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By Nicholas Bakalar Electroconvulsive therapy, or ECT, can be effective for the treatment of major depression and is just as safe as antidepressant drugs combined with psychotherapy, a large new study concludes. The procedure, once referred to as electroshock therapy, has a controversial and largely unfavorable history. This was partly due to inaccurate portrayals in popular books and films like “One Flew Over the Cuckoo’s Nest,” and partly the result of real problems with the earliest versions of the procedure, which used strong electrical currents and no anesthesia. Today, ECT is performed under general anesthesia, and the doctor, working with an anesthesiologist and a nurse, applies a weak electric current to the brain (usually about 0.8 amperes at 120 volts) for one to six seconds. This causes a seizure inside the brain, but because of the anesthesia, the patient does not experience muscular contractions. The seizure leads to brain changes that relieve symptoms of depression and certain other mental illnesses. Usually, doctors administer a series of ECT treatments over a period of days or weeks. The only painful part of the procedure is the insertion of an intravenous line before anesthesia. There can be side effects afterward, including temporary memory loss, confusion or transitory headaches and muscle aches. Doctors debate whether ECT can cause long-term memory problems distinct from the memory problems that can be caused by depression itself. For this new study, published in Lancet Psychiatry, Canadian researchers used the records of 10,016 adults whose depression was severe enough that they spent three or more days in the hospital. Half of them had received ECT, while the other half were treated with drugs and psychotherapy. Their average age was 57, and about two-thirds were women. The researchers tracked how each group fared in the 30 days after they were discharged from the hospital. © 2021 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: 27999 - Posted: 09.18.2021

By Husseini Manji, Joseph Hayes Depression affects more than 264 million people of all ages globally. The World Health Organization ranks depression as one of the most debilitating diseases to society. It is the leading cause of disability worldwide and the psychiatric diagnosis most commonly associated with suicide, which accounts for nearly 800,000 deaths globally each year. Individuals suffering from depression may face an inability to manage life’s demands and maintain social connections, affecting all aspects of their experiences, from school and employment to relationships and overall quality of life. When it comes to treatment, approximately one third of those suffering from depression do not respond to two or more antidepressants and are considered treatment-resistant. Treatment-resistant depression is a chronic condition that places an increased emotional, functional and economic burden on the individual, their loved ones and society. It is also associated with greater morbidity, higher health care costs and various comorbid conditions. While a number of antidepressants exist, they all work through changing the levels of brain-signaling molecules called monoaminergic neurotransmitters. New drug development for depression had stalled for a number of years, and many pharmaceutical companies have withdrawn from neuroscience entirely. But recent scientific advances have led to the development of novel antidepressants working via completely different mechanisms. The brain is the most advanced, adaptive information processing system in existence—in large part because of its tremendous plasticity. Scientists have been building upon these neuroscience advances to develop completely novel, rapid-acting antidepressants. In this regard, considerable evidence has demonstrated that the regulation of two receptors—AMPA and NMDA—on many neurons that respond to the neurotransmitter glutamate control changes in the tiny junctions, or synapses, between neurons. © 2021 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 4: Development of the Brain
Link ID: 27991 - Posted: 09.15.2021

James M. Gaines Young macaques given the popular antidepressant fluoxetine for two years had lower levels of certain fatty acids and other lipids in their brains than ones not given the drug, finds a recent study (July 28) in International Journal of Molecular Sciences. The findings may help explain why younger people sometimes experience adverse side effects when taking the drug. Fluoxetine, often sold under the brand name Prozac, is a prescription medication that can be given to adults as well as children as young as 7 or 8 years old. But there’s not good literature on the long-term impact of fluoxetine and other psychoactive drugs that we use to treat adult symptoms in the young brain, says Bita Moghaddam, a behavioral neuroscientist at Oregon Health & Science University who was not involved in the study, “so [it] was really nice to see that there is this level of focus.” While genes and neurotransmitters may get the lion’s share of the attention in neuroscience research, brains are mostly made of up fats and other lipids. But lipids, it turns out, can be hard to study. So, when University of California Davis brain scientist Mari Golub and her colleagues wanted to know what was going on with the fats in the brains of the monkeys they were studying, they reached out to the brain lab at the Skoltech Institute of Science and Technology in Moscow where Anna Tkachev—the lead author on the new paper—works. “We happen to specialize in lipids in particular,” says Tkachev. For years, Golub and her colleagues had been using macaques to investigate the effects of fluoxetine. The antidepressant can be an effective treatment for maladies such as depression and obsessive-compulsive disorder. However, some studies suggest that the drug can occasionally cause serious, long-term side effects, and perhaps counter-intuitively for an antidepressant, it’s been linked to an increased risk of suicidal thinking and behavior, particularly in young people. © 1986–2021 The Scientist.

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 13: Memory and Learning
Link ID: 27988 - Posted: 09.13.2021

As I lean back in the leather recliner, my limbs feel heavy. The strong dose of ketamine I've just taken is making it harder to move, so I struggle to put on my headphones and eyeshades. Soothing music lulls me into deep relaxation, as my consciousness starts to float away from my body and into a world of swirling lights, colours and images. I'm not at a new-age music festival, or in a seedy underground drug den. This fully-legal experience is taking place under medical supervision at Field Trip Health in Toronto, a clinic that offers psychedelic-assisted therapy for those suffering treatment-resistant mental illnesses like depression and PTSD. The clinic, which was the first of its kind in Canada, opened last year. Since then, similar clinics have opened in Quebec, Alberta, Saskatchewan, B.C., and Nova Scotia. Ketamine was first approved for use in Canada and the U.S. as a general anesthetic more than 50 years ago. Since then it has gained a reputation as a party drug, with names like Special K or Vitamin K. Today, it's increasingly being used as a fast-acting and effective treatment for depression. But it isn't without controversy. I've dealt with bouts of depression and suicidal thoughts for about as long as I can remember. By the fall of 2020, after months of isolation due to the COVID-19 pandemic had taken their toll, my depression was as bad as it had ever been. ©2021 CBC/Radio-Canada.

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: 27873 - Posted: 06.26.2021

An analysis of survey data from more than 280,000 young adults ages 18-35 showed that cannabis (marijuana) use was associated with increased risks of thoughts of suicide (suicidal ideation), suicide plan, and suicide attempt. These associations remained regardless of whether someone was also experiencing depression, and the risks were greater for women than for men. The study published online today in JAMA Network Open and was conducted by researchers at the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health. “While we cannot establish that cannabis use caused the increased suicidality we observed in this study, these associations warrant further research, especially given the great burden of suicide on young adults,” said NIDA Director Nora Volkow, M.D., senior author of this study. “As we better understand the relationship between cannabis use, depression, and suicidality, clinicians will be able to provide better guidance and care to patients.” The number of adults in the United States who use cannabis more than doubled from 22.6 million in 2008 to 45.0 million in 2019, and the number of daily or near-daily users almost tripled from 3.6 million to 9.8 million in 2019. Over the same time span, the number of adults with depression also increased, as did the number of people who reported suicidal ideation or plan or who died by suicide. To date, however, the relationship between trends in cannabis use and suicidality is not well understood. The current study sought to fill this gap.

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: 27866 - Posted: 06.23.2021

By Bill Hathaway A massive genome-wide association study (GWAS) of genetic and health records of 1.2 million people from four separate data banks has identified 178 gene variants linked to major depression, a disorder that will affect one of every five people during their lifetimes. The results of the study, led by the U.S. Department of Veterans Affairs (V.A.) researchers at Yale University School of Medicine and University of California-San Diego (UCSD), may one day help identify people most at risk of depression and related psychiatric disorders and help doctors prescribe drugs best suited to treat the disorder. The study was published May 27 in the journal Nature Neuroscience. For the study, the research team analyzed medical records and genomes collected from more than 300,000 participants in the V.A.’s Million Veteran Program (MVP), one of the largest and most diverse databanks of genetic and medical information in the world. These new data were combined in a meta-analysis with genetic and health records from the UK Biobank, FinnGen (a Finland-based biobank), and results from the consumer genetics company 23andMe. This part of the study included 1.2 million participants. The researchers crosschecked their findings from that analysis with an entirely separate sample of 1.3 million volunteers from 23andMe customers. When the two sets of data from the different sources were compared, genetic variants linked to depression replicated with statistical significance for most of the markers tested. Copyright © 2021 Yale University

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 13: Memory and Learning
Link ID: 27833 - Posted: 05.29.2021

By Andrew Jacobs It’s been a long, strange trip in the four decades since Rick Doblin, a pioneering psychedelics researcher, dropped his first hit of acid in college and decided to dedicate his life to the healing powers of mind-altering compounds. Even as antidrug campaigns led to the criminalization of Ecstasy, LSD and magic mushrooms, and drove most researchers from the field, Dr. Doblin continued his quixotic crusade with financial help from his parents. Dr. Doblin’s quest to win mainstream acceptance of psychedelics took a significant leap forward on Monday when the journal Nature Medicine published the results of his lab’s study on MDMA, the club drug popularly known as Ecstasy and Molly. The study, the first Phase 3 clinical trial conducted with psychedelic-assisted therapy, found that MDMA paired with counseling brought marked relief to patients with severe post-traumatic stress disorder. The results, coming weeks after a New England Journal of Medicine study that highlighted the benefits of treating depression with psilocybin, the psychoactive ingredient in magic mushrooms, have excited scientists, psychotherapists and entrepreneurs in the rapidly expanding field of psychedelic medicine. They say it is only a matter of time before the Food and Drug Administration grants approval for psychoactive compounds to be used therapeutically — for MDMA as soon as 2023, followed by psilocybin a year or two later. After decades of demonization and criminalization, psychedelic drugs are on the cusp of entering mainstream psychiatry, with profound implications for a field that in recent decades has seen few pharmacological advancements for the treatment of mental disorders and addiction. The need for new therapeutics has gained greater urgency amid a national epidemic of opioid abuse and suicides. © 2021 The New York Times Company

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: 27817 - Posted: 05.12.2021

By Paul E. Greenberg Since the early 1990s, I, together with my colleagues, have been studying the economic burden of adults with major depressive disorders (MDD). Over that time, we have tracked shifts in the prevalence of this disease; in the makeup of those suffering from it; and in the nature of treatment both for the disease itself and for the host of comorbidities, such as pain and anxiety disorders, that accompany it. We have then used these data as the basis for calculating the incremental economic burden of adults with MDD—that is, the additional costs traceable to those suffering from the disease in terms of both medical treatment and workplace productivity impacts. Our most recent study was just published in a special issue of PharmacoEconomics (which I also co-edited) that presents new research on the economics of MDD. By focusing on one year during the Great Recession (2010) and another after a long macroeconomic expansion (2018), our analysis provides a helpful profile of the changing economic effects of this widespread and pernicious illness. We report our latest estimates showing that the incremental economic burden of adults with MDD was $326 billion in 2018, 38 percent higher than in 2010. But our work goes deeper than simply providing an economic calculator. This research offers a multifaceted lens through which we can gain a better understanding of how the myriad effects of the illness manifest themselves. Importantly, we find that only 11 percent of the overall burden of illness was attributable to the direct medical costs of treating MDD itself, while the costs of treating comorbid medical conditions made up 24 percent. Another 4 percent was due to suicide-related costs, while fully 61 percent of the total burden in 2018 resulted from a combination of elevated workplace absenteeism and presenteeism (that is, reduced productivity as a result of working while sick). This striking imbalance between medical expenditures to treat either MDD or its comorbidities on the one hand and workplace-related costs on the other is one aspect of the story that has changed dramatically since 2010, when medical costs were equivalent to workplace costs. © 2021 Scientific American,

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: 27806 - Posted: 05.08.2021

By Christina Caron Finding a therapist can be a tough and time-consuming process involving multiple phone calls, waiting lists and insurance hurdles. But what if you were able to walk into your corner drugstore for a bottle of shampoo and also had the option of scheduling a walk-in session for mental health treatment? That’s the future that CVS, the largest retail pharmacy in the United States, is envisioning. Since January the company has added licensed clinical social workers trained in cognitive behavioral therapy to 13 locations in the Houston, Philadelphia and Tampa metro areas. The providers will offer mental health assessments, referrals and counseling either in person or via telehealth, a CVS spokeswoman said, and this spring the company plans to expand to 34 locations in those same regions. The social workers are available during the day, and also on evenings and weekends in the company’s MinuteClinics, which provide a variety of nonemergency health care services either via walk-in or by appointment. The hours are more flexible than what therapists might normally offer, and the social workers partner with the clinic’s nurse practitioners and pharmacists to give prescriptions when needed, said Dr. Daniel Knecht, the vice president of clinical product at CVS Health. CVS is just one of a growing number of retailers who are recognizing the unmet need for mental health providers and hoping to fill the gap. On Thursday, Walmart announced it is acquiring MeMD, which offers online medical and mental health care. Walmart currently provides counseling via Walmart Health, a health center located in a separate building alongside Walmart Supercenters. In Georgia, Walmart Health offers in-person mental health counseling and in Arkansas customers can receive online counseling. Later this year, counseling services will become available at Walmart Health locations in Illinois and Florida, a spokeswoman said. © 2021 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: 27805 - Posted: 05.08.2021

By Rachel Schraer People diagnosed with Covid-19 in the previous six months were more likely to develop depression, dementia, psychosis and stroke, researchers have found. A third of those with a previous Covid infection went on to develop or have a relapse of a psychological or neurological condition. But those admitted to hospital or in intensive care had an even higher risk. The study authors pointed to both the effects of stress, and the virus having a direct impact on the brain. UK scientists looked at the electronic medical records of more than half a million patients in the US, and their chances of developing one of 14 common psychological or neurological conditions, including: Anxiety and mood disorders were the most common diagnosis among those with Covid, and these were more likely to be down to the stress of the experience of being very ill or taken to hospital, the researchers explained. Conditions like stroke and dementia were more likely to be down to the biological impacts of the virus itself, or of the body's reaction to infection in general. Covid-19 was not associated with an increased risk of Parkinson's or Guillain-Barré syndrome (a risk from flu). Cause and effect The study, published in the Lancet Psychiatry journal, was observational. So the researchers couldn't say whether Covid had caused any of the diagnoses - and some people would have had a stroke or depression in the next six months regardless. But by comparing a group of people who had had Covid-19 with two groups - with flu and with other respiratory infections respectively - the researchers at the University of Oxford concluded Covid was associated with more subsequent brain conditions than other respiratory illnesses. © 2021 BBC.

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 13: Memory and Learning
Link ID: 27760 - Posted: 04.08.2021

By Benedict Carey When I joined the Science staff in 2004, reporters in the department had a saying, a reassuring mantra of sorts: “People will always come to the science section, if only to read about progress.” I think about that a lot as I say goodbye to my job, covering psychiatry, psychology, brain biology and big-data social science, as if they were all somehow related. The behavior beat, as it’s known, allowed tremendous freedom: I wrote about the mental upsides of binge drinking, playing the lotto and sports fandom. I covered basic lab research, the science of learning and memory, the experience of recurrent anguish, through the people who had to live with it. And much, much more. Like most science reporters, I had wanted to report on something big, to have a present-at-the-creation run that would shake up our understanding of mental health problems. At minimum, I expected research that would help people in distress improve their lives. But during my tenure, the science informing mental health care did not proceed smoothly along any trajectory. On the one hand, the field attracted enormous scientific talent, and there were significant discoveries, particularly in elucidating levels of consciousness in brain injury patients who appear unresponsive; and in formulating the first persuasive hypothesis of a cause for schizophrenia, based in brain biology. On the other hand, the science did little to improve the lives of the millions of people living with persistent mental distress. Almost every measure of our collective mental health — rates of suicide, anxiety, depression, addiction deaths, psychiatric prescription use — went the wrong direction, even as access to services expanded greatly. What happened? After 20 years covering the field, here and at The Los Angeles Times, I have a few theories, and some ideas on what might be required to turn things around. © 2021 The New York Times Company

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: 27757 - Posted: 04.03.2021

By Perri Klass, M.D. When parents bring their children in for medical care these days, there is no such thing as a casual, “Hey, how’s it going?” We doctors walk into every exam room prepared to hear a story of sadness and stress, or at the very least, of coping and keeping it together in this very hard year, full of isolation, loss, tragedy and hardship, with routines disrupted and comfort hard to come by. Parents have carried heavy burdens of stress and responsibility, worrying about themselves but also watching their children struggle, and there is worldwide concern about depression and suicidality among young people. But it isn’t only the adults and the young adults and teenagers who are suffering and sad; young children can also experience depression, but it can look very different, which makes it challenging for parents — or doctors — to recognize it and provide help. Rachel Busman, a clinical psychologist at the Child Mind Institute in New York City, said that it can be hard to think about depression in younger children because we picture childhood as a time of innocence and joy. But as many as 2 to 3 percent of children ages 6 to 12 can have serious depression, she said. And children with anxiety disorders, which are present in more than 7 percent of children aged 3 to 17, are also at risk for depression. Dr. Helen Egger, until recently the chair of child and adolescent psychiatry at N.Y.U. Langone Health, said that according to her epidemiologic research, between 1 and 2 percent of young children — as young as 3 — are depressed Depression was originally conceived of as an adult problem. Maria Kovacs, professor of psychiatry at the University of Pittsburgh School of Medicine, said that in the 1950s and ’60s, there were child psychiatrists who believed that children did not have sufficient ego development to feel depression, but that research that she and other colleagues did in the ’70s showed that “school age children can suffer from diagnosable depression.” © 2021 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 13: Memory and Learning
Link ID: 27756 - Posted: 04.03.2021

Alexandra Jones In the summer of 1981, when he was 13, Grant crashed a trail motorbike into a wall at his parents’ house in Cambridgeshire. He’d been hiding it in the shed, but “it was far too powerful for me, and on my very first time starting it in the garden, I smashed it into a wall”. His mother came outside to find the skinny teenager in a heap next to the crumpled motorbike. “I was in a lot of trouble.” Grant hadn’t given this childhood memory much thought in the intervening years, but one hot August day in 2019, it came back to him with such clarity that, at 53, now a stocky father of two, he suddenly understood it as a clue to his dangerously unhealthy relationship with alcohol. The day before, a team of specialists at the Royal Devon and Exeter hospital had given him an intravenous infusion of ketamine, a dissociative hallucinogen, in common use as an anaesthetic since the 1970s, and more recently one of a group of psychedelic drugs being hailed as a silver bullet in the fight to save our ailing mental health. To date, more than 100 patients with conditions as diverse as depression, PTSD and addiction have been treated in research settings across the UK, using a radical new intervention that combines psychedelic drugs with talking therapy. What was once a fringe research interest has become the foundation of a new kind of healthcare, one that, for the first time in modern psychiatric history, purports to not only treat but actually cure mental ill health. And if advocates are to be believed, that cure will be available on the NHS within the next five years. © 2021 Guardian News & Media 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: 27732 - Posted: 03.13.2021

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