Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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By Tina Rosenberg When Ebola ends, the people who have suffered, who have lost loved ones, will need many things. They will need ways to rebuild their livelihoods. They will need a functioning health system, which can ensure that future outbreaks do not become catastrophes. And they will need mental health care. Depression is the most important thief of productive life for women around the world, and the second-most important for men. We sometimes imagine it is a first-world problem, but depression is just as widespread, if not more so, in poor countries, where there is a good deal more to be depressed about. And it is more debilitating, as a vast majority of sufferers have no safety net. Health care for all must include mental health care. It’s hard to believe but both Liberia and Sierra Leone have only a single psychiatrist. The Ebola crisis has exposed these countries’ malignant neglect of their health systems. People can’t get care for diarrhea and malaria. How will these countries take care of an epidemic of depression? This isn’t really a medical question. We know how to treat depression. What we don’t know yet is how to make effective treatment cheap, culturally appropriate, convenient and non-stigmatizing — all needed to get treatment out to millions and millions of people. But some researchers are finding out. They are doing so despite the fact that growing attention to this issue hasn’t been accompanied by money. The U.S. National Institute of Mental Health last year provided just $24.5 million for global mental health efforts, and the Canadian government’s Grand Challenges Canada, which is said to have the largest portfolio of mental health innovation in developing countries, has spent only $28 million on them since it began in 2010. © 2014 The New York Times Company
Link ID: 20404 - Posted: 12.08.2014
By Neuroskeptic | An important new study could undermine the concept of ‘endophenotypes’ – and thus derail one of the most promising lines of research in neuroscience and psychiatry. The findings are out now in Psychophysiology. Unusually, an entire special issue of the journal is devoted to presenting the various results of the study, along with commentary, but here’s the summary paper: Knowns and unknowns for psychophysiological endophenotypes by Minnesota researchers William Iacono, Uma Vaidyanathan, Scott Vrieze and Stephen Malone. In a nutshell, the researchers ran seven different genetic studies to try to find the genetic basis of a total of seventeen neurobehavioural traits, also known as ‘endophenotypes’. Endophenotypes are a hot topic in psychiatric neuroscience, although the concept is somewhat vague. The motivation behind interest in endophenotypes comes mainly from the failure of recent studies to pin down the genetic cause of most psychiatric syndromes: endophenotypes_A Essentially an endophenotype is some trait, which could be almost anything, which is supposed to be related to (or part of) a psychiatric disorder or symptom, but which is “closer to genetics” or “more biological” than the disorder itself. Rather than thousands of genes all mixed together to determine the risk of a psychiatric disorder, each endophenotype might be controlled by only a handful of genes – which would thus be easier to find.
Close to 8 percent of Americans have depression of some kind, but only about a third of those are getting treated for it, a major federal survey finds. The most depressed group? Women ages 40 to 59. More than 12 percent of women that age say they're depressed. The least? Teenage boys. Just 4 percent of them have been diagnosed with depression. "During 2009-2012, 7.6 percent of Americans aged 12 and over had depression (moderate or severe depressive symptoms in the past 2 weeks)," Laura Pratt and Debra Brody of the National Center for Health Statistics wrote. "About 3 percent of Americans aged 12 and over had severe depressive symptoms," they added. "Of those with severe symptoms, 35 percent reported having contact with a mental health professional in the past year." This is troubling, because depression is difficult to treat and does best when people are given a combination of drugs and counseling. People living below the poverty level were more than twice as likely to have depression than people making more money. Almost 43 percent of people with severe depressive symptoms reported serious difficulties in work, home and social activities.
Link ID: 20383 - Posted: 12.03.2014
By Nicholas Bakalar Short-term psychotherapy may be an effective way to prevent repeated suicide attempts. Using detailed Danish government health records, researchers studied 5,678 people who had attempted suicide and then received a program of short-term psychotherapy based on needs, including crisis intervention, cognitive therapy, behavioral therapy, and psychodynamic and psychoanalytic treatment. They compared them with 17,034 people who had attempted suicide but received standard care, including admission to a hospital, referral for treatment or discharge with no referral. They were able to match the groups in more than 30 genetic, health, behavioral and socioeconomic characteristics. The study is online in Lancet Psychiatry. Treatment focused on suicide prevention and comprised eight to 10 weeks of individual sessions. Over a 20-year follow-up, 16.5 percent of the treated group attempted suicide again, compared with 19.1 percent of the untreated group. In the treated group, 1.6 percent died by suicide, compared with 2.2 percent of the untreated. “Suicide is a rare event,” said the lead author, Annette Erlangsen, an associate professor at the Johns Hopkins Bloomberg School of Public Health, “and you need a huge sample to study it. We had that, and we were able to find a significant effect.” The authors estimate that therapy prevented 145 suicide attempts and 30 deaths by suicide in the group studied. © 2014 The New York Times Company
Link ID: 20379 - Posted: 12.02.2014
By EUGENIA BONE I TRIED magic mushrooms out of curiosity and in middle age. I’d been on the amateur mycological circuit for a couple of years, but hallucinogenic species were rarely mentioned at the foraging expeditions and conferences I attended. It’s almost as if they were the black sheep of mycology: embarrassing to serious taxonomy jocks. I read some books on the subject, but most were tripper’s guides that didn’t utilize, um, specific language or current science. Psychoactive mushrooms had been in a kind of scientific ghetto ever since they were criminalized in 1968. But now the drug derived from the mushroom, psilocybin, is finally being re-examined for its medical applications. A study published last month in the Journal of the Royal Society Interface compared M.R.I.s of the brains of subjects injected with psilocybin with scans of their normal brain activity. The brains on psilocybin showed radically different connectivity patterns between cortical regions (the parts thought to play an important role in consciousness). The researchers mapped out these connections, revealing the activity of new neural networks between otherwise disconnected brain regions. The researchers suspect that these unusual connections may be responsible for the synesthetic experience trippers describe, of hearing colors, for example, and seeing sounds. The part of the brain that processes sound may be connecting to the part of the brain that processes sight. The study’s leader, Paul Expert at King’s College London, told me that his team doubted that this psilocybin-induced connectivity lasted. They think they are seeing a temporary modification of the subject’s brain function. © 2014 The New York Times Company
By Anna North What is depression? Anyone who has dealt with the condition knows what it can feel like — but what causes it, what sustains it, and what’s the best way to make it subside? Despite the prevalence of the disorder — in one Centers for Disease Control and Prevention study, 9.1 percent of adults met the criteria for depression — experts haven’t fully answered these questions. And to fully do so, some say we need new ways of thinking about depression entirely. For Turhan Canli, a professor of integrative neuroscience at Stony Brook University, that means looking at the possibility that depression could be caused by an infection. “I’ve always been struck by the fact that the treatment options did not seem to have dramatically improved over the course of decades,” Dr. Canli told Op-Talk. “I always had a feeling that somehow we seem to be missing the actual treatment of the disease.” He was intrigued by research showing a connection between depression and inflammation in the body, and he started to think about the known causes of inflammation — among them pathogens like bacteria, viruses and parasites. In a paper published in the journal Biology of Mood and Anxiety Disorders, he lays out his case for rethinking depression as a response to infection. He notes that the symptoms of depression are similar to those of infection: “Patients experience loss of energy; they commonly have difficulty getting out of bed and lose interest in the world around them. Although our Western conceptualization puts affective symptoms front-and-center, non-Western patients who meet DSM criteria for major depression report primarily somatic symptoms.” © 2014 The New York Times Company
Daniel Freeman and Jason Freeman “Although it is a waste of time to argue with a paranoid patient about his delusions, he may still be persuaded to keep them to himself, to repress them as far as possible and to forgo the aggressive action they might suggest, in general to conduct his life as if they did not exist.” This quote from Clinical Psychiatry, a hugely influential textbook in the 1950s and 1960s, epitomises the way in which unusual mental states were generally understood for much of the 20th century. Delusions (such as paranoid thoughts) and hallucinations (hearing voices, for example) were of interest purely as symptoms of psychosis, or what used to be called madness. Apart from their utility in diagnosis, they were deemed to be meaningless: the incomprehensible effusions of a diseased brain. Or in the jargon: “empty speech acts, whose informational content refers to neither world nor self”. There’s a certain irony here, of course, in experts supposedly dedicated to understanding the way the mind works dismissing certain thoughts as unworthy of attention or explanation. The medical response to these phenomena, which were considered to be an essentially biological problem, was to eradicate them with powerful antipsychotic drugs. This is not to say that other strategies weren’t attempted: in one revealing experiment in the 1970s, patients in a ward for “paranoid schizophrenics” in Vermont, US, were rewarded with tokens for avoiding “delusional talk”. These tokens could be exchanged for items including “meals, extra dessert, visits to the canteen, cigarettes, time off the ward, time in the TV and game room, time in bedroom between 8am and 9pm, visitors, books and magazines, recreation, dances on other wards.” (It didn’t work: most patients modified their behaviour temporarily, but “changes in a patient’s delusional system and general mental status could not be detected by a psychiatrist”.) © 2014 Guardian News and Media Limited
Link ID: 20369 - Posted: 11.29.2014
by Bethany Brookshire We all experience stress, but some handle it better than others. A lot of research has focused on what makes animals and people susceptible to stress and how that, in turn, can trigger depression. It makes sense to study the condition, not the people that don’t experience it. Depression and susceptibility are the broken state. Resilience seems normal by comparison. But resilience is not just the absence of susceptibility. It turns out that a protein called beta-catenin plays an active role in resilience. A new study, from Eric Nestler’s laboratory at the Mount Sinai School of Medicine in New York City, also identifies a large number of new targets that could help scientists understand why some people are susceptible to stress — and how they might be made more resilient. “When people study stress responses, we often just assume that in an animal that’s stressed, there’s an active process that creates these depression-like behaviors,” says Andre Der-Avakian, a neuroscientist at the University of California, San Diego. “But this study and studies from others have shown that resilience is also an active process.” The nucleus accumbens is an area of the brain most often linked with reward and pleasure from items we enjoy, such as food or drugs. But the area also shows changes in people with depression. “It makes sense — here’s a region important in responding to rewards,” Nestler explains. “One of the symptoms of people with depression is that they don’t derive pleasure from things in life.” © Society for Science & the Public 2000 - 2014
By David Tuller Patients with chronic fatigue syndrome are accustomed to disappointment. The cause of the disorder remains unknown; it can be difficult to diagnose, and treatment options are few. Research suggesting that an infection from a mouse virus may cause it raised hopes among patients a few years ago, but the evidence fell apart under closer scrutiny. Many patients are still told to seek psychiatric help. But two recent studies — one from investigators at Stanford a few weeks ago and another from a Japanese research team published earlier this year — have found that the brains of people with chronic fatigue syndrome differ from those of healthy people, strengthening the argument that serious physiological dysfunctions are at the root of the condition. “You’ve got two different groups that have independently said, ‘There’s something going on in the brain that is aberrant,’ ” said Leonard Jason, a psychologist at DePaul University in Chicago who studies the condition, also called myalgic encephalomyelitis and widely known as M.E./C.F.S. “I think you have a growing sense that this illness should be taken seriously.” Both studies were small, however, and their results must be replicated before firm conclusions can be drawn. Still, other studies presented at scientific conferences this year also have demonstrated physiological dysfunctions in these patients. In the most recent study, published by the journal Radiology, researchers at Stanford University compared brain images of 15 patients with the condition to those of 14 healthy people. The scientists found differences in both the white matter, the long, cablelike nerve structures that transmit signals between parts of the brain, and the gray matter, the regions where these signals are processed and interpreted. The most striking finding was that in people with the disorder, one neural tract in the white matter of the right hemisphere appeared to be abnormally shaped, as if the cablelike nerve structures had crisscrossed or changed in some other way. Furthermore, the most seriously ill patients exhibited the greatest levels of this abnormality. © 2014 The New York Times Company
By Michelle Roberts Health editor, BBC News online The brain has a weak spot for Alzheimer's disease and schizophrenia, according to UK scientists who have pinpointed the region using scans. The brain area involved develops late in adolescence and degenerates early during ageing. At the moment, it is difficult for doctors to predict which people might develop either condition. The findings, in the journal PNAS, hint at a potential way to diagnose those at risk earlier, experts say. Although they caution that "much more research is needed into how to bring these exciting discoveries into the clinic". The Medical Research Council team who carried out the study did MRI brain scans on 484 healthy volunteers aged between eight and 85 years. The researchers, led by Dr Gwenaëlle Douaud of Oxford University, looked at how the brain naturally changes as people age. The images revealed a common pattern - the parts of the brain that were the last to develop were also the first to show signs of age-related decline. These brain regions - a network of nerve cells or grey matter - co-ordinate "high order" information coming from the different senses, such as sight and sound. When the researchers looked at scans of patients with Alzheimer's disease and scans of patients with schizophrenia they found the same brain regions were affected. The findings fit with what other experts have suspected - that although distinct, Alzheimer's and schizophrenia are linked. Prof Hugh Perry of the MRC said: "Early doctors called schizophrenia 'premature dementia' but until now we had no clear evidence that the same parts of the brain might be associated with two such different diseases. This large-scale and detailed study provides an important, and previously missing, link between development, ageing and disease processes in the brain. BBC © 2014
By Pippa Stephens Health reporter, BBC News Women are more likely than men to display symptoms of depression when in a position of authority at work, according to US scientists. In men, authority, such as the ability to hire and fire people, decreases depressive symptoms, the study said. The study, published in the Journal of Health and Social Behaviour, looked at 2,800 middle-aged men and women. One expert said the study showed the need for more women in authority and more varied female role models. Scientists at the University of Texas at Austin interviewed 1,300 male and 1,500 female graduates from Wisconsin high schools over the phone in 1993 and 2004, when they were aged about 54 and 64. Researchers asked participants about job authority and about the number of days in the past week they felt depressive symptoms, such as feeling sad and thinking one's life is a failure. When the job included hiring, firing and influencing pay, women were predicted to have a 9% increased rate of depressive symptoms than women without authority. Meanwhile, men had a 10% decreased rate of depressive symptoms. The study said it controlled for other factors that could cause depression, such as hours worked per week, whether people had flexible hours and how often workers were checked by a supervisor. Scientists also said men were more likely to decide when to start and finish work than women and were less frequently monitored by their advisers. Lead researcher Tetyana Pudrovska said: "These women have more education, higher incomes, more prestigious occupations, and higher levels of job satisfaction and autonomy than women without job authority. Yet they have worse mental health than lower status women." BBC © 2014
By Tom Shroder After more than 30 years in which psychedelics were considered dangerous remnants of the 1960s, the drugs have begun to make a comeback, this time as potential remedies for a host of tough-to-treat maladies. Pilot studies and clinical trials of LSD, psilocybin, ketamine and MDMA have shown that the drugs, often in combination with talk therapy, can be given safely under medical supervision and may help people dealing with opiate and tobacco addiction, alcoholism, anxiety, depression and post-traumatic stress disorder, or PTSD. That these investigations have shown potential is not surprising to many researchers. A generation of scientists and practitioners had used psychedelics successfully with thousands of patients until the research was banned in 1970, after the drugs were embraced by an exploding counterculture that seemed to threaten the status quo. In the panicked reaction, psychedelics were listed along with heroin in the highest rungs of prohibition. Ironically, this failed to stop recreational use but it shut the science down cold. As one researcher put it, “It was as if psychedelic drugs had become undiscovered.” But a small cadre of psychiatrists and researchers, often risking careers and reputations, pushed to bring psychedelics back to the lab and the clinic. Their persistence paid off. Beginning in the 1990s, the Food and Drug Administration approved the first human clinical studies of psychedelic drugs in a quarter of a century. By 2004, the first FDA-approved trial of the medicinal use of a psychedelic drug, in this case a trial of MDMA-assisted therapy for PTSD involving 24 subjects, was underway. Now such studies are proliferating.
Emily Anthes Anna's life began to unravel in 2005 when her husband of 30 years announced that he had fallen in love with another woman. “It had never even occurred to me that my marriage could ever end,” recalls Anna, a retired lawyer then living in Philadelphia, Pennsylvania. “It was pretty shocking.” Over the course of several months, Anna stopped wanting to get up in the morning. She felt tired all the time, and consumed by negative thoughts. “'I'm worthless.' 'I messed up everything.' 'It's all my fault.'” She needed help, but her first therapist bored her and antidepressants only made her more tired. Then she found Cory Newman, director of the Center for Cognitive Therapy at the University of Pennsylvania, who started her on a different kind of therapy. Anna learned how to obsess less over her setbacks and give herself more credit for her triumphs. “It was so helpful to talk to someone who steered me to more positive ways of thinking,” says Anna, whose name has been changed at her request. Cognitive therapy, commonly known as cognitive behavioural therapy (CBT), aims to help people to identify and change negative, self-destructive thought patterns. And although it does not work for everyone with depression, data have been accumulating in its favour. “CBT is one of the clear success stories in psychotherapy,” says Stefan Hofmann, a psychologist at Boston University in Massachusetts. Antidepressant drugs are usually the first-line treatment for depression. They are seen as a quick, inexpensive fix — but clinical trials reveal that only 22–40% of patients emerge from depression with drugs alone. Although there are various approaches to psychotherapy, CBT is the most widely studied; a meta-analysis1 published this year revealed that, depending on how scientists measure outcomes, between 42% and 66% of patients no longer meet the criteria for depression after therapy. © 2014 Nature Publishing Group
Link ID: 20306 - Posted: 11.13.2014
Heidi Ledford If the extent of human suffering were used to decide which diseases deserve the most medical attention, then depression would be near the top of the list. More than 350 million people are affected by depression, making it one of the most common disorders in the world. It is the biggest cause of disability, and as many as two-thirds of those who commit suicide have the condition. But although depression is common, it is often ignored. Three-quarters of people with depression in the United Kingdom go undiagnosed or untreated — and even if the disorder is diagnosed, today's medications will work well for only about half of those who seek help. “It's unbelievable,” says Tom Foley, a psychiatrist at Newcastle University, UK. “If that was the case in cancer care, it would be an absolute scandal.” The comparison between depression and cancer is a common one. Cancer, too, is a terrible blight: it affects more than 32 million people and kills some 8 million a year, many more than depression. But at least in developed countries, the vast majority of people with recognized cancers do receive treatment. In research, too, depression has failed to keep up with cancer. Cancer research today is a thriving field, unearthing vast catalogues of disease-associated mutations, cranking out genetically targeted therapies and developing sophisticated animal models. Research into depression, meanwhile, seems to have floundered: once-hopeful therapies have failed in clinical trials, genetic studies have come up empty-handed. The field is still struggling to even define the disease — and overcome the stigma associated with it. © 2014 Nature Publishing Grou
Link ID: 20305 - Posted: 11.13.2014
By Julia Calderone Antidepressant use among Americans is skyrocketing. Adults in the U.S. consumed four times more antidepressants in the late 2000s than they did in the early 1990s. As the third most frequently taken medication in the U.S., researchers estimate that 8 to 10 percent of the population is taking an antidepressant. But this spike does not necessarily signify a depression epidemic. Through the early 2000s pharmaceutical companies were aggressively testing selective serotonin reuptake inhibitors (SSRIs), the dominant class of depression drug, for a variety of disorders—the timeline below shows the rapid expansion of FDA-approved uses. As the drugs' patents expired, companies stopped funding studies for official approval. Yet doctors have continued to prescribe them for more ailments. One motivating factor is that SSRIs are a fairly safe option for altering brain chemistry. Because we know so little about mental illness, many clinicians reason, we might as well try the pills already on the shelf. Doctors commonly use antidepressants to treat many maladies they are not approved for. In fact, studies show that between 25 and 60 percent of prescribed antidepressants are actually used to treat nonpsychological conditions. The most common and well-supported off-label uses of SSRIs include: Abuse and dependence ADHD (in children and adolescents) Anxiety disorders Autism (in children) Bipolar disorder Eating disorders Fibromyalgia Neuropathic pain Obsessive-compulsive disorder Premenstrual dysphoric disorder © 2014 Scientific American
Link ID: 20300 - Posted: 11.11.2014
BY Laura Sanders The first time Nathan Whitmore zapped his brain, he had a college friend standing by, ready to pull the cord in case he had a seizure. That didn’t happen. Instead, Whitmore started experimenting with the surges of electricity, and he liked the effects. Since that first cautious attempt, he’s become a frequent user of, and advocate for, homemade brain stimulators. Depending on where he puts the electrodes, Whitmore says, he has expanded his memory, improved his math skills and solved previously intractable problems. The 22-year-old, a researcher in a National Institute on Aging neuroscience lab in Baltimore, writes computer programs in his spare time. When he attaches an electrode to a spot on his forehead, his brain goes into a “flow state,” he says, where tricky coding solutions appear effortlessly. “It’s like the computer is programming itself.” Whitmore no longer asks a friend to keep him company while he plugs in, but he is far from alone. The movement to use electricity to change the brain, while still relatively fringe, appears to be growing, as evidenced by a steady increase in active participants in an online brain-hacking message board that Whitmore moderates. This do-it-yourself community, some of whom make their own devices, includes people who want to get better test scores or crush the competition in video games as well as people struggling with depression and chronic pain, Whitmore says. As reckless as it sounds to juice a brain at home with a 9-volt battery and 40 dollars’ worth of spare parts, this technology’s buzz is based on legit science. Small laboratory studies suggest that carefully controlled brain stimulation can boost a person’s memory and math abilities, hone attention and fast-track learning. The U. S. military is interested and is funding studies to test brain stimulation as a way to boost soldiers’ alertness and vigilance. The technique may even be a viable treatment for pernicious mental disorders such as major depression, according to other laboratory-based studies. © Society for Science & the Public 2000 - 2014.
By Erin Allday Stanford researchers have found some striking abnormalities in the brains of people with chronic fatigue syndrome, a frustrating and debilitating condition for which there is no known cause and no treatment that’s widely effective. The findings, published Wednesday in the journal Radiology, could improve diagnosis and spark new scientific understanding of the disease. Perhaps even more noteworthy, the results — if they can be confirmed with larger studies — could provide some of the first objective evidence that chronic fatigue syndrome is a severe illness that causes real physiological damage. That would be a major step for patients and their advocates, who still suffer under the stigma of having a condition that for decades was ignored or not taken seriously. “If this finding holds, it will be exciting because yes, we’ve found something that has never been found before. But there’s this additional layer of looking at a disease that was completely ostracized. So there’s also this component of validation,” said Dr. Jose Montoya, an infectious disease specialist who helped establish a chronic fatigue syndrome team at Stanford School of Medicine a decade ago. Montoya was the senior author of the Stanford study. For patients, Montoya said, “It’s almost like we’re saying, 'You were right all along. Hopefully this will put you where you deserve to be, in a real clinic with treatments.’” There are limitations to the study, Montoya said. Most notably, the sample size is fairly small, with 15 chronic fatigue patients and 14 healthy control subjects.
Link ID: 20256 - Posted: 10.29.2014
By Michael Hedrick I have a hard time making friends. Getting to trust people well enough to call them a friend takes a lot of work. It’s especially hard when you are living with schizophrenia and think everyone is making fun of you. Schizophrenia is the devil on your shoulder that keeps whispering in your ear and, no matter what you try, the little demon won’t stop. He hasn’t stopped in the almost nine years I’ve lived with the illness, and he’s not about to stop now. He’s just quieted down a bit. I’d call him my companion but that would imply a degree of friendship, and there’s no way in hell I’m the little devil’s friend. I have plenty of acquaintances, and a couple hundred “friends” on Facebook. But real friends, mostly family, I can count on one hand. For me, making friends is like climbing a vertical rock wall with no ropes, requiring a degree of thrill-seeking, and a good deal of risk. For someone to be my friend, they have to accept that I’m crazy, and even getting to the point of telling them that is daunting when all you hear is the devil’s whispering that they’re making snap judgments about you or will be going back to their real friends and laughing about you. But interestingly, in my efforts to make friends, coffee shops have helped. The simple routine of going to get your fix of liquid energy every day provides a sort of breeding ground for community. You see these people every day,whether you like it or not and, over time, friendships form. I used to live in a small town called Niwot, about five miles down the highway from Boulder, where I now live. Every morning around 6 I would go to Winot Coffee, the small independent coffee shop, and every morning, without fail, there was a guy my age sitting outside with his computer smoking clove cigarettes. Given the regularity of seeing him every morning, and given that we were some of the only 20-somethings in town, we got to talking. © 2014 The New York Times Company
Link ID: 20240 - Posted: 10.25.2014
Scientists say they have identified the underlying reason why some people are prone to the winter blues, or seasonal affective disorder (SAD). People with Sad have an unhelpful way of controlling the "happy" brain signalling compound serotonin during winter months, brain scans reveal. As the nights draw in, production of a transporter protein ramps up in Sad, lowering available serotonin. The work will be presented this week at a neuropsychopharmacology conference. The University of Copenhagen researchers who carried out the trial say their findings confirm what others have suspected - although they only studied 11 people with Sad and 23 healthy volunteers for comparison. Using positron emission tomography (PET) brain scans, they were able to show significant summer-to-winter differences in the levels of the serotonin transporter (SERT) protein in Sad patients. The Sad volunteers had higher levels of SERT in the winter months, corresponding to a greater removal of serotonin in winter, while the healthy volunteers did not. Winter depression Lead researcher, Dr Brenda Mc Mahon, said: "We believe that we have found the dial the brain turns when it has to adjust serotonin to the changing seasons. BBC © 2014
by Amy Standen The important thing is that Meghan knew something was wrong. When I met her, she was 23, a smart, wry young woman living with her mother and stepdad in Simi Valley, about an hour north of Los Angeles. Meghan had just started a training program to become a respiratory therapist. Concerned about future job prospects, she asked NPR not to use her full name. Five years ago, Meghan's prospects weren't nearly so bright. At 19, she had been severely depressed, on and off, for years. During the bad times, she'd hide out in her room making thin, neat cuts with a razor on her upper arm. "I didn't do much of anything," Meghan recalls. "It required too much brain power." "Her depression just sucked the life out of you," Kathy, Meghan's mother, recalls. "I had no idea what to do or where to go with it." One night in 2010, Meghan's mental state took an ominous turn. Driving home from her job at McDonald's, she found herself fascinated by the headlights of an oncoming car. "I had the weird thought of, you know, I've never noticed this, but their headlights really look like eyes." To Meghan, the car seemed malicious. It wanted to hurt her. Kathy tried to reason with her. "Honey, you know it's a car, right? You know those are headlights," she recalls pressing her daughter. "You understand that this makes no sense, right?" © 2014 NPR
Link ID: 20223 - Posted: 10.21.2014