Smoking "rots" the brain by damaging memory, learning and reasoning, according to researchers at King's College London. A study of 8,800 people over 50 showed high blood pressure and being overweight also seemed to affect the brain, but to a lesser extent. Scientists involved said people needed to be aware that lifestyles could damage the mind as well as the body. Their study was published in the journal Age and Ageing. Researchers at King's were investigating links between the likelihood of a heart attack or stroke and the state of the brain. Data about the health and lifestyle of a group of over-50s was collected and brain tests, such as making participants learn new words or name as many animals as they could in a minute, were also performed. They were all tested again after four and then eight years. Decline The results showed that the overall risk of a heart attack or stroke was "significantly associated with cognitive decline" with those at the highest risk showing the greatest decline. It also said there was a "consistent association" between smoking and lower scores in the tests. BBC © 2012

Keyword: Drug Abuse; Neurotoxins
Link ID: 17534 - Posted: 11.26.2012

A substance made by the body when it uses fat as fuel could provide a new way of treating epilepsy, experts hope. Researchers in London who have been carrying out preliminary tests of the fatty acid treatment, report their findings in Neuropharmacology journal. They came up with the idea because of a special diet used by some children with severe, drug resistant epilepsy to help manage their condition. The ketogenic diet is high in fat and low in carbohydrate. The high fat, low carbohydrate diet is thought to mimic aspects of starvation by forcing the body to burn fats rather than carbohydrates. Although often effective, the diet has attracted criticism, as side-effects can be significant and potentially lead to constipation, hypoglycaemia, retarded growth and bone fractures. By pinpointing fatty acids in the ketogenic diet that are effective in controlling epilepsy, researchers hope they can develop a pill for children and adults that could provide similar epilepsy control without the side-effects. In early trials, the scientists, from Royal Holloway and University College London, say they have identified fatty acids that look like good candidates for the job. They found that not only did some of the fatty acids outperform a regular epilepsy medication called valproate in controlling seizures in animals, they also had fewer side-effects. BBC © 2012

Keyword: Epilepsy; Obesity
Link ID: 17533 - Posted: 11.24.2012

By Carrie Arnold Researchers have untangled some of the neurological events that may ultimately lead to Alzheimer's disease. Two new studies show that a protein implicated in this form of dementia can infect other neurons to spread disease across the brain. These problematic proteins clump together, which can lead to cognitive problems. A protein's shape—the way its chains of amino acids fold—determines its function. If a protein misfolds, its structure and function change. In Alzheimer's, researchers have long suspected that misfolded versions of a protein called amyloid-beta might travel from cell to cell and cause more amyloid-beta proteins to take on a deformed shape. To test this idea, biophysicist Jan Stöhr of the University of California, San Francisco, and his colleagues injected synthetic amyloid-beta proteins into the brains of mice and found that plaques began to form in less than six months. Even when the synthetic proteins were injected into only one side of the brain, over time plaques materialized throughout the organ, the researchers found. “If these aggregates are not cleared by the brain, they will start to recruit more amyloid-beta peptides into the diseased conformation, and the spread throughout the brain begins,” Stöhr says. The results appeared in the June Proceedings of the National Academy of Sciences USA. In a separate study using a cell culture, a team of researchers led by Martin Hallbeck of Linköping University in Sweden tracked amyloid-beta transmission from neuron to neuron for the first time. The results, published in the June 27 Journal of Neuroscience, also show that neurons containing misfolded amyloid-beta can cause neighboring, connected neurons to break down, eventually infecting the entire culture. © 2012 Scientific American,

Keyword: Alzheimers
Link ID: 17532 - Posted: 11.24.2012

By ANAHAD O'CONNOR Health officials are warning parents not to use a special device designed to help keep babies in certain positions as they sleep. The device, called a sleep positioner, has been linked to at least 13 deaths in the last 15 years, officials with two federal agencies said on Wednesday. “We urge parents and caregivers to take our warning seriously and stop using these sleep positioners,” Inez Tenenbaum, the chairman of the Consumer Product Safety Commission, said in a statement. The sleep positioner devices come primarily in two forms. One is a flat mat with soft bolsters on each side. The other, known as a wedge-style positioner, looks very similar but has an incline, keeping a child in a very slight upright position. Makers of the devices claim that by keeping infants in a specific position as they sleep, they can prevent several conditions, including acid reflux and flat head syndrome, a deformation caused by pressure on one part of the skull. Many are also marketed to parents as a way to help reduce a child’s risk of sudden infant death syndrome, or SIDS, which kills thousands of babies every year, most between the ages of 2 months and 4 months. But the devices have never been shown in studies to prevent SIDS, and they may actually raise the likelihood of sudden infant death, officials say. One of the leading risk factors for sudden infant death is placing a baby on his or her stomach at bedtime, and health officials have routinely warned parents to lay babies on their backs. They even initiated a “Back to Sleep” campaign in the 1990s, which led to a sharp reduction in sudden infant deaths. Copyright 2012 The New York Times Company

Keyword: Sleep; Development of the Brain
Link ID: 17531 - Posted: 11.24.2012

by Greg Miller Hitting the wall in the middle of a busy work day is nothing unusual, and a caffeine jolt is all it takes to snap most of us back into action. But people with certain sleep disorders battle a powerful urge to doze throughout the day, even after sleeping 10 hours or more at night. For them, caffeine doesn't touch the problem, and more potent prescription stimulants aren't much better. Now, a study with a small group of patients suggests that their condition may have a surprising source: a naturally occurring compound that works on the brain much like the key ingredients in chill pills such as Valium and Xanax. The condition is known as primary hypersomnia, and it differs from the better known sleep disorder narcolepsy in that patients tend to have more persistent daytime sleepiness instead of sudden "sleep attacks." The unknown cause and lack of treatment for primary hypersomnia has long frustrated David Rye, a neurologist at Emory University in Atlanta. "A third of our patients are on disability," he says, "and these are 20- and 30-year-old people." Rye and colleagues began the new study with a hunch about what was going on. Several drugs used to treat insomnia promote sleep by targeting receptors for GABA, a neurotransmitter that dampens neural activity. Rye hypothesized that his hypersomnia patients might have some unknown compound in their brains that does something similar, enhancing the activity of so-called GABAA receptors. To try to find this mystery compound, he and his colleagues performed spinal taps on 32 hypersomnia patients and collected cerebrospinal fluid (CSF), the liquid that bathes and insulates the brain and spinal cord. Then they added the patients' CSF to cells genetically engineered to produce GABAA receptors, and looked for tiny electric currents that would indicate that the receptors had been activated. © 2010 American Association for the Advancement of Science

Keyword: Sleep
Link ID: 17530 - Posted: 11.24.2012

By NICHOLAS BAKALAR Everyone yawns. And we start yawning even before we are born. Now, using ultrasound video recordings, researchers have worked out a technique to distinguish prenatal yawns from the simple mouth openings that we also engage in well before birth. For the study, published on Wednesday in PLoS One, scientists scanned 15 healthy fetuses, eight girls and seven boys, at 24, 28, 32 and 36 weeks’ gestation. They distinguished yawns from jaw openings by the timing of the action and shape of the fetuses’ mouths. In all, they counted 56 yawns and 27 non-yawn mouth openings. By 36 weeks, the yawning had completely disappeared. Why fetuses yawn is unclear — for that matter, it is unclear why adults yawn. In any case, the study’s lead author, Nadja Reissland, a developmental psychologist at Durham University in England, said that yawning in a fetus is different from yawning in adults. “When you see a fetus yawning, it’s not because it’s tired,” she said. “The yawning itself might have some kind of function in healthy development. Fetuses yawn, and then as they develop they stop yawning. There’s something special in yawning.” Copyright 2012 The New York Times Company

Keyword: Development of the Brain; Sleep
Link ID: 17529 - Posted: 11.24.2012

By Wray Herbert In 2009 a regiment of Danish soldiers, the Guard Hussars, was deployed for a six-month tour in Afghanistan's arid Helmand province, a Taliban stronghold. They were stationed along with British soldiers—270 in all—at a forward operating base called Armadillo. Although none of the Guard Hussars were killed during the tour of duty, they nonetheless experienced many horrors of battle. A commander was seriously injured by a roadside bomb, and a night patrol ended in a firefight that killed and dismembered several Taliban combatants. The Guard Hussars' war experience is graphically depicted in the award-winning documentary film Armadillo, which debuted in 2010. It follows the soldiers from their emotional farewells in Denmark through their months in combat and, finally, back to joyous homecomings and family reunions. The film is a study of the inner lives of young men as they experience the excitement and camaraderie, the tedium and—mostly—the terror and trauma of war. Coincidentally, these same soldiers were also the subject of another, very different kind of study. At the same time that the film was being shot, the men were part of a larger group of Danish soldiers who were being scientifically observed and tested for emerging symptoms of post-traumatic stress disorder, or PTSD. A large team of Danish and American psychological scientists, led by Dorthe Berntsen of Aarhus University, wanted to do what had never been done before in this field of research: instead of studying soldiers who were already suffering from PTSD, they decided to assess young recruits before they were sent off to war, when they were still relatively unscathed, then to record them during the war experience, and finally to follow them back home and through several months of readjustment. In this way, the scientists hoped to see why some soldiers develop PTSD and others do not and how the symptoms of the disorder progress. © 2012 Scientific American

Keyword: Stress; Development of the Brain
Link ID: 17528 - Posted: 11.24.2012

by Douglas Heaven Blind people could soon be able to read street signs using an implant that translates the alphabet into Braille and beams an image of the Braille directly to visual neurons at the back of the eye. The implant is a modified version of a class of devices called retinal prostheses, which are used to restore partial sight to people with retinitis pigmentosa. A degenerative eye disease that kills the photoreceptor cells in the retina, RP tends to affect people in early adulthood and can lead to blindness, but leaves intact the neurons that carry visual signals to the brain. Prostheses such as the Argus II, manufactured by Second Sight in Sylmar, California, convert video from a camera mounted on a pair of glasses into electronic signals "displayed" on a 10-by-6 grid of electrodes implanted over a person's retina. This gives users a pixellated view of the world, allowing them to distinguish light and dark regions and even detect features such as doorways. But deciphering letters and words with the prosthesis is slow because of its low resolution. To make this more practical, Thomas Lauritzen of Second Sight and colleagues have come up with a modified version of the Argus II that presents the user with Braille. Since Braille represents letters and numbers as dots in a 3-by-2 grid, it can be displayed using the electrode array of existing Argus implants. The modified implant was tried out on a Braille-reading volunteer who already uses the Argus II. Tested on single letters and words of up to four letters, transmitted in Braille to the retinal implant, he correctly identified the letters 89 per cent of the time and words 60 to 80 per cent of the time. © Copyright Reed Business Information Ltd.

Keyword: Vision; Robotics
Link ID: 17527 - Posted: 11.24.2012

Dan Jones As diagnoses of autism spectrum disorder rise, the need for effective therapies has increased in urgency. Today, a paper in Nature describes two ways of reversing autism-like symptoms in a new mouse model of the condition1. Autism spectrum disorder (ASD) affects up to 1 in 110 people. Although a few drugs have shown promise in mouse models, none is able to treat the core social deficits common to ASD in humans. A team of researchers led by Nahum Sonenberg of McGill University in Montreal, Quebec, created a new model of mouse autism, and then reversed its symptoms. They began by genetically engineering mice so that they lacked the gene Eif4ebp2. The 4E-BP2 protein that this produces suppresses the translation of certain messenger RNAs, so knocking out Eif4ebp2 allows the proteins that these mRNAs produce to be synthesized at above normal levels. Mice lacking Eif4ebp2 exhibit many autism-like symptoms, including poor social interaction, altered communication and repetitive behaviours. Sonenberg and his co-workers found that one group of proteins that proliferates in the absence of Eif4ebp2 is the neuroligins (NLGNs), which sit in the membrane of neurons and help to create and maintain the connections, or synapses, between nerve cells. When the authors examined mouse brain slices, they discovered that overproduction of NLGNs results in synapses that are prone to overstimulation, establishing a ‘hyperconnectivity’ that many researchers believe underlies the symptoms of ASD. © 2012 Nature Publishing Group

Keyword: Autism
Link ID: 17526 - Posted: 11.24.2012

Flora Graham, deputy editor, newscientist.com These glowing shapes aren't the ears of a rave-happy Vulcan - they're slices from a mouse's brain. The slice on the right is from a mouse that lacks a gene called Arl13b - the same gene whose mutation causes Joubert syndrome in humans. This is a rare neurological condition that is linked with autism-spectrum disorders and brain structure malformations. Without Arl13b, the nerve cells known as interneurons can't find the right destination in the cerebral cortex during the brain's development. Since the interneurons don't end up in the right places, they can't be wired up properly later on. This causes the disrupted brain development, typical of Joubert syndrome, visible in the image on the right. The researchers hope that their findings will lead to better treatments for people who have the syndrome. "Ultimately, if you're going to come up with therapeutic solutions, it's important to understand the biology of the disease," says Eva Anton of the University of North Carolina in Chapel Hill, who worked on the research, which was published in Developmental Cell last week. Journal reference: Developmental cell doi:10.1016/j.devcel.2012.09.019 © Copyright Reed Business Information Ltd

Keyword: Autism
Link ID: 17525 - Posted: 11.24.2012

By ALISSA QUART THIS fall, science writers have made sport of yet another instance of bad neuroscience. The culprit this time is Naomi Wolf; her new book, “Vagina,” has been roundly drubbed for misrepresenting the brain and neurochemicals like dopamine and oxytocin. Earlier in the year, Chris Mooney raised similar ire with the book “The Republican Brain,” which claims that Republicans are genetically different from — and, many readers deduced, lesser to — Democrats. “If Mooney’s argument sounds familiar to you, it should,” scoffed two science writers. “It’s called ‘eugenics,’ and it was based on the belief that some humans are genetically inferior.” Sharp words from disapproving science writers are but the tip of the hippocampus: today’s pop neuroscience, coarsened for mass audiences, is under a much larger attack. Meet the “neuro doubters.” The neuro doubter may like neuroscience but does not like what he or she considers its bastardization by glib, sometimes ill-informed, popularizers. A gaggle of energetic and amusing, mostly anonymous, neuroscience bloggers — including Neurocritic, Neuroskeptic, Neurobonkers and Mind Hacks — now regularly point out the lapses and folly contained in mainstream neuroscientific discourse. This group, for example, slammed a recent Newsweek article in which a neurosurgeon claimed to have discovered that “heaven is real” after his cortex “shut down.” Such journalism, these critics contend, is “shoddy,” nothing more than “simplified pop.” Additionally, publications from The Guardian to the New Statesman have published pieces blasting popular neuroscience-dependent writers like Jonah Lehrer and Malcolm Gladwell. The Oxford neuropsychologist Dorothy Bishop’s scolding lecture on the science of bad neuroscience was an online sensation last summer. © 2012 The New York Times Company

Keyword: Brain imaging
Link ID: 17524 - Posted: 11.24.2012

The search for genes predisposing people to depression has taken an unexpected twist, according to Canadian researchers who found a clue in an obesity gene. Studies on families and twins suggest depression has a genetic component, but for 15 years, scientists haven't been able to find genes associated with the illness. Researchers at McMaster University in Hamilton, Ont., took a different approach by testing how obesity genes may be linked with depression. "We found the first gene predisposing to depression with consistent results," said David Meyre, an associate professor in clinical epidemiology and biostatistics at McMaster and a Canada Research Chair in genetic epidemiology. In Monday's issue of the journal Molecular Psychiatry, Meyre and his co-authors reported that a variant of the FTO gene may be associated with a lower risk of depression independent of the gene's effect on obesity. The common perception is that obese people become depressed because of their appearance and poor self-esteem or discrimination. Another common thought is that those who are depressed are less likely to be physically active or follow healthy eating habits. Taking antidepressants can also lead to weight gain. But the genetic findings challenge that thinking, Meyre said, since those with the genetic mutation predisposing to obesity were protected from depression. "This suggests that the FTO gene may have a broader role than initially thought with an effect on depression and other common psychiatric disorders," the researchers wrote. © CBC 2012

Keyword: Obesity; Depression
Link ID: 17523 - Posted: 11.21.2012

By Simon J Makin “One hundred repetitions three nights a week for four years – sixty-two thousand four hundred repetitions make one truth.” These are the thoughts of Bernard Maxwell as he reflects on The World State’s sleep-teaching technique, hypnopaedia, in Aldous Huxley’s Brave New World, before concluding: “Idiots!” Huxley was using the idea to explore social conditioning and control in a dystopian future, rather than what we might call “useful” learning, but the promise of effortless learning while we sleep is an idea that refuses to go away, as evidenced by the continued existence of dubious sleep learning “courses”. The possibility was dismissed scientifically in the 1950s after an experiment showing that people who were played the answers to a list of questions while they slept could not recall any of them the next day, unless they had also shown electrical brain activity indicating they were waking up. But evidence is now growing that the sleeping brain can, in fact, be taught in certain, limited ways. The most striking demonstration of this comes from a recent study published in Nature Neuroscience, in which people learned to associate sounds with smells while they were asleep. Pleasant and unpleasant odours were paired with different sounds played to sleeping participants and their “sniff responses” were measured. Pleasant smells provoked stronger sniffs and when the sounds paired with these smells were later played alone they still provoked stronger sniffs than those that had been paired with unpleasant odours. This was true both while the participants were still asleep and after they awoke and, unsurprisingly, they had no awareness of having learned anything. This is a limited form of learning known as conditioning, famous since Pavlov and his dog, and it can’t be used for learning anything as complex as, say, language vocab. © 2012 Scientific American

Keyword: Sleep; Learning & Memory
Link ID: 17522 - Posted: 11.21.2012

By Linda Carroll It took almost two years for Nicole Delien’s family to find someone who could explain the mysterious illness that was making their little girl “sleep” for as long as 64 days. During those excruciating 21 months doctors diagnosed everything from West Nile to epilepsy. Some even suggested that Nicole’s parents might be drugging her or somehow manipulating her sleep – an accusation that led to a report to Child Protective Services. Finally, when the family was at their wits end, they found Dr. Michael Rancurello at Allegheny General Hospital in Pittsburgh, who diagnosed Nicole, 17, with an exceedingly rare disorder called Kleine-Levin Syndrome. Rancurello wasn’t an expert in the syndrome, but by chance he’d already treated several patients with the disorder that periodically sends patients into a strange state in which they alternate between long stretches of actual sleep and periods of semi conscious delirium. Nicole was 6 years old when contracted a virus that seems to have sparked her condition. “In the beginning we thought she had the flu because she had flu-like symptoms and a high fever,” Vicki Delien, Nicole’s mom, told TODAY’s Savannah Guthrie. “But then she just became, as the days progressed, more confused and lethargic. We didn’t know what was going on. “ © 2012 NBCNews.com

Keyword: Sleep; Genes & Behavior
Link ID: 17521 - Posted: 11.21.2012

By Ferris Jabr After Thanksgiving dinner, many people start to feel a little drowsy. Turkey typically gets the blame. It supposedly contains high levels of tryptophan, an amino acid that is sold in a purified form to help people fall asleep. But turkey contains about the same amount of tryptophan as chicken, beef and other meats. If Thanksgiving drowsiness is not about the main course, what is responsible? It may have more to do with the side dishes. To understand, we first need to digest a little food chemistry. To start, we get tryptophan and other essential amino acids from all the protein in our diet, not just from meat. These amino acids swim through the bloodstream, nourishing our cells. Brain cells convert tryptophan into a chemical called serotonin. This neurotransmitter helps regulate sleep and appetite and high levels of serotonin are associated with calm and relaxation. But tryptophan and other amino acids can’t access brain cells on their own—instead, teams of proteins transport amino acids across the blood-brain barrier. As it turns out, Thanksgiving side dishes probably make it easier for tryptophan to get inside the brain. © 2012 Scientific American,

Keyword: Sleep
Link ID: 17520 - Posted: 11.21.2012

By ANAHAD O'CONNOR A new study of elementary and middle school students has found that those who are the youngest in their grades score worse on standardized tests than their older classmates and are more likely to be prescribed stimulants for attention deficit hyperactivity disorder. The findings suggest that in a given grade, students born at the end of the calendar year may be at a distinct disadvantage. Those perceived as having academic or behavioral problems may in fact be lagging simply as a result of being forced to compete with classmates almost a full year older than them. For a child as young as 5, a span of one year can account for 20 percent of the child’s age, potentially making him or her appear significantly less mature than older classmates. The new study found that the lower the grade, the greater the disparity. For children in the fourth grade, the researchers found that those in the youngest third of their class had an 80 to 90 percent increased risk of scoring in the lowest decile on standardized tests. They were also 50 percent more likely than the oldest third of their classmates to be prescribed stimulants for A.D.H.D. The differences diminished somewhat over time, the researchers found, but continued at least through the seventh grade. The new study, published in the journal Pediatrics, used data from Iceland, where health and academic measures are tracked nationally and stimulant prescription rates are high and on par with rates in the United States. Previous studies carried out there and in other countries have shown similar patterns, even among college students. Copyright 2012 The New York Times Company

Keyword: ADHD; Development of the Brain
Link ID: 17519 - Posted: 11.21.2012

By David Pogue Okay, great: we can control Our phones with speech recognition and our television sets with gesture recognition. But those technologies don't work in all situations for all people. So I say, forget about those crude beginnings; what we really want is thought recognition. As I found out during research for a recent NOVA episode, it mostly appears that brain-computer interface (BCI) technology has not advanced very far just yet. For example, I tried to make a toy helicopter fly by thinking “up” as I wore a $300 commercial EEG headset. It barely worked. Such “mind-reading” caps are quick to put on and noninvasive. They listen, through your scalp, for the incredibly weak remnants of electrical signals from your brain activity. But they're lousy at figuring out where in your brain they originated. Furthermore, the headset software didn't even know that I was thinking “up.” I could just as easily have thought “goofy” or “shoelace” or “pickle”—whatever I had thought about during the 15-second training session. There are other noninvasive brain scanners—magnetoencephalography, positron-emission tomography and near-infrared spectroscopy, and so on—but each also has its trade-offs. Of course, you can implant sensors inside someone's skull for the best readings of all; immobilized patients have successfully manipulated computer cursors and robotic arms using this approach. Still, when it comes to controlling everyday electronics, brain surgery might be a tough sell. © 2012 Scientific American,

Keyword: Robotics
Link ID: 17518 - Posted: 11.21.2012

By GRETCHEN REYNOLDS Is playing football like falling in love? That question, which would perhaps not occur to most of us watching hours of the bruising game this holiday season, is the focus of a provocative and growing body of new science examining the role of oxytocin in competitive sports. Oxytocin is, famously, the “love hormone,” a brain peptide known to promote positive intersocial relations. It makes people like one another, especially in intimate relationships. New mothers are awash in oxytocin (which is involved in the labor process), and it is believed that the hormone promotes bonding between mother and infant. New-formed romantic couples also have augmented bloodstream levels of the peptide, many studies show. The original attraction between the lovers seems to prompt the release of oxytocin, and, in turn, its actions in the brain intensify and solidify the allure. Until recently, though, scientists had not considered whether a substance that promotes cuddliness and warm, intimate bonding might also play a role in competitive sports. But the idea makes sense, says Gert-Jan Pepping, a researcher at the Center for Human Movement Sciences at the University of Groningen in The Netherlands, and the author of a new review of oxytocin and competition. “Being part of a team involves emotions, as for instance when a team scores, and these emotions are associated with brain chemicals.” Copyright 2012 The New York Times Company

Keyword: Hormones & Behavior; Emotions
Link ID: 17517 - Posted: 11.21.2012

By David P. Barash Critics claim that evolutionary biology is, at best, guesswork. The reality is otherwise. Evolutionists have nailed down how an enormous number of previously unexplained phenomena—in anatomy, physiology, embryology, behavior—have evolved. There are still mysteries, however, and one of the most prominent is the origins of homosexuality. The mystery is simple enough. Its solution, however, has thus far eluded our best scientific minds. The sine qua non for any trait to have evolved is for it to correlate positively with reproductive success, or, more precisely, with success in projecting genes relevant to that trait into the future. So, if homosexuality is in any sense a product of evolution—and it clearly is, for reasons to be explained—then genetic factors associated with same-sex preference must enjoy some sort of reproductive advantage. The problem should be obvious: If homosexuals reproduce less than heterosexuals—and they do—then why has natural selection not operated against it? The paradox of homosexuality is especially pronounced for individuals whose homosexual preference is exclusive; that is, who have no inclination toward heterosexuality. But the mystery persists even for those who are bisexual, since it is mathematically provable that even a tiny difference in reproductive outcome can drive substantial evolutionary change. Copyright 2012.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 17516 - Posted: 11.21.2012

The Associated Press Chimpanzees going through a midlife crisis? It sounds like a setup for a joke. But there it is, in the title of a report published Monday in a scientific journal: "Evidence for a midlife crisis in great apes." So what do these apes do? Buy red Ferraris? Leave their mates for some cute young bonobos? Uh, no. "I believe no ape has ever purchased a sports car," said Andrew Oswald, an author of the study. But researchers report that captive chimps and orangutans do show the same low ebb in emotional well-being at midlife that some studies find in people. That suggests the human tendency toward midlife discontent may have been passed on through evolution, rather than resulting simply from the hassles of modern life, said Oswald, a professor of economics at the University of Warwick in England who presented his work Monday in the Proceedings of the National Academy of Sciences. A second study in the journal looks at a younger age group and finds that happiness in youth can lead to higher income a few years down the road. Several studies have concluded that happiness in human adults tends to follow a certain course between ages 20 and 70: It starts high and declines over the years to reach a low point in the late 40s, then turns around and rises to another peak at 70. On a graph, that's a U-shaped pattern. Some researchers question whether that trend is real, but to Oswald the mystery is what causes it. "This is one of the great patterns of human life. We're all going to slide along this U for good or ill," he said. "So what explains it?" © CBC 2012

Keyword: Emotions; Development of the Brain
Link ID: 17515 - Posted: 11.20.2012