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Ketamine Shows Promise for Hard-to-Treat Depression in New Study

By Christina Caron A new study suggests that, for some patients, the anesthetic ketamine is a promising alternative to electroconvulsive therapy, or ECT, currently one of the quickest and most effective therapies for patients with difficult-to-treat depression. The study is the largest head-to-head comparison of the two treatments. Patients who don’t respond to at least two antidepressants — about one-third of clinically depressed patients — have a condition that clinicians refer to as “treatment-resistant.” Their options for relief are limited. Doctors typically recommend up to 12 sessions of ECT, which has a long-established efficacy, but is tainted by the stigma of historical misuse and frightening Hollywood images of people strapped to tables, writhing in agony. Today’s ECT is much safer and done under general anesthesia, but the procedure remains underutilized. The study, published on Wednesday in The New England Journal of Medicine, found that ketamine, when administered intravenously, was at least as effective as ECT in patients with treatment-resistant depression who do not have psychosis. (For people with psychosis, ketamine, even in very low doses, can worsen psychosis-like symptoms.) “The results were very surprising to us,” said Dr. Amit Anand, lead author of the study and a professor of psychiatry at Harvard Medical School who studies mood disorders at Mass General Brigham. His team had initially hypothesized that ketamine would be nearly as effective as ECT. Instead, Dr. Anand said, they found that ketamine performed even better than that. This is significant in part because some patients are uncomfortable with ECT’s potential side effects, such as temporary memory loss, muscle pain or weakness. (In rare cases it can result in permanent gaps in memory.) © 2023 The New York Times Company

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: 28806 - Posted: 05.31.2023

Ketamine no better than placebo at alleviating depression

By Claudia Lopez Lloreda Ketamine is a powerful anesthetic and sometimes recreational drug that causes people to feel dissociated from their own bodies. Recent studies suggest the drug may help treat people with depression who have tried more conventional treatments without success. But there are major questions about what makes it work. Is it the weird dissociative experience? Some molecular effect on the brain? Or just the experience of being in a clinical trial? In a new study that is yet to be peer reviewed, researchers attempted to find the answer in a unique way: They gave volunteers ketamine while they were under general anesthesia, theoretically preventing the participants from going on a trip. The approach alleviated the subjects’ depression, but not any better than a placebo did. The authors interpret this as evidence that ketamine’s effects on depression are strongly tied to a patient’s experience of being seen by medical professionals. But other experts say the study’s implications may be more complicated. Ketamine causes “dissociative” effects such as out-of-body experiences. Patients sometimes also report visual and auditory hallucinations—the voices of friends and family members who aren’t there, for example. The dissociative effects of ketamine have been linked to a stronger antidepressant response, possibly by helping patients reframe their experience from an outside perspective. But it’s a problem for researchers running double-blinded clinical trials, as participants can usually tell whether they have received ketamine or a placebo. To disentangle the subjective experience of ketamine from the biochemical effects of the drug, researchers at Stanford University recruited 40 participants who were preparing to undergo general surgery and who also had mild to moderate depression. The scientists gave the volunteers ketamine or saline as placebo right after they were put under anesthesia, but before their surgery, essentially blinding them to any psychedelic or dissociative effects. Then, for the next 3 days, the researchers surveyed the participants on their depression symptoms, scoring them on such factors as sadness, loss of appetite, and lack of sleep.

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: 28789 - Posted: 05.21.2023

The great serotonin debate: do depression treatments work by boosting the happy hormone?

Hannah Devlin Daniela da Silva is feeling good. Lying cocooned under fleece blankets inside a medical scanner, her eyes are closed and her mind is focused and remarkably unperturbed by negative thoughts. Three hours earlier, the 39-year-old yoga teacher and neuroscience student was given a dose of the stimulant drug dextroamphetamine, which is often used to treat ADHD. “I’m having a serotonin increase. Oh definitely,” she predicts before entering the PET scanner. Da Silva is a healthy volunteer in a trial using a pioneering brain imaging technique designed to measure serotonin changes in the brains of living people. Last year, scientists used the scan to obtain what they claimed to be the first direct evidence that serotonin release is blunted in the brains of people with depression. The findings added fuel to a fiercely fought debate over the role of the brain chemical – if any – in depression. Just months earlier, a high-profile scientific review caused a stir when it reached the opposite conclusion that “after a vast amount of research, conducted over several decades, there is no convincing evidence” for the idea that depression is caused by a chemical imbalance in the brain. To many, it was news that the case for serotonin being implicated in depression was not already watertight. The idea of a chemical imbalance is embedded in public consciousness and has shaped the way we view mental illness. The main class of antidepressant drugs, selective serotonin reuptake inhibitors (SSRIs), are widely assumed to work by boosting serotonin levels. So the suggestion that the way we discuss, and treat, mental illness might be based on shaky foundations was disconcerting. But it also served as a wake-up call that this view of depression has failed to provide effective treatments for a substantial proportion of those affected. Serotonin is sometimes referred to as the “happy hormone”, conjuring up the image of a substance that swooshes through the brain leaving a warm glow of contentment in its wake. In reality, its biological role is complex and extends to basic functions like the regulation of sleep, intestinal activity and the formation of blood clots. In the brain, serotonin acts as a chemical messenger between neurons, but also as a form of volume control that alternately increases or decreases the level of communication between other neurons. “Put another way, serotonin fine-tunes the working of the brain, regulating how different parts of the brain communicate with each other,” says Dr James Rucker, a consultant psychiatrist at South London and Maudsley NHS foundation trust, whose research focuses on developing new treatments for depression. © 2023 Guardian News & Media Limited

Fetterman’s Disclosure of Depression Signals New Openness on Mental Health

By Sheryl Gay Stolberg and Ellen Barry Lynn Rivers, a Democrat from Michigan, opened up about her diagnosis with bipolar disorder during a radio call-in show when she first ran for Congress. Her opponents had been hinting she had mental health problems. She decided, spur of the moment, to let it out. “Finally, I just said, ‘Are you asking me if I have depression? Yes, and so do thousands and millions of other people,’” she recalled. “I was like, ‘OK, here we go. The ball is thrown at you, just hit it.’ And so I did.” That was 1994. Ms. Rivers was elected, despite a Republican tidal wave, and served four terms. Now another Democrat, Senator John Fetterman of Pennsylvania, has announced that he has entered a hospital to be treated for clinical depression. Politicians of both parties are praising him for his openness. Mental health experts say he is a powerful symbol — especially for men, who are less likely to seek treatment for depression and suffer higher rates of suicide. Yet the stigma around mental illness remains strong — especially in politics, where questions about temperament can determine a candidate’s electability. Mr. Fetterman and others face a continuing challenge: How much do they really want to say? “We’ve come a long way; people are willing to say they have a diagnosis or that they’re going to therapy,” said Patrick J. Kennedy, a scion of the political Kennedy family, who disclosed his treatment for bipolar disorder and drug abuse when he was a congressman from Rhode Island. “But we’re still not in a place where people are comfortable saying any more than that. And really the question with Senator Fetterman is: How much is he going to disclose?” Clinical depression, also called major depression, is a severe form of the disease. Symptoms may include feelings of sadness, hopelessness or guilt; angry outbursts; loss of pleasure in ordinary activities; fatigue; anxiety; reduced appetite; and thoughts of suicide. In recent years, there have been great strides in treatment. © 2023 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 28671 - Posted: 02.18.2023

A chemical imbalance doesn’t explain depression. So what does?

By Laura Sanders You’d be forgiven for thinking that depression has a simple explanation. The same mantra — that the mood disorder comes from a chemical imbalance in the brain — is repeated in doctors’ offices, medical textbooks and pharmaceutical advertisements. Those ads tell us that depression can be eased by tweaking the chemicals that are off-kilter in the brain. The only problem — and it’s a big one — is that this explanation isn’t true. The phrase “chemical imbalance” is too vague to be true or false; it doesn’t mean much of anything when it comes to the brain and all its complexity. Serotonin, the chemical messenger often tied to depression, is not the one key thing that explains depression. The same goes for other brain chemicals. The hard truth is that despite decades of sophisticated research, we still don’t understand what depression is. There are no clear descriptions of it, and no obvious signs of it in the brain or blood. The reasons we’re in this position are as complex as the disease itself. Commonly used measures of depression, created decades ago, neglect some important symptoms and overemphasize others, particularly among certain groups of people. Even if depression could be measured perfectly, the disorder exists amid myriad levels of complexity, from biological confluences of minuscule molecules in the brain all the way out to the influences of the world at large. Countless combinations of genetics, personality, history and life circumstances may all conspire to create the disorder in any one person. No wonder the science is stuck. So here, up front, is your fair warning: There will be no satisfying wrap-up at the end of this story. You will not come away with a scientific explanation for depression, because one does not exist. But there is a way forward for depression researchers, Aftab says. It requires grappling with nuances, complexity and imperfect data. © Society for Science & the Public 2000–2023.

The Cause of Depression Is Probably Not What You Think

By Joanna Thompson People often think they know what causes chronic depression. Surveys indicate that more than 80% of the public blames a “chemical imbalance” in the brain. That idea is widespread in pop psychology and cited in research papers and medical textbooks. Listening to Prozac, a book that describes the life-changing value of treating depression with medications that aim to correct this imbalance, spent months on the New York Times bestseller list. The unbalanced brain chemical in question is serotonin, an important neurotransmitter with fabled “feel-good” effects. Serotonin helps regulate systems in the brain that control everything from body temperature and sleep to sex drive and hunger. For decades, it has also been touted as the pharmaceutical MVP for fighting depression. Widely prescribed medications like Prozac (fluoxetine) are designed to treat chronic depression by raising serotonin levels. Yet the causes of depression go far beyond serotonin deficiency. Clinical studies have repeatedly concluded that the role of serotonin in depression has been overstated. Indeed, the entire premise of the chemical-imbalance theory may be wrong, despite the relief that Prozac seems to bring to many patients. If you were still of the opinion that it was simply a chemical imbalance of serotonin, then yeah, it’s pretty damning. A literature review that appeared in Molecular Psychiatry in July was the latest and perhaps loudest death knell for the serotonin hypothesis, at least in its simplest form. An international team of scientists led by Joanna Moncrieff of University College London screened 361 papers from six areas of research and carefully evaluated 17 of them. They found no convincing evidence that lower levels of serotonin caused or were even associated with depression. People with depression didn’t reliably seem to have less serotonin activity than people without the disorder. Experiments in which researchers artificially lowered the serotonin levels of volunteers didn’t consistently cause depression. Genetic studies also seemed to rule out any connection between genes affecting serotonin levels and depression, even when the researchers tried to consider stress as a possible cofactor. All Rights Reserved © 2023

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: 28647 - Posted: 01.27.2023

How antidepressants help bacteria resist antibiotics

Liam Drew The emergence of disease-causing bacteria that are resistant to antibiotics is often attributed to the overuse of antibiotics in people and livestock. But researchers have homed in on another potential driver of resistance: antidepressants. By studying bacteria grown in the laboratory, a team has now tracked how antidepressants can trigger drug resistance1. “Even after a few days exposure, bacteria develop drug resistance, not only against one but multiple antibiotics,” says senior author Jianhua Guo, who works at the Australian Centre for Water and Environmental Biotechnology at the University of Queensland in Brisbane. This is both interesting and scary, he says. Globally, antibiotic resistance is a significant public-health threat. An estimated 1.2 million people died as a direct result of it in 20192, and that number is predicted to climb. Early clues Guo became interested in the possible contributions of non-antibiotic drugs to antibiotic resistance in 2014, after work by his lab found more antibiotic-resistance genes circulating in domestic wastewater samples than in samples of wastewater from hospitals, where antibiotic use is higher. Guo’s group and other teams also observed that antidepressants — which are among the most widely prescribed medicines in the world — killed or stunted the growth of certain bacteria. They provoke “an SOS response”, Guo explains, triggering cellular defence mechanisms that, in turn, make the bacteria better able to survive subsequent antibiotic treatment. © 2023 Springer Nature Limited

Antidepressants can cause ‘emotional blunting’

Hannah Devlin Science correspondent Widely used antidepressants cause “emotional blunting”, according to research that offers new insights into how the drugs may work and their possible side-effects. The study found that healthy volunteers became less responsive to positive and negative feedback after taking a selective serotonin reuptake inhibitor (SSRI) drug for three weeks. The “blunting” of negative emotions could be part of how the drugs help people recover from depression, but could also explain a common side-effect. The work’s senior author, Prof Barbara Sahakian of the University of Cambridge, said: “In a way, this may be in part how they work. They take away some of the emotional pain that people who experience depression feel, but unfortunately it seems that they also take away some of the enjoyment.” The findings could help patients make better informed choices about their medication, she said, but added “there is no doubt that antidepressants are beneficial” for many patients. According to the NHS more than 8.3 million patients in England received an antidepressant drug in 2021-22. SSRIs are among the most widely used, and are effective for the majority of, although not all, patients. Some people on the medication report feeling emotionally dull or no longer finding things as pleasurable, with one study suggesting this applied to 40-60% of people taking the drug. However, it has been unclear whether this symptom is a drug side-effect or a symptom of depression. The latest work suggests that the drug alone can produce emotional blunting. In the study, published in the journal Neuropsychopharmacology, 66 volunteers were given either the SSRI drug, escitalopram, or a placebo for at least 21 days before doing a set of cognitive tests. © 2023 Guardian News & Media Limited

She was headed to a locked psych ward. Then an ER doctor made a startling discovery.

By Sandra G. Boodman The 23-year-old patient arrived in the back of a police car and was in four point restraints — hands and feet strapped to a gurney — when emergency physician Elizabeth Mitchell saw her at a Los Angeles hospital early on March 17. Chloe R. Kral was being held on a 5150, shorthand in California for an emergency psychiatric order that allows people deemed dangerous to themselves or others to be involuntarily confined for 72 hours. She had spent the previous six months at a private treatment center receiving care for bipolar disorder and depression. Chloe had improved and was set to move to transitional housing when she suddenly became combative and threatened to harm staff and kill herself. Police had taken her to the emergency room at Cedars-Sinai Marina del Rey Hospital before a planned transfer to a mental hospital. Chloe, Mitchell recalled, was “mumbling about Rosa Parks” when they met. She managed to tell the doctor that she hadn’t used drugs or alcohol, but was otherwise incoherent. “We get a lot of psychiatric patients, and they’re just waiting for placement,” Mitchell said. But something indefinable — Mitchell characterized it as “maybe gut instinct” honed by nearly two decades of practice — prompted her to order a CT scan of Chloe’s head to better assess her mental status. When she pulled up the image, Mitchell gasped. “I had never seen anything like it,” she said. She rounded up her colleagues and “made everyone in the whole ER come look.” “I was speechless,” she said. “All I could think was ‘How did no one figure this out?’ ”

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 28603 - Posted: 12.21.2022

Study finds first direct evidence of a link between low serotonin and depression

Hannah Devlin Science correspondent Scientists claim to have found the first direct evidence that people with depression have a reduced capacity for releasing serotonin in the brain. The findings from a brain-imaging study reignite a debate within psychiatry over the so-called serotonin hypothesis of depression and challenge the conclusions of an influential review published in July that found “no clear evidence” that low serotonin levels are responsible. The latest work, led by scientists at Imperial College London, suggested that people with depression have a decreased serotonin response. “This is the first direct evidence that the release of serotonin is blunted in the brains of people with depression,” said Prof Oliver Howes, a consultant psychiatrist based at Imperial College and King’s College London, and a co-author. “People have been debating this question for 60 years, but it’s all been based on indirect measures. So this is a really important step.” The serotonin hypothesis arose from evidence from postmortem brains and blood samples that suggested a serotonin deficit could be involved in depression. The theory provides a plausible biological mechanism for how the main class of antidepressant drugs, selective serotonin reuptake inhibitors (SSRIs), are effective, and is why the brain chemical is sometimes referred to as a “happy hormone”. However, there is not yet conclusive evidence that serotonin abnormalities are the underlying cause of depression and resolving this question is seen as crucial to providing better treatments. The latest paper adds weight to the view that serotonin plays a role and demonstrates a new brain imaging technique that could pave the way to a better understanding of why SSRI drugs fail to help an estimated 10% to 30% of patients. “It’s the closest anyone has been able to get so far,” said Howes. “It’s hard to measure these transmitters in the brains of living people. We can’t put a pipette in there and take a sample. This is the closest we’re likely to come.” © 2022 Guardian News & Media Limited o

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: 28541 - Posted: 11.05.2022

Psychedelic mushroom dose can treat stubborn depression,

By Leo Sands Psilocybin, the active hallucinogen found in psychedelic mushrooms — also known as “magic mushrooms” — can effectively alleviate a severe bout of depression when administered in a single dose and combined with talk therapy, a new clinical study found. Adults with depression who were administered a single 25-miligram dose of psilocybin were more likely to experience significant improvements in their mental health — both immediately and for up to three months — than others who were randomly assigned smaller doses of the same drug, said the peer-reviewed study, which was published Wednesday in the New England Journal of Medicine. “There’s something about the psychedelic experience that leads to a rapid resolution of depression symptoms,” said James Rucker, a consultant psychiatrist at King’s College London who worked on the trial. “We don’t really know what that is at the moment, but it’s very different to standard antidepressants.” The trial’s findings could be an encouraging sign for the 16 million Americans estimated each year by the Centers for Disease Control and Prevention to have depression, many of whom struggle to find treatments that work for them. Its authors hope the study — which was relatively small, with just 79 participants receiving the 25 mg dose — will pave the way for eventual regulatory approval of psilocybin by the Food and Drug Administration for use as a drug against depression. The new study randomly assigned 233 adults with depression three doses of psilocybin — 25 mg, 10 mg and 1 mg — across 22 sites in 10 countries. The authors found that the group given the largest dose recorded the most significant improvements in their depression, both immediately and for several weeks after.

Smiling faces might help the drug ketamine keep depression at bay

Jon Hamilton Computer games designed to boost self-esteem appear to prolong the antidepressant benefits of the mind-bending anesthetic ketamine. A recent study of 154 people found that those who played games featuring smiling faces and positive messages remained free of depression up to three months after a ketamine infusion, a team reports in the American Journal of Psychiatry. People who got ketamine alone tended to relapse after a week or two. The results are important because "we need new approaches that help people get feeling better faster and help them stay feeling better," says Rebecca Price, an author of the study and an associate professor of psychiatry and psychology at the University of Pittsburgh. Established drugs like Prozac and Zoloft can take weeks to ease depression, and don't work for every patient. Ketamine can offer immediate relief, but the effects often fade after a few days or weeks. "And then returning for infusions over and over to keep that relief going can end up being really burdensome and costly," Price says, "and just isn't accessible to all patients." So Price and a team of researchers wanted to find a way to make ketamine's antidepressant effects last longer. They decided to focus on a common symptom of depression: low self-esteem and self-loathing. The team drew on research suggesting that ketamine temporarily causes certain brain areas to enter a state in which they form lots of new connections. During this period, the brain seems to be more receptive to learning and change. "So we tried to use that window of opportunity just after ketamine to strengthen associations specifically between the idea of me, myself, and positive information and attributes," Price says. © 2022 npr

Is It Safe to Drink Alcohol While Taking S.S.R.I.s?

By Jyoti Madhusoodanan Q: I recently started taking an S.S.R.I. antidepressant, but I have been confused about whether it’s safe to drink alcohol. Some internet sources say it’s fine, others say to avoid drinking completely. Help! For many health care providers who treat anxiety and depression, the concern about whether it’s safe — or even advised — to drink alcohol while taking an antidepressant is a common one. “Patients tell me all the time, ‘I’m going to be drinking with friends tonight, so I skipped a dose,’” said Dr. Sarah Ramsay Andrews, a psychiatrist at the Johns Hopkins University School of Medicine. But skipping a dose is never a good idea, said Dr. Jody Glance, an addiction medicine specialist at the University of Pittsburgh Medical Center Western Behavioral Health — even if you’re going out for cocktails with friends. “When people stop taking their medicines for a day or two, they often don’t resume, and that can lead to a relapse of anxiety or depression.” Besides, she added, how safe it is to drink while on antidepressants depends on the kind of antidepressant you’re taking — and for most people taking selective serotonin reuptake inhibitors (or S.S.R.I.s), an occasional drink likely won’t do much harm. There are, however, caveats to keep in mind. S.S.R.I. medications — which include citalopram (Celexa), sertraline (Zoloft) and escitalopram (Lexapro) — are the most commonly prescribed class of antidepressants. They are typically used to help treat depression, and can also be effective for other conditions like anxiety, obsessive compulsive disorder, certain phobias and even premenstrual dysphoric disorder. They work by increasing the levels of the brain chemical serotonin — which is thought to influence your mood and emotions, among other things — by blocking its removal after it carries messages in the brain. But unlike many other medications used to treat mood disorders — like the anxiety medication alprazolam (Xanax) or the tricyclic antidepressant amitriptyline (Elavil) — S.S.R.I.s are less likely to interact with alcohol than other kinds of drugs, Dr. Glance said. © 2022 The New York Times Company

These LSD-based drugs seem to help mice with anxiety and depression — without the trip

Jon Hamilton Drugs like magic mushrooms and LSD can act as powerful and long-lasting antidepressants. But they also tend to produce mind-bending side-effects that limit their use. Now, scientists report in the journal Nature that they have created drugs based on LSD that seem to relieve anxiety and depression – in mice – without inducing the usual hallucinations. "We found our compounds had essentially the same antidepressant activity as psychedelic drugs," says Dr. Bryan Roth, an author of the study and a professor of pharmacology at UNC Chapel Hill School of Medicine. But, he says, "they had no psychedelic drug-like actions at all." The discovery could eventually lead to medications for depression and anxiety that work better, work faster, have fewer side effects, and last longer. The success is just the latest involving tripless versions of psychedelic drugs. One previous effort created a hallucination-free variant of ibogaine, which is made from the root bark of a shrubby plant native to Central Africa known as the iboga tree. "It's very encouraging to see multiple groups approach this problem in different ways and come up with very similar solutions," says David E. Olson, a chemical neuroscientist at the University of California, Davis, who led the ibogaine project. The new drug comes from a large team of scientists who did not start out looking for an antidepressant. They had been building a virtual library of 75 million molecules that include an unusual structure found in a number of drugs, including the psychedelics psilocybin and LSD, a migraine drug (ergotamine), and cancer drugs including vincristine. The team decided to focus on molecules that affect the brain's serotonin system, which is involved in regulating a person's mood. But they still weren't looking for an antidepressant. Roth recalls that during one meeting, someone asked, "What are we looking for here anyway? And I said, well, if nothing else, we'll have the world's greatest psychedelic drugs." © 2022 npr

Psychedelics researchers balance trippyness with scientific rigor

Daniel Merino & Josjan Zijlmans As research into psychedelics and their medical uses makes a comeback, scientists are having to deal with the legacy – both scientific and social – of a 40-year nearly total freeze on psychedelics research. In this episode of “The Conversation Weekly” podcast, we speak with three experts about the early rise and fall of psychedelics in Western science and culture, how the mystical and often vague language of the ‘60s and '70s still pervades research today and what it’s like to actually run clinical trials using psilocybin. According to a poll done in the summer of 2022, nearly 30% of U.S. residents have tried at least one psychedelic drug in their lifetime. Whether from personal experience, hearing about the experiences of friends or widespread depictions in the media, many people will have either tried to describe a psychedelic trip or heard someone else describe one. The language commonly used in these descriptions is, for lack of a better word, often quite trippy. “A key function of the ego is to identify differentiation,” says Robin Carhart-Harris, a neurologist and psychologist at the University of California, San Francisco, and one of the world’s leading psychedelics researchers. “And when that function breaks down, it’s replaced with a sense of de-differentiation, a sense of unity, like everything is interconnected in a web of relationships. That’s not nothingness, it’s sort of everythingness.” Many psychedelics researchers use an approach called “the mystical framework” to assess psychedelic experiences. Researchers who use this framework give participants in psychedelics studies a survey as a way to define and categorize the experience. The survey asks participants to rate how strongly they felt certain phenomena during their trip, including feelings like the “certainty of encounter with ultimate reality (in the sense of being able to 'know’ and ‘see’ what is really real at some point during your experience).” © 2010–2022, The Conversation US, Inc.

Psilocybin as mental health therapy? Here’s what I found.

Perspective by Steven Petrow A few weeks ago, I mentioned to a friend that I was interested in learning more about psychedelics, especially how they might help me with depression and anxiety. That’s a broad category of plant medicines including psilocybin (“magic”) mushrooms, MDMA (ecstasy), DMT (Dimitri or the Businessman’s Trip), ketamine (“special K”) and some others. I’d been hesitant to be open about my search, because I’m old enough to remember the warnings about “bad trips” that scramble your brain. Imagine my surprise when my friend told me he’d recently taken his first “trip,” which he described as life-changing. I asked him — a real estate developer living in Northern California, married with kids — why he decided to try a psychedelic substance. “My work felt increasingly stale and meaningless,” he explained to me over a beer. “Despite a massive amount of reflection and coaching around how to break the rut, I felt as though I was still off track.” He and the others who have used these medicines spoke on the condition of anonymity because most of these psychedelics are Schedule I substances, meaning they are illegal to manufacture, buy, possess or distribute. When I confided my interest in psychedelics to a few other friends, several said they had tried the drugs and experienced several benefits: from easing anxiety to finding spiritual insights to combating depression and, among some with cancer, helping to reduce the fear of dying. They are hardly outliers. According to a new YouGovAmerica study, “one in four Americans say they’ve tried at least one psychedelic drug,” amounting to some 72 million U.S. adults. (The study included the medicines mentioned earlier, plus LSD, mescaline and salvia.) Was I missing a beat by not getting onboard?

Have we been treating depression the wrong way for decades?

Adam Miller · CBC News · A new analysis of the cause of depression has seemingly upended what we know about this common condition and challenged the use of antidepressants. But it may also leave patients with more questions than answers as the science evolves. A systematic umbrella review of 17 studies published in Molecular Psychology on July 20 looked at the decades-old theory that depression is caused by low serotonin, and found there was "no consistent evidence" of "an association between serotonin and depression." The theory that depression is caused by a chemical imbalance in the brain has been around since the 1960s. But for years, many experts have doubted this, feeling it oversimplified a complex condition. "The serotonin theory is very old and has been very popular since the '90s, when the pharmaceutical industry started promoting it," said Dr. Joanna Moncrieff, a psychiatry professor at University College London and lead author of the study. "But since about 2005, probably a bit before then, there's been sort of rumours that actually the evidence isn't very strong, or it's inconsistent. Some studies are positive, some studies are negative, but no one's really got that evidence together anywhere." Moncrieff and her team set out to challenge the serotonin theory in a systematic review of available research. They also went a step further in their conclusion by suggesting that antidepressants are ineffective at treating depression — and have largely worked as a placebo. ©2022 CBC/Radio-Canada.

U.K. Advises Coming off Antidepressants Very, Very Slowly

By Sarah Wild In 2015, psychiatrist Mark Horowitz tried to come off his antidepressants. He reduced his dosage by a set proportion over the course of several months, which is much longer than what the United Kingdom’s guidelines recommended. But in the process of tapering, he experienced a storm of new symptoms, including anxiety, dizziness, and bouts of insomnia. “I’d wake in the morning, feeling like I was being chased by an animal on the edge of a cliff,” he says. Ultimately, he felt he had no choice but to go back on his medication. As it happened, Horowitz had recently completed a Ph.D. on the neurobiology of antidepressants. During his training, he recalls, his professors had told him that stopping antidepressants was fairly easy. Their view was supported by the scientific literature, which had found that any withdrawal symptoms were minor and faded quickly. Experiences such as Horowitz’s were considered an anomaly. But a series of widely reported studies published over the past seven years suggest that discontinuation symptoms are common and can be severe, including everything from panic attacks and flu-like symptoms to electric shock sensations in the head. The longer people remain on antidepressants and the higher their dose, the more likely they are to experience withdrawal symptoms. Each year, millions of people begin taking antidepressants. They have been shown to help anxiety sufferers feel calmer and lift the moods of those with severe depression and balance their emotions. For many, the intervention is lifesaving. Yet even today, few physicians inform their patients about the potential difficulties of coming off the medication. Most national guidelines suggest a slow taper, but there is little to no guidance on precisely how to do this. Patients who experience intense withdrawal symptoms may end up remaining on antidepressants or turning to online peer support groups for help.

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Ismaeel Yunusa Taking oxycodone at the same time as certain selective serotonin reuptake inhibitors (SSRIs), a commonly prescribed class of antidepressant, can increase the risk of opioid overdose, according to a study my colleagues and I published. Doctors prescribe the opioid oxycodone to treat moderate to severe pain after surgeries and injuries or certain conditions like cancer. Opioids are also a common drug of abuse. In the U.S., over 70% of drug overdose deaths in 2019 involved an opioid. Because many patients with depression also experience chronic pain, opioids are often coprescribed with antidepressants like SSRIs. Prior research has shown that certain SSRIs, namely fluoxetine (Prozac or Sarafem) and paroxetine (Paxil, Pexeva or Brisdelle), can strongly inhibit a liver enzyme crucial to the proper breakdown of drugs in the body, including oxycodone. The resulting increased concentration of oxycodone in the blood may lead to accidental overdose. To see whether different types of SSRIs might affect a patient’s risk of overdosing on oxycodone, my colleagues and I examined data from three large U.S. health insurance claims databases. We included over 2 million adults who began taking oxycodone while using SSRIs between 2000 and 2020. The average age of the group was around 50, and a little over 72% were women. A little over 30% were taking the SSRIs paroxetine and fluoxetine. We found that patients taking paroxetine or fluoxetine had a 23% higher risk of overdosing on oxycodone than those using other SSRIs. © 2010–2022, The Conversation US, Inc.

This Nerve Influences Nearly Every Internal Organ. Can It Improve Our Mental State?

By Christina Caron In recent years, the vagus nerve has become an object of fascination, especially on social media. The vagal nerve fibers, which run from the brain to the abdomen, have been anointed by some influencers as the key to reducing anxiety, regulating the nervous system and helping the body to relax. TikTok videos with the hashtag “#vagusnerve” have been viewed more than 64 million times and there are nearly 70,000 posts with the hashtag on Instagram. Some of the most popular ones feature simple hacks to “tone” or “reset” the vagus nerve, in which people plunge their faces into ice water baths or lie on their backs with ice packs on their chests. There are also neck and ear massages, eye exercises and deep-breathing techniques. Now, wellness companies have capitalized on the trend, offering products like “vagus massage oil,” vibrating bracelets and pillow mists, that claim to stimulate the nerve, but that have not been endorsed by the scientific community. Researchers who study the vagus nerve say that stimulating it with electrodes can potentially help improve mood and alleviate symptoms in those who suffer from treatment-resistant depression, among other ailments. But are there other ways to activate the vagus nerve? Who would benefit most from doing so? And what exactly is the vagus nerve, anyway? Here’s a look at what we know so far. The term “vagus nerve” is actually shorthand for thousands of fibers. They are organized into two bundles that run from the brain stem down through each side of the neck and into the torso, branching outward to touch our internal organs, said Dr. Kevin J. Tracey, a neurosurgeon and president of the Feinstein Institutes for Medical Research, Northwell Health’s research center in New York. Imagine something akin to a tree, whose limbs interact with nearly every organ system in the body. (The word “vagus” means “wandering” in Latin.) The vagus nerve picks up information about how the organs are functioning and also sends information from the brain stem back to the body, helping to control digestion, heart rate, voice, mood and the immune system. For those reasons, the vagus nerve — the longest of the 12 cranial nerves — is sometimes referred to as an “information superhighway.” Dr. Tracey compared it to a trans-Atlantic cable. “It’s not a mishmash of signals,” he said. “Every signal has a specific job.” © 2022 The New York Times Company

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