Chapter 11. Emotions, Aggression, and Stress
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The invaders put on a disguise and infiltrate the nest with dark plans: to kill the queen and enslave the kingdom. Usually when ants take pupae from other colonies as future slaves all hell breaks loose in ensuing battles. The enslaved individuals sometimes even strike back against their overlords. It’s a relatively dramatic affair, usually resulting in the aggressive slave-makers carrying the pupae back to their own colony, says Terrence McGlynn at California State University. But a species of ant found in the eastern US, Temnothorax pilagens, does things differently. It is the first ant species known to waltz into a colony and enslave others without killing, and one of a few that take not only pupae but adult workers, too. “This was extremely surprising as ants are usually able to detect foreign species or even individuals from a different colony through their chemical profile and react aggressively towards them,” says Isabelle Kleeberg at Johannes Gutenberg-Universität Mainz, Germany, whose team has found how they get away with it. Kleeberg tracked the behaviour of T. pilagens and their preferred slave species, Temnothorax ambiguus, in 43 raiding experiments using colour-marked individuals. In each experiment the colonies of these two ant species, each housed in a plastic box, were placed 12 centimetres apart from each other. © Copyright Reed Business Information Ltd.
What if belief in God and prejudice against immigrants could be altered by magnetic energy? That’s the question researchers sought to explore in a study published Wednesday in the journal Social Cognitive and Affective Neuroscience. The “magnetic energy” comes in the form of transcranial magnetic stimulation (TMS), a noninvasive procedure that uses a metal coil to send pulses to the brain. By activating certain regions of the brain, doctors have used it for things like measuring the damage of a stroke or—increasingly—treating depression. These researchers sought to do the opposite—to temporarily disable one part of the brain (the part that responds to threats) and measure its effect on beliefs and prejudices connected to them. To do this, researchers from Britain’s University of York teamed up with UCLA to find 39 politically moderate college undergraduates who were divided into two groups. The first was given a “love-level sham” dose of TMS that had no effect on their brains. The second got a hit of magnetic energy strong enough to temporarily shut down their posterior medial frontal cortex. The pMFC, as this area near the forehead is known, is the part of the brain that identifies problems and—after measuring the level of threat—generates a response to them. Testing the effect of shutting down the part of the brain that forms judgments based on threats required first presenting threats. After receiving their respective doses of TMS, participants were asked to respond to questions about their own death. Previous studies have shown the threat of death is capable of directly affecting a person’s belief in religion. Therefore, shutting down the part of the brain that registers this threat—they theorized—would reduce the need to believe in God.
Link ID: 21525 - Posted: 10.17.2015
Could brain inflammation be to blame for schizophrenia? People with the disorder seem to have more active immune cells inside their brains, and now this activity has been spotted even before the disorder develops. This link could be a breakthrough in developing new treatments that better target the causes of the disorder. The idea that the immune system might play a part in schizophrenia was first floated 10 years ago. Since then, a couple of studies have found that people with schizophrenia seem to have more active microglia – the immune cells of the brain. Peter Bloomfield at Imperial College London wondered if this increased immune system activity might be detectable before a person is diagnosed with schizophrenia. His team examined 14 people who had been identified as being at “ultra-high risk” of developing the disorder – they had already seen a doctor about symptoms like paranoia or hallucinations, but hadn’t yet had a psychotic episode. Typically, between 20 and 35 per cent of such individuals will go on to be diagnosed with schizophrenia. By injecting a dye that labels active cells and using a PET scanner, Bloomfield’s team compared the activity of these people’s microglial cells with those of people with schizophrenia, as well as healthy people. They found increased microglial activity in both those who had schizophrenia, and those who had been classified as ultra-high risk. “What’s interesting is that the level of activity correlated with the severity of symptoms,” says Bloomfield. During the study, two of the 14 at ultra-high risk went on to develop schizophrenia and schizotypal disorder – these people had the highest levels of microglial activity, says Bloomfield. © Copyright Reed Business Information Ltd.
By ANDREW SOLOMON INEXPLICABLE violence is the hardest kind to accept. The human wish to insert logic where there is none often drives bystanders to psychic violence of their own. This happened again last week, after it was reported that the shooter at Umpqua Community College in Oregon, Christopher Harper-Mercer, who killed nine people and injured several others, may have been autistic. Although there is no established connection between autism and murder, some eagerly leapt to causality and scapegoating. The killer’s “diagnosis” was based primarily on posts on Yahoo made over the last decade by his mother, Laurel Harper, in which she characterized both herself and her son as having Asperger’s syndrome — a category no longer in medical use that describes autistic people with advanced verbal skills. Mr. Harper-Mercer attended a school that caters to children with special needs, including autism. While Ms. Harper is not a doctor, her descriptions of her son across his childhood are consistent with the syndrome. A Facebook page called “Families Against Autistic Shooters” ranted about “the soulless, dead eyes of autistic children,” and characterized them as “cold, calculating killing machines with no regard for human life!” Its author announced: “What do all shooters over the last few years have in common? A lack of empathy and compassion due to Autism!” If Mr. Harper-Mercer were rumored to have been diabetic or afflicted with male-pattern baldness, no such “explanations” of his behavior would have surfaced. But despite a huge increase in awareness of autism among the public, those with the condition are often subject to this type of disparagement. This was evident in both the Facebook page and the response to it by Facebook’s management, who, despite the site’s anti-bullying policy, initially refused to remove it on grounds that it did not target named individuals. “Families Against Autistic Shooters” remained accessible until last Monday, by which time escalating media attention and a petition on Change.org with nearly 5,000 signatures embarrassed administrators into action. For the time it was viewable, the page stigmatized a population far more likely to be attacked than to attack, far less likely to receive justice when injured, and far more likely to be misunderstood. © 2015 The New York Times Company
A new drug for multiple sclerosis can cut relapses by almost 50% more than the current standard treatment, its manufacturer claims, raising the hopes of sufferers of the disease. The Swiss pharmaceutical giant Roche announced the headline results for its drug, ocrelizumab, but has not published the detailed outcome of its trials. The announcement was warmly welcomed by patients, not least because Roche claims the drug also has an impact on a form of the disease, called primary-progressive, which affects 10-15% of people with MS in the UK and for which there are no treatments. Roche claimed it cut disability in those patients by nearly a quarter. “These phase three trial results will provide a great deal of hope for people with primary-progressive MS, who currently don’t have any treatments available that can slow down the worsening of their condition,” said Nick Rijke, the MS Society’s executive director for policy and research. “Finding effective treatments for multiple sclerosis is our number one priority at the MS Society and this is a big moment. The drug was compared in the trials with Rebif, an established drug made by Merck that reduces relapses by about a third. Ocrelizumab – which does not yet have a brand name – was said to cut annual relapses by 46% and 47% compared with Rebif in the two trials. The biggest advantage, however, may be that it is claimed to cause fewer side effects than the established drug. © 2015 Guardian News and Media Limited
By Erika Hayasaki For 40 years, Joel Dreyer was a respected psychiatrist who oversaw a clinic for troubled children, belonged to an exclusive country club, and doted on his four daughters and nine grandchildren. Then, suddenly, he became a major drug dealer. Why? In the 1980s, psychiatrist Joel Dreyer was a fixture on Detroit’s WXYZ Channel 7. His commercials promoting his treatment center, InnerVisions, which he named after the Stevie Wonder album, sometimes ran up to five times a day. In one ad, Dreyer blocks a bartender from serving a mug of beer to a patron and says, “Don’t let your marriage or your job suffer from alcohol or drugs.” In another, Dreyer, in a navy pinstriped suit with a white pocket square, looks into the camera, his expression concerned and sympathetic. “Don’t you want to talk to someone who will listen?” he asks. “Someone who won’t pass judgment? Someone who cares? Come talk to me.” InnerVisions, which was based in Southfield, a suburb northwest of Detroit, had a staff of 80 physicians, psychologists, and therapists and took up two floors of a high-rise. It had made Dreyer not only a public figure but also wealthy. He maintained a side career as an expert witness. Attorneys called on him because he was smart, charming, and persuasive. Dreyer mostly testified for the defense, and with each high-profile case, his celebrity grew. Between the clinic, trial work, and his private practice, he was earning as much as $450,000 a year. Dreyer loved to be the center of attention. He would sometimes ride to work on a motorcycle in a bejeweled Elvis outfit to entertain his colleagues.
Allison Aubrey We might not be able to remember every stressful episode of our childhood. But the emotional upheaval we experience as kids — whether it's the loss of a loved one, the chronic stress of economic insecurity, or social interactions that leave us tearful or anxious — may have a lifelong impact on our health. In fact, a study published this week in the Journal of the American College of Cardiology indicates that emotional distress during childhood — even in the absence of high stress during adult years — can increase the risk of developing heart disease and metabolic disorders such as diabetes in adulthood. Robert Wood Johnson Foundation Shots - Health News Take The ACE Quiz — And Learn What It Does And Doesn't Mean "We know that the childhood period is really important for setting up trajectories of health and well-being," explains Ashley Winning, an author of the study and postdoctoral research fellow in social and behavioral sciences at the Harvard T.H. Chan School of Public Health. To assess the connection between childhood stress and the risk of disease, Winning and her colleagues analyzed data from the 1958 British Birth Cohort Study, a long-running study that documented the diets, habits and emotional health of thousands of British children born during the same week that year. As the children entered school, the classroom became the laboratory for observation. © 2015 NPR
By Nicholas Bakalar Agitation and aggression are common in Alzheimer’s patients, and there is no known safe and effective treatment. Now researchers report that a combination drug already in use for treating certain neurological problems may be a better remedy. Dextromethorphan is a cough suppressant commonly found in over-the-counter cough medicines, and quinidine is a drug used to control heart rhythm disorders. In combination, they are used to treat certain neurological disorders involving involuntary movement of the facial muscles. The scientists randomized 152 Alzheimer’s patients to a 10-week course of dextromethorphan-quinidine and 127 to placebo. Researchers then rated them using a well-validated scale that measures aggression and agitation. The study is in the Sept. 22 issue of JAMA. Aggression scores declined to 3.8 from 7.1 in the dextromethorphan-quinidine group and to 5.3 from 7.0 in those who took a placebo. Then the researchers re-randomized those who did not respond to placebo to receive either drugs or placebo, and found similar encouraging results for the drug combination. “Fifty-five percent of the people who were on drugs had a 50 percent reduction in their agitation,” said the lead author, Dr. Jeffrey L. Cummings, director of the Cleveland Clinic Lou Ruvo Center for Brain Health. “That’s a lot when a patient is striking and hitting and cussing. There are no currently approved treatments for agitation, and we’re very enthusiastic about this finding.” © 2015 The New York Times Company
By Sarah C. P. Williams Looking at photos of starving refugees or earthquake victims can trigger a visceral sense of empathy. But how, exactly, do we feel others’ agony as our own? A new study suggests that seeing others in pain engages some of the same neural pathways as when we ourselves are in pain. Moreover, both pain and empathy can be reduced by a placebo effect that acts on the same pathways as opioid painkillers, the researchers found. “This study provides one of the most direct demonstrations to date that first-hand pain and pain empathy are functionally related,” says neurobiologist Bernadette Fitzgibbon of Monash University in Melbourne, Australia, who was not involved in the new research. “It’s very exciting.” Previous studies have used functional magnetic resonance imaging (fMRI) scans to show that similar areas of the brain are activated when someone is in pain and when they see another person in pain. But overlaps on a brain scan don’t necessarily mean the two function through identical pathways—the shared brain areas could relate to attention or emotional arousal, among other things, rather than pain itself. Social neuroscientist Claus Lamm and colleagues at the University of Vienna took a different approach to test whether pain and empathy are driven by the same pathways. The researchers first divided about 100 people into control or placebo groups. They gave the placebo group a pill they claimed to be an expensive, over-the-counter painkiller, when in fact it was inactive. This well-established placebo protocol is known to function similarly to opioid painkillers, while avoiding the drugs’ side effects. © 2015 American Association for the Advancement of Science.
By Sarah C. P. Williams When the human body needs extra energy, the brain tells fat cells to release their stores. Now, for the first time, researchers have visualized the nerves that carry those messages from brain to fat tissue. The activation of these nerves in mice, they found, helps the rodents lose weight—an observation that could lead to new slimming treatments for obese people. “The methods used here are really novel and exciting,” says neuroendocrinologist Heike Muenzberg-Gruening of Louisiana State University’s Pennington Biomedical Research Center in Baton Rouge, who was not involved in the new study. “Their work has implications for obesity research and also for studying these nerves in other tissues.” Diagrams of the chatter between the brain and fat tissues have long included two-way arrows: Fat cells produce the hormone leptin, which travels to the brain to lower appetite and boost metabolism. In turn, the brain sends signals to the fat cells when it’s time to break down their deposits of fatty molecules, such as lipids, into energy. Researchers hypothesized that there must be a set of nerve cells that hook up to traditional fat tissue to carry these messages, but they’d never been able to indisputably see or characterize them. Now they have. Thanks to two forms of microscopy, neurobiologist Ana Domingos, of the Instituto Gulbenkian de Ciência in Oeiras, Portugal, produced images showing bundles of nerves clearly enveloping fat cells in mice. She and her colleagues went on to show, using various stains, that the nerves were a type belonging to the sympathetic nervous system that stretches outward from the spinal cord and keeps the body’s systems in balance. © 2015 American Association for the Advancement of Science
Link ID: 21448 - Posted: 09.26.2015
Dark puffy eyes, a feeling of deep exhaustion, and a foul mood to match – we’ve all experienced the side effects of a lack of sleep. It’s no wonder that sleep-deprivation has been used as a method of torture. Our brains seem to lose the ability to distinguish between the innocuous and emotional in such circumstances, turning us into overreacting, exhausted wrecks. We all know that a good night’s sleep is vital for a day of clear thinking, but exactly why sleep is so important remains a mystery. Talma Hendler of Tel Aviv University in Israel is particularly interested in how lack of sleep leaves us with a short emotional fuse. “We know that sleep affects our emotional behaviour, but we don’t know how,” she says. To investigate further, Hendler and her colleagues kept 18 adults awake all night. “It took a great effort,” she says. “During the night, we repeatedly measured their sleepiness, and unsurprisingly they got more and more tired.” The volunteers were put through two rounds of tests while their brains were scanned, both the day after a good night’s sleep and after being awake for 24 hours. In one test, volunteers were asked to give the direction in which yellow dots moved on a screen. In each case, the dots were laid over a potentially distracting picture that was either positively emotional (of a kitten or a couple in love, for example), negatively emotional (such as a mutilated body or a snake) or neutral (such as a cow or spoon). © Copyright Reed Business Information Ltd.
Ian Sample Science editor Government lawyers are seeking to block compensation payments to people who developed the devastating sleep disorder, narcolepsy, as a result of a faulty swine flu vaccine. The Pandemrix vaccine made by GlaxoSmithKline (GSK) was given to 6 million people in Britain and millions more across Europe during the 2009-10 swine flu pandemic, but was withdrawn when doctors noticed a rise in narcolepsy cases among those who received the jab. In June, a 12-year-old boy was awarded £120,000 by a court that ruled he had been left severely disabled by narcolepsy caused by Pandemrix. The win ended a three-year battle with the government that argued his illness was not serious enough to warrant compensation. Narcolepsy is a permanent condition that can cause people to fall asleep dozens of times a day, even when they are in mid-conversation. Some suffer from night terrors and a problem with muscular control called cataplexy that can lead them to collapse on the spot. The boy, who remains anonymous, has become disruptive at school because he is so tired and finds it almost impossible to socialise. He needs to take several naps in the school day and cannot shower unattended or take a bus alone. He may never be able to drive as an adult. © 2015 Guardian News and Media Limited
HOW would you punish a murderer? Your answer will depend on how active a certain part of your brain happens to be. Joshua Buckholtz at the University of Harvard and his colleagues gave 66 volunteers scenarios involving a fictitious criminal called John. Some of his crimes were planned. In others, he was experiencing psychosis or distress – for example, his daughter’s life under threat. The volunteers had to decide how responsible John was for each crime and the severity of his punishment on a scale of 0 to 9. Before hearing the stories, some of the volunteers received magnetic stimulation to a brain region involved in decision-making, called the dorsolateral prefrontal cortex (DLPFC), which dampened its activity. The others were given a sham treatment. Inhibiting the DLPFC didn’t affect how responsible the volunteers thought John was for the crimes, or the punishment he should receive when he was not culpable for his actions. But they meted out a much less severe punishment than the control group when John had planned his crime (Neuron, doi.org/7rh). “By altering one process in the brain, we can alter our judgements,” says Christian Ruff at the Swiss Federal Institute of Technology in Zurich. In the justice system, the judgment stage to determine guilt is separated from sentencing, says James Tabery at the University of Utah. “It turns out that our brains work in a similar fashion.” © Copyright Reed Business Information Ltd.
By Jessica Schmerler Selfies, headshots, mug shots — photos of oneself convey more these days than snapshots ever did back in the Kodak era. Most digitally minded people continually post and update pictures of themselves at professional, social media and dating sites such as LinkedIn, Facebook, Match.com and Tinder. For better or worse, viewers then tend to make snap judgments about someone’s personality or character from a single shot. As such, it can be a stressful task to select the photo that conveys the best impression of ourselves. For those of us seeking to appear friendly and trustworthy to others, a new study underscores an old, chipper piece of advice: Put on a happy face. A newly published series of experiments by cognitive neuroscientists at New York University is reinforcing the relevance of facial expressions to perceptions of characteristics such as trustworthiness and friendliness. More importantly, the research also revealed the unexpected finding that perceptions of abilities such as physical strength are not dependent on facial expressions but rather on facial bone structure. The team’s first experiment featured photographs of 10 different people presenting five different facial expressions each. Study subjects rated how friendly, trustworthy or strong the person in each photo appeared. A separate group of subjects scored each face on an emotional scale from “very angry” to “very happy.” And three experts not involved in either of the previous two ratings to avoid confounding results calculated the facial width-to-height ratio for each face. An analysis revealed that participants generally ranked people with a happy expression as friendly and trustworthy but not those with angry expressions. Surprisingly, participants did not rank faces as indicative of physical strength based on facial expression but graded faces that were very broad as that of a strong individual. © 2015 Scientific American
Link ID: 21436 - Posted: 09.24.2015
Rachel Ehrenberg If not for a broken piece of lab equipment and a college crush, Steve Ramirez might never have gone into neuroscience. As an undergraduate at Boston University his interests were all over the place: He was taking a humanities course and classes in philosophy and biochemistry while working several hours a week in a biology lab. When the lab’s centrifuge, a device that spins liquids, broke, Ramirez had to use one in another lab. “I was trying to make small talk with this girl who was using the centrifuge, ‘What’s your major?’ kind of thing,” Ramirez recalls. Hearing of his myriad interests, the student suggested that Ramirez talk with neuroscientist Paul Lipton. That led to a conversation with Howard Eichenbaum, a leading memory researcher. Eichenbaum told him that everything Ramirez was interested in was about the brain. “Everything from the pyramids to putting a man on the moon, it’s all the product of the human brain, which is kind of crazy when you think about it,” Ramirez says. Studying “the most interdisciplinary organ in existence,” as Ramirez calls it, was a natural fit. While working in Eichenbaum’s lab, Ramirez got turned on to how the brain forms memories. Those explorations led to a Ph.D. program at MIT in the lab of Nobel laureate Susumu Tonegawa, where Ramirez focused on the individual brain cells that hold specific memories. © Society for Science & the Public 2000 - 2015.
By MATTHEW HUTSON ANGER is a primal and destructive emotion, disrupting rational discourse and inflaming illogical passions — or so it often seems. Then again, anger also has its upsides. Expressing anger, for example, is known to be a useful tool in negotiations. Indeed, in the past few years, researchers have been learning more about when and how to deploy anger productively. Consider a forthcoming paper in the November issue of the Journal of Experimental Social Psychology. Researchers tested the effectiveness of expressing anger in three types of negotiations: those that are chiefly cooperative (say, starting a business with a partner), chiefly competitive (dissolving a shared business) or balanced between the two (selling a business to a buyer). In two experiments, negotiators made greater concessions to those who expressed anger — but only in balanced situations. When cooperating, hostility seems inappropriate, and when competing, additional heat only flares tempers. But in between, anger appears to send a strategically useful signal. What does that signal communicate? According to a 2009 paper in Proceedings of the National Academy of Sciences, anger evolved to help us express that we feel undervalued. Showing anger signals to others that if we don’t get our due, we’ll exert harm or withhold benefits. As they anticipated, the researchers found that strong men and attractive women — those who have historically had the most leverage in threatening harm and conferring benefits, respectively — were most prone to anger. The usefulness of anger in extracting better treatment from others seems to be something we all implicitly understand. A 2013 paper in the journal Cognition and Emotion found that when people were preparing to enter a confrontational negotiation, as opposed to a cooperative one, they took steps to induce anger in themselves (choosing to listen to aggressive versus happy music, for example). © 2015 The New York Times Company
Link ID: 21426 - Posted: 09.21.2015
By Sarah C. P. Williams Immune cells are usually described as soldiers fighting invading viruses and bacteria. But they may also be waging another battle: the war against fat. When mice lack a specific type of immune cell, researchers have discovered, they become obese and show signs of high blood pressure, high cholesterol, and diabetes. The findings have yet to be replicated in humans, but they are already helping scientists understand the triggers of metabolic syndrome, a cluster of conditions associated with obesity. The new study “definitely moves the field forward,” says immunologist Vishwa Deep Dixit of the Yale School of Medicine, who was not involved in the work. “The data seem really solid.” Scientists already know that there is a correlation between inflammation—a heightened immune response—and obesity. But because fat cells themselves can produce inflammatory molecules, distinguishing whether the inflammation causes weight gain or is just a side effect has been tricky. When he stumbled on this new cellular link between obesity and the immune system, immunologist Yair Reisner of the Weizmann Institute of Science in Rehovot, Israel, was studying something completely different: autoimmune diseases. An immune molecule called perforin had already been shown to kill diseased cells by boring a hole in their outer membrane. Reisner’s group suspected that dendritic cells containing perforin might also be destroying the body’s own cells in some autoimmune diseases. To test the idea, Reisner and his colleagues engineered mice to lack perforin-wielding dendritic cells, and then waited to see whether they developed any autoimmune conditions. © 2015 American Association for the Advancement of Science
A choir of Canadians with Parkinson's disease is helping researchers test how well the performers regain facial movement to express emotions. Tremors and difficulty walking are often the most noticeable symptoms of Parkinson's disease, which affects about one in 500 people in Canada. Those with the disease may also have limited facial movement, which hampers the ability to express themselves. For people with Parkinson's who have "masked face syndrome," it can be difficult for others to decipher how they're feeling. That's because we unknowingly mimic or mirror each other during interaction to connect. "Within a hundred milliseconds of seeing someone else smile or frown, we are smiling or frowning," said Frank Russo, a psychology professor at Ryerson University in Toronto. "We're mirroring what the other person is doing. And that's one of the things that is absent in Parkinson's. It's the absence of mirroring that is leading to some of the deficit in understanding other people's emotions." Having a static face can leave people with Parkinson's seem cold and aloof as they also show deficits in understanding other people's emotions. The patient can then become emotionally disconnected from others. Studying the 28 members of the Parkinson's choir has bolstered Russo's thinking that singing, facial expressions and social communications are interconnected. So far Russo has found that mirroring effect or mimicry was restored among choir participants who sang for 13 weeks. ©2015 CBC/Radio-Canada.
By Bruce Bower Lemurs don’t yawn in the face of danger. They wait a few minutes after perils have passed before breaking into breathy mouth gapes. Lemurs in a southern Madagascar reserve yawned frequently within 10 minutes of fighting with other lemurs, surviving attacks by predatory birds and coming close to snakes, tourists or other potential dangers, primatologist Elisabetta Palagi of the University of Pisa in Italy and her colleagues report August 28 in the American Journal of Primatology. Lemurs largely stopped yawning after that brief outburst. This pattern held for 13 ring-tailed lemurs and 15 Verreaux’s sifakas tracked daily for three months in 2011. Recurring dangers that lemurs learn to escape or avoid elicit moderate, brief anxiety, the researchers suspect. Yawning amps up as animals rapidly return to calmness, much as it increases when lemurs take rest breaks during the day, Palagi’s team says. Many physiological and social forces contribute to yawning, they add. Citations A. Zannella et al. Testing yawning hypotheses in wild populations of two strepsirrhine species: Propithecus verreauxi and Lemur catta. American Journal of Primatology. Published August 28, 2015. doi:10.1002/ajp.22459. © Society for Science & the Public 2000 - 2015.
Link ID: 21387 - Posted: 09.09.2015
Sara Reardon Antipsychotic drugs are widely used to blunt aggressive behaviour in people with intellectual disabilities who have no history of mental illness, a UK survey of medical records finds, even though the medicines may not have a calming effect. The finding is worrisome because antipsychotic drugs can cause severe side effects such as obesity or diabetes. Psychiatry researcher Rory Sheehan and colleagues1 at University College London studied data from 33,016 people with intellectual disabilities from general-care practices in the United Kingdom over a period of up to 15 years. The researchers found that 71% of 9,135 people who were treated with antipsychotics had never been diagnosed with a severe mental illness, and that the drugs were more likely to be prescribed to those who displayed problematic behaviours. “We suspected that this would be the case, but we didn’t know the true extent,” Sheehan says. “We should be worried because the rates are high,” says James Harris, a psychiatrist at Johns Hopkins University in Baltimore, Maryland. But he adds that it is hard to determine whether treatment with antipsychotics is appropriate without knowing what other forms of treatment were available to people in the study. It is possible that medication was the only option available or that it was used to dampen a person's behaviour enough that they could participate in therapy or other types of treatment. Evidence suggests that the drugs are not effective at treating aggressive and disruptive behaviour, says psychiatrist Peter Tyrer of Imperial College London. I © 2015 Nature Publishing Group