating insight into the cultural mores of his community, growing up on the streets, and the racism he has faced throughout his life. Now a distinguished scientist, he reflects on his childhood with a new understanding, applying his scientific knowledge to reassess the path that led him to a career in academia, while avoiding the circle of drugs, addiction and prison in which many of his family and friends got caught up. © 2013 Guardian News and Media Limited

Keyword: Drug Abuse
Link ID: 18462 - Posted: 08.06.2013

By Bahar Gholipour, Children with Asperger's syndrome show patterns of brain connectivity distinct from those of children with autism, according to a new study. The findings suggest the two conditions, which are now in one category in the new psychiatry diagnostic manual, may be biologically different. The researchers used electroencephalography (EEG) recordings to measure the amount of signaling occurring between brain areas in children. They had previously used this measure of brain connectivity to develop a test that could distinguish between children with autism and normally developing children. "We looked at a group of 26 children with Asperger's, to see whether measures of brain connectivity would indicate they're part of autism group, or they stood separately," said study researcher Dr. Frank Duffy, a neurologist at Boston's Children Hospital. The study also included more than 400 children with autism, and about 550 normally developing children, who served as controls. At first, the test showed that children with Asperger's and those with autism were similar: both showed weaker connections, compared with normal children, in a region of the brain's left hemisphere called the arcuate fasciculus, which is involved in language. However, when looking at connectivity between other parts of the brain, the researchers saw differences. Connections between several regions in the left hemisphere were stronger in children with Asperger's than in both children with autism and normally developing children. © 2013 Yahoo! Inc

Keyword: Autism; Brain imaging
Link ID: 18461 - Posted: 08.06.2013

By NICK BILTON Scientists haven’t yet found a way to mend a broken heart, but they’re edging closer to manipulating memory and downloading instructions from a computer right into a brain. Researchers from the Riken-M.I.T. Center for Neural Circuit Genetics at the Massachusetts Institute of Technology took us closer to this science-fiction world of brain tweaking last week when they said they were able to create a false memory in a mouse. The scientists reported in the journal Science that they caused mice to remember receiving an electrical shock in one location, when in reality they were zapped in a completely different place. The researchers weren’t able to create entirely new thoughts, but they applied good or bad feelings to memories that already existed. “It wasn’t so much writing a memory from scratch, it was basically connecting two different types of memories. We took a neutral memory, and we artificially updated that to make it a negative memory,” said Steve Ramirez, one of the M.I.T. neuroscientists on the project. It may sound insignificant and perhaps not a nice way to treat mice, but it is not a dramatic leap to imagine that one day this research could lead to computer-manipulation of the mind for things like the treatment of post-traumatic stress disorder, Mr. Ramirez said. Technologists are already working on brain-computer interfaces, which will allow us to interact with our smartphones and computers simply by using our minds. And there are already gadgets that read our thoughts and allow us to do things like dodge virtual objects in a computer game or turn switches on and off with a thought. Copyright 2013 The New York Times Company

Keyword: Robotics; Learning & Memory
Link ID: 18460 - Posted: 08.06.2013

by Helen Thomson We all get lost sometimes. Luckily, specialised cells in the brain that help animals find their way have now been identified in humans for the first time. The discovery could lead to better treatments for people who have problems navigating. We know that animals use three cell types to navigate the world. Direction cells fire only when an animal is facing a particular direction, place cells fire only in a particular location, and grid cells fire at regular intervals as an animal moves around. To understand how grid cells work, imagine the carpet in front of you has a grid pattern of interlocking triangles. One grid cell will fire whenever you reach the corner of any triangle in that grid. Shift the grid pattern along ever so slightly to another section of the carpet, and another grid cell will be responsible for firing every time you reach the corners of that grid's triangles – and so on. Grid cells send information to place cells and both kinds of cell send information to the hippocampus – responsible for memory formation. Together, this network of activity helps form a mental representation of an animal's location in its environment. Direction and place cells have been identified in humans but the existence of grid cells has so far only been hinted at in brain scans. To find out whether these cells do exist in humans, Joshua Jacobs at Drexel University in Philadelphia, Pennsylvania, and colleagues tested 14 people who had already had electrodes implanted in their brains for epilepsy therapy. © Copyright Reed Business Information Ltd.

Keyword: Learning & Memory
Link ID: 18459 - Posted: 08.05.2013

By Luciana Gravotta Small gains now or big rewards later? The conundrum plagues every decision we make, whether we are investing or dieting. Now researchers find that men and women use different strategies to make such choices. Researchers use gambling games to understand what we do when immediate rewards are pitted against long-term gains. Most of these games find no major differences in how men and women play. An experimental setup called the Iowa Gambling Task (IGT), however, finds consistent—and large—differences between the behavior of men and women: men are better at figuring out the strategy that reaps the bigger payoff. Players are given four decks of cards, and they choose one card at a time from any deck they want. Each card has a win or loss amount on it, and each deck has its own unique payout pattern. Two of the decks contain cards that dole out large or frequent rewards, but consistently choosing cards from these decks leads to losses in the long run. The other two decks provide a modest amount of cash per win but less loss over time, so they offer long-term gains for players who pick from them most frequently. These patterns are carefully obscured so that the winning strategy is not obvious. A review published in February in Behavioural Brain Research finds that men focus on the big picture, watching their total earnings and quickly homing in on which of the decks will lead to gains in the long run. Women focus on details such as the frequencies of wins and losses for each deck, missing the overall impact each deck has on their total balance. Sensitive to losses, women tend to switch to a different deck as soon as they are pinged with a setback, making it more difficult for them to identify the prize deck. © 2013 Scientific American

Keyword: Sexual Behavior; Emotions
Link ID: 18458 - Posted: 08.05.2013

By CHRISTINE MONTROSS PROVIDENCE, R.I. — M is a 33-year old woman who swallowed silverware. She wasn’t psychotic, or out of touch with reality. She knew it was not a good idea to swallow forks and knives and she wasn’t trying to kill herself. In fact, each time she ingested utensils, she went to the emergency room so that doctors could remove them from her esophagus and stomach. Then the hospital transferred M to the psychiatric unit, where she was assigned to my care. Enlarge This Image Robert Frank Hunter When I met M she had already been hospitalized 72 times. She’d swallowed silverware — and batteries — before. Sometimes she inserted sharp objects or large doses of medication into her vagina. There are psychiatric patients who cut or burn themselves in an attempt to relieve mental anguish; M did both of these things, too, periodically, but she had primarily developed a maladaptive habit of ingesting or inserting dangerous objects into her body as a means of coping with stress. Each time, she said, she felt better afterward. Then she brought herself to the emergency room for treatment. M’s case is dramatic. But she is one of countless psychiatric patients who have nowhere to turn for care, other than the E.R. It is well known that millions of uninsured Americans, who can’t afford regular medical care, use the country’s emergency rooms for primary health care. The costs — to patients’ health, to their wallets, and to the health care system — are well documented. Less visible is the grievous effect this shift is having on psychiatric care and on the mentally ill. © 2013 The New York Times Company

Keyword: Schizophrenia
Link ID: 18457 - Posted: 08.05.2013

Steve Connor A gene thought to be involved in nerve development can double the risk of schizophrenia when it is damaged, according to a pioneering study into one of most costly mental illnesses. The findings are further evidence of a genetic basis for schizophrenia – which affects about one in every 100 people at some time of their lives – and could lead to a greater understanding of the physical faults that might lead to the psychiatric disorder in some susceptible people. The chronic, long-term illness, which results in persistent delusions and hallucinations, is estimated to cost the NHS about £2bn a year in care and treatment alone. But the extra burden on patients, their families and the criminal justice system is thought to be at least twice as high. Scientists said the genetic fault they have discovered is also associated with a separate inherited disorder that results in learning difficulties and autism. This link, they said, is probably the result of them sharing a common biological pathway at the genetic level. The gene linked to schizophrenia, called TOP3B, is normally involved in unwinding the DNA double helix to allow other genes to function, especially when the nerve cells of the brain are developing, both in the womb and during the crucial first years of life. © independent.co.uk

Keyword: Schizophrenia; Genes & Behavior
Link ID: 18456 - Posted: 08.05.2013

By Andrea Anderson In spring a band of brainy rodents made headlines for zipping through mazes and mastering memory tricks. Scientists credited the impressive intellectual feats to human cells transplanted into their brains shortly after birth. But the increased mental muster did not come from neurons, the lanky nerve cells that swap electrical signals and stimulate muscles. The mice benefited from human stem cells called glial progenitors, immature cells poised to become astrocytes and other glia cells, the supposed support cells of the brain. Astrocytes are known for mopping up excess neuro-transmitters and maintaining balance in brain systems. During the past couple of decades, however, researchers started suspecting astrocytes of making more complex cognitive contributions. In the 1990s the cells got caught using calcium to accomplish a form of nonelectrical signaling. Studies since then have revealed how extensively astrocytes interact with neurons, even coordinating their activity in some cases. Perhaps even more intriguing, our astrocytes are enormous compared with the astrocytes of other animals—20 times larger than rodent astrocytes—and they make contact with millions of neurons apiece. Neurons, on the other hand, are nearly identical in all mammals, from rodents to great apes like us. Such clues suggest astrocytes could be evolutionary contributors to our outsized intellect. The new study, published in March in Cell Stem Cell, tested this hypothesis. A subset of the implanted human stem cells matured into rotund, humanlike astrocytes in the animals' brains, taking over operations from the native mouse astrocytes. When tested under a microscope, these human astrocytes accomplished calcium signaling at least three times faster than the mouse astrocytes did. The enhanced mice masterfully memorized new objects, swiftly learned to link certain sounds or situations to an unpleasant foot shock, and displayed unusually savvy maze navigation—signs of mental acuity that surpassed skills exhibited by either typical mice or mice transplanted with glial progenitor cells from their own species. © 2013 Scientific American

Keyword: Glia; Learning & Memory
Link ID: 18455 - Posted: 08.05.2013

Josh Howgego When it comes to our sense of smell, we are all experiencing the world in very different ways. Scientists already know that humans' sensitivity to smelly molecules varies considerably from person to person (see: 'Soapy taste of coriander linked to genetic variants'). But evidence that genetic variations — as opposed to habit, culture or other factors — underlie these differences has been hard to come by. Geneticist Richard Newcomb of the New Zealand institute for Plant and Food Research in Auckland and his colleagues searched for olfactory genes by testing 187 people’s sensitivity to ten chemicals found in everyday food, including the molecules that give distinctive smells to blue cheese, apples and violets. They found that, as expected, the smelling abilities of their subjects varied. The team then sequenced the subjects’ genomes and looked for differences that could predict people’s ability to detect each chemical through smell. For four of the ten chemicals, the researchers identified clusters of genes that convincingly predicted smelling ability, as they report today in Current Biology1. The study could not conclude whether similar genetic associations exist for the other six compounds, or whether factors other than genes play a role in those cases. Previously, only five regions of the genome had been shown to affect olfactory ability when they undergo mutations, so Newcomb’s study has nearly doubled the number of genetic associations known to influence smell. And because there is nothing special about the chemicals they studied, Newcomb says that it is logical to think the findings would extend to lots of scents, meaning that people experience the plethora of chemicals surrounding them in endlessly different ways. © 2013 Nature Publishing Group

Keyword: Chemical Senses (Smell & Taste); Genes & Behavior
Link ID: 18454 - Posted: 08.03.2013

By CARL ZIMMER “Monogamy is a problem,” said Dieter Lukas of the University of Cambridge in a telephone news conference this week. As Dr. Lukas explained to reporters, he and other biologists consider monogamy an evolutionary puzzle. In 9 percent of all mammal species, males and females will share a common territory for more than one breeding season, and in some cases bond for life. This is a problem — a scientific one — because male mammals could theoretically have more offspring by giving up on monogamy and mating with lots of females. In a new study, Dr. Lukas and his colleague Tim Clutton-Brock suggest that monogamy evolves when females spread out, making it hard for a male to travel around and fend off competing males. On the same day, Kit Opie of University College London and his colleagues published a similar study on primates, which are especially monogamous — males and females bond in over a quarter of primate species. The London scientists came to a different conclusion: that the threat of infanticide leads males to stick with only one female, protecting her from other males. Even with the scientific problem far from resolved, research like this inevitably turns us into narcissists. It’s all well and good to understand why the gray-handed night monkey became monogamous. But we want to know: What does this say about men and women? As with all things concerning the human heart, it’s complicated. © 2013 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 18453 - Posted: 08.03.2013

An experimental treatment for alcohol dependence works better in individuals who possess specific combinations of genes that regulate the function and binding of serotonin, a brain chemical affected by the treatment, according to a study supported by the National Institutes of Health. A report of the finding appears online in the American Journal of Psychiatry. “This study is another important step toward personalized treatments for alcohol dependence,” says Kenneth R. Warren, Ph.D., acting director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), which funded the study. “A personalized approach based on a person’s genetic makeup is increasingly being investigated for delivering optimum treatment to the ‘right’ patient.” Ondansetron is a medication currently used to treat nausea and vomiting, often following chemotherapy. It works by blocking serotonin-3 receptors, and has shown potential as a treatment for defined subpopulations with alcohol dependence. In previous studies, Professor Bankole Johnson, D.Sc., M.D., and his team at the University of Virginia, Charlottesville, have shown that variations in genes that encode the serotonin transporter, a protein that regulates the concentration of serotonin between nerve cells, can significantly influence drinking intensity. They have also shown that the effectiveness of ondansetron therapy among people with alcohol dependence is influenced by variations of the serotonin transporter gene.

Keyword: Drug Abuse; Genes & Behavior
Link ID: 18452 - Posted: 08.03.2013