Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Sandra G. Boodman, As the jet hurtled toward New York’s John F. Kennedy International Airport on New Year’s Day 2013, the clinical psychologist watched her 16-year-old daughter warily, praying there would be no recurrence of the girl’s inexplicable and bizarre behavior. The previous night, while walking down a street in Spain where the family had spent Christmas, the teenager suddenly began yelling that the traditional New Year’s Eve fireworks were actually bombs. On the flight home, the girl seemed entirely normal. Her mother thought the high school junior might have had a panic attack, stressed by her upcoming college search and impending wisdom teeth extraction. But the uneventful flight brought a short-lived relief. Five days later, the teenager was hospitalized for treatment of what appeared to be a severe psychotic break. And for the next six weeks, the news seemed to get worse as a more ominous diagnosis emerged — and with it the specter of death. “Every day seemed like a horror story,” said Carmen, a psychoanalyst who practices in New York and whose last name, along with that of her daughter, Mia, is being withheld at her request to protect her professional privacy. For Lara Marcuse, a neurologist at Mount Sinai Hospital in Manhattan who treated Mia during her hospitalization, those weeks were filled with tension and anxiety that deepened as she worried that the teenager might not survive her sudden illness. “If she was my age,” said Marcuse, who is 44, “Mia would either be dead, in a coma or in a state psychiatric center.” Instead Mia, now 18, has fully recovered. She recently had a part in her high school play, is anticipating graduation and looking forward to entering college in September. © 1996-2014 The Washington Post
Link ID: 19548 - Posted: 04.29.2014
By MATTHEW PERRONE WASHINGTON (AP) — The Food and Drug Administration announced Friday it will convene a public meeting in October to review the risks of psychiatric and behavioral side effects with Pfizer’s anti-smoking drug Chantix. The agency said in a federal notice it will convene its panel of psychiatric drug experts to discuss the pill’s risks and how to best manage them. Since 2009 Chantix has carried the government’s strongest safety warning — a ‘‘black box’’ label — because of links to hostility, agitation, depression and suicidal thoughts. The warning was added after the FDA received dozens of reports of suicide and hundreds of reports of suicidal behavior among patients taking the smoking-cessation drug. At that time, the FDA also required Pfizer to conduct additional studies to determine the extent of the side effects. A spokeswoman for Pfizer said Friday that the company recently submitted new data to the FDA comparing the drug’s psychiatric safety to placebo and other anti-smoking techniques. The FDA first began investigating potential side effects with Chantix in 2007, the year after the twice-a-day pill hit the market. The drug’s labeling tells patients to stop taking Chantix immediately if they experience agitation, depressed mood, suicidal thinking and other behavioral changes. Doctors are advised to weigh the drug’s risks against its potential benefits in helping patients quit smoking.
by Michael Slezak Could preventing the brain shrinkage associated with depression be as simple as blocking a protein? Post-mortem analysis of brain tissue has shown that the dendrites that relay messages between neurons are more shrivelled in people with severe depression than in people without the condition. This atrophy could be behind some of the symptoms of depression, such as the inability to feel pleasure. As a result, drugs that help repair the neuronal connections, like ketamine, are under investigation. But how this shrinkage occurs has remained a mystery, limiting researchers' ability to find ways of stopping it. Ronald Duman at Yale University wondered whether a protein called REDD1, which was recently shown to reduce myelin, the fatty material that protects neurons, was the key. To find out, his team bred rats unable to produce REDD1 and exposed them to a prolonged period of unpredictable stress. In normal rats, this stress resulted in depressive-like behaviour and brain shrinkage, but Duman's rats were unaffected. In contrast, rats engineered to overproduce REDD1 became depressed and had brain shrinkage, even without being stressed. What's more, injecting normal rats with a stress hormone boosted levels of REDD1 in the brain. Giving them a drug that blocked the production of stress hormones stopped them producing the protein, even when they were externally stressed. Taken together, the experiments show that REDD1 is necessary to produce the brain shrinkage seen in stressed rats, and that stress hormones are involved in its production – offering a possible way to prevent the shrinkage. © Copyright Reed Business Information Ltd
Link ID: 19532 - Posted: 04.24.2014
By Melissa Healy The nature of psychological resilience has, in recent years, been a subject of enormous interest to researchers, who have wondered how some people endure and even thrive under a certain amount of stress, and others crumble and fall prey to depression. The resulting research has underscored the importance of feeling socially connected and the value of psychotherapy to identify and exercise patterns of thought that protect against hopelessness and defeat. But what does psychological resilience look like inside our brains, at the cellular level? Such knowledge might help bolster peoples' immunity to depression and even treat people under chronic stress. And a new study published Thursday in Science magazine has made some progress in the effort to see the brain struggling with -- and ultimately triumphing over -- stress. A group of neuroscientists at Mount Sinai's Icahn School of Medicine in New York focused on the dopaminergic cells in the brain's ventral tegmentum, a key node in the brain's reward circuitry and therefore an important place to look at how social triumph and defeat play out in the brain. In mice under stress because they were either chronically isolated or rebuffed or attacked by fellow littermates, the group had observed that this group of neurons become overactive. It would logically follow, then, that if you don't want stressed mice (or people) to become depressed, you would want to avoid hyperactivity in that key group of neurons, right? Actually, wrong, the researchers found. In a series of experiments, they saw that the mice who were least prone to behave in socially defeated ways when under stress were actually the ones whose dopaminergic cells in the ventral tegmental area displayed the greatest levels of hyperactivity in response to stress. And that hyperactivity was most pronounced in the neurons that extended from the tegmentum into the nearby nucleus accumbens, also a key node in the brain's reward system.
Scientists have traced vulnerability to depression-like behaviors in mice to out-of-balance electrical activity inside neurons of the brain’s reward circuit and experimentally reversed it – but there’s a twist. Instead of suppressing it, researchers funded by the National Institutes of Health boosted runaway neuronal activity even further, eventually triggering a compensatory self-stabilizing response. Once electrical balance was restored, previously susceptible animals were no longer prone to becoming withdrawn, anxious, and listless following socially stressful experiences. “To our surprise, neurons in this circuit harbor their own self-tuning, homeostatic mechanism of natural resilience,” explained Ming-Hu Han, Ph.D External Web Site Policy., of the Icahn School of Medicine at Mount Sinai, New York City, a grantee of the NIH’s National Institute of Mental Health (NIMH) and leader of the research team. Han and colleagues report on their discovery April 18, 2014 in the journal Science. Prior to the new study, the researchers had turned resilience to social stress on and off by using pulses of light to manipulate reward circuit neuronal firing rates in genetically engineered mice – optogenetics. But they didn’t know how resilience worked at the cellular level. To find out, they focused on electrical events in reward circuit neurons of mice exposed to a social stressor. Some mice that experience repeated encounters with a dominant animal emerge behaviorally unscathed, while others develop depression-like behaviors.
By DORIS IAROVICI, M.D. “I think our experiment failed,” the young graduate student told me, referring to our attempt to take her off the antidepressant she’d been on for seven years. She was back in my campus office after a difficult summer break, and as she talked about feeling unsettled and upset, I wondered about the broader experiment playing out on college campuses across the country. Antidepressants are an excellent treatment for depression and anxiety. I’ve seen them improve — and sometimes save — many young lives. But a growing number of young adults are taking psychiatric medicines for longer and longer periods, at the very age when they are also consolidating their identities, making plans for the future and navigating adult relationships. Are we using good scientific evidence to make decisions about keeping these young people on antidepressants? Or are we inadvertently teaching future generations to view themselves as too fragile to cope with the adversity that life invariably brings? My patient had started medication as a college freshman, after she’d become depressed and spent much of her time in bed. She was forced to take a medical leave but improved quickly, returned to school and graduated. She married soon after and worked for a few years, feeling well all the while. Professional guidelines recommend six to nine months of medicine for first episodes of depression. But my patient had never been advised to stop taking it. She reluctantly agreed to my recommendation to taper off her antidepressant. © 2014 The New York Times Company
Link ID: 19502 - Posted: 04.17.2014
On Wednesday morning we woke to the news that a passenger ferry had sunk off the coast of South Korea, with at least four people confirmed dead and 280 unaccounted for. Meanwhile, though the search has continued for the missing Malaysia Airlines plane, relatives' hopes of a safe landing have long since been extinguished. Human tragedies like these are the stuff of daily news, but we rarely hear about the long-term psychological effects on survivors and the bereaved, who may experience the symptoms of post-traumatic stress disorder for years after their experience. Although most people have heard of PTSD, few will have a clear idea of what it entails. The American Psychiatric Association's Diagnostic and Statistical Manual (DSM) defines a traumatic event as one in which a person "experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others". PTSD is marked by four types of responses to the trauma. First, patients repeatedly relive the event, either in the form of nightmares or flashbacks. Second, they seek to avoid any reminder of the traumatic event. Third, they feel constantly on edge. Fourth, they are plagued with negative thoughts and low mood. According to one estimate, almost 8% of people will develop PTSD during their lifetime. Clearly trauma (and PTSD) can strike anyone, but the risks of developing the condition are not equally distributed. Rates are higher in socially disadvantaged areas, for instance. Women may be twice as likely to develop PTSD as men. This is partly because women are at greater risk of the kinds of trauma that commonly produce PTSD (rape, for example). Nevertheless – and for unknown reasons – when exposed to the same type of trauma, women are more susceptible to PTSD than men. © 2014 Guardian News and Media Limited
By BENEDICT CAREY The relationship had become intolerably abusive, and after a stinging phone call one night, it seemed there was only one way to end the pain. Enough wine and pills should do the job — and would have, except that paramedics barged through the door, alerted by her lover. “I very rarely tell the story in detail publicly, it’s so triggering and sensational,” said Dese’Rae L. Stage, 30, a photographer and writer living in Brooklyn who tried to kill herself in 2006. “I talk about what led up to it, how helpless I felt — and what came after.” The nation’s oldest suicide prevention organization, the American Association of Suicidology, decided in a vote by its board last week to recognize a vast but historically invisible portion of its membership: people, like Ms. Stage, who tried to kill themselves but survived. About a million American adults a year make a failed attempt at suicide, surveys suggest, far outnumbering the 38,000 who succeed, and in the past few years, scores of them have come together on social media and in other forums to demand a bigger voice in prevention efforts. Plans for speakers bureaus of survivors willing to tell their stories are well underway, as is research to measure the effect of such testimony on audiences. For decades, mental health organizations have featured speakers with schizophrenia, bipolar disorder and depression. But until now, suicide has been virtually taboo, because of not only shame and stigma, but also fears that talking about the act could give others ideas about how to do it. “This is a real shift you’re seeing,” said Heidi Bryan, 56, of Neenah, Wis., who has been speaking for years about suicide attempts she made in the 1990s. “For people working in suicide prevention, they always told us not to talk about our own experience, like they were afraid to tip us over the edge or something. Honestly, we’re the ones who know what works and what doesn’t.” © 2014 The New York Times Company
Link ID: 19481 - Posted: 04.14.2014
|By Scott O. Lilienfeld and Hal Arkowitz A rabble-rousing patient on a psychiatric ward is brought into a room and strapped to a gurney. He is being punished for his defiance of the head nurse's sadistic authority. As he lies fully awake, the psychiatrist and other staff members place electrodes on both sides of his head and pass a quick jolt of electricity between them. Several orderlies hold the patient down while he grimaces in pain, thrashes uncontrollably and lapses into a stupor. This scene from the 1975 Academy Award–winning film One Flew Over the Cuckoo's Nest, starring Jack Nicholson as the rebellious patient, has probably shaped the general public's perceptions of electroconvulsive therapy (ECT) far more than any scientific description. As a result, many laypeople regard ECT as a hazardous, even barbaric, procedure. Yet most data suggest that when properly administered, ECT is a relatively safe and often beneficial last-resort treatment for severe depression, among other forms of mental illness. One Flew Over the Cuckoo's Nest is far from the only negative portrayal of ECT in popular culture. In a 2001 survey of 24 films featuring the technique, psychiatrists Andrew McDonald of the University of Sydney and Garry Walter of Northern Sydney Central Coast Health of New South Wales reported that the depictions of ECT are usually pejorative and inaccurate. In most cases, ECT is delivered without patients' consent and often as retribution for disobedience. The treatment is typically applied to fully conscious and terrified patients. Following the shocks, patients generally lapse into incoherence or a zombielike state. In six films, patients become markedly worse or die. Probably as a result of such portrayals, the general public holds negative attitudes toward ECT. © 2014 Scientific American
Link ID: 19475 - Posted: 04.12.2014
By NICHOLAS BAKALAR A new study adds to the evidence that the use of antidepressants during pregnancy is associated with a higher risk of premature birth, though many factors most likely play a role and the relationship is complex. Researchers reviewed data from 41 studies, some of which controlled for factors like smoking, alcohol or coffee drinking, weight gain during pregnancy, and other behavioral and health issues. They found no increase in the risk of early birth with the use of antidepressants during the first trimester, a 53 percent higher risk over all and a 96 percent higher risk with antidepressant use late in pregnancy. Depression itself is a risk factor for premature births, and a few studies tried to account for this by using, as a control, a group of women with a diagnosis of depression who did not take antidepressants during their pregnancy. Generally, researchers still found a higher, though diminished, risk from taking antidepressants. The review was published in March in PLOS One. Does this mean that all pregnant women should avoid these drugs? No, said the senior author, Dr. Adam C. Urato, an assistant professor of maternal-fetal medicine at Tufts University. Risks and benefits have to be balanced, he said. “It’s very complex, and depends on the severity of the disease,” Dr. Urato added. “The point is that we have to get the right information out so that we can let pregnant women make an informed decision.” © 2014 The New York Times Company
By BARBARA EHRENREICH MY atheism is hard-core, rooted in family tradition rather than adolescent rebellion. According to family legend, one of my 19th-century ancestors, a dirt-poor Irish-American woman in Montana, expressed her disgust with the church by vehemently refusing last rites when she lay dying in childbirth. From then on, we were atheists and rationalists, a stance I perpetuated by opting, initially, for a career in science. How else to understand the world except as the interaction of tiny bits of matter and mathematically predictable forces? There were no gods or spirits, just our own minds pressing up against the unknown. But something happened when I was 17 that shook my safely rationalist worldview and left me with a lifelong puzzle. Years later, I learned that this sort of event is usually called a mystical experience, and I can see in retrospect that the circumstances had been propitious: Thanks to a severely underfunded and poorly planned skiing trip, I was sleep-deprived and probably hypoglycemic that morning in 1959 when I stepped out alone, walked into the streets of Lone Pine, Calif., and saw the world — the mountains, the sky, the low scattered buildings — suddenly flame into life. There were no visions, no prophetic voices or visits by totemic animals, just this blazing everywhere. Something poured into me and I poured out into it. This was not the passive beatific merger with “the All,” as promised by the Eastern mystics. It was a furious encounter with a living substance that was coming at me through all things at once, too vast and violent to hold on to, too heartbreakingly beautiful to let go of. It seemed to me that whether you start as a twig or a gorgeous tapestry, you will be recruited into the flame and made indistinguishable from the rest of the blaze. I felt ecstatic and somehow completed, but also shattered. © 2014 The New York Times Company
By LISA SANDERS, M.D. On Thursday, we challenged Well readers to solve the mystery of a 23-year-old man with episodes of aggressive, manic behavior that couldn’t be controlled. Nearly 1,000 readers wrote in with their take on this terrifying case. More than 300 of you got the right class of disease, and 21 of you nailed the precise form of the disorder. Amazing! The correct diagnosis is … Variegate porphyria The first person with the correct answer was Francis Graziano, a 23-year-old recent graduate of the University of Michigan. His major in neuroscience really gave him a leg up on this case, he told me. He recalled a case he read of a young Vietnam veteran with symptoms of porphyria. He’s a surgical technician right now, waiting to hear where he’ll be going to medical school next year. Strong work, Dr.-to-be Graziano! The Diagnosis: The word porphyria comes from the ancient Greek word for purple, “porphyra,” because patients with this disease can have purplish-red urine, tears or saliva. The porphyrias are a group of rare genetic diseases that develop in patients born without the machinery to make certain essential body chemicals, including one of the most important parts of blood known as heme. This compound makes up the core of the blood component hemoglobin. (The presence of heme is why blood is red.) Patients who can’t make heme correctly end up with too much of its chemical precursors, known as porphyrins. The excess porphyrins injure tissues throughout the body, but especially in the nervous system. The disorder is characterized by frequent episodes of debilitating back or abdominal pain and is often accompanied by severe psychiatric symptoms. Patients with porphyria do not respond to most psychiatric medications. Indeed, many of these drugs make the symptoms of porphyria worse. © 2014 The New York Times Company
Link ID: 19448 - Posted: 04.05.2014
David Adam The day the Brazilian racing driver Ayrton Senna died in a crash, I was stuck in the toilet of a Manchester swimming pool. The door was open, but my thoughts blocked the way out. It was May 1994. I was 22 and hungry. After swimming a few lengths of the pool, I had lifted myself from the water and headed for the locker rooms. Going down the steps, I had scraped the back of my heel on the sharp edge of the final step. It left a small graze through which blood bulged into a blob that hung from my broken skin. I transferred the drop to my finger and a second swelled to take its place. I pulled a paper towel from above the sink to press to my wet heel. The blood on my finger ran with the water as it dripped down my arm. My eyes followed the blood. And the anxiety, of course, rushed back, ahead even of the memory. My shoulders sagged. My stomach tightened. Four weeks earlier, I had pricked my finger on a screw that stuck out from a bus shelter's corrugated metal. It was a busy Saturday afternoon and there had been lots of people around. Any one of them, I thought, could easily have injured themselves in the way I had. What if one had been HIV positive? They could have left infected blood on the screw, which then pierced my skin. That would put the virus into my bloodstream. I knew the official line was that transmission was impossible this way – the virus couldn't survive outside the body – but I also knew that, when pressed for long enough, those in the know would weaken the odds to virtually impossible. They couldn't be absolutely sure. In fact, several had admitted to me there was a theoretical risk. © 2014 Guardian News and Media Limited
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 19447 - Posted: 04.05.2014
By James Gallagher Health and science reporter, BBC News The illegal party drug ketamine is an "exciting" and "dramatic" new treatment for depression, say doctors who have conducted the first trial in the UK. Some patients who have faced incurable depression for decades have had symptoms disappear within hours of taking low doses of the drug. The small trial on 28 people, reported in the Journal of Psychopharmacology, shows the benefits can last months. Experts said the findings opened up a whole new avenue of research. Depression is common and affects one-in-10 people at some point in their lives. Antidepressants, such as prozac, and behavioural therapies help some patients, but a significant proportion remain resistant to any form of treatment. A team at Oxford Health NHS Foundation Trust gave patients doses of ketamine over 40 minutes on up to six occasions. Eight showed improvements in reported levels of depression, with four of them improving so much they were no longer classed as depressed. Some responded within six hours of the first infusion of ketamine. Lead researcher Dr Rupert McShane said: "It really is dramatic for some people, it's the sort of thing really that makes it worth doing psychiatry, it's a really wonderful thing to see. He added: "[The patients] say 'ah this is how I used to think' and the relatives say 'we've got x back'." Dr McShane said this included patients who had lived with depression for 20 years. Stressed man The testing of ketamine has indentified some serious side-effects The duration of the effect is still a problem. Some relapse within days, while others have found they benefit for around three months and have since had additional doses of ketamine. There are also some serious side-effects including one case of the supply of blood to the brain being interrupted. Doctors say people should not try to self-medicate because of the serious risk to health outside of a hospital setting. BBC © 2014
|By Hal Arkowitz and Scott O. Lilienfeld A commercial sponsored by Pfizer, the drug company that manufactures the antidepressant Zoloft, asserts, “While the cause [of depression] is unknown, depression may be related to an imbalance of natural chemicals between nerve cells in the brain. Prescription Zoloft works to correct this imbalance.” Using advertisements such as this one, pharmaceutical companies have widely promoted the idea that depression results from a chemical imbalance in the brain. The general idea is that a deficiency of certain neurotransmitters (chemical messengers) at synapses, or tiny gaps, between neurons interferes with the transmission of nerve impulses, causing or contributing to depression. One of these neurotransmitters, serotonin, has attracted the most attention, but many others, including norepinephrine and dopamine, have also been granted supporting roles in the story. Much of the general public seems to have accepted the chemical imbalance hypothesis uncritically. For example, in a 2007 survey of 262 undergraduates, psychologist Christopher M. France of Cleveland State University and his colleagues found that 84.7 percent of participants found it “likely” that chemical imbalances cause depression. In reality, however, depression cannot be boiled down to an excess or deficit of any particular chemical or even a suite of chemicals. “Chemical imbalance is sort of last-century thinking. It's much more complicated than that,” neuroscientist Joseph Coyle of Harvard Medical School was quoted as saying in a blog by National Public Radio's Alix Spiegel. © 2014 Scientific American
Link ID: 19432 - Posted: 04.01.2014
By Lenny Bernstein After 60 years of refusing, the people who run the Golden Gate Bridge are moving toward installing a suicide barrier, the New York Times reports. As soon as May, the Golden Gate Bridge, Highway and Transportation District is expected to approve construction of a steel mesh net 20 feet below the California landmark’s sidewalk. A record 46 people jumped to their deaths from the span in 2013, and another 118 were stopped before they could. According to the Times, they have tended to be younger than in the past. Experts have long known, and good research shows, that barriers are highly effective at halting suicides, the 10th-leading cause of death in the United States at 38,364 fatalities in 2010. This is true not just of bridges or other high places: locking up firearms and individually bubble-wrapping pills both limit suicides by those methods, said Jill Harkavy-Friedman, vice president of research for the American Foundation for Suicide Prevention. The key is the characteristics of a person on the verge of committing suicide, even someone who has been contemplating it for a while. Suicides are impulsive acts, and the people who commit them are not thinking clearly, have trouble solving problems, have difficulty shifting gears and weigh risks differently. If thwarted in that first, impulsive attempt, they often do not adjust and seek another way to take their lives, Harkavy-Friedman said. “In a suicidal crisis, it’s all about time,” she said. “They’re going to grab whatever is available. They don’t change gears if that is thwarted, because they have rigid thinking in that moment. They’re not thinking about dying. They’re thinking about ending the pain. © 1996-2014 The Washington Post
Link ID: 19423 - Posted: 03.29.2014
By NICHOLAS BAKALAR A large study has linked several common anti-anxiety drugs and sleeping pills to an increased risk of death, although it’s not certain the drugs were the cause. For more than seven years, researchers followed 34,727 people who filled prescriptions for anti-anxiety medications like Valium and Xanax, or sleep aids like Ambien, Sonata and Lunesta, comparing them with 69,418 controls who did not. After adjusting for a wide variety of factors, the researchers found that people who took the drugs had more than double the risk of death. The study appears online in BMJ. The researchers tried to account for the use of other prescribed drugs, age, smoking, alcohol use, socioeconomic status, and other health and behavioral characteristics. Most important, the investigators also controlled for sleep disorders, anxiety disorders and other psychiatric illnesses, all of which are risk factors for mortality. The lead author, Dr. Scott Weich, a professor of psychiatry at the University of Warwick, said that while he and his colleagues were careful to account for as many potential risks as possible, they were not able to control for the severity of the illnesses suffered by the study participants. Still, he said, the research “adds to an accumulating body of evidence that these drugs are dangerous.” He added: “I prescribe these drugs, and they are difficult to come off. The less time you spend on them the better.” © 2014 The New York Times Company
by Colin Barras What a nerve! Skin cells taken from people with bipolar disorder have been turned into brain cells. These in turn are offering up clues about the changes in the brain that drive the disorder, and may also provide a way to test new treatments. About three in every 100 people develop bipolar disorder – a mental illness characterised by episodes of depression and euphoria. But the condition remains poorly understood. That's because it would be too invasive to obtain and study viable nerve cells from the brains of people with the condition. There are also no good animal models, because bipolar disorder – although highly heritable – has, for the most part, not been linked to any specific genes that can be studied using animals. "People say the condition is probably the result of a lot of small contributions by multiple genes," says Sue O'Shea at the University of Michigan in Ann Arbor. Now O'Shea and her colleagues may have found an ethical way to make a genetic model of the condition. First, they took skin samples from 22 people with bipolar disorder and 10 healthy volunteers. They induced these adult skin cells to return to a stem-cell-like state, creating what are called induced pluripotent stem cells (iPSCs) and then encouraged these cells to mature into neurons. O'Shea was surprised to find that neurons derived from people with bipolar disorder grew differently from those from people without the condition. "I was expecting it would take decades of careful science before we would find any real differences," she says. © Copyright Reed Business Information Ltd.
By Gisela Telis, Jodi Corbitt had been battling depression for decades and by 2010 had resigned herself to taking antidepressant medication for the rest of her life. Then she decided to start a dietary experiment. To lose weight, the 47-year-old Catonsville, Md., mother stopped eating gluten, a protein found in wheat and related grains. Within a month she had shed several pounds — and her lifelong depression. “It was like a veil lifted and I could see life more clearly,” she recalled. “It changed everything.” Corbitt had stumbled into an area that scientists have recently begun to investigate: whether food can have as powerful an impact on the mind as it does on the body. Research exploring the link between diet and mental health “is a very new field; the first papers only came out a few years ago,” said Michael Berk, a professor of psychiatry at the Deakin University School of Medicine in Australia. “But the results are unusually consistent, and they show a link between diet quality and mental health.” “Diet quality” refers to the kinds of foods that people eat, how often they eat them and how much of them they eat. In several studies, including a 2011 analysis of more than 5,000 Norwegians, Berk and his collaborators have found lower rates of depression, anxiety and bipolar disorder among those who consumed a traditional diet of meat and vegetables than among people who followed a modern Western diet heavy with processed and fast foods or even a health-food diet of tofu and salads. © 1996-2014 The Washington Post
Link ID: 19403 - Posted: 03.25.2014
By Ariana Eunjung Cha, Millions of ordinary Americans are now able to walk into a marijuana dispensary and purchase bags of pot on the spot for a variety of medical ailments. But if you’re a researcher like Sue Sisley, a psychiatrist who studies post- traumatic stress disorder, getting access to the drug isn’t nearly so easy. That’s because the federal government has a virtual monopoly on growing and cultivating marijuana for scientific research, and getting access to the drug requires three separate levels of approval. Marijuana offers hope for 6-year-old girl with rare condition: In marijuana, Lydia Schaeffer’s family members think they might have found a treatment that works. Now, they are trying to help legalize the drug. Sisley’s fight to get samples for her study — now in its fourth month — illuminates the complex politics of marijuana in the United States. While 20 states and the District have made medical marijuana legal — in Colorado and Washington state the drug is also legal for recreational use — it remains among the most tightly controlled substances under federal law. For scientists, that means extra steps to obtain, transport and secure the drug — delays they say can slow down their research by months or even years. © 1996-2014 The Washington Post