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By WINNIE HU Ruth Brunn finally said yes to marijuana. She is 98. She pops a green pill filled with cannabis oil into her mouth with a sip of vitamin water. Then Ms. Brunn, who has neuropathy, settles back in her wheelchair and waits for the jabbing pain in her shoulders, arms and hands to ebb. “I don’t feel high or stoned,” she said. “All I know is I feel better when I take this.” Ms. Brunn will soon have company. The nursing home in New York City where she lives, the Hebrew Home at Riverdale, is taking the unusual step of helping its residents use medical marijuana under a new program to treat various illnesses with an alternative to prescription drugs. While the staff will not store or administer pot, residents are allowed to buy it from a dispensary, keep it in locked boxes in their rooms and take it on their own. From retirement communities to nursing homes, older Americans are increasingly turning to marijuana for relief from aches and pains. Many have embraced it as an alternative to powerful drugs like morphine, saying that marijuana is less addictive, with fewer side effects. For some people, it is a last resort when nothing else helps. Marijuana, which is banned by federal law, has been approved for medical use in 29 states, including New York, and the District of Columbia. Accumulating scientific evidence has shown its effectiveness in treating certain medical conditions. Among them: neuropathic pain, severe muscle spasms associated with multiple sclerosis, unintentional weight loss, and vomiting and nausea from chemotherapy. There have also been reports that pot has helped people with Alzheimer’s disease and other types of dementia as well as Parkinson’s disease. © 2017 The New York Times Company

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: 23255 - Posted: 02.20.2017

Jon Hamilton Researchers have created mice that appear impervious to the lure of cocaine. Even after the genetically engineered animals were given the drug repeatedly, they did not appear to crave it the way typical mice do, a team reports in Nature Neuroscience. "They didn't keep going into the room where they received the cocaine and they seemed to be just as happy exploring all around the cage," says Shernaz Bamji, a professor in the Department of Cellular and Physiological Sciences at the University of British Columbia in Vancouver. "Addiction is a form of learning," Bamji says. And somehow, these mice never learned to associate the pleasurable feelings produced by cocaine with the place where they received the drug. The result was startling because the scientists thought these mice would be especially susceptible to addiction. "We repeated the experiment several times to see if we had made a mistake," Bamji says. The reason for the team's surprise had to do with proteins that affect learning. The animals had been genetically engineered to produce high levels of proteins called cadherins in the brain's "reward circuit," which plays an important role in addiction. And genetic studies have suggested that people with high levels of cadherins are more susceptible to drug addiction. Cadherins act a bit like glue, binding cells together. Usually this glue enhances learning by strengthening the connections, or synapses, between brain cells. © 2017 npr

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 23228 - Posted: 02.14.2017

By Abigail Zuger, M.D. It was in 2011 that the Centers for Disease Control first drew public attention to the ongoing nationwide opioid crisis. Much earnest commentary has explored the roots of this new killer epidemic since then, focusing on the broad highway between heroin and pain pills, and the online pharmacies, pill mills, and bad-apple doctors who fueled the two-way traffic and enabled catastrophe. Forgive me for rolling my eyes. Anyone with a prescription pad and a shred of common sense saw this whole thing coming down the pike decades ago, a speeding 18-wheeler, tires squealing, no brakes. Furthermore, it has long been clear that while the bad medical apples certainly did their share of damage, there is not a health policy guru or medical school dean in the country whose sins of omission and commission are not also partly responsible. Call it an epidemic of unconscious collusion or, as Dr. Anna Lembke bluntly states, a nation’s doctors “trapped in a system gone mad.” In less than 200 pages, this may be the most important medical book of the decade for finally getting the story of the opioid epidemic exactly right. As far as I am concerned, “Drug Dealer, M.D.,” in less than 200 unassuming, readable, and carefully referenced pages, may be the most important medical book of the decade for finally getting the story of this epidemic exactly right. And it’s not the medical bad apples Lembke is talking about in her title — it’s every doctor in the country. Copyright 2017 Undark

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: 23218 - Posted: 02.13.2017

By KATHARINE Q. SEELYE and ABBY GOODNOUGH MANCHESTER, N.H. — Chad Diaz began using heroin when he was 12. Now 36 and newly covered by Medicaid under the Affordable Care Act, he is on Suboxone, a substitute opioid that eases withdrawal symptoms and cravings, and he is slowly pulling himself together. “This is the best my life has gone in many, many years,” Mr. Diaz, a big man wearing camouflage, said as he sat in a community health center here. If Congress and President Trump succeed in dismantling the Affordable Care Act, he will have no insurance to pay for his medication or counseling, and he fears he will slide back to heroin. “If this gets taken from me, it’s right back to Square 1,” he said. “And that’s not a good place. I’m scary when I’m using. I don’t care who I hurt.” As the debate over the fate of the health law intensifies, proponents have focused on the lifesaving care it has brought to people with cancer, diabetes and other physical illnesses. But the law has also had a profound, though perhaps less heralded, effect on mental health and addiction treatment, vastly expanding access to those services by designating them as “essential benefits” that must be covered through the A.C.A. marketplaces and expanded Medicaid. The Center on Budget and Policy Priorities, a left-leaning research group, calculates that 2.8 million people with substance use disorders, including 220,000 with opioid disorders, have coverage under the A.C.A. As the opioid epidemic continues to devastate communities nationwide, public health officials say the law has begun to make a critical difference in their ability to treat and rehabilitate people. © 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: 23215 - Posted: 02.11.2017

By Catherine Offord As an undergraduate at Auburn University in the early 2000s, Jeremy Day was thinking of becoming an architect. But an opportunity to work on a research project investigating reward learning in rodents changed the course of his career. “It really hooked me,” he says. “It made me immediately wonder what mechanisms were underlying that behavior in the animal’s brain.” It’s a question Day has pursued ever since. In 2004, he enrolled in a PhD program at the University of North Carolina at Chapel Hill and began studying neural reward signaling under the mentorship of neuroscientist Regina Carelli. “He was a stellar student by all accounts,” Carelli recalls. “He was very clear on the type of work he wanted to do, even that early on in his career.” Focusing on the nucleus accumbens, a brain region involved in associative learning, Day measured dopamine levels in rats undergoing stimulus-reward experiments. Although a rat’s brain released dopamine on receipt of a reward early in training, Day found that, as the rodent became accustomed to specific cues predicting those rewards, this dopamine spike shifted to accompany the cues instead, indicating a changing role for the chemical during learning.1 Day completed his PhD in 2009, but realized that to better understand dopamine signaling and errors in the brain’s reward system that lead to addiction, he would need a broader skill set. “I had a strong background in systems neuroscience, but my training in molecular neuroscience was not as strong,” he explains. So he settled on “a field that I knew almost nothing about?”—epigenetics—and joined David Sweatt’s lab at the University of Alabama at Birmingham (UAB) as a postdoc. For someone used to a field where “data come in as it’s happening,” Day says, “transitioning to a molecular lab where you might do an assay and you don’t get an answer for a week or two was a culture shock.” © 1986-2017 The Scientist

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 23203 - Posted: 02.09.2017

Hannah Devlin Science correspondent It sounds like torment for the smoker attempting to quit: handling packets of cigarettes and watching footage of people smoking, without being allowed to light up. However, scientists believe that lengthy exposure to environmental triggers for cravings could be precisely what smokers need to help them quit. The technique, known as extinction therapy, targets the harmful Pavlovian associations that drive addiction with the aim of rapidly “unlearning” them. The latest study, by scientists at the Medical University of South Carolina, found that after two one-hour sessions people smoked significantly fewer cigarettes one month after treatment compared to a control group. The study was not an unqualified success – many participants still relapsed after treatment – but the authors believe the work could pave the way for new approaches to treating addiction. Michael Saladin, the psychologist who led the work, said: “When I initially saw the results from this study it was pretty eye-opening.” In smokers, environmental triggers have typically been reinforced thousands of times so that the sight of a lighter, for instance, becomes inextricably linked to the rush of nicotine that the brain has learned will shortly follow. After quitting an addictive substance, these associations fade slowly over time, but people often flounder in the first days and weeks when cravings are most powerful. Saladin and others believe it is possible to fast-track this process in carefully designed training sessions, to help people over the initial hurdle. © 2017 Guardian News and Media Limited

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 23187 - Posted: 02.04.2017

Elizabeth Eaton Electronic cigarettes may increase the risk of heart disease, researchers at UCLA report. The team found that two risk factors for heart disease were elevated in 16 e-cigarette users compared with 18 nonsmokers. “The pattern was spot-on” for what has been seen in heart attack patients and those with heart disease and diabetes, says cardiologist Holly Middlekauff, a coauthor of the study published online February 1 in JAMA Cardiology. But because the study only looked at a small number of people, the results are not definitive — just two or three patients can skew results, John Ambrose, a cardiologist with the University of California, San Francisco cautions. Plus, he says, some of the e-cigarette users in the study used to smoke tobacco, which may have influenced the data. Even so, Ambrose called the study interesting, noting that “the medical community just doesn’t have enough information” to figure out if e-cigarettes are dangerous. E-cigarette smokers in the study had heartbeat patterns that indicated high levels of adrenaline — also known as epinephrine — in the heart, a sign of heart disease risk. Researchers also found signs of increased oxidative stress, an imbalance of certain protective molecules that can cause the hardening and narrowing of arteries. © Society for Science & the Public 2000 - 2017.

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: 23180 - Posted: 02.02.2017

Meghan Rosen New X-ray crystallography images reveal how an LSD molecule gets trapped within a protein that senses serotonin, a key chemical messenger in the brain. The protein, called a serotonin receptor, belongs to a family of proteins involved in everything from perception to mood. The work is the first to decipher the structure of such a receptor bound to LSD, which gets snared in the protein for hours. That could explain why “acid trips” last so long, study coauthor Bryan Roth and colleagues report January 26 in Cell. It’s “the first snapshot of LSD in action,” he says. “Until now, we had no idea how it worked at the molecular level.” But the results might not be that relevant to people, warns Cornell University biophysicist Harel Weinstein. Roth’s group didn’t capture the main target of LSD, a serotonin receptor called 5-HT2A, instead imaging the related receptor 5-HT2B. That receptor is “important in rodents, but not that important in humans,” Weinstein says. Roth’s team has devoted decades to working on 5-HT2A, but the receptor has “thus far been impossible to crystallize,” he says. Predictions of 5-HT2A’s structure, though, are very similar to that of 5-HT2B, he says. LSD, or lysergic acid diethylamide, was first cooked up in a chemist’s lab in 1938. It was popular (and legal) for recreational use in the early 1960s, but the United States later banned the drug (also known as blotter, boomer, Purple Haze and electric Kool-Aid). |© Society for Science & the Public 2000 - 201

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: 23175 - Posted: 02.01.2017

By Roni Jacobson The psychedelic drug ibogaine is known for two things: its reputation in some circles as a panacea for addiction and the visceral hallucinations it induces. Positive anecdotes abound from people who have sought out the illegal drug at underground clinics. Just one dose, they say, brings near-instant relief from cravings and withdrawal symptoms, a veritable miracle for seemingly intractable addictions. But the side effects of this plant-derived substance can be dangerous or even deadly. Now, with encouraging evidence from animal studies, drugs are being developed to replicate ibogaine's impact on addiction without the side effects. A drug that is chemically related to ibogaine but lacks its hallucinogenic properties is set to begin phase II clinical trials in California early this year. If the results continue to be promising, addiction treatment as we know it could change radically. For decades research on ibogaine has been stymied by its classification as a Schedule I drug, the most tightly regulated category. Yet the results of animal studies have been intriguing. In May 2016 a meta-analysis examining 32 such studies, mostly in mice and rats, found that ibogaine reduced self-administration of cocaine, opioids and alcohol. An earlier study from 2015 found that noribogaine, the substance that ibogaine breaks down to when ingested, reduced self-administration of nicotine in addicted rats by 64 percent. Now Savant HWP, a pharmaceutical company in California, has developed a drug called 18-MC, a compound chemically related to ibogaine, which it hopes will produce the antiaddictive properties without triggering hallucinations. They are betting that the “trip” is not a necessary component of the therapy—an idea shared by some academics. © 2017 Scientific American,

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: 23170 - Posted: 01.31.2017

By Andrew Joseph, Public health officials on Thursday said they had detected a bizarre cluster of cases in which patients in Massachusetts developed amnesia over the past few years — a highly unusual syndrome that could be connected to opioid use. The officials have identified only 14 cases so far. But officials said it’s possible that clinicians have simply missed other cases. The patients were all relatively young — they ranged in age from 19 to 52. Thirteen of the 14 patients identified had a substance use disorder, and the 14th patient tested positive for opioids and cocaine on a toxicology screen. “What we’re concerned about is maybe a contaminant or something else added to the drug might be triggering this,” said Dr. Alfred DeMaria, the state epidemiologist at the Massachusetts Department of Public Health and an author of the new report. “Traditionally there’s no evidence that the drugs themselves can do this.” The pattern emerged when Dr. Jed Barash, a neurologist at Lahey Hospital and Medical Center in Burlington, Mass., reported four of the amnesia cases to the state’s public health department. The department then sent out an alert to specialists, including neurologists and emergency physicians, asking about similar cases, ultimately identifying 10 more from 2012 to 2016 at hospitals in eastern Massachusetts. (The patients included one person who lived in New Hampshire and one person who was visiting Massachusetts from Washington state.) © 2017 Scientific American,

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 23163 - Posted: 01.28.2017

Amy Maxmen The acid tests of 1960s San Francisco have morphed into something quite different in today’s Silicon Valley. Mind-altering trips have given way to subtle productivity boosts purportedly caused by tiny amounts of LSD or other psychedelic drugs. Fans claim that this ‘microdosing’ boosts creativity and concentration, but sceptics doubt that ingesting or inhaling one-tenth of the normal dose could have an effect. Science could soon help to settle the matter. Researchers have finally mapped the 3D structure of LSD in its active state — and the details, published today in Cell1, indicate the key to the chemical’s potency1. Another team reports today in Current Biology2 that it has pinpointed the molecular go-between that creates the perception of deep meaning experienced during acid trips — a feeling that the writer Aldous Huxley once described as “solidarity with the Universe”. “This is what we dreamed of doing when I was a graduate student in the seventies,” says Gavril Pasternak, a pharmacologist at Memorial Sloan Kettering Cancer Center in New York City who has spent decades studying the receptor proteins in the brain that mediate the activity of opioids and psychedelic drugs. “Work like this expands our understanding of how these receptors work.” In 1972, researchers revealed LSD’s shape by mapping the arrangement of atoms in its crystallized form3. But in the decades since, they’ve struggled to reveal the crystal structure of a receptor grasping a molecule of LSD or another psychedelic drug. This active configuration is key to understanding how drugs work, because their action depends on how they cling to molecules in the body. © 2017 Macmillan Publishers Limited,

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: 23157 - Posted: 01.27.2017

Hannah Devlin Science correspondent Scientists believe that a radical treatment involving the tranquilliser ketamine could help overcome alcohol addiction by “erasing” drink-related memories. Psychologists based at University College London are testing whether a one-off dose of the drug could help hazardous drinkers who are trying to reduce their alcohol intake. Alcohol addiction is notoriously difficult to treat, and there are few effective therapies available. Using a recreational drug to treat addiction may sound counterintuitive, but the researchers say there is a growing body of research suggesting that ketamine can be used to disrupt harmful patterns of behaviour. Ravi Das, one of the lead researchers, said: “There is evidence that it could be useful as a treatment for alcoholism.” Crucially, ketamine can disrupt the formation of memories, and scientists believe that this property could be harnessed to over-write the memories that drive addiction and harmful patterns of behaviour. “Memories that you form can be hijacked by drugs in some people,” said Das. “If you were an alcoholic you might have a strong memory of being in a certain place and wanting to drink. Those memories get continuously triggered by things in the environment that you can’t avoid.” For instance, seeing a glass of beer, hearing the clinking of glasses or even arriving home from work may trigger memories of the rewarding sensation of taking a drink – and might prompt a person to follow this urge. © 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: 23146 - Posted: 01.25.2017

By Bob Grant More and more Americans are using cannabis both for medicinal and recreational purposes, but scientists still know little about the drug’s effects on human physiology, according to a National Academies report released this month (January 12). Part of this knowledge gap owes to the fact that cannabis is classified as a Schedule I drug under the US Controlled Substances Act. In the eyes of the federal government, marijuana is a dangerous substance—on par with heroin—that “has no currently accepted medical use in treatment in the United States.” But researchers in Canada are not far ahead of their US counterparts, even though cannabis has since 2001 been functionally legal for medicinal use at the federal level there. See “National Academies Detail the State of Weed Science” “I wish I could say that [legalizing medical marijuana] had led to more research” in Canada, said Mark Ware, a McGill University pain management physician who has researched the safety and efficacy of cannabinoids for the past 18 years. “I think there’s certainly a willingness to be able to document real world use of cannabis under a legal framework.” Ware, who served as a reviewer on the National Academies report, added that while there are several public registries that track the legal use of cannabis among Canadians, experimental evidence on the effects of that use are lacking. “The clinical trials, I think for most people that’s an expensive undertaking,” he said. “There are still questions around who owns the intellectual property, who’s going to sponsor the trials. . . . Those remain barriers even in a legal framework as to the cost of that kind of research and the drug development piece of it.” © 1986-2017 The Scientist

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: 23145 - Posted: 01.25.2017

By Nicole Kobie Getting drunk could make it harder to enter your password – even if your brainwaves are your login. Brainwave authentication is one of many biometric measures touted as an alternative to passwords. The idea is for a person to authenticate their identity with electroencephalogram (EEG) readings. For example, instead of demanding a passcode, a computer could display a series of words on a screen and measure the user’s response via an EEG headset. EEG signatures are unique and are more complex than a standard password, making them difficult to hack. But while research suggests that EEG readings can authenticate someone’s identity with accuracy rates around 94 per cent, there could be confounding factors – including whether you’ve had a few too many drinks. Tommy Chin, a security researcher at cybersecurity consultancy firm Grimm, and Peter Muller, a graduate student at the Rochester Institute of Technology, decided to test this theory experimentally, by analysing people’s brainwaves before and after drinking shots of Fireball, a cinnamon-flavoured whisky. “Brainwaves can be easily manipulated by external influences such as drugs [like] opioids, caffeine, and alcohol,” Chin says. “This manipulation makes it a significant challenge to verify the authenticity of the user because they drank an immense amount of alcohol or caffeinated drink.” © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23123 - Posted: 01.19.2017

Tina Rosenberg It has been nearly 30 years since the first needle exchange program opened in the United States, in Takoma, Wash., in 1988. It was a health measure to prevent injecting drug users from sharing needles, and therefore spreading H.I.V. and hepatitis. The idea was controversial, to say the least. Many people felt — and still feel — that it enables drug use and sends a message that drug use is O.K. and can be done safely. Today the evidence is overwhelming that needle exchange prevents disease, increases use of drug treatment by winning users’ trust and bringing them into the health system, and does not increase drug use. Its utility has won over some critics. When Vice President-elect Mike Pence was governor of Indiana, he authorized needle exchange programs as an emergency response to an H.I.V. outbreak. “I do not support needle exchange as antidrug policy, but this is a public health emergency,” he said at a news conference in 2015. Needle exchange saved New York City from a generalized H.I.V. epidemic. In 1990, more than half of injecting drug users had H.I.V. Then in 1992, needle exchange began — and by 2001, H.I.V. prevalence had fallen to 13 percent. America has another epidemic now: overdose deaths from opioids, heroin and fentanyl, a synthetic opioid so powerful that a few grains can kill. A thousand people died of overdose in the city last year — three times the number who were killed in homicides. Nationally, drug overdose has passed firearms and car accidents as the leading cause of injury deaths. If there is a way to save people from overdose death without creating harm, we should do it. Yet there is a potent weapon that we’re ignoring: the supervised injection room. According to a report by the London-based group Harm Reduction International, 90 supervised injection sites exist around the world: in Canada, Australia and eight countries in Europe. Scotland and Ireland plan to open sites this year. In the United States, state officials in New York, California and Maryland, and city officials in Seattle (where a task force recommended two sites), San Francisco, New York City, Ithaca, N.Y., and elsewhere, are discussing such facilities. © 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: 23120 - Posted: 01.18.2017

By Catherine Caruso If you give a mouse a beer, he’s going to ask for a cookie—and another, and another. If you give a person enough beer, she might find herself wolfing down a plate of greasy nachos. But why does binge drinking make us binge eat as well? The reason may lie not in the stomach but in the brain, recent research suggests. A study published today in Nature Communications found alcohol activated brain cells that control hunger, sending drunk mice scampering for snacks even when they were not really hungry. Researchers from The Francis Crick Institute Mill Hill Laboratory in London got mice drunk, then tagged and recorded the electrical activity in brain cells linked to hunger, uncovering a neural mechanism that could explain why the animals ate significantly more after binge-drinking sessions even though their bodies did not need the calories. Although hunger pangs in our stomach usually alert us that it is time to eat, the impulse to consume food originates in our brains, and brain cells located in the hypothalamus called agouti-related protein (AgRP) neurons play a key role in controlling hunger. A previous study showed that when AgRP neurons are activated, mice almost immediately seek out food and start eating, even if their stomachs are full. By contrast, when AgRP neurons are deactivated, hungry mice will not eat. AgRP neurons play a similar role in human hunger: Under natural conditions they are activated when our bodies need calories, signaling to us that we should find food. Something different happens, however, when alcohol is involved. Although alcohol is second only to fat in caloric density, previous studies have shown drinking causes humans to eat more, a paradox that made lead authors Craig Blomeley and Sarah Cains and colleagues wonder whether the brain could be to blame. © 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: 23083 - Posted: 01.11.2017

By Virginia Smart, CBC News A controversial Canadian program that gives a regulated, hourly dose of wine to alcoholics to help manage their addiction and keep them safe has caught the attention of health care researchers in Australia. The managed alcohol programs (MAPs) that have sparked the international interest have been giving new hope and new lives to many alcoholics struggling with homelessness and troubles with addiction in communities from British Columbia to Ontario. Kate Dolan, a professor at the National Drug and Alcohol Research Centre at the University of New South Wales in Australia, has visited programs in Ottawa and Vancouver and was impressed. "We used to lead the world in harm reduction services," Dolan tells the fifth estate, but "the alcohol field has not progressed as much as the illicit drug use field." Research led Dolan to Ottawa's MAP. She found MAPs to be cost-effective through reductions in spending on health care and emergency services. Participants also significantly reduce their alcohol consumption and learn a sense of community. The Pour Lucia Ali monitors 'The Pour,' the hourly distribution of a prescribed dose of alcohol dictated by the in-house nurse at the Oaks, a residence for stabilized alcoholics in Ottawa. (CBC) When participants arrive at a MAP, Dolan wrote in her study, "it is all about me, myself and I." But as they progress, they lose the "chip on their shoulder and open up." ©2016 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: 23061 - Posted: 01.06.2017

By Don Lattin In the fall of 1965, a 33-year-old father of three named Arthur King—a patient on the alcoholics ward at Baltimore’s Spring Grove Hospital—swallowed an LSD pill and laid back on his bed in a special unit called “Cottage Thirteen.” Sanford Unger, the chief of psychosocial research at the Johns Hopkins University School of Medicine, knelt beside King’s bed, holding his hand and reassuring the patient as he started to feel the drug’s mind-altering effects. This was not a normal psychotherapy session. During his 12-hour experience, designed to help stop his destructive drinking habit, King sat on the edge of the bed and looked at the photo of his son that he’d brought. Suddenly, the child became alive in the picture, which initially frightened him. Then King noticed that a lick of his son’s hair was out of place, so he stroked the photo, putting the errant strands back in place. His fear vanished. Later, Unger held out a small vase with a single red rose. King looked at the flower, which seemed to be opening and closing, as though it were breathing. At one point, Unger asked him whether he’d like to go out to a bar and have a few drinks. King didn’t say anything but was shocked when the rose suddenly turned black and dropped dead before his eyes. He never picked up another drink. Arthur King was one of thousands of research subjects who were given LSD, psilocybin, and mescaline as therapeutic tools in the 1950s and 1960s, often with government support and with promising results. But by the time King was enjoying his sobriety, the backlash against psychedelic testing had already begun. By the mid-1970s, the legal exploration of the therapeutic benefits of psychedelic drugs was over.

Related chapters from BP7e: 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: 23048 - Posted: 01.03.2017

Linda Bauld January is a time for New Year’s resolutions and if you’re one of the world’s one billion smokers, your resolution may be to stop smoking. For some people, this year’s quit attempt might involve an electronic cigarette, and a recent study in England, published in the BMJ, suggested that these devices helped at least 18,000 smokers to stop in 2015 who would not otherwise have done so. That’s very good news, but will there be as many quit attempts in 2017 as there have been in the past with e-cigarettes? I’m not so sure. Since I last wrote about e-cigarettes in this column one year ago, headlines about the dangers of these devices have continued to appear and show no sign of abating. The result is clear. More people believe today, compared with a year ago, that e-cigarettes are as harmful as smoking. In fact these incorrect perceptions have risen year on year, from fewer than one in ten adults in Great Britain in 2013 to one in four this past summer. Surveys of smokers show similar patterns, with an increasing proportion believing that e-cigarettes are more or equally harmful than tobacco. Yet we know that these harm perceptions are wrong. There is now very strong evidence, from a range of studies, that vaping - inhaling nicotine without the combustion involved in smoking - is far less risky than smoking cigarettes. Just a few months ago this body of evidence was brought together by the Royal College of Physicians who published an authoritative report analysing dozens of studies and concluded that the hazard to health arising from long term vapour inhalation from e-cigarettes is unlikely to exceed 5% of the harm from smoking tobacco. The RCP, and since then other UK doctor’s organisations such as the Royal College of General Practitioners, have made clear that it is important to promote the use of e-cigarettes, along with other non-tobacco nicotine products (like Nicotine Replacement Therapy such as gum or inhalators) to smokers who are trying to quit. The work of these organisations is underpinned by a consensus statement endorsed by many of the main health charities and public health bodies in the UK. They agree that vaping is safer than smoking, and while these products are not risk free and should not be promoted to children or never smokers, they have a legitimate and positive role to play in tobacco control. © 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: 23046 - Posted: 01.02.2017

By KEVIN DEUTSCH An anesthetic commonly used for surgery has surpassed heroin to become the deadliest drug on Long Island, killing at least 220 people there in 2016, according to medical examiners’ records. The drug, fentanyl, is a synthetic opioid, which can be 100 times more potent than morphine. The numbers from Long Island are part of a national pattern, as fentanyl fatalities have already surpassed those from heroin in other parts of the country, including New England, as its use has skyrocketed. Part of the reason for the increase is economic — because fentanyl can be manufactured in the lab, it is much cheaper and easier than cultivating heroin. In New York City, more than 1,000 people are expected to die from drug overdoses this year — the first recorded four-digit death total in city history, according to statistics compiled by the Department of Health and Mental Hygiene. Nearly half of all unintentional drug overdose deaths in the city since July have involved fentanyl, the health department said. The medical examiners of Long Island’s two counties, Nassau and Suffolk, compiled the new numbers. “Fentanyl has surpassed heroin as the most commonly detected drug in fatal opioid overdoses,” Dr. Michael J. Caplan, the Suffolk County medical examiner, said in a written statement about the statistics, which were obtained by The New York Times ahead of their release. “The influx of illicitly manufactured fentanyl from overseas is a nationwide issue that requires a multidisciplinary intervention from all levels of government.” Nationwide, recorded deaths from opioids surpassed 30,000 in 2015, according to data compiled by the Centers for Disease Control and Prevention. And overdoses caused by synthetic opioids like fentanyl increased by 72.2 percent in 2015 over 2014 — one of the deadliest year-over-year surges for any drug in United States history, the same data shows. © 2016 The New York Times Company

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: 23032 - Posted: 12.29.2016