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Stephen Cave For centuries, philosophers and theologians have almost unanimously held that civilization as we know it depends on a widespread belief in free will—and that losing this belief could be calamitous. Our codes of ethics, for example, assume that we can freely choose between right and wrong. In the Christian tradition, this is known as “moral liberty”—the capacity to discern and pursue the good, instead of merely being compelled by appetites and desires. The great Enlightenment philosopher Immanuel Kant reaffirmed this link between freedom and goodness. If we are not free to choose, he argued, then it would make no sense to say we ought to choose the path of righteousness. Today, the assumption of free will runs through every aspect of American politics, from welfare provision to criminal law. It permeates the popular culture and underpins the American dream—the belief that anyone can make something of themselves no matter what their start in life. As Barack Obama wrote in The Audacity of Hope, American “values are rooted in a basic optimism about life and a faith in free will.” So what happens if this faith erodes? The sciences have grown steadily bolder in their claim that all human behavior can be explained through the clockwork laws of cause and effect. This shift in perception is the continuation of an intellectual revolution that began about 150 years ago, when Charles Darwin first published On the Origin of Species. Shortly after Darwin put forth his theory of evolution, his cousin Sir Francis Galton began to draw out the implications: If we have evolved, then mental faculties like intelligence must be hereditary. But we use those faculties—which some people have to a greater degree than others—to make decisions. So our ability to choose our fate is not free, but depends on our biological inheritance. © 2016 by The Atlantic Monthly Group.
Link ID: 22228 - Posted: 05.18.2016
George Johnson At the Science of Consciousness conference last month in Tucson, I was faced with a quandary: Which of eight simultaneous sessions should I attend? In one room, scientists and philosophers were discussing the physiology of brain cells and how they might generate the thinking mind. In another, the subject was free will — real or an illusion? Next door was a session on panpsychism, the controversial (to say the least) idea that everything — animal, vegetable and mineral — is imbued at its subatomic roots with mindlike qualities. Running on parallel tracks were sessions titled “Phenomenal Consciousness,” the “Neural Correlates of Consciousness” and the “Extended Mind.” For much of the 20th century, the science of consciousness was widely dismissed as an impenetrable mystery, a morass of a problem that could be safely pursued only by older professors as they thought deep thoughts in their endowed chairs. Beginning in the 1990s, the field slowly became more respectable. There is, after all, a gaping hole in science. The human mind has plumbed the universe, concluding that it is precisely 13.8 billion years old. With particle accelerators like the Large Hadron Collider at CERN, scientists have discovered the vanishingly tiny particles, like the Higgs boson, that underpin reality. But there is no scientific explanation for consciousness — without which none of these discoveries could have been made. © 2016 The New York Times Company
Link ID: 22227 - Posted: 05.18.2016
Andrea Hsu Scientists and doctors say the case is clear: The best way to tackle the country's opioid epidemic is to get more people on medications that have been proven in studies to reduce relapses and, ultimately, overdoses. Yet, only a fraction of the more than 4 million people believed to abuse prescription painkillers or heroin in the U.S. are being given what's called medication-assisted treatment. One reason is the limited availability of the treatment. But it's also the case that stigma around the addiction drugs has inhibited their use. Methadone and buprenorphine, two of the drugs used for treatment, are themselves opioids. A phrase you often hear about medication-assisted treatment is that it's merely replacing one drug with another. While doctors and scientists strongly disagree with that characterization, it's a view that's widespread in recovery circles. Now, the White House is pushing to change the landscape for people seeking help. In his 2017 budget, President Obama has asked Congress for $1.1 billion in new funding to address the opioid epidemic, with almost all of it geared toward expanding access to medication-assisted treatment. The White House is also highlighting success stories. At the National Prescription Drug Abuse and Heroin Summit held in Atlanta in March, President Obama appeared on stage with Crystal Oertle, a 35-year-old mother of two from Ohio. Oertle spoke of her spiral into addiction, which began with prescription painkillers and progressed to heroin. She tried unsuccessfully to quit on her own several times, before being prescribed buprenorphine a year ago. © 2016 npr
Keyword: Drug Abuse
Link ID: 22226 - Posted: 05.18.2016
By Sarah Kaplan You probably wouldn't be surprised if a scientist told you that your genes influence when you hit puberty, how tall you are, what your BMI will be and whether you're likely to develop male pattern baldness. But what if he said that the same gene could hold sway over all four things? That finding comes from a study published Monday in the journal Nature Genetics. Using data from dozens of genome-wide association studies (big scans of complete sets of DNA from many thousands of people), researchers at the New York Genome Center and the genetic analysis company 23andMe found examples of single "multitasking" genes that influence diverse and sometimes seemingly disparate traits. The scientists say that the links they uncovered could help researchers understand how certain genes work, and figure out better ways of treating some of the health problems they might control. "Most studies tend to go one disease at a time," said Joseph Pickrell, a professor at Columbia University and the New York Genome Center's lead investigator on the project. "But if we can try to make these sorts of connections between what you might think of as unrelated traits ... that gives us another angle of attack to understand the connections between these different diseases." To start, Pickrell and his team sought out genome-wide association studies (GWAS) identifying particular genetic variants associated with 42 different traits. Many had to do with diseases (for example, studies that linked certain genes to the risk of developing Alzheimer's or type 2 diabetes) and other personal health traits (body mass index, blood type, cholesterol levels).
Keyword: Genes & Behavior
Link ID: 22225 - Posted: 05.18.2016
Zoe Cormier A hallucinogenic drug derived from magic mushrooms could be useful in treating depression, the first safety study of this approach has concluded. Researchers from Imperial College London gave 12 people psilocybin, the active component in magic mushrooms. All had been clinically depressed for a significant amount of time — on average 17.8 years. None of the patients had responded to standard medications, such as selective serotonin re-uptake inhibitors (SSRIs), or had electroconvulsive therapy. One week after receiving an oral dose of psilocybin, all patients experienced a marked improvement in their symptoms. Three months on, five patients were in complete remission. “That is pretty remarkable in the context of currently available treatments,” says Robin Carhart-Harris, a neuropsychopharmacologist at Imperial College London and first author of the latest study, which is published in The Lancet Psychiatry1. The equivalent remission rate for SSRIs is around 20%. The study's authors are not suggesting that psilocybin should be a treatment of last resort for depressed patients. “Our conclusion is more sober than that — we are simply saying that this is doable,” says Carhart-Harris. “We can give psilocybin to depressed patients, they can tolerate it, and it is safe. This gives us an initial impression of the effectiveness of the treatment.” © 2016 Nature Publishing Group
By Simon Oxenham The “cuddle chemical”. The “moral molecule”. Oxytocin has quite a reputation – but much of what we thought about the so-called “love hormone” may be wrong. Oxytocin is made by the hypothalamus and acts on the brain, playing a role in bonding, sex and pregnancy. But findings that a sniff of the hormone is enough to make people trust each other more are being called into question after a string of studies failed to replicate classic experiments. Paul Zak at the Centre for Neuroeconomic Studies in Claremont, California, made his moral molecule hypothesis famous in 2011 when he memorably squirted a syringe of the hormone into the air while delivering a TED talk. When people sniff oxytocin before playing a money-lending game, it increases how much they trust each other, he explained. But several teams have been unable to replicate his finding. Last November, Gideon Nave at the California Institute of Technology in Pasadena and his colleagues reviewed studies of oxytocin, and concluded that the effect of nasal squirts of the hormone on trust are not reliably different from zero. Nave’s team aren’t the only ones calling the moral molecule hypothesis into question. In 2012, Moïra Mikolajczak at the Catholic University of Louvain (UCL) in Belgium and her colleagues published their own seminal findings backing a link between trust and oxytocin. They found that when people filled out an anonymous questionnaire about their sex lives and fantasies, they were less likely to seal the envelopes they returned them in if given a nasal dose of oxytocin beforehand. © Copyright Reed Business Information Ltd.
A bionic body is closer than you think By Dwayne Godwin, Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2016 Scientific American
Link ID: 22222 - Posted: 05.17.2016
By JONATHAN BALCOMBE Washington — IN March, two marine biologists published a study of giant manta rays responding to their reflections in a large mirror installed in their aquarium in the Bahamas. The two captive rays circled in front of the mirror, blew bubbles and performed unusual body movements as if checking their reflection. They made no obvious attempt to interact socially with their reflections, suggesting that they did not mistake what they saw as other rays. The scientists concluded that the mantas seemed to be recognizing their reflections as themselves. Mirror self-recognition is a big deal. It indicates self-awareness, a mental attribute previously known only among creatures of noted intelligence like great apes, dolphins, elephants and magpies. We don’t usually think of fishes as smart, let alone self-aware. As a biologist who specializes in animal behavior and emotions, I’ve spent the past four years exploring the science on the inner lives of fishes. What I’ve uncovered indicates that we grossly underestimate these fabulously diverse marine vertebrates. The accumulating evidence leads to an inescapable conclusion: Fishes think and feel. Because fishes inhabit vast, obscure habitats, science has only begun to explore below the surface of their private lives. They are not instinct-driven or machinelike. Their minds respond flexibly to different situations. They are not just things; they are sentient beings with lives that matter to them. A fish has a biography, not just a biology. Those giant manta rays have the largest brains of any fish, and their relative brain-to-body size is comparable to that of some mammals. So, an exception? Then you haven’t met the frillfin goby. © 2016 The New York Times Company
Dara Mohammadi As the small motorboat chugs to a halt, three travellers, wind-beaten from the three-hour journey along the Atrato river, step on to the muddy banks of Bellavista, an otherwise inaccessible town in the heart of the heavily forested north-west of Colombia. They swing their hessian bags – stuffed with bedsheets, dried beans and cuddly toys – to their shoulders and clamber up a dusty path. Tucked inside the bag of one of the travellers, neuropsychologist Sonia Moreno, is the reason they are here: a wad of unfinished, hand-drawn charts of family trees. The people whose names are circled on the charts have Huntington’s disease, an incurable genetic brain disorder that usually starts between the ages of 35 and 45 years. It begins with personality changes that can make them aggressive, violent, uninhibited, anxious and depressed. The disease progresses slowly, robbing them first of the control of their body, which jerks and twists seemingly of its own will, and then their ability to walk, talk and think until, about 20 years after the symptoms first begin, they die. Their children, each of whom has a 50% chance of inheriting the disease, watch and wait to see if it will happen to them. It is in this way that the disease strangles families. With Moreno is Ignacio Muñoz-Sanjuan, vice president of translational biology at CHDI Foundation, a US nonprofit research organisation that aims to find ways to prevent or slow down the progression of the disease. The foundation spent $140m–$150m (£97m-£104m) on research last year, but Muñoz-Sanjuan is not here on official business. He’s here for Factor-H, an initiative he founded four years ago to help with the other end of the problem – poor families with Huntington’s struggling in Latin America. © 2016 Guardian News and Media Limited o
By CLYDE HABERMAN At respected research centers in the United States and other countries, scientists have spent much of their professional lives in drug rehabilitation. It is not because they themselves struggle with addiction. What they are trying to rehabilitate are the drugs. Their focus is on mind-altering compounds that fell far from grace nearly half a century ago, LSD prominent among them. Along with other psychedelics, it was outlawed by the federal government, damned as bearing a high potential for abuse and offering no accepted medical benefit. But in recent years, researchers have sought to rescue hallucinogens from exile by examining their efficacy in treating certain disorders of the mind, and perhaps even in understanding the nature of consciousness and spirituality. The work of these scientists now draws the attention of Retro Report, a series of video documentaries that examine major news stories of the past and their enduring significance. Psychoactive substances, often derived from mushrooms, have been part of human cultures from Central and South America to the Sahara for thousands of years. But there is no need to look that far back; 1938 will do. That was when Albert Hofmann, a Swiss chemist searching for a drug to combat circulatory ailments, happened to synthesize lysergic acid diethylamide: LSD or, more familiarly, acid. Five years later, Dr. Hofmann, who died in 2008 at age 102, accidentally ingested a small dose of his creation and discovered its mind-blowing potential as he embarked on the first known acid trip. Many more such journeys would follow, for him and for countless others. © 2016 The New York Times Company
By Julia Shaw You see a crime take place. You are interviewed about it. You give a statement about what you saw. Do you think that at a later date you would be able to detect whether someone had tampered with your statement? Or re-written parts of it? This is currently a hot topic in the UK, where a very recently published inquiry into the so-called Hillsborough disaster, in which 96 people were crushed to death during a soccer match in 1989, found that testimonies had been deliberately altered by police. Research published earlier this year by the false memory dream team at the University of California, looked directly into the implications of such police (mis)conduct. They found that it is possible that changed statements can go unnoticed by the person who gave the original testimony, and may even develop into a false memory that accommodates the false account. To describe this effect, the researchers came up with the term "memory blindness"—the phenomenon of failing to recognize our own memories. The term was intended to mirror the ‘choice blindness’ literature. Choice blindness is forgetting choices that we have made. The researchers wanted to know “Can choice blindness have lasting effects on eyewitness memory?” To examine this, PhD Student Kevin Cochran and his colleagues conducted two experiments. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22218 - Posted: 05.16.2016
Rae Ellen Bichell For Tim Goliver and Luther Glenn, the worst illness of their lives started in the same way — probably after having a stomach bug. Tim was 21 and a college student at the University of Michigan. He was majoring in English and biology and active in the Lutheran church. "I was a literature geek," says Tim. "I was really looking forward to my senior year and wherever life would take me." Luther was in his 50s. He'd spent most of his career as a U.S. military policeman and was working in security in Washington, D.C. He'd recently separated from his wife and had just moved into a new house with his two daughters, who were in their 20s. Both men recovered from their stomach bugs, but a few days later they started to feel sluggish. "Here we are trying to unpack, prepare ourselves for new life together and I'm flat out, dead tired," says Luther. He fell asleep in the car one morning and never made it out of the garage. Then he fell in the bathroom. For Tim, it started to feel like running a marathon just to lift a spoonful of soup. One morning, he tried to comb his hair and realized he couldn't lift his arm above his shoulder. "At that moment I started to freak out," he says. Both men got so weak that their families had to wheel them into the emergency room in wheelchairs. They got the same diagnosis: Guillain-Barre syndrome, a neurological disorder which can leave people paralyzed for weeks. © 2016 npr
By John Horgan Speakers at the 2016 Tucson consciousness conference suggested that “temporal nonlocality” or other quantum effects in the brain could account for free will. But what happens when the brain is immersed in a hot tub? This is the second of four posts on “The Science of Consciousness” in Tucson, Arizona, which lasted from April 26 to April 30. (See Further Reading for links to other posts.) Once again, I’m trying to answer the question: What is it like to be a skeptical journalist at a consciousness conference? -- John Horgan DAY 2, THURSDAY, APRIL 28. HOT TUBS AND QUANTUM INCOHERENCE Breakfast on the patio with Stuart Kauffman, who has training in… almost everything. Philosophy, medicine, science. We’ve bumped heads in the past, but we’re friendly now. In his mid-70s, Stu is still obsessed with--and hacking away at--the biggest mysteries. We talk about… almost everything. Quantum mechanics, the origin of life, materialism, free will, God, the birth and death of his daughter, the death of his wife, his re-marriage, predictability versus possibility. As Stu speaks, his magnificent, weathered face looks happy/sad, arrogant/anxious. Superposition of emotions. He tells me about his brand-new book, Humanity in a Creative Universe, in which he outlines a perspective that can help lift us out of our spiritual crisis. Who saves the savior? I scoot to a morning session, “Consciousness and Free Will.” I hope it will supply me with ammo for my defenses of free will. I can do without God, but not free will. © 2016 Scientific American, a Division of Nature America, Inc.
Link ID: 22216 - Posted: 05.16.2016
By Adam Gopnik On a bitter, soul-shivering, damp, biting gray February day in Cleveland—that is to say, on a February day in Cleveland—a handless man is handling a nonexistent ball. Igor Spetic lost his right hand when his forearm was pulped in an industrial accident six years ago and had to be amputated. In an operation four years ago, a team of surgeons implanted a set of small translucent “interfaces” into the neural circuits of his upper arm. This afternoon, in a basement lab at a Veterans Administration hospital, the wires are hooked up directly to a prosthetic hand—plastic, flesh-colored, five-fingered, and articulated—that is affixed to what remains of his arm. The hand has more than a dozen pressure sensors within it, and their signals can be transformed by a computer into electric waves like those natural to the nervous system. The sensors in the prosthetic hand feed information from the world into the wires in Spetic’s arm. Since, from the brain’s point of view, his hand is still there, it needs only to be recalled to life. Now it is. With the “stimulation” turned on—the electronic feed coursing from the sensors—Spetic feels nineteen distinct sensations in his artificial hand. Above all, he can feel pressure as he would with a living hand. “We don’t appreciate how much of our behavior is governed by our intense sensitivity to pressure,” Dustin Tyler, the fresh-faced principal investigator on the Cleveland project, says, observing Spetic closely. “We think of hot and cold, or of textures, silk and cotton. But some of the most important sensing we do with our fingers is to register incredibly minute differences in pressure, of the kinds that are necessary to perform tasks, which we grasp in a microsecond from the feel of the outer shell of the thing. We know instantly, just by touching, whether to gently squeeze the toothpaste or crush the can.”
Keyword: Pain & Touch
Link ID: 22215 - Posted: 05.14.2016
By JONAH BROMWICH It’s relatively easy to determine when someone is too drunk to drive. If a driver’s blood-alcohol level is 0.08 percent or higher, that person is considered legally impaired. But a study says that measuring the effects of marijuana on drivers is far trickier, and that blood tests are an unreliable indication of impairment by cannabis. As more states consider legalizing the substance, that presents a challenge to legislators seeking to create laws on driving while impaired by marijuana. The study, commissioned by the AAA Foundation for Traffic Safety, found that laws in six states that legally assess impairment by measuring how much THC (the active ingredient in marijuana) is in a person’s blood are not supported by science. “There is no concentration of the drug that allows us to reliably predict that someone is impaired behind the wheel in the way that we can with alcohol,” said Jake Nelson, AAA’s director of traffic safety advocacy and research. Lawmakers in those states looked to policies on drunken driving for cues on how to legislate against driving while high. But the body absorbs alcohol and cannabis in different ways, the study said. While drunkenness directly correlates to alcohol in the bloodstream, cannabis impairment takes place only when THC makes its way into the fatty tissue of the brain. Regular marijuana users, including those who take the drug medicinally, often show no signs of impairment after using, according to Jolene Forman, a staff lawyer for the Drug Policy Alliance, a drug-reform advocacy group. She also said that marijuana can stay in the blood for hours, days and even weeks after its effects wear off. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22214 - Posted: 05.14.2016
Bret Stetka Last year, in an operating room at the University of Toronto, a 63-year-old women with Alzheimer's disease experienced something she hadn't for 55 years: a memory of her 8-year-old self playing with her siblings on their family farm in Scotland. The woman is a patient of Dr. Andres Lozano, a neurosurgeon who is among a growing number of researchers studying the potential of deep brain stimulation to treat Alzheimer's and other forms of dementia. If the approach pans out it could provide options for patients with fading cognition and retrieve vanished memories. Right now, deep brain stimulation is used primarily to treat Parkinson's disease and tremor, for which it's approve by the Food and Drug Administration. DBS involves delivering electrical impulses to specific areas of the brain through implanted electrodes. The technique is also approved for obsessive-compulsive disorder and is being looked at for a number of other brain disorders, including depression, chronic pain and, as in Lozano's work, dementia. In 2008 Lozano's group published a study in which an obese patient was treated with deep brain stimulation of the hypothalamus. Though no bigger than a pea, the hypothalamus is a crucial bit of brain involved in appetite regulation and other bodily essentials such as temperature control, sleep and circadian rhythms. It seemed like a reasonable target in trying to suppress excessive hunger. To the researcher's surprise, following stimulation the patient reported a sensation of deja vu. He also perceived feeling 20 years younger and recalled a memory of being in a park with friends, including an old girlfriend. With increasing voltages his memories became more vivid. He remembered their clothes. © 2016 npr
Keyword: Learning & Memory
Link ID: 22213 - Posted: 05.14.2016
By Nicholas Bakalar Exposure to pesticides may increase the risk for amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, a new study has found. The study, in JAMA Neurology, included 156 patients with A.L.S. and 128 controls. All participants completed questionnaires providing information on age, sex, ethnicity, education, marital status, residential history, occupational history, smoking and military service. The researchers used the information on residence and occupation to estimate long-term exposure to pesticides, and then took blood samples to determine serum levels of 122 persistent environmental pollutants. The scientists divided exposure into four time periods: ever exposed, exposed in the last 10 years, exposed 10 to 30 years ago, and exposed more than 30 years ago. Exposure to pesticides at any time was associated with a fivefold increased relative risk for A.L.S. compared to no exposure. Even exposure more than 30 years ago tripled the risk. Military service was associated with double the risk, confirming findings of previous studies. “This is an association, not causality,” cautioned the senior author, Dr. Eva L. Feldman, a professor of neurology at the University of Michigan. “We found that people with A.L.S. were five times more likely to have been exposed to pesticides, but we don’t want people to conclude that pesticides cause A.L.S.” © 2016 The New York Times Company
Laura Sanders Brain waves during REM sleep solidify memories in mice, scientists report in the May 13 Science. Scientists suspected that the eye-twitchy, dream-packed slumber known as rapid eye movement sleep was important for memory. But REM sleep’s influence on memory has been hard to study, in part because scientists often resorted to waking people or animals up — a stressful experience that might influence memory in different ways. Richard Boyce of McGill University in Montreal and colleagues interrupted REM sleep in mice in a more delicate way. Using a technique called optogenetics, the researchers blocked a brain oscillation called theta waves in the hippocampus, a brain structure involved in memory, during REM sleep. This light touch meant that the mice stayed asleep but had fewer REM-related theta waves in their hippocampi. Usually, post-learning sleep helps strengthen memories. But mice with disturbed REM sleep had memory trouble, the researchers found. Curious mice will spend more time checking out an object that’s been moved to a new spot than an unmoved object. But after the sleep treatment, the mice seemed to not remember objects’ earlier positions, spending equal time exploring an unmoved object as one in a new place. These mice also showed fewer signs of fear in a place where they had previously suffered shocks. Interfering with theta waves during other stages of sleep didn’t seem to cause memory trouble, suggesting that something special happens during REM sleep. R. Boyce et al. Causal evidence for the role of REM sleep theta rhythm in contextual memory consolidation. Science. Vol. 352, p. 812, May 13, 2016. doi: 10.1126/science.aad5252. © Society for Science & the Public 2000 - 2016.
By Emily Underwood One of the telltale signs of Alzheimer’s disease (AD) is sticky plaques of ß-amyloid protein, which form around neurons and are thought by a large number of scientists to bog down information processing and kill cells. For more than a decade, however, other researchers have fingered a second protein called tau, found inside brain cells, as a possible culprit. Now, a new imaging study of 10 people with mild AD suggests that tau deposits—not amyloid—are closely linked to symptoms such as memory loss and dementia. Although this evidence won’t itself resolve the amyloid-tau debate, the finding could spur more research into new, tau-targeting treatments and lead to better diagnostic tools, researchers say. Scientists have long used an imaging technique called positron emission tomography (PET) to visualize ß-amyloid deposits marked by radioactive chemical tags in the brains of people with AD. Combined with postmortem analyses of brain tissue, these studies have demonstrated that people with AD have far more ß-amyloid plaques in their brains than healthy people, at least as a general rule. But they have also revealed a puzzle: Roughly 30% of people without any signs of dementia have brains “chock-full” of ß-amyloid at autopsy, says neurologist Beau Ances at Washington University in St. Louis in Missouri. That mystery has inspired many in the AD field to ask whether a second misfolded protein, tau, is the real driver of the condition’s neurodegeneration and symptoms, or at least an important accomplice. Until recently, the only ways to test that hypothesis were to measure tau in brain tissue after a person died, or in a sample of cerebrospinal fluid (CSF) extracted from a living person by needle. But in the past several years, researchers have developed PET imaging agents that can harmlessly bind to tau in the living brain. The more tau deposits found in the temporal lobe, a brain region associated with memory, the more likely a person was to show deficits on a battery of memory and attention tests, the team reports today in Science Translational Medicine. © 2016 American Association for the Advancement of Science.
Erika Check Hayden The largest-ever genetics study in the social sciences has turned up dozens of DNA markers that are linked to the number of years of formal education an individual completes. The work, reported this week in Nature, analysed genetic material from around 300,000 people. “This is good news,” says Stephen Hsu, a theoretical physicist at Michigan State University in East Lansing, who studies the genetics of intelligence. “It shows that if you have enough statistical power you can find genetic variants that are associated with cognitive ability.” Yet the study’s authors estimate that the 74 genetic markers they uncovered comprise just 0.43% of the total genetic contribution to educational achievement (A. Okbay et al. Nature http://dx.doi.org/10.1038/nature17671; 2016). By themselves, the markers cannot predict a person’s performance at school. And because the work examined only people of European ancestry, it is unclear whether the results apply to those with roots in other regions, such as Africa or Asia. The findings have proved divisive. Some researchers hope that the work will aid studies of biology, medicine and social policy, but others say that the emphasis on genetics obscures factors that have a much larger impact on individual attainment, such as health, parenting and quality of schooling. © 2016 Nature Publishing Group