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By David Tuller Patients with chronic fatigue syndrome are accustomed to disappointment. The cause of the disorder remains unknown; it can be difficult to diagnose, and treatment options are few. Research suggesting that an infection from a mouse virus may cause it raised hopes among patients a few years ago, but the evidence fell apart under closer scrutiny. Many patients are still told to seek psychiatric help. But two recent studies — one from investigators at Stanford a few weeks ago and another from a Japanese research team published earlier this year — have found that the brains of people with chronic fatigue syndrome differ from those of healthy people, strengthening the argument that serious physiological dysfunctions are at the root of the condition. “You’ve got two different groups that have independently said, ‘There’s something going on in the brain that is aberrant,’ ” said Leonard Jason, a psychologist at DePaul University in Chicago who studies the condition, also called myalgic encephalomyelitis and widely known as M.E./C.F.S. “I think you have a growing sense that this illness should be taken seriously.” Both studies were small, however, and their results must be replicated before firm conclusions can be drawn. Still, other studies presented at scientific conferences this year also have demonstrated physiological dysfunctions in these patients. In the most recent study, published by the journal Radiology, researchers at Stanford University compared brain images of 15 patients with the condition to those of 14 healthy people. The scientists found differences in both the white matter, the long, cablelike nerve structures that transmit signals between parts of the brain, and the gray matter, the regions where these signals are processed and interpreted. The most striking finding was that in people with the disorder, one neural tract in the white matter of the right hemisphere appeared to be abnormally shaped, as if the cablelike nerve structures had crisscrossed or changed in some other way. Furthermore, the most seriously ill patients exhibited the greatest levels of this abnormality. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 20355 - Posted: 11.25.2014

By Pippa Stephens Health reporter, BBC News Women are more likely than men to display symptoms of depression when in a position of authority at work, according to US scientists. In men, authority, such as the ability to hire and fire people, decreases depressive symptoms, the study said. The study, published in the Journal of Health and Social Behaviour, looked at 2,800 middle-aged men and women. One expert said the study showed the need for more women in authority and more varied female role models. Scientists at the University of Texas at Austin interviewed 1,300 male and 1,500 female graduates from Wisconsin high schools over the phone in 1993 and 2004, when they were aged about 54 and 64. Researchers asked participants about job authority and about the number of days in the past week they felt depressive symptoms, such as feeling sad and thinking one's life is a failure. When the job included hiring, firing and influencing pay, women were predicted to have a 9% increased rate of depressive symptoms than women without authority. Meanwhile, men had a 10% decreased rate of depressive symptoms. The study said it controlled for other factors that could cause depression, such as hours worked per week, whether people had flexible hours and how often workers were checked by a supervisor. Scientists also said men were more likely to decide when to start and finish work than women and were less frequently monitored by their advisers. Lead researcher Tetyana Pudrovska said: "These women have more education, higher incomes, more prestigious occupations, and higher levels of job satisfaction and autonomy than women without job authority. Yet they have worse mental health than lower status women." BBC © 2014

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 20343 - Posted: 11.21.2014

By Tom Shroder After more than 30 years in which psychedelics were considered dangerous remnants of the 1960s, the drugs have begun to make a comeback, this time as potential remedies for a host of tough-to-treat maladies. Pilot studies and clinical trials of LSD, psilocybin, ketamine and MDMA have shown that the drugs, often in combination with talk therapy, can be given safely under medical supervision and may help people dealing with opiate and tobacco addiction, alcoholism, anxiety, depression and post-traumatic stress disorder, or PTSD. That these investigations have shown potential is not surprising to many researchers. A generation of scientists and practitioners had used psychedelics successfully with thousands of patients until the research was banned in 1970, after the drugs were embraced by an exploding counterculture that seemed to threaten the status quo. In the panicked reaction, psychedelics were listed along with heroin in the highest rungs of prohibition. Ironically, this failed to stop recreational use but it shut the science down cold. As one researcher put it, “It was as if psychedelic drugs had become undiscovered.” But a small cadre of psychiatrists and researchers, often risking careers and reputations, pushed to bring psychedelics back to the lab and the clinic. Their persistence paid off. Beginning in the 1990s, the Food and Drug Administration approved the first human clinical studies of psychedelic drugs in a quarter of a century. By 2004, the first FDA-approved trial of the medicinal use of a psychedelic drug, in this case a trial of MDMA-assisted therapy for PTSD involving 24 subjects, was underway. Now such studies are proliferating.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20321 - Posted: 11.18.2014

Emily Anthes Anna's life began to unravel in 2005 when her husband of 30 years announced that he had fallen in love with another woman. “It had never even occurred to me that my marriage could ever end,” recalls Anna, a retired lawyer then living in Philadelphia, Pennsylvania. “It was pretty shocking.” Over the course of several months, Anna stopped wanting to get up in the morning. She felt tired all the time, and consumed by negative thoughts. “'I'm worthless.' 'I messed up everything.' 'It's all my fault.'” She needed help, but her first therapist bored her and antidepressants only made her more tired. Then she found Cory Newman, director of the Center for Cognitive Therapy at the University of Pennsylvania, who started her on a different kind of therapy. Anna learned how to obsess less over her setbacks and give herself more credit for her triumphs. “It was so helpful to talk to someone who steered me to more positive ways of thinking,” says Anna, whose name has been changed at her request. Cognitive therapy, commonly known as cognitive behavioural therapy (CBT), aims to help people to identify and change negative, self-destructive thought patterns. And although it does not work for everyone with depression, data have been accumulating in its favour. “CBT is one of the clear success stories in psychotherapy,” says Stefan Hofmann, a psychologist at Boston University in Massachusetts. Antidepressant drugs are usually the first-line treatment for depression. They are seen as a quick, inexpensive fix — but clinical trials reveal that only 22–40% of patients emerge from depression with drugs alone. Although there are various approaches to psychotherapy, CBT is the most widely studied; a meta-analysis1 published this year revealed that, depending on how scientists measure outcomes, between 42% and 66% of patients no longer meet the criteria for depression after therapy. © 2014 Nature Publishing Group

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20306 - Posted: 11.13.2014

Heidi Ledford If the extent of human suffering were used to decide which diseases deserve the most medical attention, then depression would be near the top of the list. More than 350 million people are affected by depression, making it one of the most common disorders in the world. It is the biggest cause of disability, and as many as two-thirds of those who commit suicide have the condition. But although depression is common, it is often ignored. Three-quarters of people with depression in the United Kingdom go undiagnosed or untreated — and even if the disorder is diagnosed, today's medications will work well for only about half of those who seek help. “It's unbelievable,” says Tom Foley, a psychiatrist at Newcastle University, UK. “If that was the case in cancer care, it would be an absolute scandal.” The comparison between depression and cancer is a common one. Cancer, too, is a terrible blight: it affects more than 32 million people and kills some 8 million a year, many more than depression. But at least in developed countries, the vast majority of people with recognized cancers do receive treatment. In research, too, depression has failed to keep up with cancer. Cancer research today is a thriving field, unearthing vast catalogues of disease-associated mutations, cranking out genetically targeted therapies and developing sophisticated animal models. Research into depression, meanwhile, seems to have floundered: once-hopeful therapies have failed in clinical trials, genetic studies have come up empty-handed. The field is still struggling to even define the disease — and overcome the stigma associated with it. © 2014 Nature Publishing Grou

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20305 - Posted: 11.13.2014

By Julia Calderone Antidepressant use among Americans is skyrocketing. Adults in the U.S. consumed four times more antidepressants in the late 2000s than they did in the early 1990s. As the third most frequently taken medication in the U.S., researchers estimate that 8 to 10 percent of the population is taking an antidepressant. But this spike does not necessarily signify a depression epidemic. Through the early 2000s pharmaceutical companies were aggressively testing selective serotonin reuptake inhibitors (SSRIs), the dominant class of depression drug, for a variety of disorders—the timeline below shows the rapid expansion of FDA-approved uses. As the drugs' patents expired, companies stopped funding studies for official approval. Yet doctors have continued to prescribe them for more ailments. One motivating factor is that SSRIs are a fairly safe option for altering brain chemistry. Because we know so little about mental illness, many clinicians reason, we might as well try the pills already on the shelf. Doctors commonly use antidepressants to treat many maladies they are not approved for. In fact, studies show that between 25 and 60 percent of prescribed antidepressants are actually used to treat nonpsychological conditions. The most common and well-supported off-label uses of SSRIs include: Abuse and dependence ADHD (in children and adolescents) Anxiety disorders Autism (in children) Bipolar disorder Eating disorders Fibromyalgia Neuropathic pain Obsessive-compulsive disorder Premenstrual dysphoric disorder © 2014 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20300 - Posted: 11.11.2014

BY Laura Sanders The first time Nathan Whitmore zapped his brain, he had a college friend standing by, ready to pull the cord in case he had a seizure. That didn’t happen. Instead, Whitmore started experimenting with the surges of electricity, and he liked the effects. Since that first cautious attempt, he’s become a frequent user of, and advocate for, homemade brain stimulators. Depending on where he puts the electrodes, Whitmore says, he has expanded his memory, improved his math skills and solved previously intractable problems. The 22-year-old, a researcher in a National Institute on Aging neuroscience lab in Baltimore, writes computer programs in his spare time. When he attaches an electrode to a spot on his forehead, his brain goes into a “flow state,” he says, where tricky coding solutions appear effortlessly. “It’s like the computer is programming itself.” Whitmore no longer asks a friend to keep him company while he plugs in, but he is far from alone. The movement to use electricity to change the brain, while still relatively fringe, appears to be growing, as evidenced by a steady increase in active participants in an online brain-hacking message board that Whitmore moderates. This do-it-yourself community, some of whom make their own devices, includes people who want to get better test scores or crush the competition in video games as well as people struggling with depression and chronic pain, Whitmore says. As reckless as it sounds to juice a brain at home with a 9-volt battery and 40 dollars’ worth of spare parts, this technology’s buzz is based on legit science. Small laboratory studies suggest that carefully controlled brain stimulation can boost a person’s memory and math abilities, hone attention and fast-track learning. The U. S. military is interested and is funding studies to test brain stimulation as a way to boost soldiers’ alertness and vigilance. The technique may even be a viable treatment for pernicious mental disorders such as major depression, according to other laboratory-based studies. © Society for Science & the Public 2000 - 2014.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 20266 - Posted: 11.01.2014

By Erin Allday Stanford researchers have found some striking abnormalities in the brains of people with chronic fatigue syndrome, a frustrating and debilitating condition for which there is no known cause and no treatment that’s widely effective. The findings, published Wednesday in the journal Radiology, could improve diagnosis and spark new scientific understanding of the disease. Perhaps even more noteworthy, the results — if they can be confirmed with larger studies — could provide some of the first objective evidence that chronic fatigue syndrome is a severe illness that causes real physiological damage. That would be a major step for patients and their advocates, who still suffer under the stigma of having a condition that for decades was ignored or not taken seriously. “If this finding holds, it will be exciting because yes, we’ve found something that has never been found before. But there’s this additional layer of looking at a disease that was completely ostracized. So there’s also this component of validation,” said Dr. Jose Montoya, an infectious disease specialist who helped establish a chronic fatigue syndrome team at Stanford School of Medicine a decade ago. Montoya was the senior author of the Stanford study. For patients, Montoya said, “It’s almost like we’re saying, 'You were right all along. Hopefully this will put you where you deserve to be, in a real clinic with treatments.’” There are limitations to the study, Montoya said. Most notably, the sample size is fairly small, with 15 chronic fatigue patients and 14 healthy control subjects.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20256 - Posted: 10.29.2014

Scientists say they have identified the underlying reason why some people are prone to the winter blues, or seasonal affective disorder (SAD). People with Sad have an unhelpful way of controlling the "happy" brain signalling compound serotonin during winter months, brain scans reveal. As the nights draw in, production of a transporter protein ramps up in Sad, lowering available serotonin. The work will be presented this week at a neuropsychopharmacology conference. The University of Copenhagen researchers who carried out the trial say their findings confirm what others have suspected - although they only studied 11 people with Sad and 23 healthy volunteers for comparison. Using positron emission tomography (PET) brain scans, they were able to show significant summer-to-winter differences in the levels of the serotonin transporter (SERT) protein in Sad patients. The Sad volunteers had higher levels of SERT in the winter months, corresponding to a greater removal of serotonin in winter, while the healthy volunteers did not. Winter depression Lead researcher, Dr Brenda Mc Mahon, said: "We believe that we have found the dial the brain turns when it has to adjust serotonin to the changing seasons. BBC © 2014

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 20225 - Posted: 10.21.2014

By David Bornstein Shortly after the birth of her daughter, Andrea became severely depressed. She was 17 at the time and she didn’t fully understand what she was going through; she just felt like a failure. “I felt like I didn’t want to be alive,” she recalls. “I felt like I didn’t deserve to be alive. I felt like a bad person and a bad mother, and I was never going to get any better.” When her baby persisted in crying, she felt her frustration mount quickly. “I was hitting a boiling point,” she says. “I was at a point where I didn’t want to deal with anything. Sometimes I would just let her cry — but then I would feel very bad afterwards.” Depression is the most common health problem women face. In the United States, outside of obstetrics, it is the leading cause of hospitalizations among women ages 15 to 44. It’s estimated that 20 percent to 25 percent of women will experience depression during their lifetimes, and about one in seven will experience postpartum depression. For low-income women, the rates are about twice as high. As my colleague Tina Rosenberg has reported, the World Health Organization ranks depression as the most burdensome of all health conditions affecting women (as measured by lost years of productive life). Postpartum depressions are often assumed to be associated with hormonal changes in women. In fact, only a small fraction of them are hormonally based, said Cindy-Lee Dennis, a professor at the University of Toronto and a senior scientist at Women’s College Research Institute, who holds a Canada Research Chair in Perinatal Community Health. The misconception is itself a major obstacle, she adds. Postpartum depression is often not an isolated form of depression; nor is it typical. “We now consider depression to be a chronic condition,” Dennis says. “It reoccurs in approximately 30 to 50 percent of individuals. And a significant proportion of postpartum depression starts during the pregnancy but is not detected or treated to remission. We need to identify symptoms as early as possible, ideally long before birth.” © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 20221 - Posted: 10.20.2014

A drug being studied as a fast-acting mood-lifter restored pleasure-seeking behavior independent of — and ahead of — its other antidepressant effects, in a National Institutes of Health trial. Within 40 minutes after a single infusion of ketamine, treatment-resistant depressed bipolar disorder patients experienced a reversal of a key symptom — loss of interest in pleasurable activities — which lasted up to 14 days. Brain scans traced the agent’s action to boosted activity in areas at the front and deep in the right hemisphere of the brain. “Our findings help to deconstruct what has traditionally been lumped together as depression,” explained Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health. “We break out a component that responds uniquely to a treatment that works through different brain systems than conventional antidepressants — and link that response to different circuitry than other depression symptoms.” This approach is consistent with the NIMH’s Research Domain Criteria project, which calls for the study of functions – such as the ability to seek out and experience rewards – and their related brain systems that may identify subgroups of patients in one or multiple disorder categories. Zarate and colleagues reported on their findings Oct. 14, 2014 in the journal Translational Psychiatry. Although it’s considered one of two cardinal symptoms of both depression and bipolar disorder, effective treatments have been lacking for loss of the ability to look forward to pleasurable activities, or anhedonia. Long used as an anesthetic and sometimes club drug, ketamine and its mechanism-of-action have lately been the focus of research into a potential new class of rapid-acting antidepressants that can lift mood within hours instead of weeks.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20218 - Posted: 10.18.2014

|By Brian Bienkowski and Environmental Health News On his farm in Iowa, Matt Peters worked from dawn to dusk planting his 1,500 acres of fields with pesticide-treated seeds. “Every spring I worried about him,” said his wife, Ginnie. “Every spring I was glad when we were done.” In the spring of 2011, Ginnie Peters' “calm, rational, loving” husband suddenly became depressed and agitated. “He told me ‘I feel paralyzed’,” she said. “He couldn’t sleep or think. Out of nowhere he was depressed.” A clinical psychologist spoke to him on the phone and urged him to get medical help. “He said he had work to do, and I told him if it’s too wet in the morning to plant beans come see me,” Mike Rossman said. “And the next day I got the call.” Peters took his own life. He was 55 years old. No one knows what triggered Peters’ sudden shift in mood and behavior. But since her husband’s death, Ginnie Peters has been on a mission to not only raise suicide awareness in farm families but also draw attention to the growing evidence that pesticides may alter farmers’ mental health. “These chemicals that farmers use, look what they do to an insect. It ruins their nervous system,” Peters said. “What is it doing to the farmer?” Farming is a stressful job – uncontrollable weather, physical demands and economic woes intertwine with a personal responsibility for land that often is passed down through generations. But experts say that some of the chemicals used to control pests may make matters worse by changing farmers’ brain chemistry. © 2014 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20171 - Posted: 10.07.2014

By Gretchen Reynolds Exercise may help to safeguard the mind against depression through previously unknown effects on working muscles, according to a new study involving mice. The findings may have broad implications for anyone whose stress levels threaten to become emotionally overwhelming. Mental health experts have long been aware that even mild, repeated stress can contribute to the development of depression and other mood disorders in animals and people. Scientists have also known that exercise seems to cushion against depression. Working out somehow makes people and animals emotionally resilient, studies have shown. But precisely how exercise, a physical activity, can lessen someone’s risk for depression, a mood state, has been mysterious. So for the new study, which was published last week in Cell, researchers at the Karolinska Institute in Stockholm delved into the brains and behavior of mice in an intricate and novel fashion. Mouse emotions are, of course, opaque to us. We can’t ask mice if they are feeling cheerful or full of woe. Instead, researchers have delineated certain behaviors that indicate depression in mice. If animals lose weight, stop seeking out a sugar solution when it’s available — because, presumably, they no longer experience normal pleasures — or give up trying to escape from a cold-water maze and just freeze in place, they are categorized as depressed. And in the new experiment, after five weeks of frequent but intermittent, low-level stress, such as being restrained or lightly shocked, mice displayed exactly those behaviors. They became depressed. The scientists could then have tested whether exercise blunts the risk of developing depression after stress by having mice run first. But, frankly, from earlier research, they knew it would. They wanted to parse how. So they bred pre-exercised mice. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 20145 - Posted: 10.01.2014

by Bethany Brookshire Isaac Newton famously showed that in physics, every action has an equal and opposite reaction. A similar push-and-pull of positive and negative inputs also exists in our brains. Brain cells can send out excitatory chemical signals, and they can also receive inhibitory chemical signals, putting the brakes on further signaling. This delicate balance of excitation and inhibition allows our brains to function normally and to react to the world around us. A new study shows that the same neurons contribute excitatory and inhibitory chemical signals in a brain area linked with how we process disappointment, and that antidepressants might be able to change this delicate molecular dance and stop some of the negative thought cycles associated with depression. But while the work finds an association, it’s not yet proof that the balance of these chemicals holds the key to relieving depressive symptoms. The study, published September 19 in Science, focuses on the lateral habenula. This tiny area makes up the “stalk” connecting the pineal gland to the rest of the brain. It receives inputs from areas of the brain important in reward and emotional processing, including the basal ganglia. Some areas of the brain appear to specialize in predicting rewards, showing increases in activity in response to enjoyable things such as food, sex or drugs. Activity in these areas lets us know when things are about to get good. But for every high there is a low. The lateral habenula is thought to play a role in how we process negative events: Getting a lemon on the slot machine again or the empty inbox on your dating site. Studies in monkeys and other animals have shown that increased activity in the habenula is linked to depressive behaviors, and treatment with antidepressants decreases this activity. In addition, a study in rats and a 2009 case study in a human patient showed that deep-brain stimulation in the lateral habenula could relieve symptoms of depression. © Society for Science & the Public 2000 - 2014.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20125 - Posted: 09.27.2014

By CLYDE HABERMAN When it came to pharmacological solutions to life’s despairs, Aldous Huxley was ahead of the curve. In Huxley’s 1932 novel about a dystopian future, the Alphas, Betas and others populating his “Brave New World” have at their disposal a drug called soma. A little bit of it chases the blues away: “A gramme” — Huxley was English, remember, spelling included — “is better than a damn.” With a swallow, negative feelings are dispelled. Prozac, the subject of this week’s video documentary from Retro Report, is hardly soma. But its guiding spirit is not dissimilar: A few milligrams of this drug are preferable to the many damns that lie at the core of some people’s lives. Looking back at Prozac’s introduction by Eli Lilly and Company in 1988, and hopscotching to today, the documentary explores the enormous influence, both chemical and cultural, that Prozac and its brethren have had in treating depression, a concern that gained new resonance with the recent suicide of the comedian Robin Williams. In the late 1980s and the 90s, Prozac was widely viewed as a miracle pill, a life preserver thrown to those who felt themselves drowning in the high waters of mental anguish. It was the star in a class of new pharmaceuticals known as S.S.R.I.s — selective serotonin reuptake inhibitors. Underlying their use is a belief that depression is caused by a shortage of the neurotransmitter serotonin. Pump up the levels of this brain chemical and, voilà, the mood lifts. Indeed, millions have embraced Prozac, and swear by it. Depression left them emotionally paralyzed, they say. Now, for the first time in years, they think clearly and can embrace life. Pharmacological merits aside, the green-and-cream pill was also a marvel of commercial branding, down to its market-tested name. Its chemical name is fluoxetine hydrochloride, not the most felicitous of terms. A company called Interbrand went to work for Eli Lilly and came up with Prozac. “Pro” sounds positive. Professional, too. “Ac”? That could signify action. As for the Z, it suggests a certain strength, perhaps with a faint high-techy quality. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20098 - Posted: 09.22.2014

By Douglas Main Researchers have created a blood test that they have used to accurately diagnose depression in a small sample of people, and they hope that with time and funding it could be used on a widespread basis. It is the first blood test—and thus the first “objective” gauge—for any type of mental disorder in adults, says study co-author Eva Redei, a neuroscientist at Northwestern University in Evanston, Ill. Outside experts caution, however, that the results are preliminary, and not close to ready for use the doctor’s office. Meanwhile, diagnosing depression the “old-fashioned way” through an interview works quite well, and should only take 10 to 15 minutes, says Todd Essig, a clinical psychologist in New York. But many doctors are increasingly overburdened and often not reimbursed for taking the time to talk to their patients, he says. The test works by measuring blood levels of nine different types of RNA, a chemical that the body uses to process DNA. Besides accurately diagnosing depression, which affects perhaps 10 percent of American adults and is becoming more common, the technique may also be able to tell who could benefit from talk therapy and who may be vulnerable to the condition in the first place. In a study describing the test, published in the journal Translational Psychiatry, the scientists recruited 32 patients who were diagnosed with depression using a clinical interview, the standard technique. They also got 32 non-depressed patients to participate as a control group. © 2014 Newsweek LLC

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20084 - Posted: 09.17.2014

By ANNA FELS THE idea of putting a mind-altering drug in the drinking water is the stuff of sci-fi, terrorist plots and totalitarian governments. Considering the outcry that occurred when putting fluoride in the water was first proposed, one can only imagine the furor that would ensue if such a thing were ever suggested. The debate, however, is moot. It’s a done deal. Mother Nature has already put a psychotropic drug in the drinking water, and that drug is lithium. Although this fact has been largely ignored for over half a century, it appears to have important medical implications. Lithium is a naturally occurring element, not a molecule like most medications, and it is present in the United States, depending on the geographic area, at concentrations that can range widely, from undetectable to around .170 milligrams per liter. This amount is less than a thousandth of the minimum daily dose given for bipolar disorders and for depression that doesn’t respond to antidepressants. Although it seems strange that the microscopic amounts of lithium found in groundwater could have any substantial medical impact, the more scientists look for such effects, the more they seem to discover. Evidence is slowly accumulating that relatively tiny doses of lithium can have beneficial effects. They appear to decrease suicide rates significantly and may even promote brain health and improve mood. Yet despite the studies demonstrating the benefits of relatively high natural lithium levels present in the drinking water of certain communities, few seem to be aware of its potential. Intermittently, stories appear in the scientific journals and media, but they seem to have little traction in the medical community or with the general public. The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20077 - Posted: 09.15.2014

Being bullied regularly by a sibling could put children at risk of depression when they are older, a study led by the University of Oxford suggests. Around 7,000 children aged 12 were asked if they had experienced a sibling saying hurtful things, hitting, ignoring or lying about them. The children were followed up at 18 and asked about their mental health. A charity said parents should deal with sibling rivalry before it escalates. Previous research has suggested that victims of peer bullying can be more susceptible to depression, anxiety and self-harm. This study claims to be the first to examine bullying by brothers or sisters during childhood for the same psychiatric problems in early adulthood. Researchers from the Universities of Oxford, Warwick and Bristol and University College London sent questionnaires to thousands of families with 12-year-old children in 2003-04 and went back to them six years later to assess their mental health. If they had siblings they were asked about bullying by brothers and sisters. The questionnaire said: "This means when a brother or sister tries to upset you by saying nasty and hurtful things, or completely ignores you from their group of friends, hits, kicks, pushes or shoves you around, tells lies or makes up false rumours about you." Most children said they had not experienced bullying. Of these, at 18, 6.4% had depression scores in the clinically significant range, 9.3% experienced anxiety and 7.6% had self-harmed in the previous year. The 786 children who said they had been bullied by a sibling several times a week were found to be twice as likely to have depression, self-harm and anxiety as the other children. BBC © 2014

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 20044 - Posted: 09.08.2014

Greta Kaul, Stanford researchers say poor sleep may be an independent risk factor for suicide in adults over 65. Researchers used data from a previous epidemiological study to compare the sleep quality of 20 older adults who committed suicide and 400 who didn't, over 10 years. Researchers found that those who didn't sleep well were 1.4 times more likely to commit suicide within a decade. Older adults have disproportionately high suicide rates in the first place, especially older men. The Stanford researchers believe that on its own, sleeping poorly could be a risk factor for suicide later in life. It may even be a more powerful predictor of suicide risk than symptoms of depression. They found that the strongest predictor of suicide was the combination of bad sleep and depression. Unlike many biological, psychological and social risk factors for suicide, sleep disorders tend to be treatable, said Rebecca Bernert, the lead author of the study. Sleep disorders are also less stigmatized than other suicide risk factors. Bernert is now studying whether treating insomnia is effective in preventing depression and suicide. The study was published in JAMA Psychiatry in August. © 2014 Hearst Communications, Inc.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 20024 - Posted: 09.03.2014

By RONI CARYN RABIN Pregnant women often go to great lengths to give their babies a healthy start in life. They quit smoking, skip the chardonnay, switch to decaf, forgo aspirin. They say no to swordfish and politely decline Brie. Yet they rarely wean themselves from popular selective serotonin reuptake inhibitor antidepressants like Prozac, Celexa and Zoloft despite an increasing number of studies linking prenatal exposure to birth defects, complications after birth and even developmental delays and autism. Up to 14 percent of pregnant women take antidepressants, and the Food and Drug Administration has issued strong warnings that one of them, paroxetine (Paxil), may cause birth defects. But the prevailing attitude among doctors has been that depression during pregnancy is more dangerous to mother and child than any drug could be. Now a growing number of critics are challenging that assumption. “If antidepressants made such a big difference, and women on them were eating better, sleeping better and taking better care of themselves, then one would expect to see better birth outcomes among the women who took medication than among similar women who did not,” said Barbara Mintzes, an associate professor at the University of British Columbia School of Population and Public Health. “What’s striking is that there’s no research evidence showing that.” On the contrary, she said, “when you look for it, all you find are harms.” S.S.R.I.s are believed to work in part by blocking reabsorption (or reuptake) of serotonin, altering levels of this important neurotransmitter in the brain and elsewhere in the body. Taken by a pregnant woman, the drugs cross the placental barrier, affecting the fetus. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 20020 - Posted: 09.02.2014