Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

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by Emilie Reas Paranoia. Munchies. Giggles. Sleepiness. Memory loss. Although the effects of cannabinoids–the active components of marijuana–are familiar to many, their neurobiological substrates are poorly characterized. Perhaps the effect of greatest interest to both neuroscientists and to cannabis users hoping to preserve their cognitive function, is short-term memory impairment that often accompanies marijuana use. Our partial understanding of its physiological and behavioral effects is not for want of studies into its neural effects. Ample research has shown a range of changes to neurotransmission, receptors, ion channels and mitochondria following cannabinoid exposure. However, knowledge of its cellular and molecular properties alone cannot offer a complete picture of its system-wide effects leading to cognitive and behavioral changes. A recent study published in PLOS Computational Biology took a novel approach to address this issue, combining computational modeling with electrophysiological brain recordings from rats performing a memory task, to unravel the dynamics of neural circuits under the influence of cannabinoids. To assess memory changes induced by cannabinoids, the scientists injected tetrahydrocannabinol (THC), the main psychoactive compound in marijuana, into rats before they performed a “delayed-nonmatch-to-sample” working memory task. In this task, rats are cued with one of two levers, and after a delay, are required to select the opposite lever. Compared to sober sessions, performance under THC was impaired by 12%, confirming the all-too-familiar memory impairment associated with cannabis use. THC alters hippocampal activity

Keyword: Learning & Memory; Drug Abuse
Link ID: 24087 - Posted: 09.21.2017

Paula Span In the summer, Henry Wrenn-Meleck likes to sit on the stoop of his building on the Upper West Side of Manhattan, observing the passing urban parade. One day in late July, “one of my neighbors could see something was wrong,” he recently recalled. “I was sort of rolling around, obviously in a lot of pain. He said, ‘I have to call 911,’ and he did.” Mr. Wrenn-Meleck, 63, an independent music publisher and dealer in rare guitars, spent three weeks in a hospital, being treated for trauma from a fall he does not recall. But the underlying problem was “40 years of being a very serious alcoholic,” he said. “My body finally said no more.” Discharged from the hospital after detoxing, Mr. Wrenn-Meleck went to the New Jewish Home in Manhattan for physical therapy. He also entered its geriatric substance abuse recovery program where, he found, he was one of the younger participants. Epidemiologists at the National Institute on Alcohol Abuse and Alcoholism last month reported a jarring trend: Problem drinking is rising fast among older Americans. Their study, published in JAMA Psychiatry, compared data from a national survey taken in 2001 and 2002 and again in 2012 and 2013, each time with about 40,000 adults. Drinking had increased in every age group, the researchers found. Those over 65 remained far less likely to drink than younger people — about 55 percent of older participants told interviewers they’d imbibed in the past year. Still, that was a 22 percent increase over the two periods, the greatest rise in any age group. More troublingly, the proportion of older adults engaged in “high-risk drinking” jumped 65 percent, to 3.8 percent. The researchers’ definition: for a man, downing five or more standard drinks in a day (each containing 14 grams of alcohol) at least weekly during the past year; for a woman, four such drinks in a day.

Keyword: Drug Abuse
Link ID: 24066 - Posted: 09.15.2017

By Diana Kwon Lying in a room at Imperial College London, surrounded by low lighting and music, Kirk experienced a vivid recollection of visiting his sick mother before she passed away. “I used to go and see my mum in the hospital quite a lot,” recalls Kirk, a middle-aged computer technician who lives in London (he requested we use only his first name). “And a lot of the time she’d be asleep . . . [but] she’d always sense I was there, and after about five minutes she’d wake up, and we’d interact. I kind of went through that again—but it was a kind of letting go.” Kirk choked up slightly while retelling his experience. “It’s still a little bit emotional,” he says. “The thing I realized [was that] I didn’t want to let go. I wanted to hold on to the grief, because that was the only connection I had with my mum.” While this may sound like an ordinary therapy session, it was not what you would typically expect. Kirk was experiencing the effects of a 25-mg dose of psilocybin—the active ingredient in psychedelic “magic” mushrooms—which he had ingested as part of a 2015 clinical trial investigating the drug’s therapeutic potential. After his mother died, Kirk says, he fell into a “deep, dark pit of grief.” Despite antidepressants and regular sessions with a therapist, his condition was not improving. “I was stuck in it for years,” he recalls. So when he heard Imperial College London was recruiting participants for an upcoming trial studying the impact of psilocybin on depression, Kirk decided to sign up. © 1986-2017 The Scientist

Keyword: Depression; Drug Abuse
Link ID: 24064 - Posted: 09.14.2017

By Michelle Roberts Health editor, BBC News online There is "surprisingly limited" evidence that light drinking during pregnancy poses any risk to the baby, say UK researchers. They reviewed all the available studies done on the topic since the 1950s and found no convincing proof that a drink or two a week is harmful. The Bristol University team stress this does not mean it is completely safe. They say women should avoid all alcohol throughout pregnancy "just in case", as per official guidelines. But women who have had small amounts to drink in pregnancy should be reassured that they are unlikely to have harmed their baby. The Chief Medical Officer for the UK, Prof Dame Sally Davies, updated her advice last year to advocate total abstinence. Before that, pregnant women had been told they could drink one or two units - equivalent to one or two small glasses of wine - a week. There is no proven safe amount that women can drink during pregnancy, although the risks of drinking heavily in pregnancy are well known. Getting drunk or binge drinking during pregnancy increases the risk of miscarriage and premature birth and can lead to mental and physical problems in the baby, called foetal alcohol syndrome. The risks associated with light drinking, however, are less clear. Dr Luisa Zuccolo and colleagues found 26 relevant studies on the topic. Their review found no overwhelming proof of harm - but, in seven of the studies, light drinking was associated, on average, with an 8% higher risk of having a small baby, compared with drinking no alcohol at all. The review, in BMJ Open, also notes it appeared to increase the risk of having a premature birth. © 2017 BBC.

Keyword: Development of the Brain; Drug Abuse
Link ID: 24057 - Posted: 09.12.2017

By JOSH KATZ The first governmental account of nationwide drug deaths in 2016 shows overdose deaths growing even faster than previously thought. Drug overdoses killed roughly 64,000 people in the United States last year, according to the first governmental account of nationwide drug deaths to cover all of 2016. It’s a staggering rise of more than 22 percent over the 52,404 drug deaths recorded the previous year — and even higher than The New York Times’s estimate in June, which was based on earlier preliminary data. Drug overdoses are expected to remain the leading cause of death for Americans under 50, as synthetic opioids — primarily fentanyl and its analogues — continue to push the death count higher. Drug deaths involving fentanyl more than doubled from 2015 to 2016, accompanied by an upturn in deaths involving cocaine and methamphetamines. Together they add up to an epidemic of drug overdoses that is killing people at a faster rate than the H.I.V. epidemic at its peak. This is the first national data to break down the growth by drug and by state. We’ve known for a while that fentanyls were behind the growing count of drug deaths in some states and counties. But now we can see the extent to which this is true nationally, as deaths involving synthetic opioids, mostly fentanyls, have risen to more than 20,000 from 3,000 in just three years. Deaths involving prescription opioids continue to rise, but many of those deaths also involved heroin, fentanyl or a fentanyl analogue. There is a downward trend in deaths from prescription opioids alone. At the same time, there has been a resurgence in cocaine and methamphetamine deaths. Many of these also involve opioids, but a significant portion of drug deaths — roughly one-third in 2015 — do not. © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 24027 - Posted: 09.02.2017

By Colin Hendrie and Alisdair Pickles The current global crisis of depressive illness has a simple root cause: a failure of treatment. This is the result of a broken scientific process that has for nearly 70 years fallen short in delivering the drug therapies it was set up to provide. Given existing antidepressants don’t work for many people, the excitement surrounding the development of a new class of treatments from recreational drugs such as magic mushrooms is understandable. But there are strong reasons to doubt they will have the kind of impact hoped for. Instead, we are more likely to be seeing the latest episode in a long-running saga of repeated disappointment. This saga began when antidepressant use became widespread in the 1950s and 1960s. It was hoped they would have the same transformative effect on mental illness that antibiotics had on non-viral infectious diseases. As it turned out, antidepressants were only of value to some people with depression. Studies involving thousands of people with the condition reveal that the proportion seeing a clinically significant response to antidepressants is often very similar to that seen with a placebo, which is about 40 per cent. In double-blind, placebo-controlled studies, antidepressants don’t fare well. This helps to explain why, by the end of the 20th century, Big Pharma was floundering over the development of new drugs for depression. In 2010, many companies stopped such work. © Copyright New Scientist Ltd.

Keyword: Depression; Drug Abuse
Link ID: 24017 - Posted: 08.31.2017

By Meredith Wadman Luca Rossi tried to hang himself in a bedroom in Perugia, Italy, in 2012. Suspended by his belt from a wardrobe, he had begun to choke when his fiancée unexpectedly walked in. He struggled to safety, defeated even in this intended last act. The 35-year-old physician had everything to live for: a medical career, plans for a family, and supportive parents. But Rossi* was addicted to crack cocaine. He had begun his habit not long after medical school, confidently assuming that he could control the drug. Now, it owned him. Once ebullient and passionate, he no longer smiled or cried. He knew he might be endangering his patients, but even that didn’t matter. He was indifferent to all except obtaining his next fix. “It pushes you to suicide because it fills you with your own emptiness,” he says. In the first months after his near suicide, Rossi didn’t drop his $3500-a-month habit. Early in 2013, he learned that his fiancée was pregnant. Frightened by impending fatherhood, he smoked even more. He didn’t—couldn’t—stop. Then, in April 2013, Rossi’s father, a chemist, happened upon a local newspaper article describing work just published in Nature. Neuroscientists led by Antonello Bonci and Billy Chen at the National Institute on Drug Abuse (NIDA) in Baltimore, Maryland, had studied rats trained to seek cocaine compulsively—animals so powerfully addicted that they tolerated repeated electric shocks to their feet to get their fixes. The rats had also been genetically engineered so that their neurons could be controlled with light. When the researchers stimulated the animals’ brains in an area that regulates impulse control, the rats essentially kicked their habit. “They would almost instantaneously stop searching for cocaine,” Bonci says. © 2017 American Association for the Advancement of Science

Keyword: Brain imaging; Drug Abuse
Link ID: 24013 - Posted: 08.30.2017

Nicola Davis An article suggesting that sugar should be considered an addictive substance, and could even be on a par with abusive drugs such as cocaine, has sparked a furious backlash with experts describing the claims as “absurd”. In a narrative review published in the British Journal of Sports Medicine the authors write that sugar could act as a gateway to alcohol and other addictive substances, adding that like sugar, like cocaine and opium, is refined from plants to yield pure white crystals – a process they say “significantly adds to its addictive properties.” Too much sugar could increase depression risk in men, study suggests Read more The article was co-authored by cardiovascular research scientist James J DiNicolantonio and cardiologist James H O’Keefe, both from Saint Luke’s Mid America Heart Institute in Kansas, together with William Wilson – a physician with the nonprofit US group practice Lahey Health. “Consuming sugar produces effects similar to that of cocaine, altering mood, possibly through its ability to induce reward and pleasure, leading to the seeking out of sugar,” they write, citing rodent studies which show that sweetness is preferred even over cocaine, and that mice can experience sugar withdrawal. Speaking to the Guardian, DiNicolantonio said that the consumption of sugar was a grave concern. “In animals, it is actually more addictive than even cocaine, so sugar is pretty much probably the most consumed addictive substance around the world and it is wreaking havoc on our health.” © 2017 Guardian News and Media Limited

Keyword: Drug Abuse; Obesity
Link ID: 23999 - Posted: 08.26.2017

By Emily Underwood It doesn’t take long for tropical zebrafish to get hooked on hydrocodone. Within a week, they will risk their lives thousands of times per hour to get a dose of the opioid, shows the first study that let the fish themselves choose when to take a hit. To train them, researchers released 1.5 milligrams of hydrocodone per liter of water every time they swam over a shallow platform. The drug quickly filtered out of the tank, so they had to keep going back if they wanted to maintain their high. After just 5 days, the trained fish were visiting the opioid-delivering platform almost 2000 times every 50 minutes, the team reports online today in Behavioral Brain Research. When no drug was present, they visited the platform only about 200 times. Fish normally avoid shallow water, where they’re more likely to be spotted by predators. But over and over again, the jonesing zebrafish left the safety of deep water for the shallow platform. When the team rigged the tank so it took several visits to get a hit, the fish ramped up their efforts, returning as many as 20 times for one dose. Previous studies have shown that zebrafish exposed to opioids become stressed and anxious when the drug is taken away, displaying symptoms of withdrawal. But this is the first time scientists have shown that zebrafish will expend effort—and even court danger—to get a dose. Because zebrafish and humans share the same opioid receptor in their brains, as well as neurotransmitters such as dopamine and serotonin that signal pleasure and reward, the team hopes to use them to screen for new treatments for opioid addiction. © 2017 American Association for the Advancement of Science

Keyword: Drug Abuse
Link ID: 23998 - Posted: 08.26.2017

By Jessica Hamzelou People who use methamphetamine are almost five times more likely to have a stroke caused by a bleed in the brain, many of which are fatal. “We can add stroke to the list of terrible and devastating things that methamphetamine does,” says Damian Zuloaga, of the University at Albany, New York. Beyond the signature tooth decay known as “meth mouth”, methamphetamine also increases heart rate and blood pressure, and can trigger heart attacks. The drug can lead to psychosis, and has been linked to anxiety disorders, depression, and problems with movement similar to those seen in Parkinson’s disease. A handful of studies have also linked methamphetamine use to strokes. To explore further, Julia Lappin and her colleagues at the Australian National Drug and Alcohol Research Centre in Sydney sifted through published research on the topic. The team specifically looked for research into people under the age of 45 – a group less likely to be affected by age-related causes of stroke. They assessed the results of 77 studies in total. Most of these studies were conducted in the US, where, in 2012, around 1.2 million people reported using methamphetamine in the past year. Several of the studies the team looked at reported that strokes are responsible for between one and five per cent of methamphetamine-related deaths. And other studies found that methamphetamine was to blame for between two and six per cent of all strokes caused by a blockage in the brain’s blood flow in under 45s. © Copyright New Scientist Ltd.

Keyword: Drug Abuse; Stroke
Link ID: 23988 - Posted: 08.24.2017

Richard Harris It's always appealing to think that there could be an easy technical fix for a complicated and serious problem. For example, wouldn't it be great to have a vaccine to prevent addiction? "One of the things they're actually working on is a vaccine for addiction, which is an incredibly exciting prospect," said Dr. Tom Price, secretary of Health and Human Services. He was talking to reporters earlier this week, after the White House discussed the recommendations from a government commission tasked with suggesting ways to cope with the nation's opioid epidemic. Trump Says He Intends To Declare Opioid Crisis National Emergency But, as is so often the case, there's no quick fix on the horizon for an epidemic that is now killing more Americans than traffic accidents. Researchers have been working on vaccines against addictive drugs, including nicotine, cocaine and heroin, for almost two decades. "Like any other vaccine, you inject the vaccine and you use your immune system to produce antibodies," says Dr. Ivan Montoya, acting director of the division of Therapeutics and Medical Consequences at the National Institute on Drug Abuse. "In this case, the antibodies are against the drugs of abuse." © 2017 npr

Keyword: Drug Abuse
Link ID: 23980 - Posted: 08.22.2017

By Aggie Mika | In a report published today (August 16) in Nature, researchers uncover the mechanisms by which the psychoactive and addictive drug fenethylline, trade name Captagon, exerts its potent stimulating effects. Essentially, one component of the drug, theophylline, boosts the effects of another, amphetamine. “This combination greatly enhances amphetamine’s properties,” says coauthor and Scripps Research Institute researcher Kim Janda in a press conference this week, Reuters reports. “So this now makes sense why it’s being so heavily abused.” In exploring fenethylline’s mode of action, the researchers came upon a method to vaccinate against the drug in mice using small, antibody-eliciting molecules called haptens that target the drug’s chemical components. Once antibodies for a specific chemical are prompted by a vaccine, they bind to and prevent it from interacting with its receptors in the body, thus preventing the effects of the drug driven by that chemical. Fenethylline’s use is mostly confined to the Middle East, where approximately 40 percent of young adult drug users in Saudi Arabia are addicted to the drug, the authors write in their report. According to Reuters, the drug initially sparked Janda’s interest because of its use by Islamic State jihadists. According to the San Diego Union-Tribune, “Syrian civil war combatants and Islamic State terrorists have reportedly used the drug to boost their fighting ability and to lessen fear.” © 1986-2017 The Scientist

Keyword: Drug Abuse; Neuroimmunology
Link ID: 23971 - Posted: 08.18.2017

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

Keyword: Drug Abuse
Link ID: 23954 - Posted: 08.14.2017

By Kerry Grens The popular chemogenetic technique for controlling cells does not operate in vivo in the way scientists had assumed. Reporting in Science yesterday (August 3), researchers show that CNO, a drug used in the DREADDs method (designer receptors exclusively activated by designer drugs), is not actually responsible for the effects scientists observe. Rather, it’s clozapine, a metabolite of CNO with numerous cellular targets, that binds the receptors. These results make it imperative for researchers to do proper controls with clozapine, and indicate that they should change their protocols altogether. “I’m glad I don’t own stock in CNO,” says Scott Sternson, a neuroscientist at the Janelia Research Campus. “There’s no reason to use CNO anymore.” Although it may be the end of CNO in these studies, coauthor Mike Michaelides of the National Institute on Drug Abuse tells The Scientist the results don’t necessarily mean the end of DREADDs. In fact, his findings might simplify things. Rather than using CNO, researchers can just administer clozapine instead because it’s the real actuator of the technique. “If they use proper controls, then hopefully it should be fine,” he says. The idea behind DREADDs is that a receptor is introduced into cells that will only respond to a particular drug, in this case CNO. Likewise, the drug will only target that receptor. The technique allows researchers to control neural activity. Michaelides says that although it’s a commonly used method, no one had done the critical experiments to observe CNO interacting directly with DREADDs in vivo. © 1986-2017 The Scientist

Keyword: Miscellaneous
Link ID: 23931 - Posted: 08.08.2017

/ By Robin Lloyd While broadly welcomed by public health advocates as an important step to further curb tobacco use, many of the commitments in a new plan to tackle the problem, announced last Friday by Food and Drug Administration Commissioner Scott Gottlieb, actually involve gathering more input for future policies, rather than taking action now. “We expect to take meaningful steps in 2017 to advance important regulatory components that address the key aspects of this new policy,” FDA spokesman Michael Felberbaum said in an email message to Undark. “We do not have any additional details to share at this time.” That strikes some public health advocates as a bit of foot-dragging. “A lot of these issues they’re raising that they say they have to consider have been considered, have been researched, have been studied,” says Eric Lindblom, director for tobacco control and food and drug law at the O’Neill Institute for National and Global Health Law at Georgetown University. Lindblom has a long resume for developing tobacco control policies to improve public health, including a 2011-2014 stint at the FDA’s Center for Tobacco Products. “FDA saying that ‘We’re going to look into nicotine reduction,’ without also saying, ‘We’re going to issue a proposed rule before the end of this year, or before June of next year,’ just opens the door to continued discussion and talking and all the rest, without actually ever getting anything done,” Lindblom said. Copyright 2017 Undark

Keyword: Drug Abuse
Link ID: 23928 - Posted: 08.08.2017

by Kate Travis Nearly 5 percent of U.S. adults misused prescription opioids in 2015, a new study shows. Based on the National Survey on Drug Use and Health, an in-person survey of more than 50,000 people, researchers estimated that 91.8 million, or 37.8 percent, of adults used prescription opioids in 2015. Some 11.5 million people misused the painkillers and 1.9 million people reported opioid dependence or abuse, Beth Han of the Substance Abuse and Mental Health Services Administration in Rockville, Md., and colleagues report online August 1 in Annals of Internal Medicine. Among people reporting opioid misuse, nearly 60 percent used the painkillers without a prescription, 22 percent took a bigger dose than prescribed, about 15 percent used them more frequently than directed, and 13 percent of people used them for longer than directed. Relieving pain was the most commonly cited reason for misusing opioids — for 66 percent of people reporting misuse and nearly 49 percent of those with opioid dependence or abuse. These results underscore the urgent need for better approaches to pain management, the authors conclude. As part of the efforts to curb the nation’s opioid epidemic — and pain problem — scientists are searching for safer opioids and opioid alternatives. Misuse motivators Pain relief was the top reason cited for misusing or abusing opioid painkillers. Other reasons included to relax, sleep or get high. B. Han et al/Annals of Internal Medicine 2017 © Society for Science & the Public 2000 - 2017.

Keyword: Drug Abuse
Link ID: 23907 - Posted: 08.02.2017

By Laurie McGinley and William Wan An electronic cigarette is demonstrated in Chicago. (AP Photo/Nam Y. Huh, File) The Food and Drug Administration said Friday it wants to reduce the nicotine in cigarettes to make them less addictive. The unexpected announcement sent shares of tobacco companies plummeting and sparked praise among some public health advocates. If successful, the effort would be the first time the government has tried to get the Americans to quit cigarettes by reaching beyond warning labels or taxes to attacking the actual addictive substance inside. The FDA rolled out a second major announcement at the same time: It is delaying for several years a key regulation affecting cigars and e-cigarettes, including flavored vaping products that studies show are especially enticing to youth. Specifically, it postponed the requirement that such products be approved by the agency. FDA’s commissioner Scott Gottlieb said both actions are part of a comprehensive plan to eventually wean smokers off conventional cigarettes and steer them toward less harmful alternative forms of nicotine like vaping. “The overwhelming amount of death and disease attributable to tobacco is caused by addiction to cigarettes — the only legal consumer product that, when used as intended, will kill half of all long-term users,” he said. Some health proponents, however, expressed caution, pointing out that the nicotine-reduction proposal could take years to enact and could be derailed by major hurdles, including the significant lobbying power of tobacco industry. © 1996-2017 The Washington Post

Keyword: Drug Abuse
Link ID: 23893 - Posted: 07.29.2017

People who drink three to four times a week are less likely to develop type 2 diabetes than those who never drink, Danish researchers suggest. Wine appears to be particularly beneficial, probably as it plays a role in helping to manage blood sugar, the study, published in Diabetologia, says. They surveyed more than 70,000 people on their alcohol intake - how much and how often they drank. But experts said this wasn't a "green light" to drink more than recommended. And Public Health England warned that consuming alcohol contributed to a vast number of other serious diseases, including some cancers, heart and liver disease. "People should keep this in mind when thinking about how much they drink," a spokeswoman said. Prof Janne Tolstrup, from the National Institute of Public Health of the University of Southern Denmark, who led the research, said: "We found that drinking frequency has an independent effect from the amount of alcohol taken. "We can see it's a better effect to drink the alcohol in four portions rather than all at once." After around five years, study participants were followed up and a total of 859 men and 887 women group had developed diabetes - either type 1 or the more common type 2. The researchers concluded that drinking moderately three to four times a week reduced a woman's risk of diabetes by 32% while it lowered a man's by 27%, compared with people drinking on less than one day a week. Findings also suggest that not all types of alcohol had the same effect. Wine appeared to be particularly beneficial because polyphenols, particularly in red wine, play a role in helping to manage blood sugar. © 2017 BBC.

Keyword: Drug Abuse
Link ID: 23892 - Posted: 07.29.2017

By BENEDICT CAREY Dr. Herbert Needleman, whose studies of children exposed to low levels of lead prompted regulations that limited or banned the metal in a range of common products, like gasoline and paint, and set a standard for the modern study of environmental toxins, died on July 18 in Pittsburgh. He was 89. His son, Dr. Joshua Needleman, said the cause was lung failure resulting from edema, an excess of fluid. Dr. Needleman was working at a community psychiatric clinic in North Philadelphia after medical school when he met a young man who would become a touchstone for a crusading career. The boy approached Dr. Needleman and explained his ambitions, which were large, even as the boy struggled with words. He was bright and open; nonetheless he had deficits that struck Dr. Needleman as similar to those found in children with lead poisoning. “I thought, how many of these kids who are coming to the clinic are in fact a missed case of lead poisoning?” he said in a later interview. His clinic office overlooked a school playground; the view gave him an idea. Doctors had long known that exposure to high doses of lead caused mental lapses, even permanent brain damage and death. But what about the low-level exposure that many children, like the ones playing in the yard, absorbed every day — merely by living in older urban neighborhoods thick with lead paint and industrial contamination? No one knew. No one could study the effects carefully, because the available tests for lead exposure were of hair, blood, or fingernails — each flawed in its own way. Bone is the most accurate long-term repository: Once absorbed into the body, lead circulates in the blood and accumulates in the skeleton. But taking bone samples — biopsies — is painful and hardly justifiable for the sake of a hypothesis, especially in young children. Yet Dr. Needleman had seen an earlier study of lead poisoning, a small one, which measured accumulated lead exposure in teeth. Teeth are a part of the human skeleton. And young children shed them. “That was the insight that changed everything,” said Dr. Bernard Goldstein, former dean of the University of Pittsburgh’s graduate school of public health. “Herb became the Tooth Fairy.” © 2017 The New York Times Company

Keyword: Neurotoxins; Development of the Brain
Link ID: 23887 - Posted: 07.28.2017

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

Keyword: Drug Abuse; Obesity
Link ID: 23870 - Posted: 07.25.2017