By Daniel Bergner If severe mental illness, untreated, underlies the feeling of encroaching anarchy and menace around the homeless encampments of San Francisco or in the subways of New York City, then the remedy appears obvious. Let’s rescue those who, as New York’s mayor, Eric Adams, says, “slip through the cracks” of our mental health care systems; let’s give people “the treatment and care they need.” It sounds so straightforward. It sounds like a clear way to lower the odds of tragic incidents occurring, like the chokehold killing of Jordan Neely, a homeless, psychiatrically troubled man, or the death of Michelle Alyssa Go, who was pushed off a Times Square subway platform to her death by a homeless man with schizophrenia. Improving order and safety in public spaces and offering compassionate care seem to be convergent missions. But unless we confront some rarely spoken truths, that convergence will prove illusory. The problems with the common-sense approach, as it’s currently envisioned, run beyond the proposed solutions we usually read about: funding more beds on hospital psychiatric wards, establishing community-based programs to oversee treatment when people are released from the hospital and providing housing for those whose mental health is made increasingly fragile by the constant struggle for shelter. The most difficult problems aren’t budgetary or logistical. They are fundamental. They involve the involuntary nature of the care being called for and the flawed antipsychotic medications that are the mainstay of treatment for people dealing with the symptoms of psychosis, like hallucinatory voices or paranoid delusions, which can come with a range of severe psychiatric conditions. © 2023 The New York Times Company

Keyword: Schizophrenia
Link ID: 28810 - Posted: 06.03.2023

John Michael Streicher Opioid drugs such as morphine and fentanyl are like the two-faced Roman god Janus: The kindly face delivers pain relief to millions of sufferers, while the grim face drives an opioid abuse and overdose crisis that claimed nearly 70,000 lives in the U.S. in 2020 alone. Scientists like me who study pain and opioids have been seeking a way to separate these two seemingly inseparable faces of opioids. Researchers are trying to design drugs that deliver effective pain relief without the risk of side effects, including addiction and overdose. One possible path to achieving that goal lies in understanding the molecular pathways opioids use to carry out their effects in your body. How do opioids work? The opioid system in your body is a set of neurotransmitters your brain naturally produces that enable communication between neurons and activate protein receptors. These neurotransmitters include small proteinlike molecules like enkephalins and endorphins. These molecules regulate a tremendous number of functions in your body, including pain, pleasure, memory, the movements of your digestive system and more. Analysis of the world, from experts Opioid neurotransmitters activate receptors that are located in a lot of places in your body, including pain centers in your spinal cord and brain, reward and pleasure centers in your brain, and throughout the neurons in your gut. Normally, opioid neurotransmitters are released in only small quantities in these exact locations, so your body can use this system in a balanced way to regulate itself. The opioids your body produces and opioid drugs bind to the same receptors. The problem comes when you take an opioid drug like morphine or fentanyl, especially at high doses for a long time. These drugs travel through the bloodstream and can activate every opioid receptor in your body. You’ll get pain relief through the pain centers in your spinal cord and brain. But you’ll also get a euphoric high when those drugs hit your brain’s reward and pleasure centers, and that could lead to addiction with repeated use. When the drug hits your gut, you may develop constipation, along with other common opioid side effects. Targeting opioid signal transduction How can scientists design opioid drugs that won’t cause side effects? One approach my research team and I take is to understand how cells respond when they receive the message from an opioid neurotransmitter. Neuroscientists call this process opioid receptor signal transduction. Just as neurotransmitters are a communication network within your brain, each neuron also has a communication network that connects receptors to proteins within the neuron. When these connections are made, they trigger specific effects like pain relief. So, after a natural opioid neurotransmitter or a synthetic opioid drug activates an opioid receptor, it activates proteins within the cell that carry out the effects of the neurotransmitter or the drug. © 2010–2023, The Conversation US, Inc.

Keyword: Drug Abuse; Pain & Touch
Link ID: 28809 - Posted: 06.03.2023

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

Keyword: Depression; Drug Abuse
Link ID: 28806 - Posted: 05.31.2023

By Scientific American Custom Media Megan Hall: How does the stomach tell the brain it’s full? How do cells in our body grow and divide? James Rothman realized that the fundamental biology behind these processes are basically the same. In 2010, he shared The Kavli Prize in Neuroscience with Richard Scheller and Thomas Südhof for their work detailing how nerve cells communicate with each other on a microscopic level. Three years later, he received the Nobel Prize. Hall: James Rothman was pleasantly surprised when he received The Kavli Prize in Neuroscience. James Rothman: I'd always thought of myself as a biochemist first and a cell biologist second. And I never really thought of myself as a neuroscientist. Hall: He did apply to a neuroscience program in grad school… Rothman: It all just made a whole lot of sense, except for the fact that I wasn't admitted. Hall: But James is not the kind of person to worry about labels. In fact, he’s explored a range of scientific disciplines. As an undergrad at Yale, he studied physics, maybe in part because he grew up in the 50s. Rothman: Scientists and doctors were really the most admired in the 1950s. And it was the physicists in particular. Einstein, Oppenheimer, people like that. Hall: But his father worried about his career options, so he convinced James to try a biology course. Rothman: And I just fell in love. Hall: So, he ditched physics and decided to go to Harvard Medical School to learn more about biology. Rothman: In the end I never finished medical school. Hall: But, while he was there, he stumbled upon his life’s work. Rothman: I was a first-year medical student and I was listening to a lecture in our course on histology and cell biology. Hall: The professor was showing images that had been captured by scientists only a few decades before. They showed, for the first time, how complex the cell is. Rothman: The cell is not just, like a dumb little liquid inside. It's a highly organized place. It's more like a city than anything else. © 2023 Scientific American,

Keyword: Biomechanics
Link ID: 28805 - Posted: 05.31.2023

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.

Keyword: Depression; Drug Abuse
Link ID: 28789 - Posted: 05.21.2023

By David Ovalle It had been four days since Kevin Hargrove last took the medication that stilled his dangerous cravings. He awoke with a queasy stomach and achy muscles, then vomited on the sidewalk as he set off from his encampment under a D.C. bridge this month. Hargrove recently changed his Medicare-funded insurance company and was unable to fill his prescription for buprenorphine, the medication he has taken for years to treat his opioid addiction. The withdrawals proved too much. The 66-year-old found a dealer on the street, paid $6 for two pills he believed were codeine painkillers and washed them down with a can of Olde English 800 malt liquor. Less than an hour later, Hargrove passed out inside his sister’s Columbia Heights apartment, overdosing on what was suspected to be fentanyl. “Don’t tell me!” his sister cried. “You’ve been doing so well!” Hargrove’s story illustrates the challenges often faced by those struggling with opioid addiction — especially people of color — in receiving buprenorphine, a medication that public health experts believe should play a critical role in curbing an addiction-and-overdose crisis fueled by fentanyl. His overdose happened this month as a newly published national study from the Harvard T.H. Chan School of Public Health showed that White patients are up to 80 percent more likely to receive buprenorphine than Black patients, and that Black patients receive a more limited supply. “There are lots of totally counterproductive insurance restrictions on this drug, particularly for populations in which the need is the greatest,” said the study’s lead author, Michael L. Barnett, an associate professor of health policy and management at Harvard’s School of Public Health.

Keyword: Drug Abuse
Link ID: 28788 - Posted: 05.21.2023

By Meredith Wadman A groundbreaking epidemiological study has produced the most compelling evidence yet that exposure to the chemical solvent trichloroethylene (TCE)—common in soil and groundwater—increases the risk of developing Parkinson’s disease. The movement disorder afflicts about 1 million Americans, and is likely the fastest growing neurodegenerative disease in the world; its global prevalence has doubled in the past 25 years. The report, published today in JAMA Neurology, involved examining the medical records of tens of thousands of Marine Corps and Navy veterans who trained at Marine Corps Base Camp Lejeune in North Carolina from 1975 to 1985. Those exposed there to water heavily contaminated with TCE had a 70% higher risk of developing Parkinson’s disease decades later compared with similar veterans who trained elsewhere. The Camp Lejeune contingent also had higher rates of symptoms such as erectile dysfunction and loss of smell that are early harbingers of Parkinson’s, which causes tremors; problems with moving, speaking, and balance; and in many cases dementia. Swallowing difficulties often lead to death from pneumonia. About 90% of Parkinson’s cases can’t be explained by genetics, but there have been hints that exposure to TCE may trigger it. The new study, led by researchers at the University of California, San Francisco (UCSF), represents by far the strongest environmental link between TCE and the disease. Until now, the entire epidemiological literature included fewer than 20 people who developed Parkinson’s after TCE exposure. The Camp Lejeune analysis “is exceptionally important,” says Briana De Miranda, a neurotoxicologist at the University of Alabama at Birmingham who studies TCE’s pathological impacts in the brains of rats. “It gives us an extremely large population to assess a risk factor in a very carefully designed epidemiological study.”

Keyword: Parkinsons; Neurotoxins
Link ID: 28785 - Posted: 05.18.2023

By Jan Hoffman Despite the continuing rise in opioid overdose deaths, one of the most effective treatments for opioid addiction is still drastically underprescribed in the United States, especially for Black patients, according to a large new study. From 2016 through 2019, scarcely more than 20 percent of patients diagnosed with opioid use disorder filled prescriptions for buprenorphine, the medication considered the gold standard in opioid addiction treatment, despite repeated visits to health care providers, according to the study, which was published Wednesday in the New England Journal of Medicine. Within six months following a high-risk event like an overdose, white patients filled buprenorphine prescriptions up to 80 percent more often than Black patients, and up to 25 percent more often than Latino patients, the study found. Rates of use for methadone, another effective treatment, were generally even lower. “It was disheartening to see that buprenorphine or methadone treatments were so low, even among patients who just left the hospital with an overdose or other addiction-related issue,” said Dr. Michael L. Barnett, the lead author, who teaches health policy and management at Harvard. “And not only that, but people of color received lifesaving treatment at a fraction of the rate that white patients did.” Access to medical care, a reason often used to explain racial disparities in treatment, was not necessarily at work here, said Dr. Barnett, an associate professor at the Harvard T.H. Chan School of Public Health. Noting that all the patients regardless of race encountered doctors roughly once a month, he said, “There are two mechanisms left that could explain disparities this large. One is where people of color get their health care, which we know is highly segregated, and another is racial differences in patient trust and demand for buprenorphine.“ Buprenorphine, often marketed under the brand name Suboxone, is a synthetic opioid that satisfies a patient’s cravings for other opioids and prevents withdrawal, without providing a high. It was approved for addiction treatment by the Food and Drug Administration more than two decades ago, but still faces some resistance and stigma because it, too, is an opioid. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 28779 - Posted: 05.13.2023

Tess McClure Every few months, Cohen “Coey” Irwin lies on his back and lets the walls close in. Lights move overhead, scanning over the tattoos covering his cheeks. He lies suspended, his head encased by a padded helmet, ears blocked, as his body is shunted into a tunnel. The noise begins: a rhythmic crashing, loud as a jackhammer. For the next hour, an enormous magnet will produce finely detailed images of Irwin’s brain. Irwin has spent much of his adult life addicted to smoking methamphetamine – or P, as the drug is known in New Zealand. He knows its effects intimately: the euphoria, the paranoia, the explosive violence, the energy, the tics that run through his neck and lips. Stepping outside the MRI machine, however, he can get a fresh view for the first time – looking in from the outside at what the drug has done to his internal organs. New Zealanders are some of the world’s biggest meth takers: wastewater testing has placed it in the top four consumers worldwide. The country’s physical isolation – 4,000km from the nearest major ports – makes importing hard drugs challenging and costly, but meth can be manufactured relatively cheaply and easily, and is derived from available pharmaceuticals. Almost a third of middle-aged New Zealanders have tried the drug, a University of Otago study found in 2020. In the backroom of Mātai research centre, Irwin thinks back to when it all started. He was a teenager when he tried P for the first time – trying to impress a girl on New Year’s Eve, in his home town of Porirua, Wellington. The girlfriend didn’t last, but the drug was love at first puff, he says, and would become one of the defining relationships of his life. “I remember it was the next day, the sun had risen, I was still awake with the people at the table I’d been smoking with. And I was instantly trying to find ways: how can we make money to get more?” Within a few years, he would be smoking every day. © 2023 Guardian News & Media Limited

Keyword: Drug Abuse; Brain imaging
Link ID: 28772 - Posted: 05.06.2023

By Aimee Cunningham Fentanyl, a deadly synthetic opioid, is killing a growing number of children and teens in the United States. More than 1,500 kids under the age of 20 died from fentanyl in 2021, four times as many as in 2018, says epidemiologist Julie Gaither of the Yale School of Medicine, who will present the data May 1 at the Pediatric Academic Societies meeting in Washington, D.C. The fentanyl deaths account for nearly all of the opioid-related deaths in this age group in 2021. Fentanyl is a lab-made opioid used for pain treatment that is 30 to 50 times more potent than heroin, making it lethal at a much smaller dose. The drug is also manufactured and sold illegally and is increasingly found contaminating counterfeit prescription drugs, or entirely replacing the drug a buyer expects to get (SN: 5/1/18). “That’s primarily the story of what’s happening among teenagers,” says pediatrician and addiction provider Sarah Bagley of the Boston University Chobanian & Avedisian School of Medicine. They intend to purchase and use one kind of drug or substance but unknowingly ingest fentanyl. “People are not anticipating that they are going to be exposed to fentanyl, and then they are, and that results in an overdose.” Some of the signs that a person is experiencing an overdose include falling asleep, losing consciousness, gurgling or choking sounds and weak or no breathing. “This change in the drug supply, where you just have a much more potent opioid, is really driving it all,” says Bagley, who was not involved in the work. © Society for Science & the Public 2000–2023.

Keyword: Drug Abuse
Link ID: 28758 - Posted: 04.29.2023

By Geoffrey Giller From the brightly colored poison frogs of South America to the prehistoric-looking newts of the Western US, the world is filled with beautiful, deadly amphibians. Just a few milligrams of the newt’s tetrodotoxin can be fatal, and some of those frogs make the most potent poisons found in nature. In recent years, scientists have become increasingly interested in studying poisonous amphibians and are starting to unravel the mysteries they hold. How is it, for example, that the animals don’t poison themselves along with their would-be predators? And how exactly do the ones that ingest toxins in order to make themselves poisonous move those toxins from their stomachs to their skin? Even the source of the poison is sometimes unclear. While some amphibians get their toxins from their diet, and many poisonous organisms get theirs from symbiotic bacteria living on their skin, still others may or may not make the toxins themselves — which has led scientists to rethink some classic hypotheses. Over the long arc of evolution, animals have often turned to poisons as a means of defense. Unlike venoms — which are injected via fang, stinger, barb, or some other specialized structure for offensive or defensive purposes — poisons are generally defensive toxins a creature makes that must be ingested or absorbed before they take effect. Amphibians tend to store their poisons in or on their skin, presumably to increase the likelihood that a potential predator is deterred or incapacitated before it can eat or grievously wound them. Many of their most powerful toxins — like tetrodotoxin, epibatidine and the bufotoxins originally found in toads — are poisons that interfere with proteins in cells, or mimic key signaling molecules, thus disrupting normal function. © 2023 Annual Reviews

Keyword: Neurotoxins
Link ID: 28757 - Posted: 04.29.2023

By Christina Jewett and Julie Creswell New York, California and several other states announced a $462 million settlement with Juul Labs on Wednesday, resolving lawsuits claiming that the company aggressively marketed its e-cigarettes to young people and fueled a vaping crisis. The agreement brings many of the company’s legal woes to a conclusion, with settlements reached with 47 states and territories, and 5,000 individuals and local governments. Juul is in the middle of a trial in Minnesota, an unusual case in which a settlement has not been reached. But the company’s efforts to broker deals over the lawsuits have cost it nearly $3 billion so far, an enormous sum for a company still seeking official regulatory approval to keep selling its products. The latest settlement resolved the claims of New York, California, Colorado, the District of Columbia, Illinois, Massachusetts and New Mexico. It follows other lawsuit settlements that took Juul to task for failing to warn young users that the high levels of nicotine in their e-cigarettes would prove addictive. California contended in its lawsuit that for months, Juul did not disclose in its advertising that its devices contained nicotine. It detailed the company’s early marketing efforts, which included handing out free samples of the e-cigarettes in 2015 at trendy events, including a “Nocturnal Wonderland” in San Bernardino and a “Movies All Night Slumber Party” in Los Angeles. The New York lawsuit noted that the company embraced the use of social media hashtags like #LightsCameraVapor. Attorneys general in those states conducted investigations that they said had found that Juul executives were aware that their initial marketing lured teenage users into buying its sleek vaping pens, but did little to address the problem as the adolescent vaping rate exploded. In New York City and the Hamptons, the company held glamorous parties and “falsely led consumers to believe that its vapes were safer than cigarettes and contained less nicotine,” Letitia James, New York’s attorney general, said in a press event Wednesday. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 28740 - Posted: 04.15.2023

By Bruce Bower Human hair recovered in a Mediterranean island cave has yielded Europe’s oldest direct evidence of people taking hallucinogenic drugs, researchers say. By around 3,000 years ago, visitors at Es Càrritx cave on Menorca — perhaps shamans who performed spiritual and healing rituals — consumed plants containing mind-altering and vision-inducing substances, say archaeologist Elisa Guerra-Doce of the University of Valladolid in Spain and colleagues. Signs of human activity at the cave, including more than 200 human graves arrayed in a chamber at the entrance, were previously dated to between around 3,600 and 2,800 years ago. Researchers had also found a hoard of objects in a small pit within an inner cave chamber, including six wooden containers, each containing locks of human hair. Chemical analyses of one container’s locks, possibly from more than one person, detected three psychoactive plant substances that had been ingested and absorbed into the hair over nearly a year, the scientists report April 6 in Scientific Reports. Two substances, atropine and scopolamine from nightshade plants, induce disorientation, hallucinations and altered physical sensations. Another, ephedrine, boosts energy and alertness. Shamans would have known how to handle and consume these potentially toxic plants safely, the investigators say. Individuals intent on preserving ancient traditions hid hair and other ritually significant objects at Es Càrritx as Menorca’s growing population spurred social changes between 3,000 and 2,800 years ago, the researchers speculate. Burial rituals had included dyeing strands of hair on corpses a reddish color and later cutting off some locks to be put in containers left near graves. © Society for Science & the Public 2000–2023.

Keyword: Drug Abuse
Link ID: 28733 - Posted: 04.09.2023

By David Marchese As the founding director of the Johns Hopkins Center for Psychedelic and Consciousness Research, Dr. Roland Griffiths has been a pioneer in investigating the ways in which psychedelics can help treat depression, addiction and, in patients with a life-threatening cancer diagnosis, psychological distress. He has also looked at how the use of psychedelics can produce transformative and long-lasting feelings of human interconnectedness and unity. One could surely classify his achievements using various medical and scientific terms, but I’ll just put it like this: Griffiths has expanded the knowledge of how we might better learn to live. Now he is learning to die. Griffiths, who is 76, has been diagnosed with Stage 4 metastatic colon cancer. It’s a diagnosis, in all likelihood terminal, that for him has brought forth transcendently positive feelings about existence and what he calls the great mystery of consciousness. “We all know that we’re terminal,” says Griffiths, who since being diagnosed has established an endowment at Johns Hopkins to study psychedelics and their potential for increasing human flourishing. “So I believe that in principle we shouldn’t need this Stage 4 cancer diagnosis to awaken. I’m excited to communicate, to shake the bars and tell people, ‘Come on, let’s wake up!’ ” Can we start with your current prognosis? [Laughs.] Prognosis is a 50 percent chance that I’ll make it to Halloween.1 1 Soon after we spoke, Griffiths was removed from the drug trial he was participating in because of a lack of positive results. That likely means his survival timeline is now shorter than it was at the time of our interview. And how are you feeling about that? In spite of that, life has been more beautiful, more wonderful than ever. When I first got that diagnosis, because I work out regularly, I watch my diet, I sleep well, this came out of left field. There was this period in which it felt like I was going to wake up and say, “Boy, that was” — to put it in psychedelic language — “a bummer, a bad dream.” But soon after that I started to contemplate the different psychological states that would be naturally forthcoming with a diagnosis like mine: depression, anxiety, denial, anger, or adopting some belief system of religious outcomes, which as a scientist I was not cut out to do. I went through those, exploring what life would be like if I inhabited those reactions, and I quickly concluded that that was not a wise way to live. I have a long-term meditation practice. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 28729 - Posted: 04.09.2023

By Brian Gallagher One question for Christopher Timmermann, a cognitive neuroscientist at the Centre for Psychedelic Research at Imperial College London, where he leads the DMT Research Group and focuses on the nature of consciousness. What happens to my brain on the psychedelic DMT? The DMT experience is one in which people report going into a different dimension, an alternate reality that feels convincingly real, even more real than this everyday reality. One that has a spiritual significance. In that DMT experience, they sometimes encounter beings. In our latest study we looked at brain scans using fMRI and EEG, and found that this feeling of immersion appears to be underpinned by a dysregulation of the systems in the human brain—in the prefrontal cortex, in the temporal cortices—involved in planning, decision making, and semantics. The way in which we construct meaning, essentially. The brain usually functions in this modular, organized, hierarchical way. You have different networks and systems that crystallize as we grow older. What we see with DMT (specifically N,N-Dimethyltryptamine) is that the systems that generate complex behaviors and tasks stop working in this specialized fashion. They start to work in synchrony with the rest of the brain. The specialization is interrupted. The hierarchy is dysregulated, flattens out. What you have as a result is a more integrated connectivity in the brain. In our day-to-day lives, we have a very good demarcation of what happens inside us versus what happens outside. The sensory areas of the brain that allow us to engage with the external world are very much separated from the reflective areas of the brain that allow us to engage with ourselves. Not on DMT. What we see is that this separation, that usually divides these two poles of organization of the brain, starts to mesh together. The neurons are firing in sync. © 2023 NautilusNext Inc.,

Keyword: Drug Abuse; Depression
Link ID: 28713 - Posted: 03.23.2023

By Freda Kreier The only cure to being drunk is to wait it out. But that might not always be the case: Injecting drunk mice with a naturally occurring hormone helped them sober up more quickly than they otherwise would have, a new study shows. Mice that received a shot of FGF21 — a hormone made by the liver — woke up from a drunken stupor roughly twice as fast as those that didn’t, researchers report in the March 7 Cell Metabolism. The find could one day be used to help treat alcohol poisoning, a sometimes-deadly side effect of heavy drinking that lands millions of people in the emergency room every year, says molecular endocrinologist David Mangelsdorf. The sobering effect of FGF21 isn’t the first time the hormone has been linked to drinking. Scientists have previously shown that livers ramp up production of this hormone when alcohol floods the bloodstream. And while FGF21 doesn’t help break down alcohol, researchers have found that the hormone can help protect livers from the toxic effects of liquor while dampening the desire to continue drinking in mice and monkeys. Those findings made Mangelsdorf, of the University of Texas Southwestern Medical Center in Dallas, and his colleagues curious whether FGF21 also plays a role in recovering from too much alcohol. So the team fed mice enough alcohol to knock them out and waited to see how long it took for them to wake up. © Society for Science & the Public 2000–2023.

Keyword: Drug Abuse; Hormones & Behavior
Link ID: 28711 - Posted: 03.23.2023

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

Keyword: Depression; Emotions
Link ID: 28703 - Posted: 03.15.2023

Martha Bebinger For two decades — as opioid overdose deaths rose steadily — the federal government limited access to buprenorphine, a medication that addiction experts consider the gold-standard for treating patients with an opioid use disorder. Study after study shows it helps people continue addiction treatment while reducing the risk of overdose, and death. Clinicians who wanted to prescribe the medicine had to complete an 8-hour training. They could only treat a limited number of patients and had to keep special records. They were given a Drug Enforcement Administration (DEA) registration number starting with X, a designation that many doctors say made them a target for drug enforcement audits. "Just the process associated with taking care of our patients with a substance use disorder made us feel like, 'boy, this is dangerous stuff,'" says Dr. Bobby Mukkamala, who chairs the American Medical Association's task force on substance use disorder. "The science doesn't support that but the rigamarole suggested that." That rigamarole is mostly gone. Congress eliminated what became known as the "X-waiver" in legislation President Biden signed late last year. Now begins what some addiction experts are calling a truth serum moment. Was the X-waiver and the burdens that came with it the real reason only about 7% of clinicians in the U.S. were cleared to prescribe buprenorphine? Or was it an excuse that masked hesitation about treating addiction, if not outright disdain for these patients? There's great optimism among some leaders that getting rid of the X-waiver will expand access to buprenorphine and reduce overdoses. One study from 2021 shows taking buprenorphine reduces the risk by 50%. The medication is an opioid that produces much weaker effects than heroin or fentanyl and reduces cravings for those deadlier drugs. © 2023 npr

Keyword: Drug Abuse
Link ID: 28691 - Posted: 03.08.2023

By McKenzie Prillaman Psychedelics go beneath the cell surface to unleash their potentially therapeutic effects. These drugs are showing promise in clinical trials as treatments for mental health disorders (SN: 12/3/21). Now, scientists might know why. These substances can get inside nerve cells in the cortex — the brain region important for consciousness — and tell the neurons to grow, researchers report in the Feb. 17 Science. Several mental health conditions, including depression and post-traumatic stress disorder, are tied to chronic stress, which degrades neurons in the cortex over time. Scientists have long thought that repairing the cells could provide therapeutic benefits, like lowered anxiety and improved mood. Psychedelics — including psilocin, which comes from magic mushrooms, and LSD — do that repairing by promoting the growth of nerve cell branches that receive information, called dendrites (SN: 11/17/20). The behavior might explain the drugs’ positive outcomes in research. But how they trigger cell growth was a mystery. It was already known that, in cortical neurons, psychedelics activate a certain protein that receives signals and gives instructions to cells. This protein, called the 5-HT2A receptor, is also stimulated by serotonin, a chemical made by the body and implicated in mood. But a study in 2018 determined that serotonin doesn’t make these neurons grow. That finding “was really leaving us scratching our heads,” says chemical neuroscientist David Olson, director of the Institute for Psychedelics and Neurotherapeutics at the University of California, Davis. © Society for Science & the Public 2000–2023.

Keyword: Drug Abuse; Depression
Link ID: 28673 - Posted: 02.18.2023

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.

Keyword: Depression
Link ID: 28670 - Posted: 02.15.2023