Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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By Janet Davison, CBC News Jason Novick has seen the darkness that mental health disorders can create. The 27-year-old Toronto man has also seen how advocacy — by himself and by others — has been vital in helping him cope with bipolar disorder, general anxiety disorder, mania and depression, particular during the stressful transition from his teenage years to leaving home for post-secondary school. "Mental health awareness … is still an issue that’s largely misunderstood," he said in a recent interview. "There’s a lot of [post-secondary] administrative workers and professors and program co-ordinators and what have you who won’t know the first thing about such issues, so your best ally is probably going to be yourself a lot of the time." Another ally can also be a caring friend or family member who steps up to help others understand the larger situation. Novick remembers going with his mother to "set the record straight" with a college professor. They wanted to explain to the instructor that it was his mental health that was his problem, not any lack of interest in the course. "It was my mental health that was causing me to be so withdrawn, that was causing me to be so unmotivated. I was passionate about the subject, but I was not passionate about life and living." Novick, who says he contemplated suicide at one point and has been in closed hospital wards three times because of his disorders, is much more passionate about life and living now, particularly after having completed an inpatient program at the Centre for Addiction and Mental Health in Toronto. © CBC 2013
By JAMES GORMAN Worldwide, 100,000 people have electrical implants in their brains to treat the involuntary movements associated with Parkinson’s disease, and scientists are experimenting with the technique for depression and other disorders. But today’s so-called deep brain stimulation only treats — it does not monitor its own effectiveness, partly because complex ailments like depression do not have defined biological signatures. The federal Defense Advanced Research Projects Agency, known as Darpa, announced Thursday that it intended to spend more than $70 million over five years to jump to the next level of brain implants, either by improving deep brain stimulation or by developing new technology. Justin Sanchez, Darpa program manager, said that for scientists now, “there is no technology that can acquire signals that can tell them precisely what is going on with the brain.” And so, he said, Darpa is “trying to change the game on how we approach these kinds of problems.” The new program, called Systems-Based Neurotechnology and Understanding for the Treatment of Neuropsychological Illnesses, is part of an Obama administration brain initiative, announced earlier this year, intended to promote innovative basic neuroscience. Participants in the initiative include Darpa, as well as the National Institutes of Health and the National Science Foundation. The announcement of Darpa’s goal is the first indication of how that research agency will participate in the initiative. The money is expected to be divided among different teams, and research proposals are now being sought. Darpa’s project is partly inspired by the needs of combat veterans who suffer from mental and physical conditions, and is the first to invest directly in researching human illness as part of the brain initiative. © 2013 The New York Times Company
Amanda Mascarelli Duplication of a single gene — and too much of the corresponding protein in brain cells — causes mice to have seizures and display manic-like behaviour, a study has found. But a widely used drug reversed the symptoms, suggesting that it could also help some people with hyperactivity who do not respond to common treatments. Smooth functioning at the synapses, the junctions between brain cells, is crucial to functions that control everything from social etiquette to everyday decision-making. It is increasingly thought that some neuropsychiatric disorders are caused by function of the synapses going awry1, and indeed researchers have found that neuropsychiatric conditions such as schizophrenia and autism can sometimes be traced to missing, mutated or duplicated copies of SHANK32, a gene that encodes one of the 'architectural' proteins that help to ensure that messages are relayed properly between cells. Some people with attention deficit hyperactivity disorder (ADHD), Asperger's syndrome or schizophrenia have an extra copy of a wider region of DNA that contains SHANK33. To explore the role of SHANK3, Huda Zoghbi, a neurogeneticist at Baylor College of Medicine in Houston, Texas, and her colleagues created mice with duplicate copies of the gene. “The mouse was remarkably hyperactive, running around like mad,” says Zoghbi. But the animals did not respond to stimulant medications typically used to treat ADHD. Instead, their hyperactivity grew much worse. “That’s when we knew this was not typical ADHD,” says Zoghbi. The study is published today in Nature4. © 2013 Nature Publishing Group
by Bruce Bower Thomas Jefferson defended the right to pursue happiness in the Declaration of Independence. But that’s so 237 years ago. Many modern societies champion everyone’s right to be happy pretty much all the time. Good luck with that, says psychologist Joseph Forgas of the University of New South Wales in Sydney. A lack of close friends, unfulfilled financial dreams and other harsh realities leave many people feeling lonely and forlorn a lot of the time. But there’s a mental and social upside to occasional downers that often goes unappreciated. “Bad moods are seen in our happiness-focused culture as representing a problem, but we need to be aware that temporary, mild negative feelings have important benefits,” Forgas says. Growing evidence suggests that gloomy moods improve key types of thinking and behavior, Forgas asserts in a new review paper aptly titled “Don’t worry, be sad!” For good evolutionary reasons, positive and negative moods subtly recruit thinking styles suited to either benign or troubling situations, he says. Each way of dealing with current circumstances generally works well, if imperfectly. New and recent studies described by Forgas in the June Current Directions in Psychological Science illustrate some of the ways in which periods of sadness spontaneously recruit a detail-oriented, analytical thinking style. Morose moods have evolved as early-warning signs of problematic or dangerous situations that demand close attention, these reports suggest. © Society for Science & the Public 2000 - 2013.
By Lary C. Walker Clumps of proteins twisted into aberrant shapes cause the prion diseases that have perplexed biologists for decades. The surprises just keep coming with a new report that the simple clusters of proteins responsible for Mad Cow and other prions diseases may, without help from DNA or RNA, be capable of changing form to escape the predations of drugs that target their eradication. Prion drug resistance could be eerily similar to that found in cancer and HIV—and may have implications for drug development for Alzheimer’s and Parkinson’s, neurodegenerative diseases also characterized by misfolded proteins. Prion diseases include scrapie, chronic wasting disease and bovine spongiform encephalopathy (mad cow disease) in nonhuman species, and Creutzfeldt-Jakob disease and fatal insomnia in humans. They are unusual in that they can arise spontaneously, as a result of genetic mutations, or, in some instances, through infection. Remarkably, the infectious agent is not a microbe or virus, but rather the prion itself, a clump of proteins without genetic material. The noxious agents originate when a normally generated protein – called the prion protein – mistakenly folds into a stable, sticky, and potentially toxic shape. When the misfolded protein contacts other prion protein molecules, they too are corrupted and begin to bind to one another. In the ensuing chain reaction, the prions grow, break apart, and spread; within the nervous system, they relentlessly destroy neurons, ultimately, and invariably, leading to death. © 2013 Scientific American
Anne Trafton, MIT News Office Schizophrenia patients usually suffer from a breakdown of organized thought, often accompanied by delusions or hallucinations. For the first time, MIT neuroscientists have observed the neural activity that appears to produce this disordered thinking. The researchers found that mice lacking the brain protein calcineurin have hyperactive brain-wave oscillations in the hippocampus while resting, and are unable to mentally replay a route they have just run, as normal mice do. Mutations in the gene for calcineurin have previously been found in some schizophrenia patients. Ten years ago, MIT researchers led by Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, created mice lacking the gene for calcineurin in the forebrain; these mice displayed several behavioral symptoms of schizophrenia, including impaired short-term memory, attention deficits, and abnormal social behavior. In the new study, which appears in the Oct. 16 issue of the journal Neuron, Tonegawa and colleagues at the RIKEN-MIT Center for Neural Circuit Genetics at MIT’s Picower Institute for Learning and Memory recorded the electrical activity of individual neurons in the hippocampus of these knockout mice as they ran along a track. Previous studies have shown that in normal mice, “place cells” in the hippocampus, which are linked to specific locations along the track, fire in sequence when the mice take breaks from running the course. This mental replay also occurs when the mice are sleeping. These replays occur in association with very high frequency brain-wave oscillations known as ripple events.
Link ID: 18798 - Posted: 10.17.2013
Ewen Callaway As a new study in the British Medical Journal reveals that 1 in 2000 people in the UK may harbour the infectious prion protein which causes variant Creutzfeldt–Jakob disease (vCJD), Nature explains what this means. The usually fatal condition is the human form of bovine spongiform encepalpoathy — dubbed 'mad cow disease' in the UK after an outbreak of the disease in the 1980s. Both diseases are caused by misfolded proteins called prions, which induce other proteins in the brain to clump, eventually destoying neurons. Humans are thought to contract the disease by consuming beef containing infected bovine brain or other central nervous system tissue. But it also spreads through blood transfusions, and some worry that the prion disease is transmitted via contaminated surgical instruments . The BSE outbreak in the 1980s and 1990s led to a surge in British vCJD cases, and a total of 177 have been detected in the UK to date, with just one in the last two years. Cases of vCJD peaked in 2000, leading some scientists to speculate that the disease takes about a decade to develop. Yet other studies of different forms of CJD suggest its incubation time could be much longer — indicating that many Britons may be carrying the infection without symtoms. Studies have come to varying conclusions as to just how many people harbour the abnormal prion protein (PrP) that causes vCJD. Surveys of tens of thousands of appendices and tonsil, discarded after surgery, have come up with prevalence rates ranging from 1 in 40001 to 1 in 10,0002 to 03. © 2013 Nature Publishing Group
Link ID: 18795 - Posted: 10.16.2013
by Simon Makin A drug similar to ketamine has been shown to work as an antidepressant, without the psychosis-like side effects associated with the party drug. In 2000, ketamine was seen to alleviate depression almost immediately in people for whom other treatments had failed. Larger clinical trials have since corroborated the findings. The drawback is that ketamine can cause hallucinations and other psychotic symptoms, making it unsuitable for use as a treatment. These effects also make it difficult to conduct randomised, placebo-controlled trials – the gold standard in clinical medicine – as it is obvious which participants have been given the drug. This meant that there was a possibility that the beneficial effects seen in previous trials were inflated. So a team led by Gerard Sanacora of Yale University and Mike Quirk of pharmaceutical firm AstraZeneca looked for an alternative compound. They decided to test lanicemine, a drug originally developed to treat epilepsy that targets the same brain receptors as ketamine. The team gave 152 people with moderate-to-severe depression and a history of poor response to antidepressants either lanicemine or a placebo three times a week, for three weeks. They were allowed to continue taking any medications they were already on. Before and after the trial the participants' level of depression was rated on a 60-point scale. After three weeks, those taking lanicemine were less depressed by an average of 13.5 points – 5.5 points better than those who took the placebo. The improvement was still statistically significant up to two weeks after the treatment ended. Dizziness was the only common side effect. © Copyright Reed Business Information Ltd.
Mind over matter. New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules. While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain. Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.) While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons. © 2013 American Association for the Advancement of Science.
Link ID: 18781 - Posted: 10.12.2013
Children whose mothers are depressed during pregnancy have a small increased risk of depression in adulthood, according to a UK study. Medical treatment during pregnancy could lower the risk of future mental health problems in the child, say researchers at Bristol University. The study followed the offspring of more than 8,000 mothers who had postnatal or antenatal depression. The risk is around 1.3 times higher than normal at age 18, it found. The study is published in JAMA Psychiatry. Lead researcher Dr Rebecca Pearson told the BBC: "Depression in pregnancy should be taken seriously and treated in pregnancy. It looks like there is a long-term risk to the child, although it is small." She said it was an association, not a causal link, and needed further investigation. Prof Carmine Pariante of King's College London's Institute of Psychiatry said the development of an individual's mental health did not start at birth but in the uterus. "The message is clear - helping women who are depressed in pregnancy will not only alleviate their suffering but also the suffering of the next generation." Prof Celso Arango of Gregorio Maranon General University Hospital, Madrid, said stress hormones may affect the child's development in the womb. "Women with depression would ideally be treated before getting pregnant, but if they are already pregnant when diagnosed with depression it is even more important that they are treated as it will impact on the mother and child." The researchers think different factors may be involved in antenatal and postnatal depression, with environmental factors such as social support having a bigger impact in postnatal depression. BBC © 2013
Alison Abbott In a sign that psychiatric-disease research is entering a new era, the pharmaceutical giant Novartis has hired an expert in neural circuitry, rather than pharmacology, to head its relaunched neuroscience division. The appointment of 42-year-old Ricardo Dolmetsch, who has spent his entire career in academic research, signifies a radical policy shift for the company, as it moves away from conventional neurotransmitter research to concentrate on analysing the neural circuitry that causes brain diseases. The decision suggests Novartis is confident that after years of fruitless research in the field, revolutionary advancements in, for example, genetic and stem-cell technologies will pay dividends. The company intends to hire 100 new staff members for the department over the next 3 years. But the move is risky: even if it pans out, new drugs for common disorders such as schizophrenia could be decades away from reaching the market. Dolmetsch, a former senior director at the Allen Institute for brain Science in Seattle, Washington, who has also worked at Stanford University School of Medicine in California, says that his new role gives him access to previously unimaginable resources. “I had this idea that big pharma was a slow, plodding, conservative giant,” he says. “I was surprised by the depth of science at Novartis.” An expert in autism spectrum disorder, he was also attracted by the prospect of contributing to the development of therapies — something that academic institutions are poorly equipped to do — particularly because one of his own sons has autism. There was “not much enthusiasm” for studying disease at the Allen Institute, which focuses instead on basic research into brain science, he says. © 2013 Nature Publishing Group
by Linda Geddes There's little doubt that smoking during pregnancy is bad for the baby. But besides stunting growth and boosting the risk of premature birth, it seems that tobacco smoke leaves a lasting legacy on the brain. Children whose mothers smoked during pregnancy have altered brain growth, which may put them at greater risk of anxiety and depression. Hanan El Marroun at Erasmus Medical Center in Rotterdam, the Netherlands, and her colleagues had previously seen impaired brain growth in babies born to women who smoked throughout their pregnancy, although no differences were seen if women stopped smoking soon after learning that they were pregnant. The question was whether these changes were permanent, or would correct themselves as the child developed. So El Marroun's team used MRI to look at the brains of 113 children aged between 6 and 8 years old whose mothers smoked during pregnancy, and another 113 children whose mums did not. The children's behavioural and emotional functioning was also tested. Depression link Those whose mothers smoked throughout pregnancy had smaller total brain volumes and reduced amounts of grey and white matter in the superior frontal cortex, an area involved in regulating moods. What's more, these structural differences correlated with symptoms of depression and anxiety in the children. Not every child whose mother smoked showed these symptoms, and the study could not definitively prove cause and effect. However, because we already know that smoking is bad for babies, pregnant women should continue to be advised not to smoke, El Marroun says. © Copyright Reed Business Information Ltd.
By Gary Stix Psychological depression is more than an emotional state. Good evidence for that comes from emerging new uses for a technology already widely prescribed for Parkinson’s patients. The more neurologists and surgeons learn about the aptly named deep brain stimulation, the more they are convinced that the currents from the technology’s implanted electrodes can literally reboot brain circuits involved with the mood disorder. Thomas Schlaepfer, a psychiatrist from the University of Bonn Hospital and a leading expert in researching deep brain stimulation, describes in the interview that follows the workings of the technique and why it may help the severely depressed. Can you explain what deep brain stimulation is and what it is currently used for? Deep brain stimulation refers to the implantation of very small electrodes in both hemispheres of the brain, which are connected to a neurostimulator, usually placed under the skin on the right chest. This device is in size and function very similar to a heart pacemaker. It allows stimulations of different pulse width and frequency. Depending on the chosen stimulation parameters the electrodes in the brain are able to “neuromodulate” – to reversibly alter the function – of the surrounding brain tissue. Deep brain stimulation has gained widespread acceptance as a successful treatment for tremor associated with Parkinson’s disease. More than 80,000 patients worldwide have been treated with this method. Some see deep brain stimulation as a much less invasive and fully reversibly alternative to historical neurosurgical interventions, which require tiny amounts of brain tissue to be destroyed in order to have clinical effects. © 2013 Scientific American
Link ID: 18747 - Posted: 10.05.2013
By NICHOLAS BAKALAR Depression may be an independent risk factor for Parkinson’s disease, a new study has found. In a retrospective analysis, researchers followed 4,634 patients with depression and 18,544 matched controls for 10 years. To rule out the possibility that depression is an early symptom of Parkinson’s disease, their analysis excluded patients who received a diagnosis of depression within five years of their Parkinson’s diagnosis. The average age of people with depression was 41, while it was 64 for those with both depression and Parkinson’s. The study, published online in Neurology, found that 66 patients with depression, or 1.42 percent, developed Parkinson’s disease, compared with 97, or 0.52 percent, among those who were not depressed. After controlling for age, sex, diabetes, hypertension and other factors, the researchers found clinical depression was associated with more than three times the risk for Parkinson’s disease. “Our paper does not convey the message that all depression leads to Parkinson’s disease,” said the senior author, Dr. Albert C. Yang, a professor of psychiatry at the National Yang-Ming University in Taiwan. “But particularly the depressed elderly and those with difficult-to-treat depression should be alert to the possibility of neurological disease and Parkinson’s.” Copyright 2013 The New York Times Company
By Travis Riddle Humans like being around other humans. We are extraordinarily social animals. In fact, we are so social, that simply interacting with other people has been shown to be use similar brain areas as those involved with the processing of very basic rewards such as food, suggesting that interacting with people tends to make us feel good. However, it doesn’t take much reflection to notice that the way people interact with each other has radically changed in recent years. Much of our contact happens not face-to-face, but rather while staring at screen-based digital representations of each other, with Facebook being the most prominent example. This raises a very fundamental question – how does online interaction with other people differ from interacting with people in person? One possible way these two interaction styles might differ is through how rewarding we find them to be. Does interacting with Facebook make us feel good as does interacting with people in real life? A recent paper suggests that the answer is “probably not.” In fact, the data from this paper suggest that the more we interact with Facebook, the worse we tend to feel. Researchers recruited participants from around a college campus. The participants initially completed a set of questionnaires, including one measuring their overall satisfaction with life. Following this, participants were sent text messages 5 times a day for two weeks. For each text, participants were asked to respond to several questions, including how good they felt at that moment, as well as how much they had used Facebook, and how much they had experienced direct interaction with others, since the last text. At the end of the two weeks, participants completed a second round of questionnaires. Here, the researchers once again measured participants’ overall satisfaction with life. © 2013 Scientific American
by Linda Geddes They say the early bird catches the worm, but night owls may be missing far more than just a tasty snack. Researchers have discovered the first physical evidence of structural brain differences that distinguish early risers from people who like to stay up late. The differences might help to explain why night owls seem to be at greater risk of depression. Around 10 per cent of people qualify as morning people or larks, and a further 20 per cent are night owls – with the rest of us falling somewhere in between. Your lark or night owl status is called your chronotype. Previous studies have suggested that night owls experience worse sleep, more tiredness during the day and consume greater amounts of tobacco and alcohol. This has prompted some to suggest that they are suffering from a form of chronic jet lag. To investigate further, Jessica Rosenberg at RWTH Aachen University in Germany and colleagues used diffusion tensor imaging to scan the brains of 16 larks, 23 night owls and 20 intermediate chronotypes. They found a reduction in the integrity of night owls' white matter – brain tissue largely comprised of fatty insulating material that speeds up the transmission of nerve signals – in areas associated with depression. "We think this could be caused by the fact that late chronotypes suffer from this permanent jet lag," says Rosenberg, although she cautions that further studies are needed to confirm cause and effect. © Copyright Reed Business Information Ltd.
By BRANDON A. GAUDIANO PROVIDENCE, R.I. — PSYCHOTHERAPY is in decline. In the United States, from 1998 to 2007, the number of patients in outpatient mental health facilities receiving psychotherapy alone fell by 34 percent, while the number receiving medication alone increased by 23 percent. This is not necessarily for a lack of interest. A recent analysis of 33 studies found that patients expressed a three-times-greater preference for psychotherapy over medications. As well they should: for patients with the most common conditions, like depression and anxiety, empirically supported psychotherapies — that is, those shown to be safe and effective in randomized controlled trials — are indeed the best treatments of first choice. Medications, because of their potential side effects, should in most cases be considered only if therapy either doesn’t work well or if the patient isn’t willing to try counseling. So what explains the gap between what people might prefer and benefit from, and what they get? The answer is that psychotherapy has an image problem. Primary care physicians, insurers, policy makers, the public and even many therapists are largely unaware of the high level of research support that psychotherapy has. The situation is exacerbated by an assumption of greater scientific rigor in the biologically based practices of the pharmaceutical industries — industries that, not incidentally, also have the money to aggressively market and lobby for those practices. For the sake of patients and the health care system itself, psychotherapy needs to overhaul its image, more aggressively embracing, formalizing and promoting its empirically supported methods. My colleague Ivan W. Miller and I recently surveyed the empirical literature on psychotherapy in a series of papers we edited for the November edition of the journal Clinical Psychology Review. It is clear that a variety of therapies have strong evidentiary support, including cognitive-behavioral, mindfulness, interpersonal, family and even brief psychodynamic therapies (e.g., 20 sessions). © 2013 The New York Times Company
Link ID: 18722 - Posted: 09.30.2013
If you look at the facts and figures on the mental health charity Mind's website, you'll find that around 1 in 4 people will experience some sort of mental health problem each year. About 10% of these people will see their doctor and be diagnosed as having a mental health problem, and of this group, a small proportion will in turn be referred to specialist psychiatric care. Of these people, precisely none resemble the breathtakingly ignorant costumes that have recently been withdrawn from Tesco and Asda. If you want to know what someone with a mental health issue looks like, just look around you. One of the most common types of mental health issue is anxiety – about 9% of people in Britain meet the criteria for mixed anxiety and depression, for example. We all feel anxious from time to time, and that's not necessarily a bad thing. Isaac Marks and Randy Nesse argued in 1994 that anxiety is an important emotion that has been shaped during the course of human evolution. If we are in a potentially dangerous environment, being anxious increases our awareness of our surroundings and puts us in a state of physiological readiness to deal with any threats. However, when an anxiety response kicks in too often, and in situations where it is not needed, it becomes a debilitating problem. In serious cases, anxiety can make it incredibly hard for the person to function. There's now a wealth of research that is trying to tap into the mechanisms involved in both sub-clinical and clinical forms of anxiety. By understanding what happens when we become anxious, we might be able to get a clearer idea of how and why things go wrong in anxiety disorders. For example, a new study published this week in the Journal of Neuroscience has suggested one potential contributing factor – how smells are processed. © 2013 Guardian News and Media Limited
By REED ABELSON THE first time Melissa Morelli was taken to the hospital, she was suicidal and cutting herself, her mother says. She was just 13, and she had been transferred to a psychiatric hospital, where she stayed for more than a week. Her doctors told her mother, Cathy Morelli, that it was not safe for Melissa to go home. But the family’s health insurance carrier would not continue to pay for her to remain in the hospital. The second time, the same thing happened. And the third and the fourth. Over the course of five months, Ms. Morelli took Melissa to the hospital roughly a dozen times, and each time the insurance company, Anthem Blue Cross, refused to pay for hospital care. “It was just a revolving door,” Ms. Morelli said. “You had not been getting better in a significant way,” Anthem explained in one letter sent directly to Melissa, then 14, in July 2012. “It does not seem likely that doing the same thing will help you get better.” Desperate to get help for her daughter, Ms. Morelli sought the assistance of Connecticut state officials and an outside reviewer. She eventually won all her appeals, and Anthem was forced to pay for the care it initially denied. All told, Melissa spent nearly 10 months in a hospital; she is now at home. Anthem, which would not comment on Melissa’s case, says its coverage decisions are based on medical evidence. Melissa’s treatment did not come cheap: it ultimately cost hundreds of thousands of dollars, Ms. Morelli said. Patients often find themselves at odds with health insurers, but the battles are perhaps nowhere so heated as with the treatment of serious mental illness. © 2013 The New York Times Company
By Michelle Roberts Health editor, BBC News online People prescribed anti-depressants should be aware they could be at increased risk of type 2 diabetes, say UK researchers. The University of Southampton team looked at available medical studies and found evidence the two were linked. But there was no proof that one necessarily caused the other. It may be that people taking anti-depressants put on weight which, in turn, increases their diabetes risk, the team told Diabetes Care journal. Or the drugs themselves may interfere with blood sugar control. Their analysis of 22 studies involving thousands of patients on anti-depressants could not single out any class of drug or type of person as high risk. Prof Richard Holt and colleagues say more research is needed to investigate what factors lie behind the findings. And they say doctors should keep a closer check for early warning signs of diabetes in patients who have been prescribed these drugs. With 46 million anti-depressant prescriptions a year in the UK, this potential increased risk is worrying, they say. Prof Holt said: "Some of this may be coincidence but there's a signal that people who are being treated with anti-depressants then have an increased risk of going on to develop diabetes. BBC © 2013