Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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By John Horgan Transcranial magnetic stimulation is becoming an increasingly popular treatment for depression in spite of a lack of objective evidence of effectiveness. Illustration: National Institute of Mental Health. Delving into the history of treatments for mental illness can be depressing. Rather than developing ever-more-potent therapies, psychiatrists and others in the mental-health industry seem merely to recycle old ones. Consider, for example, therapies that stimulate the brain with electricity. In 1901, H. Lewis Jones, a physician, stated in the Journal of Mental Science: "The employment of electricity in medicine has passed through many vicissitudes, being at one time recognized and employed at the hospitals, and again being neglected, and left for the most part in the hands of ignorant persons, who continue to perpetrate the grossest impositions in the name of electricity. As each fresh important discovery in electric science has been reached, men’s minds have been turned anew to the subject, and interest in its therapeutic properties has been stimulated. Then after extravagant hopes and promises of cure, there have followed failures, which have thrown the employment of this agent into disrepute, to be again after time revived and brought into popular favor." Jones’s concerns could apply to our era, when electro-cures for mental illness have once again been "brought into popular favor." Below I briefly review the evidence—or lack thereof--for five electrotherapies: transcranial magnetic stimulation, cranial electrotherapy stimulation, vagus-nerve stimulation, deep-brain stimulation and electroconvulsive therapy.
Link ID: 21092 - Posted: 06.25.2015
By Tina Rosenberg Elle is a mess. She’s actually talented, attractive and good at her job, but she feels like a fraud — convinced that today’s the day she’ll flunk a test, lose a job, mess up a relationship. Her colleague Moody also sabotages himself. He’s a hardworking, nice person, but loses friends because he’s grumpy, oversensitive and gets angry for no reason. If you suffer from depression or anxiety as Elle and Moody do, spending time with them could help. They are characters in a free online program of cognitive behavioral therapy called MoodGYM, which leads users through quizzes and exercises — therapy without the therapist. Cognitive behavioral therapy is a commonly used treatment for depression, anxiety and other conditions. With it, the therapist doesn’t ask you about your mother — or look at the past at all. Instead, a cognitive behavioral therapist aims to give patients the skills to manage their moods by helping them identify unhelpful thoughts like “I’m worthless,” “I’ll always fail” or “people will always let me down.” Patients learn to analyze them and replace them with constructive thoughts that are more accurate or precise. For example, a patient could replace “I fail at everything” with “I succeed at things when I’m motivated and I try hard.” That new thought in turn changes feelings and behaviors. The success of cognitive behavioral therapy is well known; many people consider it the most effective therapy for depression. What is not widely known, at least in the United States, is that you don’t need a therapist to do it. Scores of studies have found that online C.B.T. works as well as conventional face-to-face cognitive behavioral therapy – as long a there is occasional human support or coaching. “For common mental disorders like anxiety and depression, there is no evidence Internet-based treatment is less effective than face-to-face therapy,” said Pim Cuijpers, professor of clinical psychology at the Vrije Universiteit Amsterdam and a leading researcher on computer C.B.T. © 2015 The New York Times Company
Link ID: 21076 - Posted: 06.20.2015
By Michael Hedrick I’ve had a little success dating in the nearly 10 years I’ve lived with schizophrenia. But there are a lot of obstacles. Schizophrenia is a terrifying word for many people. It conjures up ideas of murderous intent, lack of control and a host of other scary things. I live with this word, though; I am the word. But it is not a word you can just drop into a conversation and follow with “It’s not a big deal, though.” I seem to fall in love easily, but it’s always with girls who don’t feel the same way about me. I have seen more rejection than I care to admit, putting myself on the line like that, and it’s been a chore for me not to let my emotions get the best of me. If it’s not outright rejection, it seems to be something else that always seems to happen. I can remember one date I went on some months back. She was a big girl with blonde hair and eyes that had that squinty “I’m up to no good” look. We met over Match.com, and I was struck by how much time she spent going to Phish shows. Her profile was scattered with a number of bands that I had loved at different points in my life. She was a teacher, and she mentioned in her profile something along the lines that because of her love of sparkles, arts-and- crafts, and rainbows, she was a 6-year-old in a woman’s body. Before I knew it, I was asking if she wanted to go get a beer. She said yes, a little too eagerly I thought. I got to the restaurant about 15 minutes early and ordered a beer, apprehensive knowing that eventually I would have to tell her about my illness. Soon enough she walked in, and I was struck by the fact that she seemed a little disappointed to be there. There was no smile as she sat down to join me. © 2015 The New York Times Company
Link ID: 21051 - Posted: 06.15.2015
Sara Reardon Traumatic experiences, such as those encountered during warfare, can cause long-lasting stress. Tweaking the immune system could be key to treating, or even preventing, post-traumatic stress disorder (PTSD). Research in rodents suggests that immunizing animals can lessen fear if they are later exposed to stress. Researchers have known for some time that depression and immune-system health are linked and can affect each other. Early clinical trials have shown that anti-inflammatory drugs can reduce symptoms of depression1, raising hopes that such treatments might be useful in other types of mental illness, such as PTSD. “I think there’s kind of a frenzy about inflammation in psychiatry right now,” says Christopher Lowry, a neuroscientist at the University of Colorado Boulder. He presented results of experiments probing the link between fearful behaviour and immune response at a meeting in Victoria, Canada, last week of the International Behavioral Neuroscience Society. Studies of military personnel suggest that immune function can influence the development of PTSD. Soldiers whose blood contains high levels of the inflammatory protein CRP before they are deployed2, or who have a genetic mutation that makes CRP more active3, are more likely to develop the disorder. To directly test whether altering the immune system affects fear and anxiety, Lowry and colleagues injected mice with a common bacterium, Mycobacterium vaccae, three times over three weeks to modulate their immune systems. The scientists then placed these mice, and a control group of unimmunized mice, in cages with larger, more aggressive animals. © 2015 Nature Publishing Group
Boer Deng A genetic variant protected some practitioners of cannibalism from prion disease. Scientists who study a rare brain disease that once devastated entire communities in Papua New Guinea have described a genetic variant that appears to stop misfolded proteins known as prions from propagating in the brain1. Kuru was first observed in the mid-twentieth century among the Fore people of Papua New Guinea. At its peak in the late 1950s, the disease killed up to 2% of the group's population each year. Scientists later traced the illness to ritual cannibalism2, in which tribe members ate the brains and nervous systems of their dead. The outbreak probably began when a Fore person consumed body parts from someone who had sporadic Creutzfeldt-Jakob disease (CJD), a prion disease that spontaneously strikes about one person in a million each year. Scientists have noted previously that some people seem less susceptible to prion diseases if they have an amino-acid substitution in a particular region of the prion protein — codon 1293. And in 2009, a team led by John Collinge — a prion researcher at University College London who is also the lead author of the most recent analysis — found another protective mutation among the Fore, in codon 1274. The group's latest work, reported on 10 June in Nature1, shows that the amino-acid change that occurs at this codon, replacing a glycine with a valine, has a different and more powerful effect than the substitution at codon 129. The codon 129 variant confers some protection against prion disease only when it is present on one of the two copies of the gene that encodes the protein. But transgenic mice with the codon-127 mutation were completely resistant to kuru and CJD regardless of whether they bore one or two copies of it. The researchers say that the mutation in codon 127 appears to confer protection by preventing prion proteins from becoming misshapen. © 2015 Nature Publishing Group,
Link ID: 21043 - Posted: 06.13.2015
Owning a cat as a kid could put you at risk for schizophrenia and bipolar disorder later on because of parasites found in feline feces, new research says. Previous studies have linked the parasite toxoplasma gondii (T. gondii) to the development of mental disorders, and two more research papers published recently provide further evidence. Researchers from the Academic Medical Centre in Amsterdam looked at more than 50 studies and found that a person infected with the parasite is nearly twice as likely to develop schizophrenia. The other study, led by Dr. Robert H. Yolken of Johns Hopkins University School of Medicine in Baltimore, confirmed the results of a 1982 questionnaire that found half of people who had a cat as a kid were diagnosed with mental illnesses later in life compared to 42% of those who didn't grow up with a cat. "Cat ownership in childhood has now been reported in three studies to be significantly more common in families in which the child is later diagnosed with schizophrenia or another serious mental illness," the authors said in a press release. The findings were published in Schizophrenia Research and Acta Psychiatrica Scandinavica. T. gondii, which causes the disease toxoplasma, is especially risky for pregnant women and people with weak immune symptoms. The parasite can also be found in undercooked meat and unwashed fruits and vegetables.
Angus Chen The genetic underpinnings of psychosis are elusive and diffuse. There are hundreds of common genetic mutations scattered throughout the human genome that each bump up by just a tiny bit the risk of developing a mental illness like schizophrenia. Many people carry some set of those genes, but most don't end up with a psychotic disorder. Instead, a study suggests, they might be getting a small creative boost. Meghan, 23, began experiencing hallucinations at 19. "Driving home, cars' headlights turned into eyes. The grills on the cars turned into mouths and none of them looked happy. It would scare the crap out of me," Meghan says. Those genetic changes may persist in human DNA because they confer benefits, according Dr. Kári Stefánsson, a neurologist and CEO of a biological research company called deCODE Genetics, which conducted the study published in Nature Neuroscience Monday. "They are found in most of us, and they're common because they either confer or in the past conferred some reproductive advantage," he says. The advantage of having a more creative mind, he suggests, might help explain why these genes persist, even as they increase the risk of developing debilitating disorders, such as schizophrenia. It's an idea from the ancients. The philosopher Aristotle famously opined that genius and madness go hand in hand. Psychiatric studies have to some degree supported the adage. Studies of more than 1 million Swedish people in 2011 and 2013 found that people who had close relatives with schizophrenia or bipolar disorder were much more likely to become creative professionals. (The patients with mental illness were not themselves more creative, with the exception of some who had bipolar disorder.) What's more, studies that looked at healthy people who carry genetic markers associated with a psychotic disorder found their brains work slightly differently than others who lack those genetic markers. © 2015 NPR
by Helen Thomson For the first time, scientists have discovered a mechanism in humans that could explain how your lifestyle choices may impact your children and grandchildren's genes. Mounting evidence suggests that environmental factors such as smoking, diet and stress, can leave their mark on the genes of your children and grandchildren. For example, girls born to Dutch women who were pregnant during a long famine at the end of the second world war had twice the usual risk of developing schizophrenia. Likewise, male mice that experience early life stress give rise to two generations of offspring that have increased depression and anxiety, despite being raised in a caring environment. This has puzzled many geneticists, as genetic information contained in sperm and eggs is not supposed to be affected by the environment, a principle called the August Weismann barrier. But we also know the activity of our own genes can be changed by our environment, through epigenetic mechanisms . These normally work by turning a gene on or off by adding or subtracting a methyl group to or from its DNA. These methyl groups can inactivate genes by making their DNA curl up, so that enzymes can no longer access the gene and read its instructions. Such epigenetic mechanisms are high on the list of suspects when it comes to explaining how environmental factors that affect parents can later influence their children, such as in the Dutch second world war study, but just how these epigenetic changes might be passed on to future generations is a mystery. © Copyright Reed Business Information Ltd.
Steve Connor Scientists have linked the condition with variations in the DNA of genes known to be involved in stimulating or inhibiting the passing of chemical messages across the tiny gaps or “synapses” between nerve cells in the brain. They said the findings are part of a wider body of evidence pointing to the genetic causes of schizophrenia which is known to have a strong inherited component as well as being influenced by a person’s environment and upbringing. “We’re finally starting to understand what goes wrong in schizophrenia. Our study marks a significant step towards understanding the biology underpinning schizophrenia, which is an incredible complex condition and has up until very recently kept scientists largely mystified as to is origins,” said Andrew Pocklington of Cardiff University. “We now have what we hope is a pretty sizeable piece of the jigsaw puzzle that will help us to develop a coherent model of the disease, while helping us to rule out some of the alternatives,” said Dr Pocklington, the lead author of the study published in the journal Neuron. “A reliable model of disease is urgently needed to direct future efforts in developing new treatments, which haven’t really improved a great deal since the 1970s,” he said. © independent.co.uk
By Rachael Rettner and LiveScience Mathematician John Nash, who died May 23 in a car accident, was known for his decades-long battle with schizophrenia—a struggle famously depicted in the 2001 Oscar-winning film "A Beautiful Mind." Nash had apparently recovered from the disease later in life, which he said was done without medication. But how often do people recover from schizophrenia, and how does such a destructive disease disappear? Nash developed symptoms of schizophrenia in the late 1950s, when he was around age 30, after he made groundbreaking contributions to the field of mathematics, including the extension of game theory, or the math of decision making. He began to exhibit bizarre behavior and experience paranoia and delusions, according to The New York Times. Over the next several decades, he was hospitalized several times, and was on and off anti-psychotic medications. But in the 1980s, when Nash was in his 50s, his condition began to improve. In an email to a colleague in the mid-1990s, Nash said, "I emerged from irrational thinking, ultimately, without medicine other than the natural hormonal changes of aging," according to The New York Times. Nash and his wife Alicia died, at ages 86 and 82, respectively, in a crash on the New Jersey Turnpike while en route home from a trip on which Nash had received a prestigious award for his work. © 2015 Scientific American
Link ID: 21018 - Posted: 06.06.2015
By ANDREW SOLOMON At the beginning of spring in 2013, Mary Guest, a lively, accomplished 37-year-old woman, fell in love, became pregnant and married after a short courtship. At the time, Mary taught children with behavioral problems in Portland, Ore., where she grew up. Her supervisor said that he had rarely seen a teacher with Mary’s gift for intuiting students’ needs. “Mary was a powerful person,” he wrote to her mother, Kristin. “Around Mary, one felt compassion, drive, calmness and support.” Mary had struggled with depression for much of her life. Starting in her 20s, she would sometimes say to Kristin that she just wanted to die. “She would always follow up by saying, ‘But you don’t need to worry, Mama,’ ” Kristin told me. “ ‘I don’t have a plan, and I don’t intend to do anything.’ ” In recent years, Mary and her mother went for a walk once a week, and Mary would describe the difficulties she was having. She was helped somewhat by therapy and by antidepressant and antianxiety medications, which blunted her symptoms. Mary’s friends appreciated her wacky sense of humor and her engaging wit. Colleagues said that her moods never impinged on her work; in fact, few of them knew what she was dealing with. Yet for years Mary worried that she would never be in a stable relationship and experience love or a family of her own. She said plaintively to Kristin, “I think I would be a really good mother.” So when she discovered that she was pregnant, she was delighted, and she expected the experience to be blissful. She decided to discontinue her antidepressants, having read about their potential danger for a growing fetus. Given her history of severe depression, she was monitored closely by a psychiatric nurse practitioner, who told her that she could call anytime for an immediate prescription. But Mary elected to stay off medication.
By Tori Rodriguez Heart disease and depression often go hand in hand. Long-term studies have found that people with depression have a significantly higher risk of subsequent heart disease, and vice versa. Recent research has revealed that the link begins at an early age and is probably caused by chronic inflammation. A new study in the November 2014 issue of Psychosomatic Medicine by researchers in the U.S., Australia and China examined data from an ongoing study of health among Australians. The researchers looked at the scores of 865 young adults on a questionnaire that assesses depression symptoms and other measures of mental health. They also examined measurements of the internal diameter of the blood vessels of the retina, a possible marker of early cardiovascular disease. After controlling for sex, age, smoking status and body mass index, the investigators found that participants with more symptoms of depression and anxiety had wider retinal arterioles than others, which could reflect the quality of blood vessels in their heart and brain. “We don't know if the association is causal,” explains study co-author Madeline Meier, a psychology professor at Arizona State University. “But our findings suggest that symptoms of depression and anxiety may identify youth at risk for cardiovascular disease.” Other research shows that people with depression have more inflammation throughout their body and nervous system. “One theory is that stress and inflammation could play a causal role in depression,” Meier says. Such chronic inflammation is also a risk factor for cardiovascular disease. The relationship is complex: in some people, inflammation seems to precede depression and heart disease; in others, the disorders seem to cause or exacerbate the inflammation. © 2015 Scientific American
Boer Deng The ability of the bizarre prion protein to cause an array of degenerative brain conditions may help solve a puzzle in Alzheimer's research — why the disease sometimes kills within a few years, but usually causes a slow decline that can take decades. By adopting tools used to study the prion protein, PrP, researchers have found variations in the shape of a protein involved in Alzheimer’s that may influence how much damage it causes in the brain. At the Prion 2015 meeting, held on 26–29 May in Fort Collins, Colorado, neuroscientist Lary Walker described how he has borrowed a technique from prion research to study different ‘strains’ of the amyloid-β protein, which accumulates in clumps in the brains of people with Alzheimer’s. It may be that differences between the strains account for variations in the disease’s symptoms and rate of progression. “The Alzheimer’s field has not been paying enough attention to what’s happening in the prion field,” says Walker, who is based at Emory University in Atlanta, Georgia. Similarities between rare prion diseases and common neurodegenerative diseases such as Alzheimer’s have been noted for decades: both are thought to involve proteins in the nervous system that change shape and clump together. In prion diseases, a misfolded, often foreign, protein induces cascading malformation of the native prion protein in a patient’s brain. In Alzheimer’s, proteins called tau and amyloid-β accumulate within and around nerve cells, though what triggers that process — and the role of the deposits in the disease — is unclear. © 2015 Nature Publishing Group,
Jon Hamilton Antidepressant drugs that work in hours instead of weeks could be on the market within three years, researchers say. "We're getting closer and closer to having really, truly next-generation treatments that are better and quicker than existing ones," says Dr. Carlos Zarate, a researcher at the National Institute of Mental Health. The new drugs are based on the anesthetic ketamine, which is also a popular club drug known as Special K. Unlike current antidepressants, which can take weeks to work, ketamine-like drugs have an immediate effect. They also have helped people with depression who didn't respond to other medications. The drug that is furthest along is esketamine, a chemical variant of ketamine that has been designated a potential breakthrough by the Food and Drug Administration. Esketamine is poised to begin Phase 3 trials, and the drug's maker, Johnson & Johnson, plans to seek FDA approval in 2018. Ketamine, used as a tranquilizer for animals and as an anesthetic in humans, is also being tested as a treatment for depression. Another ketamine-like drug on the horizon is rapastinel. It has completed Phase 2 studies, which showed "rapid, substantial, and sustained reductions in depressive symptoms," according to the drug's maker, Naurex. "I think it's highly probable that we'll see some version of one of these treatments being approved in the relatively near future," says Dr. Gerard Sanacora, director of the Yale Depression Research Program. "In my mind it is the most exciting development in mood disorder treatment in the last 50 years." © 2015 NPR
Link ID: 20999 - Posted: 05.30.2015
Stacey Vanek Smith I'm in a booth with a computer program called Ellie. She's on a screen in front of me. Ellie was designed to diagnose post-traumatic stress disorder and depression, and when I get into the booth she starts asking me questions — about my family, my feelings, my biggest regrets. Emotions seem really messy and hard for a machine to understand. But Skip Rizzo, a psychologist who helped design Ellie, thought otherwise. When I answer Ellie's questions, she listens. But she doesn't process the words I'm saying. She analyzes my tone. A camera tracks every detail of my facial expressions. The doctor may see you now "Contrary to popular belief, depressed people smile as many times as non-depressed people," Rizzo says. "But their smiles are less robust and of less duration. It's almost like polite smiles rather than real, robust, coming from your inner-soul type of a smile." Ellie compares my smile to a database of soldiers who have returned from combat. Is my smile genuine? Is it forced? Ellie also listens for pauses. She watches to see whether I look off to the side or down. If I lean forward, she notices. All this analysis seems to work: In studies, Ellie could detect signs of PTSD and depression about as well as a large pool of psychologists. Jody Mitic served with the Canadian forces in Afghanistan. He lost both of his feet to a bomb. And Mitic remembers that Ellie's robot-ness helped him open up. "Ellie seemed to just be listening," Mitic says. "A lot of therapists, you can see it in their eyes, when you start talking about some of the grislier details of stuff that you might have seen or done, they are having a reaction." © 2015 NPR
Dan Sung A 10-year study has revealed a startling link between high levels of anxiety and an increased risk of death from liver disease. The research, carried out by scientists at the University of Edinburgh, took account for obvious sociological and physiological factors such as alcohol consumption, obesity, diabetes and class, but still the data pointed to a clear relationship between the psychological conditions of stress and depression and the physical health of the hepatic system. There were over 165,000 participants surveyed for mental distress. They were each tracked for over a decade during which time the causes of death for those who passed on were recorded and categorised. What was found was that those who’d scored highly for signs of depression and stress were far more likely to suffer fatal liver disease. “This study provides further evidence for the important links between mind and body, and of the damaging effects psychological distress can have on physical wellbeing,” said Dr Tom Russ of the Centre for Clinical Brain Sciences. The work did not uncover any reasons for direct cause and effect but is the first to identify such a link between mental states and liver damage. Previous research has described how psychological conditions can lead to increased risk of cardiovascular disease which, in turn, may develop into obesity, raised blood pressure and then eventually to liver failure but, with this methodology controlling for such factors, it appears that the link is more direct than was previously thought.
By Will Lippincott In January 2012, two weeks after my discharge from a psychiatric hospital in Connecticut, I made a plan to die. My week in an acute care unit that had me on a suicide watch had not diminished my pain. Back in New York, I stormed out of my therapist’s office and declared I wouldn’t return to the treatment I’d dutifully followed for three decades. Nothing was working, so what was the point? I fit the demographic profile of the American suicide — white, male and entering middle age with a history of depression. Suicide runs in families, research tells us, and it ran in mine. My father killed himself at age 49 in April 1990. A generation before, an aunt of his took her life; before her, there were others. Shame runs in families, too, and no one in mine talked much about mental illness. The first time I was hospitalized for wanting to kill myself, as a teenager, my dad visited me a few days in. I made an effort to greet him with a firm handshake; he shared a few jokes with me. Dad was visibly concerned and told me he loved me. Only after his suicide a few years later did I learn that he, too, had been hospitalized, for depression, when he was in his early 20s. Setting out to start my own life after college, I felt that suicide was a clear and present opportunity, one that glowed more brightly during my depressive episodes. But I had an ambitious plan to beat it. I’d be a performer: work hard, keep my goals in the line of sight at all times, and make as much money as I could. Professional success would be my first line of defense to keep hopelessness at bay. In parallel, I’d find excellent doctors and be a compliant patient, take my meds and show up for talk therapy. And for a long time, through my 20s and 30s, that plan worked. © 2015 The New York Times Company
Link ID: 20949 - Posted: 05.19.2015
Nick Davis Mood disorders such as depression are devastating to sufferers, and hugely costly to treat. The most severe form of depression, often called clinical depression or major depressive disorder (MDD), increases the person’s likelihood of suicide and contributes significantly to a person’s disability-adjusted life years (DALYs), a measure of quality of life taking into account periods of incapacity. The healthcare burden of MDD is large in most countries, especially when the person requires a stay in hospital. Putting these factors together, it’s clear we need to develop effective treatments to combat depression. The mechanisms of depressive disorders are not well understood, and it seems likely that there is no single cause. Most modern therapies use drugs that target neurotransmitters – the chemicals that carry signals between neurons. For example, the class of drugs known as SSRIs, or selective serotonin reuptake inhibitors, prevent the neurotransmitter serotonin from being reabsorbed by a neuron; this means that more serotonin is available to wash around between the nerve cells, and is more likely to activate cells in the brain networks that area affected in MDD. But SSRIs and other drugs are not a pharmacological ‘free lunch’. Drug treatments for depression are ineffective for many people, cause side-effects, and may lose their therapeutic effect over time. For these reasons, many researchers are searching for alternative treatments for MDD that overcome these problems, and are more effective or less unpleasant. One potential treatment involves the use of pulses of magnetic energy over the head to target the brain’s mood circuits. This technique, called transcranial magnetic stimulation (TMS), may potentially address some of the problems of pharmaceutical treatments, but we still don’t know exactly how it works, or how effective it will be in treating MDD. © 2015 Guardian News and Media Limited
Link ID: 20946 - Posted: 05.18.2015
John Crace After over a year working in Westminster as this paper’s parliamentary sketchwriter, I thought I had learned a thing or two about bearpits. That was before I agreed to second Prof Allan Young in speaking against the motion that “This House believes that the long-term use of psychiatric medications is causing more harm than good”. It turned out that politicians are almost models of decency compared to psychiatrists fighting their own corner. I had wondered why I had been invited. I have no scientific knowledge of the subject under discussion; all I had to offer was my own personal experience of living with episodes of depression and acute anxiety for more than 20 years. For me, a combination of medication and therapy has proved effective; not so effective as to prevent recurrences of these mental health problems all together, but effective enough for me to have managed them without having to return as an in-patient at the psychiatric hospital I wound up in 20 years earlier. I could perhaps have done more to look after myself, I suppose. I could have given up my Spurs season ticket. But apart from that … Having raised concerns about my credentials, I was assured that it was important to have a patient’s voice heard. I thought so, too. So I agreed. But on the way home from the debate last night, I did wonder if the reason I had been asked was because everyone else had turned them down. Things didn’t get off to a great start, when there was a pre-debate vote in the packed theatre at King’s College’s Institute of Psychiatry, Psychology and Neuroscience, which had apparently sold out within hours of the tickets being made available in March. 126 people – a mixture of mental health practitioners, students and members of the public – believed the motion to be correct; 28 abstained, and only 64 were on my side. © 2015 Guardian News and Media Limited
Link ID: 20936 - Posted: 05.16.2015
Haroon Siddique Long-term depression in people over 50 could more than double their risk of suffering a stroke, with the risk remaining significantly higher even after the depression allays, research suggests. The US study of more than 16,000 people, which documented 1,192 strokes, found that onset of recent depression was not associated with higher stroke risk, suggesting the damage is done by depressive symptoms accumulating over time. The study’s lead author, Paola Gilsanz, from Harvard University’s TH Chan School of Public Health, said: “Our findings suggest that depression may increase stroke risk over the long term. Looking at how changes in depressive symptoms over time may be associated with strokes allowed us to see if the risk of stroke increases after elevated depressive symptoms start or if risk goes away when depressive symptoms do. We were surprised that changes in depressive symptoms seem to take more than two years to protect against or elevate stroke risk.” The research, published on Wednesday in the Journal of the American Heart Association, used data from between 1998 and 2010 from the Health and Retirement Study, which interviews a panel of representative Americans aged over 50 every two years, on their depressive symptoms, history of stroke, and stroke risk factors. Gilsanz, with colleagues from universities in Washington, California and Minnesota, and Bronx Partners for Healthy Communities, found that people with high depressive symptoms at two consecutive interviews had a 114% higher risk of suffering a first stroke, compared with people without depression at either interview. Those who had depressive symptoms at one interview but not at the next had a 66% higher risk. © 2015 Guardian News and Media Limited