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Heavy drinkers are putting themselves at risk of dementia, according to the largest study of its kind ever conducted. Research published in the Lancet Public Health journal provides powerful evidence that people who drink enough to end up in hospital are putting themselves at serious risk of vascular dementia and Alzheimer’s disease. It will also raise questions for moderate drinkers about the possible long-term consequences of their social habit. The study, which used the French National Hospital Discharge database, looked at more than a million people diagnosed with dementia between 2008 and 2013. More than a third – 38% of the 57,000 cases of early-onset dementia – were directly alcohol-related and 18% had an additional diagnosis of alcohol use disorders. Overall, alcohol use disorders were associated with a three times greater risk of all types of dementia. Dr Sara Imarisio, head of research at Alzheimer’s Research UK, said: “As this study only looked at the people who had been admitted to hospital due to chronic heavy drinking, it doesn’t reveal the full extent of the link between alcohol use and dementia risk. Previous research has indicated that even moderate drinking may have a negative impact on brain health and people shouldn’t be under the impression that only drinking to the point of hospitalisation carries a risk.” Experts said the new research should change attitudes. “What is most surprising about this paper is that it has taken us so long to recognise that alcohol misuse and dependence are such potent risk factors for the development of dementia,” said Robert Howard, professor of old age psychiatry at University College London.

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: 24682 - Posted: 02.21.2018

Dean Burnett The internet is a weird place. Part of this is due to how things linger rather than disappear, as they tended to do with more “traditional” media. Nowadays, people’s jobs can (rightly or wrongly) be endangered for tweets they wrote years ago. The adage about “today’s news is tomorrow’s fish and chip papers” seems no longer to apply. This is particularly true when a headline or story from years ago can be found by a group or community on a social network that missed it previously, so they share it widely and it ends up in your feeds long after it’s been “forgotten”. It can be a bit confusing for those of us who grew up solely with televised news. It’s like watching the weekend football roundup when it’s suddenly interrupted by a report that the Berlin Wall has come down. Case in point: yesterday I saw several examples of a story from 2015 about how scientists have discovered that cheese triggers the same part of the brain as hard drugs. A lot of people seem to be sharing this again (even me, thinking it was new). You’d assume someone well-versed in neuroscience like myself would easily recognise an old story like this. So why didn’t I? Stories like this are hardly uncommon. You can barely go a month without some study or report describing something supposedly innocuous as having the same effect on the brain, or activating the same brain regions, as drugs of abuse, be it sugar, pornography, religion, sex, Facebook, music, or, apparently, cheese. Give it a week, something else will be cited as stimulating our brains just like the most powerful narcotics. Maybe walking on crunchy leaves or taking your bra off after a long day will be described as the equivalent of inhaling a bin-bag full of cocaine? © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Attention and Consciousness
Link ID: 24658 - Posted: 02.14.2018

By Marc Lewis Over the past year and a half, Scientific American has published a number of fine articles arguing that addiction is not a disease, that drugs are not the cause of addiction, and that social and societal factors are fundamental contributors to opioid addiction in general and the overdose crisis in particular. The dominant view, that addiction is a disease resulting from drug use, is gradually being eroded by these and other incisive critiques. Yet the disease model and its corollaries still prevail in the domains of research, policy setting, knowledge dissemination and treatment delivery, more in the United States than in any other country in the developed world. You might wonder: what are we waiting for? The disease model remains dominant in the U.S. because of its stakeholders. First, the rehab industry, worth an estimated $35 billion per year, uses the disease nomenclature in a vast majority of its ads and slogans. Despite consistently low success rates, that's not likely to stop because it pulls in the cash. Second, as long as addiction is labeled a disease, medical insurance providers can be required to pay for it. Of course they do so as cheaply as possible, to the detriment of service quality, but they at least save governments the true costs of dealing with addiction through education, social support, employment initiatives and anti-poverty mechanisms. Third, the National Institute on Drug Abuse (NIDA), a part of the National Institutes of Health (NIH) that funds roughly 90 percent of addiction research worldwide, is a medically oriented funder and policy setter, as are the American Society of Addiction Medicine and other similar bodies. © 2018 Scientific American

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: 24642 - Posted: 02.10.2018

Kratom, a coffee-like plant native to southeast Asia which has similar properties to heroin and morphine is readily available in Canada. (Earth Kratom) U.S. health authorities say an herbal supplement promoted as an alternative pain remedy contains the same chemicals found in opioids, the addictive family of drugs at the centre of a national addiction crisis. The U.S. Food and Drug Administration analysis, published Tuesday, makes it more likely that the supplement, kratom, could be banned by the federal government. The FDA also said it has identified 44 reports of death involving kratom since 2011, up from 36 reported in November. Sold in various capsules and powders, kratom has gained popularity in the U.S. as a treatment for pain, anxiety and drug dependence. Proponents argue that the substance is safer than opioid painkillers like OxyContin and Vicodin, which have contributed to an epidemic of drug abuse. More than 63,000 Americans died in 2016 from drug overdoses, mostly from opioids. FDA Commissioner Scott Gottlieb reiterated that there are no FDA-approved medical uses for kratom, which is derived from a plant native to Southeast Asia. "Claiming that kratom is benign because it's 'just a plant' is shortsighted and dangerous," Gottlieb said in a statement. "It's an opioid. And it's an opioid that's associated with novel risks because of the variability in how it's being formulated, sold and used recreationally." ©2018 CBC/Radio-Canada.

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: 24628 - Posted: 02.07.2018

Beth Marsh, Lilla Porffy, Meryem Grabski, Will Lawn January 2018 has come to an end and with it the month that people increasingly use to abstain from alcohol. It is still unknown whether Dry January has a lasting effect on drinking behaviours, and people with an alcohol dependency problem should always seek support from their GP before going through detox. Nonetheless, Dry January undoubtedly drives a critical conversation about alcohol use and provides an opportunity for us to reconsider our relationship with alcohol (one of the main goals of the charity Alcohol Concern, who support the challenge). While overall alcohol consumption in the UK is falling, alcohol abuse still represents the fifth biggest risk factor for illness, death and disability across all ages. With current treatments often failing to prevent relapse in the long term, researchers are investigating the possibility of using ketamine combined with psychological therapy to help people stay dry, and not just for January. Despite its often cited use as a recreational drug and “horse-tranquilizer” ketamine is also the most widely used anaesthetic in humans. Administered appropriately in a controlled and safe medical environment, ketamine may also have benefits in the treatment of drug problems. Evidence for this originally came from a research group in Russia in the 1980s. In this study, patients who had alcohol problems were given three weekly ketamine treatments in conjunction with psychological therapy. After one year, 66% of patients who underwent this treatment regime were abstinent, in comparison to 24% of patients who received treatment as usual, without any ketamine. This abstinence rate is much greater than those documented with any other relapse prevention method. © 2018 Guardian News and Media Limited

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: 24619 - Posted: 02.06.2018

By Kendall Powell “It’s impossible that we still struggle to decide if coffee is healthy or unhealthy,” says Giuseppe Grosso, a nutritional epidemiologist at the University of Catania in Italy: Good for hypertension one week. Bad for hypertension the next. To address this vexing situation, Grosso and his colleagues collected all studies on the health effects of coffee, systematically reviewed the evidence, then offered up their bottom line in the Annual Review of Nutrition. Specifically, they looked at 127 meta-analyses, which lump together and statistically analyze studies on similar topics. A few of the studies were randomized controlled trials on coffee or caffeine administration, but most were observational studies of real-world coffee and caffeine consumption habits. (None of the review’s authors were paid by any food or beverage company.) For each meta-analysis, the team calculated the strength of the study’s designs and conclusions and then ranked its evidence for relationships between coffee and health on a scale from “convincing” all the way down to “limited.” No studies showed a “convincing” level of evidence — not surprisingly, since observational studies lack the rigor of ­gold-standard trials that use placebo controls. But several found “probable” evidence that coffee-drinking is associated with a decreased risk of many common cancers — including breast, colorectal, colon, endometrial and prostate — with a 2 to 20 percent reduction in risk, depending on the cancer type. © 1996-2018 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: 24612 - Posted: 02.05.2018

Emmarie Huetteman Dr. Andrey Ostrovsky's family did not discuss what killed his uncle in 2015. The man was young, not quite two weeks past his 45th birthday, when he died, and had lost touch with loved ones in his final months. At the time, Ostrovsky wondered if his uncle had perhaps killed himself. Almost two years later, Ostrovsky was Medicaid's chief medical officer, grappling professionally with an opioid crisis that kills about 115 Americans each day, when he learned the truth: His uncle had died of a drug overdose. Family members knew the uncle's life had been turbulent for a while before his death; they'd watched as he divorced his wife and became estranged from his 4-year-old daughter and eventually lost his job as a furniture store manager. But Ostrovsky wanted to better understand what had happened to the man — his stepfather's younger brother. So last fall, when he found himself in southeastern Florida, where his uncle had died, Ostrovsky contacted one of the uncle's friends for what he expected would be a quick cup of coffee. Instead the friend "let loose," revealing that he and Ostrovsky's uncle had been experimenting with a variety of drugs the night of the death. It was the tragic culmination of more than a decade of substance abuse — a pattern of behavior much of the family knew nothing about. An autopsy showed there were opiates and cocaine in his uncle's system, Ostrovsky later learned. © 2018 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: 24572 - Posted: 01.26.2018

By Alex Therrien Health reporter, BBC News Smokers need to quit cigarettes rather than cut back on them to significantly lower their risk of heart disease and stroke, a large BMJ study suggests. People who smoked even one cigarette a day were still about 50% more likely to develop heart disease and 30% more likely to have a stroke than people who had never smoked, researchers said. They said it showed there was no safe level of smoking for such diseases. But an expert said people who cut down were more likely to stop. Cardiovascular disease, not cancer, is the greatest mortality risk for smoking, causing about 48% of smoking-related premature deaths. While the percentage of adults in the UK who smoked had been falling, the proportion of people who smoked one to five cigarettes a day had been rising steadily, researchers said. Their analysis of 141 studies, published in the BMJ, indicates a 20-a-day habit would cause seven heart attacks or strokes in a group of 100 middle-aged people. But if they drastically cut back to one a day it would still cause three heart attacks, the research suggests. The researchers said men who smoked one cigarette a day had about a 48% higher risk of developing coronary heart disease and were 25% more likely to have a stroke than those who had never smoked. For women, it was higher - 57% for heart disease and 31% for stroke. Prof Allan Hackshaw at the UCL Cancer Institute at University College London, who led the study, told the BBC: "There's been a trend in quite a few countries for heavy smokers to cut down, thinking that's perfectly fine, which is the case for things like cancer. "But for these two common disorders, which they're probably more likely to get than cancer, it's not the case. They've got to stop completely." © 2018 BBC.

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: 24563 - Posted: 01.25.2018

Patti Neighmond Kids who vape and use other forms of e-cigarettes are likely to try more harmful tobacco products like regular cigarettes, but e-cigarettes do hold some promise for helping adults quit. That's according to the National Academies of Science, Engineering and Medicine, which published a comprehensive public health review of more than 800 studies on e-cigarettes on Tuesday. "There is conclusive evidence that most products emit a variety of potentially toxic substances. However the number and intensity is highly variable," says David Eaton, who heads the committee that wrote the report. He is also the dean and vice provost of the graduate school of the University of Washington, Seattle. "In some circumstances, such as their use by nonsmoking adolescents and young adults, their adverse effects clearly warrant concern. In other cases, such as when adult smokers use them to quit smoking, they offer an opportunity to reduce smoking-related illness." In fact, 15 of the studies NAS reviewed found that when teens and young adults use e-cigarettes, they are more likely to try regular tobacco within a year. "We found that kids who tried e-cigarettes, hookah, or smokeless tobacco or cigars — any non-cigarette tobacco product — were all twice as likely to try cigarettes a year later, compared to kids who hadn't used any of those other tobacco products," says Shannon Lea Watkins, a public policy researcher at University of California, San Francisco. Watkins and her colleagues also found that the effects of using non-cigarette products compound: "Kids using two or more non-cigarette products were four times as likely to report using cigarettes a year later." © 2018 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: 24561 - Posted: 01.24.2018

By Dina Fine Maron One evening this past fall a patient stumbled into the emergency room at Brigham and Women’s Hospital in Boston. “I don’t feel so…” she muttered, before losing consciousness. Her breathing was shallow and her pupils were pinpoints, typical symptoms of an opioid overdose. Her care team sprang into action. They injected her with 0.4 milligram of naloxone, an overdose antidote—but she remained unresponsive. They next tried one milligram, then two, then four. In total they used 12 milligrams in just five minutes, says Edward Boyer, the physician overseeing her care that night. Yet the patient still had trouble breathing. They put a tube down her throat and hooked her to a ventilator. Twenty minutes later she woke up—angry and in drug withdrawal, but alive. The patient, whose identifying details may have been altered to protect patient confidentiality, had apparently injected herself with a synthetic opioid such as fentanyl right outside of the hospital building. That gave her just enough time to seek help. But many users of synthetic opioids are not so lucky. These drugs, which bear little chemical resemblance to any opioid derived from the opium poppy, are much more powerful than poppy-based heroin and semisynthetic opioids such as oxycodone or hydrocodone. Thus, the standard dose of naloxone employed by first responders (and sold in bystander overdose kits) is often not potent enough to save a synthetic opioid user’s life. © 2018 Scientific American

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 24505 - Posted: 01.09.2018

Nicola Davis The prospect of a non-addictive alternatives to morphine and other opioids has moved a step closer as scientists say they have cracked a key challenge in developing safe and effective substitute painkillers. Overuse of highly addictive opioids has led to a health crisis across the world, especially in the US where more than 60,000 people died after overdoses in 2016 alone; president Donald Trump has declared the epidemic a public health emergency. Researchers looking for alternatives examined a receptor protein that interacts with opioids in the brain, and have now revealed its structure as it binds to a molecule related to morphine. While the structure of the receptor had previously been reported, this is the first time scientists have unveiled its structure as it interacts with a drug. The development, they say, could prove pivotal. The protein, known as the kappa opioid receptor, is one of four that interacts with opioids, but – crucially – while it can trigger pain-killing effects, it is not linked to problems including constipation, addiction risk and death as a result of overdose. “Tens of thousands of people are dying every year in the US because of opioid overdoses; in the last year more than 50,000 people died. That is as many as died in the Vietnam war in the US. It is a terrible, terrible crisis,” said Bryan Roth, co-author of the research from the University of North Carolina at Chapel Hill. © 2018 Guardian News and Media Limited

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24497 - Posted: 01.06.2018

By Alfonso Serrano Elvis Alonzo began smoking cannabis as a last resort. Three years as a Marine Corps officer and 13 years with the Glendale Police Department in Arizona—where he was exposed to murders, suicides and people dying in his arms—had left him emotionally crippled. Toward the end of his police service, doctors diagnosed Alonzo with post-traumatic stress disorder and prescribed various medications to temper his nightmares and flashbacks. The drugs “turned me into a zombie,” he says. “I was so out of it that I couldn’t even drive, so they (the police department) had to medically retire me.” Alonzo stopped showering. His wife left him, and he nearly lost his house. Then a friend suggested he try marijuana to relieve his symptoms. “It’s been a godsend,” he says. “It curbs my anxiety, and it makes me sleep fantastic for at least four hours. It needs to be studied.” Thousands of military veterans have echoed Alonzo’s claim for years. They have pressured federal and state legislators to legalize medicinal cannabis and ease rules on research into the plant’s apparent therapeutic properties, arguing that it could help reduce suicide rates among former soldiers. Backed by overwhelming public support for broader legalization, their demands are starting to resonate in statehouses across the country. This past November, New York Gov. Andrew Cuomo chose Veterans Day to make PTSD a qualifying condition for the state’s tightly controlled medical marijuana program. New York joined seven other states this year—and 27 overall—that include PTSD in their lists of conditions that qualify for medical cannabis. © 2018 Scientific America

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: 24491 - Posted: 01.05.2018

/ By Robin Lloyd Most Americans drink safely and in moderation, as many of us could attest earlier this week. But a steady annual increase in trips made to emergency rooms as a result of drinking alcohol added up to 61 percent more visits in 2014 compared with 2006, according to a study published this week in the journal Alcoholism: Clinical and Experimental Research. The increase is alarming but also a bit mysterious to neuroscientist Aaron White, one of the study’s authors, in part because the same nine-year period showed a mere 2 percent increase in per capita alcohol consumption overall, and an 8 percent increase in the number of emergency room visits for any reason. White and his four co-authors, three of whom work with him at the National Institute on Alcohol Abuse and Alcoholism, have yet to understand what’s behind the dramatic increase in alcohol-related ER visits. “The lowest hanging fruit in terms of hypotheses is that there must be an increase in risky drinking in some people,” White says. “Even though that is not showing up in increases in overall per capita consumption, it’s enough to drive the increase in alcohol-related emergency department visits.” But there is no strong evidence for a national increase in binge drinking, he added. The new finding comes from an analysis of a nationally representative data set that includes information on about 30 million visits to U.S. hospital-based emergency departments annually, from 945 hospitals in 33 states and Washington, D.C. Copyright 2018 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: 24490 - Posted: 01.05.2018

Linda Bauld Search for the term ‘vaping’ online and you’d be forgiven for thinking that it is an activity fraught with risks. The top stories relate to health problems, explosions and that vaping leads to smoking in teenagers. For the average smoker seeking information on vaping, a quick internet search offers little reassurance. Might as well continue smoking, the headlines imply, if these products are so dangerous. But the reality is that they are not. In the past year, more than any other, the evidence that using an e-cigarette is far safer than smoking has continued to accumulate. 2017 saw the publication of the first longer term study of vaping, comparing toxicant exposure between people who’d stopped smoking and used the products for an average of 16 months, compared with those who continued to smoke. Funded by Cancer Research UK, the study found large reductions in carcinogens and other toxic compounds in vapers compared with smokers, but only if the user had stopped smoking completely. A further recent study compared toxicants in vapour and smoke that can cause cancer, and estimated excess cancer risk over a lifetime from smoking cigarettes or vaping. Most of the available data on e-cigarettes in this study suggested a cancer risk from vaping around 1% of that from smoking. E-cigarettes are less harmful than smoking because they don’t contain tobacco. Inhaling burnt tobacco - but also chewing it - is hugely damaging to human health. Remove the tobacco and the combustion and it is hardly surprising that risk is reduced. That doesn’t mean e-cigarettes are harmless. But it does mean that we can be relatively confident that switching from smoking to vaping will have health benefits. © 2017 Guardian News and Media Limited

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: 24474 - Posted: 12.30.2017

By Simon Makin The brain's reward system learns the actions that produce positive outcomes, such as obtaining food or sex. It then reinforces the desire to initiate those behaviors by inducing pleasure in anticipation of the relevant action. But in some circumstances this system can become oversensitized to pleasurable but harmful behaviors, producing pathological impulses like drug addiction, binge eating and compulsive gambling. But what if we could spot impulsive urges in the brain and intervene to prevent the act? This is the promise of a new study published December 18 in Proceedings of the National Academy of Sciences, led by neurosurgeon Casey Halpern, of Stanford University. His team identified a “signature” of impulsive urges in part of the brain's reward-learning circuitry, the nucleus accumbens. Delivering electrical pulses to this region on detecting this activity reduced binge-eating behavior in mice. They also observed the same signature in a human brain, suggesting the technique has potential for treating a range of conditions involving compulsive behaviors. “We've identified a brain biomarker of loss of control,” Halpern says. “If we can use that to prevent any of these potentially dangerous actions, we can help a lot of people.” Researchers used a variation on deep-brain stimulation (DBS) in their experiments, a well-established treatment to diminish the shaking present in Parkinson's disease that is also showing promise in other conditions including depression and obsessive-compulsive disorder. Exactly how DBS has beneficial effects is still being debated, but there can be side effects. When treating movement disorders, patients may experience tingling and muscle contraction, says neurosurgeon Tipu Aziz of the University of Oxford. The long-term consequences in other regions are unknown but could include seizures, or effects on cognition, he says. © 2017 Scientific American,

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24441 - Posted: 12.20.2017

Angus Chen Psychedelic drugs are getting a makeover, with scientists exploring their potential in treating debilitating conditions like cluster headaches, addiction or anxiety, with promising results. That's despite the fact that very few researchers are legally allowed to study psychedelics, largely because of LSD's decades-old reputation as a counterculture drug that sparked bad trips. Back in the 1960s, LSD was touted as a tool to shed social conventions and fast-forward to enlightenment – or as LSD advocate Timothy Leary memorably said, "Turn on, tune in, drop out." He was hardly the first to feel the chemical's allure. Back in the 1930s, Swiss chemist Albert Hofmann had shelved LSD after first testing it as a treatment for heart disease. But he couldn't shake the feeling that there was something more to it. After accidentally ingesting a bit and having a mild psychedelic experience, Hofmann decided to go further. He eats 250 micrograms of LSD and, scientist that he is, starts journaling his experience. He only gets one entry down before he starts having really intense hallucinations. As he bikes home, he feels like time and space are standing still and objects around him are warping and wavering in weird shapes. In the 1930's, Albert Hofmann accidentally ingested LSD during an experiment, which led him to experience a psychedelic reaction. © 2017 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: 24435 - Posted: 12.18.2017

By SHEILA KAPLAN Chris Beekman, whose company sells the dietary supplement Opiate Detox Pro, does not understand what all the fuss is about. “If it works, it works,” Mr. Beekman, the owner of NutraCore Health Products, said in an interview. “If it doesn’t, it doesn’t.” His customers, addicts trying to shake a dependence on opioids, can always get their money back, he said. Opiate Detox Pro’s label says, “Opioid addiction ease,” and the company’s website claims, “Our ingredients are the most effective on the market for treating withdrawal symptoms.” Mr. Beekman said he did not have scientific evidence to prove that the product worked, and would not be conducting research to buttress the company’s claims. “It’s just not going to happen,” he said, citing what he called the prohibitive cost of scientific studies and clinical trials. Peter Lurie thinks that is an unacceptable position from someone who sells supplements that purport to treat addiction. Dr. Lurie, a former Food and Drug Administration official, runs the nonprofit Center for Science in the Public Interest, which on Friday urged the F.D.A. and the Federal Trade Commission to crack down on businesses that target addicts with products that make unproven health claims. The F.D.A. has already zeroed in on another supplement, kratom, a botanical substance that has been promoted as a safe substitute for opioids and an adjunct to opioid use. Last month, the agency issued a public health advisory for kratom, warning that the product carried “deadly risks,” and linked about three dozen deaths to it. Earlier, the agency had ordered that kratom imports be seized and told companies to take it out of supplements. In general, the agency can fine companies that make and distribute them, or take other enforcement actions. In the past few weeks, reacting to other agency warnings, Amazon has stopped making available some products claiming to assist in opioid withdrawal. © 2017 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: 24410 - Posted: 12.09.2017

Paula Span Jeannie Cox currently enjoys a flavor called Coffee & Cream when she vapes. She’s also fond of White Lotus, which tastes “kind of fruity.” She buys those nicotine-containing liquids, along with her other e-cigarette supplies, at Mountain Oak Vapors in Chattanooga, Tenn., where she lives. A retired secretary in her 70s, she’s often the oldest customer in the shop. Not that she cares. What matters is that after ignoring decades of doctors’ warnings and smoking two packs a day, she hasn’t lit up a conventional cigarette in four years and four months. “Not one cigarette,” she said. “Vaping took its place.” Like Ms. Cox, some smokers have been able to stop smoking by switching to e-cigarettes, and many are trying. A recent study by the Centers for Disease Control and Prevention found that more smokers now attempt to quit by using e-cigarettes as a partial or total substitute for cigarettes than by using nicotine gum or lozenges, prescription medications or several other more established methods. Her success is what researchers disdainfully call “anecdotal evidence,” however. There’s “no conclusive evidence” that e-cigarettes help people stop smoking long-term, said Brian King, deputy director of the C.D.C.’s Office of Smoking and Health. At the moment, therefore, neither the C.D.C., the Food and Drug Administration nor the United States Preventive Services Task Force has approved or recommended e-cigarettes for smoking cessation. In fact, the rise of e-cigarettes has generated contentious debate among public health officials and advocates. But while the proportion of Americans who smoke continues to decrease — down to 15.1 percent in 2015 — the decline has stalled among older adults. © 2017 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: 24409 - Posted: 12.09.2017

Aimee Cunningham To halt the misuse of opioids, it may help to slash the number of pills prescribed, a new study suggests. Five months after the implementation of new opioid prescription guidelines at a University of Michigan hospital, roughly 7,000 fewer pills went home with patients — a drop that might reduce the risk of accessible pills leading to substance abuse. But the opioid reduction didn’t leave patients who had undergone a routine surgery with more pain, the team reports online December 6 in JAMA Surgery. “The decline in opioid volume after the intervention was dramatic,” says physician Mark Bicket of Johns Hopkins University School of Medicine, who was not involved in the study. Around 50 percent of people who misuse opioids get the drugs from a friend or relative for free, while 22 percent obtain them from a doctor, according to the U.S. Department of Health and Human Services. Michael Englesbe, a surgeon at the University of Michigan in Ann Arbor, says that part of doing a better job of managing patients’ pain “will be preventing chronic opioid use after surgical care and making sure fewer pills get into the community.” Englesbe and colleagues looked at 170 people who had a minimally invasive surgery to remove their gall bladders at the University of Michigan hospital from 2015 to 2016. All had received a prescription for opioids. Of those patients, 100 completed a survey detailing how much of the prescription they took, whether they also used a common painkiller such as ibuprofen or acetaminophen, and how they rated their pain during the first week after surgery. © Society for Science & the Public 2000 - 2017.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 24400 - Posted: 12.07.2017

By DOUGLAS QUENQUA If you grew up as part of the D.A.R.E. generation — kids of the 1980s and ’90s who learned about drugs from alarmist public service announcements — you know all too well the dangers of so-called gateway drugs. Go to bed with marijuana or beer, you were taught, and risk waking up with cocaine or heroin. Three decades later, scientists and politicians still debate whether using “soft” drugs necessarily leads a person down a slippery slope to the harder stuff. Critics note that marijuana has, in some cases, been shown to actually prevent people from abusing other substances. And even D.A.R.E. now acknowledges that the overwhelming majority of people who smoke pot or drink never graduate to pills and powders. But new research is breathing fresh life into the perennially controversial theory, and the timing seems apt. As marijuana legalization and the opioid epidemic sweep across the country, parents are once again questioning the root causes of addiction. And politicians opposed to legalization, including Attorney General Jeff Sessions and Gov. Chris Christie of New Jersey, have routinely used the gateway effect as their chief argument against reform. A Columbia University study published in November in Science Advances showed that rats exposed to alcohol were far more likely than other rats to push a lever that released cocaine. The researchers also found that the alcohol suppressed two genes that normally act as cutoff switches for the effects of cocaine, creating a “permissive environment” for the drug within the rodents’ brains. A similar study from 2011 — conducted by some of the same researchers, most notably Denise Kandel, who helped formulate the gateway theory in 1975 — produced comparable findings using nicotine and mice. © 2017 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: 24399 - Posted: 12.07.2017