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By Megan Scudellari Neuropharmacology postdoc Nick DiPatrizio was stumped. His advisor, University of California, Irvine, researcher Daniele Piomelli, had discovered eight years earlier that hungry rats have high levels of endocannabinoids, endogenous molecules that bind to the same receptors as the active ingredient in marijuana. Now, in 2009, DiPatrizio was trying to identify exactly where and how those molecules were controlling food intake in rats. But under specific feeding conditions, he couldn’t locate any changes in endocannabinoid levels in the brain, which is flush with endocannabinoid receptors and the obvious place to look for behavioral signals. Piomelli gently chastised his mentee. “He said, ‘You’re being neurocentric. Remember, there’s a body attached to the head. Look in the other organs of the body,’ ” recalls DiPatrizio. So the young scientist persisted, and eventually discovered that hunger—and the taste of fat—leads to increased endocannabinoid levels in the jejunum, a part of the small intestine. Endocannabinoid signaling in the gut, not the brain, was controlling food intake in the rodents in response to tasting fats.1 The evolution of endocannabinoid research has mirrored DiPatrizio’s early thinking: ever since the first endocannabinoid receptor was identified in the late 1980s, the field has been overwhelmingly focused on the central nervous system. The main endocannabinoid receptor, CB1, was first discovered in a rat brain and is now known to be among the most abundant G protein–coupled receptors in neurons there. Plus, cannabis is well-known for its psychotropic effects. “That has led the research field to be very CNS-oriented,” says Saoirse O’Sullivan, who studies endocannabinoids at the University of Nottingham in the U.K. © 1986-2017 The Scientist

Related chapters from BP7e: 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: 23870 - Posted: 07.25.2017

Laurel Hamers A common blood sugar medication or an extra dose of a thyroid hormone can reverse signs of cognitive damage in rats exposed in utero to alcohol. Both affect an enzyme that controls memory-related genes in the hippocampus, researchers report July 18 in Molecular Psychiatry. That insight might someday help scientists find an effective human treatment for fetal alcohol spectrum disorders, which can cause lifelong problems with concentration, learning and memory. “At this moment, there’s really no pharmaceutical therapy,” says R. Thomas Zoeller, a neurobiologist at the University of Massachusetts Amherst. Fetal alcohol syndrome disorders may affect up to 5 percent of U.S. kids, according to estimates from the U.S. Centers for Disease Control and Prevention. Scientists don’t know exactly why alcohol has such a strong effect on developing brains. But the lower thyroid hormone levels commonly induced by alcohol exposure might be one explanation, suggests study coauthor Eva Redei, a psychiatrist at Northwestern University Feinberg School of Medicine in Chicago. “The mother has to supply the thyroid hormones for brain development,” says Redei. So, pregnant women who drink might not be providing their fetuses with enough hormones for normal brain development. That could disrupt the developing hippocampus, a brain region involved in learning and memory. To counter alcohol’s effects, Redei and her colleagues gave doses of thyroxine, a thyroid hormone, to newborn rats that had been exposed to alcohol before birth. (That timing coincides developmentally with the third trimester of pregnancy in humans.) The amount of alcohol fed to the rat moms corresponded roughly to a woman drinking a glass or two of wine a day. |© Society for Science & the Public 2000 - 2017

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; 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: 23849 - Posted: 07.19.2017

By PERRI KLASS, M.D. We want to believe we’re raising our kids to think for themselves, and not to do dumb or unhealthy things just because the cool kids are doing them. But research shows that when it comes to smoking, children are heavily influenced by some of the folks they consider the coolest of the cool: actors in movies. “There’s a dose-response relationship: The more smoking kids see onscreen, the more likely they are to smoke,” said Dr. Stanton Glantz, a professor and director of the University of California, San Francisco, Center for Tobacco Control Research and Education. He is one of the authors of a new study that found that popular movies are showing more tobacco use onscreen. “The evidence shows it’s the largest single stimulus,” for smoking, he said; “it overpowers good parental role modeling, it’s more powerful than peer influence or even cigarette advertising.” He said that epidemiological studies have shown that if you control for all the other risk factors of smoking (whether parents smoke, attitudes toward risk taking, socioeconomic status, and so on), younger adolescents who are more heavily exposed to smoking on film are two to three times as likely to start smoking, compared with the kids who are more lightly exposed. Those whose parents smoke are more likely to smoke, he said, but exposure to smoking in movies can overcome the benefit of having nonsmoking parents. In one study, the children of nonsmoking parents with heavy exposure to movie smoking were as likely to smoke as the children of smoking parents with heavy movie exposure. To Dr. Glantz, and the other people who study this topic, that makes smoking in movies an “environmental toxin,” a factor endangering children. © 2017 The New York Times Company

Related chapters from BP7e: 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: 23844 - Posted: 07.18.2017

Nicola Davis People who drink coffee have a lower risk of dying from a host of causes, including heart disease, stroke and liver disease, research suggests – but experts say it’s unclear whether the health boost is down to the brew itself. The connection, revealed in two large studies, was found to hold regardless of whether the coffee was caffeinated or not, with the effect higher among those who drank more cups of coffee a day. But scientists say that the link might just be down to coffee-drinkers having healthier behaviours. “It is plausible that there is something else behind this that is causing this relationship,” said Marc Gunter, a co-author of one of the studies, from the International Agency for Research on Cancer. But, he added, based on the consistency of the results he would be surprised if coffee itself didn’t play a role in reducing the risk of death. About 2.25bn cups of coffee are consumed worldwide every day. While previous studies have suggested coffee might have health benefits, the latest research involves large and diverse cohorts of participants. The first study looked at coffee consumption among more than 185,000 white and non-white participants, recruited in the early 1990s and followed up for an average of over 16 years. The results revealed that drinking one cup of coffee a day was linked to a 12% lower risk of death at any age, from any cause while those drinking two or three cups a day had an 18% lower risk, with the association not linked to ethnicity. © 2017 Guardian News and Media Limited

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Brain Asymmetry, Spatial Cognition, and Language
Link ID: 23823 - Posted: 07.11.2017

Hannah Devlin A Catholic priest, a Rabbi and a Buddhist walk into a bar and order some magic mushrooms. It may sound like the first line of a bad joke, but this scenario is playing out in one of the first scientific investigations into the effects of psychedelic drugs on religious experience – albeit in a laboratory rather than a bar. Scientists at Johns Hopkins University in Baltimore have enlisted two dozen religious leaders from a wide range of denominations, to participate in a study in which they will be given two powerful doses of psilocybin, the active ingredient in magic mushrooms. Dr William Richards, a psychologist at Johns Hopkins University in Baltimore, Maryland who is involved in the work, said: “With psilocybin these profound mystical experiences are quite common. It seemed like a no-brainer that they might be of interest, if not valuable, to clergy.” The experiment, which is currently under way, aims to assess whether a transcendental experience makes the leaders more effective and confident in their work and how it alters their religious thinking. Despite most organised religions frowning on the use of illicit substances, Catholic, Orthodox and Presbyterian priests, a Zen Buddhist and several rabbis were recruited. The team has yet to persuade a Muslim imam or Hindu priest to take part, but “just about all the other bases are covered,” according to Richards. After preliminary screening, including medical and psychological tests, the participants have been given two powerful doses of psilocybin in two sessions, one month apart. © 2017 Guardian News and Media Limited

Related chapters from BP7e: Chapter 18: Attention and Higher Cognition; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 14: Attention and Consciousness; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23814 - Posted: 07.09.2017

Elana Gordon By the time Elvis Rosado was 25, he was addicted to opioids and serving time in jail for selling drugs to support his habit. "I was like, 'I have to kick this, I have to break this,' " he says. For Rosado, who lives in Philadelphia, drugs had become a way to disassociate from "the reality that was life." He'd wake up physically needing the drugs to function. His decision to finally stop using propelled him into another challenging chapter of his addiction and one of the most intense physical and mental experiences he could have imagined: detoxing. "The symptoms are horrific," Rosado says. There are recovery and treatment centers that can help people quit using drugs — in fact, it's a multi-billion-dollar industry. But this help can be expensive, and waiting lists for state and city-funded programs are often extremely long. So can detoxing on your own be the solution? In most cases, the answer is no. In fact, a growing movement within the field of addiction medicine is challenging the entire notion of detox and the assumption that when people cleanse themselves of chemicals, they're on the road to recovery. Article continues after sponsorship "That's a really pernicious myth, and it has erroneous implications," says Dr. Frederic Baurer, president of the Pennsylvania Society of Addiction Medicine. But at the time, Rosado says, he needed to end his "longtime love affair" with codeine. Like Oxycontin and morphine, it's an opioid. In jail, these drugs were easily available, Rosado recalls, through friends and cell mates. © 2017 npr

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23803 - Posted: 07.04.2017

By RONI CARYN RABIN It may be the most palatable advice you will ever get from a doctor: Have a glass of wine, a beer or a cocktail every day, and you just might prevent a heart attack and live longer. But the mantra that moderate drinking is good for the heart has never been put to a rigorous scientific test, and new research has linked even modest alcohol consumption to increases in breast cancer and changes in the brain. That has not stopped the alcoholic beverage industry from promoting the alcohol-is-good-for-you message by supporting scientific meetings and nurturing budding researchers in the field. Now the National Institutes of Health is starting a $100 million clinical trial to test for the first time whether a drink a day really does prevent heart attacks. And guess who is picking up most of the tab? Five companies that are among the world’s largest alcoholic beverage manufacturers — Anheuser-Busch InBev, Heineken, Diageo, Pernod Ricard and Carlsberg — have so far pledged $67.7 million to a foundation that raises money for the National Institutes of Health, said Margaret Murray, the director of the Global Alcohol Research Program at the National Institute on Alcohol Abuse and Alcoholism, which will oversee the study. The decision to let the alcohol industry pay the bulk of the cost has raised concern among researchers who track influence-peddling in science. “Research shows that industry-sponsored research almost invariably favors the interests of the industry sponsor, even when investigators believe they are immune from such influence,” said Marion Nestle, a professor of nutrition and food studies at New York University who is the author of several books on the topic, including “Food Politics: How the Food Industry Influences Nutrition and Health.” © 2017 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23800 - Posted: 07.04.2017

By Wallis Snowdon, Ariel Fournier The seizure of a controversial drug in Edmonton is evidence that more research is required on kratom as a possible antidote in Alberta's deadly opioid epidemic, says a leading researcher in the field. "Everything has to be taken with caution, but does that mean you take it off the streets?" said Susruta Majumdar, a chemist who has worked on numerous studies into the drug. "Probably not," said Majumdar, who works in the department of neurology at Sloan Kettering Cancer Center in New York. "It's a little premature to ban it right away and take it out of the public scenario because very little research has been done. It's a weak alkaloid but we need to be cautious about it." In a news release Tuesday, Health Canada said it had seized unauthorized kratom products from two Edmonton head shops. The packets were confiscated from a store called Jupiter on Whyte Avenue and from another called Bogart's Pipes and Papers on 132nd Avenue. Kratom is a coffee-like plant native to southeast Asia. The drug is traditionally consumed by chewing on the leaves, but can also be ingested as a capsule or powder or as a tea. Health Canada said the herbal product has been linked to both "narcotic and stimulant-like effects," and may pose serious health risks including nausea, vomiting, seizures, and liver toxicity. ©2017 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23799 - Posted: 07.01.2017

ByMaia Szalavitz George Sarlo is throwing cash at research into how drugs like magic mushrooms can help people overcome trauma like his own. Deep in the Mexican jungle, in a village so remote it's only accessible by boat, 74-year-old venture capitalist George Sarlo waited to meet his father. It was the fall of 2012, and Sarlo knew his quest seemed absurd. After all, his father had been dead for decades, and he had no connection to this region of rainforests and beaches and its indigenous peoples. As the financier watched a shaman prepare a ceremonial cup of bitter brown ayahuasca, he couldn't believe that he'd agreed to swallow this nauseating psychedelic brew for a second time. But he had traveled for 12 hours—via plane, boat, and finally on foot—to this primeval place, a newly-built gazebo-like wood platform without walls. He had expressed his intentions in a group therapy session in preparation; he had eaten a special, bland diet and even halted other medications. He also trusted his friend, Dr. Gabor Maté, a fellow Hungarian Holocaust survivor, who led the therapy and had arranged the trip. Maté is perhaps best known for his book, In the Realm of Hungry Ghosts, which explores his work with extremely traumatized injection drug users in Vancouver. He's been offering psychedelic therapy to trauma survivors since learning about the potential of ayahuasca in 2008.

Related chapters from BP7e: 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: 23798 - Posted: 07.01.2017

Hannah Devlin Doctors in Bristol are set to begin the world’s first clinical study into the use of MDMA to treat alcohol addiction. Researchers are testing whether a few doses of the drug, in conjunction with psychotherapy, could help patients overcome addiction more effectively than conventional treatments. The small trial was granted ethical approval a few weeks ago and the team expects to give the first dose of MDMA, the active ingredient in ecstasy pills, within the next two months. Ben Sessa, a clinical psychiatrist on the trial and senior research fellow at Imperial College London said: “We know that MDMA works really well in helping people who have suffered trauma and it helps to build empathy. Many of my patients who are alcoholics have suffered some sort of trauma in their past and this plays a role in their addiction.” Twenty patients, recruited through the recreational drug and alcohol services in Bristol, will be given the drug in capsule form during two supervised treatment sessions. The participants will be heavy drinkers – typically consuming the equivalent of five bottles of wine a day – who have relapsed into alcoholism repeatedly after trying other forms of treatment. “After 100 years of modern psychiatry our treatments are really poor,” said Sessa, speaking at the Breaking Convention conference in London. “The chances of relapse for these patients are really high – 90% at three years. No one has ever given MDMA to treat alcoholism before.” © 2017 Guardian News and Media Limited

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23797 - Posted: 07.01.2017

By ABBY GOODNOUGH WASHINGTON — The Senate leadership’s efforts to salvage the Republican health care bill have focused in part on adding $45 billion for states to spend on opioid addiction treatment. That is a big pot of money. But addiction specialists said it was drastically short of what would be needed to make up for the legislation’s deep cuts to Medicaid, which has provided treatment for hundreds of thousands of people caught up in a national epidemic of opioid abuse. The new money would most likely flow to states in the form of grants over 10 years, averaging out to $4.5 billion per year. With hundreds of people dying every week from overdoses of heroin, fentanyl and opioid painkillers, some specialists say a fixed amount of grant money is simply inadequate compared with the open-ended funding stream that Medicaid provides to treat all who qualify for the coverage. “When it comes to other illnesses like breast cancer or heart disease, we’d never rely solely on grants for treatment — because we know that grants are not substitutes for health coverage,” said Linda Rosenberg, president and chief executive of the National Council for Behavioral Health, which represents treatment providers. “Addiction is no different.” The Affordable Care Act vastly expanded access to addiction treatment by designating those services as “essential benefits.” That means they had to be covered through both an expansion of Medicaid to far more low-income adults and the marketplaces set up under the law for people to buy private plans. Both the House and Senate health bills would effectively end the expansion and cap federal Medicaid spending, resulting in the loss of coverage for millions of people, according to the Congressional Budget Office. © 2017 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23796 - Posted: 07.01.2017

By Kathryn Casteel It’s no secret that heroin has become an epidemic in the United States. Heroin overdose deaths have risen more than sixfold in less than a decade and a half.1 Yet according to one of the most widely cited sources of data on drug use, the number of Americans using heroin has risen far more slowly, roughly doubling during the same time period.2 Most major researchers believe that source, the National Survey on Drug Use and Health, vastly understates the increase in heroin use. But many rely on the survey anyway for a simple reason: It’s the best data they have. Several other sources that researchers once relied on are no longer being updated or have become more difficult to access. The lack of data means researchers, policymakers and public health workers are facing the worst U.S. drug epidemic in a generation without essential information about the nature of the problem or its scale. “We’re simply flying blind when it comes to data collection, and it’s costing lives,” said John Carnevale, a drug policy expert who served at the federal Office of National Drug Control Policy under both Republican and Democratic administrations. There is anecdotal evidence of how patterns of drug use are changing, Carnevale said, and special studies conducted in various localities are identifying populations of drug users. “But the national data sets we have in place now really don’t give us the answers that we need,” he said.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23792 - Posted: 06.30.2017

By Chris Brown, Chris Corday, All it took was a single beer for Murray's Shaw life to unravel. The moment came on a bike holiday in January 2016 in San Diego while he was with some friends from the Vancouver area. After almost 20 years sober, the community college instructor from New Westminster, B.C., cracked open a cold one at the end of a long ride. Fourteen months later, he died alone in a hotel room in Vancouver's Downtown Eastside. Fentanyl overdose was the coroner's conclusion. "He wasn't making a choice with a rational mind. He was depressed and he was battling this impulse to use," said his wife, Sasha Wood, who offered to tell her husband's story to CBC News in the hopes it might help other families dealing with substance abuse issues. Fentanyl has become a scourge across the country, but B.C. has been hit the hardest: an average of four people have died of drug overdose every day in 2017. Wood said the events that led to Shaw's death illustrate much that's wrong with how the Canadian health care system treats those with an addiction. 'I just thought he could stop' Shaw had problems with alcohol in his 20s and got into trouble with the law. But Wood, 49, says he sought treatment and turned his life around. He stopped drinking completely, went to university and worked toward a PhD. ©2017 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23769 - Posted: 06.24.2017

By SAM QUINONES COVINGTON, KY. — Not long ago, I visited a Narcotics Anonymous meeting where men with tattoos and short-cropped hair sat in a circle and talked out their errors. One had lived under an overpass, pimping his girlfriend’s daughter for cash to buy heroin. As the thought brought him to tears, his neighbor patted his shoulder. Others owned to stealing from grandparents, to losing jobs and children. Soon, most in the room — men with years of street addiction behind them — were wiping their eyes. What made the meeting remarkable, however, was not the stories, but where it was taking place. Unit 104 is a 70-man pod in Kenton County Detention Center in northern Kentucky, across the Ohio River from Cincinnati. The unit, and an equivalent one for women, is part of a new approach to jail made necessary by our nationwide epidemic of opiate addiction. Drug overdoses are now the leading cause of death among Americans under 50. As the country has awakened to that epidemic, a new mantra has emerged: “We can’t arrest our way out of this,” accompanied by calls for more drug-addiction treatment. Yet the opiate epidemic has swamped our treatment-center infrastructure. Only one in 10 addicts get the treatment they need, according to a 2016 surgeon general’s report. New centers are costly to build, politically difficult to find real estate for and beyond the means of most uninsured street addicts, anyway. So where can we quickly find cheap new capacity for drug treatment accessible to the street addict? Jail is one place few have thought to look. Jails typically house inmates awaiting trial or serving up to a year for a misdemeanor crime. Many inmates are drug addicts. They vegetate for months, trading crime stories in an atmosphere of boredom and brutality. Any attempt at treatment is usually limited to a weekly visit by a pastor or an Alcoholics Anonymous volunteer. When inmates are released, they’re in the clothes they came in with, regardless of the weather, and have no assistance to re-enter the real world. This kind of jail has always been accepted as an unavoidable fixed cost of government. © 2017 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23754 - Posted: 06.20.2017

By ABBY GOODNOUGH WASHINGTON — Weeks before the presidential election, at a packed rally in New Hampshire, Donald J. Trump recounted the story of a young woman and her boyfriend who had fatally overdosed within a year of each other. He promised not just a border wall to keep drugs out, but also more access to treatment. “We’re going to take care of it,” he said of the opioid addiction epidemic, which has disproportionately hit states that were crucial to his election victory. “What’s taking so long?” Five months into his term, though, President Trump has enthusiastically supported a health care bill that would deeply cut the Medicaid program that has provided treatment to thousands of addicted Americans. He has yet to fill the nation’s top public health and drug policy jobs. And while he has appointed a bipartisan commission on the opioid crisis, which held its first official meeting on Friday, it remains to be seen how much attention the panel can command from Mr. Trump’s turbulent administration. Some addiction specialists say that waiting for a commission’s recommendations when hundreds of people are dying each week — and when countless groups around the country have studied the issue already — is wasting time. What is really needed, the specialists say, is the type of concerted, emergency action that public health officials have used to fight outbreaks of infectious diseases. “There really isn’t anything this commission is going to figure out that we don’t know already,” said Dr. Andrew Kolodny, who directs opioid policy research at Brandeis University’s Heller School for Social Policy and Management. “What we need is an enormous federal investment in expanding access to addiction treatment, and for the different federal agencies that have a piece of this problem to be working in a coordinated fashion.” © 2017 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23750 - Posted: 06.17.2017

Rob Stein The Food and Drug Administration requested Thursday that the drugmaker Endo Pharmaceuticals stop selling Opana ER — its extended-release version of Opana. The FDA says the move marks the first time the agency has taken steps to remove an opioid from the market because of "public health consequences of abuse." An increasing number of people, the FDA says, are abusing the powerful prescription pills by crushing, dissolving and injecting them. The sharing of needles by these drug users has fueled an outbreak of associated infectious diseases — HIV, hepatitis C and another serious blood disorder. "We are facing an opioid epidemic — a public health crisis, and we must take all necessary steps to reduce the scope of opioid misuse and abuse," says Dr. Scott Gottlieb, the FDA's commissioner, in announcing the move. "We will continue to take regulatory steps when we see situations where an opioid product's risks outweigh its benefits, not only for its intended patient population but also in regard to its potential for misuse and abuse," Gottlieb says. Dangers Of Opana Opioid Painkiller Outweigh Benefits, FDA Panel Says In a written statement, Endo says the company is "reviewing the request and is evaluating the full range of potential options as we determine the appropriate path forward." The company defended its drug, a version of the medicine oxymorphone hydrochloride, citing the opioid's effectiveness in alleviating pain and Endo's efforts to prevent abuse. © 2017 npr

Related chapters from BP7e: 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: 23725 - Posted: 06.09.2017

Nicola Davis Drinking even moderate amounts of alcohol can damage the brain and impair cognitive function over time, researchers have claimed. While heavy drinking has previously been linked to memory problems and dementia, previous studies have suggested low levels of drinking could help protect the brain. But the new study pushes back against the notion of such benefits. “We knew that drinking heavily for long periods of time was bad for brain health, but we didn’t know at these levels,” said Anya Topiwala, a clinical lecturer in old age psychiatry at the University of Oxford and co-author of the research. Alcohol is a direct cause of seven ​​forms of cancer, finds study Read more Writing in the British Medical Journal, researchers from the University of Oxford and University College London, describe how they followed the alcohol intake and cognitive performance of 550 men and women over 30 years from 1985. At the end of the study the team took MRI scans of the participants’ brains. None of the participants were deemed to have an alcohol dependence, but levels of drinking varied. After excluding 23 participants due to gaps in data or other issues, the team looked at participants’ alcohol intake as well as their performance on various cognitive tasks, as measured at six points over the 30 year period.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23718 - Posted: 06.07.2017

By JOSH KATZ AKRON, Ohio — Drug overdose deaths in 2016 most likely exceeded 59,000, the largest annual jump ever recorded in the United States, according to preliminary data compiled by The New York Times. The death count is the latest consequence of an escalating public health crisis: opioid addiction, now made more deadly by an influx of illicitly manufactured fentanyl and similar drugs. Drug overdoses are now the leading cause of death among Americans under 50. Although the data is preliminary, the Times’s best estimate is that deaths rose 19 percent over the 52,404 recorded in 2015. And all evidence suggests the problem has continued to worsen in 2017. Because drug deaths take a long time to certify, the Centers for Disease Control and Prevention will not be able to calculate final numbers until December. The Times compiled estimates for 2016 from hundreds of state health departments and county coroners and medical examiners. Together they represent data from states and counties that accounted for 76 percent of overdose deaths in 2015. They are a first look at the extent of the drug overdose epidemic last year, a detailed accounting of a modern plague. The initial data points to large increases in drug overdose deaths in states along the East Coast, particularly Maryland, Florida, Pennsylvania and Maine. In Ohio, which filed a lawsuit last week accusing five drug companies of abetting the opioid epidemic, we estimate overdose deaths increased by more than 25 percent in 2016. “Heroin is the devil’s drug, man. It is,” Cliff Parker said, sitting on a bench in Grace Park in Akron. Mr. Parker, 24, graduated from high school not too far from here, in nearby Copley, where he was a multisport athlete. In his senior year, he was a varsity wrestler and earned a scholarship to the University of Akron. Like his friends and teammates, he started using prescription painkillers at parties. It was fun, he said. By the time it stopped being fun, it was too late. Pills soon turned to heroin, and his life began slipping away from him. © 2017 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23712 - Posted: 06.06.2017

Meghan Rosen The first thing you’ll notice is the noise. Monitors beep steadily, relentlessly, ready to sound a car-alarm blare if a baby is in trouble. The air has an astringent odor — not clean exactly, but reminiscent of an operating room (there’s one next door). Ceiling lights shine fluorescent white. Half are off, but glare from the monitors throws out extra light. It’s midday on a Friday, but it’ll be just as bright at midnight. Here on the fourth floor of Yale New Haven Children’s Hospital, 10 tiny beds hold 10 tiny infants, each with Band-Aid–like patches stuck to their bodies to continuously monitor health. Between beds, nurses squeeze through narrow aisles crammed with folding chairs and plastic incubators. This space, one of five in the hospital’s neonatal intensive care unit, has the people and equipment needed to keep sick babies alive — heart rate monitors, oxygen tanks, IV poles to deliver medications. Until recently, Yale’s NICU and hundreds like it across the country were considered the place to be for newborns withdrawing from opioid drugs. But now, as the number of drug-dependent babies surges, doctors here and elsewhere are searching for better options. “We’re really focused on trying to get these kids out of the NICU,” says Yale pediatrician Matthew Grossman. “We’re looking at moms and the dads as the first line of treatment.” The nationwide rate of babies withdrawing from opioids has soared — up nearly 400 percent from 2000 to 2012. The booming numbers are the bleak by-product of the United States’ ongoing battle with the drugs: Sales of prescription opioid pain relievers alone quadrupled from 1999 to 2010, and overdose deaths tripled from 2000 to 2014. © Society for Science & the Public 2000 - 2017

Related chapters from BP7e: 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: 23689 - Posted: 06.01.2017

By Catherine Caruso If you give a mouse a beer, he is going to want a cookie—and another, and another. If you give a person enough beer, she might find herself wolfing down a plate of greasy nachos or some other caloric snack. A study published in January in Nature Communications helps to explain why binge drinking, in both mice and humans, so often leads to binge eating even though alcohol is, itself, high in calories. In the first part of the study, neuroscientists Craig Blomeley and Sarah Cains, both at the Francis Crick Institute Mill Hill Laboratory in London, injected mice with the equivalent of roughly two bottles of wine once a day for three consecutive days, mimicking a weekend of heavy drinking. Sure enough, the inebriated mice ate far more than sober mice in a control group. To figure out why, the researchers then exposed thin-sliced postmortem mouse brains to alcohol and measured the resulting neural activity using fluorescent tags and electrodes. They found that ethanol exposure alters calcium exchange in the cells, causing specialized nerve cells called agouti-related protein (AgRP) neurons to fire more frequently and easily. These neurons normally fire when our body needs calories, and research has shown that activating them artificially will cause mice to chow down even when they are full. The study results suggest that alcohol activates AgRP neurons in the brain, giving drunk mice the munchies. The same is likely true for humans because this brain circuitry has been highly conserved across mammal species, Cains says: “I don't doubt that AgRP neurons are activated in humans, and that's why you see this effect.” © 2017 Scientific American

Related chapters from BP7e: 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: 23645 - Posted: 05.22.2017