Chapter 4. Development of the Brain

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By Taylor Majewski Rachel Nuwer’s “I Feel Love: MDMA and the Quest for Connection in a Fractured World,” is clearly aimed at a broad audience. It will resonate with readers who have experienced MDMA recreationally, probably at a rave, or therapeutically, probably to heal the emotional aftereffects of deep-seated trauma. Or both. But it’s also intended for readers who have never touched the drug, colloquially known as ecstasy or molly. Perhaps it’s especially for them. “I Feel Love” belongs to a growing family of nonfiction accounts of the fraught history of psychedelics and why, through compelling anecdotes and the latest science, we should reconsider them. Nuwer, a science journalist, chronicles the hopeful story of something both small and large — MDMA, the compound, and MDMA, the drug that’s repeatedly brought humans together across decades, continents, politics, and moral panics. The book is a natural successor to Michael Pollan’s 2018 bestseller “How to Change Your Mind,” which covered the mystical and medical benefits of LSD and psilocybin, and paved the way for a psychedelic renaissance of sorts, Nuwer writes in the introduction, “no such modern telling exists for MDMA.” Now, it does. “I Feel Love” is, above all, a time capsule. Nuwer begins with a crucial asterisk: “MDMA, also known as Ecstasy or Molly, is currently an illegal drug.” Today, most journalism around psychedelics is stipulated with this simple fact. Despite their potential to heal, drugs like psilocybin, LSD, and MDMA are still classified as Schedule I, the Drug Enforcement Administration’s highest category for controlled substances with no medical use, with a high potential for abuse. For MDMA specifically, that might be about to change.

Keyword: Drug Abuse
Link ID: 28922 - Posted: 09.23.2023

Kimberlee D'Ardenne Dopamine seems to be having a moment in the zeitgeist. You may have read about it in the news, seen viral social media posts about “dopamine hacking” or listened to podcasts about how to harness what this molecule is doing in your brain to improve your mood and productivity. But recent neuroscience research suggests that popular strategies to control dopamine are based on an overly narrow view of how it functions. Dopamine is one of the brain’s neurotransmitters – tiny molecules that act as messengers between neurons. It is known for its role in tracking your reaction to rewards such as food, sex, money or answering a question correctly. There are many kinds of dopamine neurons located in the uppermost region of the brainstem that manufacture and release dopamine throughout the brain. Whether neuron type affects the function of the dopamine it produces has been an open question. Recently published research reports a relationship between neuron type and dopamine function, and one type of dopamine neuron has an unexpected function that will likely reshape how scientists, clinicians and the public understand this neurotransmitter. Dopamine is involved with more than just pleasure. Dopamine neuron firing Dopamine is famous for the role it plays in reward processing, an idea that dates back at least 50 years. Dopamine neurons monitor the difference between the rewards you thought you would get from a behavior and what you actually got. Neuroscientists call this difference a reward prediction error. Understand new developments in science, health and technology, each week Eating dinner at a restaurant that just opened and looks likely to be nothing special shows reward prediction errors in action. If your meal is very good, that results in a positive reward prediction error, and you are likely to return and order the same meal in the future. Each time you return, the reward prediction error shrinks until it eventually reaches zero when you fully expect a delicious dinner. But if your first meal was terrible, that results in a negative reward prediction error, and you probably won’t go back to the restaurant. Dopamine neurons communicate reward prediction errors to the brain through their firing rates and patterns of dopamine release, which the brain uses for learning. They fire in two ways. © 2010–2023, The Conversation US, Inc.

Keyword: Drug Abuse; Learning & Memory
Link ID: 28917 - Posted: 09.21.2023

By Jim Crotty The opioid crisis continues to rage across the U.S., but there are some positive, if modest, signs that it may be slowing. Overdose deaths due to opioids are flattening in many places and dropping in others, awareness of the dangers of opioid abuse continues to increase, and more than $50 billion in opioid settlement funds are finally making their way to state and local governments after years of delay. There is still much work to be done, but all public health emergencies eventually subside. Then what? First, it’s important to realize that synthetic opioids like fentanyl will never fully disappear from the drug supply. They are too potent, too addictive, and perhaps most importantly, too lucrative. Opioids, like Covid-19, are here to stay, consistently circulating in the community but at more manageable levels. More alarming is what may take its place. Since 2010, overdoses involving both stimulants and fentanyl have increased 50-fold. Experts suggest this dramatic rise in polysubstance use represents a “fourth wave” in the opioid crisis, but what if it is really the start of a new wave of an emerging stimulant crisis? Substance abuse tends to move in cycles. Periods with high rates of depressant drug use (like opioids) are almost always followed by ones with high rates of stimulant drug use (like methamphetamine and cocaine), and vice versa. The heroin crisis of the 1960s and 1970s was followed by the crack epidemic of the 1980s and 1990s, which gave way to the current opioid epidemic. As the think tank scholar Charles Fain Lehman quipped, “As with fashion, so with drugs — whatever the last generation did, the next generation tends to abhor.” The difference now is the primacy of synthetic drugs — that is, illicit substances created in a lab that are designed to mimic the effects of naturally occurring drugs.

Keyword: Drug Abuse
Link ID: 28916 - Posted: 09.21.2023

Neurotransmitters are the words our brain cells use to communicate with one another. For years, researchers relied on tools that provided limited temporal and spatial resolution to track changes in the fast chemical chat between neurons. But that started to change about ten years ago for glutamate—the most abundant excitatory neurotransmitter in vertebrates that plays an essential role in learning, memory, and information processing—when scientists engineered the first glutamate fluorescent reporter, iGluSnFR, which provided a readout of neurons’ fast glutamate release. In 2013, researchers at the Howard Hughes Medical Institute collaborated with scientists from other institutions to develop the first generation of iGluSnFR.1 To create the biosensor, the team combined a bacteria-derived glutamate binding protein, Gltl, a wedged fluorescent GFP protein, and a membrane-targeting protein that anchors the reporter to the surface of the cell. Upon glutamate binding, the Gltl protein changes its conformation, increasing the fluorescence intensity of GFP. In their first study, the team showcased the utility of the biosensor for monitoring glutamate levels by demonstrating selective activation by glutamate in cell cultures. By conducting experiments with brain cells from the C. elegans worm, zebrafish, and mice, they confirmed that the reporter also tracked glutamate in vivo, a finding that set iGluSnFR apart from existing glutamate sensors. The first iGluSnFR generation allowed researchers to study glutamate dynamics in different biological systems, but the indicator could not detect small amounts of the neurotransmitter or keep up with brain cells’ fast glutamate release bouts. Making improvements © 1986–2023 The Scientist.

Keyword: Brain imaging
Link ID: 28901 - Posted: 09.10.2023

By Matt Richtel More than one-fifth of people who use cannabis struggle with dependency or problematic use, according to a study published on Tuesday in The Journal of the American Medical Association Network Open. The research found that 21 percent of people in the study had some degree of cannabis use disorder, which clinicians characterize broadly as problematic use of cannabis that leads to a variety of symptoms, such as recurrent social and occupational problems, indicating impairment and distress. In the study, 6.5 percent of users suffered moderate to severe disorder. Cannabis users who experience more severe dependency tended to be recreational users, whereas less severe but still problematic use was associated roughly equally with medical and recreational use. The most common symptoms among both groups were increased tolerance, craving, and uncontrolled escalation of cannabis use. ImageA person holding a lit joint while bags of cannabis sit on a black table in the Cannabis use is rising nationwide as more states have legalized it. The new findings align with prior research, which has found that around 20 percent of cannabis users develop cannabis use disorder. The condition can be treated with detoxification and abstinence, therapies and other treatments that work with addictive behaviors. The new study drew its data from nearly 1,500 primary care patients in Washington State, where recreational use is legal, in an effort to explore the prevalence of cannabis use disorder among both medical and nonmedical users. The research found that 42 percent of cannabis users identified themselves solely as medical users; 25 percent identified as nonmedical users, and 32 percent identified as both recreational and medical users. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 28888 - Posted: 08.30.2023

David Cox In June 2021, 32-year-old actor Kate Hyatt travelled to a farmhouse near Great Malvern in Worcerstershire for a plant medicine retreat that she hoped would improve her mental health after a difficult time during the pandemic lockdowns. While there, she is believed to have taken a substance called wachuma, or San Pedro cactus, a powerful hallucinogen used by Indigenous people in the Andes for thousands of years. But Hyatt did not experience relief; instead, her mental health worsened. Three months later, she described being in “some sort of psychotic break” and feeling as if her brain was going to explode. Later that autumn she took her own life. At the subsequent inquest, the coroner’s report linked her worsening symptoms to the hallucinogens she had consumed. Such tragedies represent the darker side of the psychedelics renaissance. These cases are often forgotten amid the feverish anticipation surrounding the therapeutic potential of these drugs, combined with exhaustive media coverage, the rapid rise of a billion-dollar industry – ranging from venture capital-backed startups to wellness retreats – and the hype around last year’s Netflix series How to Change Your Mind (based on Michael Pollan’s bestselling book). Yet without careful monitoring and scrutiny of who receives them, this class of drugs – which includes LSD, MDMA (commonly known as ecstasy or molly) and psilocybin (the active ingredient of magic mushrooms) – can be dangerous. There is evidence that they can destabilise vulnerable individuals who have experienced a previous psychotic episode or have a family history of psychosis. The substances are illegal to distribute and possess in the UK, although they are often obtained on the hidden market. Scientific researchers and biotechnology companies are able to use them in clinical trials only after obtaining a Home Office licence and applying extensive security arrangements. © 2023 Guardian News & Media Limited

Keyword: Depression; Drug Abuse
Link ID: 28873 - Posted: 08.19.2023

By David Ovalle The evolving overdose crisis in the United States is making another lethal turn, federal disease trackers reported Wednesday: Increasingly, people dying from opioids are also using stimulants such as cocaine and methamphetamine. An analysis by the Centers for Disease Control and Prevention shows that between 2011 and 2021, the age-adjusted rate of overdose deaths involving opioids and cocaine nearly quintupled, far outpacing the rate of deaths involving only cocaine. In 2021 alone, nearly 80 percent of the 24,486 cocaine overdose deaths recorded in the United States also involved an opioid. Experts say it represents the latest wave of the nation’s drug epidemic. For many users injecting or smoking fentanyl for some time, “adding a stimulant makes the drug feel like it did in the beginning,” said Daniel Ciccarone, a professor of addiction medicine at the University of California at San Francisco who has been studying the simultaneous use of stimulants and opioids. The federal analysis adds clarity to the staggering number of drug poisonings, largely driven by fentanyl, which can be up to 50 times more powerful than heroin. The CDC estimates that in 2022, more than 110,000 people succumbed to overdoses, edging past the previous year but representing a plateau from earlier spikes. Preliminary CDC data also suggest a slight increase in deaths in 2022 involving opioids taken with cocaine and psychostimulants such as meth. “These aren’t mutually exclusive categories. Someone can die of more than one drug,” said CDC researcher Merianne Rose Spencer, who led the analysis. The international cocaine market has thrived despite shutdowns associated with the coronavirus pandemic, according to the U.N.’s Global Report on Cocaine 2023, with record production in Latin America, new trafficking hubs in Africa and increased seizures.

Keyword: Drug Abuse
Link ID: 28848 - Posted: 07.19.2023

By Tammy Worth In two decades as a pediatrician, Jason Reynolds has had no success treating patients with opioid use disorder by sending them to rehab. But five years ago, when his Massachusetts practice, Wareham Pediatric Associates PC, became the first in the state to offer medication therapy to adolescent patients, he saw dramatic results. The first patient he treated with medication, a young man named Nate, had overdosed on opioids twice in the 24-hour period before seeing Reynolds. But that patient has had no opioid relapses since starting drug therapy. Reynolds’ success received a lot of media attention, and one interviewer, he recalls, asked Nate if any of his friends would also consider starting the treatment. Reynolds is among a small minority of pediatricians using medication to treat opioid use disorder in adolescents. Fewer than 2 percent of all physicians prescribing the medications are pediatricians, and many youth rehabilitation facilities don’t offer them at all. Medication for opioid use disorder (MOUD) uses buprenorphine or methadone to reduce cravings and withdrawal symptoms, or naltrexone to block the high that users would otherwise get if they decided to use opioids. Though MOUD is often used to treat adults, several barriers have prevented it from being adopted more widely for youth. Reynolds and a handful of other practitioners across the country are now working to provide education and training to other health care providers, hoping to increase use of this life-saving treatment. Opioid use among US youth is on the rise nationally, with diagnoses increasing from 0.26 per 100,000 person-years in 2001 to 1.51 in 2014. Overdose deaths have also spiked, more than doubling among youth ages 14 to 18, from 492 in 2019 to 1,146 in 2021. © 2023 Annual Reviews

Keyword: Drug Abuse; Development of the Brain
Link ID: 28844 - Posted: 07.06.2023

Alaina Demopoulos It was in 1975, when Carl Resnikoff and his girlfriend, Judith Gipson, took a bucolic ferry ride to Sausalito, a city located on the north end of Golden Gate Bridge, that a revolution in youth culture, music, emotion and imagination would take place. It was on that ride that the two undergraduates took capsules filled with MDMA powder for the very first time. Resnikoff, a biophysics major at Berkeley, had synthesized the drug himself. As the boat cut through the water of the San Francisco Bay, Gipson began to feel “a floating sense of euphoria … like some guy could come walking up to us asking for help and his guts are spilling out, and we’d be grooving on how beautiful it was.’” According to Rachel Nuwer’s book I Feel Love: MDMA and the Quest for Connection in a Fractured World, Resnikoff and his girlfriend’s romp was the first-ever documented instance of people taking MDMA recreationally. Nuwer is a science journalist who covered clinical trials for MDMA use in treating post-traumatic stress disorder (PTSD). While cannabis and psilocybin have undergone rebrands of late, going from countercultural tokens to the mainstream, she believes that the public is starting to open up to MDMA, too. “MDMA deserves its own story,” Nuwer said. “I wanted to bring together the history, culture, politics and science of the drug all in one place. This book is for anyone who’s interested in the drug, whether it’s someone who’s taken it 500 times on the dancefloor or who’s using it therapeutically for the first time.” Nuwer believes that MDMA will “follow the path of cannabis”, becoming legal medicinally first, then decriminalized, and perhaps fully legalized for all types of use. That cycle may have already started: three clinical trials have found that MDMA, which is also called ecstasy, can speed the recovery of PTSD. FDA approval for therapeutic use could come as early as next year. © 2023 Guardian News & Media Limited

Keyword: Drug Abuse
Link ID: 28834 - Posted: 06.28.2023

By Yasemin Saplakoglu Enough pints of beer can have you falling off your bar stool or loudly reciting lyrics to early 2000s jams to total strangers, because alcohol can get past one of the strongest defenses in the body. If you’ve ever been drunk, high or drowsy from allergy medication, you’ve experienced what happens when some molecules defeat the defense system called the blood-brain barrier and make it into the brain. Embedded in the walls of the hundreds of miles of capillaries that wind through the brain, the barrier keeps most molecules in the blood from ever reaching sensitive neurons. Much as the skull protects the brain from external physical threats, the blood-brain barrier protects it from chemical and pathogenic ones. While it’s a fantastic feat of evolution, the barrier is very much a nuisance for drug developers, who have spent decades trying to selectively overcome it to deliver therapeutics to the brain. Biomedical researchers want to understand the barrier better because its failures seem to be the key to some diseases and because manipulating the barrier could help improve the treatment of certain conditions. It’s really there to control the environment for proper brain function. “We’ve learned a lot over the last decade,” said Elizabeth Rhea, a research biologist at the University of Washington Medicine Memory and Brain Wellness Center. But “we’re definitely still facing challenges in getting substrates and therapeutics across.” Protection, but Not a Fortress Like the rest of the body, the brain needs circulating blood to deliver essential nutrients and oxygen and to carry away waste. But blood chemistry constantly fluctuates, and brain tissue is extremely sensitive to its chemical environment. Neurons rely on precise releases of ions to communicate — if ions could flow freely out of the blood, that precision would be lost. Other types of biologically active molecules can also twang the delicate neurons, interfering with thoughts, memories and behaviors. All Rights Reserved © 2023

Keyword: Drug Abuse
Link ID: 28831 - Posted: 06.21.2023

Sara Reardon Psychedelic drugs are promising treatments for many mental-health conditions, but researchers don’t fully understand why they have such powerful therapeutic effects. Now, a study in mice suggests that psychedelics all work in the same way: they reset the brain to a youthful state in which it can easily absorb new information and form crucial connections between neurons1. The findings raise the prospect that psychedelic drugs could allow long-term changes in many types of behavioural, learning and sensory system that are disrupted in mental-health conditions. But scientists caution that more research needs to be done to establish how the drugs remodel brain connections. The study was published on 14 June in Nature. Psychedelics such as MDMA (also known as ecstasy), ketamine and psilocybin — the active ingredient in magic mushrooms — are known for producing mind-altering effects, including hallucinations in some cases. But each compound affects a different biochemical pathway in the brain during the short-term ‘trip’, leaving scientists to wonder why so many of these drugs share the ability to relieve depression2, addiction and other difficult-to-treat conditions in the long term. Gül Dölen, a neuroscientist at Johns Hopkins University in Baltimore, Maryland, and her colleagues sought answers by studying how psychedelics affect social behaviour in mice. Mice can learn to associate socializing with positive feelings, but only during an adolescent ‘critical period’, which closes as they become adults. The scientists trained mice to associate one ‘bedroom’ in their enclosure with mousy friends and another room with solitude. They could then examine how psychedelics affected the rodents’ room choices — a proxy for whether the drug affects the critical period. © 2023 Springer Nature Limited

Keyword: Depression; Drug Abuse
Link ID: 28825 - Posted: 06.17.2023

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