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By Cathleen O’Grady People who take tiny amounts of LSD, “magic mushrooms,” and related drugs report a range of benefits, from more creativity to improved psychological well-being. But do these microdoses—typically less than 10% of the amount that causes a true psychedelic experience—actually benefit the mind? That’s been a hard question to answer. Placebo-controlled trials are tricky to pull off, because psychedelics are so tightly regulated. Now, researchers have come up with a creative workaround: They’ve enlisted microdosing enthusiasts to hide their drugs in gel capsules and mix them up with empty capsules. The upshot of this “self-blinding” study: Microdosing did lead to improvements in psychological well-being—but so did the placebo capsules. “The benefits are real,” says lead author Balázs Szigeti, a neuroscientist at Imperial College London. “But they are not caused by the pharmacological effects of microdosing.” The findings, however, are “the least interesting thing about this study,” says Noah Haber, a study design specialist at Stanford University. The “very, very clever” method of self-blinding pushes the boundaries of what can be investigated using randomized placebo controls, he says. Getting the new study off the ground wasn’t easy. Obtaining ethical approval to enroll psychedelic-taking volunteers was a “long and difficult process,” Szigeti says. And then he had to go out and find those volunteers, which he did by reaching out to microdosing communities, giving talks at psychedelic societies, and holding an “ask me anything” discussion on Reddit. Szigeti eventually garnered more than 1600 sign-ups, but once potential participants realized they’d have to procure their own psychedelics, interest ebbed, and only 246 ended up in the experiment. © 2021 American Association for the Advancement of Science.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27721 - Posted: 03.06.2021

By Kim Tingley The brain is an electrical organ. Everything that goes on in there is a result of millivolts zipping from one neuron to another in particular patterns. This raises the tantalizing possibility that, should we ever decode those patterns, we could electrically adjust them to treat neurological dysfunction — from Alzheimer’s to schizophrenia — or even optimize desirable qualities like intelligence and resilience. Of course, the brain is so complex, and so difficult to access, that this is much easier to imagine than to do. A pair of studies published in January in the journal Nature Medicine, however, demonstrate that electrical stimulation can address obsessive-compulsive urges and symptoms of depression with surprising speed and precision. Mapping participants’ brain activity when they experienced certain sensations allowed researchers to personalize the stimulation and modify moods and habits far more directly than is possible through therapy or medication. The results also showed the degree to which symptoms that we tend to categorize as a single disorder — depression, for example — may involve electrical processes that are unique to each person. In the first study, a team from the University of California, San Francisco, surgically implanted electrodes in the brain of a woman whose severe depression had proved resistant to other treatments. For 10 days, they delivered pulses through the electrodes to different areas of the brain at various frequencies and had the patient record her level of depression, anxiety and energy on an iPad. The impact of certain pulses was significant and nuanced. “Within a minute, she would say, ‘I feel like I’m reading a good book,’” says Katherine W. Scangos, a psychiatrist and the study’s lead author. The patient described the effect of another pulse as “less cobwebs and cotton.” © 2021 The New York Times Company

Related chapters from BN: 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: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27712 - Posted: 02.28.2021

By Gary Stix A consensus has emerged in recent years that psychotherapies—in particular, cognitive behavioral therapy (CBT)—rate comparably to medications such as Prozac and Lexapro as treatments for depression. Either option, or the two together, may at times alleviate the mood disorder. In looking more closely at both treatments, CBT—which delves into dysfunctional thinking patterns—may have a benefit that could make it the better choice for a patient.The reason may be rooted in our deep evolutionary past. Scholars suggest humans may become depressed to help us focus attention on a problem that might cause someone to fall out of step with family, friends, clan or the larger society—an outcast status that, especially in Paleolithic times, would have meant an all-but-certain tragic fate. Depression, by this account, came about as a mood state to make us think long and hard about behaviors that may have caused us to become despondent because some issue in our lives is socially problematic. A recent article in American Psychologist, the flagship publication of the American Psychological Association, weighs what the possible evolutionary origins of depression might mean for arguments about the merits of psychotherapy versus antidepressants. In the article, Steven D. Hollon, a professor of psychology at Vanderbilt University, explores the implications of helping a patient come to grips with the underlying causes of a depression—which is the goal of CBT, and is also in line with an evolutionary explanation. The anodyne effects of an antidepressant, by contrast, may divert a patient from engaging in the reflective process for which depression evolved—a reason perhaps that psychotherapy appears to produce a more enduring effect than antidepressants. Scientific American spoke with Hollon about his ideas on the topic.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27696 - Posted: 02.17.2021

By Warren Cornwall Prozac might need a new warning label: “Caution: This antidepressant may turn fish into zombies.” Researchers have found that long-term exposure to the drug makes guppies act more alike, wiping out some of the typical behavioral differences that distinguish them. That could be a big problem when the medication—technically named fluoxetine—washes into streams and rivers, potentially making fish populations more vulnerable to predators and other threats. In recent decades, scientists have uncovered a plethora of ways that pharmaceuticals affect animals in the lab and in the wild, such as by altering courtship, migration, and anxiety. The drugs find their way into the environment through water that pours from sewage treatment plants, which is rarely filtered to remove the chemicals. But the findings are usually based on an average taken from combining measurements of all the individual animals in a group. Giovanni Polverino, a behavioral ecologist at the University of Western Australia, Perth, and colleagues wondered whether this calculation obscured important but subtle insights about individual animals. Did the drug change behavior similarly in all the creatures in a group? Or were certain kinds of “personalities” affected more strongly? To find out, Polverino’s team captured 3600 guppies (Poecilia reticulata)—a common silvery fish often used in labs that grows to half the length of an average human’s pinkie—from a creek in northeastern Australia. In the laboratory, the fish and their offspring—as many as six generations—spent 2 years in tanks filled with either freshwater, water with fluoxetine at levels common in the wild, or a higher dose similar to places near sewage outflows. © 2021 American Association for the Advancement of Science.

Related chapters from BN: 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: Development of the Brain
Link ID: 27685 - Posted: 02.13.2021

by Peter Hess A new engineered protein that glows in the presence of serotonin enables researchers to track the neurotransmitter’s levels and location in the brains of living mice, according to a new study. This ‘serotonin sensor’ could help elucidate serotonin’s role in autism, experts say. Serotonin helps regulate mood, circulation and digestion, among other functions. Some people with autism have elevated levels of serotonin in their blood. Other evidence links serotonin to social behavior in mice. “Serotonin is wildly important both for basic research and human health. And for the longest time, ways to measure it were very indirect,” says co-lead researcher Loren Looger, professor of neuroscience at the University of California, San Diego. “Only with sensors like this can one follow it in vivo, which is critical.” Unlike other tools for measuring serotonin, the sensor can also show changes in serotonin activity over time, making it an exciting tool for autism research, says Jeremy Veenstra-VanderWeele, professor of psychiatry at Columbia University, who was not involved in the study. “This tool will make it possible to understand the relationships between serotonin release and complex behaviors, including in different genetic mouse models related to autism,” he says. “I imagine that this tool will come into fairly broad use.” Programmable protein: The new sensor originated from one described last year that detects a different neurotransmitter, acetylcholine. Looger and his team used a computer algorithm to redesign the acetylcholine-binding portion of the sensor protein so that it could attach to serotonin instead. © 2021 Simons Foundation

Related chapters from BN: 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: Development of the Brain
Link ID: 27680 - Posted: 02.08.2021

Paul Tullis On a sunny day in London in 2015, Kirk Rutter rode the Tube to Hammersmith Hospital in hopes of finally putting an end to his depression. Rutter had lived with the condition off and on for years, but the burden had grown since the death of his mother in 2011, followed by a relationship break-up and a car accident the year after. It felt as if his brain was stuck on what he describes as “an automatic circuit”, repeating the same negative thoughts like a mantra: “‘Everything I do turns to crap.’ I actually believed that,” he recalls. The visit to Hammersmith was a preview. He would be returning the next day to participate in a study, taking a powerful hallucinogen under the guidance of Robin Carhart-Harris, a psychologist and neuroscientist at Imperial College London. Years of talking therapy and a variety of anti-anxiety medications had failed to improve Rutter’s condition, qualifying him for the trial. “Everyone was super nice, like really lovely, and especially Robin,” Rutter recalls. Carhart-Harris led him to a room with a magnetic resonance imaging (MRI) machine, so researchers could acquire a baseline of his brain activity. Then he showed Rutter where he would spend his time while on the drug. Carhart-Harris asked him to lie down and played him some of the music that would accompany the session. He explained that he would have on hand a drug that could neutralize the hallucinogen, if necessary. Then the two practised a grounding technique, to help calm Rutter in the event that he became overwhelmed. Without warning, Rutter burst into tears. “I think I knew this was going to be unpacking a lot — I was carrying a bit of a load at the time,” Rutter says. © 2021 Springer Nature Limited

Related chapters from BN: 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: Development of the Brain
Link ID: 27670 - Posted: 01.30.2021

Research shows that hallucinogens can be highly effective treatments for anxiety, depression, addiction, and trauma. Here's everything you need to know: Aren't psychedelic drugs illegal? Under federal and most states' laws, they are, but a push to legalize or decriminalize the drugs is gaining momentum. On Election Day, Oregon voters made their state the first to legalize the active ingredient in "magic mushrooms" — psilocybin — for mental health therapy in a controlled setting with a therapist. Washington, D.C., voters passed Initiative 81, making the city at least the fifth to decriminalize magic mushrooms. Similar legislation has been proposed in California, Vermont, and Iowa. Last summer, Canada issued four terminally ill patients exemptions to take psilocybin for end-of-life anxiety and depression. British Columbia resident Mona Strelaeff, 67, got an exemption for treatment for trauma, addiction, depression, and anxiety. "All the unresolved trauma," Strelaeff said, "it came back and I was beyond terrified, shaking uncontrollably, and crying." She said that psilocybin therapy helped her conquer "those tough memories" and today she "ain't afraid of jack (s---)." How does psychedelic therapy work? Participants usually take psilocybin or LSD in a relaxing setting, lying down with blindfolds and headphones on, listening to music. Trained supervisors encourage them to "go inward and to kind of experience whatever is going to come up," said Alan Davis, who studies psychedelics at Johns Hopkins University. Bad psilocybin trips are rare — Johns Hopkins and NYU researchers conducted 500 sessions without observing any "serious adverse effects" — but they can occur. Advocates say careful dose control, supervision, and controlled settings are very important. Psilocybin sessions typically last between four and six hours, while LSD sessions go on for 12. Robin Carhart-Harris, who runs the Centre for Psychedelic Research at Imperial College in London, theorized that such sessions can "reboot" the brain in a way similar to a near-death or intense spiritual experience. ® 2021 The Week Publications Inc.,

Related chapters from BN: 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: Development of the Brain
Link ID: 27667 - Posted: 01.27.2021

Kayt Sukel Psychedelic drugs conjure images of tie-dyed tee shirts, Woodstock, and Vietnam War protests. While early research into the properties of drugs like psilocybin (magic mushrooms) and lysergic acid diethylamide (LSD) during the middle of the 20th century suggested therapeutic potential for diverse mental health conditions, their role in the 1960s anti-war and counterculture movement made them suspect by law enforcement. Not long after American psychologist Timothy Leary called for people to “turn on, tune in, and drop out,” endorsing the regular use of psychedelic drugs for health and well-being, the federal Controlled Substances Act classified them as highly dangerous Schedule 1 compounds, or drugs with “no currently accepted medical use and a high potential for abuse.” “Initially, psychedelics showed quite a lot of promise for treating a wide range of mental health conditions—in particular, addiction and post-traumatic stress disorder (PTSD),” says Anil Seth, co-director of the Sackler Centre for Consciousness Science at the University of Sussex in the United Kingdom. “There’s long been a blame game going regarding what led to these drugs being outlawed, mostly focusing on people like Timothy Leary promoting indiscriminate use of what we know are quite powerful drugs. But the end result was that, despite their promise, it became nearly impossible for anyone to do any research at all on them.” Over the past decade, however, there has been a revival of psychopharmacology and neuroscience research into the effects of psychedelic drugs. In fact, despite continuing legal barriers and funding challenges involved with using these banned drugs in research studies—many researchers wait years for Food and Drug Administration approvals and require funding from non-governmental agencies to move forward—several unique research centers, including the Centre for Psychedelic Research at Imperial College London and Johns Hopkins University’s Center for Psychedelics and Consciousness Research, are now actively studying LSD, psilocybin, and dimethyltryptamine (DMT), from both basic science and clinical perspectives. © 2021 The Dana Foundation

Related chapters from BN: 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: Development of the Brain
Link ID: 27646 - Posted: 01.15.2021

By Benedict Carey At a recent visit to the Veterans Affairs clinic in the Bronx, Barry, a decorated Vietnam veteran, learned that he belonged to a very exclusive club. According to a new A.I.-assisted algorithm, he was one of several hundred V.A. patients nationwide, of six million total, deemed at imminent risk of suicide. The news did not take him entirely off guard. Barry, 69, who was badly wounded in the 1968 Tet offensive, had already made two previous attempts on his life. “I don’t like this idea of a list, to tell you the truth — a computer telling me something like this,” Barry, a retired postal worker, said in a phone interview. He asked that his surname be omitted for privacy. “But I thought about it,” Barry said. “I decided, you know, OK — if it’s going to get me more support that I need, then I’m OK with it.” For more than a decade, health officials have watched in vain as suicide rates climbed steadily — by 30 percent nationally since 2000 — and rates in the V.A. system have been higher than in the general population. The trends have defied easy explanation and driven investment in blind analysis: machine learning, or A.I.-assisted algorithms that search medical and other records for patterns historically associated with suicides or attempts in large clinical populations. Doctors have traditionally gauged patients’ risks by looking at past mental health diagnoses and incidents of substance abuse, and by drawing on experience and medical instinct. But these evaluations fall well short of predictive, and the artificially intelligent programs explore many more factors, like employment and marital status, physical ailments, prescription history and hospital visits. These algorithms are black boxes: They flag a person as at high risk of suicide, without providing any rationale. But human intelligence isn’t necessarily better at the task. “The fact is, we can’t rely on trained medical experts to identify people who are truly at high risk,” said Dr. Marianne S. Goodman, a psychiatrist at the Veterans Integrated Service Network in the Bronx, and a clinical professor of medicine at the Icahn School of Medicine at Mount Sinai. “We’re no good at it.” © 2020 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27600 - Posted: 11.30.2020

By Jelena Kecmanovic Across the spectrum, mental health problems seem to be on the rise. One-quarter of Americans reported moderate to severe depression this summer and another quarter said they suffered from mild depression, a recent study reported. These findings are similar to surveys done by the Census Bureau and the Centers for Disease Control and Prevention. A third of Americans now show signs of clinical anxiety or depression, Census Bureau finds. Former first lady Michelle Obama highlighted the problem for many when she said in August that she has been dealing with “low-grade depression.” As a psychologist, I hear almost daily how the combination of coronavirus, racial unrest, economic uncertainty and political crisis are leading many people to feel a lot worse than usual. “It is not at all surprising that we are seeing the significant increase in distress. It’s a normal reaction to an abnormal situation,” said Judy Beck, president of the Beck Institute for Cognitive Behavior Therapy in Philadelphia and author of the widely used mental health textbook “Cognitive Behavior Therapy: Basics and Beyond.” But an important difference exists between having depressive symptoms — such as sadness, fatigue and loss of motivation — and a full-blown major depressive episode that can affect your ability to function at work and home for weeks or months. The amount and duration of the symptoms, as well as the degree to which they impair one’s life all play a role in diagnosing clinical depression. Extensive research suggests that certain ways of thinking and behaving can hasten the plunge into clinical depression, while others can prevent it. As we head into winter, which can stress the coping skills of many people, here are some strategies that can help you resist the depressive downward spiral. 1. Reduce overthinking. When we feel down, we tend to think about the bad things repeatedly, often trying to figure out why they’ve happened. Research shows that some people are especially prone to this kind of “depressive rumination.” They overanalyze everything, hoping to think their way out of feeling bad, and fret about consequences of their sadness.

Related chapters from BN: 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: 27599 - Posted: 11.30.2020

By Linda Searing The “baby blues” that women can experience after giving birth usually go away within a week or two, but it now appears that more severe depressive symptoms, known as postpartum depression, may affect some new mothers for at least three years. Research from the National Institutes of Health, which tracked 4,866 women for three years after childbirth, found that about 25 percent of the women reported moderate to high levels of depressive symptoms at some point and that the remaining 75 percent experienced low-level depressive symptoms throughout the study. The “baby blues” typically include such symptoms as mood swings, anxiety and trouble sleeping, whereas postpartum depression symptoms — generally more intense and longer lasting — may include excessive crying, overwhelming fatigue, loss of appetite, difficulty bonding with the baby, feelings of inadequacy, hopelessness and more. The NIH research, published in the journal Pediatrics, encourages pediatricians to screen their tiny patients’ mothers for depressive symptoms during the children’s regular checkups, noting that “mothers’ mental health is critical to children’s well-being and development.” The researchers note that maternal depression increases a child’s risk for cognitive, emotional and behavioral problems. Getting treatment, however, should not only ease a mother’s symptoms but also improve her child’s odds for a favorable developmental outcome.

Related chapters from BN: 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 4: Development of the Brain
Link ID: 27573 - Posted: 11.10.2020

By Nicholas Bakalar A mother’s psychological distress during pregnancy may increase the risk for asthma in her child, a new study suggests. Researchers had the parents of 4,231 children fill out well-validated questionnaires on psychological stress in the second trimester of pregnancy, and again three years later. The mothers also completed questionnaires at two and six months after giving birth. The study, in the journal Thorax, found that 362 of the mothers and 167 of the fathers had clinically significant psychological distress during the mothers’ pregnancies. When the children were 10 years old, parents reported whether their child had ever been diagnosed with asthma. As an extra measure, the researchers tested the children using forced expiratory volume, or FEV, a standard clinical test of lung function. After controlling for age, smoking during pregnancy, body mass index, a history of asthma and other factors, they found that maternal depression and anxiety during pregnancy was significantly associated with both diagnoses of asthma and poorer lung function in their children. There was no association between childhood asthma and parents’ psychological distress in the years after pregnancy, and no association with paternal psychological stress at any time. “Of course, this could be only one of many causes of asthma,” said the lead author, Dr. Evelien R. van Meel of Erasmus University in Rotterdam, “but we corrected for many confounders, and we saw the effect only in mothers. This seems to suggest that there’s something going on in the uterus. But this is an observational study, and we can’t say that it’s a causal effect.” © 2020 The New York Times Company

Related chapters from BN: 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 4: Development of the Brain
Link ID: 27534 - Posted: 10.21.2020

By John Horgan One of the most impressive, disturbing works of science journalism I’ve encountered is Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America, published in 2010. In the book, which I review here, award-winning journalist Robert Whitaker presents evidence that medications for mental illness, over time and in the aggregate, cause net harm. In 2012, I brought Whitaker to my school to give a talk, in part to check him out. He struck me as a smart, sensible, meticulous reporter whose in-depth research had led him to startling conclusions. Since then, far from encountering persuasive rebuttals of Whitaker’s thesis, I keep finding corroborations of it. If Whitaker is right, modern psychiatry, together with the pharmaceutical industry, has inflicted iatrogenic harm on millions of people. Reports of surging mental distress during the pandemic have me thinking once again about Whitaker’s views and wondering how they have evolved. Below he answers some questions. —John Horgan
 Horgan: When and why did you start reporting on mental health? Whitaker: It came about in a very roundabout way. In 1994, I had co-founded a publishing company called CenterWatch that covered the business aspects of the “clinical trials industry,” and I soon became interested in writing about how financial interests were corrupting drug trials. Risperdal and Zyprexa had just come to market, and after I used a Freedom of Information request to obtain the FDA’s review of those two drugs, I could see that psychiatric drug trials were a prime example of that corruption. In addition, I had learned of NIMH-funded research that seemed abusive of schizophrenia patients, and in 1998, I co-wrote a series for the Boston Globe on abuses of patients in psychiatric research. My interest was in that broader question of corruption and abuse in research settings, and not specific to psychiatry. © 2020 Scientific American

Related chapters from BN: 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
Link ID: 27531 - Posted: 10.19.2020

By Lisa Grossman Clues from a chemical — Science News, October 3, 1970 An experimental drug’s effects on the sexual behavior of certain animals is arousing interest among investigators.… The drug, para-chlorophenylalanine … reduces the level of a naturally occurring neurochemical, serotonin, in the brain of rats, mice and dogs.… Little is known about how serotonin acts in the brain, and investigators quickly recognized that PCPA could be used to study this brain chemical. Update PCPA helped e­stablish serotonin’s role in regulating sexual desire, as well as sleep, appetite and mood. The chemical messenger has become key to one common class of antidepressant drugs called selective serotonin r­euptake inhibitors. Identified in 1974, SSRIs work by increasing the brain’s serotonin levels. But such drugs can hinder sexual desire. One SSRI that failed to relieve depression in humans found a second life as a treatment for sexual dysfunction. Approved by the U.S. Food and Drug Administration in 2015, this “little pink pill,” sold as Addyi, may boost sex drive in women by lowering serotonin in the brain’s reward centers. H.A. Croft. Understanding the role of serotonin in female hypoactive sexual desire disorder and treatment options. Journal of Sexual Medicine. Vol. 14, December 2017, p. 1575. Doi: 10.1016/j.jsxm.2017.10.068. © Society for Science & the Public 2000–2020.

Related chapters from BN: 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: 27497 - Posted: 09.30.2020

Chris Woolston Signs of depression among graduate students in the United States have apparently doubled during the COVID-19 pandemic, according to a survey that drew responses from more than 15,000 graduate and 30,000 undergraduate students at 9 US research universities. The survey, conducted by the Student Experience in the Research University (SERU) Consortium — a collaboration between the University of California, Berkeley (UC Berkeley), and the University of Minnesota Twin Cities in Minneapolis — found that indications of anxiety among graduate students rose by 50% this year compared with last year. “It’s very alarming that so many students are suffering from mental-health issues,” says Igor Chirikov, director of SERU and a senior researcher in higher education with the Center for Studies in Higher Education at UC Berkeley. “The pandemic has obviously had a big impact.” The survey, which ran from 18 May to 20 July, used simple two-item questionnaires — the Generalized Anxiety Disorder-2 and Patient Health Questionnaire-2 — to screen for symptoms of anxiety disorders and major depression. Thirty-nine per cent of graduate students (a group that includes law- and medical-school students) screened positive for anxiety, and 32% screened positive for depression. When the same screening questions were asked in March to July 2019, 26% of graduate students had signs of anxiety and 15% showed depression symptoms. © 2020 Springer Nature Limited

Related chapters from BN: 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: 27427 - Posted: 08.20.2020

Jon Hamilton The Food and Drug Administration has approved a variant of the anesthetic and party drug ketamine for suicidal patients with major depression. The drug is a nasal spray called Spravato and it contains esketamine, a chemical cousin of ketamine. In 2019, the FDA approved Spravato for patients with major depressive disorder who hadn't responded to other treatments. Now, the agency is adding patients who are having suicidal thoughts or have recently attempted to harm themselves or take their own lives. "Spravato is the first approved antidepressant medication that's been able to demonstrate a reduction in symptoms of major depressive disorder within 24 hours after the first dose," says Dr. Michelle Kramer, a psychiatrist and vice president of U.S. neuroscience, medical affairs at Janssen Pharmaceuticals, which makes the drug. Janssen is part of Johnson & Johnson. The drug's quick action is potentially important for suicidal patients because "existing drugs typically can take weeks or longer before you really get noticeable clinical benefit," says Dr. Gerard Sanacora, a professor of psychiatry at Yale University and director of Yale's depression research program. He was involved in the studies leading to the FDA approval and has consulted for Janssen. So a dose of esketamine "could potentially get a person out of a difficult, horrible situation when they're feeling so overwhelmed," says Dr. Charles Conway, a professor of psychiatry at Washington University School of Medicine in St. Louis who wasn't involved in the study. "This could be a significant improvement in how we can help people who have intense suicidal thinking." © 2020 npr

Related chapters from BN: 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 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27416 - Posted: 08.12.2020

By Hannah Sparks For communities with a low rate of depression and suicide, there may be something in the water, according to a new study. A comprehensive analysis of findings from previous studies has revealed that regions where the public drinking water contains a high level of naturally occurring lithium — a mineral used most often for the treatment of depression and bipolar disorder — also boast a lower rate of suicide than other areas. The review included all prior research on the effects of lithium, as well as regional water samples and suicide data from 1,286 locales in Austria, Greece, Italy, Lithuania, the UK, Japan and the United States. “Naturally occurring lithium in drinking water may have the potential to reduce the risk of suicide and may possibly help in mood stabilization, particularly in populations with relatively high suicide rates and geographical areas with a greater range of lithium concentration in the drinking water,” the authors concluded in their report. Denoted as “Li” on the periodic table, the element is found in varying concentrations in crops, rocks, soil and ground water — thus how it seeps into our water supply. In a statement on the King’s College London website, lead study author and chairman of epidemiology and public health at Brighton and Sussex Medical School Anjum Memon said, “It is promising that higher levels of trace lithium in drinking water may exert an anti-suicidal effect and have the potential to improve community mental health.” The results, published in the British Journal of Psychiatry, “are also consistent with the finding in clinical trials that lithium reduces suicide and related behaviors in people with a mood disorder,” said Allan Young, a professor at King’s College’s Institute of Psychiatry, Psychology & Neuroscience.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27408 - Posted: 08.08.2020

By Matthew Sitman As I read George Scialabba’s new book How To Be Depressed, I recalled that I’d been introduced to his writing almost a decade ago by a schizophrenic, manic-depressive homeless man. R. might have protested that term—technically, he lived in a small garage that a fellow parishioner at the church we all attended let him use. It was shocking to visit him there for the first time; nearly every square inch of the place was filled with musty stacks of the New York Review of Books, assorted newspapers, and books, leaving only a narrow path that led to a mattress. Before adding something to one of these piles, he’d open his latest acquisition and run his finger down its pages, searching for matches or “sparks” that might cause a destructive fire—a phobia caused by a traumatic incident in R.’s childhood. My friends and I tried to look after R., taking him to dinner or paying his phone bill or letting him do laundry in our homes. I was drawn to R. partly because I couldn’t help but see some of myself in him, and had a gnawing fear that his plight would one day be my own. He was, in his way, an intellectual, who actually read at least a few of the periodicals he collected and enjoyed arguing about politics. I’d often see him in the local used bookstore I frequented, and that must have been where he pressed Scialabba’s What Are Intellectuals Good For? into my hands. “This is the good shit,” he solemnly professed, and he was right. R. had been an alcoholic, and I’d gleaned that when he finally kicked booze the withdrawal caused a breakdown from which he’d never quite recovered. I knew I sometimes drank too much, too, and for the wrong reasons—enough to watch myself. We shared both hypochondria and a dread of visiting the doctor. I wasn’t a manic depressive, but for much of the time I knew R. I was in the throes of the worst severe depression of my life. © 2020 Commonweal Magazine.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27365 - Posted: 07.15.2020

Amy Fleming Taking a stroll with Shane O’Mara is a risky endeavour. The neuroscientist is so passionate about walking, and our collective right to go for walks, that he is determined not to let the slightest unfortunate aspect of urban design break his stride. So much so, that he has a habit of darting across busy roads as the lights change. “One of life’s great horrors as you’re walking is waiting for permission to cross the street,” he tells me, when we are forced to stop for traffic – a rude interruption when, as he says, “the experience of synchrony when walking together is one of life’s great pleasures”. He knows this not only through personal experience, but from cold, hard data – walking makes us healthier, happier and brainier. We are wandering the streets of Dublin discussing O’Mara’s book, In Praise of Walking, a backstage tour of what happens in our brains while we perambulate. Our jaunt begins at the grand old gates of his workplace, Trinity College, and takes in the Irish famine memorial at St Stephen’s Green, the Georgian mile, the birthplace of Francis Bacon, the site of Facebook’s new European mega-HQ and the salubrious seaside dwellings of Sandymount. O’Mara, 53, is in his element striding through urban landscapes – from epic hikes across London’s sprawl to more sedate ambles in Oxford, where he received his DPhil – and waxing lyrical about science, nature, architecture and literature. He favours what he calls a “motor-centric” view of the brain – that it evolved to support movement and, therefore, if we stop moving about, it won’t work as well. © 2020 Read It Later, Inc.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 27364 - Posted: 07.15.2020

By Erica Rex In 2012, I had my first psychedelic experiences, as a subject in a clinical trial at Johns Hopkins University School of Medicine’s Behavioral Pharmacology Research Unit. I was given two doses of psilocybin spaced a month apart to treat my cancer-related depression. During one session, deep within the world the drug evoked, I found myself inside a steel industrial space. Women were bent over long tables, working. I became aware of my animosity towards my two living siblings. A woman seated at the end of a table wearing a net cap and white clothes, turned and handed me a tall Dixie cup. “You can put that in here,” she said. The cup filled itself with my bilious, sibling-directed feelings. “We’ll put it over there.” She turned and placed the cup matter-of-factly on a table at the back of the room. Then she went back to her tasks. Whenever I speak with her, Mary Cosimano, the director of guide/facilitator services at Johns Hopkins Center for Psychedelic and Consciousness Research, mentions the women in the chamber and the cup. My experience struck a chord. For me, the women in the chamber have become a transcendent metaphor for emotional healing. “I’ve thought about having a necklace made, with the cup, as a momento,” she said the last time I saw her at a conference. “Have you thought about it?” Prior to their 1971 prohibition, psilocybin and LSD were administered to approximately 40,000 patients, among them people with terminal cancer, alcoholics and those suffering from depression and obsessive-compulsive disorder. The results of the early clinical studies were promising, and more recent research has been as well. The treatment certainly helped me. Eight years after my sessions, researchers continue to prove the same point again and again in an ongoing effort to turn psychedelic drug therapy into FDA-sanctioned medical treatment. This can’t happen soon enough. © 2020 Scientific American,

Related chapters from BN: 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 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27361 - Posted: 07.14.2020