Chapter 12. Psychopathology: The Biology of Behavioral Disorders
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Amy Maxmen The acid tests of 1960s San Francisco have morphed into something quite different in today’s Silicon Valley. Mind-altering trips have given way to subtle productivity boosts purportedly caused by tiny amounts of LSD or other psychedelic drugs. Fans claim that this ‘microdosing’ boosts creativity and concentration, but sceptics doubt that ingesting or inhaling one-tenth of the normal dose could have an effect. Science could soon help to settle the matter. Researchers have finally mapped the 3D structure of LSD in its active state — and the details, published today in Cell1, indicate the key to the chemical’s potency1. Another team reports today in Current Biology2 that it has pinpointed the molecular go-between that creates the perception of deep meaning experienced during acid trips — a feeling that the writer Aldous Huxley once described as “solidarity with the Universe”. “This is what we dreamed of doing when I was a graduate student in the seventies,” says Gavril Pasternak, a pharmacologist at Memorial Sloan Kettering Cancer Center in New York City who has spent decades studying the receptor proteins in the brain that mediate the activity of opioids and psychedelic drugs. “Work like this expands our understanding of how these receptors work.” In 1972, researchers revealed LSD’s shape by mapping the arrangement of atoms in its crystallized form3. But in the decades since, they’ve struggled to reveal the crystal structure of a receptor grasping a molecule of LSD or another psychedelic drug. This active configuration is key to understanding how drugs work, because their action depends on how they cling to molecules in the body. © 2017 Macmillan Publishers Limited,
By Anil Ananthaswamy People with post-traumatic stress disorder often get flashbacks that can be triggered by an innocuous smell or sound. Now a study that linked unrelated memories and separated them again, suggests that one day we may be able to decouple memories and prevent flashbacks in people with PTSD. Individual memories are stored in groups of neurons – an idea first proposed by psychologist Donald Hebb in 1949. Only now are we developing sophisticated techniques for examining these ensembles of neurons. To see whether two independent memories can become linked, Kaoru Inokuchi at the University of Toyama in Japan, and colleagues used a standard method for creating memories in mice. When mice are exposed to pain, they can learn to link this with associated stimuli, a taste, for example. The team trained mice to form two separate fear memories. First, the mice learned to avoid the sugary taste of saccharine. Whenever they licked a bottle filled with saccharine solution, they were injected with lithium chloride, which induces nausea. Disconnecting memories A few days later, the same mice were taught to associate a tone with a mild electric shock. This caused the mice to freeze whenever they heard it, even if it wasn’t followed with a shock. They remembered the tone as a traumatic experience. © Copyright Reed Business Information Ltd.
By Nathaniel P. Morris In the 20th century, the deinstitutionalization of mental health care took patients out of long-term psychiatric facilities with the aim that they might return to the community and lead more fulfilling lives. But in our rush to shut down America’s asylums, we failed to set up adequate outpatient services for the mentally ill, who now often fend for themselves on the streets or behind bars. According to recent surveys, the number of state psychiatric beds has fallen from over 550,000 in 1955 to fewer than 38,000 in 2016. Meanwhile, research conducted by the Treatment Advocacy Center estimates over 355,000 inmates in America’s prisons and jails suffered from severe mental illness in 2012. Last year, a report by the Department of Housing and Urban Development found that over 100,000 Americans who experienced homelessness also suffered from severe mental illness. Mental health advocates point to a number of failures, such as limited funding for outpatient care and a lack of political foresight, that may have led to this situation. Yet emerging community-based approaches to mental health care are providing hope for the severely mentally ill—as well as some constraints. Court-ordered care for patients with severe mental illness, known as assisted outpatient treatment or AOT, is spreading nationwide. In December, President Obama signed into law the landmark 21st Century Cures Act, bipartisan legislation that bolsters funding for medical research and reshapes approval processes for drugs and medical devices. The law also supports a number of mental health reforms, including millions in federal incentives for states to develop AOT. © 2017 Scientific American
Joseph Palamar On Nov. 30 the FDA approved a Phase III clinical trial to confirm the effectiveness of treating post-traumatic stress disorder (PTSD) with MDMA, also known as Ecstasy. This news appeared in headlines throughout the world, as it represents an important – yet somewhat unorthodox – advance in PTSD treatment. However, the media have largely been referring to Ecstasy – the street name for this drug – as the treatment in this trial, rather than MDMA (3,4-methylenedioxymethamphetamine). This can lead to misunderstanding, as recreational Ecstasy use is a highly stigmatized behavior. Using this terminology may further misconceptions about the study drug and its uses. While Ecstasy is in fact a common street name for MDMA, what we call Ecstasy has changed dramatically since it became a prevalent recreational drug. Ecstasy now has a very different meaning – socially and pharmacologically. It is understandable why the media have referred to this drug as Ecstasy rather than MDMA. Not only has much of the public at least heard of Ecstasy (and would not recognize MDMA), but this also increases shock value and readership. But referring to a therapeutic drug by its street name (such as Ecstasy) is misleading – especially since MDMA is known to be among the most popular illicit drugs used at nightclubs and dance festivals. This leads some to assume that street drugs are being promoted and provided to patients, perhaps in a reckless manner. © 2010–2017, The Conversation US, Inc.
Claudia Dreifus Geneticists tell us that somewhere between 1 and 5 percent of the genome of modern Europeans and Asians consists of DNA inherited from Neanderthals, our prehistoric cousins. At Vanderbilt University, John Anthony Capra, an evolutionary genomics professor, has been combining high-powered computation and a medical records databank to learn what a Neanderthal heritage — even a fractional one — might mean for people today. We spoke for two hours when Dr. Capra, 35, recently passed through New York City. An edited and condensed version of the conversation follows. Q. Let’s begin with an indiscreet question. How did contemporary people come to have Neanderthal DNA on their genomes? A. We hypothesize that roughly 50,000 years ago, when the ancestors of modern humans migrated out of Africa and into Eurasia, they encountered Neanderthals. Matings must have occurred then. And later. One reason we deduce this is because the descendants of those who remained in Africa — present day Africans — don’t have Neanderthal DNA. What does that mean for people who have it? At my lab, we’ve been doing genetic testing on the blood samples of 28,000 patients at Vanderbilt and eight other medical centers across the country. Computers help us pinpoint where on the human genome this Neanderthal DNA is, and we run that against information from the patients’ anonymized medical records. We’re looking for associations. What we’ve been finding is that Neanderthal DNA has a subtle influence on risk for disease. It affects our immune system and how we respond to different immune challenges. It affects our skin. You’re slightly more prone to a condition where you can get scaly lesions after extreme sun exposure. There’s an increased risk for blood clots and tobacco addiction. To our surprise, it appears that some Neanderthal DNA can increase the risk for depression; however, there are other Neanderthal bits that decrease the risk. Roughly 1 to 2 percent of one’s risk for depression is determined by Neanderthal DNA. It all depends on where on the genome it’s located. © 2017 The New York Times Company
About 11 per cent of Canadians aged 15 to 24 experienced depression at some point in their lives, and fewer than half of them sought professional help for a mental health condition over the previous year, according to Statistics Canada. The information was released Wednesday in the agency's Health Reports, and is based on data from the 2012 Canadian Community Health Survey Mental Health. The report was based on 4,031 respondents aged 15 to 24, which when extrapolated represents more than 4.4 million young people. Canadians 15 to 24 years old had a higher rate of depression than any other age group. Suicide is the second leading cause of death (after accidents), accounting for nearly a quarter of deaths in the 15-24 category, Statistics Canada said. An estimated 14 per cent of respondents reported having had suicidal thoughts at some point in their lives. The figure includes six per cent having that thought in the past 12 months. As well, 3.5 per cent had attempted suicide, according to the data. Report author Leanne Findlay said the findings confirm people with depression or suicidal thoughts are increasingly likely to seek professional help. Young people in the study were more likely to turn to friends or family, and when they did, generally felt they received a lot or some help. Factors such as perceived ability to deal with stress and "negative social interactions" — for instance, feeling others were angry with you — were related to depression and suicidal thoughts. Symptoms of depression include feeling sad or having trouble sleeping that last two weeks or more, Findlay said. "Knowledge of these risk and protective factors may facilitate early intervention," Findlay concluded. ©2017 CBC/Radio-Canada.
Mi Zhang, David Mohr, Jingbo Meng Depression is the leading mental health issue on college campuses in the U.S. In 2015, a survey of more than 90,000 students at 108 American colleges and universities found that during the previous year, more than one-third of them had felt so depressed at some point that it was difficult to function. More than two-thirds had felt hopeless in the preceding academic year. Today’s college students are dealing with depression at an alarmingly high rate, and are increasingly seeking help from on-campus mental health services. Depression is also an underlying cause of other common problems on college campuses, including alcohol and substance abuse, eating disorders, self-injury, suicide and dropping out of school. But university counseling centers, the primary sources for students to get mental health care, are struggling to meet this rising demand. First, it can take a long time for clinicians to gain a full picture of what students are experiencing: Depressed students’ accounts of their symptoms are often inaccurate and incomplete. In addition, budget constraints and limited office hours mean the number of clinicians on campus has not grown, and in some cases has shrunk, despite increasing demand. There simply are not enough university clinicians available to serve every student – and few, if any, at critical times like nights and weekends. The number of students on counseling waiting lists doubled from 2010 to 2012. This can leave students waiting long periods without help. In the worst cases, this can have lifelong – or life-ending – consequences. Using mobile technology for mental illness diagnosis and treatment is becoming a hot research topic nowadays because of the pervasiveness of mobile devices and their behavior-tracking capabilities. Building on others’ work, we have found a way to enhance counseling services with mobile technology and big data analytics. It can help students and clinicians alike, by offering a new tool for assessing depression that may shed increased light on a condition that is challenging to study. © 2010–2017, The Conversation US, Inc.
Link ID: 23103 - Posted: 01.14.2017
Jonathan Sadowsky Carrie Fisher’s ashes are in an urn designed to look like a Prozac pill. It’s fitting that in death she continues to be both brash and wryly funny about a treatment for depression. The public grief over Carrie Fisher’s death was not only for an actress who played one of the most iconic roles in film history. It was also for one who spoke with wit and courage about her struggle with mental illness. In a way, the fearless General Leia Organa on screen was not much of an act. Carrie Fisher at a screening of ‘Catastrophe’ at the Tribeca Film Festival in April 2016. PBG/AAD/STAR MAX/IPx via AP Fisher’s bravery, though, was not just in fighting the stigma of her illness, but also in declaring in her memoir “Shockaholic” her voluntary use of a stigmatized treatment: electroconvulsive therapy (ECT), often known as shock treatment. Many critics have portrayed ECT as a form of medical abuse, and depictions in film and television are usually scary. Yet many psychiatrists, and more importantly, patients, consider it to be a safe and effective treatment for severe depression and bipolar disorder. Few medical treatments have such disparate images. I am a historian of psychiatry, and I have published a book on the history of ECT. I had, like many people, been exposed only to the frightening images of ECT, and I grew interested in the history of the treatment after learning how many clinicians and patients consider it a valuable treatment. My book asks the question: Why has this treatment been so controversial? © 2010–2017, The Conversation US, Inc.
Link ID: 23102 - Posted: 01.14.2017
By Amy Ellis Nutt Martin M. Katz might never have begun his groundbreaking scientific career were it not for a quirk in his vision: He was colorblind. As a budding chemist in college, that flaw forced him to reconsider his options. The result, eventually, was a PhD in psychology from the University of Texas in 1955. He went on to become a key figure in neuropsychopharmacology. Katz, who died Jan. 12 at age 89, spent more than two decades at the National Institute of Mental Health. Among his accomplishments: In a multi-institutional collaborative project at NIMH, developing a behavioral methodology to study the effects of new antidepressant drugs; designing the Katz Adjustment Scales, which created an easy-to-use checkoff method for laypeople to observe and measure over time the symptoms of mentally ill patients and track their behavioral changes from treatment; and creating the multivantage model of measurement, which insisted on the necessity of assessing patient, family, and professional views of patient symptoms and experience. The Post spoke with Katz last month. Q: You’ve said you think a lot of your success was fortuitous. How so? A: I was looking for a job in California [after graduate school], but I didn’t want to do clinical work. That was my problem. So I went back to Texas to do a postdoc. A woman who was the dean of the school was experimenting with nutrition of underfed Latino kids in Texas schools. She wanted to get a psychometric background on these kids. That was really the beginning of my career.
Link ID: 23092 - Posted: 01.13.2017
Sarah Boseley Health editor No new drugs for depression are likely in the next decade, even though those such as Prozac work for little more than half of those treated and there have been concerns over their side-effects, say scientists. Leading psychiatrists, some of whom have been involved in drug development, say criticism of the antidepressants of the Prozac class, called the SSRIs (selective serotonin reuptake inhibitors), is partly responsible for the pharmaceutical industry’s reluctance to invest in new drugs – even though demand is steadily rising. But the main reason, said Guy Goodwin, professor of psychiatry at Oxford University, is that the the NHS and healthcare providers in other countries do not want to pay the bill for new drugs that will have to go through expensive trials. The antidepressants that GPs currently prescribe work for only about 58% of people, but they are cheap because they are out of patent. Why 'big pharma' stopped searching for the next Prozac Pharma giants have cut research on psychiatric medicine by 70% in 10 years, so where will the next ‘wonder drug’ come from? “We are not going to get any more new drugs for depression in the next decade simply because the pharmaceutical industry is not investing in research,” said Goodwin. “It can’t make money on these drugs. It costs approximately $1bn to do all the trials before you launch a new drug. “There is also a failure of the science. It has to get more understanding of how these things work before they can improve them.” © 2017 Guardian News and Media Limited
Link ID: 23086 - Posted: 01.12.2017
By Sally Adee Now we know – zapping the brain with electricity really does seem to improve some medical conditions, meaning it may be a useful tool for treating depression. Transcranial direct current stimulation (tDCS) involves using electrodes to send a weak current across the brain. Stimulating brain tissue like this has been linked to effects ranging from accelerated learning to improving the symptoms of depression and faster recovery from strokes. Thousands of studies have suggested the technique may be useful for everything from schizophrenia and Parkinson’s to tinnitus and autism. However, replicating such studies has generally been difficult, and two recent analyses found no evidence that tDCS is effective, leading some to say that the technique is largely a sham. “There are too many folks out there right now who are using electrical brain stimulation in a cavalier way,” says Michael Weisend, a tDCS researcher at Rio Grande Neuroscience in Santa Fe, New Mexico. “At best it has an effect that’s poorly understood, at worst it could be dangerous.” Now a review has weighed up the best available evidence. It has found that depression, addiction and fibromyalgia are most likely to respond to tDCS treatment. Jean-Pascal Lefaucheur, a neurophysiologist at Henri Mondor Hospital in Paris, France, and his team concluded this by sifting through all tDCS studies so far. Unlike the two previous analyses, this one didn’t lump together studies of variable sizes and designs. Instead, the team chose only studies that were placebo-controlled, used tDCS as a daily medical treatment, and involved at least 10 participants. © Copyright Reed Business Information Ltd.
Link ID: 23079 - Posted: 01.10.2017
Joanne Silberner For a revolutionary, Deepali Vishwakarma of Bhopal, India, is more quiet and reflective than you might expect. She's in her 30s, small, with a round face that holds intense brown eyes and a shy grin. Vishwakarma is a lay counselor — a well-trained community member who goes out daily to fight what novelist William Styron once called a "howling tempest in the brain." She's part of an effort by the Indian nonprofit group Sangath to provide mental health treatment to poor people in India and to show that people with much less training than a psychiatrist or psychologist can deliver effective care. Vishwakarma had 40 hours of training for her role as a counselor. So her counseling is definitely revolutionary. And some mental health observers wonder if it might work in the U.S. But it's a controversial approach. Critics say the use of lay counselors means that patients receive substandard care. Tell that to Vishwakarma. In a typical week, she may meet with 25 people, and in her several years as a counselor, patients who've stuck with her, as most have, have done well. The patients have been diagnosed with serious depression (or stress or tension, as it's more often called in India), or alcoholism, and every so often, someone with schizophrenia. She's been trained to listen and to assign specific tasks to her patients. She might tell someone who's feeling really low to go for a daily walk, or go out and play soccer, or work in the garden or listen to the radio. For depression, it means thinking about anything other than that paralyzing howling tempest. For schizophrenia, it means helping people, many of whom are on medication, adjust to living in society. © 2017 npr
Link ID: 23056 - Posted: 01.05.2017
By LESLEY ALDERMAN Here’s a New Year’s challenge for the mind: Make this the year that you quiet all those negative thoughts swirling around your brain. All humans have a tendency to be a bit more like Eeyore than Tigger, to ruminate more on bad experiences than positive ones. It’s an evolutionary adaptation that helps us avoid danger and react quickly in a crisis. But constant negativity can also get in the way of happiness, add to our stress and worry level and ultimately damage our health. And some people are more prone to negative thinking than others. Thinking styles can be genetic or the result of childhood experiences, said Judith Beck, a psychologist and the president of the Beck Institute for Cognitive Behavior Therapy in Bala Cynwyd, Pa. Children may develop negative thinking habits if they have been teased or bullied, or experienced blatant trauma or abuse. Women, overall, are also more likely to ruminate than men, according to a 2013 study. “We were built to overlearn from negative experiences, but under learn from positive ones,” said Rick Hanson, a psychologist and senior fellow at the Greater Good Science Center at the University of California, Berkeley. But with practice you can learn to disrupt and tame negative cycles. The first step to stopping negative thoughts is a surprising one. Don’t try to stop them. If you are obsessing about a lost promotion at work or the results of the presidential election, whatever you do, don’t tell yourself, “I have to stop thinking about this.” “Worry and obsession get worse when you try to control your thoughts,” Dr. Beck said. Instead, notice that you are in a negative cycle and own it. Tell yourself, “I’m obsessing about my bad review.” Or “I’m obsessing about the election.” © 2017 The New York Times Company
By Don Lattin In the fall of 1965, a 33-year-old father of three named Arthur King—a patient on the alcoholics ward at Baltimore’s Spring Grove Hospital—swallowed an LSD pill and laid back on his bed in a special unit called “Cottage Thirteen.” Sanford Unger, the chief of psychosocial research at the Johns Hopkins University School of Medicine, knelt beside King’s bed, holding his hand and reassuring the patient as he started to feel the drug’s mind-altering effects. This was not a normal psychotherapy session. During his 12-hour experience, designed to help stop his destructive drinking habit, King sat on the edge of the bed and looked at the photo of his son that he’d brought. Suddenly, the child became alive in the picture, which initially frightened him. Then King noticed that a lick of his son’s hair was out of place, so he stroked the photo, putting the errant strands back in place. His fear vanished. Later, Unger held out a small vase with a single red rose. King looked at the flower, which seemed to be opening and closing, as though it were breathing. At one point, Unger asked him whether he’d like to go out to a bar and have a few drinks. King didn’t say anything but was shocked when the rose suddenly turned black and dropped dead before his eyes. He never picked up another drink. Arthur King was one of thousands of research subjects who were given LSD, psilocybin, and mescaline as therapeutic tools in the 1950s and 1960s, often with government support and with promising results. But by the time King was enjoying his sobriety, the backlash against psychedelic testing had already begun. By the mid-1970s, the legal exploration of the therapeutic benefits of psychedelic drugs was over.
By KATHARINE Q. SEELYE BROOKLINE, Mass. — When Michael Dukakis lost the presidential election in 1988, his wife, Kitty, felt as if she had been squashed in a compactor, all the air forced out of her. Her even-keeled husband went back to work as governor of Massachusetts; she started binge drinking. “An alcoholic can contain himself for only so long,” Mrs. Dukakis would later write. “When a crisis hits, the restraints snap.” Her drinking masked a long-smoldering depression that eventually led her to receive electroconvulsive therapy, also known as electroshock therapy or ECT. Like most people, she had no idea that the procedure was still used. She thought it a relic, scrapped after it was depicted as an instrument of torture in the 1975 movie “One Flew Over the Cuckoo’s Nest.” But Mrs. Dukakis was desperate. Rehabilitation, talk therapy and antidepressants had failed to ease her crippling depression, so in 2001, at age 64, she turned to shock therapy. To her amazement, it helped. After the first treatment, Mrs. Dukakis wrote, “I felt alive,” as if a cloud had lifted — so much so that when Mr. Dukakis picked her up at Massachusetts General Hospital, she astonished him by proposing that they go out to dinner. “I was so shocked I almost drove off Storrow Drive,” Mr. Dukakis recalled. “I had left this wife of mine at the hospital a basket case just the night before.” Now, 15 years later, the Dukakises have emerged as the nation’s most prominent evangelists for electroconvulsive therapy. Truth be told, there is not much competition. Few boldface names who have had the treatment will acknowledge as much; the stigma is still too great. Exceptions include Carrie Fisher, the actress and writer who died Tuesday, and Dick Cavett, the talk-show host; both have openly discussed their positive experiences. Electroconvulsive therapy is not a one-and-done procedure. Mrs. Dukakis, 80, still receives maintenance treatment every seven or eight weeks. She said that she had minor memory lapses but that the treatment had banished her demons and that she no longer drank, smoked or took antidepressants. © 2017 The New York Times Company
Link ID: 23047 - Posted: 01.02.2017
By Nicole Mortillaro Post-traumatic stress disorder can be a debilitating condition. It's estimated that it affects nearly one in 10 Canadian veterans who served in Afghanistan. Now, there's promising research that could lead to the treatment of the disorder. Following a particularly traumatic event — one where there is the serious threat of death or a circumstance that was overwhelming — we often exhibit physical symptoms immediately. But the effects in our brains actually take some time to form. That's why symptoms of PTSD — reliving an event, nightmares, anxiety — don't show up until some time later. Research has shown that, after such an event, the hippocampus — which is important in dealing with emotions and memory — shrinks, while our amygdala — also important to memory and emotions — becomes hyperactive. In earlier research, Sumantra Chattarji from the National Centre for Biological Sciences (NCBS) and the Institute for Stem Cell Biology and Regenerative Medicine (inStem), in Bangalore, India, discovered that traumatic events cause new nerve connections to form in the amygdala, which also causes hyperactivity. This plays a crucial role in people dealing with post-traumatic stress disorder. Chattarji has been studying changes in the brain after traumatic events for more than a decade. In an earlier study, he concluded that a single stress event had no immediate event on the amygdala of rats. However, 10 days later, the rats exhibited increased anxiety. There were even changes to the brain, and, in particular the amygdala. So Chattarji set out to see if there was a way to prevent these changes. Post-traumatic stress disorder can seriously affect those who have served in the military. New research may help to one day prevent that. (Shamil Zhumatov/Reuters) The new research focused on a particular cell receptor in the brain, called N-Methyl-D-Aspartate Receptor (NMDA-R), which is crucial in forming memories. ©2016 CBC/Radio-Canada.
By Alice Callahan Can psychiatric medications alter the mother-baby bond? I am having a baby in a month and am on an antidepressant, antipsychotic and mood stabilizer. I don't feel a natural instinct to mother or connect to my baby yet. Could it be because of my medications? It’s normal for expectant parents to worry if they don’t feel a strong connection to the baby right away. “Those kinds of mixed fears and anxieties are really common in most pregnancies, certainly first pregnancies,” said Dorothy Greenfeld, a licensed clinical social worker and professor of obstetrics and gynecology at Yale School of Medicine. Bonding is a process that takes time, and while it can begin in pregnancy, the relationship between parent and child mostly develops after birth. Psychiatric conditions, and the medicines used to treat them, can complicate the picture. Antidepressants, the most widely used class of psychiatric drugs, do not seem to interfere with a woman’s attachment to the fetus during pregnancy, as measured by the amount of time the mother spends thinking about and planning for the baby, a 2011 study in the Archives of Women’s Mental Health found. On the other hand, the study found that women with major depression in pregnancy had lower feelings of maternal-fetal attachment, and this sense of disconnection intensified with more severe symptoms of depression. “Depression can definitely affect a person’s ability to bond with their baby, to feel those feelings of attachment, which is why we encourage treatment so strongly,” said Dr. Amy Salisbury, the study leader and a professor of pediatrics and psychiatry at the Alpert Medical School at Brown University. “That’s more likely to interfere than the medication itself.” There is less research on the effects of other types of mental health medications on mother-baby bonding, but psychiatric medications can have side effects that might interfere with parenting. For example, a small percentage of people taking mood-stabilizing medications have feelings of apathy, and that could hinder the bonding process, said Dr. Salisbury. And some mental health medications, depending on dosage and combination, might make a person feel too sedated. But again, letting mental illness go untreated is likely far riskier for both the mother and the baby. © 2016 The New York Times Company
By BENEDICT CAREY She was all there, all the time: exuberant in describing her mania, savage and tender when recalling her despair. And for decades, she gracefully wore the legacy of her legendary role as Princess Leia, worshiped by a generation of teenage girls as the lone female warrior amid the galactic male cast of the “Star Wars” trilogy. In her long, openhearted life, the actress and author Carrie Fisher brought the subject of bipolar disorder into the popular culture with such humor and hard-boiled detail that her death on Tuesday triggered a wave of affection on social media and elsewhere, from both fans and fellow bipolar travelers, whose emotional language she knew and enriched. She channeled the spirit of people like Patty Duke, who wrote about her own bipolar illness, and Kitty Dukakis, who wrote about depression and alcoholism, and turned it into performance art. Ms. Fisher’s career coincided with the growing interest in bipolar disorder itself, a mood disorder characterized by alternating highs and lows, paralyzing depressions punctuated by flights of exuberant energy. Her success fed a longstanding debate on the relationship between mental turmoil and creativity. And her writing and speaking helped usher in a confessional era in which mental disorders have entered the pop culture with a life of their own: Bipolar is now a prominent trait of another famous Carrie, Claire Danes’s character Carrie Mathison in the Showtime television series “Homeland.” “She was so important to the public because she was telling the truth about bipolar disorder, not putting on airs or pontificating, just sharing who she is in an honest-to-the-bone way,” said Judith Schlesinger, a psychologist and author of “The Insanity Hoax: Exposing the Myth of the Mad Genius.” © 2016 The New York Times Company
Link ID: 23035 - Posted: 12.29.2016
By Kelly Servick The “mad cow disease” epidemic that killed more than 200 people in Europe peaked more than a decade ago, but the threat it poses is still real. Eating meat contaminated with bovine spongiform encephalopathy and its hallmark misshapen proteins, called prions, can cause a fatal and untreatable brain disorder, variant Creutzfeldt-Jakob disease (vCJD). Thousands of Europeans are thought to be asymptomatic carriers, and they can spread prions through blood donations. So for years, researchers have sought a test to safeguard blood supplies. This week, two teams bring that goal closer. They describe methods for detecting prions in blood that proved highly accurate in small numbers of samples from infected people and controls. “There is new technology to go forward, and it looks promising,” says Jonathan Wadsworth, a biochemist who studies prion disease at University College London. “These are definitely very welcome papers.” Analyses of discarded appendix and tonsil samples suggest that as many as one in 2000 people in the United Kingdom carries abnormal prions—misfolded variations of a naturally abundant protein, which prompt surrounding healthy proteins to fold and clump abnormally. No one knows how many of these carriers will ever develop vCJD; incubation periods as long as 50 years have been reported. Once symptoms occur—first depression and hallucinations, and eventually dementia and loss of motor control—patients survive about a year. Four people are known to have contracted vCJD through a blood transfusion from an infected donor. © 2016 American Association for the Advancement of Science.
Link ID: 23007 - Posted: 12.22.2016
By STEVEN PETROW “So why did you stop drinking?” my friend Brad asked recently when we were out for dinner. “You never seemed to have a drinking problem.” The question surprised me, coming as it did a full two years after my decision to take a “break” from alcohol. He was scanning the wine list, and I sensed he was hoping I’d share a bottle of French rosé with him. So I decided to tell him the truth. “To get my depression back under control.” In my late 50s, my longstanding depression had started to deepen, albeit imperceptibly at first. I continued drinking moderately, a couple of glasses of wine most days of the week, along with a monthly Manhattan. Then two dark and stormy months really shook me up, leaving me in a black hole of despair as depression closed in. At my first therapy appointment, the psychopharmacologist listened to me attentively, then said bluntly: “Stop drinking for a month.” The shrink wanted to know whether I was in control of my drinking or my drinking was in control of me. He explained that we become more sensitive to the depressant effects of alcohol as we age, especially in midlife, when our body chemistry changes and we’re more likely to be taking various medications that can interact with alcohol and one another. On doctor’s orders, I went cold turkey off alcohol. When I returned a month later and volunteered that I hadn’t touched a drink since our last visit, he was satisfied that I didn’t have “an active alcohol problem” and told me I could drink in what he considered moderation: No more than two glasses of wine a day, and never two days in a row. He also suggested I keep a log. © 2016 The New York Times Company