Links for Keyword: Depression

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By Moises Velasquez-Manoff In May of 2017, Louise decided that her life was just too difficult, so she’d end it. In the previous four years, three siblings and a half-sibling had died, two from disease, one from fire and one from choking. Close friends had moved away. She felt painfully, unbearably alone. It would be the fourth time Louise (I’m using her middle name to protect her privacy), then 68, would attempt suicide, and she was determined to get it right. She wrote a letter with instructions on where to find important documents and who should inherit what. She packed up her jewelry and artwork, addressing each box to particular friends and family members. Then she checked into a motel — homes where people have committed suicide lose value and she didn’t want hers to sell below market — put a plastic sheet on the bed, lay down and swallowed what she figured was an overdose of prescription pills with champagne. A few days later, she woke up in a psychiatric ward in Albuquerque. The motel maid had found her. “I was very upset I had failed,” she told me recently. So she tried to cut her wrists with a bracelet she was wearing — unsuccessfully. The suicide rate has been rising in the United States since the beginning of the century, and is now the 10th leading cause of death, according to the Centers for Disease Control and Prevention. It’s often called a public health crisis. And yet no new classes of drugs have been developed to treat depression (and by extension suicidality) in about 30 years, since the advent of selective serotonin reuptake inhibitors like Prozac. The trend most likely has social causes — lack of access to mental health care, economic stress, loneliness and despair, the opioid epidemic, and the unique difficulties facing small-town America. These are serious problems that need long-term solutions. But in the meantime, the field of psychiatry desperately needs new treatment options for patients who show up with a stomach full of pills. Now, scientists think that they may have found one — an old anesthetic called ketamine that, at low doses, can halt suicidal thoughts almost immediately. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25746 - Posted: 12.03.2018

Ashley P. Taylor Electrically stimulating the lateral orbitofrontal cortex, a brain area behind the eyes, improves the moods of people with depression, according to a study published yesterday (November 29) in Current Biology. The technique used by the researchers, led by Edward Chang of the University of California, San Francisco, is called deep brain stimulation (DBS), in which surgically implanted electrodes send electrical pulses to particular areas of the brain. The approach is already in use as a treatment for movement disorders such as Parkinson’s disease and tremors. But results on its ability to treat depression have been mixed, as NPR reports. The researchers worked with 25 epilepsy patients who already had electrodes implanted into their brains as part of their treatments. Many of the study participants also had signs of depression as evaluated by mood tests the researchers administered, Science News reports. The investigators tried stimulating many areas of the brain, and they found that jolts to the lateral orbitofrontal cortex made patients with signs of depression—but not others who didn’t have symptoms—feel better right away. “Wow, I feel a lot better. . . . What did you guys do?” study coauthor Kristin Sellers recalls a patient exclaiming after receiving the stimulation, she tells NPR. “Only the people who had symptoms [of depression] to start with improved their mood, which suggests that perhaps the effect of what we’re doing is to normalize activity that starts off abnormal,” adds another coauthor, Vikram Rao.

Related chapters from BN8e: Chapter 18: Attention and Higher Cognition; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 14: Attention and Consciousness; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 25742 - Posted: 12.03.2018

Jon Hamilton There's new evidence that mild pulses of electricity can relieve depression — if they reach the right target in the brain. A study of 25 people with epilepsy found that those who had symptoms of depression felt better almost immediately when doctors electrically stimulated an area of the brain just above the eyes, a team reported Thursday in the journal Current Biology. These people were in the hospital awaiting surgery and had wires inserted into their brains to help doctors locate the source of their seizures. Several of the patients talked about the change they felt when the stimulation of the lateral orbitofrontal cortex began, says Kristin Sellers, an author of the paper and a postdoctoral researcher at the University of California, San Francisco. One person's response was: "Wow, I feel a lot better. ... What did you guys do?" The stimulation only lasted a few minutes. After it stopped, the effect on mood quickly faded. To be sure that the effect was real, the researchers also pretended to stimulate the lateral OFC in the same patients without actually running current through the tiny wires implanted in their brains. In those sham treatments, there was no discernible change. DBS is an approved treatment for tremors, including those associated with Parkinson's disease. But results with depression have been less consistent, and DBS isn't approved for this purpose by the Food and Drug Administration. © 2018 npr

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 25735 - Posted: 11.30.2018

By Roni Caryn Rabin A. A deficiency of vitamin B12 can cause neurological and psychiatric problems that “can progress if left untreated, and can lead to irreversible damage,” said Dr. Donald Hensrud, director of the Mayo Clinic’s Healthy Living Program. Fortunately, it can be reversed fairly easily with vitamin pills or injections. Vitamin B12 is required for proper red blood cell formation, nerve function and DNA synthesis. It is naturally present in fish, meat, eggs and dairy products, as well as some fortified breakfast cereals and nutritional yeast products. Strict vegans who avoid animal products can develop a deficiency of B12 over time if they don’t take a supplement. But two-thirds of cases occur in the elderly, who are susceptible because they may not absorb adequate amounts of B12 from foods but who are not routinely tested, Dr. Hensrud said. Consequences of B12 deficiency can cause a range of symptoms that include fatigue, weakness, constipation, loss of appetite and weight loss. Other symptoms include difficulty maintaining balance, depression, confusion, dementia, poor memory and soreness in the mouth or tongue. B12 deficiency may also result in a form of anemia called megaloblastic anemia, which can also result from a deficiency of folic acid, another B vitamin. If anemia is detected on blood tests, levels of both vitamins should be checked. Neurological symptoms can, however, occur in the absence of anemia. Early treatment is critical to avoid potentially irreversible damage. Older adults are susceptible to B12 deficiency because they may have decreased secretion of hydrochloric acid in the stomach, which makes it difficult to absorb B12. Also vulnerable to B12 deficiency are those with gastrointestinal disorders like celiac disease or Crohn’s disease; those who have had weight loss or other gastrointestinal surgery; and those who use certain acid reflux drugs or the diabetes drug metformin. Individuals with pernicious anemia, which affects up to 2 percent of older adults, are also susceptible. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25732 - Posted: 11.30.2018

At 35, Sharon Jakab knew something was wrong when she started hallucinating. "I saw my grandmother on the wall in the room. She was talking to me. I wasn't sleeping, and I was a mess," she says from her home in Burlington, Ont. Jakab had been suffering from postpartum depression following the birth of her daughter. About a year and a half later, Jakab had another episode of postpartum depression following an ectopic pregnancy. It became so bad, she was suicidal. "There was a gun in the house and there were cartridges. I was all set to kill myself." She had to suicide-proof her home by taking away all dangerous objects, even skates, which have sharp blades. Now 61, Jakab has been in and out of hospitals, dealing with what she calls "waves of depression" that have lasted most of her adult life. She's tried about a dozen medications, including the antipsychotic drug clozapine. "Clozapine really helped me a lot, but I still suffered from depression, psychosis and mania." Because standard treatment like medication and therapy weren't effective, Jakab was diagnosed with treatment-resistant depression, a severe form of depression that close to a million Canadians experience. Electroconvulsive therapy or ECT, better known as shock treatment, is still considered the go-to treatment but comes with the common side effect of memory loss. So doctors are now exploring less invasive experimental approaches like brain stimulation that rewires the brain's circuits. ©2018 CBC/Radio-Canada

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 25718 - Posted: 11.26.2018

A countrywide shortage of a common antidepressant medication has caused alarm among doctors, pharmacists and patients with mental illnesses. Nearly a dozen pharmacies in Saskatoon and Regina have told CBC News that they have run out of bupropion— both the brand-name product Wellbutrin and its generic counterparts — and can't get more from their suppliers. More than 12,000 patients in Saskatchewan take bupropion, according to the Ministry of Health. National figures are not readily available. The prescription antidepressant is used to treat major depressive disorder and seasonal affective disorder. "This might have been the drug that gave you the energy to live your life, do the things you needed to do, get on with your job, do your studies," said Dr. Sara Dungavell, a Saskatoon psychiatrist. She said she fielded anxious phone calls from patients about the shortage. Two pharmaceutical companies that produce generic bupropion are reporting a shortage or anticipated shortage on the Health Canada website. The company that manufactures Wellbutrin, Bausch Health, reported its shortage to Health Canada six weeks ago. On Thursday, it told CBC News it had resolved its shortage, and Canadian pharmacies would receive the drug "imminently," depending on delivery schedules. By Saturday afternoon, pharmacies in Calgary, Saskatoon, Regina and Winnipeg said they had yet to receive a shipment, and their pharmacists said it was still listed as unavailable in their system. ©2018 CBC/Radio-Canada

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25702 - Posted: 11.20.2018

By Benedict Carey A generation ago, depression was viewed as an unwanted guest: a gloomy presence that might appear in the wake of a loss or a grave disappointment and was slow to find the door. The people it haunted could acknowledge the poor company — I’ve been a little depressed since my father died — without worrying that they had become chronically ill. Today, the condition has been recast in the medical literature as a darker, more permanent figure, a monster in the basement poised to overtake the psyche. For decades, researchers have debated the various types of depression, from mild to severe to “endogenous,” a rare, near-paralyzing despair. Hundreds of studies have been conducted, looking for markers that might predict the course of depression and identify the best paths to recovery. But treatment largely remains a process of trial and error. A drug that helps one person can make another worse. The same goes for talk therapies: some patients do very well, others don’t respond at all. “If you got a depression diagnosis, one of the most basic things you want to know is, what are the chances of my life returning to normal or becoming optimal afterward?” said Jonathan Rottenberg, a professor of psychology at the University of South Florida. “You’d assume we’d have an answer to that question. I think it’s embarrassing that we don’t.” In a paper in the current issue of Perspectives on Psychological Science, Dr. Rottenberg and his colleagues argue that, in effect, the field has been looking for answers in the wrong place. In trying to understand how people with depression might escape their condition, scientists have focused almost entirely on the afflicted, overlooking a potentially informative group: people who once suffered from some form of depression but have more or less recovered. Indeed, while this cohort almost certainly exists — every psychiatrist and psychologist knows someone in it — it is so neglected that virtually nothing is known about its demographics, how well its members are faring and, fundamentally, how many individuals it contains. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25603 - Posted: 10.23.2018

Sasa Woodruff Ryan "China" McCarney has played sports his entire life, but sometimes he has to force himself to show up on the field to play pick-up soccer with his friends. "I'm dreading and I'm anticipating the worst. But I do it anyway. And then, it's a euphoric sensation when you're done with it because you end up having a great time," says McCarney. McCarney was just 22 when he had his first panic attack. As a college and professional baseball player, he says getting help was stigmatized. It took him six years to get professional support. He still struggles with depression and social anxiety, but says exercising helps him — especially when it's with his teammates. Research shows exercise can ease things like panic attacks or mood and sleep disorders, and a recent study in the journal, Lancet Psychiatry, found that popular team sports may have a slight edge over the other forms of physical activity. The researchers analyzed CDC survey data from 1.2 million adults and found — across age, gender, education status and income — people who exercised reported fewer days of bad mental health than those who didn't. And those who played team sports reported the fewest. One of the study's authors, Adam Chekroud, an assistant adjunct professor at Yale's School of Medicine, thinks team activity could add another layer of relief for sufferers of mental illness. He says there are biological, cognitive and social aspects to mental illness. "Some sports might just be hitting on more of those elements than other sports," he says. "If you just run on a treadmill for example, it's clear that you're getting that biological stimulation. But perhaps there are other elements of depression that you're not going to be tapping into." © 2018 npr

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25597 - Posted: 10.22.2018

By Erin Blakemore Are you depressed? If you’re not sure, it’s no surprise. Perpetual sadness isn’t the only symptom. Anger, back pain, sleep disturbances and even indecisiveness could all be signs of depression. One in six adults will experience depression in their life, but you can’t get help if you’re not sure you need it. Your doctor can screen for depression, so it’s worth asking on your next visit. Isolation and social withdrawal are common among people with depression. But it’s still possible to seek help during these periods. If you can’t face the thought of visiting your doctor, you can find information and assistance on your computer or smartphone. Screening for Mental Health’s online screening program gives a brief survey. It then tells you whether your answers are consistent with depression and provides materials to bring to your next doctor’s visit and a list of resources. Although it’s not a formal diagnosis, it’s a place to start to seek help. Crisis Text Line can connect you with a trained crisis counselor who can take you from crisis to cool down, all via text. The service is free and confidential. It’s available to people experiencing any kind of crisis. Text HOME to 741741 to get started. The National Alliance on Mental Illness can also connect you to mental-health resources, including help for depression. Visit nami.org/Find-Support or call the NAMI Helpline, 800-950-NAMI, between 10 a.m. and 6 p.m. Eastern. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25537 - Posted: 10.08.2018

By Benedict Carey Dr. Bernard J. Carroll, whose studies of severe depression gave psychiatry the closest thing it has to a “blood test” for a mental disorder, and who later became one of the field’s most relentless critics, helping to expose pervasive corruption in academic research, died on Sept. 10 at his home in Carmel, Calif. He was 77. His wife, Sylvia Carroll, said the cause was lung cancer. Dr. Carroll was all of 28 when he published a paper that seemed to herald a new age of psychiatry, one rooted in biology rather than Freudian theory. Trained both in endocrinology and psychiatry, he applied a test from that first specialty — the dexamethasone suppression test, or DST — to people with mood problems. The test measures the body’s ability to suppress its own surges of cortisol, a stress hormone. In a 1968 article in The British Medical Journal, Dr. Carroll announced that when the test was administered to people with the severest species of depression — a paralyzing gloom then called melancholia, or endogenous depression — their bodies were shown to have trouble suppressing the hormone. People with other kinds of mood disorders had normal scores. The test did not mean that failure to suppress cortisol caused depression, just that it was associated with it. “I thought of it as a confirmatory test, to support a diagnosis, not to make one,” Dr. Carroll, known as Barney, said, in a recent interview in his home, “and possibly as a way to monitor progress in treatment.” It didn’t happen. In 1980, experts revising psychiatry’s influential diagnostic manual eliminated distinctions in kinds of depression. Melancholia was lumped with many other mild and moderate conditions under the classification “major depressive disorder.” Soon after, modern antidepressants hit the market, and pharmaceutical companies paid top academics around the world to help interpret studies, massage data and promote their products. The field chased the drugs, and the money, and learned nothing about the biology of mental disorders. © 2018 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25531 - Posted: 10.05.2018

By Laura M. Holson Researchers from Johns Hopkins University have recommended that psilocybin, the active compound in hallucinogenic mushrooms, be reclassified for medical use, potentially paving the way for the psychedelic drug to one day treat depression and anxiety and help people stop smoking. The suggestion to reclassify psilocybin from a Schedule I drug, with no known medical benefit, to a Schedule IV drug, which is akin to prescription sleeping pills, was part of a review to assess the safety and abuse of medically administered psilocybin. Before the Food and Drug Administration can be petitioned to reclassify the drug, though, it has to clear extensive study and trials, which can take more than five years, the researchers wrote. The analysis was published in the October print issue of Neuropharmacology, a medical journal focused on neuroscience. The study comes as many Americans shift their attitudes toward the use of some illegal drugs. The widespread legalization of marijuana has helped demystify drug use, with many people now recognizing the medicinal benefits for those with anxiety, arthritis and other physical ailments. Psychedelics, like LSD and psilocybin, are illegal and not approved for medical or recreational use. But in recent years scientists and consumers have begun rethinking their use to combat depression and anxiety. “We are seeing a demographic shift, particularly among women,” said Matthew Johnson, an associate professor of psychiatry and behavioral sciences at Johns Hopkins and one of the study’s authors. Among the research he has conducted, he said, “we’ve had more females in our studies.” © 2018 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25530 - Posted: 10.04.2018

By Michael Shermer Anthony Bourdain (age 61). Kate Spade (55). Robin Williams (63). Aaron Swartz (26). Junior Seau (43). Alexander McQueen (40). Hunter S. Thompson (67). Kurt Cobain (27). Sylvia Plath (30). Ernest Hemingway (61). Alan Turing (41). Virginia Woolf (59). Vincent van Gogh (37). By the time you finish reading this list of notable people who died by suicide, somewhere in the world another person will have done the same, about one every 40 seconds (around 800,000 a year), making suicide the 10th leading cause of death in the U.S. Why? According to the prominent psychologist Jesse Bering of the University of Otago in New Zealand, in his authoritative book Suicidal: Why We Kill Ourselves (University of Chicago Press, 2018), “the specific issues leading any given person to become suicidal are as different, of course, as their DNA—involving chains of events that one expert calls ‘dizzying in their variety.’” Indeed, my short list above includes people with a diversity of ages, professions, personality and gender. Depression is commonly fingered in many suicide cases, yet most people suffering from depression do not kill themselves (only about 5 percent Bering says), and not all suicide victims were depressed. “Around 43 percent of the variability in suicidal behavior among the general population can be explained by genetics,” Bering reports, “while the remaining 57 percent is attributable to environmental factors.” Having a genetic predisposition for suicidality, coupled with a particular sequence of environmental assaults on one's will to live, leads some people to try to make the pain stop. In Bering's case, it first came as a closeted gay teenager “in an intolerant small Midwestern town” and later with unemployment at a status apex in his academic career (success can lead to unreasonably high standards for happiness, later crushed by the vicissitudes of life). Yet most oppressed gays and fallen academics don't want to kill themselves. “In the vast majority of cases, people kill themselves because of other people,” Bering adduces. “Social problems—especially a hypervigilant concern with what others think or will think of us if only they knew what we perceive to be some unpalatable truth—stoke a deadly fire.” © 2018 Scientific American

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25529 - Posted: 10.04.2018

Sarah Boseley Health editor Half of all those taking antidepressants experience withdrawal problems when they try to give them up and for millions of people in England, these are severe, according to a new review of the evidence commissioned by MPs. Guidance from the National Institute of Health and Care Excellence (Nice), which says withdrawal symptoms “are usually mild and self-limiting over about one week” urgently needs to be changed, say the review authors. Dr James Davies from the University of Roehampton and Prof John Read from the University of East London say the high rate of withdrawal symptoms may be part of the reason people are staying on the pills for longer. They cannot cope, so carry on taking the drugs, or their doctors assume they have relapsed and write another prescription. The review was commissioned by the all-party parliamentary group for prescribed drug dependence and follows a long debate about the Nice guidance, which critics say is out of date. Modern antidepressants of the SSRI class, such as Prozac (fluoxetine) and Seroxat (paroxetine), were marketed in part on their safety. People were unable to harm themselves by overdosing as they could on benzodiazepines like valium and stopping the drugs was said to be easier. There have been plenty of anecdotal accounts of withdrawal symptoms, which include dizziness, vertigo, nausea, insomnia, headaches, tiredness and difficulties concentrating. But the Nice guidance said in 2004 that the withdrawal symptoms were slight and short-lived and was re-adopted without further evidence in 2009. It is similar to the US guidance, which says symptoms usually resolve within one to two weeks. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25524 - Posted: 10.03.2018

By Megan Thielking, Walk into Kalypso Wellness Centers in San Antonio, Texas, and you might be treated with one of five “proprietary blends” of ketamine. They’re not cheap—$495 per infusion—and not covered by insurance, but the company offers a “monthly” membership program to cut costs and advertises discounts for members of the military and first responders. Kalypso promotes ketamine, long used as an anesthetic during surgery and more recently as a club drug, as a treatment for more than two dozen conditions, including depression, chronic pain, and migraines. “Congratulations on resetting your life!!!” it cheerily tells patients on a form they’re handed after an infusion. Starting with just one office 19 months ago, Kalypso has expanded rapidly to meet surging patient demand for ketamine and now oversees two other Texas clinics and offices in North Carolina and New York. It recruits customers through online ads and radio spots, and even by visiting support groups for pain patients, people with depression, first responders, and grieving parents who have lost children. Advertisement “You name it, we’ve done it,” said clinic co-founder and anesthesiologist Dr. Bryan Clifton. An investigation by STAT shows that Kalypso’s sweeping claims are hardly uncommon in the booming ketamine treatment business. Dozens of free-standing clinics have opened across the U.S. in recent years to provide the drug to patients who are desperate for an effective therapy and hopeful ketamine can help. But the investigation found wide-ranging inconsistencies among clinics, from the screening of patients to the dose and frequency of infusions to the coordination with patients’ mental health providers. A number of clinics stray from recommendations issued last year by the American Psychiatric Association. © 2018 Scientific American

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25500 - Posted: 09.27.2018

Denis Campbell Health policy editor Eating junk food increases the risk of becoming depressed, a study has found, prompting calls for doctors to routinely give dietary advice to patients as part of their treatment for depression. In contrast, those who follow a traditional Mediterranean diet are much less likely to develop depression because the fish, fruit, nuts and vegetables that diet involves help protect against Britain’s commonest mental health problem, the research suggests. Published in the journal Molecular Psychiatry, the findings have come from an analysis by researchers from Britain, Spain and Australia who examined 41 previous studies on the links between diet and depression. “A pro-inflammatory diet can induce systemic inflammation, and this can directly increase the risk for depression,” said Dr Camille Lassale, the study’s lead author. Bad diet heightens the risk of depression to a significant extent, she added. The analysis found that foods containing a lot of fat or sugar, or was processed, lead to inflammation of not just the gut but the whole body, known as “systemic inflammation”. In that respect the impact of poor diet is like that of smoking, pollution, obesity and lack of exercise. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 25494 - Posted: 09.26.2018

By — Linda Searing More than 1 of every 3 college freshmen across the globe — 35 percent — show symptoms of one of the common mental-health disorders, according to new research published by the American Psychological Association. The research was based on World Health Organization data on 13,984 full-time freshman students from 19 colleges in eight countries — Australia, Belgium, Germany, Mexico, Northern Ireland, South Africa, Spain and the United States. The two most common disorders found were major depression (affecting 21 percent of the students) and generalized anxiety disorder (19 percent). The students were also screened for panic disorder, mania, drug abuse and alcohol abuse or dependence. Although the study, published in the Journal of Abnormal Psychology, found that symptoms started years before college — generally at about age 14 — in most cases, the life changes and stresses that may occur as students enter their college years could exacerbate symptoms. The study’s authors, and other experts, say that to help manage their mental-health condition, students should check whether their campus counseling centers, or local psychologists, offer group or individual cognitive behavioral therapy, or CBT. But the lead author said that because the number of students needing mental-health treatment “far exceeds the resources of most [campus] counseling centers,” students and colleges should consider supplementing services with “Internet-based interventions” that studies have shown to be effective, including online CBT. © 1996-2018 The Washington Post

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 25482 - Posted: 09.24.2018

By Knvul Sheikh Humans and other mammals react to stressful situations through a series of well-orchestrated evolutionary adaptations. When faced with a predator looking for its next meal, or with worry of losing a job, our bodies release a cascade of stress hormones. Our heart rate spikes, breath quickens, muscles tense up and beads of sweat appear. This so-called “fight-or-flight” response served our ancestors well, but its continual activation in our modern-day lives comes with a cost. Scientists are starting to realize stress often exacerbates several diseases, including depression, diabetes, cardiovascular disease, HIV/AIDS and asthma. One theory is hoping to explain the link between stress and such widespread havoc by laying the blame on an unexpected source—the microscopic powerhouses inside each cell. Each of our cells contains hundreds of small bean-shaped mitochondria — subcellular structures, or organelles, that provide the energy needed for normal functioning. Mitochondria have their own circular genome with 37 genes. We inherit this mitochondrial DNA only from our mothers, so the makeup of the DNA’s code stays relatively consistent from one generation to the next. But our fight-or-flight response places extreme demands on the mitochondria. All of a sudden, they need to produce much more energy to fuel a faster heartbeat, expanding lungs and tensing muscles, which leaves them vulnerable to damage. Unlike DNA in the cell’s nucleus, though, mitochondria have limited repair mechanisms. And recent animal studies have shown chronic stress not only leads to mitochondrial damage in brain regions such as the hippocampus, hypothalamus and cortex, it also results in mitochondria releasing their DNA into the cell cytoplasm, and eventually into the blood. © 2018 Scientific American,

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25448 - Posted: 09.14.2018

By Bernardo Kastrup, Edward F. Kelly A long-awaited resurgence in psychedelic research is now under way and some of its early results have been startling. Whereas most scientists expected the mind-boggling experiences of psychedelic states to correlate with increased brain activity,a landmark study from 2012 found the opposite to be the case. Writing in this magazine, neuroscientist Christof Koch expressed the community’s collective surprise. These unexpected findings have since been repeatedly confirmed with a variety of psychedelic agents and measures of brain activity (2013,2015,2016, 2017). Under the mainstream physicalist view that brain activity is, or somehow generates, the mind, the findings certainly seem counterintuitive: How can the richness of experience go up when brain activity goes down? Understandably, therefore, researchers have subsequently endeavored to find something in patterns of brain activity that reliably increases in psychedelic states. Alternatives include brain activity variability, functional coupling between different brain areas and, most recently, a property of brain activity variously labeled as “complexity,” “diversity,” “entropy” or “randomness”—terms viewed as approximately synonymous. The problem is that modern brain imaging techniques do detect clear spikes in raw brain activity when sleeping subjects dream even of dull things such as staring at a statue or clenching a hand. So why are only decreasesin brain activity conclusively seen when subjects undergo psychedelic experiences, instead of dreams? Given how difficult it is to find one biological basis for consciousness, how plausible is it that two fundamentally different mechanisms underlie conscious experience in the otherwise analogous psychedelic and dreaming states? © 2018 Scientific American

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25414 - Posted: 09.04.2018

Sarah Boseley Health editor Erica Avey, 27, microdosed on LSD for eight months, using an analogue that was legal in Germany, where she was living. “I started microdosing essentially because I was in a really depressed stage of my life. It was for mental health reasons – mood balancing, mood management. It was hard for me to leave my apartment and do normal things as a human being,” she said. Depression or sadness are very common reasons for starting; Avey was unusual only in that she could be open about it. Her workplace knew and thought it was fine. “As long as I wasn’t out of control or permanently high at work they were quite OK.” She took about 15 micrograms (a whole tab is 100 micrograms). “That was a good amount for me. Some people take as little as six,” she said. She adopted a popular protocol – one day on, three days off. It worked for her. “It definitely had the effect I wanted,” she said. “It lifted me out of a pretty deep depression. I’m still trying to wrap my head around what it has done to me in the long-term. I think it has changed me.” She had been “pretty negative”, she said, mindlessly going through social media, plagued with obsessive thoughts. “I’m able to be more mindful of my emotions. If I’m feeling sad, that’s OK. I don’t obsess anymore. I don’t dwell on it. I don’t get worked up about it.” © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25407 - Posted: 09.01.2018

Jon Hamilton A new study suggests that ketamine, an increasingly popular treatment for depression, has something in common with drugs like fentanyl and oxycodone. The small study found evidence that ketamine's effectiveness with depression, demonstrated in many small studies over the past decade, comes from its interaction with the brain's opioid system. A Stanford University team reported their findings Wednesday in The American Journal of Psychiatry. "We think ketamine is acting as an opioid," says Alan Schatzberg, one of the study's authors and a professor of psychiatry and behavioral sciences at Stanford. "That's why you're getting these rapid effects." Until now, most researchers have attributed ketamine's success to its effect on the brain's glutamate system, which is involved in learning and memory. The opioid system, in contrast, controls pain, reward, and addictive behaviors. Ketamine is an anesthetic that is frequently given to children in the emergency room. It is also a popular but illicit party drug that can cause an out-of-body experience at high doses. And in the past few years, ketamine has seen increasing use as an off-label treatment that doctors prescribe for patients with severe depression that doesn't respond to other drugs. Unlike conventional antidepressants like Prozac, which can take weeks to work, an infusion or nasal administration of ketamine typically produces results in hours. © 2018 npr

Related chapters from BN8e: 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: The Biology of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 25397 - Posted: 08.29.2018