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By Rachel Nuwer In an important step toward medical approval, MDMA, the illegal drug popularly known as Ecstasy or Molly, was shown to bring relief to those suffering from severe post-traumatic stress disorder when paired with talk therapy. Of the 90 people who took part in the new study, which is expected to be published later this month in Nature Medicine, those who received MDMA during therapy experienced a significantly greater reduction in the severity of their symptoms compared with those who received therapy and an inactive placebo. Two months after treatment, 67 percent of participants in the MDMA group no longer qualified for a diagnosis of PTSD, compared with 32 percent in the placebo group. MDMA produced no serious adverse side effects. Some participants temporarily experienced mild symptoms like nausea and loss of appetite. “This is about as excited as I can get about a clinical trial,” said Gul Dolen, a neuroscientist at Johns Hopkins University School of Medicine, who was not involved in the research. “There is nothing like this in clinical trial results for a neuropsychiatric disease.” Before MDMA-assisted therapy can be approved for therapeutic use, the Food and Drug Administration needs a second positive Phase 3 trial, which is currently underway with 100 participants. Approval could come as early as 2023. Mental health experts say that this research — the first Phase 3 trial conducted on psychedelic-assisted therapy — could pave the way for further studies on MDMA’s potential to help address other difficult-to-treat mental health conditions, including substance abuse, obsessive compulsive disorder, phobias, eating disorders, depression, end-of-life anxiety and social anxiety in autistic adults. © 2021 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: 27804 - Posted: 05.05.2021

Ariana Remmel Scientists in search of psychedelic drug treatments have developed a way to determine whether a molecule is likely to cause hallucinations, without testing it on people or animals. Growing evidence suggests that psychedelic compounds, which are active in the brain, have potential to treat psychiatric illnesses such as post-traumatic stress disorder (PTSD), but researchers are trying to find out whether there is a way to keep the beneficial properties of these drugs without the hallucinogenic side effects, which can complicate treatment. It is currently almost impossible to predict whether a potential drug will cause hallucinations before it is tested on animals or people. “That really slows down drug discovery,” says David Olson, a chemical neuroscientist at the University of California, Davis. To address this, a team led by Olson and neuroscientist Lin Tian, also at Davis, designed a fluorescent sensor to predict whether a molecule is hallucinogenic, based on the structure of a brain receptor targeted by psychedelics. Using their approach, the researchers identified a psychedelic-like molecule without hallucinogenic properties that they later found had antidepressant activity in mice1. The discovery adds “more fuel for the fire” of efforts to make drugs from psychedelic-like molecules without side effects, says Bryan Roth, a molecular pharmacologist at the University of North Carolina School of Medicine in Chapel Hill. © 2021 Springer Nature Limited

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: 27798 - Posted: 05.01.2021

By Nambi Ndugga and Austin Frakt American deaths from misuse of substances, including alcohol, have increased over the past two decades, but not uniformly across various demographic groups. Overall rates of alcohol abuse and related deaths have consistently and significantly increased for white non-Hispanic Americans, while Black Americans have experienced a much slower and less significant incline, and some other groups have had declines. More recently, alcohol use has been up during the pandemic, with one study showing a greater increase in misuse among women than among men. (For men, heavy drinking is considered more than four drinks per day and 14 drinks per week, and for women, more than three drinks per day and seven drinks per week, according to the National Institute on Alcohol Abuse and Alcoholism.) “Alcohol kills many more people than many may realize,” said Yusuf Ransome, an assistant professor at Yale’s School of Public Health. “It is a major contributor to deaths linked to physical injuries, interpersonal violence, motor vehicle crashes, self-harm and other harmful outcomes.” One reason for this might be that alcohol is often viewed as socially acceptable. “Alcohol use has been normalized because it is consumed sometimes at family and communal gatherings, casual outings, and that’s the type of drinking that is typically seen or showed within the media,” he said. “We rarely see the long-term health impacts of excessive alcohol use, nor do we show the acute dangers of alcohol misuse and abuse.” Between 2000 and 2016, according to research published in JAMA, alcohol-related deaths continually increased for white men (2.3 percent per year on average) and white women (4.1 percent), with middle-aged white Americans accounting for the highest increase in deaths. Rapid increases during this period in mortality related to alcohol and drugs like opioids among white Americans — particularly those without a college degree — have been termed “deaths of despair.” Sign up for The Upshot Newsletter: Analysis that explains politics, policy and everyday life, with an emphasis on data and charts. © 2021 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27779 - Posted: 04.21.2021

Greg Rosalsky Last month, New Jersey Governor Phil Murphy signed three bills making it official: marijuana will soon be growing legally in the gardens of the Garden State for anyone over 21 to enjoy. The bills follow through on a marijuana legalization ballot initiative that New Jerseyans approved overwhelmingly last year. New Jersey is now one of a dozen states, plus the District of Columbia, which have let loose the magic dragon — and more states, like Virginia, may be on the way. It's been almost a decade since Colorado and Washington legalized marijuana. That's given economists and other researchers enough time to study the effects of the policy. Here are some of the most interesting findings: Legalization didn't seem to substantially affect crime rates — Proponents of legalizing weed claimed it would reduce violent crimes. Opponents said it would increase violent crimes. A study by the CATO Institute finds, "Overall, violent crime has neither soared nor plummeted in the wake of marijuana legalization." Legalization seems to have little or no effect on traffic accidents and fatalities — Opponents of marijuana legalization argued it would wreak havoc on the road. A few studies have found that's not the case. Economists Benjamin Hansen, Keaton S. Miller & Caroline Weber, for instance, found evidence suggesting it had no effect on trends in traffic fatalities in both Colorado and Washington. © 2021 npr

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27734 - Posted: 03.17.2021

By Matt Richtel Texas has one of the most restrictive medical marijuana laws in the country, with sales allowed only by prescription for a handful of conditions. That hasn’t stopped Lukas Gilkey, chief executive of Hometown Hero CBD, based in Austin, Texas. His company sells joints, blunts, gummy bears, vaping devices and tinctures that offer a recreational high. In fact, business is booming online as well, where he sells to many people in other states with strict marijuana laws. But Mr. Gilkey says that he is no outlaw, and that he’s not selling marijuana, just a close relation. He’s offering products with a chemical compound — Delta-8-THC — extracted from hemp. It is only slightly chemically different from Delta 9, which is the main psychoactive ingredient in marijuana. And that small distinction, it turns out, may make a big difference in the eyes of the law. Under federal law, psychoactive Delta 9 is explicitly outlawed. But Delta-8-THC from hemp is not, a loophole that some entrepreneurs say allows them to sell it in many states where hemp possession is legal. The number of customers “coming into Delta 8 is staggering,” Mr. Gilkey said. “You have a drug that essentially gets you high, but is fully legal,” he added. “The whole thing is comical.” The rise of Delta 8 is a case study in how industrious cannabis entrepreneurs are pulling apart hemp and marijuana to create myriad new product lines with different marketing angles. They are building brands from a variety of potencies, flavors and strains of THC, the intoxicating substance in cannabis, and of CBD, the nonintoxicating compound that is often sold as a health product. With Delta 8, entrepreneurs also believe they have found a way to take advantage of the country’s fractured and convoluted laws on recreational marijuana use. It’s not quite that simple, though. Federal agencies, including the Drug Enforcement Administration, are still considering their options for enforcement and regulation. © 2021 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27714 - Posted: 02.28.2021

By Tom Bartlett The stimulant hexedrone — known more commonly as “bath salts” — is the kind of drug Carl Hart believes would be ideal to take right before a hellish academic reception or departmental holiday party. He’ll do cocaine and ecstasy from time to time and is a fan of the opioids oxycodone and morphine for the “pleasurable calmness” they induce. But after a long day, there are few things that Hart, a neuroscientist and psychology professor at Columbia University, enjoys more than a few lines of heroin by the fireplace. Hart has long pushed back against what he sees as the demonization of certain drugs and those who take them, particularly Black users, who are incarcerated at higher rates than white users. He has questioned the prevailing opinion that methamphetamine interferes with cognition and presented findings that suggest marijuana has minimal impact on the working memory of regular smokers. In his 2013 memoir, High Price: A Neuroscientist’s Journey of Self-Discovery That Challenges Everything You Know About Drugs and Society, Hart makes the case for decriminalizing narcotics and argues that “we’re too afraid of these drugs and of what we think they do.” In a 2014 talk at the TEDMed conference, he argued that “science should be driving our drug policy and our drug education, even if that makes you and me uncomfortable.” In his new book, Drug Use for Grown-Ups: Chasing Liberty in the Land of Fear, the former chairman of Columbia’s psychology department goes a step further, revealing that he has used — and continues to use — a number of illegal drugs. In fact, Hart recently said on a podcast that he was on methamphetamine when he delivered that TEDMed talk and that he’s given some of his best interviews the day after using heroin. Hart, who is 54, tried heroin for the first time in his 40s and has used it regularly — and responsibly, he contends — for years. “I am an unapologetic drug user,” he writes. “I take drugs as part of my pursuit of happiness, and they work. I am a happier and better person because of them.” He is not, he writes, an addict, and his book is not about addiction. Hart says that his stressful recent stint as department chairman was more damaging to his health than any substance he has ingested. © 2021 The Chronicle of Higher Education

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27709 - Posted: 02.28.2021

By Linda Searing People who smoke even occasionally are more likely than nonsmokers to have a serious type of stroke caused by a ruptured blood vessel — 27 percent more likely if they smoke up to 20 packs a year, according to research published in the journal Stroke. The average American smoker, according to the Centers for Disease Control and Prevention, smokes 14 cigarettes daily, which means about 255 packs a year. The type of stroke examined by the researchers, known as a subarachnoid hemorrhage, occurs when a weakened blood vessel ruptures and bleeds into the space between a person’s brain and skull. Most often, this results from an aneurysm, an abnormal bulge in a blood vessel. A subarachnoid hemorrhage is not as common as an ischemic stroke, which is caused by a blood clot, but it also can lead to neurological problems or be life-threatening without immediate treatment to stop the bleeding. To focus on the effect that smoking may have on people’s risk for this type of stroke, the researchers analyzed data on 408,609 adults, about a third of whom smoked regularly. During the study period, 904 participants had a subarachnoid hemorrhage. The more people smoked, the greater their risk for this type of stroke, prompting the American Stroke Association to note that the findings “provide evidence for a causal link” between smoking and subarachnoid hemorrhage. washingtonpost.com © 1996-2021

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 15: Language and Lateralization
Link ID: 27707 - Posted: 02.28.2021

By Nicholas Bakalar A large analysis looked at hundreds of factors that may influence the risk of heart failure and found one dietary factor in particular that was associated with a lower risk: drinking coffee. Heart failure, sometimes called congestive heart failure, occurs when the heart muscle becomes weakened and can no longer pump blood efficiently. It can be caused by high blood pressure, heart valve disease, heart attack, diabetes and other diseases and conditions. The analysis included extensive, decades-long data from three large health studies with 21,361 participants, and used a method called machine learning that uses computers to find meaningful patterns in large amounts of data. “Usually, researchers pick things they suspect would be risk factors for heart failure — smoking, for example — and then look at smokers versus nonsmokers,” said the senior author, Dr. David P. Kao, an assistant professor of medicine at the University of Colorado. “But machine learning identifies variables that are predictive of either increased or decreased risk, but that you haven’t necessarily thought of.” Using this technique, Dr. Kao and his colleagues found 204 variables that are associated with the risk for heart failure. Then they looked at the 41 strongest factors, which included, among others, smoking, marital status, B.M.I., cholesterol, blood pressure and the consumption of various foods. The analysis is in Circulation: Heart Failure. In all three studies, coffee drinking was associated more strongly than any other dietary factor with a decreased long-term risk for heart failure. Drinking a cup a day or less had no effect, but two cups a day conferred a 31 percent reduced risk, and three cups or more reduced risk by 29 percent. There were not enough subjects who drank more than three cups daily to know if more coffee would decrease the risk further. © 2021 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27701 - Posted: 02.23.2021

By Linda Searing A surge in the number of U.S. residents who have died of a drug overdose — 81,230 in the 12 months ending last May — set a record for the most such deaths in a one-year span, according to a report issued by the Centers for Disease Control and Prevention. Overall, drug overdose deaths jumped by 18 percent from the previous year, with increases recorded in 46 states (by more than 20 percent in 25 of those states) and just four states recording a decrease. Deaths attributed to synthetic opioids, mainly fentanyl, increased 38 percent nationwide, but 98 percent in 10 western states. Overdose deaths tied to cocaine use, often involving co-use or mixing with fentanyl or heroin, increased about 26 percent, and deaths linked to psychostimulants, such as methamphetamine, increased 35 percent. The CDC noted that the death rate from drug overdoses accelerated as the coronavirus pandemic set in, disrupting daily life and leading to isolation, depression, anxiety and economic distress for many, including people with a substance use disorder. In a health alert, the CDC urged broader distribution and use of naloxone, a medication that can block the effects of an overdose, as well as expanded prevention and treatment for those struggling with drug use. A free and confidential hotline, offering information and treatment referral, can be reached by calling the Substance Abuse and Mental Health Services Administration at 800-662-4357.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27663 - Posted: 01.27.2021

By Katherine J. Wu For a lesson in euphoria, look no further than a house cat twined around a twig of silver vine. When offered a snipping of the plant, which contains chemicals similar to the ones found in catnip, most domesticated felines will purr, drool and smoosh their faces into its intoxicating leaves and stems, then zonk out in a state of catatonic bliss. But the ecstatic rush might not be the only reason felines flock to these plants, new research suggests. Compounds laced into plants like silver vine and catnip might also help cats ward off mosquitoes, equipping them with a DIY pest repellent that’s far more fun to apply than a greasy coat of DEET. Other papers have pointed to the insect-deterring effects of catnip and similar plants. But the new study, published Wednesday in the journal Science Advances, is the first to draw a direct link between the plants and their protective effects on cats. “It’s a really interesting observation, that such a well-known behavior could be having this unappreciated benefit for cats,” said Laura Duvall, a mosquito researcher at Columbia University in New York who wasn’t involved in the study. Botanically speaking, catnip and silver vine are distant cousins. But both contain iridoids, a suite of chemicals that seem to potently tickle pleasure circuits in cats. To pinpoint the evolutionary roots of this plant-feline connection, a team of researchers led by Masao Miyazaki, a biochemist and veterinary scientist at Iwate University in Japan, corralled a menagerie of cats — some domestic, some wild — and monitored their responses to an iridoid extracted from silver vine, which thrives in many mountainous parts of Asia. Presented with scraps of paper dosed with iridoid, most of the cats initiated a ritualized rolling and rubbing. Some cats were so eager to engage with the compounds that they climbed up the sides of their cages — some of which were nearly four feet tall — to anoint themselves with chemical-soaked paper secured to the ceiling. © 2021 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 27662 - Posted: 01.23.2021

Jon Hamilton Root extracts from the African shrub iboga have long been used in traditional healing rituals and more recently as an experimental treatment for depression and to reduce drug cravings in addiction. Scientists now are working on a version of the extract that doesn't cause heart attacks or hallucinations as side effects. Steeve Jordan/AFP via Getty Images A chemically tweaked version of the psychedelic drug ibogaine appears to relieve depression and addiction symptoms without producing hallucinations or other dangerous side effects. The results of a study in rodents suggest it may be possible to make psychedelic drugs safe enough to become mainstream treatments for psychiatric disorders, the authors report Wednesday in the journal Nature. "What we need is a medicine that is so safe that you can take it home and put it in your medicine cabinet just like you would aspirin," says David Olson, the paper's senior author and an assistant professor at the University of California, Davis. "And that's really what we were trying to achieve." The success with ibogaine is "a promising first step," says Gabriela Manzano, a postdoctoral fellow at Weill Cornell Medicine in New York and a co-author of a commentary on the study. "This provides a road map on how we could start tweaking these chemical compounds to make them very useful in the clinic," she says. "Keep the good parts, get rid of the bad parts." For decades, psychedelic drugs, including ketamine and psilocybin, have shown promise in treating people with mental health problems including addiction, depression and post-traumatic stress disorder. But doctors and researchers have been wary of using the drugs because of their side effects. © 2020 npr

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 0: ; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27621 - Posted: 12.12.2020

By Abby Goodnough PHILADELPHIA — Steven Kelty had been addicted to crack cocaine for 32 years when he tried a different kind of treatment last year, one so basic in concept that he was skeptical. He would come to a clinic twice a week to provide a urine sample, and if it was free of drugs, he would get to draw a slip of paper out of a fishbowl. Half contained encouraging messages — typically, “Good job!” — but the other half were vouchers for prizes worth between $1 and $100. “I’ve been to a lot of rehabs, and there were no incentives except for the idea of being clean after you finished,” said Mr. Kelty, 61, of Winfield, Pa. “Some of us need something to motivate us — even if it’s a small thing — to live a better life.” The treatment is called contingency management, because the rewards are contingent on staying abstinent. A number of clinical trials have found it highly effective in getting people addicted to stimulants like cocaine and methamphetamine to stay in treatment and to stop using the drugs. But outside the research arena and the Department of Veterans Affairs, where Mr. Kelty is a patient, it is nearly impossible to find programs that offer such treatment — even as overdose deaths involving meth, in particular, have soared. There were more than 16,500 such deaths last year, according to preliminary data, more than twice as many as in 2016. Early data suggests that overdoses have increased even more during the coronavirus pandemic, which has forced most treatment programs to move online. Researchers say that one of the biggest obstacles to contingency management is a moral objection to the idea of rewarding someone for staying off drugs. That is one reason publicly funded programs like Medicaid, which provides health coverage for the poor, do not cover the treatment. Some treatment providers are also wary of giving prizes that they say patients could sell or trade for drugs. Greg Delaney, a pastor and the outreach coordinator at Woodhaven, a residential treatment center in Ohio, said, “Until you’re at the point where you can say, ‘I can make a good decision with this $50,’ it’s counterproductive.” © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 0: ; Chapter 13: Memory and Learning
Link ID: 27556 - Posted: 10.28.2020

R. Douglas Fields As I opened my copy of Science at home one night, an unfamiliar word in the title of a new study caught my eye: dopaminylation. The term refers to the brain chemical dopamine’s ability, in addition to transmitting signals across synapses, to enter a cell’s nucleus and control specific genes. As I read the paper, I realized that it completely upends our understanding of genetics and drug addiction. The intense craving for addictive drugs like alcohol and cocaine may be caused by dopamine controlling genes that alter the brain circuitry underlying addiction. Intriguingly, the results also suggest an answer to why drugs that treat major depression must typically be taken for weeks before they’re effective. I was shocked by the dramatic discovery, but to really understand it, I first had to unlearn some things. “Half of what you learned in college is wrong,” my biology professor, David Lange, once said. “Problem is, we don’t know which half.” How right he was. I was taught to scoff at Jean-Baptiste Lamarck and his theory that traits acquired through life experience could be passed on to the next generation. The silly traditional example is the mama giraffe stretching her neck to reach food high in trees, resulting in baby giraffes with extra-long necks. Then biologists discovered we really can inherit traits our parents acquired in life, without any change to the DNA sequence of our genes. It’s all thanks to a process called epigenetics — a form of gene expression that can be inherited but isn’t actually part of the genetic code. This is where it turns out that brain chemicals like dopamine play a role. All genetic information is encoded in the DNA sequence of our genes, and traits are passed on in the random swapping of genes between egg and sperm that sparks a new life. Genetic information and instructions are coded in a sequence of four different molecules (nucleotides abbreviated A, T, G and C) on the long double-helix strand of DNA. The linear code is quite lengthy (about 6 feet long per human cell), so it’s stored neatly wound around protein bobbins, similar to how magnetic tape is wound around spools in cassette tapes. All Rights Reserved © 2020

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 0: ; Chapter 4: Development of the Brain
Link ID: 27555 - Posted: 10.28.2020

By Jane E. Brody Do you have the heart to safely smoke pot? Maybe not, a growing body of medical reports suggests. Currently, increased smoking of marijuana in public, even in cities like New York where recreational use remains illegal (though no longer prosecuted), has reinforced a popular belief that this practice is safe, even health-promoting. “Many people think that they have a free pass to smoke marijuana,” Dr. Salomeh Keyhani, professor of medicine at the University of California, San Francisco, told me. “I even heard a suggestion on public radio that tobacco companies should switch to marijuana because then they’d be selling life instead of selling death.” But if you already are a regular user of recreational marijuana or about to become one, it would be wise to consider medical evidence that contradicts this view, especially for people with underlying cardiovascular diseases. Well: Get the best of Well, with the latest on health, fitness and nutrition. Compared with tobacco, marijuana smoking causes a fivefold greater impairment of the blood’s oxygen-carrying capacity, Dr. Keyhani and colleagues reported. In a review of medical evidence, published in January in the Journal of the American College of Cardiology, researchers described a broad range of risks to the heart and blood vessels associated with the use of marijuana. The authors, led by Dr. Muthiah Vaduganathan, cardiologist at Brigham and Women’s Hospital in Boston, point out that “marijuana is becoming increasingly potent, and smoking marijuana carries many of the same cardiovascular health hazards as smoking tobacco.” Edible forms of marijuana have also been implicated as a possible cause of a heart attack, especially when high doses of the active ingredient THC are consumed. © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 0:
Link ID: 27550 - Posted: 10.26.2020

By Eddie Jacobs How would you feel about a new therapy for your chronic pain, which—although far more effective than any available alternative—might also change your religious beliefs? Or a treatment for lymphoma that brings one in three patients into remission, but also made them more likely to vote for your least preferred political party? These seem like idle hypothetical questions about impossible side effects. After all, this is not how medicine works. But a new mental health treatment, set to be licensed next year, poses just this sort of problem. Psychotherapy assisted by psilocybin, the psychedelic compound in “magic mushrooms,” seems to be remarkably effective in treating a wide range of psychopathologies, but also causes a raft of unusual nonclinical changes not seen elsewhere in medicine. Although its precise therapeutic mechanisms remain unclear, clinically relevant doses of psilocybin can induce powerful mystical experiences more commonly associated with extended periods of fasting, prayer or meditation. Arguably, then, it is unsurprising that it can generate long-lasting changes in patients: studies report increased prosociality and aesthetic appreciation, plus robust shifts in personality, values and attitudes to life, even leading some atheists to find God. What’s more, these experiences appear to be a feature, rather than a bug, of psilocybin-assisted psychotherapy, with the intensity of the mystical experience correlating with the extent of clinical benefit. © 2020 Scientific American,

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 0: ; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27521 - Posted: 10.12.2020

By Linda Searing U.S. deaths from overdoses of cocaine, a powerfully addictive stimulant, numbered 14,666 in 2018, the most recent year tallied, according to a new report from the Centers for Disease Control and Prevention. The rate of overdose deaths remained stable from 2009 through 2013, the report found, but then headed upward at about 27 percent each year from 2013 through 2018. That rate increase represents about 2½ times more cocaine-related deaths in 2018 than in 2014. Although the report does not address potential causes of the increase in cocaine overdose deaths, the Drug Enforcement Administration has said increased availability of the drug, “in large part due to record levels of coca cultivation and cocaine production in Colombia,” has led to increased usage in the United States. The CDC report says that the rate of overdose deaths from cocaine was higher among men than women and more common among middle-aged people (35 to 44 years old), those living in urban rather than rural areas, and people residing in the Northeast region. In addition, the rate of overdose deaths attributed to cocaine laced with a synthetic opioid such as fentanyl increased faster in recent years than did overdose deaths from purely cocaine. Cocaine overdoses can cause breathing problems, high blood pressure, hallucinations and extreme agitation, as well as seizures, heart attacks and strokes.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 0:
Link ID: 27520 - Posted: 10.12.2020

Ken Solt & Oluwaseun Akeju The state of dissociation is commonly described as feeling detached from reality or having an ‘out of body’ experience. This altered state of consciousness is often reported by people who have psychiatric disorders arising from devastating trauma or abuse. It is also evoked by a class of anaesthetic drug, and can occur in epilepsy. The neurological basis of dissociation has been a mystery, but writing in Nature, Vesuna et al.1 describe a localized brain rhythm that underlies this state. Their findings will have far-reaching implications for neuroscience. The authors first recorded brain-wide neuronal activity in mice using a technique called widefield calcium imaging. They studied changes in these brain rhythms in response to a range of drugs that have sedative, anaesthetic or hallucinogenic properties, including three that induce dissociation — ketamine, phencyclidine (PCP) and dizocilpine (MK801). Only the dissociative drugs produced robust oscillations in neuronal activity in a brain region called the retrosplenial cortex. This region is essential for various cognitive functions, including episodic memory and navigation2. The oscillations occurred at a low frequency, of about 1–3 hertz. By contrast, non-dissociative drugs such as the anaesthetic propofol and the hallucinogen lysergic acid diethylamide (LSD) did not trigger this rhythmic retrosplenial activity. Vesuna et al. examined the active cells in more detail using a high-resolution approach called two-photon imaging. This analysis revealed that the oscillations were restricted to cells in layer 5 of the retrosplenial cortex. The authors then recorded neuronal activity across multiple brain regions. Normally, other parts of the cortex and subcortex are functionally connected to neuronal activity in the retrosplenial cortex; however, ketamine caused a disconnect, such that many of these brain regions no longer communicated with the retrosplenial cortex. © 2020 Springer Nature Limited

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 0: ; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27481 - Posted: 09.19.2020

Jon Hamilton Scientists used light to control the firing of specific cells to artificially create a rhythm in the brain that acted like the drug ketamine enjoynz/Getty Images Out-of-body experiences are all about rhythm, a team reported Wednesday in the journal Nature. In mice and one person, scientists were able to reproduce the altered state often associated with ketamine by inducing certain brain cells to fire together in a slow, rhythmic fashion. "There was a rhythm that appeared, and it was an oscillation that appeared only when the patient was dissociating," says Dr. Karl Deisseroth, a psychiatrist and neuroscientist at Stanford University. Dissociation is a brain state in which a person feels separated from their own thoughts, feelings and body. It is common in people who have some mental illnesses or who have experienced a traumatic event. It can also be induced by certain drugs, including ketamine and PCP (angel dust). The study linking dissociation to brain rhythms represents "a big leap forward in understanding how these drugs produce this unique state," says Dr. Ken Solt, an anesthesiologist at Harvard Medical School and Massachusetts General Hospital. Solt is the co-author of an article that accompanied the study but was not involved in the research. The finding also could be a step toward finding non-drug methods to control states of consciousness, Solt says. Deisseroth's lab made the discovery while studying the brains of mice that had been given ketamine or other drugs that cause dissociation. The team was using technology that allowed them to monitor the activity of cells throughout the brain. © 2020 npr

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 0: ; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27480 - Posted: 09.19.2020

By Nicholas Bakalar The incidence of hip fracture has decreased steadily over the past 40 years, but a new analysis suggests that new osteoporosis drugs have made only a small contribution to the trend. The report, published in JAMA Internal Medicine, included 10,552 men and women and their offspring followed since 1970. Every five years through 2010, the researchers recorded the number of hip fractures in people over 60. They found that the incidence of hip fractures decreased by 67 percent over those years, and rates were lower in people born later. The bone-strengthening bisphosphonates, like Fosamax (introduced in 1995) and Boniva (introduced in 2003), cut the fracture incidence by about 4.8 percent, the researchers estimate. But smoking decreased to 15 percent of participants in 2010, from 38 percent in 1970, and heavy drinking declined to 4.5 percent, from 7 percent. Both are significant risk factors for fracture. Other risk factors, like being underweight and early menopause, were stable over the years. “Smoking cessation accounts for about 90 percent of the decline in the age-adjusted decrease,” said the lead author, Dr. Timothy Bhattacharyya, an orthopedic surgeon with the National Institutes of Health. Other factors that may have played a role included estrogens, which were approved for osteoporosis treatment in 1988, and bone mineral density testing, which first became available in the 1990s. But “we didn’t observe any effect from estrogens or bone mineral density testing,” Dr. Bhattacharyya said. © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27406 - Posted: 08.08.2020

Craig W. Stevens Even as the COVID-19 pandemic cripples the economy and kills hundreds of people each day, there is another epidemic that continues to kill tens of thousands of people each year through opioid drug overdose. Opioid analgesic drugs, like morphine and oxycodone, are the classic double-edged swords. They are the very best drugs to stop severe pain but also the class of drugs most likely to kill the person taking them. In a recent journal article, I outlined how a combination of state-of-the-art molecular techniques, such as CRISPR gene editing and brain microinjection methods, could be used to blunt one edge of the sword and make opioid drugs safer. I am a pharmacologist interested in the way opioid drugs such as morphine and fentanyl can blunt pain. I became fascinated in biology at the time when endorphins – natural opioids made by our bodies – were discovered. I have been intrigued by the way opioid drugs work and their targets in the brain, the opioid receptors, for the last 30 years. In my paper, I propose a way to prevent opioid overdoses by modifying an opioid user’s brain cells using advanced technology. Opioid receptors stop breathing Opioids kill by stopping a person from breathing (respiratory depression). They do so by acting on a specific set of respiratory nerves, or neurons, found in the lower part of the brain that contain opioid receptors. Opioid receptors are proteins that bind morphine, heroin and other opioid drugs. The binding of an opioid to its receptor triggers a reaction in neurons that reduces their activity. Opioid receptors on pain neurons mediate the pain-killing, or analgesic, effects of opioids. When opioids bind to opioid receptors on respiratory neurons, they slow breathing or, in the case of an opioid overdose, stop it entirely. © 2010–2020, The Conversation US, Inc.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27401 - Posted: 08.06.2020