By ADAM NAGOURNEY and RICK LYMAN LOS ANGELES — In the heart of Northern California’s marijuana growing region, the sheriff’s office is inundated each fall with complaints about the stench of marijuana plots or the latest expropriation of public land by growers. Its tranquil communities have been altered by the emergence of a wealthy class of marijuana entrepreneurs, while nearly 500 miles away in Los Angeles, officials have struggled to regulate an explosion of medical marijuana shops. But at a time when polls show widening public support for legalization — recreational marijuana is about to become legal in Colorado and Washington, and voter initiatives are in the pipeline in at least three other states — California’s 17-year experience as the first state to legalize medical marijuana offers surprising lessons, experts say. Warnings voiced against partial legalization — of civic disorder, increased lawlessness and a drastic rise in other drug use — have proved unfounded. Instead, research suggests both that marijuana has become an alcohol substitute for younger people here and in other states that have legalized medical marijuana, and that while driving under the influence of any intoxicant is dangerous, driving after smoking marijuana is less dangerous than after drinking alcohol. Although marijuana is legal here only for medical use, it is widely available. There is no evidence that its use by teenagers has risen since the 1996 legalization, though it is an open question whether outright legalization would make the drug that much easier for young people to get, and thus contribute to increased use. And though Los Angeles has struggled to regulate marijuana dispensaries, with neighborhoods upset at their sheer number, the threat of unsavory street traffic and the stigma of marijuana shops on the corner, communities that imposed early and strict regulations on their operations have not experienced such disruption. © 2013 The New York Times Company

Keyword: Drug Abuse
Link ID: 18840 - Posted: 10.28.2013

If you were stung by a bark scorpion, the most venomous scorpion in North America, you’d feel something like the intense, painful jolt of being electrocuted. Moments after the creature flips its tail and injects venom into your skin, the intense pain would be joined by a numbness or tingling in the body part that was stung, and you might experience a shortness of breath. The effect of this venom on some people—small children, the elderly or adults with compromised immune systems—can even trigger frothing at the mouth, seizure-like symptoms, paralysis and potentially death. Based solely on its body size, the four-inch-long furry grasshopper mouse should die within minutes of being stung—thanks to the scorpion’s venom, which causes temporary paralysis, the muscles that allow the mouse to breathe should shut down, leading to asphyxiation—so you’d think the rodent would avoid the scorpions at all costs. But if you put a mouse and a scorpion in the same place, the rodent’s reaction is strikingly brazen. If stung, the four-inch-long rodent might jump back for a moment in surprise. Then, after a brief pause, it’ll go in for the kill and devour the scorpion piece by piece: This predatory behavior isn’t the result of remarkable toughness. As scientists recently discovered, the mouse has evolved a particularly useful adaptation: It’s immune to both the pain and paralytic effects that make the scorpion’s venom so toxic. Although scientists long knew that the mouse, native to the deserts of the American Southwest, preys upon a range of non-toxic scorpions, “no one had ever really asked whether they attack and kill really toxic scorpions,” says Ashlee Rowe of Michigan State University, who led the new study published today in Science.

Keyword: Pain & Touch; Evolution
Link ID: 18839 - Posted: 10.28.2013

Who would win in a fight: a bark scorpion or a grasshopper mouse? It seems like an easy call. The bark scorpion (Centruroides sculpturatus) delivers one of the most painful stings in the animal kingdom—human victims have compared the experience to being branded. The 25-gram grasshopper mouse (Onychomys torridus) is, well, a mouse. But as you can see in the video above, grasshopper mice routinely kill and eat bark scorpions, blissfully munching away even as their prey sting them repeatedly (and sometimes right in the face). Now, scientists have discovered why the grasshopper mice don’t react to bark scorpion stings: They simply don’t feel them. Evolutionary neurobiologist Ashlee Rowe at the University of Texas, Austin, has been studying the grasshopper mice’s apparent superpower since she was in graduate school. For the new study, she milked venom from nearly 500 bark scorpions and started experimenting. When she injected the venom into the hind paws of regular laboratory mice, the mice furiously licked the site for several minutes. But when she injected the same venom into grasshopper mice, they licked their paws for just a few seconds and then went about their business, apparently unfazed. In fact, the grasshopper mice appeared to be more irritated by injections of the saline solution Rowe used as a control. Rowe knew that grasshopper mice weren’t entirely impervious to pain—they reacted to injections of other painful chemicals such as formalin, just not the bark scorpion venom. To find out what was going on, she and her team decided to determine how the venom affects the grasshopper mouse’s nervous system, in particular the parts responsible for sensing pain. © 2013 American Association for the Advancement of Science

Keyword: Pain & Touch; Neurotoxins
Link ID: 18838 - Posted: 10.26.2013

By HELENE STAPINSKI IN an office of the American Museum of Natural History, a team of scientists, artists and multimedia experts were discussing what had poisoned Skippy, a cute Jack Russell terrier that had keeled over sick in his virtual backyard. Was it the chocolate he found in the garbage can? Did a snake, or a black widow spider, bite him? Or was a poisonous cane toad to blame? Skippy is just one of many victims in the museum’s show, “The Power of Poison,” opening Nov. 16, to which the staff was busy applying finishing touches. Using iPads, visitors can examine the circumstances surrounding Skippy’s fictional poisoning and, controlling their experience individually, take a crack at solving the mystery. But because the museum is popular with small children, Skippy does not die. Instead, his animated eyes turn into Xs, he runs erratically around the yard, he drools and he vomits a bit. Eventually, though, Skippy rallies to full health. “We were not going to make this a scary show,” said the exhibit’s curator, Dr. Mark Siddall. “Instead you walk out saying, ‘Wow. That was cool.’ ” Dr. Siddall spent two hours enthusiastically discussing poison and its properties at the museum recently, walking through some of the show’s highlights. The exhibit, which takes a look at poison’s role in nature, myth, medicine and human history, examines killer caterpillars, zombie ants and deadly vipers. It also looks at the possible victims, like the heavily slumbering Snow White. Plus the age-old question of what killed Cleopatra. Was it an asp, or something else? And while we’re at it, was Napoleon really poisoned with arsenic? © 2013 The New York Times Company

Keyword: Neurotoxins
Link ID: 18837 - Posted: 10.26.2013

by Linda Geddes Anaesthetics usually knock you out like a light. But by slowing the process down so that it takes 45 minutes to become totally unresponsive, researchers have discovered a new signature for unconsciousness. The discovery could lead to more personalised methods for administering anaesthetics and cut the risks associated with being given too high or too low a dose. It also sheds new light on what happens to our brain when we go under the knife. Hundreds of thousands of people are anaesthetised every day, yet researchers still don't fully understand what's going on in the anaesthetised brain. Nor is there a direct way of measuring when someone is truly unresponsive. Instead, anaesthetists rely on indirect measures such as heart and breathing rate, and monitoring reflexes. To investigate further, Irene Tracey and her colleagues at Oxford University slowed the anaesthesia process down. Instead of injecting the anaesthetic propofol in one go, which triggers unconsciousness in seconds, the drug was administered gradually so that it took 45 minutes for 16 volunteers to become fully anaesthetised. Their brain activity was monitored throughout using electroencephalography (EEG). The study was then repeated on 12 of these volunteers using functional magnetic resonance imaging (fMRI). EEG recordings revealed that before the volunteers became completely unresponsive to external stimuli they progressed through a sleep-like state characterised by slow-wave oscillations – a hallmark of normal sleep, in which neurons cycle between activity and inactivity. As the dose of anaesthetic built up, more and more neurons fell into this pattern, until a plateau was reached when no more neurons were recruited, regardless of the dose administered. © Copyright Reed Business Information Ltd.

Keyword: Consciousness; Sleep
Link ID: 18836 - Posted: 10.26.2013

By JAMES GORMAN Worldwide, 100,000 people have electrical implants in their brains to treat the involuntary movements associated with Parkinson’s disease, and scientists are experimenting with the technique for depression and other disorders. But today’s so-called deep brain stimulation only treats — it does not monitor its own effectiveness, partly because complex ailments like depression do not have defined biological signatures. The federal Defense Advanced Research Projects Agency, known as Darpa, announced Thursday that it intended to spend more than $70 million over five years to jump to the next level of brain implants, either by improving deep brain stimulation or by developing new technology. Justin Sanchez, Darpa program manager, said that for scientists now, “there is no technology that can acquire signals that can tell them precisely what is going on with the brain.” And so, he said, Darpa is “trying to change the game on how we approach these kinds of problems.” The new program, called Systems-Based Neurotechnology and Understanding for the Treatment of Neuropsychological Illnesses, is part of an Obama administration brain initiative, announced earlier this year, intended to promote innovative basic neuroscience. Participants in the initiative include Darpa, as well as the National Institutes of Health and the National Science Foundation. The announcement of Darpa’s goal is the first indication of how that research agency will participate in the initiative. The money is expected to be divided among different teams, and research proposals are now being sought. Darpa’s project is partly inspired by the needs of combat veterans who suffer from mental and physical conditions, and is the first to invest directly in researching human illness as part of the brain initiative. © 2013 The New York Times Company

Keyword: Depression; Parkinsons
Link ID: 18835 - Posted: 10.26.2013

By James Gallagher Health and science reporter, BBC News The mocked "obesity excuse" of being born with a slow metabolism is actually true for some people, say researchers. A team at the University of Cambridge has found the first proof that mutated DNA does indeed slow metabolism. The researchers say fewer than one in 100 people are affected and are often severely obese by early childhood. The findings, published in the journal Cell, may lead to new obesity treatments even for people without the mutation. Scientists at the Institute of Metabolic Science, in Cambridge, knew that mice born without a section of DNA, a gene called KSR2, gained weight more easily. But they did not know what effect it may be having in people, so they analysed the DNA of 2,101 severely obese patients. Some had mutated versions of KSR2. It had a twin effect of increasing their appetite while their slowing metabolism. "You would be hungry and wanting to eat a lot, you would not want to move because of a slower metabolism and would probably also develop type 2 diabetes at a young age," lead researcher Prof Sadaf Farooqi told the BBC. She added: "It slows the ability to burn calories and that's important as it's a new explanation for obesity." BBC © 2013

Keyword: Obesity; Genes & Behavior
Link ID: 18834 - Posted: 10.26.2013

By NELSON GRAVES Six years ago I suffered a stroke that forced me to relearn how to walk. The other day I ran a half-marathon. Strokes strike with stealth, but for me it was not entirely a surprise. During a physical in Milan in 2007, the doctor listened to my heart, then ordered an electrocardiogram. “Fair enough,” I reassured myself. “I’m 52 years old, and it’s no use taking anything for granted.” The nurse furrowed her brow as she studied the first read-out, then conducted a second, longer EKG. I put my shirt back on and returned to the doctor’s office. “I have some news for you,” he said. “You have atrial fibrillation. AF for short.” He wrote down the two words and explained they meant an irregular beating of the heart’s upper chambers. “It’s not life threatening. But it increases the risk of stroke six-fold.” I was too young to have a stroke. “I work 12-hour days, play squash three times a week and haven’t missed a day of work in 24 years,” I said. My attention piqued, I could now hear my heart’s irregular beat as I lay my head on my pillow. That must explain the dizziness when I get up at night to go to the bathroom. Or the fatigue at the end of a squash match. So when, on a September afternoon in Tokyo, my head began to spin wildly and I could hardly speak, I knew what was happening. After an ambulance ride to the hospital and an M.R.I., I heard the doctor say, “You’ve had a cerebral embolism.” That would be a stroke. Copyright 2013 The New York Times Company

Keyword: Stroke
Link ID: 18833 - Posted: 10.26.2013

by Tina Hesman Saey BOSTON — A variant in a gene involved in breaking down chemicals in smoke triples a smoker’s risk of multiple sclerosis, a study shows. Smoking increases by 30 to 50 percent a person’s risk of multiple sclerosis, a disease in which the immune system attacks a waxy coating around nerve cells. Scientists don’t know exactly how smoking contributes to the disease. Farren Briggs of the University of California, Berkeley and his colleagues searched DNA of thousands of people in Northern California, Norway and Sweden for genetic variants associated with both smoking and multiple sclerosis. The team found hundreds of variants in three genes involved in breaking down chemicals found in smoke, Briggs said October 24 at the annual meeting of the American Society of Human Genetics. In particular, people who smoke and who have two copies of a variant in the NAT1 gene have a risk of getting MS that is three times higher than that of smokers without the variant. For nonsmokers, the variant doesn’t increase MS risk. Citations F.B.S. Briggs et al. NAT1 in an important genetic effect modifier of tobacco smoke exposure in multiple sclerosis susceptibility in 5,453 individuals. American Society of Human Genetics annual meeting, Boston, October 24, 2013. Further Reading N. Seppa. Old drug may have new trick. Science News. Vol. 184, November 2, 2013, p. 16. N. Seppa. Black women may have highest multiple sclerosis rates. Science News. Vol. 183, June 15, 2013, p. 15. © Society for Science & the Public 2000 - 2013

Keyword: Multiple Sclerosis; Genes & Behavior
Link ID: 18832 - Posted: 10.26.2013

Kerri Smith Jack Gallant perches on the edge of a swivel chair in his lab at the University of California, Berkeley, fixated on the screen of a computer that is trying to decode someone's thoughts. On the left-hand side of the screen is a reel of film clips that Gallant showed to a study participant during a brain scan. And on the right side of the screen, the computer program uses only the details of that scan to guess what the participant was watching at the time. Anne Hathaway's face appears in a clip from the film Bride Wars, engaged in heated conversation with Kate Hudson. The algorithm confidently labels them with the words 'woman' and 'talk', in large type. Another clip appears — an underwater scene from a wildlife documentary. The program struggles, and eventually offers 'whale' and 'swim' in a small, tentative font. “This is a manatee, but it doesn't know what that is,” says Gallant, talking about the program as one might a recalcitrant student. They had trained the program, he explains, by showing it patterns of brain activity elicited by a range of images and film clips. His program had encountered large aquatic mammals before, but never a manatee. Groups around the world are using techniques like these to try to decode brain scans and decipher what people are seeing, hearing and feeling, as well as what they remember or even dream about. © 2013 Nature Publishing Group

Keyword: Vision; Brain imaging
Link ID: 18831 - Posted: 10.24.2013

By Tori Rodriguez The digestive tract and the brain are crucially linked, according to mounting evidence showing that diet and gut bacteria are able to influence our behavior, thoughts and mood. Now researchers have found evidence of bacterial translocation, or “leaky gut,” among people with depression. Normally the digestive system is surrounded by an impermeable wall of cells. Certain behaviors and medical conditions can compromise this wall, allowing toxic substances and bacteria to enter the bloodstream. In a study published in the May issue of Acta Psychiatrica Scandinavica, approximately 35 percent of depressed participants showed signs of leaky gut, based on blood tests. The scientists do not yet know how leaky gut relates to depression, although earlier work offers some hints. Displaced bacteria can activate autoimmune responses and inflammation, which are known to be associated with the onset of depression, lower mood and fatigue. “Leaky gut may maintain increased inflammation in depressed patients,” which could exacerbate the symptoms of depression if not treated, says Michael Maes, a research psychiatrist with affiliations in Australia and Thailand and an author of the paper. Currently leaky gut is treated with a combination of glutamine, N-acetylcysteine and zinc—believed to have anti-inflammatory or antioxidant properties—when behavioral and dietary modifications fail. © 2013 Scientific American

Keyword: Obesity
Link ID: 18830 - Posted: 10.24.2013

Amanda Mascarelli Duplication of a single gene — and too much of the corresponding protein in brain cells — causes mice to have seizures and display manic-like behaviour, a study has found. But a widely used drug reversed the symptoms, suggesting that it could also help some people with hyperactivity who do not respond to common treatments. Smooth functioning at the synapses, the junctions between brain cells, is crucial to functions that control everything from social etiquette to everyday decision-making. It is increasingly thought that some neuropsychiatric disorders are caused by function of the synapses going awry1, and indeed researchers have found that neuropsychiatric conditions such as schizophrenia and autism can sometimes be traced to missing, mutated or duplicated copies of SHANK32, a gene that encodes one of the 'architectural' proteins that help to ensure that messages are relayed properly between cells. Some people with attention deficit hyperactivity disorder (ADHD), Asperger's syndrome or schizophrenia have an extra copy of a wider region of DNA that contains SHANK33. To explore the role of SHANK3, Huda Zoghbi, a neurogeneticist at Baylor College of Medicine in Houston, Texas, and her colleagues created mice with duplicate copies of the gene. “The mouse was remarkably hyperactive, running around like mad,” says Zoghbi. But the animals did not respond to stimulant medications typically used to treat ADHD. Instead, their hyperactivity grew much worse. “That’s when we knew this was not typical ADHD,” says Zoghbi. The study is published today in Nature4. © 2013 Nature Publishing Group

Keyword: ADHD; Genes & Behavior
Link ID: 18829 - Posted: 10.24.2013

Stroke deaths and illnesses are likely to continue shifting younger, global research suggests. In the Global and Regional Burden of Stroke in 1999-2010 study published in Thursday's issue of the medical journal The Lancet, researchers take a comprehensive look at stroke rates by country and region. "Stroke burden worldwide continues to increase," Prof. Valery Feigin, director of the National Institute for Stroke and Applied Neurosciences at AUT University in New Zealand said in an interview. "It's increasing at increased pace, more than we expected, disproportionately affecting low-to middle-income countries." The proportion of stroke in people younger than 65 is substantial, Feigin's team said. More than 83,000 children and youths aged 20 years and younger are affected by stroke annually. Feigin said the epidemic of obesity, and Type 2 diabetes in children and young people is increasing worldwide, which will be important risk factors for stroke 20 or 30 years down the road. If the trends in low-income and middle-income countries continue, by 2030 there will be almost 12 million stroke deaths and 70 million stroke survivors worldwide, the researchers projected. More than 90 per cent of strokes are preventable through lifestyle changes such as improving diet, quitting smoking, reducing salt and alcohol intake, increasing physical activity and managing stress, Feigin said.

Keyword: Stroke
Link ID: 18828 - Posted: 10.24.2013

By Gary Stix The Obama administration’s neuroscience initiative highlights new technologies to better understand the workings of brain circuits on both a small and large scale. Various creatures, from roundworms to mice, will be centerpieces of that program because the human brain is too complex—and the ethical issues too intricate—to start analyzing the actual human organ in any meaningful way. But what if there were already a means to figure out how the brain wires itself up and, in turn, to use this knowledge to study what happens in various neurological disorders of early life? Reports in scientific journals have started to trickle in on the way stem cells can spontaneously organize themselves into complex brain tissue—what some researchers have dubbed mini-brains. Christopher A. Walsh, Bullard Professor of pediatrics and neurology at Harvard Medical School, talked to Scientific American about the importance of just such work for understanding brain development and neurological disease. (Also, check out the Perspective Walsh did for Science on this topic, along with Byoung-il Bae.) In order to be able to understand the way the brain solves this tremendously complex problem of wiring itself up, we need to be able to study it rigorously in the laboratory. We need some sort of model. We can’t just take humans and put them under the microscope, so we have to find some way of modeling the brain. The mouse has been tremendously useful for understanding brain wiring and how cells in the brain form. And the mouse will continue to be very useful. The mouse is particularly useful in studying cellular effects of particular genes, but, as we get smarter and smarter about what the problems are, we’re increasingly able to think, not about things that we share with mice, but the differences that distinguish us from mice. © 2013 Scientific American

Keyword: Development of the Brain; Brain imaging
Link ID: 18827 - Posted: 10.24.2013

People with Parkinson's disease are dancing at the National Ballet School as part of a study into how learning dance moves can change the brain. Anecdotally, learning to dance seems to improve motor skills in the short-term among people with Parkinson's disease, a neurological disorder that interferes with gait and balance. As part of a 12-week program, 20 people with Parkinson's disease are taking weekly dance classes at the National Ballet School in Toronto. The classes began in September. The research team is led by neuroscientist Prof. Joseph DeSouza of York University's Faculty of Health and National Ballet School instructor Rachel Bar. The volunteers are also getting a series of functional MRI scans to help researchers understand how the brain reacts and learns. "We know that balance can improve and gait can improve and even there's social benefits but we want to see why that's happening, how is it happening? To do that, we're looking inside the brain," Bar said. People aren't able to dance in scanner but they are asked to visualize the dance while listening to the accompanying music. "If you visualize a dance, theoretically you're using almost all the same neural circuitry as if you were doing it," DeDouza said. The hypothesis is that the brain of someone with Parkinson's may develop new paths around damaged areas if stimulated by the movement of dance. © CBC 2013

Keyword: Parkinsons
Link ID: 18826 - Posted: 10.23.2013

By Phil Plait Thanks to my evil twin Richard Wiseman (a UK psychologist who specializes in studying the ways we perceive things around us, and how easily we can be fooled), I saw this masterful illusion video that will keep you guessing on what’s real and what isn’t. It’s only two minutes long, so give it a gander: Cool, eh? The reason you got fooled, at least twice, is that we get confused when our three-dimensional world is translated into two dimensions. We perceive distance for nearby objects using binocular vision, which depends on the angles between our eyes and the objects. If you create a picture of an object that is carefully distorted to match those changing angles, you can fool the brain into thinking it’s seeing a real object when in fact it’s a flat representation. We’re actually very good at taking subtle cues and turning them into three-dimensional interpretations. However, because of that very sensitivity, it’s easy to throw a monkey in the wrench, messing up our perception. Still don’t believe me? Then watch this, and if it doesn’t melt your brain, I can no longer help you. Our brains are very, very easy to fool. I’ll note that the way we see color is very easy to trick, too. I wrote an article about a fantastic, astonishing color illusion back in 2009, and it spurred a lot of arguments in the comments, even when I showed clearly how it works. Amazing. © 2013 The Slate Group, LLC

Keyword: Vision
Link ID: 18825 - Posted: 10.23.2013

Special Note to Teachers: The content of the following lesson plans compares the “normal” brain to a “zombie” brain. Zombies are not real but there are plenty of diseases that effect real people and students may have people in their lives who have suffered because of them. The following lessons about neuroscience have been inspired by the book, “The Zombie Autopsies”, written by Steven C. Schlozman, M.D., and are intended to compliment it. “The Zombie Autopsies” was inspired by George Romero’s 1968 cult-classic horror film “Night of the Living Dead”. These original lessons build upon each other and have an accompanying plot line where the world is fighting a zombie apocalypse and the best and the brightest young people are being trained as medical students – with a specialty in neuroscience – with the hopes that they will be able to provide a cure to this terrible epidemic and save humanity. For a richer experience have the students read the book in class and as homework (see suggested reading schedule) along with the class activities. Although the materials are organized as a unit, lessons can be used as stand-alone or can be shaped to fit the needs of you and your students regarding time and content. For example, Lesson 3 is perfect for the day of Halloween. © 2013 MacNeil-Lehrer Productions

Keyword: Learning & Memory
Link ID: 18824 - Posted: 10.23.2013

When frogs croak, the fringe-lipped bat, Trachops cirrhosus, listens. The bats use the sounds to track and feed on amphibians and to share dining tips with neighbors. In a new study, Patricia Jones of the University of Texas at Austin and colleagues trained a few frog-eating bats to associate a cell phone ringtone with food. Some of the bats reliably got food when they heard the phone ring. Others did not. The bats that failed to get food using their own cues paid more attention to new ones that their fellow mammals shared. Social learning becomes much more important if a bat is unsuccessful at finding food, the scientists report October 22 in the Proceedings of the Royal Society B. Observing how bats forage alone and together may help scientists understand the way new hunting behaviors spread through animal populations. It may also give insight to animals’ potential for cultivating culture, the authors suggest. © Society for Science & the Public 2000 - 2013.

Keyword: Learning & Memory
Link ID: 18823 - Posted: 10.23.2013

Katherine Harmon Courage An infant's innate sense for numbers predicts how their mathematical aptitude will develop years later, a team of US researchers has found. Babies can spot if a set of objects increases or decreases in number — for instance, if the number of dots on a screen grows, even when dot size, colour and arrangement also change. But until recently, researchers could generally only determine the number sense of groups of babies, thus ruling out the ability to correlate this with later mathematics skills in individuals. In 2010, Elizabeth Brannon, a neuroscientist at Duke University in Durham, North Carolina, and her colleagues demonstrated that they could test and track infants' number sense over time1. To do this, six-month-old babies are presented with two screens. One shows a constant number of dots, such as eight, changing in appearance, and the other also shows changing dots but presents different numbers of them — eight sometimes and 16 other times, for instance. An infant who has a good primitive number sense will spend more time gazing at the screen that presents the changing number of dots. In the latest work, which is published in this week's Proceedings of the National Academy of Sciences2, Brannon's team took a group of 48 children who had been tested at six months of age and retested them three years later, using the same dot test but also other standard maths tests for preschoolers — including some that assessed the ability to count, to tell which of two numbers is larger and to do basic calculations. © 2013 Nature Publishing Group

Keyword: Attention; Development of the Brain
Link ID: 18822 - Posted: 10.22.2013

By Scott Barry Kaufman One of the longest standing assumptions about the nature of human intelligence has just been seriously challenged. According to the traditional “investment” theory, intelligence can be classified into two main categories: fluid and crystallized. Differences in fluid intelligence are thought to reflect novel, on-the-spot reasoning, whereas differences in crystallized intelligence are thought to reflect previously acquired knowledge and skills. According to this theory, crystallized intelligence develops through the investment of fluid intelligence in a particular body of knowledge. As far as genetics is concerned, this story has a very clear prediction: In the general population– in which people differ in their educational experiences– the heritability of crystallized intelligence is expected to be lower than the heritability of fluid intelligence. This traditional theory assumes that fluid intelligence is heavily influenced by genes and relatively fixed, whereas crystallized intelligence is more heavily dependent on acquired skills and learning opportunities. But is this story really true? In a new study, Kees-Jan Kan and colleagues analyzed the results of 23 independent twin studies conducted with representative samples, yielding a total sample of 7,852 people. They investigated how heritability coefficients vary across specific cognitive abilities. Importantly, they assessed the “Cultural load” of various cognitive abilities by taking the average percentage of test items that were adjusted when the test was adapted for use in 13 different countries. © 2013 Scientific American

Keyword: Intelligence; Genes & Behavior
Link ID: 18821 - Posted: 10.22.2013