Chapter 7. Life-Span Development of the Brain and Behavior
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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
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
By MAGGIE KOERTH-BAKER Between the fall of 2011 and the spring of 2012, people across the United States suddenly found themselves unable to get their hands on A.D.H.D. medication. Low-dose generics were particularly in short supply. There were several factors contributing to the shortage, but the main cause was that supply was suddenly being outpaced by demand. The number of diagnoses of Attention Deficit Hyperactivity Disorder has ballooned over the past few decades. Before the early 1990s, fewer than 5 percent of school-age kids were thought to have A.D.H.D. Earlier this year, data from the Centers for Disease Control and Prevention showed that 11 percent of children ages 4 to 17 had at some point received the diagnosis — and that doesn’t even include first-time diagnoses in adults. (Full disclosure: I’m one of them.) That amounts to millions of extra people receiving regular doses of stimulant drugs to keep neurological symptoms in check. For a lot of us, the diagnosis and subsequent treatments — both behavioral and pharmaceutical — have proved helpful. But still: Where did we all come from? Were that many Americans always pathologically hyperactive and unable to focus, and only now are getting the treatment they need? Probably not. Of the 6.4 million kids who have been given diagnoses of A.D.H.D., a large percentage are unlikely to have any kind of physiological difference that would make them more distractible than the average non-A.D.H.D. kid. It’s also doubtful that biological or environmental changes are making physiological differences more prevalent. Instead, the rapid increase in people with A.D.H.D. probably has more to do with sociological factors — changes in the way we school our children, in the way we interact with doctors and in what we expect from our kids. © 2013 The New York Times Company
Research indicates that indeed Americans girls and boys are going through puberty earlier than ever, though the reasons are unclear. Many believe our widespread exposure to synthetic chemicals is at least partly to blame, but it’s hard to pinpoint exactly why our bodies react in certain ways to various environmental stimuli. Researchers first noticed the earlier onset of puberty in the late 1990s, and recent studies confirm the mysterious public health trend. A 2012 analysis by the U.S. Centers for Disease Control and Prevention (CDC) found that American girls exposed to high levels of common household chemicals had their first periods seven months earlier than those with lower exposures. “This study adds to the growing body of scientific research that exposure to environmental chemicals may be associated with early puberty,” says Danielle Buttke, a researcher at CDC and lead author on the study. Buttke found that the age when a girl has her first period (menarche) has fallen over the past century from an average of age 16-17 to age 12-13. Earlier puberty isn’t just for girls. In 2012 researchers from the American Academy of Pediatrics (AAP) surveyed data on 4,100 boys from 144 pediatric practices in 41 states and found a similar trend: American boys are reaching puberty six months to two years earlier than just a few decades ago. African-American boys are starting the earliest, at around age nine, while Caucasian and Hispanics start on average at age 10. One culprit could be rising obesity rates. Researchers believe that puberty (at least for girls) may be triggered in part by the body building up sufficient reserves of fat tissue, signaling fitness for reproductive capabilities. Clinical pediatrician Robert Lustig of Benioff Children’s Hospital in San Francisco reports that obese girls have higher levels of the hormone leptin which in and of itself can lead to early puberty while setting off a domino effect of more weight gain and faster overall physical maturation. © 2013 Scientific American,
By Brian Palmer Myopia isn’t an infectious disease, but it has reached nearly epidemic proportions in parts of Asia. In Taiwan, for example, the percentage of 7-year-old children suffering from nearsightedness increased from 5.8 percent in 1983 to 21 percent in 2000. An incredible 81 percent of Taiwanese 15-year-olds are myopic. If you think that the consequences of myopia are limited to a lifetime of wearing spectacles—and, let’s be honest, small children look adorable in eyeglasses—you are mistaken. The prevalence of high myopia, an extreme form of the disorder, in Asia has more than doubled since the 1980s, and children who suffer myopia early in life are more likely to progress to high myopia. High myopia is a risk factor for such serious problems as retinal detachment, glaucoma, early-onset cataracts, and blindness. The explosion of myopia is a serious public health concern, and doctors have struggled to identify the source of the problem. Nearsightedness has a strong element of heritability, but the surge in cases shows that a child’s environment plays a significant role. A variety of risk factors has been linked to the disorder: frequent reading, participation in sports, television watching, protein intake, and depression. When each risk factor was isolated, however, its overall effect on myopia rates seemed to be fairly minimal. Researchers believe they are now closing in on a primary culprit: too much time indoors. In 2008 orthoptics professor Kathryn Rose found that only 3.3 percent of 6- and 7-year-olds of Chinese descent living in Sydney, Australia, suffered myopia, compared with 29.1 percent of those living in Singapore. The usual suspects, reading and time in front of an electronic screen, couldn’t account for the discrepancy. The Australian cohort read a few more books and spent slightly more time in front of the computer, but the Singaporean children watched a little more television. On the whole, the differences were small and probably canceled each other out. The most glaring difference between the groups was that the Australian kids spent 13.75 hours per week outdoors compared with a rather sad 3.05 hours for the children in Singapore. © 2013 The Slate Group, LLC.
By Christopher Wanjek and LiveScience Your liver could be "eating" your brain, new research suggests. People with extra abdominal fat are three times more likely than lean individuals to develop memory loss and dementia later in life, and now scientists say they may know why. It seems that the liver and the hippocampus (the memory center in the brain), share a craving for a certain protein called PPARalpha. The liver uses PPARalpha to burn belly fat; the hippocampus uses PPARalpha to process memory. In people with a large amount of belly fat, the liver needs to work overtime to metabolize the fat, and uses up all the PPARalpha — first depleting local stores and then raiding the rest of the body, including the brain, according to the new study. The process essentially starves the hippocampus of PPARalpha, thus hindering memory and learning, researchers at Rush University Medical Center in Chicago wrote in the study, published in the current issue of Cell Reports. Other news reports were incorrect in stating that the researchers established that obese individuals were 3.6 times more likely than lean individuals to develop dementia. That finding dates back to a 2008 study by researchers at the Kaiser Permanente Division of Research in Oakland, Calif. In another study, described in a 2010 article in the Annals of Neurology, researchers at Boston University School of Medicine found that the greater the amount of belly fat, the greater the brain shrinkage in old age. © 2013 Scientific American
By SINDYA N. BHANOO Hungry babies instinctively open their mouths as their mother’s breast or a bottle draws near. Now, researchers from England and France report that this instinct — the anticipation of touch — is a skill fetuses teach themselves in the womb. Studying scans at monthly intervals between 24 and 36 weeks of pregnancy, the scientists found that the youngest fetuses were more likely to touch their heads and that as they matured, they began to touch their mouths more. And by 36 weeks, the fetuses began to open their mouths before they touched them. The anticipation of touch is a skill a baby uses during feeding, said Nadja Reissland, a psychologist at Durham University in England, who reports the findings along with colleagues in the journal Developmental Psychobiology. “We can’t say it’s a precursor to feeding, but it’s one element of feeding,” she said. “You actually need to open your mouth in order to feed.” Premature babies may not have fully grasped this skill, Dr. Reissland said. The study could provide more information about what premature babies can do and what special care they need. “The fetus might actually be learning the limits of its body, the texture of the body and what it feels like to be a person in the womb,” she said. © 2013 The New York Times Company
Keyword: Development of the Brain
Link ID: 18786 - Posted: 10.15.2013
By JANE E. BRODY Fifty years ago, a revolution began in neonatal care that has preserved the physical and mental health, and often the lives, of thousands of babies: screening of newborns for inherited and congenital disorders. On Oct. 15, 1963, the first law requiring that all newborns be screened for phenylketonuria, or PKU, took effect in Massachusetts. PKU, an inherited metabolic disorder, afflicts one in 20,000 of the four million babies born each year in the United States. Children with PKU are missing an enzyme that converts the amino acid phenylalanine to tyrosine, and unless they remain on a special protein-restricted diet, the resulting buildup of phenylketone damages the brain and causes mental retardation and physical disabilities. Today every state tests babies at birth for PKU — and not just that. There are now more than 50 disorders that can be picked up through screening, 31 of which comprise the “core conditions” of the government’s Recommended Uniform Screening Panel. Other conditions are likely to be added to the panel in the future. All but two of them — hearing loss and critical congenital heart disease — can be detected by automated analysis of a few drops of dried blood from a heel stick done within a few days of birth. Giana Swift, a fifth grader in Sherman Oaks, Calif., was one of more than 12,500 babies who benefit from newborn screening each year. The story of her birth in October 2002 was recounted in The Times. Through a pilot screening program, Giana was found to have an inherited metabolic disorder called 3-MCC (3-methylcrotonyl-CoA carboxylase deficiency). It afflicts about 100 babies a year, rendering them unable to process the amino acid leucine. As with PKU, toxic byproducts of the unprocessed amino acid build up in the blood and damage the brain. Because she was tested at birth, Giana thrived, first on a special leucine-free baby formula, then on a diet nearly free of protein. Her grateful father, David Swift, 44, recently described Giana as “very bright, precocious, happy and a top athlete.” Copyright 2013 The New York Times Company
Kashmira Gander A team in Bristol have created an implant that encourages cells damaged by the disease to grow again. It does this through a system of tubes and catheters that pump proteins into patients’ brain once a month, potentially stopping the disease from progressing by encouraging the damaged cells to grow again. The port located behind a patient’s ear releases a protein called glial cell line-derived neurotrophic factor (GDNF). Six patients at Frenchay Hospital, Bristol, have trialled the system, and doctors are now looking for another 36 to help them continue their research. Dr Kieran Breen, director of research and innovation at Parkinson's UK, said: “For years, the potential of GDNF as a treatment for Parkinson's has remained one of the great unanswered research questions. ”This new study will take us one step closer to finally answering this question once and for all. “We believe GDNF could have the potential to unlock a new approach for treating Parkinson's that may be able to slow down and ultimately stop the progression of the condition all together. ”Currently there are very few treatments available for people with Parkinson's and none capable of stopping the condition from advancing.“ More than 127,000 people in the UK currently have the disease, which is caused when nerve cells in the brain die due to a lack of the chemical dopamine. Symptoms include slowness of movement, stiffness and tremors. © independent.co.uk
by Laura Sanders After Baby V joined our team, one of the first things people would ask is, “Are you getting any sleep?” (The answer was, and is, no.) The recurring question highlights how sorely lacking sleep is for new parents. Capitalism noticed us tired parents, too: Countless products beckon exhausted families with promises of eight, 10, even 12 hours of blissful, uninterrupted sleep. You can buy special swaddles, white noise machines, swings that sway like a moving car and books upon books that whisper contradictory secrets of how to get your baby to sleep through the night. (If you don’t have time to read them all, mother-of-twins Ava Neyer helpfully breaks down all of the advice for you.) As the owner of a stack of such books, I was intrigued by this recent review: “Behavioral sleep interventions in the first six months of life do not improve outcomes for mothers or infants: A systematic review.” Excuse me? The Sleep Sheep, the Baby Whisperer and the Sleep Lady lied to me? At the behest of the United Kingdom’s National Institute for Health Research, Australians Pamela Douglas and Peter Hill combed through the existing scientific literature on sleep interventions looking for benefits. These interventions included delaying responses to infant cues (also known by its cold-hearted name of “crying it out”), sticking to a feeding or sleeping schedule and other ways that aim to teach a baby how to fall asleep without the need to eat or be held. After analyzing 43 studies on infant sleep interventions, the team concluded that these methods weren’t beneficial for babies younger than six months, or their mothers. The studies didn’t convincingly show that interventions curb infant crying, prevent sleep or behavioral problems later or protect against maternal depression, Douglas and Hill write in the September Journal of Developmental & Behavioral Pediatrics. © Society for Science & the Public 2000 - 2013.
Children whose mothers are depressed during pregnancy have a small increased risk of depression in adulthood, according to a UK study. Medical treatment during pregnancy could lower the risk of future mental health problems in the child, say researchers at Bristol University. The study followed the offspring of more than 8,000 mothers who had postnatal or antenatal depression. The risk is around 1.3 times higher than normal at age 18, it found. The study is published in JAMA Psychiatry. Lead researcher Dr Rebecca Pearson told the BBC: "Depression in pregnancy should be taken seriously and treated in pregnancy. It looks like there is a long-term risk to the child, although it is small." She said it was an association, not a causal link, and needed further investigation. Prof Carmine Pariante of King's College London's Institute of Psychiatry said the development of an individual's mental health did not start at birth but in the uterus. "The message is clear - helping women who are depressed in pregnancy will not only alleviate their suffering but also the suffering of the next generation." Prof Celso Arango of Gregorio Maranon General University Hospital, Madrid, said stress hormones may affect the child's development in the womb. "Women with depression would ideally be treated before getting pregnant, but if they are already pregnant when diagnosed with depression it is even more important that they are treated as it will impact on the mother and child." The researchers think different factors may be involved in antenatal and postnatal depression, with environmental factors such as social support having a bigger impact in postnatal depression. BBC © 2013
Charlie Cooper Scientists have hailed an historic “turning point” in the search for a medicine that could beat Alzheimer's disease, after a drug-like compound was used to halt brain cell death in mice for the first time. Although the prospect of a pill for Alzheimer's remains a long way off, the landmark British study provides a major new pathway for future drug treatments. The compound works by blocking a faulty signal in brains affected by neurodegenerative diseases, which shuts down the production of essential proteins, leading to brain cells being unprotected and dying off. It was tested in mice with prion disease - the best animal model of human neurodegenerative disorders - but scientists said they were confident the same principles would apply in a human brain with debilitating brain diseases such as Alzheimer's or Parkinson's. The study, published today in the journal Science Translational Medicine, was carried out at the Medical Research Council's (MRC) Toxicology Unit at the University of Leicester. “It's a real step forward,” team leader Professor Giovanna Mallucci told The Independent. “It's the first time a substance has been given to mice that prevents brain disease. The fact that this is a compound that can be given orally, that gets into the brain and prevents brain disease, is a first in itself… We can go forward and develop better molecules and I can't see why preventing this process should only be restricted to mice. I think this probably will translate into other mammalian brains.” © independent.co.uk
Link ID: 18775 - Posted: 10.10.2013
By MICHAEL TORTORELLO SONOMA, Calif. — Here is a truth about children with autism: they grow up to become adults with autism. Advocates estimate that over the next decade some 500,000 such individuals will come of age in the United States. No one can say for sure what adulthood will hold for them. To start, where will everyone live and work? A 2008 Easter Seals study found that 79 percent of young adults with autism spectrum disorders continue to reside with their parents. A solid majority of them have never looked for a job. And yet the life expectancy of people with autism is more or less average. Here is another truth, then, about children with autism: they can’t stay at home forever. This realization — as obvious as it is worrying — has recently stirred the beginnings of a response from researchers, architects and, not least, parents. In 2009, a pair of academics, Kim Steele and Sherry Ahrentzen, collaborated on “Advancing Full Spectrum Housing,” a comprehensive design guideline for housing adults with autism. (An expanded book on the topic is scheduled to come out next year.) Perhaps the first development to closely follow their template is Sweetwater Spectrum, a residence for 16 adults whose abilities and disabilities span the full range of autism. The innovative $10.4 million project opened in January in the heart of California wine country, and its founding families and board hope to make Sweetwater a model for like-minded experiments across the country. “You hear about different organizations planning to do these things,” said Dr. Ahrentzen, a professor in the Shimberg Center for Housing Studies at the University of Florida, in Gainesville. But “it takes time to get all these different funding sources in place.” © 2013 The New York Times Company
Link ID: 18774 - Posted: 10.10.2013
by Bruce Bower Babies may start to learn their mother tongues even before seeing their mothers’ faces. Newborns react differently to native and foreign vowel sounds, suggesting that language learning begins in the womb, researchers say. Infants tested seven to 75 hours after birth treated spoken variants of a vowel sound in their home language as similar, evidence that newborns regard these sounds as members of a common category, say psychologist Christine Moon of Pacific Lutheran University in Tacoma, Wash., and her colleagues. Newborns deemed different versions of a foreign vowel sound to be dissimilar and unfamiliar, the scientists report in an upcoming Acta Paediatrica. “It seems that there is some prenatal learning of speech sounds, but we do not yet know how much,” Moon says. Fetuses can hear outside sounds by about 10 weeks before birth. Until now, evidence suggested that prenatal learning was restricted to the melody, rhythm and loudness of voices (SN: 12/5/09, p. 14). Earlier investigations established that 6-month-olds group native but not foreign vowel sounds into categories. Moon and colleagues propose that, in the last couple months of gestation, babies monitor at least some vowels — the loudest and most expressive speech sounds — uttered by their mothers. © Society for Science & the Public 2000 - 2013
By Helen Briggs BBC News The brain has a critical window for language development between the ages of two and four, brain scans suggest. Environmental influences have their biggest impact before the age of four, as the brain's wiring develops to process new words, say UK and US scientists. The research in The Journal of Neuroscience suggests disorders causing language delay should be tackled early. It also explains why young children are good at learning two languages. The scientists, based at King's College London, and Brown University, Rhode Island, studied 108 children with normal brain development between the ages of one and six. They used brain scans to look at myelin - the insulation that develops from birth within the circuitry of the brain. To their surprise, they found the distribution of myelin is fixed from the age of four, suggesting the brain is most plastic in very early life. Any environmental influences on brain development will be strongest in infanthood, they predict. This explains why immersing children in a bilingual environment before the age of four gives them the best chance of becoming fluent in both languages, the research suggests. BBC © 2013
Alison Abbott In a sign that psychiatric-disease research is entering a new era, the pharmaceutical giant Novartis has hired an expert in neural circuitry, rather than pharmacology, to head its relaunched neuroscience division. The appointment of 42-year-old Ricardo Dolmetsch, who has spent his entire career in academic research, signifies a radical policy shift for the company, as it moves away from conventional neurotransmitter research to concentrate on analysing the neural circuitry that causes brain diseases. The decision suggests Novartis is confident that after years of fruitless research in the field, revolutionary advancements in, for example, genetic and stem-cell technologies will pay dividends. The company intends to hire 100 new staff members for the department over the next 3 years. But the move is risky: even if it pans out, new drugs for common disorders such as schizophrenia could be decades away from reaching the market. Dolmetsch, a former senior director at the Allen Institute for brain Science in Seattle, Washington, who has also worked at Stanford University School of Medicine in California, says that his new role gives him access to previously unimaginable resources. “I had this idea that big pharma was a slow, plodding, conservative giant,” he says. “I was surprised by the depth of science at Novartis.” An expert in autism spectrum disorder, he was also attracted by the prospect of contributing to the development of therapies — something that academic institutions are poorly equipped to do — particularly because one of his own sons has autism. There was “not much enthusiasm” for studying disease at the Allen Institute, which focuses instead on basic research into brain science, he says. © 2013 Nature Publishing Group
by Linda Geddes There's little doubt that smoking during pregnancy is bad for the baby. But besides stunting growth and boosting the risk of premature birth, it seems that tobacco smoke leaves a lasting legacy on the brain. Children whose mothers smoked during pregnancy have altered brain growth, which may put them at greater risk of anxiety and depression. Hanan El Marroun at Erasmus Medical Center in Rotterdam, the Netherlands, and her colleagues had previously seen impaired brain growth in babies born to women who smoked throughout their pregnancy, although no differences were seen if women stopped smoking soon after learning that they were pregnant. The question was whether these changes were permanent, or would correct themselves as the child developed. So El Marroun's team used MRI to look at the brains of 113 children aged between 6 and 8 years old whose mothers smoked during pregnancy, and another 113 children whose mums did not. The children's behavioural and emotional functioning was also tested. Depression link Those whose mothers smoked throughout pregnancy had smaller total brain volumes and reduced amounts of grey and white matter in the superior frontal cortex, an area involved in regulating moods. What's more, these structural differences correlated with symptoms of depression and anxiety in the children. Not every child whose mother smoked showed these symptoms, and the study could not definitively prove cause and effect. However, because we already know that smoking is bad for babies, pregnant women should continue to be advised not to smoke, El Marroun says. © Copyright Reed Business Information Ltd.
By Rebecca Lanning, Everywhere I went, people asked me about my son Will. They knew he’d graduated from high school, and they wanted to know what he was doing. Smiling politely, I told them that Will had been accepted to his first-choice college. But, I always added — in case someone saw him around town — that he had deferred enrollment. He was taking a gap year, I’d say. “So what’s your son doing with his windfall of free time? Traveling abroad? Doing research?” My cheeks burned as I played along, offering sound bites. A start-up venture. A film project. Independent study. Anything to avoid the truth: that my handsome, broad-shouldered son was, probably, at that very moment, home in bed with the shutters drawn, covers pulled over his head. Officially, Will was taking a gap year. But after 13 years of school, what he needed, what he’d earned, was a nap year. Will has long suffered from learning difficulties. It took years to pinpoint a diagnosis — and even when we did, figuring out how to manage it wasn’t easy. He needed a break. So did I. Will’s problems began to surface when he was in kindergarten. “He’s not where the other children are,” his teacher whispered to me one morning. I knew what she meant. Clumsy and slow to read, Will rested his head on his desk a lot. His written work, smudgy from excessive erasing, looked like bits of crumpled trash. School was torture for Will. He couldn’t take notes, failed to turn in homework, forgot when tests were coming up. Yet on standardized tests, his verbal scores consistently exceeded the 99th percentile. I wondered why he struggled, when clearly he was bright. © 1996-2013 The Washington Post
by Linda Geddes They are identical in almost every way, except one twin is fat and the other is thin. Now a study of this rare group is shedding light on a medical mystery: how some people can be obese and perfectly healthy. Obesity usually goes hand in hand with metabolic syndrome – high blood pressure, high cholesterol and type 2 diabetes – but a minority of obese people escape this fate. To probe the fit fat phenomenon, Jussi Naukkarinen at the University of Helsinki in Finland and his colleagues turned to a registry of identical twins, picking 16 pairs whose body weight differed by 17 kilograms on average. They are a perfect model for studying such differences because they are genetically identical and have usually been raised in very similar environments. Naukkarinen's team started by looking at the siblings' body fat distribution and quickly saw that the fat twins fell into two groups: those that tended to accumulate fat within their livers, and those whose liver fat resembled that of their thin twin. Suppressed activity Next, they looked at other markers of ill-health, including insulin resistance, cholesterol, inflammation and blood pressure. These measures also divided the group. "Basically all the hallmarks of the metabolic syndrome were lacking in the group where there was no liver fat," Naukkarinen says. Researchers also compared samples of the twins' abdominal fat, or adipose tissue. In unhealthy obese twins, genes involved in inflammation were activated – genes that were not activated in their thin twin. The activity of cellular powerhouses called mitochondria seemed to be suppressed as well. But in healthy obese twins, gene expression was similar to that of the thin twin. © Copyright Reed Business Information Ltd.
By John Horgan Last spring, I kicked up a kerfuffle by proposing that research on race and intelligence, given its potential for exacerbating discrimination, should be banned. Now Nature has expanded this debate with “Taboo Genetics.” The article “looks at four controversial areas of behavioral genetics”—intelligence, race, violence and sexuality—”to find out why each field has been a flashpoint, and whether there are sound scientific reasons for pursuing such studies.” Behavioral genetics has failed to produce robust evidence linking complex traits and disorders to specific genes. The essay provides a solid overview, including input from both defenders of behavioral genetics and critics. The author, Erika Check Hayden, quotes me saying that research on race and intelligence too often bolsters “racist ideas about the inferiority of certain groups, which plays into racist policies.” I only wish that Hayden had repeated my broader complaint against behavioral genetics, which attempts to explain human behavior in genetic terms. The field, which I’ve been following since the late 1980s, has a horrendous track record. My concerns about the potential for abuse of behavioral genetics are directly related to its history of widely publicized, erroneous claims. I like to call behavioral genetics “gene whiz science,” because “advances” so often conform to the same pattern. Researchers, or gene-whizzers, announce: There’s a gene that makes you gay! That makes you super-smart! That makes you believe in God! That makes you vote for Barney Frank! The media and the public collectively exclaim, “Gee whiz!” © 2013 Scientific American