Links for Keyword: Depression

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.


Links 61 - 80 of 1376

By Ellen Barry A new book by Dr. Thomas P. Insel, who for 13 years ran the United States’ foremost mental health research institution, begins with a sort of confession. During his tenure as the “nation’s psychiatrist,” he helped allocate $20 billion in federal funds and sharply shifted the focus of the National Institute of Mental Health away from behavioral research and toward neuroscience and genetics. “I should have been able to help us bend the curves for death and disability,” Dr. Insel writes. “But I didn’t.” Dr. Insel, 70, who left N.I.M.H. in 2015, calls the advances in neuroscience of the last 20 years “spectacular” — but in the very first pages of his new book, he says that, for the most part, they haven’t yet benefited patients. His book, “Healing: Our Path From Mental Illness to Mental Health,” is not an indictment of the science to which he devoted much of his adult life. Instead, it chronicles failures in virtually every other element of our mental health system, including the ineffective delivery of care, the gutting of community health services and the reliance on police and jails for crisis services. It also calls out a paradox: that the United States, a country that leads the world in spending on medical research, also stands out for its dismal outcomes in people with mental illnesses. Indeed, over the last three decades, even as the government invested billions of dollars in better understanding the brain, by some measures, those outcomes have deteriorated. The country’s long spell without breakthrough treatments can be attributed, in part, to the complexity of the brain. Dr. Insel rose through the ranks at a time of optimism that advances in neurobiology would lead to new treatments, and as head of N.I.M.H., as he put it, he “bet big on genomics.” But 20 years later, he said the role that genes play in schizophrenia and bipolar disorder has proven to be extraordinarily complex. “Each of those variants that have been discovered just account for a tiny, tiny amount of risk, so in aggregate, they’re probably significant, but you have to put a hundred of them together,” he said. “So we started doing bigger and bigger studies to find smaller and smaller effects.” © 2022 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: 28214 - Posted: 02.23.2022

ByElizabeth Pennisi The trillions of bacteria in and on our bodies can bolster our health and contribute to disease, but just which microbes are the key actors has been elusive. Now, a study involving thousands of people in Finland has identified a potential microbial culprit in some cases of depression. The finding, which emerged from a study of how genetics and diet affect the microbiome, “is really solid proof that this association could have major clinical importance,” says Jack Gilbert, a microbial ecologist at the University of California, San Diego, who was not involved with the work. Researchers are finding ever more links between brain conditions and gut microbes. People with autism and mood disorders, for example, have deficits of certain key bacteria in their guts. Whether those microbial deficits actually help cause the disorders is unclear, but the findings have spawned a rush to harness gut microbes and the substances they produce as possible treatments for a variety of brain disorders. Indeed, researchers recently reported in Frontiers in Psychiatry that fecal transplants improved symptoms in two depressed patients. Guillaume Méric didn’t set out to find microbes that cause depression. A microbial bioinformatician at the Baker Heart & Diabetes Institute, he and his colleagues were analyzing data from a large health and lifestyle study from Finland. Part of a 40-year effort to track down underlying causes of chronic disease in Finnish people, the 2002 study assessed the genetic makeup of 6000 participants, identified their gut microbes, and compiled extensive data about their diets, lifestyles, prescription drug use, and health. Researchers tracked the health of participants until 2018. Méric and his colleagues combed the data for clues to how a person’s diet and genetics affect the microbiome. “There have been very few studies that have examined [all these factors] in such detail,” Gilbert says. Two sections of the human genome seemed to strongly influence which microbes are present in the gut, the researchers report this week in Nature Genetics. One contains the gene for digesting the milk sugar lactose, and the other helps specify blood type. (A second study, also published today in Nature Genetics, identified the same genetic loci by analyzing the relationship between the genomes and gut microbes of 7700 people in the Netherlands.) © 2022 American Association for the Advancement of Science.

Related chapters from BN: 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: 28188 - Posted: 02.05.2022

ByRobert F. Service More than 50 years after the Summer of Love, psychedelics are again the rage. This time the love comes from doctors beginning to embrace psychedelics such as LSD and psilocybin to treat depression, substance abuse, and other serious mental health conditions. But because the drugs cause hallucinations, their medical use requires intensive monitoring by clinicians. That drives up treatment costs, making psychedelics impractical for widespread therapeutic use. In recent years, researchers have begun to tweak psychedelics’ chemical structures, aiming to make analogs that retain medical usefulness but don’t cause hallucinations. Now, researchers report in Science they’ve teased apart the molecular interactions responsible for psychedelics’ antidepressive effects from those that cause hallucinations. They used that knowledge to make new compounds that appear to activate brain cellular circuits that help relieve depression without triggering a closely related pathway involved in hallucinations. So far, the compounds have only been studied in mice. But if such psychedelic analogs work in humans, they could spawn new families of pharmaceuticals. “This work is going to generate a lot of interest,” says Bryan Roth, a pharmacologist at the University of North Carolina School of Medicine, whose lab is also seeking nonhallucinogenic psychedelic analogs. The need is profound. Mental or neurological disorders are estimated to affect roughly one-quarter of U.S. adults every year, and therapies often don’t work. LSD, psilocybin (the main ingredient in magic mushrooms), and other psychedelics might do better. Studies have shown a single dose of psilocybin can offer relief from depression for months at a time, and last year, a clinical trial of 3,4-methylenedioxymethamphetamine, or ecstasy, showed it can alleviate posttraumatic stress disorder. © 2022 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: 28177 - Posted: 01.29.2022

By Emily Witt In the fall of 1972, a psychiatrist named Salvador Roquet travelled from his home in Mexico City to the Maryland Psychiatric Research Center, an institution largely funded by the United States government, to give a presentation on an ongoing experiment. For several years, Roquet had been running a series of group-therapy sessions: over the course of eight or nine hours, his staff would administer psilocybin mushrooms, morning-glory seeds, peyote cacti, and the herb datura to small groups of patients. He would then orchestrate what he called a “sensory overload show,” with lights, sounds, and images from violent or erotic movies. The idea was to push the patients through an extreme experience to a psycho-spiritual rebirth. One of the participants, an American psychology professor, described the session as a “descent into hell.” But Roquet wanted to give his patients smooth landings, and so, eventually, he added a common hospital anesthetic called ketamine hydrochloride. He found that, given as the other drugs were wearing off, it alleviated the anxiety brought on by these punishing ordeals. Clinicians at the Maryland Psychiatric Research Center had been studying LSD and other psychedelics since the early nineteen-fifties, beginning at a related institution, the Spring Grove Hospital Center. But ketamine was new: it was first synthesized in 1962, by a researcher named Calvin Stevens, who did consulting work for the pharmaceutical company Parke-Davis. (Stevens had been looking for a less volatile alternative to phencyclidine, better known as PCP.) Two years later, a doctor named Edward Domino conducted the first human trials of ketamine, with men incarcerated at Jackson State Prison, in Michigan, serving as his subjects. At higher doses, Domino noticed, ketamine knocked people out, but at lower ones it produced odd psychoactive effects on otherwise lucid patients. Parke-Davis wanted to avoid characterizing the drug as psychedelic, and Domino’s wife suggested the term “dissociative anesthetic” to describe the way it seemed to separate the mind from the body even as the mind retained consciousness. The F.D.A. approved ketamine as an anesthetic in 1970, and Parke-Davis began marketing it under the brand name Ketalar. It was widely used by the U.S. military during the Vietnam War, and remains a standard anesthetic in emergency rooms around the world. © 2021 Condé Nast.

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: 28132 - Posted: 12.31.2021

By Vanessa Barbara JUIZ DE FORA, Brazil — My first encounter with ketamine did not go well. A lifelong depressive — I picked up the habit of despairing sadness in early adulthood, and it remained faithfully with me — I’d turned to a more experimental form of treatment: ketamine infusions, in which a kindly anesthesiologist funnels the drug into a sad person’s veins for around 50 minutes and hopes it perks her up. Forty-five minutes into my first session, I rather anxiously asked my partner, who was in the room with me, if our 3-year-old daughter was fine. He decided it was the perfect time for a joke. Our daughter, he answered, was safe at home — and as a matter of fact, he added, she was already a very independent 15-year-old. I panicked. While under the strong, dissociative effect of the drug, patients sometimes enter what’s called a k-hole, in which their sense of time and space is distorted or eliminated. In that state of oblivion, I found it entirely plausible that my daughter was not a toddler anymore, but a strong-willed teenager. I became very distressed. My heartbeat accelerated. The anesthesiologist hurriedly ended the session as my partner said: “I’m kidding! Sorry! She’s still 3!” It was an inauspicious start, but I was determined to make the best of it. Ketamine, long used as an anesthetic but better known as an illegal party drug and, of course, a horse tranquilizer, has in recent years been gaining traction as an antidepressant. People have written enthusiastic accounts of their experiences, and researchers and psychiatrists, in a cascade of studies, have pointed to its possible benefits, not least the speed with which it can alleviate symptoms. Today, hundreds of clinics around the world provide infusions to people who have found little, if any, improvement with other treatments. That’s where I come in. Over the years, apart from the good old psychotropic medications, I have tried several types of talk therapy, meditation, acupuncture, singing lessons, bungee jumping and transcranial magnetic stimulation. (I still have sweet memories of the woodpecker sounds tapped into my brain.) © 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: 28130 - Posted: 12.29.2021

L. Carol Ritchie U.S. Surgeon General Vivek Murthy has a warning about the mental health of young people. Murthy told Morning Edition that children and young adults were already facing a mental health crisis before the coronavirus pandemic began: One in three high school students reported persistent feelings of sadness or hopelessness, a 40% increase from 2009 to 2019, he said. Suicide rates went up during that time by 57% among youth ages 10 to 24. During the pandemic, rates of anxiety and depression have increased, he said. The pandemic has made the issues behind the mental health crisis only worse, he said. "This is a critical issue that we have to do something about now," he said. "We can't wait until after the pandemic is over." Murthy, who issued an advisory called "Protecting Youth Mental Health," also cites gun violence, the specter of climate change, racism and social conflict as sources of stress. "We also have to recognize that kids increasingly are experiencing bullying, not just in school but online, that they're growing up in a popular culture and a media culture that reminds kids often that they aren't good-looking enough, thin enough, popular enough, rich enough, frankly, just not enough," he said. Article continues after sponsor message "Even to this day, even though I have parents who I know unconditionally loved me, I never felt comfortable telling them about it because I thought that this was my fault. I don't want that to be the reality for my children, who are 4 and 5 and growing up, you know, in this very complicated world." © 2021 npr

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: 28101 - Posted: 12.08.2021

By Laura Sanders Kanu Caplash was lying on a futon in a medical center in Connecticut, wearing an eye mask and listening to music. But his mind was far away, tunneling down through layer upon layer of his experiences. As part of a study of MDMA, a psychedelic drug also known as molly or ecstasy, Caplash was on an inner journey to try to ease his symptoms of post-traumatic stress disorder. On this particular trip, Caplash, now 22, returned to the locked bathroom door of his childhood home. As a kid, he used to lock himself in to escape the yelling adults outside. But now, he was both outside the locked door, knocking, and inside, as his younger, frightened self. He started talking to his younger self. “I open the door, and my big version picks up my younger version of myself, and literally carries me out,” he says. “I carried myself out of there and drove away.” That self-rescue brought Caplash peace. “I got out of there. I’m alive. It’s all right. I’m OK.” For years, Caplash had experienced flashbacks, nightmares and insomnia from childhood trauma. He thought constantly about killing himself, he says. His experiences while on MDMA changed his perspective. “I still have the memory, but that anger and pain is not there anymore.” Caplash’s transcendent experiences, spurred by three therapy sessions on MDMA, happened in 2018 as part of a research project on PTSD. Along with a handful of other studies, that research suggests that when coupled with psychotherapy, mind-altering drugs bring some people immediate, powerful and durable relief. © Society for Science & the Public 2000–2021.

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: 28099 - Posted: 12.04.2021

By Kelly Servick For patients whose depression resists treatment with drugs and electroconvulsive therapy, surgically implanted wires that stimulate the brain might bring relief. But in recent years, two randomized, controlled trials of this approach, known as deep brain stimulation (DBS), were halted after underwhelming results in interim analyses. “It was like the air was let out of the room,” Sameer Sheth, a neurosurgeon at Baylor College of Medicine, says of those results. “It was a big let-down.” Now, researchers are testing more sophisticated, personalized DBS techniques they hope will yield stronger results. The tests to date have involved just one or a few patients, far from proof of effectiveness. But researchers hope they’ll inform larger studies that finally cement the effectiveness of DBS in depression. “With all these irons in the fire … we will hopefully build up enough understanding and evidence,” says Sheth, an author of a case study published this week. DBS is already approved in the United States to treat epilepsy, obsessive compulsive disorder, and movement disorders such as Parkinson’s disease. Could it also shift patterns of abnormal activity in neural circuits that may drive depression symptoms? Early studies without control groups yielded promising results, but two randomized, controlled trials, sponsored by the medical device companies Medtronic and St. Jude Medical, Inc. (which was later acquired by Abbott Laboratories) did not show significant benefits after several months of DBS, teams reported in 2015 and 2017. Long-term follow-up of participants has revived some optimism. For example, many people in the 30-participant Medtronic trial improved over 1 year or more—beyond the timeline of the initial study, says Stanford University psychiatrist Mahendra Bhati, a co-investigator. Last month, he and colleagues published a follow-up study of eight trial patients, most of whom continue to use their implant about 10 years later. About one-half have had at least a 50% improvement over their pretreatment score on a depression scale. © 2021 American Association for the Advancement of Science.

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: 28089 - Posted: 11.24.2021

Chloe Tenn Depression affects almost 300 million people globally, and is considered a leading cause of disability by the World Health Organization. As with many diseases, studies that have searched for genetic variations associated with depression have been conducted primarily in people of European ancestry, and there is limited data available on genes linked to depression in non-European ancestry groups. Finding such genetic variations can not only help in assessing individuals’ likelihood of developing depression, but potentially provide insight into how to treat the mental illness by pinpointing the genes and proteins that underlie it. See “Our Aching Brains” Researchers have now conducted the largest genomic study to date on depression in a non-European population, focusing on participants with East Asian ancestry. In a study published on September 29 in JAMA Psychiatry, they reveal that not only were a majority of genetic variants associated with depression in European populations not applicable in East Asian ancestral cohorts, but novel indicators emerged in East Asians that had not been discovered in studies on Europeans. The study’s authors caution that the existing knowledge on genetic risk factors for depression is not generalizable to a global population. “I think it’s a strikingly ambitious effort,” says Andrew Ryder, a cultural-clinical psychologist who specializes in East Asian cultures at Concordia University in Montreal who was unaffiliated with the study. “I see this research as establishing that, even in the hard science aspects of studying humanity, you can’t ignore the social world and the potential influence of culture. . . . It’s too easy for people to assume if we’re doing something scientific, it must be true of people everywhere in the world, rather than building culture into their sense of how their science works.” © 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: 28076 - Posted: 11.17.2021

Sarah Marsh and Hannah Devlin A growing number of private clinics are offering ketamine for depression, according to experts who warn of a potential “wild west” of providers with no national register of patients’ treatment being integrated into overall NHS care. At least six private providers in the UK offer the drug for depression. In March the first service that also includes psychotherapy opened in Bristol, charging £6,000 for a course of low-dose treatments and talking therapy. But health experts expressed concern about creating a two-tier system in which the novel treatment is unavailable to NHS patients. They also warned of “doctor shopping”, where patients go to a ketamine clinic one day and another the next without health professionals being able to keep track of who is getting the drug. Scientists said the NHS healthcare watchdog was taking too long to update its guidance informing clinical practice on prescribing antidepressants in the UK. It was last updated in 2009. Ketamine has a reputation as a party drug because of its short-term dissociative effects but is licensed as an anaesthetic. When abused, the drug can cause long-term problems such as ulcers, pain in the bladder and kidney problems. But it has shown potential in depression treatment trials for those who are resistant to other treatments. Because ketamine is licensed to be used by doctors as an anaesthetic it can be prescribed off-licence for depression, which is what is happening in private clinics. To be prescribed on the NHS, it would need to be approved by the National Institute for Health and Care Excellence (Nice) as a cost-effective treatment. Ketamine would also need to be authorised by the Medicines and Healthcare Regulatory Agency to be marketed as a treatment for depression. © 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: 28073 - Posted: 11.13.2021

By Brianna Randall Inside the Big Sky Ketamine Care clinic in Missoula, Montana, a woman relaxes in a leather recliner as soothing classical music pipes through the speakers. She watches nature scenes flicker across a TV screen as a low dose of ketamine drips into her arm for 40 minutes. A nurse monitors vitals and sits beside the woman as her mind drifts — and hopefully heals. The Montana business is just one example of the recent boom in ketamine treatment, which uses a sedative also known as an animal tranquilizer or a club drug nicknamed “Special K.” This alternative therapy option for treating mood disorders has grown in popularity as patients and medical providers look to fast-acting options for the 264 million people worldwide who suffer from depression. It’s the only legal psychedelic currently available in the U.S., though psilocybin was recently legalized for therapy in Oregon. Providers and many researchers say ketamine can alleviate anxiety or depression symptoms, including suicidality, in a matter of hours; commonly prescribed oral antidepressants, like Zoloft or Prozac, on the other hand, often take weeks before they kick-in. Still, along with its promise in psychiatric treatment, ketamine faces cultural distrust and lingering questions, especially surrounding its main side effect: feeling high, or a dissociated sense that you are separate from your mind, body and surroundings. Scientists still don’t know the exact pathways by which ketamine alleviates mood disorders, but recent research about how ketamine works in the brain — as well as how best to use it in clinical settings — may help overcome some of the distrust. © 2021 Kalmbach Media Co.

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: 28048 - Posted: 10.23.2021

By Jane E. Brody It’s no surprise that when a person gets a diagnosis of heart disease, cancer or some other life-limiting or life-threatening physical ailment, they become anxious or depressed. But the reverse can also be true: Undue anxiety or depression can foster the development of a serious physical disease, and even impede the ability to withstand or recover from one. The potential consequences are particularly timely, as the ongoing stress and disruptions of the pandemic continue to take a toll on mental health. The human organism does not recognize the medical profession’s artificial separation of mental and physical ills. Rather, mind and body form a two-way street. What happens inside a person’s head can have damaging effects throughout the body, as well as the other way around. An untreated mental illness can significantly increase the risk of becoming physically ill, and physical disorders may result in behaviors that make mental conditions worse. In studies that tracked how patients with breast cancer fared, for example, Dr. David Spiegel and his colleagues at Stanford University School of Medicine showed decades ago that women whose depression was easing lived longer than those whose depression was getting worse. His research and other studies have clearly shown that “the brain is intimately connected to the body and the body to the brain,” Dr. Spiegel said in an interview. “The body tends to react to mental stress as if it was a physical stress.” Despite such evidence, he and other experts say, chronic emotional distress is too often overlooked by doctors. Commonly, a physician will prescribe a therapy for physical ailments like heart disease or diabetes, only to wonder why some patients get worse instead of better. © 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: 28034 - Posted: 10.13.2021

By Laura Sanders A personalized brain implant eased the crushing symptoms of a woman’s severe depression, allowing her to once again see the beauty of the world. “It’s like my lens on the world changed,” said Sarah, the research volunteer who requested to be identified by her first name only. The technology, described October 4 in Nature Medicine, brings researchers closer to understanding how to detect and change brain activity in ultraprecise ways (SN: 2/10/19). The device was bespoke; it was built specifically for Sarah’s brain. The details of the new system may not work as a treatment for many other people, says Alik Widge, a psychiatrist and neural engineer at the University of Minnesota in Minneapolis. Still, the research is “a really significant piece of work,” he says, because it points out a way to study how brain activity goes awry in depression. Researchers at the University of California, San Francisco implanted temporary thin wire electrodes into Sarah’s brain. The 36-year-old woman had suffered from severe depression for years. These electrodes allowed researchers to monitor the brain activity that corresponded to Sarah’s depression symptoms — a pattern that the researchers could use as a biomarker, a signpost of trouble to come. In Sarah’s case, a particular sign emerged: a fast brain wave called a gamma wave in her amygdala, a brain structure known to be involved in emotions. With this biomarker in hand, the researchers then figured out where to stimulate the brain to interrupt Sarah’s distressing symptoms. A region called the ventral capsule/ventral striatum, or VC/VS, seemed to be the key. That’s not surprising; previous research suggests the region is involved with feeling good and other emotions. When researchers applied tiny jolts of electrical current to this region, Sarah’s mood improved. © Society for Science & the Public 2000–2021.

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: 28022 - Posted: 10.06.2021

By Christina Caron For about 1 in 20 people in the northern half of the United States, cooling temperatures and shorter, darker days may signal the onset of seasonal affective disorder, or SAD, a type of depression that typically arrives in the fall or winter, then goes away in the spring. Unlike mild cases of the “winter blues,” SAD symptoms make it difficult to function. It tends to start with so-called “vegetative symptoms”: an increased appetite and a craving for carbohydrates like french fries or ice cream, the urge to sleep longer hours, difficulty getting up in the morning and feeling wiped out at work. Then, in three to four weeks, “the mood plummets,” said Michael Terman, a professor of clinical psychology at Columbia University and an expert in seasonal affective disorder. Patients with SAD develop major depression, which includes persistent feelings of sadness, withdrawal from friends and family and a loss of interest in activities that were once enjoyable. Researchers don’t yet know why some people develop SAD and others do not, but the disorder is believed to run in families and is more common among women. SAD develops in the fall and winter because shorter daylight hours and less sunlight shift the body’s internal clock, and certain mood-regulating hormones, like serotonin, oscillate with the seasons. The good news is that because SAD is tied to the changing seasons, “you can predict its onset and ward it off,” Dr. Terman said. If you have already started experiencing vegetative symptoms — for example you are sleeping longer and having more difficulty waking up — or if you already know you are susceptible to seasonal affective disorder, experts said it’s best to start implementing preventive measures before major depression sets in. © 2021 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 28018 - Posted: 10.02.2021

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