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By James Gallagher Health editor, BBC News website Higher rates of obesity and ill-health have been found in shift workers than the general population. Health Survey for England data showed they were in worse health despite often being young. The lead researcher told the BBC that the rise of zero-hours contracts may be increasing the numbers doing shift work and could raise "pretty serious problems" for the nation's health. Scientists said it was "fairly clear now" that shift work was unhealthy. The report, by the Health and Social Care Information Centre, showed 33% of men and 22% of women of working age were doing shift work. They defined shifts as employment outside 0700-1900. Rachel Craig, the research director for the Health Survey for England, told the BBC: "Overall, people who are doing shift work are not quite as healthy as their counterparts doing regular working hours." The data showed 30% of shift workers were obese, compared with 24% of men and 23% of women doing normal hours. Meanwhile, 40% of men and 45% of women on shifts had long-standing health conditions such as back-pain, diabetes or chronic obstructive pulmonary disease compared with 36% and 39% of the rest of the population. Younger people Shift working is most common in the 16-24 age group with nearly half of men and a third of women having this working pattern. The rates fell with age so that fewer than a third of men and a fifth of women were working shifts after the age of 55. Ms Craig said that, overall, young people should be in better health: "You'd expect less ill-health and fewer long-standing conditions that reflect lifestyle like obesity, so it makes it an even stronger relationship [between shifts and poor health]." BBC © 2014
|By Marissa Fessenden Songbirds stutter, babble when young, become mute if parts of their brains are damaged, learn how to sing from their elders and can even be "bilingual"—in other words, songbirds' vocalizations share a lot of traits with human speech. However, that similarity goes beyond behavior, researchers have found. Even though humans and birds are separated by millions of years of evolution, the genes that give us our ability to learn speech have much in common with those that lend birds their warble. A four-year long effort involving more than 100 researchers around the world put the power of nine supercomputers into analyzing the genomes of 48 species of birds. The results, published this week in a package of eight articles in Science and 20 papers in other journals, provides the most complete picture of the bird family tree thus far. The project has also uncovered genetic signatures in song-learning bird brains that have surprising similarities to the genetics of speech in humans, a finding that could help scientists study human speech. The analysis suggests that most modern birds arose in an impressive speciation event, a "big bang" of avian diversification, in the 10 million years immediately following the extinction of dinosaurs. This period is more recent than posited in previous genetic analyses, but it lines up with the fossil record. By delving deeper into the rich data set, research groups identified when birds lost their teeth, investigated the relatively slow evolution of crocodiles and outlined the similarities between birds' and humans' vocal learning ability, among other findings. © 2014 Scientific American,
By Candy Schulman My mother’s greatest fear was Alzheimer’s. She got Lewy body dementia, or LBD, instead. This little known, oddly named, debilitating illness afflicts an estimated 1.3 million Americans, the actor and comedian Robin Williams possibly among them. It is often misdiagnosed because its signs, such as hallucinations and body rigidity, do not seem like those of dementia, but in the end it robs people of themselves even more painfully. I first noticed my mother’s cognitive difficulties when she was 88. Until then, she’d led an extraordinarily active life: She was a competitive golfer with a bureau full of trophies, a painter and a sculptor. Every Hanukkah she hosted a lively feast for her eight grandchildren and nine great-grandchildren. This time, though, she needed my help planning, shopping and cooking. She was having difficulty with the guest list, trying to write every family member’s name on a piece of paper, adding up the numbers to see how many potatoes to buy for latkes. Her concentration became frayed and she kept ripping it up and starting again, close to tears. Several months before that, she had sent me a Mother’s Day card that was illustrated with childlike prose, colorful illustrations and glitter hearts. The poem on the cover was printed in a playful purple font: “For you, Mom. For kissing my boo-boos, for wiping my face. . . . For calming my fears with your loving embrace.” On Mother’s Day and the rest of the year, Mom added in a shaky script, “thanks.”
Link ID: 20422 - Posted: 12.16.2014
|By Emilie Reas If you carried a gene that doubled your likelihood of getting Alzheimer's disease, would you want to know? What if there was a simple lifestyle change that virtually abolished that elevated risk? People with a gene known as APOE e4 have a higher risk of cognitive impairment and dementia in old age. Even before behavioral symptoms appear, their brains show reduced metabolism, altered activity and more deterioration than those without the high-risk gene. Yet accumulating research is showing that carrying this gene is not necessarily a sentence for memory loss and confusion—if you know how to work it to your advantage with exercise. Scientists have long known that exercise can help stave off cognitive decline. Over the past decade evidence has mounted suggesting that this benefit is even greater for those at higher genetic risk for Alzheimer's. For example, two studies by a team in Finland and Sweden found that exercising at least twice a week in midlife lowers one's chance of getting dementia more than 20 years later, and this protective effect is stronger in people with the APOE e4 gene. Several others reported that frequent exercise—at least three times a week in some studies; up to more than an hour a day in others—can slow cognitive decline only in those carrying the high-risk gene. Furthermore, for those who carry the gene, being sedentary is associated with increased brain accumulation of the toxic protein beta-amyloid, a hallmark of Alzheimer's. More recent studies, including a 2012 paper published in Alzheimer's & Dementia and a 2011 paper in NeuroImage, found that high-risk individuals who exercise have greater brain activity and glucose uptake during a memory task compared with their less active counterparts or with those at low genetic risk. © 2014 Scientific American
By Nicholas Bakalar Poor sleep in older adults may be linked to brain changes associated with dementia, a new study has found. Researchers studied 167 men who underwent sleep tests in 1999 and died by 2010. The study, in Neurology, recorded sleep duration, periods of waking up and episodes of apnea, and used pulse oximetry to measure oxygen saturation of their blood. On autopsy, they found that those in the highest one-quarter for duration of sleep at oxygen saturation of less than 95 percent were almost four times as likely to have higher levels microinfarcts, small areas of dead tissue caused by deprivation of blood supply, as those in the lowest one-quarter. Compared with those in the lowest 25 percent for duration of slow-wave (deep) sleep, those in the highest one-quarter were about a third as likely to have moderate or high levels of generalized brain atrophy. “Prior studies have shown an association between certain types of sleep disturbance and dementia,” said the lead author, Dr. Rebecca P. Gelber, an epidemiologist with the Veterans Administration in Hawaii. “These lesions may help explain the association.” © 2014 The New York Times Company
|By Ingrid Wickelgren Confusion is one symptom of a concussion. But confusion may also characterize decisions about how soon to let an athlete play after taking a hit to the head. Sizing up symptoms such as dizziness and nausea is subjective, after all. Now a study suggests that a blood test could objectively determine whether or not the damage is bad enough to put a player on the bench. The work is in the Journal of Neurotrauma. [Robert Siman et al, Serum SNTF Increases in Concussed Professional Ice Hockey Players and Relates to the Severity of Post Concussion Symptoms] A strong blow to the head causes chemical changes within nerve cells that damage their structural proteins. Among the debris is a protein fragment called SNTF—which in more severe cases, spills into the bloodstream. The new study followed 20 professional hockey players who got concussions with symptoms that lasted six days or more. And blood levels of SNTF were much higher one hour to six days later than were levels of the protein fragment in eight other athletes who had gotten concussions that cleared up within five days. Levels were also low in 45 non-concussed players tested during the pre-season. A blood test for SNTF might thus forecast recovery time from a head injury. Combined with other neurological tests, levels of this molecule could help doctors tell athletes when it’s safe to suit up again. © 2014 Scientific American
Keyword: Brain Injury/Concussion
Link ID: 20419 - Posted: 12.16.2014
By David Noonan It was the day before Christmas, and the normally busy MIT laboratory on Vassar Street in Cambridge was quiet. But creatures were definitely stirring, including a mouse that would soon be world famous. Steve Ramirez, a 24-year-old doctoral student at the time, placed the mouse in a small metal box with a black plastic floor. Instead of curiously sniffing around, though, the animal instantly froze in terror, recalling the experience of receiving a foot shock in that same box. It was a textbook fear response, and if anything, the mouse’s posture was more rigid than Ramirez had expected. Its memory of the trauma must have been quite vivid. Which was amazing, because the memory was bogus: The mouse had never received an electric shock in that box. Rather, it was reacting to a false memory that Ramirez and his MIT colleague Xu Liu had planted in its brain. “Merry Freaking Christmas,” read the subject line of the email Ramirez shot off to Liu, who was spending the 2012 holiday in Yosemite National Park. The observation culminated more than two years of a long-shot research effort and supported an extraordinary hypothesis: Not only was it possible to identify brain cells involved in the encoding of a single memory, but those specific cells could be manipulated to create a whole new “memory” of an event that never happened. “It’s a fantastic feat,” says Howard Eichenbaum, a leading memory researcher and director of the Center for Neuroscience at Boston University, where Ramirez did his undergraduate work. “It’s a real breakthrough that shows the power of these techniques to address fundamental questions about how the brain works.” In a neuroscience breakthrough, the duo implanted a false memory in a mouse
By Bruce Bower In the movie Roxanne, Steve Martin plays a lovesick guy who mocks his own huge schnoz by declaring: “It’s not the size of a nose that’s important. It’s what’s in it that matters.” Scientists demonstrated the surprising truth behind that joke this year: People can whiff an average of more than 1 trillion different odors, regardless of nose size (SN: 4/19/14, p. 6). No one had systematically probed how many scents people can actually tell apart. So a team led by Leslie Vosshall of Rockefeller University in New York City asked 26 men and women to discriminate between pairs of scents created from mixes of 128 odor molecules. Volunteers easily discriminated between smells that shared as much as 51 percent of their odor molecules. Errors gradually rose as pairs of scents became chemically more alike. Vosshall’s group calculated that an average participant could tell apart a minimum of more than 1 trillion smells made up of different combinations of 30 odor molecules. Really good smellers could have detected way more than 1 trillion odor mixtures, the scientists said. Smell lags behind sight and hearing as a sense that people need to find food, avoid dangers and otherwise succeed at surviving. Still, detecting the faint odor of spoiled food and other olfactory feats must have contributed to the success of Homo sapiens over the last 200,000 years. Perhaps many animals can whiff the difference between a trillion or more smells. For now, odor-detection studies modeled on Vosshall’s approach have been conducted only with humans. © Society for Science & the Public 2000 - 2014.
Keyword: Chemical Senses (Smell & Taste)
Link ID: 20417 - Posted: 12.16.2014
by Andy Coghlan It may not sound very appetising, but an edible powder made from waste excreted by bacteria in our guts may help people to avoid gaining weight. Stabilising a person's weight could have a major health impact, says Gary Frost of Imperial College London, because as people on Western diets grow older, they tend to put on between 0.3 and 0.8 kilograms per year on average. A fatty acid called propionate is released when the bacteria in our gut digest fibre. Propionate makes people feel full by activating cells in the large intestine that produce the satiety hormones GLP-1 and PYY: these tell the brain that it's time to stop eating. But to trigger a big enough dose of this appetite-suppressing signal from gut bacteria alone, people would have to eat extremely large amounts of fibre. To get around that, Frost and his team made the molecule in a concentrated form called inulin-propionate ester (IPE). "That gives you eight times the amount of someone following a typical Western diet," he says. To test its appetite-stemming properties, the team gave powdered IPE, mixed in with fruit juice or a milkshake, to a group of overweight volunteers every day for six months. A type of ordinary fibre was given to another set of people, who acted as controls. Only one of the 25 volunteers taking IPE put on more than 3 per cent of their body weight over that time, compared with six of the 24 controls. One reason for this might be that the IPE recipients ate around 9 per cent less over the six months. © Copyright Reed Business Information Ltd.
Link ID: 20416 - Posted: 12.13.2014
|By Lindsey Konkel For 28 years, Bill Gilmore lived in a New Hampshire beach town, where he surfed and kayaked. “I’ve been in water my whole life,” he said. “Before the ocean, it was lakes. I’ve been a water rat since I was four.” Now Gilmore can no longer swim, fish or surf, let alone button a shirt or lift a fork to his mouth. Earlier this year, he was diagnosed with amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease. In New England, medical researchers are now uncovering clues that appear to link some cases of the lethal neurological disease to people’s proximity to lakes and coastal waters. About five years ago, doctors at a New Hampshire hospital noticed a pattern in their ALS patients—many of them, like Gilmore, lived near water. Since then, researchers at Dartmouth-Hitchcock Medical Center have identified several ALS hot spots in lake and coastal communities in New England, and they suspect that toxic blooms of blue-green algae—which are becoming more common worldwide—may play a role. Now scientists are investigating whether breathing a neurotoxin produced by the algae may raise the risk of the disease. They have a long way to go, however: While the toxin does seem to kill nerve cells, no research, even in animals, has confirmed the link to ALS. As with all ALS patients, no one knows what caused Bill Gilmore’s disease. He was a big, strong guy—a carpenter by profession. One morning in 2011, his arms felt weak. “I couldn’t pick up my tools. I thought I had injured myself,” said Gilmore, 59, who lived half his life in Hampton and now lives in Rochester, N.H. © 2014 Scientific American
by Colin Barras It's not just great minds that think alike. Dozens of the genes involved in the vocal learning that underpins human speech are also active in some songbirds. And knowing this suggests that birds could become a standard model for investigating the genetics of speech production – and speech disorders. Complex language is a uniquely human trait, but vocal learning – the ability to pick up new sounds by imitating others – is not. Some mammals, including whales, dolphins and elephants, share our ability to learn new vocalisations. So do three groups of birds: the songbirds, parrots and hummingbirds. The similarities between vocal learning in humans and birds are not just superficial. We know, for instance, that songbirds have specialised vocal learning brain circuits that are similar to those that mediate human speech. What's more, a decade ago we learned that FOXP2, a gene known to be involved in human language, is also active in "area X" of the songbird brain – one of the brain regions involved in those specialised vocal learning circuits. Andreas Pfenning at the Massachusetts Institute of Technology and his colleagues have now built on these discoveries. They compared maps of genetic activity – transcriptomes – in brain tissue taken from the zebra finch, budgerigar and Anna's hummingbird, representing the three groups of vocal-learning birds. © Copyright Reed Business Information Ltd.
By Gail Sullivan Chemicals found in food and common household products have been linked to lower IQ in kids exposed to high levels during pregnancy. Previous research linked higher exposure to chemicals called "phthalates" to poor mental and motor development in preschoolers. This study was said to be the first to report a link between prenatal exposure to the chemicals and childhood development. Researchers from Columbia University’s Mailman School of Public Health studied exposure to five types of phthalates, which are sometimes referred to as “hormone disruptors” or “endocrine disruptors.” Among these, di-n-butyl phthalate (DnBP) is used in shower curtains, raincoats, hairspray, food wraps, vinyl and pill coating, among other things — but according to the EPA, the largest source of exposure may be seafood. Di-isobutyl phthalate (DiBP) and Butylbenzyl phthalate (BBzP) are added to plastics to make them flexible. These chemicals may also used in makeup, nail polish, lacquer and explosives. The researchers linked prenatal exposure to phthalates to a more than six-point drop in IQ score compared with kids with less exposure. The study, “Persistent Associations between Maternal Prenatal Exposure to Phthalates on Child IQ at Age 7 Years," was published Wednesday in the journal PLOS One. "The magnitude of these IQ differences is troubling," one of the study’s authors, Robin Whyatt, said in a press release. "A six- or seven-point decline in IQ may have substantial consequences for academic achievement and occupational potential."
by Andy Coghlan To catch agile prey on the wing, dragonflies rely on the same predictive powers we use to catch a ball: that is, anticipating by sight where the ball will go and readying body and hand to snatch it from mid-air. Until now, dragonflies were thought to catch their prey without this predictive skill, instead blindly copying every steering movement made by their prey, which can include flies and bees. Now, sophisticated laboratory experiments have tracked the independent body and eye movements of dragonflies as they pursue prey, showing for the first time that dragonflies second guess where their prey will fly to next and then steer their flight accordingly. Throughout the pursuit, they lock on to their target visually while they orient their bodies and flight path for ultimate interception, rather than copying each little deviation in their prey's flight path in the hope of ultimately catching up with it. "The dragonfly lines up its body axis in the flight direction of the prey, but keeps the eyes in its head firmly fixed on the prey," says Anthony Leonardo of the Howard Hughes Medical Institute in Ashburn, Virginia. "It enables the dragonfly to catch the prey from beneath and behind, the prey's blind spot," he says. © Copyright Reed Business Information Ltd.
Link ID: 20412 - Posted: 12.13.2014
|By Claudia Wallis Touch a hot frying pan and the searing message of pain sprints up to your brain and back down to your hand so fast that the impulse to withdraw your fingers seems instantaneous. That rapid-fire signal begins in a heat-sensing molecule called a TRPV1 channel. This specialized protein is abundant on the surface of sensory nerve cells in our fingers and elsewhere and is a shape-shifter that can take an open or closed configuration. Heat opens a central pore in the molecule, so do certain spider toxins and capsaicin—the substance that gives chili peppers their burn. Once the pore is open, charged ions of sodium and calcium flow into the nerve cell, triggering the pain signal. Ouch! As neuroscientist-journalist Stephani Sutherland explains in “Pain that Won’t Quit,” in the December Scientific American, researchers have long been interested in finding ways to moderate the action of this channel—and other ion channels—in patients who suffer from chronic pain. Shutting down the TRPV1 channel completely, however, is not an option because it plays a vital role in regulating body temperature. In two papers published in Nature in December 2013 investigators at the University of California, San Francisco, gave pain researchers a big leg up in understanding TRPV1. They revealed, in exquisite atomic detail, the structure of the channel molecule (from a rat) using an electron cryomicroscope, an instrument designed to explore the 3-D structure of molecules at very low temperatures. One of those investigators, Yifan Cheng, also created this colorful animation, showing how the molecule looks when the channel is open. © 2014 Scientific American
Keyword: Pain & Touch
Link ID: 20411 - Posted: 12.13.2014
By Dr. Mitesh Popat It’s common knowledge that eating better, exercising more, limiting alcohol intake and not smoking can lead to a healthier, longer life. For many, sustaining healthy behaviors is not easy. For diabetics, maintaining healthy behaviors is even more challenging, although it is critical. If well managed, the disease can be held in check; if not, it can be devastating, leading to kidney failure, blindness, stroke and even death. It may be a surprise that there is strong association between depression, anxiety and diabetes. Not only can depression and anxiety seriously affect the ability to manage the disease, but there also is evidence that, for some, depression plays a role in actually causing diabetes. Research indicates that depression is unrecognized and untreated in approximately two-thirds of patients with diabetes. Whether cause or effect, the medical profession needs to do more to address the psychological issues associated with the disease. As a family medicine physician, I see the association on daily basis. Some patients are so overwhelmed by the necessary daily self-care that comes with diabetes that they become highly anxious and depressed. Others who are suffering from complications or are having trouble managing their blood sugar levels may feel a loss of control and get anxious or depressed. These symptoms are often compounded in people who live in poverty, including the low-income Latinos, African Americans and seniors whom we care for at Marin Community Clinics. Diabetes has become an epidemic in these groups. Working three jobs and constantly worrying about making ends meet can trigger depression and anxiety in anyone. Add to that the need to adopt a disciplined healthy lifestyle, and it can be a real struggle.
Link ID: 20410 - Posted: 12.13.2014
By Gary Stix Our site recently ran a great story about how brain training really doesn’t endow you instantly with genius IQ. The games you play just make you better at playing those same games. They aren’t a direct route to a Mensa membership. Just a few days before that story came out—Proceedings of the National Academy of Sciences—published a report that suggested that playing action video games, Call of Duty: Black Ops II and the like—actually lets gamers learn the essentials of a particular visual task (the orientation of a Gabor signal—don’t ask) more rapidly than non-gamers, a skill that has real-world relevance beyond the confines of the artificial reality of the game itself. As psychologists say, it has “transfer effects.” Gamers appear to have learned how to do stuff like home in quickly on a target or multitask better than those who inhabit the non-gaming world. Their skills might, in theory, make them great pilots or laparoscopic surgeons, not just high scorers among their peers. Action video games are not billed as brain training, but both Call of Duty and nominally accredited training programs like Lumosity are both structured as computer games. So that leads to the question of what’s going on here? Every new finding about brain training as B.S. appears to be contradicted by another that points to the promise of cognitive exercise, if that’s what you call a session with Call of Duty. It may boil down to a realization that the whole story about exercising your neurons to keep the brain supple may be a lot less simple than proponents make it out to be. © 2014 Scientific American
Keyword: Learning & Memory
Link ID: 20409 - Posted: 12.13.2014
By Nsikan Akpan Gut surgery is often the only option for life-threatening obesity and diabetes, but what if doctors could cut the pounds without using a knife? Scientists have engineered an antiobesity drug that rivals the dramatic benefits seen with surgery, dropping excess body weight by a third. Though the work was done only in rodents, the drug is the first to influence three obesity-related hormones in the gut at once. Bariatric surgery, including gastric bypass, typically involves limiting food intake by removing part of the stomach or intestines. Yet it does more than shrink the size of patient’s stomach or intestines. It also changes the release of multiple gut-related hormones, explains clinical endocrinologist Stephen O'Rahilly of the University of Cambridge in the United Kingdom, who wasn’t involved with the study. That’s important, because years of eating a diet high in fat and sugar can throw a person’s metabolism into disarray. Cells undergo genetic reprogramming that negatively impacts how they process sugar and store fat, locking in obesity. This pattern makes it harder and harder to lose weight, even if a person changes their diet and begins exercising. Bariatric surgery interrupts that cycle by stimulating the production of several hormones that reduce blood sugar, burn fat, and curb appetite. (It may also change the composition of the gut’s microbes.) Three of these hormones are called glucagon-like peptide-1 (GLP-1), gastric inhibitory peptide (GIP), and glucagon. Cells in your gut release GLP-1 and GIP after a meal to keep your body’s blood sugar levels in a normal range. GLP-1 also curbs appetite, signaling to your brain that you are full. In type 2 diabetes, the body stops responding to GLP-1 and GIP, which contributes to hyperglycemia, or too much blood sugar. Hyperglycemia causes the devastating hallmarks of diabetes, such as kidney injury, cardiovascular disease, and nerve damage. © 2014 American Association for the Advancement of Science.
Link ID: 20408 - Posted: 12.10.2014
By ANDREW POLLACK It is either the most exciting new treatment for depression in years or it is a hallucinogenic club drug that is wrongly being dispensed to desperate patients in a growing number of clinics around the country. It is called ketamine — or Special K, in street parlance. While it has been used as an anesthetic for decades, small studies at prestigious medical centers like Yale, Mount Sinai and the National Institute of Mental Health suggest it can relieve depression in many people who are not helped by widely used conventional antidepressants like Prozac or Lexapro. And the depression seems to melt away within hours, rather than the weeks typically required for a conventional antidepressant. But some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials, and they are alarmed that clinics are springing up to offer ketamine treatments, charging hundreds of dollars for sessions that must be repeated many times. “We don’t know what the long-term side effects of this are,” said Dr. Anthony J. Rothschild, a professor of psychiatry at the University of Massachusetts Medical School. Some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials. Credit Sandy Huffaker for The New York Times Pharmaceutical companies hope to solve the problem by developing drugs that work like ketamine but without the side effects, which are often described as out-of-body experiences. © 2014 The New York Times Company
by Helen Thomson Zapping your brain might make you better at maths tests – or worse. It depends how anxious you are about taking the test in the first place. A recent surge of studies has shown that brain stimulation can make people more creative and better at maths, and can even improve memory, but these studies tend to neglect individual differences. Now, Roi Cohen Kadosh at the University of Oxford and his colleagues have shown that brain stimulation can have completely opposite effects depending on your personality. Previous research has shown that a type of non-invasive brain stimulation called transcranial direct current stimulation (tDCS) – which enhances brain activity using an electric current – can improve mathematical ability when applied to the dorsolateral prefrontal cortex, an area involved in regulating emotion. To test whether personality traits might affect this result, Kadosh's team tried the technique on 25 people who find mental arithmetic highly stressful, and 20 people who do not. They found that participants with high maths anxiety made correct responses more quickly and, after the test, showed lower levels of cortisol, an indicator of stress. On the other hand, individuals with low maths anxiety performed worse after tDCS. "It is hard to believe that all people would benefit similarly [from] brain stimulation," says Cohen Kadosh. He says that further research could shed light on how to optimise the technology and help to discover who is most likely to benefit from stimulation. © Copyright Reed Business Information Ltd.
Ian Sample, science editor Electrical brain stimulation equipment – which can boost cognitive performance and is easy to buy online – can have bad effects, impairing brain functioning, research from scientists at Oxford University has shown. A steady stream of reports of stimulators being able to boost brain performance, coupled with the simplicity of the devices, has led to a rise in DIY enthusiasts who cobble the equipment together themselves, or buy it assembled on the web, then zap themselves at home. In science laboratories brain stimulators have long been used to explore cognition. The equipment uses electrodes to pass gentle electric pulses through the brain, to stimulate activity in specific regions of the organ. Roi Cohen Kadosh, who led the study, published in the Journal of Neuroscience, said: “It’s not something people should be doing at home at this stage. I do not recommend people buy this equipment. At the moment it’s not therapy, it’s an experimental tool.” The Oxford scientists used a technique called transcranial direct current stimulation (tDCS) to stimulate the dorsolateral prefrontal cortex in students as they did simple sums. The results of the test were surprising. Students who became anxious when confronted with sums became calmer and solved the problems faster than when they had sham stimulation (the stimulation itself lasted only 30 seconds of the half hour study). The shock was that the students who did not fear maths performed worse with the same stimulation.