Links for Keyword: Depression

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By Jack Turban Fourteen-year-old Nicole, whose name I changed for her privacy, told her mother every day for years that she wanted to end her own life. Between suicide attempts were more psychiatric hospital visits than she or her mother could count. She refused to get out of bed, shower, or go to school, missing sixty school days in a single year. In one visit with her therapist, she admitted to praying every night that she would not wake up the next morning. After countless psychiatrists and psychotherapists were unable to improve her depression, her mother converted a bathroom cabinet into a locked safe, containing all of the sharp objects and pills in the house. Her parents were certain it was only a matter of time until Nicole killed herself. Today, a now seventeen-year-old Nicole greets me with a big smile. Her blonde hair is pulled back into a ponytail to reveal her bright blue eyes. She tells me she hasn’t missed a day of school and is preparing for college. Blushing, she lets me know that her first date is coming up, a prom date to be precise. For the first time in years, she is happy and wants to live. What happened to cause this dramatic change? In December, Nicole started infusions of a psychedelic drug called ketamine. Though she had failed to respond to endless medication trials for her depression (selective serotonin reuptake inhibitors, mirtazapine, topiramate, antipsychotics, and lithium to name just a few), ketamine cleared her depression within hours. The effect lasts about two weeks before she needs a new infusion. © 2017 Scientific America

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23850 - Posted: 07.19.2017

Dean Burnett Antidepressants; the go-to treatment for depression, or generalised anxiety. It’s incredible when you think about it, the fact that you can have a debilitating mood disorder, take a few pills, and feel better. It’s unbelievable that medical science has progressed so far that we now fully understand how the human brain produces moods and other emotions, so can manipulate them with designer drugs. That’s right, it is unbelievable. Because it isn’t the case. The fact that antidepressants are now so common is something of a mixed blessing. On one hand, anything that helps reduce stigma and lets those afflicted know they aren’t alone can only be helpful. Depression is incredibly common, so this awareness can literally save many lives. On the other hand, familiarity does not automatically mean understanding. Nearly everyone has a smartphone these days, but how many people, if pushed, could construct a touchscreen? Not many, I’d wager. And so it is with depression and antidepressants. For all the coverage and opinion pieces produced about them, the details around how they work remain somewhat murky and elusive. Actually, in the case of antidepressants, it’s more a question of why they work, rather than how. Most antidepressants, from the earliest Trycyclics and Monamine Oxidase inhibitors, to the ubiquitous modern day selective serotonin reuptake inhibitors (SSRIs), work by increasing the levels of specific neurotransmitters in the brain, usually by preventing them from being broken down and reabsorbed into the neurons, meaning they linger in the synapses longer, causing more activity, so “compensating” for the reduced overall levels. Antidepressants make the remaining neurotransmitters work twice as hard, so overall activity is more “normal”, so to speak. © 2017 Guardian News and Media Limited

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23822 - Posted: 07.11.2017

Deborah Orr Most people know about SSRIs, the antidepressant drugs that stop the brain from re-absorbing too much of the serotonin we produce, to regulate mood, anxiety and happiness. And a lot of people know about these drugs first hand, for the simple reason that they have used them. Last year, according to NHS Digital, no fewer than 64.7m antidepressant prescriptions were given in England alone. In a decade, the number of prescriptions has doubled. On Tuesday I joined the throng, and popped my first Citalopram. It was quite a thing – not least because, like an idiot, I dropped my pill about 90 minutes before curtain up for the Royal Shakespeare Company’s production of The Tempest at the Barbican. That’s right. This isn’t just mental illness: this is metropolitan-elite mental illness. It was a pretty overwhelming theatrical experience. The first indication that something was up came as I approached my local tube station. I noticed that I was in a state of extreme dissociation, walking along looking as though I was entirely present in the world yet feeling completely detached from it. I had drifted into total mental autopilot. Luckily, I was able to recognise my fugue. It’s a symptom of my condition, which, as I’ve written before, is complex post-traumatic stress disorder. The drug-induced dissociation was more intense than I’m used to when it’s happening naturally. I use the word advisedly. Much of what is thought of as illness is actually an extreme and sensible protective reaction to unbearable interventions from outside the self. © 2017 Guardian News and Media Limited

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 14: Attention and Consciousness
Link ID: 23818 - Posted: 07.09.2017

By Clare Wilson A patient-led movement is helping people taking psychiatric medicines to hack their dosing regimens so they can wean themselves off the drugs without any side effects. Now a Dutch website that sells kits to help people do this is about to launch an English-language site, triggering safety concerns among UK regulators and doctors. Some people find it impossible to stop taking certain antidepressants and anti-anxiety medicines such as valium because, unless the dose is reduced very gradually, they get severe mental and physical side-effects. The problem is these medicines aren’t sold in small enough tablets to allow for tapering. This has prompted some people to flout mainstream medical advice and use DIY methods for reducing their doses, such as grinding up tablets and dissolving them in water, or breaking open capsules of tiny beads and counting them out. The UK mental health charity Mind advises people who want to stop taking antidepressants of some techniques to try, but recommends they get advice from their doctor or pharmacist first. To help people taper their dose more easily, a Dutch medical charity, called Cinderella Therapeutics, creates personalised “tapering kits”, with precisely weighed out tablets in labelled packets that gradually reduce over several months. The website recommends people do this under medical supervision and must first receive a doctor’s prescription. © Copyright New Scientist Ltd.

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23817 - Posted: 07.09.2017

Martha Mills So, it turns out I’m getting better at depression. That isn’t to say I’ve stopped suffering it, or that it is any less debilitating when it sneaks up after a two-year hiatus and pile-drives me into a blistering agony of mental carpet burns topped with a patronising tousle of the bed-hair, like a nostalgic school bully. No, what’s “better” about me is spotting it and moving quicker through the self-blame method of diagnosis. We all have down days, and that’s what you hope these are. Only they stopped being a day or two of feeling blue that can be whiled away with the distraction of a conspiratorial sofa and questionable DVD collection, and have merged into weeks since you were last able to feel anything but disappointment on waking up, and the choice between showering or just smelling like a tramp’s undercarriage has gone beyond struggle into pure resignation. Being especially practised at denial, I decided that I, a mere mortal with a solid history of depressive episodes since childhood, could fake my way out of this oncoming tsunami of debilitating black fog using the advice that people who have never experienced depression trot out – an experiment that could surely only succeed [sidelong glance to camera]. I would improve my diet and exercise, force myself to take up hobbies, I would “soldier on until it passed” and thrust myself (reluctantly) into social situations. I even tried “looking on the bright side” but it turned out to just be glare on my TV. © 2017 Guardian News and Media Limited

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23795 - Posted: 07.01.2017

By Catherine Caruso, More than half of all opioid prescriptions in the United States are written for people with anxiety, depression, and other mood disorders, according to a new study that questions how pain is treated in this vulnerable population. People with mood disorders are at increased risk of abusing opioids, and yet they received many more prescriptions than the general population, according to an analysis of data from 2011 and 2013. “We’re handing this stuff out like candy,” said Dr. Brian Sites, of Dartmouth-Hitchcock Medical Center, the senior author of the study. Opioid prescribing in the U.S. quadrupled between 1999 and 2015, and during that time over 183,000 people died from overdoses related to prescription opioids, according to the CDC. Sites said more research is needed to understand whether opioids are being overprescribed to adults with mood disorders. “If you want to come up with social policy to address the need to decrease our out-of-control opioid prescribing, this would be the population you want to study, because they’re getting the bulk of the opioids, and then they are known to be at higher risk for the bad stuff,” he said. The study, published Monday in the Journal of the American Board of Family Medicine, tapped a U.S. health survey that gathered data from providers and facilities on prescription medications, health status, and basic demographics for about 51,000 adults. It found that 19 percent of the 38.6 million Americans with mood disorders use prescription opioids, compared to 5 percent of the general population — a difference that remained even when the researchers controlled for factors such as physical health, level of pain, age, sex and race. © 2017 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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23779 - Posted: 06.27.2017

By JANE E. BRODY It’s perfectly normal for someone to feel anxious or depressed after receiving a diagnosis of a serious illness. But what if the reverse occurs and symptoms of anxiety or depression masquerade as an as-yet undiagnosed physical disorder? Or what if someone’s physical symptoms stem from a psychological problem? How long might it take before the true cause of the symptoms is uncovered and proper treatment begun? Psychiatric Times, a medical publication seen by some 50,000 psychiatrists each month, recently published a “partial listing” of 47 medical illnesses, ranging from cardiac arrhythmias to pancreatic cancer, that may first present as anxiety. Added to that was another “partial listing” of 30 categories of medications that may cause anxiety, including, ironically, popular antidepressants like selective serotonin reuptake inhibitors, or S.S.R.I.s. These lists were included in an article called “Managing Anxiety in the Medically Ill” meant to alert mental health practitioners to the possibility that some patients seeking treatment for anxiety or depression may have an underlying medical condition that must be addressed before any emotional symptoms are likely to resolve. Doctors who treat ailments like cardiac, endocrine or intestinal disorders would do well to read this article as well lest they do patients a serious disservice by not recognizing an emotional cause of physical symptoms or addressing the emotional components of a physical disease. © 2017 The New York Times Company

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: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 23773 - Posted: 06.26.2017

/ By Joshua C. Kendall Dr. Joshua A. Gordon, the new director of the National Institute of Mental Health, took office in the final year of Barack Obama’s presidency. But he has this much in common with Obama’s successor: He has little patience for incremental reforms. As Gordon defines it, the job involves both advocating for the mental health needs of Americans and developing science to guide policymakers and clinicians. A 49-year-old psychiatrist who made his reputation as a brilliant researcher of mice with mutations that mimic human mental disorders, Gordon is convinced that radical changes are needed in the treatment of illnesses like schizophrenia. In an interview in his office at the NIMH campus in Bethesda, Maryland, he lamented that while modest improvements have been made in patient care over the last few decades, we don’t know enough about the brain to “even begin to imagine what the transformative treatments of tomorrow will be like.” Few psychiatrists would disagree that change is overdue. Take depression: Current approaches, which employ drugs like Prozac or cognitive-behavioral therapy, or a combination of the two, can relieve major symptoms in only some patients. The hope is that “precision medicine” — treatments targeted to the specific biological makeup of the patient — can do for psychiatry what scientists like Gordon’s Nobel Prize-winning mentors J. Michael Bishop and Harold E. Varmus did for cancer treatment a generation ago. Unfortunately, as Gordon is well aware, mental illness is particularly challenging in this regard. In contrast to many types of cancer, where one genetic mutation can cause unregulated cell growth, psychiatric diseases rarely stem from any single faulty gene; instead, they are typically rooted in a complex interplay of genetic, environmental, and cultural factors. Copyright 2017 Undark

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23751 - Posted: 06.17.2017

By Sam Wong Microdosing, the practice of regularly taking small amounts of psychedelic drugs to improve mood and performance, has been taking off over the past few years. But the fact that these drugs are illegal makes it difficult to research their effects and possible health consequences. There are no rigorous clinical trials to see whether microdosing works (see “Microdosers say tiny hits of LSD make your work and life better”). Instead, all we have are anecdotes from people like Janet Lai Chang, a digital marketer based in San Francisco. She will present her experience of microdosing at the Quantified Self conference in Amsterdam from 17 to 18 June. When did you start microdosing? I started in February 2016. I wanted to understand how my brain works and how it might work differently with the influence of psilocybin [the active ingredient in magic mushrooms]. What else did you hope to achieve? I had been struggling with a lot of social anxiety. It was really preventing me from advancing professionally. I was invited to give a talk at Harvard University and a TedX talk in California. I didn’t feel ready. I felt all this anxiety. I procrastinated until the last minute and then didn’t do it. It was one of my biggest regrets. What doses did you take? At first I was taking 0.2 grams of mushrooms every day, with a day or two off at the weekend. In August, I had a month off. From October to April, it was a few times a week. How did it affect you? I was less anxious, less depressed, more open, more extroverted. I was more present in the moment. It’s harder to get into the flow of the focused solo work that I’m normally really good at. But it’s good for the social aspect. © Copyright New Scientist Ltd.

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23743 - Posted: 06.15.2017

By ALEX WILLIAMS This past winter, Sarah Fader, a 37-year-old social media consultant in Brooklyn who has generalized anxiety disorder, texted a friend in Oregon about an impending visit, and when a quick response failed to materialize, she posted on Twitter to her 16,000-plus followers. “I don’t hear from my friend for a day — my thought, they don’t want to be my friend anymore,” she wrote, appending the hashtag #ThisIsWhatAnxietyFeelsLike. Thousands of people were soon offering up their own examples under the hashtag; some were retweeted more than 1,000 times. You might say Ms. Fader struck a nerve. “If you’re a human being living in 2017 and you’re not anxious,” she said on the telephone, “there’s something wrong with you.” It was 70 years ago that the poet W.H. Auden published “The Age of Anxiety,” a six-part verse framing modern humankind’s condition over the course of more than 100 pages, and now it seems we are too rattled to even sit down and read something that long (or as the internet would say, tl;dr). Anxiety has become our everyday argot, our thrumming lifeblood: not just on Twitter (the ur-anxious medium, with its constant updates), but also in blogger diaries, celebrity confessionals (Et tu, Beyoncé?), a hit Broadway show (“Dear Evan Hansen”), a magazine start-up (Anxy, a mental-health publication based in Berkeley, Calif.), buzzed-about television series (like “Maniac,” a coming Netflix series by Cary Fukunaga, the lauded “True Detective” director) and, defying our abbreviated attention spans, on bookshelves. With two new volumes analyzing the condition (“On Edge: A Journey Through Anxiety,” by Andrea Petersen, and “Hi, Anxiety,” by Kat Kinsman) following recent best-sellers by Scott Stossel (“My Age of Anxiety”) and Daniel Smith (“Monkey Mind”), the anxiety memoir has become a literary subgenre to rival the depression memoir, firmly established since William Styron’s “Darkness Visible” and Elizabeth Wurtzel’s “Prozac Nation” in the 1990s and continuing today with Daphne Merkin’s “This Close to Happy.” © 2017 The New York Times Company

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: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 23732 - Posted: 06.12.2017

By JULIA FIERRO A few months ago, I gave a reading at a local bookstore. A small but enthusiastic crowd attended, and I confessed to the audience filled with emerging writers that I had, in my 20s and early 30s, stopped writing for eight years, and that I had accepted I’d never write again. Then someone asked, “How did you return to writing?” I decided to tell the truth: Zoloft. I began flipping light switches on and off (always in fives) in third grade. My frugal parents were aghast at the waste of electricity. I tried to explain. I had to flip the switches. Or else something bad would happen, to me, to them. We were all in danger — my younger brother, my school friends, even my pets. I assumed that my fears were rational and that my school friends were like me, worrying all the time. As my obsessions accumulated, the dread throbbed more insistently, and my rituals became more complex. I counted in fives all day at school, my teeth clicking in time so much my teacher grew annoyed by the sound, and when the last school bell rang, my jaw was sore. My nightly prayers became a chant I had to recite 20, then 50 and, later, 100 times. Now that I am a mother, it astounds me that I was able to hide my rituals from my family — but I felt I had no choice. As the daughter of an Italian immigrant who survived unimaginable horrors — poverty, plague, war, domestic violence, the death of his baby sister because of a lack of basic health care — I heard one word over and over again. “Forte.” Strength. Weakness or, to be more specific, showing or admitting to weakness, seemed both un-Italian and un-American. I was raised in a historic whaling village on Long Island. Every year our grade school class field-tripped to the town museum, where we heard stories about courageous Dutch and English settlers who harpooned and lanced whales before towing them ashore and using their flensing knives to cut blubber into long strips. The stories taught us that America was bedrocked with self-reliance and fortitude.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23716 - Posted: 06.07.2017

Sarah Marsh When depression takes hold of Helen it feels like she is drowning in a pool of water, unable to swim up to the world above. The 36-year-old former nurse has had mental health problems most of her life. No drugs, hospital stays or therapies have been able to help. Then one day, during yet another spell in hospital, her consultant told her about a psychiatrist treating patients with ketamine. The psychiatrist in question visited her to discuss using the drug. He warned there were no guarantees, but it had helped some patients. Since then Helen’s life has transformed. Sitting on a bench in the grounds of the hospital where her treatment began a year and a half ago, she lists everything she can do now that she could not before: take her kids to school, give them hugs, go on coffee dates. “I am managing my thoughts and that is what ketamine helps to do. It slows down my thought process so instead of being completely overwhelmed by all these immense negative thoughts and feelings … I can think, stop and breathe,” she says, nervously pulling her sleeves over her hands as she talks. She adds: “It’s still really hard but now there is a tiny fraction of a second where my thoughts are slow enough to think: ‘I can deal with this. I cannot give up.’”

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23697 - Posted: 06.02.2017

By Ariana Eunjung Cha Depression is usually considered an issue parents have to watch out for starting in the turbulent teenage years. The CW channel, full of characters with existential angst about school, friends and young love, tells us so, as do the countless parenting books about the adolescent years in every guidance counselor's office. But what if by that time it's already too late? A large new study out this week contains some alarming data about the state of children's mental health in the United States, finding that depression in many children appears to start as early as age 11. By the time they hit age 17, the analysis found, 13.6 percent of boys and a staggering 36.1 percent of girls have been or are depressed. These numbers are significantly higher than previous estimates. Understanding the risk of depression is critically important because of the close link between depressive episodes and serious issues with school, relationships and suicide. While researchers have long known about the gender gap in depression, with more adult women than men suffering from the condition, the new numbers show that whatever divergent paths boys and girls take happens even earlier than expected. Published in the journal Translational Psychiatry, the study was based on data compiled from in-person interviews with more than 100,000 children who participated in the National Survey of Drug Use and Health from 2009 to 2014. The NSDUH is an annual survey on a representative sample of the U.S. population. Among the standard questions asked are ones about insomnia, irritability, and feelings of guilt or worthlessness that researchers used to “diagnose” survey participants with depression using diagnostic criteria from the Diagnostic and Statistical Manual of Mental Disorders. Through the survey, they were able to capture a broader group of children than those who have a formal diagnosis and who may be in treatment. © 1996-2017 The Washington Post

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: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 23687 - Posted: 06.01.2017

Sara Reardon Tom Insel, former director of the US National Institute of Mental Health, is searching for new ways of addressing mental illness. Sixteen months after leaving the US National Institute of Mental Health (NIMH) for Google’s health sciences division, psychiatrist Tom Insel is on the move again. The former NIMH director, who left Google on 5 May, is starting his own company. Insel’s group, called Mindstrong, will try to infer a person’s mental-health status by analysing the way they use smartphones. Insel stepped down as NIMH director in December 2015 in order to start a mental-health program called Verily within Google’s Life Sciences group. One of the division’s goals overlaps with that of Mindstrong's: Verily intends to build tools, which could include smartphone apps or computer programs, that can recognize characteristics of mental illness using a method known as “digital phenotyping”. The method analyses factors such as a user’s word choice in communication, voice patterns when talking to digital assistants, their physical movements and location data to determine their state of mind. If a smartphone could recognize when its owner was feeling suicidal, for instance, it could potentially intervene by providing resources or alerting others. © 2017 Macmillan Publishers Limited

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23597 - Posted: 05.10.2017

A U.S.-based drug researcher who led a team that hunted through a massive database of patient records says the anesthetic ketamine shows potential as an antidepressant and should be further studied for its potential as a psychiatric drug. Doctors currently use ketamine to relieve pain during surgery and it is approved for that purpose. The drug's potential to relieve suicidal depression is also well known, but that information is based on anecdotes and small studies rather than a large clinical trial. Ruben Abagyan, a professor in the school of pharmaceutical sciences at the University of California San Diego, said ketamine is a "possible alternative treatment and definitely in particularly difficult cases." Those cases could include suicidal depression, where the weeks of treatment that traditional antidepressants require to take effect might be too long, Abagyan said. Search for beneficial signal Abagyan is the senior author of a study published in Wednesday's issue of the journal Scientific Reports, based on an analysis of a large U.S. database of adverse effect reports that were made for any reason. The U.S. Food and Drug Administration's adverse effects database, which contains over 8 million patient records of reports made for a wide range of reasons, is normally used to look for potentially harmful side-effects. But in a twist, the researchers turned this on its head, looking for reduction in depression symptoms among patients who took ketamine. "If we can look at the reduction of their complaints about depression that can be a signal for the beneficial effect of ketamine," Abagyan said. ©2017 CBC/Radio-Canada.

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23569 - Posted: 05.04.2017

Miriam E. Tucker In July 2012, a science reporter for The Washington Post, Brian Vastag, was in Wisconsin visiting his family when a high fever hit. He became instantly bedridden with flu-like symptoms that never went away. "It didn't feel like anything I'd ever had before. ... The things that distinguished it were the dizziness and the feeling of unreality in the head," Vastag says. Now, nearly five years later, the 45-year-old can no longer concentrate or read even a few sentences without becoming exhausted. A short walk to the mailbox means lying down for the rest of the day. In September, he'll qualify for Medicare due to his disability. That level of severity isn't the picture most people — including physicians — think of when they hear the term "chronic fatigue syndrome." But that was the diagnosis Vastag finally received after 18 months of visiting numerous doctors, submitting countless vials of blood and initially being misdiagnosed with West Nile virus. Actually, Vastag's condition is now termed "myalgic encephalomyelitis/chronic fatigue syndrome," or ME/CFS for short, and is estimated to affect at least 1 million people in the U.S. alone. Many with the condition dislike the name "chronic fatigue syndrome" because they feel it's trivializing and misleading, giving the impression that they're simply tired or depressed when in fact many are quite ill. Nailing down the cause — or, more likely, causes — of the illness has proven exceptionally difficult, since patients' symptoms vary tremendously. © 2017 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23561 - Posted: 05.02.2017

Elizabeth Eaton Researchers have pinpointed a gene that keeps important brain cells in mice from crossing their wires, providing a possible link between brain wiring and mood disorders like depression. Without the gene, called Pcdhαc2, mice acted more depressed, researchers report April 28 in Science. Nerve cells, or neurons, that produce the chemical messenger molecule serotonin extend long projections called axons to various parts of the brain. Serotonin released from the tips of the axons signal other neurons in these target areas to influence mood and other aspects of behavior. For efficient signaling, the axon tips must be properly spaced. In the new work, scientists from New York City, St. Louis and China found that such spacing is disrupted in mice lacking the Pcdhαc2 gene. As a result, serotonin-signaling circuits are not properly assembled and the mice exhibited behaviors indicating depression. Pcdhαc2 is found in a cluster of genes that contain the blueprints for proteins that protrude from the surface of cells. These proteins work like ID cards, says study coauthor Joseph Dougherty, a neurogeneticist at Washington University School of Medicine in St. Louis. As serotonin neuron axons branch out through the brain, they can recognize other axons carrying identical IDs and spread out to keep out of each other’s paths. This process, called tiling, evenly spaces the axons in their target areas within the brain. |© Society for Science & the Public 2000 - 2017

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 23553 - Posted: 04.29.2017

New research from the National Institutes of Health found that pairing the antidepressant amitriptyline with drugs designed to treat central nervous system diseases, enhances drug delivery to the brain by inhibiting the blood-brain barrier in rats. The blood-brain barrier serves as a natural, protective boundary, preventing most drugs from entering the brain. The research, performed in rats, appeared online April 27 in the Journal of Cerebral Blood Flow and Metabolism. Although researchers caution that more studies are needed to determine whether people will benefit from the discovery, the new finding has the potential to revolutionize treatment for a whole host of brain-centered conditions, including epilepsy, stroke,human amyotrophic lateral sclerosis (ALS), depression, and others. The results are so promising that a provisional patent application has been filed for methods of co-administration of amitriptyline with central nervous system drugs. According to Ronald Cannon, Ph.D., staff scientist at NIH’s National Institute of Environmental Health Sciences (NIEHS), the biggest obstacle to efficiently delivering drugs to the brain is a protein pump called P-glycoprotein. Located along the inner lining of brain blood vessels, P-glycoprotein directs toxins and pharmaceuticals back into the body’s circulation before they pass into the brain. To get an idea of how P-glycoprotein works, Cannon said to think of the protein as a hotel doorman, standing in front of a revolving door at a lobby entrance. A person who is not authorized to enter would get turned away, being ushered back around the revolving door and out into the street.

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: The Biology of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 23548 - Posted: 04.28.2017

Aimee Cunningham Taking antidepressants during pregnancy does not increase the risk of autism or attention-deficit/hyperactivity disorder, two new large studies suggest. Genetic or environmental influences, rather than prenatal exposure to the drugs, may have a greater influence on whether a child will develop these disorders. The studies are published online April 18 in JAMA. Clinically, the message is “quite reassuring for practitioners and for mothers needing to make a decision about antidepressant use during pregnancy,” says psychiatrist Simone Vigod, a coauthor of one of the studies. Past research has questioned the safety of expectant moms taking antidepressants (SN: 6/5/10, p. 22). “A mother’s mood disturbances during pregnancy are a big public health issue — they impact the health of mothers and their children,” says Tim Oberlander, a developmental pediatrician at the University of British Columbia in Vancouver. About one in 10 women develop a major depressive episode during pregnancy. “All treatment options should be explored. Nontreatment is never an option,” says Oberlander, who coauthored a commentary, also published in JAMA. Untreated depression during pregnancy creates risks for the child, including poor fetal growth, preterm birth and developmental problems. Some women may benefit from psychotherapy alone. A more serious illness may require antidepressants. “Many of us have started to look at longer term child outcomes related to antidepressant exposure because mothers want to know about that in the decision-making process,” says Vigod, of Women’s College Hospital in Toronto. |© Society for Science & the Public 2000 - 2017.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 14: Attention and Consciousness
Link ID: 23510 - Posted: 04.19.2017

By Andy Coghlan It tastes foul and makes people vomit. But ayahuasca, a hallucinogenic concoction that has been drunk in South America for centuries in religious rituals, may help people with depression that is resistant to antidepressants. Tourists are increasingly trying ayahuasca during holidays to countries such as Brazil and Peru, where the psychedelic drug is legal. Now the world’s first randomised clinical trial of ayahuasca for treating depression has found that it can rapidly improve mood. The trial, which took place in Brazil, involved administering a single dose to 14 people with treatment-resistant depression, while 15 people with the same condition received a placebo drink. A week later, those given ayahuasca showed dramatic improvements, with their mood shifting from severe to mild on a standard scale of depression. “The main evidence is that the antidepressant effect of ayahuasca is superior to the placebo effect,” says Dráulio de Araújo of the Brain Institute at the Federal University of Rio Grande do Norte in Natal, who led the trial. Shamans traditionally prepare the bitter, deep-brown brew of ayahuasca using two plants native to South America. The first, Psychotria viridis, is packed with the mind-altering compound dimetheyltryptamine (DMT). The second, the ayahuasca vine (Banisteriopsis caapi), contains substances that stop DMT from being broken down before it crosses the gut and reaches the brain. © Copyright Reed Business Information Ltd.

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23494 - Posted: 04.15.2017