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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

Doctors trialling the use of ketamine to treat depression are calling for the treatment to be rolled out. Ketamine is licensed to be used as an anaesthetic but has a reputation as an illegal party drug. Writing in The Lancet Psychiatry, Dr Rupert McShane, who has led a trial in Oxford, since 2011 says ketamine can work on patients with depression "where nothing has helped before". However, he is calling for a national registry to monitor its use. Dr McShane says tens of thousands of people who have not responded to other treatment could be helped by the drug. But he adds there should be a national registry for those who prescribe the treatment to monitor the results and avoid misuse of the Class B substance. Of the 101 people taking part who had failed to find a successful depression treatment, 42 of them responded to the ketamine. "The first ketamine infusion literally saved my life," says one patient. "I had felt so desperate I was going to end it all. "Subsequent ketamine treatment has enabled me to return to my job full-time. I still struggle at times but being able to work again has given me such a boost." Dr McShane hopes more doctors will use it to treat depression but fears that the UK could follow the US where there are private ketamine clinics that vary in their clinical checks. © 2017 BB

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: 23469 - Posted: 04.10.2017

Aaron E. Carroll One of the biggest American public health victories of the last decade has been the record low reached in the teenage birthrate. Along with that have been lows in rates for teenage pregnancy and abortion. Most researchers believe that improved access to contraception is a large part of this success. But news continues to focus on the concern that hormone-based contraception — like the pill or the patch — causes depression, and that this should lead us to question its wider use. A more nuanced discussion would consider both the benefits and the harms. This issue drew widespread coverage at the end of last year with a large study published in JAMA Psychiatry. Researchers tracked all women and adolescent females (ages 15 to 34) living in Denmark from 2000 through 2014. The study found that those who used hormonal contraception had significantly higher risks of also taking an antidepressant. The study broke down the increased relative risk for each hormonal method this way: combined oral contraceptives (23 percent), progestogen-only pills (34 percent), the patch (100 percent), vaginal ring (60 percent) and levonorgestrel intrauterine system (40 percent). The risks were highest in adolescents and decreased as women aged. The risks also peaked six months after the start of contraception. Needless to say, many news outlets covered this finding widely. Some portrayed it as shocking new information that should change the way we think about hormonal birth control. Others saw it as a vindication of many women who said for years that birth control had triggered their depression while scientists and doctors ignored them. But we have to acknowledge the limitations of this type of research. It’s not a controlled trial, and it’s impossible to establish causality. Women who choose to have sex could also be more likely to consider antidepressant use. © 2017 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 23439 - Posted: 04.03.2017

Amy Maxmen Before his 33-year-old son became bedridden with chronic fatigue syndrome, biochemist Ronald Davis created technologies to analyse genes and proteins faster, better and more cheaply. Now he aims his inventions at a different target: the elusive inner workings of his son’s malady. In his office at the Stanford Genome Technology Center in Palo Alto, California, Davis holds a nanofabricated cube the size of a gaming die. It contains 2,500 electrodes that measure electrical resistance to evaluate the properties of human cells. When Davis exposed immune cells from six people with chronic fatigue syndrome to a stressor — a splash of common salt — the cube revealed that they couldn’t recover as well as cells from healthy people could. Now his team is fabricating 100 more devices to repeat the experiment, and testing a cheaper alternative — a paper-thin nanoparticle circuit that costs less than a penny to make on an inkjet printer. Davis’s findings, although preliminary, are helping to propel research on chronic fatigue syndrome, also called myalgic encephalomyelitis (ME/CFS), into the scientific mainstream. Physicians used to dismiss the disease as psychosomatic, but studies now suggest that it involves problems in the chemical reactions, or pathways, within cells. “We now have a great deal of evidence to support that this is not only real, but a complex set of disorders,” says Ian Lipkin, an epidemiologist at Columbia University in New York City. “We are gathering clues that will lead to controlled clinical trials.” © 2017 Macmillan Publishers Limited,

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: 23420 - Posted: 03.29.2017

By Melissa Banigan Twenty years ago, I started experiencing what turned into a long list of seemingly unrelated health issues. Headaches, depression, insomnia, peripheral neuropathy, fatigue, joint pain, chest pain, shortness of breath, a lesion on my spine and a variety of uncomfortable gastrointestinal ailments. Over the past five years, things went from bad to worse as I also became lactose-intolerant, developed mild vitiligo (a condition that leads to loss of skin pigmentation) and major vertigo, experienced a series of low-grade fevers and started to have some memory loss that I referred to as brain fogs. Doctors told me that as an overworked single mother of 40, I might just need to figure out ways to get more sleep and relax. Some of what was happening, they said, might be attributed to the normal processes of aging. What was happening, however, didn’t feel normal. Always a voracious reader and a writer by profession, I could no longer focus on work, read even a page of a book or grip a pen long enough to write a grocery list. I often felt too exhausted to keep plans with friends. When I did pull myself off my couch to see them, I couldn’t concentrate on conversations, so I sequestered myself in my apartment and let my friendships fade. I had been a runner, a swimmer and a hiker, but just walking up a flight of stairs made me lose my breath so completely that I succumbed to inactivity. I did everything the doctors asked me to do. I changed my diet and sleep schedule, went to a physical therapist and saw specialists in neurology and rheumatology and even a mental-health therapist. I then also turned to massage therapists, herbalists and an acupuncturist. © 1996-2017 The Washington Post

Related chapters from BP7e: 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: 23408 - Posted: 03.27.2017

By Anil Ananthaswamy People who have chronic pain are more likely to experience mood disorders, but it’s not clear how this happens. Now a study in mice has found that chronic pain can induce genetic changes in brain regions that are linked to depression and anxiety, a finding that may lead to new treatments for pain. “At least 40 per cent of patients who suffer from severe forms of chronic pain also develop depression at some point, along with other cognitive problems,” says Venetia Zachariou of the Icahn School of Medicine at Mount Sinai in New York. To see if there might be a genetic link between these conditions, Zachariou and her team studied mice with damage to their peripheral nervous system. These mice show symptoms similar to chronic pain in people – they become hypersensitive to harmless touch, and avoid other situations that might also cause them pain. Until now, pain behaviour in mice had only been studied for at most a week at a time, says Zachariou, whose team monitored their mice for 10 weeks. “At the beginning, we saw only sensory deficits and pain-like symptoms. But several weeks later, the animals developed anxiety and depression-like behaviours.” The team then examined gene activity in three regions in the mouse brains we know are associated with depression and anxiety. Analysing the nucleus accumbens, medial prefrontal cortex, and periaqueductal gray, they found nearly 40 genes where activity was significantly higher or lower than in mice without the nervous system damage. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 23402 - Posted: 03.24.2017

Jon Hamilton Gerard Sanacora, a professor of psychiatry at Yale University, has treated hundreds of severely depressed patients with low doses of ketamine, an anesthetic and popular club drug that isn't approved for depression. This sort of "off-label" prescribing is legal. But Sanacora says other doctors sometimes ask him, "How can you be offering this to patients based on the limited amount of information that's out there and not knowing the potential long-term risk?" Sanacora has a simple answer. "If you have patients that are likely to seriously injure themselves or kill themselves within a short period of time, and they've tried the standard treatments, how do you not offer this treatment?" he says. Dozens of clinics now offer ketamine to patients with depression. And a survey of providers in the U.S. and Canada showed that "well over 3,000" patients have been treated so far, Sanacora says. A number of small studies have found that ketamine can do something no other drug can: it often relieves even suicidal depression in a matter of hours in patients who have not responded to other treatments. Ketamine's potential as an antidepressant was recognized more than a decade ago. And studies done since then provide "compelling evidence that the antidepressant effects of ketamine infusion are both rapid and robust, albeit transient," according to a consensus statement from a task force of the American Psychiatric Association. Sanacora is one of the task force members. © 2017 npr

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: 23382 - Posted: 03.21.2017