Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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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
by Amy Standen The important thing is that Meghan knew something was wrong. When I met her, she was 23, a smart, wry young woman living with her mother and stepdad in Simi Valley, about an hour north of Los Angeles. Meghan had just started a training program to become a respiratory therapist. Concerned about future job prospects, she asked NPR not to use her full name. Five years ago, Meghan's prospects weren't nearly so bright. At 19, she had been severely depressed, on and off, for years. During the bad times, she'd hide out in her room making thin, neat cuts with a razor on her upper arm. "I didn't do much of anything," Meghan recalls. "It required too much brain power." "Her depression just sucked the life out of you," Kathy, Meghan's mother, recalls. "I had no idea what to do or where to go with it." One night in 2010, Meghan's mental state took an ominous turn. Driving home from her job at McDonald's, she found herself fascinated by the headlights of an oncoming car. "I had the weird thought of, you know, I've never noticed this, but their headlights really look like eyes." To Meghan, the car seemed malicious. It wanted to hurt her. Kathy tried to reason with her. "Honey, you know it's a car, right? You know those are headlights," she recalls pressing her daughter. "You understand that this makes no sense, right?" © 2014 NPR
Link ID: 20223 - 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
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.
By Jane E. Brody In the 1997 film “As Good As It Gets,” Jack Nicholson portrays Melvin Udall, a middle-aged man with obsessive-compulsive disorder who avoids stepping on cracks, locks doors and flips light switches exactly five times, and washes his hands repeatedly, each time tossing out the new bar of soap he used. He brings wrapped plastic utensils to the diner where he eats breakfast at the same table every day. Though the film is billed as a romantic comedy, Melvin’s disorder is nothing to laugh about. O.C.D. is often socially, emotionally and vocationally crippling. It can even be fatal. Four years ago, John C. Kelly, 24, killed himself in Irvington, N.Y., after a long battle with a severe form of obsessive-compulsive disorder. Mr. Kelly was a devoted baseball player, and now friends hold an annual softball tournament to raise money for the foundation established in his honor to increase awareness of the disorder. Obsessive thoughts and compulsive behaviors occur in almost every life from time to time. I have a fair share of compulsive patterns: seasonings arranged in strict alphabetical order; kitchen equipment always put back the same way in the same place; two large freezers packed with foods just in case I need them. I hold onto a huge collection of plastic containers, neatly stacked with their covers, and my closets bulge with clothes and shoes I haven’t worn in years, and probably never will again — yet cannot bring myself to give away. But these common habits fall far short of the distressing obsessions and compulsions that are the hallmarks of O.C.D.: intrusive, disturbing thoughts or fears that cannot be ignored and compel the sufferer to engage in ritualistic, irrational behaviors to relieve the resulting anxiety.
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 20208 - Posted: 10.16.2014
Patients with schizophrenia are already known to have higher rates of premature death than the general population. The study found that elevated risks of heart disease and metabolic issues such as high blood sugar in people with first episode psychosis are due to an interaction of mental illness, unhealthy lifestyle behaviors and antipsychotic medications that may accelerate these risks. Patients entered treatment with significant health concerns – including excess weight, smoking, and metabolic issues – despite an average age of only 24 years. The study identifies key opportunities for health care systems to improve the treatment of such patients with first episode psychosis. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Christoph Correll, M.D., of The Zucker Hillside Hospital, Hofstra North Shore-Long Island Jewish School of Medicine, New York, and colleagues, report their findings on Oct. 8, 2014 in JAMA Psychiatry. The study is among the first of several to report results from the Recovery After an Initial Schizophrenia Episode (RAISE) project, which was developed by NIMH to examine first episode psychosis before and after specialized treatment was offered in community settings. The researchers studied nearly 400 individuals between the ages of 15 and 40 with first episode psychosis, who presented for treatment at 34 community-based clinics across 21 states. The frequency of obesity was similar to the same age group in the general population. However, smoking and metabolic syndrome (a combination of conditions including obesity, high blood pressure, high blood sugar, and abnormal blood fats, such as cholesterol and triglycerides) were much more common.
Link ID: 20182 - Posted: 10.09.2014
By Julie Rehmeyer Eight years ago, collapsed on a neurologist’s examining table, I asked a naive question that turned out to be at the center of a long-running controversy: “So what is chronic fatigue syndrome?” I had just been diagnosed with the illness, which for six years had been gradually overtaking me. A week earlier, I had woken up barely able to walk. Fatigue hardly described what I felt. Paralysis was more like it. My legs seemed to have been amputated and replaced with tubes of liquid concrete, and just shifting them on the table made me grunt like an Olympic weightlifter. My bones hurt; my brain felt like a swollen mass. Speaking required tracking down and spearing each word individually as it scampered away from me. I felt as capable of writing an article about science — my job — as of killing a rhino with my teeth. “We don’t understand it very well,” my neurologist said, his face blank. He could recommend no tests, no treatments, no other doctors. I came to understand that, for him, the term chronic fatigue syndrome meant “I can’t help you.” My neurologist’s understanding of the illness mirrored that of many doctors, who believe two things about CFS: that it’s probably psychosomatic and that there’s nothing doctors can do for it. One survey found that nearly half of doctors thought that CFS was or might be psychosomatic, and 58 percent said there wasn’t enough information available to help them diagnose it. An examination of medical textbooks found that CFS was underrepresented, even compared with less-prevalent illnesses.
|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
|By Tori Rodriguez The safety of football continues to be a heated topic for players and parents, with mixed evidence regarding the effect of head injuries on mental illness. Past studies on the connection have often been methodologically flawed or yielded ambiguous results. Now a paper in April in the American Journal of Psychiatry, the largest study yet to investigate the link, finds that even a single head injury indeed increases the risk of later mental illness, especially if the injury occurs during adolescence. Using Danish medical registries, researchers led by physician Sonja Orlovska of the University of Copenhagen studied 113,906 people who had been hospitalized for head injuries over a 23-year period. They discovered that in addition to cognitive symptoms caused by structural damage to the brain (such as delirium), these people were subsequently more likely than the general population to develop several psychiatric illnesses. Risk increased by 65 percent for schizophrenia and 59 percent for depression. Risk was highest in the first year postinjury but remained significantly elevated throughout the next 15 years. After the team controlled for several potential confounders, such as accident proneness and a family history of psychiatric problems, they found the strongest injury-related predictor for later onset of schizophrenia, depression and bipolar disorder was a head trauma experienced between the ages of 11 and 15. “Previous studies have shown that head injury induces inflammation in the brain, which causes several changes—for example, an increased permeability of the blood-brain barrier,” Orlovska says. Normally the barrier protects the brain from potentially harmful contents in the bloodstream, but injury-induced inflammation may allow these substances access to the brain. “For some individuals, this might initiate damaging processes in the brain,” she says. © 2014 Scientific American,
Have you ever wrongly suspected that other people are out to harm you? Have you been convinced that you’re far more talented and special than you really are? Do you sometimes hear things that aren’t actually there? These experiences – paranoia, grandiosity and hallucinations in the technical jargon – are more common among the general population than is usually assumed. But are people who are susceptible simply “made that way”? Are they genetically predisposed, in other words, or have their life experiences made them more vulnerable to these things? It’s an old debate: which is more important, nature or nurture? Scientists nowadays tend to agree that human psychology is a product of a complex interaction between genes and experience – which is all very well, but where does the balance lie? Scientists (including one of the authors of this blog) recently conducted the first ever study among the general population of the relative contributions of genes and environment to the experience of paranoia, grandiosity and hallucinations. How did we go about the research? First, it is important to be clear about the kinds of experience we measured. By paranoia, we mean the unfounded or excessive fear that other people are out to harm us. Grandiosity denotes an unrealistic conviction of one’s abilities and talents. Hallucinations are sensory experiences (hearing voices, for instance) that aren’t caused by external events. Led by Dr Angelica Ronald at Birkbeck, University of London, the team analysed data on almost 5,000 pairs of 16-year-old twins. This is the classical twin design, a standard method for gauging the relative influence of genes and environment. Looking simply at family traits isn’t sufficient: although family members share many genes, they also tend to share many of the same experiences. This is why studies involving twins are so useful. © 2014 Guardian News and Media Limited
Link ID: 20147 - Posted: 10.02.2014
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
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.
Link ID: 20125 - Posted: 09.27.2014
By Dick Miller, CBC News Dan Campbell felt the bullets whiz past his head. The tracer rounds zipped between his legs. It was his first firefight as a Canadian soldier in Afghanistan. "I was completely frightened and scared like I’d never been before in my life,” he says. As the attack continued, the sights, sounds and smells started to form memories inside his brain. The fear he felt released the hormone norepinephrine, and in the complex chemistry of the brain, the memories of the battle became associated with the fear. 'I think one day, hopefully in the not-too-distant future, we will be able to delete a memory.'- Dr. Sheena Josselyn, senior scientist, Hospital For Sick Children Research Institute Six years later, a sight or sound such as a firecracker or car backfiring can remind him of that night in 2008. The fear comes back and he relives rather than remembers the moments. "It can be hard. Physically, you know, there’s the tapping foot, my heart beating,” he says. Like so many soldiers and victims of assault or people who have experienced horrific accidents, Campbell was diagnosed with post traumatic stress disorder. Now a newspaper reporter in Yellowknife, Campbell thinks one day he may get therapy. But for now he is working on his own to control the fear and anger the memories bring. © CBC 2014
|By Simon Makin The Claim Casual cannabis use harms young people's brains. The Facts A study found differences in the brains of users and nonusers, but it did not establish that marijuana use caused the variations or that they had any functional significance. The Details Researchers at Northwestern University and Harvard Medical School conducted MRI scans of two groups of 20 young adults ages 18 to 25. One group reported using marijuana at least once a week, smoking 11 joints a week on average, whereas the other had used it less than five times total and not at all during the last year. Neither group had any psychiatric disorders, and the users were psychiatrically assessed as not dependent on the drug. The study focused on two brain regions involved in processing rewards, the nucleus accumbens and the amygdala. These areas create pleasurable experiences of things such as food and sex, as well as the high associated with drugs, and have been shown to change in animals given THC, the main psychoactive component of cannabis. The researchers found that cannabis users had more gray matter density in the left nucleus accumbens and left amygdala, as well as differences in the shape of the left nucleus accumbens and right amygdala. The left nucleus accumbens also tended to be slightly larger in users. They concluded that recreational cannabis use might be associated with abnormalities in the brain's reward system. News reports have proclaimed that scientists have shown that even casual cannabis use harms young people's brains. The Caveats The most obvious problem with leaping to that conclusion is that the scans were conducted at only one point. © 2014 Scientific American
|By Corinne Iozzio Albert “Skip” Rizzo of the University of Southern California began studying virtual reality (VR) as psychological treatment in 1993. Since then, dozens of studies, his included, have shown the immersion technique to be effective for everything from post-traumatic stress disorder (PTSD) and anxiety to phobias and addiction. But a lack of practical hardware has kept VR out of reach for clinicians. The requirements for a VR headset seem simple—a high-resolution, fast-reacting screen, a field of vision that is wide enough to convince patients they are in another world and a reasonable price tag— yet such a product has proved elusive. Says Rizzo, “It’s been 20 frustrating years.” In 2013 VR stepped into the consumer spotlight in the form of a prototype head- mounted display called the Oculus Rift. Inventor Palmer Luckey’s goal was to create a platform for immersive video games, but developers from many fields—medicine, aviation, tourism—are running wild with possibilities. The Rift’s reach is so broad that Oculus, now owned by Facebook, hosted a conference for developers in September. The Rift, slated for public release in 2015, is built largely from off- the-shelf parts, such as the screens used in smartphones. A multi- axis motion sensor lets the headset refresh imagery in real time as the wearer’s head moves. The kicker is the price: $350. (Laboratory systems start at $20,000.) Rizzo has been among the first in line. His work focuses on combat PTSD. In a 2010 study, he placed patients into controlled traumatic scenarios, including a simulated battlefield, so they could confront and process emotions triggered in those situations. © 2014 Scientific American
|By Victoria Stern Many studies show that teens who use marijuana face a greater risk of later developing schizophrenia or symptoms of it, especially if they have a genetic predisposition. For instance, one 15-year study followed more than 45,000 Swedes who initially had no psychotic symptoms. The researchers determined that subjects who smoked marijuana by age 18 were 2.4 times more likely to be diagnosed with schizophrenia than their nonsmoking peers, and this risk increased with the frequency of cannabis use. The connection still held when researchers accounted for participants' use of other drugs. Yet despite these results and an uptick in marijuana use in the 1970s and 1980s, other researchers have not uncovered an increase in the incidence of schizophrenia in the general Swedish population—suggesting that perhaps people who were going to develop schizophrenia anyway were more likely to use marijuana. Another study, conducted in Australia over a 30-year period, also found no increase in schizophrenia diagnoses among the general population, despite rising rates of teen marijuana use. These authors concluded that although cannabis most likely does not cause schizophrenia, its use might trigger psychosis in vulnerable people or exacerbate an existing condition. © 2014 Scientific American
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
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
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
Link ID: 20077 - Posted: 09.15.2014
by Bethany Brookshire Post-traumatic stress disorder, or PTSD, has many different symptoms. Patients may suffer from anxiety, flashbacks, memory problems and a host of other reactions to a traumatic event. But one symptom is especially common: 70 percent of civilian patients and 90 percent of combat veterans with PTSD just can’t get a decent night’s sleep. Problems with sleep, including rapid-eye movement — or REM — sleep, have long been associated with PTSD. “We know that sleep difficulties in the weeks following trauma predict the development of PTSD, and we know that bad sleep makes PTSD symptoms worse,” says Sean Drummond, a clinical psychologist who studies sleep at the University of California at San Diego. Studies in rats show that exposing the animals to traumatic, fearful experiences such as foot shocks disrupts their REM sleep. Drummond and his research assistant Anisa Marshall wanted to connect those findings to humans. But he soon found out that in humans, it’s not fear that predicts REM sleep. Instead, it’s safety. The scientists tested this in 42 people without PTSD using a measure called fear-potentiated startle. Subjects sit in a comfortable chair with an electrode on their wrists. A screen shows blue squares or yellow squares. If participants see blue squares, they run a high risk of receiving an annoying shock to the wrist. If they see yellow squares, they can relax; no shocks are headed their way. During this time, they will also hear random, loud bursts of white noise. The scientists measure how much the subjects startle in response to the noise by measuring the strength of their eyeblinks in response to the noise. In the presence of the blue squares, the blinks become much stronger, an effect called fear-potentiated startle. With yellow squares, the blinks weaken. © Society for Science & the Public 2000 - 2014.