Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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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
By Melissa Mancini, Many veterans are turning to marijuana to ease symptoms of post traumatic stress disorder, despite concerns from the medical community about how effective pot is at treating the condition. There are a "tremendous" number of testimonials from patients with post traumatic stress disorder who say dried cannabis helps them, but there is a lack of randomized, controlled trials, said Dr. Stewart Cameron, a family physician and professor at Dalhousie University's faculty of medicine. In September 2014, the College of Family Physicians of Canada released a document to help doctors decide how to use cannabis in their practices. "They strongly recommended that it not be used for PTSD," said Cameron. "They suggested it should be reserved as a third or fourth line agent in people who suffer certain types of pain." Veterans Affairs paid out $5.2 million for medical marijuana to veterans across Canada last year. Of that, $3.4 million went to veterans in Atlantic Canada. The department could not say which ailments the veterans are treating with marijuana, because Veterans Affairs doesn't track cannabis reimbursement by condition. Medical marijuana advocate Fabian Henry says most of the 500 veterans who visited his company last year were looking for authorization to use marijuana to help with post traumatic stress disorder. Henry's company, Marijuana for Trauma, connects veterans with physicians willing to authorize medical cannabis. The organization has helped hundreds of veterans fill out forms for medical pot reimbursement from Veterans Affairs Canada. Marijuana for Trauma calls cannabis "a natural choice medicine" and says it's "proven to be effective in 85 per cent of those who suffer with PTSD." But Canadian medical authorities are far from assigning such a high efficacy rate to the drug. ©2015 CBC/Radio-Canada.
Sarah Boseley Health editor Psychiatric drugs do more harm than good and the use of most antidepressants and dementia drugs could be virtually stopped without causing harm, an expert on clinical trials argues in a leading medical journal. The views expressed in a British Medical Journal debate by Peter Gøtzsche, professor and director of the Nordic Cochrane Centre in Denmark, are strongly opposed by many experts in mental health. However, others say the debate around the use of psychiatric drugs is important and acknowledge that there has been overuse of antipsychotics to quieten aggressive patients with dementia. Gøtzsche says more than half a million people over the age of 65 die as a result of the use of psychiatric drugs every year in the western world. “Their benefits would need to be colossal to justify this, but they are minimal,” he writes. He claims that trials carried out with funding from drug companies into the efficacy of psychiatric drugs have almost all been biased, because the patients involved have usually been on other medication first. They stop their drugs and often experience a withdrawal phase prior to starting the trial drug, which then appears to have a big benefit. He also claims that deaths from suicide in clinical trials are under-reported. In trials of the modern antidepressants fluoxetine and venlafaxine, says Gøtzsche, it takes only a few extra days for depression in the placebo group – given dummy pills – to lift as much as in the group given the drugs. He argues that there is spontaneous remission of the disease over time. © 2015 Guardian News and Media Limited
By Melissa Healy contact the reporter Schizophrenia is one of psychiatry's most puzzling afflictions, with a complex of symptoms that goes far beyond its hallmark hallucinations and delusional thinking. But new research has found connections among several of schizophrenia's peculiar collection of symptoms -- including agitation and memory problems -- and linked them to a single genetic variant among the hundreds thought to heighten risk of the disorder. The findings offer new insights into the molecular basis for schizophrenia and could lead to treatments for the disease that are more targeted and more comprehensive. Published Monday in the journal Nature Neuroscience, the study looks at how a gene variant called Arp2/3 contributes to psychosis, agitation and problems of short- and long-term memory. Mice that were genetically modified to lack the Arp2/3 gene variant showed all three symptoms (although to measure psychosis in mice, scientists looked instead for an abnormal startle response that is also seen in humans in the grips of psychosis). The study's authors, led by Duke University neurobiologist Scott Soderling, then dug below those behaviors to see whether brain abnormalities linked to such behaviors had anything in common. Mice that lacked the Arp2/3 gene variant, they discovered, had not only symptoms of schizophrenia, but also several of the underlying brain abnormalities most closely linked to psychosis, agitation and memory problems seen in those with schizophrenia.
Link ID: 20895 - Posted: 05.06.2015
|By Michele Solis An individual with obsessive-compulsive disorder (OCD) is overcome with an urge to engage in unproductive habits, such as excessive hand washing or lock checking. Though recognizing these behaviors as irrational, the person remains trapped in a cycle of life-disrupting compulsions. Previous studies found that OCD patients have abnormalities in two different brain systems—one that creates habits and one that plays a supervisory role. Yet whether the anomalies drive habit formation or are instead a consequence of doing an action over and over remained unclear. To resolve this question, a team at the University of Cambridge monitored brain activity while people were actually forming new habits. Lapses in supervision are to blame, the researchers reported in a study published online in December 2014 in the American Journal of Psychiatry. They scanned 37 people with OCD and 33 healthy control subjects while they learned to avoid a mild shock by pressing on a foot pedal. Pressing the pedal became a habit for everyone, but people with OCD continued to press even when the threat of shock was over. Those with OCD showed abnormal activity in the supervisory regions important for goal-directed behavior but not in those responsible for habit formation. The finding suggests that shoring up the goal-directed systems through cognitive training might help people with OCD. The growing understanding of OCD's roots in the brain may also help convince individuals to engage in standard habit-breaking treatments, which expose a person to a trigger but prevent his or her typical response. “It's hard for people to not perform an action that their whole body is telling them to do,” says first author Claire Gillan, now at New York University. “So if you have an awareness that the habit is just a biological slip, then it makes OCD a lot less scary and something you can eventually control.” © 2015 Scientific American
By Tina Hesman Saey People with depression have more mitochondrial DNA and shorter telomeres than nondepressed people do, an international team of researchers reports online April 23 in Current Biology. Mitochondria are organelles that produce energy for cells. Mitochondria seem to become inefficient under stress, the team found, so more mitochondria may be needed to produce enough energy. Telomeres are the DNA endcaps on chromosomes that prevent the genetic material from unraveling. Short telomeres are associated with shorter life spans. The altered DNA may reflect metabolic changes associated with depression, the researchers say. Experiments with mice showed that these DNA changes are brought on by stress or by stress hormones. Four weeks after scientists stopped stressing the mice, their mitochondrial and telomere DNA had returned to normal. Those results indicate that the molecular changes are reversible. Researchers also studied DNA from more than 11,000 people to learn whether past stress was responsible for the molecular changes seen in people with depression. Depression was associated with the DNA changes, but having a stressful life was not. For instance, people who had experienced childhood sexual abuse but were not depressed did not have statistically meaningful changes to their DNA compared with people who had no history of abuse. The findings suggest that stress can change DNA but many people can bounce back. Depressed people may have a harder time recovering from the molecular damage. © Society for Science & the Public 2000 - 2015.
By Smitha Mundasad Health reporter, BBC News A mindfulness-based therapy could offer a "new choice for millions of people" with recurrent depression, a Lancet report suggests. Scientists tested it against anti-depressant pills for people at risk of relapse and found it worked just as well. The therapy trains people to focus their minds and understand that negative thoughts may come and go. In England and Wales doctors are already encouraged to offer it. Patients who have had recurrent clinical depression are often prescribed long-term anti-depressant drugs to help prevent further episodes. And experts stress that drug therapy is still essential for many. In this study, UK scientists enrolled 212 people who were at risk of further depression on a course of mindfulness-based cognitive therapy (MBCT) while carefully reducing their medication. Patients took part in group sessions where they learned guided meditation and mindfulness skills. The therapy aimed to help people focus on the present, recognise any early warning signs of depression and respond to them in ways that did not trigger further reoccurrences. Researchers compared these results to 212 people who continued to take a full course of medication over two years. By the end of the study, a similar proportion of people had relapsed in both groups. And many in the MBCT group had been tapered off their medication. Scientists say these findings suggest MBCT could provide a much-needed alternative for people who cannot or do not wish to take long-term drugs. In their report, they conclude it "may be a new choice for millions of people with recurrent depression on repeat prescriptions." © 2015 BBC
By KATIE THOMAS Last fall, an article in the American Journal of Psychiatry caught the attention of specialists who treat borderline personality disorder, an intractable condition for which no approved drug treatment exists. The article seemed to offer a glimmer of hope: The antipsychotic drug Seroquel XR reduced some of the disorder’s worst symptoms in a significant number of patients. “It was an exciting development,” recalled Mark F. Lenzenweger, a professor at Binghamton University and Weill Cornell Medical College and an expert in borderline personality disorder. In the realm of clinical trials, however, reality is sometimes far messier than the tidy summaries in medical journals. A closer look at the Seroquel XR study shows just how complicated things can get when a clinical trial involves psychiatric disorders and has its roots in intersecting and sometimes competing interests: a drug company looking to hold onto sales of a best-selling drug, a prominent academic with strong ties to the pharmaceutical industry and a university under fire for failing to protect human study subjects. The trial was paid for by AstraZeneca, the maker of Seroquel XR, and was conducted by Dr. S. Charles Schulz, the head of psychiatry at the University of Minnesota. Two of the study participants were living in a residential treatment facility for sex offenders and may have lied about their diagnosis to qualify for the trial. One of those men slipped the drugs to unwitting treatment center residents and staff, an alarming development that nevertheless did not seem to ruffle the university oversight board that is charged with looking into such episodes. The University of Minnesota’s clinical trial practices are now under intense scrutiny. In February, a panel of outside experts excoriated the university for failing to properly oversee clinical trials and for paying inadequate attention to the protection of vulnerable subjects. The review, commissioned by the university after years of criticism of its research practices, singled out Dr. Schulz and his department of psychiatry, describing “a culture of fear” that pervaded the department. © 2015 The New York Times Company
Link ID: 20814 - Posted: 04.18.2015