Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

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by Laurie McGinley The Food and Drug Administration on Thursday took the first concrete action to reduce nicotine in cigarettes to make them much less addictive, opening a regulatory process described as a “historic first step” by the agency's top official. Commissioner Scott Gottlieb unveiled an “advance notice of proposed rulemaking,” the earliest step in what promises to be a long, complicated regulatory effort to lower nicotine levels to be minimally addictive or nonaddictive. The notice, to be published Friday in the Federal Register, includes new data published in the New England Journal of Medicine on Thursday based on a possible policy scenario. That FDA-funded analysis found that slashing nicotine levels could push the smoking rate down to 1.4 percent from the current 15 percent of adults. That in turn would result in 8 million fewer tobacco-related deaths through the end of the century — which Gottlieb termed “an undeniable public health benefit.” The evaluation was based on reducing nicotine levels to 0.4 milligrams per gram of tobacco filler, FDA officials told reporters during a teleconference. Many adults try to quit smoking each year but fail because nicotine is such an addictive substance, said Mitch Zeller, director of the FDA's Center for Tobacco Products. Cutting the nicotine level would not only help them succeed, but it also could keep young people who may be experimenting with cigarettes from becoming addicted, he said. The nicotine notice will be open for public comment for 90 days. FDA officials are seeking input on what the maximum nicotine level in cigarettes should be and whether such a limit should be implemented all at once or gradually. Nicotine levels can be manipulated by leaf blending, chemical extraction and genetic engineering. © 1996-2018 The Washington Post

Keyword: Drug Abuse
Link ID: 24762 - Posted: 03.16.2018

Paula Span At first, the pills helped her feel so much better. Jessica Falstein, an artist living in the East Village in Manhattan, learned she had an anxiety disorder in 1992. It led to panic attacks, a racing pulse, sleeplessness. “Whenever there was too much stress, the anxiety would become almost intolerable, like acid in the veins,” she recalled. When a psychopharmacologist prescribed the drug Klonopin, everything brightened. “It just leveled me out,” Ms. Falstein said. “I had more energy. And it helped me sleep, which I was desperate for.” After several months, however, the horrible symptoms returned. “My body became accustomed to half a milligram, and the drug stopped working,” she said. “So then I was up to one milligram. And then two.” Her doctor kept increasing the dosage and added Ativan to the mix. Now 67, with her health and stamina in decline, Ms. Falstein has been diligently working to wean herself from both medications, part of the class called benzodiazepines that is widely prescribed for insomnia and anxiety. “They turn on you,” she said. For years, geriatricians and researchers have sounded the alarm about the use of benzodiazepines among older adults. Often called “benzos,” the problem drugs include Valium (diazepam), Klonopin (clonazepam), Xanax (alprazolam) and Ativan (lorazepam). The cautions have had scant effect: Use of the drugs has risen among older people, even though they are particularly vulnerable to the drugs’ ill effects. Like Ms. Falstein, many patients take them for years, though they’re recommended only for short periods. The chemically related “z-drugs” — Ambien, Sonata and Lunesta — present similar risks. © 2018 The New York Times Company

Keyword: Development of the Brain; Drug Abuse
Link ID: 24761 - Posted: 03.16.2018

Geoff Brumfiel Sergei Skripal and his daughter, Yulia, were found slumped on a bench in the city of Salisbury on March 4. Experts quickly assessed that Skripal — a former Russian intelligence official accused of spying for the British — had been poisoned with a nerve agent. On Monday, British Prime Minister Theresa May named the agent in a speech before Parliament. "It is now clear that Mr. Skripal and his daughter were poisoned with a military-grade nerve agent of a type developed by Russia," she said. "This is part of a group of nerve agents known as Novichok." Novichok agents are extremely rare. "As far as I know, I don't know anybody who knows how to make it except these guys in Russia," says Dan Kaszeta, a chemical weapons expert with Strongpoint Security in London. "They've been a deep, dark secret." Novichok means "newcomer" in Russian. Kaszeta says that Novichok agents were developed in the 1980s as a new weapon in the waning days of the Cold War. Novichok chemicals were designed to evade equipment carried by NATO troops. "They wanted to develop nerve agents that the West couldn't detect," he says. According to a defector's report published by the Stimson Center in 1995, they were developed at the State Scientific Research Institute of Organic Chemistry and Technology in Moscow. As the U.S. and Russia were laying the groundwork to dismantle their chemical weapons stockpiles, researchers at the institute were working in secret to develop the new Novichok chemicals. © 2018 npr

Keyword: Neurotoxins
Link ID: 24747 - Posted: 03.13.2018

By Aaron E. Carroll More people in the United States are on antidepressants, as a percentage of the population, than any other country in the world. And yet the drugs’ efficacy has been hotly debated. Some believe that the short-term benefits are much more modest than widely thought, and that harms may outweigh benefits in the long run. Others believe that they work, and that they can be life-changing. Settling this debate has been much harder than you might think. It’s not that we lack research. Many, many studies of antidepressants can be found in the peer-reviewed literature. The problem is that this has been a prime example of publication bias: Positive studies are likely to be released, with negative ones more likely to be buried in a drawer. In 2008, a group of researchers made this point by doing a meta-analysis of antidepressant trials that were registered with the Food and Drug Administration as evidence in support of approvals for marketing or changes in labeling. Companies had to submit the results of registered trials to the F.D.A. regardless of the result. These trials also tend to have less data massaging — such as the cherry-picking of outcomes — than might be possible in journals. The researchers found 74 studies, with more than 12,500 patients, for drugs approved between 1987 and 2004. About half of these trials had “positive” results, in that the antidepressant performed better than a placebo; the other half were “negative.” But if you looked only in the published literature, you’d get a much different picture. Nearly all of the positive studies are there. Only three of the negative studies appear in the literature as negative. Twenty-two were never published, and 11 were published but repackaged so that they appeared positive. © 2018 The New York Times Company

Keyword: Depression
Link ID: 24739 - Posted: 03.12.2018

Ari Shapiro Millions of Americans use opioids to relieve pain. But many also struggle with addiction. This week, a report in JAMA, the journal of the American Medical Association, found that nonopioid painkillers — like acetaminophen and ibuprofen — were as effective as opioids at treating chronic back, hip and knee pain, and with fewer side effects. The findings raise a lot of questions about the right approach to managing pain, particularly chronic pain. So earlier this week, we asked listeners on Facebook and Twitter to share their questions about treating chronic pain. For answers, NPR's Ari Shapiro turned to Dr. Ajay Wasan, professor and vice chair for pain medicine at the University of Pittsburgh Medical Center. Isn't it true that ... acetaminophen can be very damaging to the liver, particularly with daily long-term use? — Emma Juneau For treatment of chronic pain, especially arthritis pain, higher doses of acetaminophen have been recommended, and there are good studies supporting that it can be quite effective for pain. You get a cumulative effect with the higher doses. Those can also be associated with a rise in liver enzymes for some people. It would be very rare for those enzymes to reach a toxic level that would cause liver damage, but we don't know what percent of people get that little rise in liver enzymes, or the chances that a slight increase in liver enzymes will lead to liver damage. It raises a very excellent point, that nonopiate medications have some side effects as well. We know anti-inflammatories can have significant side effects — in general the side effects of opioids are greater — but both nonopioids and opioids do have side effects. © 2018 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 24735 - Posted: 03.10.2018

Simon Parkin In an unprecedented attack of candour, Sean Parker, the 38-year-old founding president of Facebook, recently admitted that the social network was founded not to unite us, but to distract us. “The thought process was: ‘How do we consume as much of your time and conscious attention as possible?’” he said at an event in Philadelphia in November. To achieve this goal, Facebook’s architects exploited a “vulnerability in human psychology”, explained Parker, who resigned from the company in 2005. Whenever someone likes or comments on a post or photograph, he said, “we… give you a little dopamine hit”. Facebook is an empire of empires, then, built upon a molecule. A neuroscientist explains: the need for ‘empathetic citizens’ - podcast Dopamine, discovered in 1957, is one of 20 or so major neurotransmitters, a fleet of chemicals that, like bicycle couriers weaving through traffic, carry urgent messages between neurons, nerves and other cells in the body. These neurotransmitters ensure our hearts keep beating, our lungs keep breathing and, in dopamine’s case, that we know to get a glass of water when we feel thirsty, or attempt to procreate so that our genes may survive our death. In the 1950s, dopamine was thought to be largely associated with physical movement after a study showed that Parkinsonism (a group of neurological disorders whose symptoms include tremors, slow movement and stiffness) was caused by dopamine deficiency. In the 1980s, that assumption changed following a series of experiments on rats by Wolfram Schultz, now a professor of neuroscience at Cambridge University, which showed that, inside the midbrain, dopamine relates to the reward we receive for an action. Dopamine, it seemed, was to do with desire, ambition, addiction and sex drive.

Keyword: Drug Abuse
Link ID: 24721 - Posted: 03.05.2018

Clayton Dalton When patients arrive in the emergency room, nearly all but those with the most minor complaints get an IV. To draw blood, give medications, or administer fluids — the IV is the way doctors and nurses gain access to the body. Putting one in is quick and simple, and it's no more painful than a mild bee sting. Yet for some patients this routine procedure becomes excruciating. On my shifts as an emergency physician, I began to notice a strange pattern. These hypersensitive patients often had a history of using opioids. Shouldn't these patients be less susceptible to pain, instead of more so? As I looked into it, I found that I was far from the first to notice the paradox of heightened pain sensitivity with opioid use. An English physician in 1870 reported on morphine's tendency to "encourage the very pain it pretends to relieve." In 1880, a German doctor named Rossbach described a similar hypersensitivity to pain with opioid dependence. A century passed before the phenomenon received serious scientific attention. That's when American scientists showed that rats exhibited increased sensitivity to pain after exposure to morphine, a phenomenon that became known as opioid-induced hyperalgesia. By the 1990s the evidence for this unusual reaction in animals was strong, but whether it occurred in humans wasn't clear. © 2018 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 24719 - Posted: 03.05.2018

By Simon Makin Ketamine has been called the biggest thing to happen to psychiatry in 50 years, due to its uniquely rapid and sustained antidepressant effects. It improves symptoms in as little as 30 minutes, compared with weeks or even months for existing antidepressants, and is effective even for the roughly one third of patients with so-called treatment-resistant depression Although there are multiple theories, researchers do not quite know how ketamine combats depression. Now, new research has uncovered a mechanism that may, in part, explain ketamine's antidepressant properties. Two studies, recently published in Nature, describe a distinctive pattern of neural activity that may drive depression in a region called the lateral habenula (LHb); Ketamine, in turn, blocks this activity in depression-prone rats. Originally licensed as an anesthetic in 1970, ketamine has since gained fame as a party drug for causing out-of-body experiences, hallucinations and other psychosislike effects. Its antidepressant properties in humans were discovered almost 20 years ago. Ketamine does not directly influence the same chemical messengers as standard antidepressants such as serotonin but rather works via interaction with another chemical, glutamate—not usually associated with mood but rather with brain plasticity. One prominent idea about how it alleviates depression is by promoting the growth of new neural connections. “We provide a new angle for people to think about how this drug works,” says neuroscientist Hailan Hu of Zhejiang University in China, leader of the team that conducted both studies. If she is right, her group may have identified multiple new lines of attack for treating a condition the World Health Organization calls the leading cause of disability worldwide. © 2018 Scientific American

Keyword: Depression; Drug Abuse
Link ID: 24718 - Posted: 03.02.2018

By Katarina Zimmer Jermaine Jones’s first memory of being a “bit of a scientist” was discovering that toilet water is actually pretty clean. While conducting a science fair pro-ject during his junior year of high school in Virginia, he learned that “you get much more varied bacteria from the toilet seat as opposed to the water,” he explains. With encouragement from his aunt, who was a biologist, Jones chose to pursue a degree in science at the University of Virginia. Over the course of several undergraduate internships, he got a taste of different fields of research, from probing decision making in mice to examining the analgesic effects of rainforest plant extracts in Brazil. By the time Jones had earned his master’s degree from Old Dominion University, he was certain that investigating drug abuse would be a good fit for his two main interests, pharmacology and psychology. For his PhD, Jones moved to Washington, D.C., where he worked on elucidating the neurobiological mechanisms of cocaine’s aversive effects in rodent models with Anthony Riley, a behavioral pharmacologist at American University. At the same time, Jones examined the effects of knocking out genes encoding the neurotransmitter transporters that the drug acts upon in mice with neuroscientists George Uhl and Scott Hall at the National Institute on Drug Abuse. For his dissertation, “he was able to show, pretty unequivocally, the role of neuro-transmitter systems in the aversive effects of cocaine in these mice,” Riley recalls.1 © 1986-2018 The Scientist

Keyword: Drug Abuse; Genes & Behavior
Link ID: 24717 - Posted: 03.02.2018

Terry Gross Antidepressants and medications for bipolar disorder can be life-changing and even lifesaving, but journalist Lauren Slater warns that the long-term side effects of these drugs are "cloaked in mystery." "As a nation, we're consuming them; we're gobbling them down," she says. "And we don't really know what we're taking into our bodies." Slater, who suffers from depression and bipolar disorder, has firsthand experience with psychotropic drugs; she has been taking medication for 35 years. Her new book, Blue Dreams, dedicates separate chapters to drugs such as Thorazine, lithium and psilocybin. Slater says she wanted to "unveil" the drugs by explaining their history, as well as how they work and the benefits and consequences for people who take them: "My goal was to almost try to make the drug into a character in and of itself. ... I wanted to bring these drugs alive." On how Thorazine changed the way mental illness was treated [Long] before Thorazine, people thought that mental illness was the result of what are called "humors" — blood, phlegm, bodily fluids that went out of whack. ... [Later, they] believed that it could be the result of hereditary genes gone wrong. But then Thorazine was invented, and that sort of was the kick-start to a whole bunch of other drugs being invented and to doctors and later the public at large thinking that mental illness was biochemical in nature. ... © 2018 npr

Keyword: Depression; Schizophrenia
Link ID: 24714 - Posted: 03.01.2018

It was disappointing to read such an uncritical description of the latest analysis of antidepressant trials that does not address doubts about the widespread use of these drugs (The drugs do work, says study of antidepressants, 22 February). The analysis consists of comparing “response” rates between people on antidepressants and those on placebo. But “response” is an artificial category that has been arbitrarily constructed out of the data actually collected, which consists of scores on depression rating scales. Analysing categories inflates differences. When scores are compared, differences are trivial, and unlikely to be clinically relevant. Moreover, even these small differences are easily accounted for by the fact that antidepressants produce more or less subtle mental and physical alterations (eg nausea, dry mouth, drowsiness and emotional blunting) irrespective of whether or not they treat depression. These enable participants to guess whether they have been allocated to antidepressant or placebo, thus enhancing the placebo effect of the active drugs. This may explain why antidepressants that cause the most noticeable alterations, such as amitriptyline, appeared to be the most effective. “Real world” studies show that people treated with antidepressants have poor outcomes and fare worse than depressed people who do not receive antidepressants. Increased prescribing will do more harm than good. Adverse effects include sexual dysfunction, which may occasionally persist after the drugs are stopped, agitation, suicidal and aggressive behaviour among younger users, prolonged and severe withdrawal effects and foetal abnormalities. The costs of encouraging more people to consider themselves as flawed and diseased are hard to quantify. © 2018 Guardian News and Media Limited

Keyword: Depression
Link ID: 24690 - Posted: 02.23.2018

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.

Keyword: Drug Abuse; Alzheimers
Link ID: 24682 - Posted: 02.21.2018

By Matt Warren The anesthesia medication ketamine has shown promise in treating depression, but its exact effects on the brain are unclear. Now, researchers have discovered that the drug changes the firing patterns of cells in a pea-size structure hidden away in the center of the brain. This could explain why ketamine is able to relieve symptoms of depression so quickly—and may provide a fresh target for scientists developing new antidepressants. “It’s a spectacular study,” says Roberto Malinow, a neuroscientist at the University of California, San Diego, who was not involved in the work. “It will make a lot of people think.” In clinical trials, ketamine appears to act much faster than existing antidepressants, improving symptoms within hours rather than weeks. “People have tried really hard to figure out why it’s working so fast, because understanding this could perhaps lead us to the core mechanism of depression,” says Hailan Hu, a neuroscientist at Zhejiang University School of Medicine in Hangzhou, China, and a senior author on the new study. Hu suspected the drug might target a tiny region in the middle of the brain called the lateral habenula, the so-called “anti–reward center.” This region inhibits nearby reward areas, which can be useful in learning; for example, if a monkey pulls a lever expecting a treat but never receives it, the lateral habenula will reduce the activity of reward areas, and the monkey will be less likely to pull the lever in the future. But research over the past decade has suggested that the area may be overactive in depression, dampening down those reward centers too much. © 2018 American Association for the Advancement of Science.

Keyword: Depression; Drug Abuse
Link ID: 24664 - Posted: 02.15.2018

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

Keyword: Drug Abuse; Attention
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

Keyword: Drug Abuse
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.

Keyword: Drug Abuse
Link ID: 24628 - Posted: 02.07.2018

By PAM BELLUCK More American children than previously thought may be suffering from neurological damage because their mothers drank alcohol during pregnancy, according to a new study. The study, published Tuesday in the journal JAMA, estimates that fetal alcohol syndrome and other alcohol-related disorders among American children are at least as common as autism. The disorders can cause cognitive, behavioral and physical problems that hurt children’s development and learning ability. The researchers evaluated about 3,000 children in schools in four communities across the United States and interviewed many of their mothers. Based on their findings, they estimated conservatively that fetal alcohol spectrum disorders affect 1.1 to 5 percent of children in the country, up to five times previous estimates. About 1.5 percent of children are currently diagnosed with autism. “This is an equally common, or more common, disorder and one that’s completely preventable and one that we are missing,” said Christina Chambers, one of the study authors and a professor of pediatrics at the University of California, San Diego. “If it truly is affecting a substantial proportion of the population, then we can do something about it. We can provide better services for those kids, and we can do a better job of preventing the disorders to begin with.” The range of fetal alcohol spectrum disorders (also called FASDs) can cause cognitive, behavioral and physical difficulties. The most severe is fetal alcohol syndrome, in which children have smaller-than-typical heads and bodies, as well as eyes unusually short in width, thin upper lips, and smoother-than-usual skin between the nose and mouth, Dr. Chambers said. A moderate form is partial fetal alcohol syndrome. Less severe is alcohol-related neurodevelopmental disorder, in which children have neurological but not physical characteristics and it is known that their mothers drank during pregnancy. © 2018 The New York Times Company

Keyword: Development of the Brain; Drug Abuse
Link ID: 24626 - 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

Keyword: Drug Abuse
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

Keyword: Drug Abuse
Link ID: 24612 - Posted: 02.05.2018

Ian Sample Science editor A nasal spray that delivers a natural painkiller to the brain could transform the lives of patients by replacing the dangerous and addictive prescription opioids that have wreaked havoc in the US and claimed the lives of thousands of people. Scientists at University College London found they could alleviate pain in animals with a nasal spray that delivered millions of soluble nanoparticles filled with a natural opioid directly into the brain. In lab tests, the animals showed no signs of becoming tolerant to the compound’s pain-relieving effects, meaning the risk of overdose should be far lower. The researchers are now raising funds for the first clinical trial in humans to assess the spray’s safety. They will start with healthy volunteers who will receive the nasal spray to see if it helps them endure the pain of immersing one of their arms in ice-cold water. “If people don’t develop tolerance, you don’t have them always having to up the dose. And if they don’t have to up the dose, they won’t get closer and closer to overdose,” said Ijeoma Uchegbu, a professor of pharmaceutical nanoscience who is leading the research through Nanomerics, a UCL startup. If the first human safety trial is successful, the scientists will move on to more trials to investigate whether the nasal spray can bring swift relief to patients with bone cancer who experience sudden and excruciating bouts of pain.

Keyword: Pain & Touch; Drug Abuse
Link ID: 24609 - Posted: 02.03.2018