Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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Imagine that, after feeling unwell for a while, you visit your GP. "Ah," says the doctor decisively, "what you need is medication X. It's often pretty effective, though there can be side-effects. You may gain weight. Or feel drowsy. And you may develop tremors reminiscent of Parkinson's disease." Warily, you glance at the prescription on the doctor's desk, but she hasn't finished. "Some patients find that sex becomes a problem. Diabetes and heart problems are a risk. And in the long term the drug may actually shrink your brain … " This scenario may sound far-fetched, but it is precisely what faces people diagnosed with schizophrenia. Since the 1950s, the illness has generally been treated using antipsychotic drugs – which, as with so many medications, were discovered by chance. A French surgeon investigating treatments for surgical shock found that one of the drugs he tried – the antihistamine chlorpromazine – produced powerful psychological effects. This prompted the psychiatrist Pierre Deniker to give the drug to some of his most troubled patients. Their symptoms improved dramatically, and a major breakthrough in the treatment of psychosis seemed to have arrived. Many other antipsychotic drugs have followed in chlorpromazine's wake and today these medications comprise 10% of total NHS psychiatric prescriptions. They are costly items: the NHS spends more on these medications than it does for any other psychiatric drug, including antidepressants. Globally, around $14.5bn is estimated to be spent on antipsychotics each year. Since the 1950s the strategy of all too many NHS mental health teams has been a simple one. Assuming that psychosis is primarily a biological brain problem, clinicians prescribe an antipsychotic medication and everyone does their level best to get the patient to take it, often for long periods. There can be little doubt that these drugs make a positive difference, reducing delusions and hallucinations and making relapse less likely – provided, that is, the patient takes their medication. © 2014 Guardian News and Media Limited
Link ID: 19336 - Posted: 03.08.2014
By BENEDICT CAREY He heard about the drug trial from a friend in Switzerland and decided it was worth volunteering, even if it meant long, painful train journeys from his native Austria and the real possibility of a mental meltdown. He didn’t have much time, after all, and traditional medicine had done nothing to relieve his degenerative spine condition. “I’d never taken the drug before, so I was feeling — well, I think the proper word for it, in English, is dread,” said Peter, 50, an Austrian social worker, in a telephone interview; he asked that his last name be omitted to protect his identity. “There was this fear that it could all go wrong, that it could turn into a bad trip.” On Tuesday, The Journal of Nervous and Mental Disease is posting online results from the first controlled trial of LSD in more than 40 years. The study, conducted in the office of a Swiss psychiatrist near Bern, tested the effects of the drug as a complement to talk therapy for 12 people nearing the end of life, including Peter. Most of the subjects had terminal cancer, and several died within a year after the trial — but not before having a mental adventure that appeared to have eased the existential gloom of their last days. “Their anxiety went down and stayed down,” said Dr. Peter Gasser, who conducted the therapy and followed up with his patients a year after the trial concluded. The new publication marks the latest in a series of baby steps by a loose coalition of researchers and fund-raisers who are working to bring hallucinogens back into the fold of mainstream psychiatry. Before research was banned in 1966 in the United States, doctors tested LSD’s effect for a variety of conditions, including end-of-life anxiety. But in the past few years, psychiatrists in the United States and abroad — working with state regulators as well as ethics boards — have tested Ecstasy-assisted therapy for post-traumatic stress; and other trials with hallucinogens are in the works. © 2014 The New York Times Company
|By Roni Jacobson Modern antipsychotic drugs are increasingly prescribed to children and adolescents diagnosed with a broad variety of ailments. The drugs help to alleviate symptoms in some disorders, such as schizophrenia and bipolar disorder, but in others their effectiveness is questionable. Yet off-label prescribing is on the rise, especially in children receiving public assistance and Medicaid. Psychotic disorders typically arise in adulthood and affect only a small proportion of children and adolescents. Off-label prescriptions, however, most often target aggressive and disruptive behaviors associated with attention-deficit hyperactivity disorder (ADHD). “What's really concerning now is that a lot of this prescription is occurring in the face of emerging evidence that there are significant adverse effects that may be worse in youth than in adults,” says David Rubin, a general pediatrician and co-director of PolicyLab at Children's Hospital of Philadelphia. Here we review the evidence for the effectiveness of antipsychotic medications commonly prescribed for five childhood conditions. But do the benefits outweigh the risks? Schizophrenia Evidence from several randomized controlled trials conducted in the past 10 years strongly suggests that antipsychotics are an effective treatment for youths with schizophrenia. Indeed, the FDA has approved five medications—risperidone, aripiprazole, olanzapine, quetiapine and paliperidone—for use in adolescents aged 13 to 17. Bipolar Disorder Recent research indicates that antipsychotics may hasten the resolution of manic and mixed episodes in children with bipolar disorder and increase the likelihood that the illness will go into remission. The FDA has approved the same set of drugs for 10- to 17-year-olds with bipolar disorder as it has for youths with schizophrenia, with the exception of paliperidone. © 2014 Scientific American
Ian Sample, science correspondent Children born to fathers over the age of 45 are at greater risk of developing psychiatric problems and more likely to struggle at school, according to the findings of a large-scale study. The research found that children with older fathers were more often diagnosed with disorders such as autism, psychosis, attention deficit hyperactivity disorder (ADHD), schizophrenia and bipolar disorder. They also reported more drug abuse and suicide attempts, researchers said. The children's difficulties seemed to affect school performance, leading to worse grades at the age of 15 and fewer years in education overall. "We were shocked when we saw the comparisons," said Brian D'Onofrio, the first author of the study at Indiana University in the US. But he added that it was impossible to be sure that older age was to blame for the problems. Scientists have reported links between fathers' age and children's cognitive performance and health before but this study suggests the risks may be more serious than previously thought. The increased risks might be caused by genetic mutations that build up in sperm as men age. Researchers at Indiana University and the Karolinska Institute in Stockholm studied medical and educational records of more than 2.6 million babies born to 1.4 million men. The group amounted to nearly 90% of births in Sweden from 1973 and 2001. Using the records, the scientists added up diagnoses for psychiatric disorders and educational achievements and compared the figures for children born to fathers of different ages. © 2014 Guardian News and Media Limited
By MICHAEL HEDRICK I still remember the first group therapy session I went to after I got out of the hospital. I was 20 and had been diagnosed as schizophrenic after a road trip that took me from Colorado to the United Nations building in New York City, my mind riddled with notions of good and evil, demons and angels, and a determination to save the world. Now I was in something of a state of shock, having come to understand that amid the delusions and paranoia that swarmed through my head I was, in reality, insane. A constant need to move felt like ants crawling over my skin, a side effect of the antipsychotic medications I had been prescribed. Every second of every day, I felt like clawing out my eyes and tearing out my hair because I just couldn’t sit still. I held up my front, though. I smiled when I thought I had to and tried to be nice to people. Laughter, however, was not something that was possible, and wouldn’t be for a long time. The group was a dual-functioning therapy technique to address both mental health issues and drug abuse. I had been assigned to it after disclosing that I had a marijuana habit. The doctors had told me that therapy groups were an integral part of my getting better. I agreed to go only to get out of the hospital prison and back home to my warm bed. I sat in a circle with a melting pot of people. There was the construction worker still wearing dusty boots and clothes splattered with mud, and the depressed sorority girl, makeup and hair still impeccable. The two had formed a friendship over their history with methamphetamine. There was the quiet bipolar Hispanic man who spoke only in short staccato sentences, and the rotund marketing guy who introduced himself by saying his drugs of choice were food, cocaine and marijuana. © 2014 The New York Times Company
Link ID: 19302 - Posted: 02.27.2014
|By Beth Skwarecki Prions, the protein family notorious for causing "mad cow" and neurodegenerative diseases like Parkinson's, can play an important role in healthy cells. "Do you think God created prions just to kill?" mused Nobel laureate Eric Kandel. "These things must have evolved initially to have a physiological function." His work on memory helped reveal that animals make and use prions in their nervous systems as part of an essential function: stabilizing the synapses that constitute long-term memories. These natural prions aren't infectious but on a molecular level they chain up exactly the same way as their disease-causing brethren. (Some researchers call them "prionlike" to avoid confusion.) This week, work from neuroscientist Kausik Si of the Stowers Institute for Medical Research, one of Kandel's former students, shows that the prion's action is tightly controlled by the cell, and can be turned on when a new long-term memory needs to be formed. Prions are proteins with two unusual properties: First, they can switch between two possible shapes, one that is stable on its own and an alternate conformation that can form chains. Second, the chain-forming version has to be able to trigger others to change shape and join the chain. Say that in the normal version the protein is folded so that one portion of the protein structure—call it "tab A"—fits into its own "slot B." In the alternate form, though, tab A is available to fit into its neighbor's slot B. That means the neighbor can do the same thing to the next protein to come along, forming a chain or clump that can grow indefinitely. © 2014 Scientific American,
Sara Reardon Freddie Lee Hall loved to gamble, although he usually lost. Winning was better: then he gladly gave the money back to the friends he'd won it from, along with all the wages he earned picking fruit in rural Florida. His friends praised him for this. It made him feel good. And Hall needed to feel good — as court documents make abundantly clear. As a child growing up in the impoverished town of Webster, Florida, he had struggled to keep up with 16 brothers and sisters, who were much smarter than he was. If he failed to understand something, his mother beat him, once while he was tied up in a bag strung over a fire. He stuttered, never learned to read and feared the dark. He was unable to live alone. “Even though he was full grown, mentally he was a child,” his sister Diana told the court. “I had hoped to protect Freddie Lee from the outside world.” But the outside world found him. In 1978, Hall and his friend Mack Ruffin decided to rob a convenience store. They needed a car, so they forced 21-year-old Karol Hurst, who was pregnant, to drive into the woods, where they raped and killed her. Later, one of the pair also shot and killed a sheriff's deputy. When the two men were caught, tried and convicted of murder, the court decided that Hall was the likely ringleader. Ruffin was eventually sentenced to life in prison; Hall was sentenced to death. Next month, after 35 years of failed appeals to have that death sentence commuted to life imprisonment, Hall will have his case heard before the US Supreme Court. His guilt is not in question: the issue is Florida's use of IQ test scores in sentencing him to death. © 2014 Nature Publishing Group,
By James Gallagher Health and science reporter, BBC News A tool for predicting the risk of clinical depression in teenage boys has been developed by researchers. Looking for high levels of the stress hormone cortisol and reports of feeling miserable, lonely or unloved could find those at greatest risk. Researchers at the University of Cambridge want to develop a way of screening for depression in the same way as heart problems can be predicted. However, their method was far less useful in girls. Teenage years and early adulthood are a critical time for mental health - 75% of disorders develop before the age of 24. But there is no way to accurately say who will or will not develop depression. Risky combination Now researchers say they have taken the "first step" towards a screening tool. Tests on 1,858 teenagers, reported in Proceedings of the National Academy of Sciences, combined hormone levels and mood questionnaires to assess risk. They showed that having both high cortisol levels and depressive mood symptoms posed a higher risk of depression than either factor alone and presented a risk of clinical depression 14 times that of those with low cortisol and no depressive symptoms. Around one in six boys was in the high-risk category and half of them were diagnosed with clinical depression during the three years of study. One of the researchers, Prof Ian Goodyer, said: "Depression is a terrible illness that will affect as many as 10 million people in the UK at some point in their lives. "Through our research, we now have a very real way of identifying those teenage boys most likely to develop clinical depression. BBC © 2014
by Ashley Yeager Humans aren’t the only ones to suffer from obsessive-compulsive disorder. Dogs can suffer from the disorder as well, with particular breeds compulsively chewing their feet, chasing their tails or sucking blankets. Now scientists say they have identified several of the genes that trigger the behavior in Doberman pinschers, bullterriers, sheepdogs and German shepherds. Four genes, CDH2, CTNNA2, ATXN1 and PGCP, involved in the communication between brain cells appear to play a role in dog OCD, researchers report February 16 in Genome Biology. The results could be used to better understand the disorder in people. © Society for Science & the Public 2000 - 2013.
by Clare Wilson AS MANY as 1 in 10 cases of schizophrenia may be triggered by an autoimmune reaction against brain cells, according to early trial results shared with New Scientist. The finding offers the possibility of gentler treatments for this devastating mental illness. Last month, doctors at a conference at the Royal Society of Medicine in London were told to consider an autoimmune cause when people first show symptoms of schizophrenia. People with schizophrenia experience symptoms of psychosis, such as hallucinations, delusions and paranoia. It affects 1 per cent of people in the West and is thought to be caused by overactive dopamine signalling pathways in the brain. Anti-psychotic drugs don't always work wellMovie Camera and have serious side effects. Previous studies had found that antibodies that target the NMDA receptor on neurons trigger brain inflammation, leading to seizures, comas – and sometimes psychosis (Annals of Neurology, doi.org/fdgnpc). In the past few years, these antibodies have also been found in the blood of people whose only symptom is psychosis. In 2010, Belinda Lennox at the University of Oxford tested 46 people with recent onset of psychosis for antibodies known to target neurons. Three people – about 6 per cent – tested positive (Neurology, doi.org/chs532). "The question is whether a larger percentage of cases might have other antibodies which we cannot yet detect," says Robin Murray at the Institute of Psychiatry in London, who wasn't involved in the research. Now Lennox is conducting a larger trial. Early results suggest other antibodies could well be involved. © Copyright Reed Business Information Ltd.
Eighteen neurological patients in North Carolina may have been exposed to an incurable and fatal disorder similar to "mad cow" disease while undergoing surgery at the Novant Health Forsyth Medical Center because surgical instruments were insufficiently sterilized, the hospital said on Monday. Surgeons operated on the 18 patients on January 18 using tools that had not been sufficiently sanitized after they were used on a man suspected of having Creutzfeldt-Jakob Disease (CJD), the hospital in Winston-Salem said in a press statement. "On behalf of the entire team at Novant Health, I apologize to the patients and their families for having caused this anxiety," Jeff Lindsay, president of the medical center, said at a news conference. CJD causes failing memory, blindness, involuntary movement and coma, and kills 90 percent of patients within one year, according to the National Institute of Neurological Disorders and Stroke. The condition is similar to mad cow disease, but is not linked to beef consumption. The incubation period — before initial symptoms surface — can last years, the statement said. After the first sign of symptoms, most patients die within four months, it said The possibility of contracting the disease through surgical exposure is very remote, the hospital said.
Link ID: 19234 - Posted: 02.11.2014
|By Simon Makin For decades two very different treatments of depression have existed side by side. Medications act on molecules, cells and synapses in the brain. Psychological therapies focus on cognition and behavior, trying to alter negatively biased thinking. Now a new theory suggests that these interventions may work in more similar ways than anyone realized, providing an opportunity to better integrate the two approaches. More important, it may help provide patients faster, more reliable relief from this crippling condition. Antidepressant drugs increase the levels of certain chemical messengers in the brain, such as serotonin and norepinephrine. Yet exactly how these neurotransmitters affect mood is unknown. “There was a missing link between the cellular, molecular and synaptic bases of these drugs, on the one hand, and what they affect in humans, which is their experiences, perceptions, memories and feelings,” says Catherine Harmer, a neuroscientist at the University of Oxford. The psychological explanation, meanwhile, describes depression in terms of distorted information processing. Depressed people are thought to process perceptions, experiences and memories with a negative bias. Many studies confirm that depressed individuals show increased sensitivity to sad faces, greater memory for negative material and reduced responsiveness to rewards as compared with healthy people. Successful therapies teach patients how to correct for this clouded vision. Harmer now believes that antidepressants may also work by altering this negative emotional processing. About a decade ago she and her colleagues tested the effects of commonly prescribed antidepressants on healthy volunteers and found that many of the drugs skewed emotional processing to the positive. Previous research had shown that antidepressants also change these measures in depressed people, but studies included only patients who had been on medication for six to eight weeks because the drugs were assumed to take that long to kick in. © 2014 Scientific American
Schizophrenia and related mental illnesses can have a devastating effect on people who suffer from them, often making it impossible for them to work or maintain normal social relationships. Antipsychotic drugs are usually the first line of defense, but they can have serious side effects. A new study concludes that psychological approaches could be an alternative for patients who either can’t or won’t take medication, although some critics continue to question the effectiveness of these interventions. Schizophrenia, which can involve hallucinations, delusions, paranoia, emotional problems, and severe difficulty focusing on daily tasks, affects about 1% of populations worldwide. More than 20 antipsychotic medications, such as risperidone, haloperidol, and clozapine, are now on the market, and they are often effective in temporarily relieving the worse symptoms. But when taken for extended periods, such drugs can cause uncontrollable muscle movements, serious weight gain, and higher risk of heart attacks. In recent years, a number of psychiatrists and psychologists have begun to advocate psychological approaches, including an approach called cognitive behavioral therapy (CBT), as an adjunct to antipsychotic drugs. With CBT, which has long been shown to be effective for depression and anxiety disorders, a therapist takes the subject through a series of guided steps designed to explore alternative interpretations and explanations of what he or she is experiencing, with the goal of changing both outlook and behavior. A schizophrenic patient who is having hallucinations might be encouraged to stop trying to fight them off or suppress them, for example, or to stop engaging with voices in his or her head, to test how strong such symptoms really are and how much control they exert over the subject’s life. The technique also involves what practitioners call “normalization”: The patient might be reassured that hearing voices and seeing things that are not there is an experience that many normal people have from time to time, thus reducing some of the anxiety that makes sufferers feel distressed and isolated. © 2014 American Association for the Advancement of Science
Link ID: 19227 - Posted: 02.08.2014
By James Gallagher Health and science reporter, BBC News Changing the way people think about and deal with schizophrenia could be as effective as drugs, say researchers. Cognitive behavioural therapy is an officially recommended treatment, but is available to less than 10% of patients in the UK with schizophrenia. A study published in the Lancet indicates CBT could help the many who refuse antipsychotic medication. Experts say larger trials are needed. About four-in-10 patients benefit from taking antipsychotic medication. But the drugs do not work for the majority and they cause side-effects such as type 2 diabetes and weight gain. Up to half of patients with schizophrenia end up not taking the drugs. The study looked at cognitive behaviour therapy in 74 people. The therapy works by identifying an individual patient's problem - such as hearing voices, paranoid thinking or no longer going out of the house - and developing techniques to deal with them. Prof Tony Morrison, director of the psychosis research unit at Greater Manchester West Mental Health Foundation Trust, said: "We found cognitive behavioural therapy did reduce symptoms and it also improved personal and social function and we demonstrated very comprehensively it is a safe and effective therapy." It worked in 46% of patients, approximately the same as for antipsychotics - although a head-to-head study directly comparing the two therapies has not been made. Douglas Turkington, professor of psychiatry at Newcastle University, said: "One of our most interesting findings was that when given the option, most patients were agreeable to trying cognitive therapy." BBC © 2014
Link ID: 19212 - Posted: 02.06.2014
By BENEDICT CAREY BETHESDA, Md. — The police arrived at the house just after breakfast, dressed in full riot gear, and set up a perimeter at the front and back. Not long after, animal rights marchers began filling the street: scores of people, young and old, yelling accusations of murder and abuse, invoking Hitler, as neighbors stepped out onto their porches and stared. It was 1997, in Decatur, Ga. The demonstrators had clashed with the police that week, at the Yerkes National Primate Research Center at nearby Emory University, but this time, they were paying a personal call — on the house of the center’s director, inside with his wife and two teenage children. “I think it affected the three of them more than it did me, honestly,” said Dr. Thomas R. Insel, shaking his head at the memory. “But the university insisted on moving all of us to a safe place for a few days, to an ‘undisclosed location.’ “I’ll say this. I learned that if you’re going to take a stand, you’re going to make some people really angry — so you’d better believe in what you’re doing, and believe it completely.” For the past 11 years, Dr. Insel, a 62-year-old brain scientist, has run an equally contentious but far more influential outfit: the National Institute of Mental Health, the world’s leading backer of behavioral health research. The job comes with risk as well as power. Patient groups and scientists continually question the agency’s priorities, and politicians occasionally snipe at its decisions. Two previous directors resigned in the wake of inflammatory statements (one on marijuana laws, one comparing urban neighborhoods to jungles), and another stepped down after repeatedly objecting to White House decisions. © 2014 The New York Times Company
Christie Nicholson reports. Advocates claim numerous health benefits for meditation, many of which are supported by studies on the practice. Still, meditation has not become part of mainstream medicine. So researchers at Johns Hopkins University analyzed 47 previously published clinical trials to narrow down the most effective use for meditation as medical therapy. The studies involved more than 3,500 patients suffering from various issues including stress, addiction, depression, anxiety, diabetes, heart disease, cancer and chronic pain. The meta-analysis is in the journal JAMA Internal Medicine. [Madhav Goyal et al, Meditation Programs for Psychological Stress and Well-being: A Systematic Review and Meta-analysis] Apparently practicing just 30 minutes of meditation per day significantly decreases the symptoms of anxiety and depression. An 8-week training program in mindfulness meditation – where participants have to focus on the current moment – led to optimal improvement in lowering anxiety, depression and pain. And the improvements continued over the six months following the training. For depression and anxiety, the effects of meditation were as strong as for those achieved by taking antidepressant medication. However, meditation failed to significantly affect any of the other conditions, such as heart disease or cancer. Nevertheless, while some might view meditation as sitting and doing nothing, doing nothing does something. © 2014 Scientific American
By Melissa Healy Adolescents treated with the antidepressant fluoxetine -- better known by its commercial name, Prozac -- appear to undergo changes in brain signaling that result in changed behavior well into adulthood, says a new study. Adult mice and rats who were administered Prozac for a stretch of mid-adolescence responded to daunting social and physical challenges with less despair than animals who passed their teen years unmedicated, a team of researchers found. But, even as adults long separated from their antidepressant days, the Prozac veterans reacted to stressful situations with greater anxiety than did the adult Prozac virgins. The latest research, published Wednesday in the Journal of Neuroscience, offers evidence that treatment with a selective serotonin reuptake inhibitor -- an SSRI antidepressant -- has long-lived effects on the developing brain. It also zeroes in on how and where fluoxetine effects those lasting changes: by modifying the cascade of chemical signals issued by the brain's ventral tegmentum -- a region active in mood regulation -- in stressful situations. Yet, the new research raises more questions than it answers, since the changes in adults who were treated with Prozac as adolescents seem contradictory. Sensitivity to stress appears to predispose one to developing depression. So how does a medication that treats depression in children and teens -- and that continues to protect them from depression as adults -- also heighten their sensitivity to stress?
By RICHARD A. FRIEDMAN, M.D. “How the Federal Government Destroyed the Mental Illness Treatment System”: That subtitle is the opening shot across the bow in this jeremiad of a book by the psychiatrist Dr. E. Fuller Torrey. It could just as well have read: “How a group of well-intentioned, starry-eyed idealists made a hash of mental health care.” You could hardly blame them for trying, though. The care of people with serious mental illness was long a national disgrace. By the 1950s, slightly more than half a million psychiatric patients resided in overcrowded and underfunded state mental hospitals, often under appalling conditions. Related Coverage Enter a group of high-minded psychiatrists with a vision to “create a brave new world, a mentally healthy America,” in Dr. Torrey’s words. Armed with little more than optimism, they helped start the National Institute of Mental Health and set in motion an ambitious agenda for the next half-century: closing the state mental hospitals, initiating a federal takeover of the mental health system, and creating a nationwide network of community mental health centers. Reform was well underway when President John F. Kennedy endorsed this new era in mental health in a 1963 speech, calling for a “bold new approach” in which “reliance on the cold mercy of custodial isolation will be supplanted by the open warmth of community concern and capability.” Those were heady days in American psychiatry, when psychoanalysis and the mental hygiene movement held sway and promised to cure all manner of ills by early intervention and improving the social environment. In hindsight, the therapeutic zeal of these professionals was impressively naïve: They were certain that severely mentally ill patients in state hospitals — many living there for decades — would magically adjust to the community and do well with outpatient treatment. How wrong they proved to be. © 2014 The New York Times Company
Link ID: 19127 - Posted: 01.14.2014
By Megan Wiegand and Slate, Tips for beating the seasonal blues are as numerous as the winter night is long. Light boxes, touted to “uplift people’s spirits” and “improve mood and energy,” offer a New-Agey-seeming solution to propel us into the cold as if it’s the first beautiful day of spring. But can sitting in front of a light for a few minutes a day actually counteract the dreariest months? Yes, in many cases. Light-box therapy has been shown to alleviate symptoms in people who suffer from seasonal affective disorder, or SAD. Symptoms of this form of depression — they can include lost interest in beloved activities, overeating, loss of energy, disrupted sleep cycles and feelings of hopelessness or guilt — typically appear in late fall or early winter and dissipate in spring. Women are twice as likely as men to seek treatment for SAD, and those farther away from the equator are more likely to be diagnosed: About 11 percent of Mainers have a clinical SAD diagnosis, but only 2 percent of Floridians report the illness, according to Kathryn Roecklein, an assistant professor of psychology at the University of Pittsburgh. One tool doctors use to treat SAD is light-box therapy. Light boxes use bright white fluorescent bulbs (or sometimes blue light) that reproduce some wavelengths of the sun’s light. They contain filters to block harmful UV rays and come in various shapes, sizes, light types and price points. © 1996-2014 The Washington Post
By Tia Ghose and LiveScience Neurons derived from schizophrenic patients. Image: Dr. Kristen Brennand, Salk Institute for Biological Studies. Some so-called jumping genes that copy and paste themselves throughout the genome may be linked to schizophrenia, new research suggests. The new study, published Jan. 2 in Neuron, suggests these jumping genes may alter how neurons (or nerve cells in the brain) form during development, thereby increasing the risk of schizophrenia, study co-author Dr. Tadafumi Kato, a neurobiologist at the RIKEN Brain Science Institute in Japan, wrote in an email. Jumping genes, or retrotransposons, are mobile genetic elements that copy and paste themselves at different places throughout the genome. About half of the human genome is made of these mysterious elements, compared with the 1 percent of genes that actually code for making proteins, Kato said. Earlier studies had found that a certain type of jumping gene, known as long interspersed nuclear element-1 (LINE-1), was active in human brain cells. Kato and his colleagues wondered whether they might play a role in mental illness. To find out, the team conducted a post-mortem analysis of 120 human brains, 13 from patients who had been diagnosed with schizophrenia. The team found a higher number of LINE-1 copies in the brains of schizophrenics compared with other groups. © 2014 Scientific American