Links for Keyword: Drug Abuse

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


Links 1 - 20 of 1689

A genetic variant found only in people of African descent significantly increases a smoker’s preference for cigarettes containing menthol, a flavor additive. The variant of the MRGPRX4 gene is five to eight times more frequent among smokers who use menthol cigarettes than other smokers, according to an international group of researchers supported by the U.S. Food and Drug Administration and the National Institutes of Health. The multiethnic study is the first to look across all genes to identify genetic vulnerability to menthol cigarettes. The paper was published online in the journal PLOS Genetics (link is external) on Feb. 15. Menthol provides a minty taste and a cooling or soothing sensation, and plays a particularly troubling role in U.S. cigarette smoking patterns. According to the FDA, nearly 20 million people in the United States smoke menthol cigarettes, which are particularly popular among African-American smokers and teen smokers. In the U.S., 86 percent of African-American smokers use menthol cigarettes, compared to less than 30 percent of smokers of European descent. In addition, menthol cigarettes may be harder to quit than other cigarettes. Although not originally the focus of the study, researchers also uncovered clues as to how menthol may reduce the irritation and harshness of smoking cigarettes. “This study sheds light on the molecular mechanisms of how menthol interacts with the body,” said Andrew Griffith, M.D., Ph.D., scientific director and acting deputy director of NIH’s National Institute on Deafness and Other Communications Disorders (NIDCD). “These results can help inform public health strategies to lower the rates of harmful cigarette smoking among groups particularly vulnerable to using menthol cigarettes.”

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 25969 - Posted: 02.18.2019

Terry Gross Growing up, neuroscientist Judith Grisel would take little sips of alcohol at family events, but it wasn't until she was 13 that she experienced being drunk for the first time. Everything changed. "It was so complete and so profound," she says. "I suddenly felt less anxious, less insecure, less inept to cope with the world. Suddenly I was full and OK in a way that I had never been." Grisel began chasing that feeling. Over the years, she struggled with alcohol, marijuana and cocaine. But along the way, she also became interested in the neuroscience of addiction. "I'm always interested in the mechanisms of things," she says. "And when I heard that I had a disease, I kind of felt naturally that that would have a biological basis, and I figured that I could study that biological basis and understand it and then maybe fix it." Now it has been 30 years without using drugs or alcohol for Grisel, a professor of psychology at Bucknell University, where she studies how addictive drugs work on the brain. Her new book is Never Enough: The Neuroscience and Experience of Addiction. Interview Highlights On how drug and alcohol abuse affects the brains of young people The changes in behavior that happen during adolescence are so important and lasting because the brain is forming permanent structures. So whatever you experience as an adolescent is going to have a much more impactful influence on the rest of your life trajectory than it would, say, if you did this at another time in development when your brain wasn't so prone to changing. © 2019 npr

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25958 - Posted: 02.13.2019

/ By Ronnie Cohen Dr. Samir Grover was taken aback when, early in his gastroenterology career, he saw one physician speak two times and present contradictory conclusions about the same medication. Each time, the speaker presented identical data on a drug used to treat inflammatory bowel disease. First, he recommended the pharmaceutical. A week later, he deemed it ineffective. “How could this exact same data be spun in two very different ways?” asked Grover, a professor at the University of Toronto. One fact did change — the drug manufacturer that sponsored and paid for the lecture. “Simply following clinical practice guidelines could lead doctors — even those who shun all industry gifts — to unwittingly dispense financially tainted medicine” It’s no secret that drug makers pay doctors to hype their products to other doctors. But few outside the halls of hospitals witness physicians bending a single set of facts in opposing ways. After watching similar acts of statistical wizardry throughout his nine years of medical practice, Grover set out to investigate a more sweeping question about conflicts of interest. Do they infect clinical practice guidelines? Professional societies produce thousands of these documents every year. They steer the decisions of health care professionals and insurance companies about how to prevent and treat an ever-widening range of conditions — from diabetes, hypertension, and heart disease to arthritis, hepatitis, cancer, and depression. Grover and his colleagues’ paper and a companion study recently published in JAMA Internal Medicine suggest that simply following clinical practice guidelines could lead doctors — even those who shun all industry gifts — to unwittingly dispense financially tainted medicine. More than half of the authors of guidelines examined in the two studies had financial conflicts of interest. In many cases, the doctors who wrote the guidelines were paid by the same companies that produced the drugs they recommended. In addition, a significant portion of the doctors who took pharmaceutical money failed to disclose the payments, many of which amounted to $10,000 or more. Copyright 2019 Undark

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25930 - Posted: 02.04.2019

/ By Jacob Appel One of the most upsetting illnesses any psychiatrist encounters is Wernicke-Korsakoff Syndrome (WKS). Caused by a deficiency of thiamine (vitamin B1), it results in devastating impairment of muscle control and memory. Able-bodied men and women develop a severe and irreversible amnesia that wipes clean their pasts and prevents them from forming new memories. Those who survive — and many patients don’t — are often relegated to nursing homes. Yet the neurological damage WKS causes is only part of what makes it so upsetting to emergency room psychiatrists; after all, many neurological and psychiatric illnesses inflict irreversible cognitive harm. The tragedy of WKS is that, with appropriate public health measures, it could be easily prevented. Historically, thiamine deficiency afflicted the indigent, prisoners of war, and societies with rice-based diets. Its most serious chronic manifestation, beriberi, can present in a “wet” form that results in cardiac overload and massive edema, or in a “dry” variant — of which WKS is a subset — that affects the peripheral nervous system, the brain, or both. In addition to amnesia, victims of WKS often display striking degrees of spontaneous confabulation, in which they volunteer personal stories that they believe to be true but are not. Prevalence rates for WKS at autopsy have been found to run as high as 2.8 percent in Australia, and between 0.1 to 2.2 percent in the U.S. Copyright 2019 Undark

Related chapters from BN8e: Chapter 17: Learning and Memory; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25923 - Posted: 02.01.2019

By Laurie McGinley E-cigarettes are almost twice as effective at helping smokers quit as nicotine replacement therapies such as lozenges and patches, according to a new study that immediately stoked the debate over whether e-cigarettes are an important smoking-cessation tool or a health menace. The study, published online Wednesday by the New England Journal of Medicine, is the first randomized trial to test the effectiveness of modern e-cigarettes vs. nicotine-replacement products, said Peter Hajek, a psychologist at Queen Mary University of London, who led the trial. The researchers found that 18 percent of the e-cigarette users were smoke-free after a year, compared with 9.9 percent of those in the nicotine-replacement group. The participants also received behavioral support to stop smoking. For years, physicians have been reluctant to recommend e-cigarettes for smoking cessation because of a lack of clinical trial data, Hajek said. “This is now likely to change,” he added in a statement. But two editorials in the same publication threw some cold water on the trial’s results. One editorial, by Boston University researchers, said e-cigarettes should be used only when Food and Drug Administration-approved treatments do not work. Those approved therapies, as well as drugs such as bupropion, have higher effectiveness rates than the new study suggested, and much more is known about their side effects, said Belinda Borrelli, a Boston University researcher who co-wrote the editorial. © 1996-2019 The Washington Post

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25918 - Posted: 01.31.2019

Ian Sample Science editor A group of volunteers who took a trip in the name of science have helped researchers uncover how LSD messes with activity in the brain to induce an altered state of consciousness. Brain scans of individuals high on the drug revealed that the chemical allows parts of the cortex to become flooded with signals that are normally filtered out to prevent information overload. The drug allowed more information to flow from the thalamus, a kind of neural gatekeeper, to a region called the posterior cingulate cortex, and it stemmed the flow of information to another part known as the temporal cortex. This disruption in communication may underpin some of the wacky effects reported by LSD users, from feelings of bliss and being at one with the universe to hallucinations and what scientists in the field refer to as “ego dissolution”, where one’s sense of self disintegrates. For the study, the researchers invited 25 healthy participants into the lab to be scanned under the influence of LSD and, on another occasion, after taking a placebo. They were shown around the scanner beforehand to ensure they felt comfortable going inside when the drug took hold. Had the machine suddenly taken on a threatening demeanour, the scans might not have come out so well. The scientists wanted to test a hypothesis first put forward more than a decade ago. It states LSD causes the thalamus to stop filtering information it relays to other parts of the brain. It is the breakdown of this filter that gives rise to the weird effects the drug induces, or so the thinking goes. © 2019 Guardian News and Media Limited

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 25910 - Posted: 01.29.2019

/ By Courtenay Harris Bond When Anna Brennan was 15 years old, her mother abandoned her in the projects of northeast Philadelphia. Her aunt eventually took her in, but Brennan struggled with anxiety and depression. She also needed to support herself, so in ninth grade she dropped out of high school and went to work at an all-night diner downtown. At 20, she met her first husband, who also lived with mental illness and had substance use issues — and gave her a tooth-marked scar in her upper right shoulder. For years, Brennan waitressed seven days a week until she had her third child, Gemma, and her back pain started, forcing her to quit. “Our approach is: ‘Your urine is positive for substances. Let’s figure out how to make this work better for you.’” A physician prescribed painkillers, and Brennan became addicted. Her habit quickly turned from buying pills, which were expensive on the street, to snorting and then injecting heroin, which came cheap and pure. Twelve years into their marriage, Brennan’s husband committed suicide. Then she lost her house. Brennan’s two older kids went to stay with her sister, and Brennan hasn’t seen them in over a year. “I’m a drug addict,” Brennan says bluntly. “She won’t give them back.” Brennan started taking Suboxone, an opioid-replacement therapy that cut her cravings and kept her from experiencing withdrawal, two different times: in 2015 and then again from 2016 to 2018. During the second round, Brennan spent more than two years making trips to Prevention Point Philadelphia on Kensington Avenue. There, she met with her case manager and the doctor who prescribed her medication. Brennan seemed poised to be a success story. But she was weighed down by the stress of coping with a drug-addicted second husband, caring for her daughter Gemma, who is autistic; and despairing that she might never see her two older children again. Copyright 2019 Undark

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25895 - Posted: 01.24.2019

/ By Dave Levitan Scientific research on the effects of marijuana is rife with holes, thanks in large part to it still being categorized at the federal level alongside drugs such as heroin and LSD. Unfortunately, when research is scarce, it becomes easier to mislead people through cherry-picked data, sneaky word choice, and misinterpreted conclusions. On virtually every issue in his 272-page book, Adam Berenson commits one of the most common logical errors: He mixes up correlation and causation. Which brings us to Alex Berenson and Malcolm Gladwell, and what happens when tidy narratives outrun the science. Two weeks ago, Berenson, a former New York Times reporter and subsequent spy novelist, published a book with the ominous title “Tell Your Children: The Truth about Marijuana, Mental Illness, and Violence.” Gladwell, meanwhile, published a feature in the New Yorker, where he is a staff writer, drawing largely on Berenson’s book and questioning the supposed consensus that weed is among the safest drugs. Combined, these two works offer a master class in statistical malfeasance and a smorgasbord of logical fallacies and data-free fear-mongering that serve only to muddle an issue that, as experts point out, needs far more good-faith research. Berenson’s main argument is relatively simple. In his book, he claims, essentially, that the existing evidence really does contain solid answers, painting a truly alarming picture about marijuana: That it can and does cause psychosis and schizophrenia. He then makes the leap that since psychosis and schizophrenia can lead to violence, marijuana itself is causing violence to increase in the United States and elsewhere. Copyright 2019 Undark

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25892 - Posted: 01.22.2019

Aimee Cunningham As public health officials tackle opioid addiction and overdoses, another class of prescription drugs has been contributing to a growing number of deaths across the United States. Benzodiazepines, such as Valium and Xanax, are commonly prescribed for anxiety and insomnia. The drugs are also highly addictive and can be fatal, especially when combined with alcohol or opioids. In the latest sign of the drug’s impact, the number of overdose deaths involving “benzos” rose from 0.54 per 100,000 in 1999 to 5.02 per 100,000 in 2017 among women aged 30 to 64, researchers report January 11 in the Morbidity and Mortality Weekly Report. That’s a spike of 830 percent, surpassed only by increases seen in overdose deaths involving synthetic opioids or heroin. Overall, there were 10,684 overdose deaths involving benzodiazepines in the United States in 2016, according to the National Institute on Drug Abuse. In 1999, the total was 1,135. Benzodiazepines have a sedating effect, and are particularly dangerous when used with other drugs that slow breathing, such as opioids and alcohol. In combination, the substances can “cause people to fall asleep and essentially never wake up again,” says Anna Lembke, an addiction psychiatrist at Stanford University School of Medicine. Benzos and opioids are often prescribed together, and opioids contribute to 75 percent of overdose deaths involving benzos. The rising number of deaths involving benzos hasn’t stopped the flow of prescriptions. The number of U.S. adults who filled a prescription for benzos rose from 8.1 million in 1996 to 13.5 million in 2013, a jump of 67 percent, a study in the American Journal of Public Health in 2016 found. The quantity of benzos acquired more than tripled over the same time. |© Society for Science & the Public 2000 - 2019.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 25882 - Posted: 01.19.2019

By Abby Goodnough WASHINGTON — A new study offers some of the strongest evidence yet of the connection between the marketing of opioids to doctors and the nation’s addiction epidemic. It found that counties where opioid manufacturers offered a large number of gifts and payments to doctors had more overdose deaths involving the drugs than counties where direct-to-physician marketing was less aggressive. The study, published Friday in JAMA Network Open, said the industry spent about $40 million promoting opioid medications to nearly 68,000 doctors from 2013 through 2015, including by paying for meals, trips and consulting fees. And it found that for every three additional payments that companies made to doctors per 100,000 people in a county, overdose deaths involving prescription opioids there a year later were 18 percent higher. Even as the opioid epidemic was killing more and more Americans, such marketing practices remained widespread. From 2013 through 2015, roughly 1 in 12 doctors received opioid-related marketing, according to the study, including 1 in 5 family practice doctors. The authors, from Boston Medical Center and New York University School of Medicine, found that counties where doctors received more industry marketing subsequently saw an increase in both the number of opioids prescribed and opioid-related overdose deaths. In response to the study, Dr. John Cullen, president of the American Academy of Family Physicians, said, “A limitation of the study, as acknowledged by the authors, is the many unknown variables that prevent drawing a direct causal link between pharmaceutical marketing and opioid-related deaths.” He added, “We’re very much aware of the critical and devastating impact of the opioid epidemic and work every day, with every patient interaction, to fight it. At the same time, we must protect the physician’s ability to provide adequate pain management.” © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25881 - Posted: 01.19.2019

By Diana Kwon o For the longest time the cerebellum, a dense, fist-size formation located at the base of the brain, never got much respect from neuroscientists. For about two centuries the scientific community believed the cerebellum (Latin for “little brain”), which contains approximately half of the brain’s neurons, was dedicated solely to the control of movement. In recent decades, however, the tide has started to turn, as researchers have revealed details of the structure’s role in cognition, emotional processing and social behavior. The longstanding interest in the cerebellum can be seen in the work of French physiologist Marie Jean Pierre Flourens—(1794–1867). Flourens removed the cerebella of pigeons and found the birds became unbalanced, although they could still move. Based on these observations, he concluded the cerebellum was responsible for coordinating movements. “[This] set the dogma that the cerebellum was involved in motor coordination,” says Kamran Khodakhah, a neuroscientist at Albert Einstein College of Medicine, adding: “For many years, we ignored the signs that suggested it was involved in other things.” One of the strongest pieces of evidence for the cerebellum’s broader repertoire emerged around two decades ago, when Jeremy Schmahmann, a neurologist at Massachusetts General Hospital, described cerebellar cognitive affective syndrome after discovering behavioral changes such as impairments in abstract reasoning and regulating emotion in individuals whose cerebella had been damaged. Since then this line of study has expanded. There has been human neuroimaging work showing the cerebellum is involved in cognitive processing and emotional control—and investigations in animals have revealed, among other things, that the structure is important for the normal development of social and cognitive capacities. Researchers have also linked altered cerebellar function to addiction, autism and schizophrenia.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 25880 - Posted: 01.19.2019

A new study in rodents has shown that the brain’s cerebellum—known to play a role in motor coordination—also helps control the brain’s reward circuitry. Researchers found a direct neural connection from the cerebellum to the ventral tegmental area (VTA) of the brain, which is an area long known to been involved in reward processing and encoding. These findings, published in Science, demonstrate for the first time that the brain’s cerebellum plays a role in controlling reward and social preference behavior, and sheds new light on the brain circuits critical to the affective and social dysfunction seen across multiple psychiatric disorders. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. “This type of research is fundamental to deepening our understanding of how brain circuit activity relates to mental illnesses,” said Joshua A. Gordon, M.D., Ph.D., director of NIMH. “Findings like the ones described in this paper help us learn more about how the brain works, a key first step on the path towards developing new treatments.” The cerebellum plays a well-recognized role in the coordination and regulation of motor activity. However, research has also suggested that this brain area contributes to a host of non-motor functions. For example, abnormalities in the cerebellum have been linked to autism, schizophrenia, and substance use disorders, and brain activation in the cerebellum has been linked to motivation, social and emotional behaviors, and reward learning, each of which can be disrupted in psychiatric disorders.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 25876 - Posted: 01.18.2019

By Benedict Carey Nearly a century after the film “Reefer Madness” alarmed the nation, some policymakers and doctors are again becoming concerned about the dangers of marijuana, although the reefers are long gone. Experts now distinguish between the “new cannabis” — legal, highly potent, available in tabs, edibles and vapes — and the old version, a far milder weed passed around in joints. Levels of T.H.C., the chemical that produces marijuana’s high, have been rising for at least three decades, and it’s now possible in some states to buy vape cartridges containing little but the active ingredient. The concern is focused largely on the link between heavy usage and psychosis in young people. Doctors first suspected a link some 70 years ago, and the evidence has only accumulated since then. In a forthcoming book, “Tell Your Children,” Alex Berenson, a former Times reporter, argues that legalization is putting a generation at higher risk of schizophrenia and other psychotic syndromes. Critics, including leading researchers, have called the argument overblown, and unfaithful to the science. Can cannabis use cause psychosis? Yes, but so can overuse of caffeine, nicotine, alcohol, stimulants and hallucinogens. Psychosis is a symptom: a temporary disorientation that resembles a waking dream, with odd, imagined sights and sounds, often accompanied by paranoia or an ominous sensation. The vast majority of people who have this kind of psychotic experience do not go on to develop a persistent condition such as schizophrenia, which is characterized by episodes of psychosis that recur for years, as well as cognitive problems and social withdrawal. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25875 - Posted: 01.18.2019

By Aaron E. Carroll Are we underestimating the harms of legalizing marijuana? Those who hold this view have been in the news recently, saying that research shows we are moving too far too fast without understanding the damage. America is in the midst of a sea change in policies on pot, and we should all be a bit nervous about unintended consequences. Vigilance is required. But it should be reasoned and thoughtful. To tackle recent claims, we should use the best methods and evidence as a starting point. Does Marijuana Increase Crime? Crime has gone up in Colorado and Washington since those states legalized marijuana. It’s reasonable to wonder about the connection, but it’s also reasonable to be skeptical about causation. The best method to investigate this may be synthetic controls. Researchers can use a weighted combination of similar groups (states that are like Colorado and Washington in a number of ways) to create a model of how those states might have been expected to perform with respect to crime without any changes in marijuana laws. Benjamin Hansen, a professor of economics at the University of Oregon, used this methodology to create a comparison group that most closely resembled the homicide trends and levels from 2000-12. “I picked those years because they were after the tremendous crime drop in the early ’90s and most predictive of crime today,” he said. “I ended in 2012 because that’s when Colorado and Washington voted to legalize marijuana.” This model showed that we might have predicted more of an increase in Colorado or Washington just based on trends seen in comparable states, even without legalization. When he compared the two states with the synthetic control, Colorado and Washington actually had lower rates after legalization than you’d expect given trends. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25860 - Posted: 01.14.2019

Ian Stewart For the first time in U.S. history, a leading cause of deaths, vehicle crashes, has been surpassed in likelihood by opioid overdoses, according to a new report on preventable deaths from the National Safety Council. Americans now have a 1 in 96 chance of dying from an opioid overdose, according to the council's analysis of 2017 data on accidental death. The probability of dying in a motor vehicle crash is 1 in 103. "The nation's opioid crisis is fueling the Council's grim probabilities, and that crisis is worsening with an influx of illicit fentanyl," the council said in a statement released Monday. Fentanyl is now the drug most often responsible for drug overdose deaths, the Centers for Disease Control and Prevention reported in December. And that may only be a partial view of the problem: Opioid-related overdoses have also been under-counted by as much as 35 percent, according to a study published last year in the journal Addiction. The council has recommended tackling the epidemic by increasing pain management training for opioid prescribers, making the potentially-lifesaving drug naloxone more widely available and expanding access to addiction treatment. While the leading causes of death in the U.S. are heart disease (1 in 6 chance) and cancer (1 in 7), the rising overdose numbers are part of distressing trend the non-profit has tracked: The lifetime odds of an American dying from a preventable, unintentional injury have gone up over the past 15 years. © 2019 npr

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25859 - Posted: 01.14.2019

Maria Temming A new smartphone app may help people who shoot up alone get medical treatment if they accidentally overdose. The app, dubbed Second Chance, monitors its user for breathing problems that foreshadow an opioid overdose (SN: 3/31/18, p. 18). In an emergency, the app could call 911 or send an SOS to friends or family who could provide opioid-counteracting medication. “Being able to track an overdose when a person may be by themselves could significantly improve the ability to save lives,” says psychiatrist Nora Volkow, director of the National Institute on Drug Abuse in Bethesda, Md., who was not involved in developing the app. More than 115 people die from an opioid overdose every day in the United States, according to the NIDA, and many victims are alone or with people who are either untrained or too impaired to help. Second Chance, described online January 9 in Science Translational Medicine, converts a smartphone’s speaker and microphone into a sonar system that works within about a meter of a user’s body. When the app is running, the phone continuously emits sound waves at frequencies too high to hear, which bounce off a user’s chest. Tracking when these echoes reach the phone allows the app to detect two possible signs of an impending overdose: slow breathing or no breathing at all. Phone a friend (or EMS) If the Second Chance app judges that a user is likely succumbing to opioids, it could call emergency contacts or medical personnel to deliver the drug naloxone, used to counteract an overdose. |© Society for Science & the Public 2000 - 2018

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25858 - Posted: 01.11.2019

By Malcolm Gladwell A few years ago, the National Academy of Medicine convened a panel of sixteen leading medical experts to analyze the scientific literature on cannabis. The report they prepared, which came out in January of 2017, runs to four hundred and sixty-eight pages. It contains no bombshells or surprises, which perhaps explains why it went largely unnoticed. It simply stated, over and over again, that a drug North Americans have become enthusiastic about remains a mystery. For example, smoking pot is widely supposed to diminish the nausea associated with chemotherapy. But, the panel pointed out, “there are no good-quality randomized trials investigating this option.” We have evidence for marijuana as a treatment for pain, but “very little is known about the efficacy, dose, routes of administration, or side effects of commonly used and commercially available cannabis products in the United States.” The caveats continue. Is it good for epilepsy? “Insufficient evidence.” Tourette’s syndrome? Limited evidence. A.L.S., Huntington’s, and Parkinson’s? Insufficient evidence. Irritable-bowel syndrome? Insufficient evidence. Dementia and glaucoma? Probably not. Anxiety? Maybe. Depression? Probably not. Then come Chapters 5 through 13, the heart of the report, which concern marijuana’s potential risks. The haze of uncertainty continues. Does the use of cannabis increase the likelihood of fatal car accidents? Yes. By how much? Unclear. Does it affect motivation and cognition? Hard to say, but probably. Does it affect employment prospects? Probably. Will it impair academic achievement? Limited evidence. This goes on for pages. © 2019 Condé Nast.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25848 - Posted: 01.08.2019

By Alex Berenson Marijuana seems to be on an unstoppable march to legalization in the United States. New York and New Jersey are racing to join the 10 states that already allow recreational use of cannabis. Some 65 percent of Americans favor legalization, and several potential Democratic candidates for president support ending federal prohibitions on marijuana. This huge shift in public attitudes comes even though most Americans do not use the drug. Only 15 percent of people over 12 used it even once in 2017, according to a large federal survey. That year, only three million people tried it for the first time. Instead, the change has been largely driven by decadeslong lobbying by marijuana legalization advocates and for-profit cannabis companies. Those groups have shrewdly recast marijuana as a medicine rather than an intoxicant. Some have even claimed that marijuana can help slow the opioid epidemic, though studies show that people who use cannabis are more likely to start using opioids later. Meanwhile, legalization advocates have squelched discussion of the serious mental health risks of marijuana and THC, the chemical responsible for the drug’s psychoactive effects. As I have seen firsthand in writing a book about cannabis, anyone who raises those concerns may be mocked as a modern-day believer in “Reefer Madness,” the notorious 1936 movie that portrays young people descending into insanity and violence after smoking marijuana. A strange disconnect has resulted. With large studies in peer-reviewed journals showing that marijuana increases the risk of psychosis and schizophrenia, the scientific literature around the drug is far more negative than it was 20 years ago. Comparing two major reports from the National Academy of Medicine, the nonprofit group that advises the federal government on health and medicine, makes the difference clear. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25843 - Posted: 01.07.2019

By: Arthur Robin Williams, M.D., and Frances R. Levin, M.D. There's no shortage of statistics about the depth of America's opioid epidemic: 72,000 overdose deaths just last year, more than 2 million with problems, and so on. But numbers only begin to tell the whole story. Beth Macy, who has spent three decades reporting on central Appalachia—which she claims is the birthplace of the modern opioid epidemic—focuses her book on social and economic trends and how they affect ordinary people. Our reviewers, colleagues at the Columbia University Division on Substance Use Disorders, are well qualified to comment. A new volume can be added to the panoply of books detailing the tragedies of the 21st century opioid epidemic. Beth Macy’s Dopesick (Little Brown & Co., 2018) is anchored in a handful of increasingly vocal and public Appalachia families afflicted by the expansion of opioid dealing into small towns and suburbs formerly thought immune to inner-city plagues of addiction. Dopesick largely reads as a human interest story, a series of intertwined portrayals of grief and terror as young family members descend into OxyContin (one quarter of the local high school students had reported trying the drug within two years of its 1996 market launch), then heroin, then synthetic opioids, reflecting the epidemic’ s tragic course. These painful and personal stories form the heart of Macy’s book and make it perhaps the most empathic of the volumes regarding the epidemic. That she can represent a major drug dealer with as much compassion as the grieving families of teenagers and young adults who died because of his trade speaks to her Southern warmth. Her shrewd tirelessness as a journalist enables her to discern the fault lines of the stories that matter most. © 2018 The Dana Foundation

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25816 - Posted: 12.23.2018

Patricia Janak Drugs of abuse have complex pharmacological effects that trigger many changes in brain function. One of these effects, the direct or indirect activation of neurons that release the neurotransmitter dopamine, is common to all drugs of abuse and has long been assumed to contribute to the development of addiction. Writing in Nature, Pascoli et al.1 report on the neurobiological mechanisms induced by the repeated activation of dopamine neurons that might explain why some drug users seek reward despite facing negative consequences — a type of compulsive behaviour that is a defining feature of human addiction2. The authors took an optogenetics approach to mimic the activation of the brain’s dopamine systems by drugs of abuse: they used laser light delivered through an optical fibre to activate dopamine neurons in the ventral tegmental area (VTA) of the brains of genetically engineered mice. The mice could directly stimulate these neurons themselves by pressing a lever, and performed this action avidly during a test period of 40 minutes a day for almost 2 weeks. On subsequent days, the mice received a brief electric shock to their feet on one-third of the lever-pressing occasions, at random. Their behaviour under this condition revealed an intriguing variability: 40% of the mice (termed renouncers) greatly reduced the frequency of lever-pressing when given foot shocks (Fig. 1a), whereas the remaining 60% (perseverers) were willing to receive painful punishment for the opportunity to self-stimulate their dopamine neurons (Fig. 1b). As some of these authors have previously shown3, the persevering mice provide a model for persistent drug use despite negative consequences, and parallel the subset of human drug users whose drug use becomes compulsive. © 2018 Springer Nature Publishing AG

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25814 - Posted: 12.22.2018