Links for Keyword: Drug Abuse
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By LIZ ALDERMAN PARIS — On a recent day in the shadow of the Arc de Triomphe, a line of 20 people spilled onto the sidewalk of a trendy new boutique, eager to get a taste of its latest gourmet offerings. A sign in the window promoted piña colada as the store’s flavor of the month. A woman wearing a Chanel jacket said she wanted to try peach. But this was no temple of gastronomy. It was one of scores of electronic cigarette shops that have been springing up by the week in Paris as well as in numerous cities across Europe and the United States. Inside the ClopiNette boutique, shoppers can choose from among more than 60 flavors of nicotine liquid — including Marlboro and Lucky Strike flavors — all in varying strengths and arranged in color-coded rows. (ClopiNette is a play on “clope,” French slang for a cigarette.) “It’s like visiting a Nespresso store,” said Anne Stephan, a lawyer specializing in health issues at a nearby law firm. What’s driving her into the store is a desire shared by many: they want to give up smoking tobacco but don’t want to kick the smoking habit. After smoking 20 cigarettes daily for 25 years and failing to quit, Ms. Stephan said she had cut down to one a day in the three months since she began puffing on a so-called e-cig. Using technology that turns nicotine-infused propylene glycol into an inhalable vapor, e-cigarettes smoke almost like the real thing, without the ashtray odor. © 2013 The New York Times Company
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18270 - Posted: 06.13.2013
by Satoshi Kanazawa in The Scientific Fundamentalist Drinking alcohol is evolutionarily novel, so the Hypothesis would predict that more intelligent people drink more alcohol than less intelligent people. The human consumption of alcohol probably originates from frugivory (consumption of fruits). Fermentation of sugars by yeast naturally present in overripe and decaying fruits produces ethanol, known to intoxicate birds and mammals. However, the amount of ethanol alcohol in such fruits ranges from trace to 5%, roughly comparable to light beer. (And you can't really get drunk on light beer.) It is nothing compared to the amount of alcohol present in regular beer (4-6%), wine (12-15%), and distilled spirits (20-95%). Human consumption of alcohol, however, was unintentional, accidental, and haphazard until about 10,000 years ago. The intentional fermentation of fruits and grain to yield ethanol arose only recently in human history. The production of beer, which relies on a large amount of grain, and that of wine, which similarly requires a large amount of grapes, could not have taken place before the advent of agriculture around 8,000 BC and the consequent agricultural surplus. Archeological evidence dates the production of beer and wine to Mesopotamia at about 6,000 BC. The origin of distilled spirits is far more recent, and is traced to Middle East or China at about 700 AD. The word alcohol - al kohl - is Arabic in origin, like many other words that begin with "al," like algebra, algorithm, alchemy, and Al Gore. Human experience with concentrations of ethanol higher than 5% that is attained by decaying fruits is therefore very recent. © Copyright 2002-2013 Sussex Directories, Inc.
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 1: An Introduction to Brain and Behavior
Link ID: 18258 - Posted: 06.12.2013
By Scicurious When I am stressed (and I’m stressed a lot of the time, as I bet a lot of you are as well), I turn to coffee. Not just to keep me going through the time when I need to get things done, but also for relaxation. For me, the smell and taste of coffee brings me thoughts of relaxing conversations with friends and other fun times. But what if the memories weren’t all the relaxing the caffeine was doing for me? What if the chronic caffeine consumption was keeping my stressful life at bay? It’s time to look at adenosine 2A receptors in the hippocampus. Don’t worry, the coffee will be back. First let’s talk about stress. Specifically, childhood stress. In small doses, stress exposure can actually be good for you, but in large, or prolonged, doses, it’s definitely not. There are effects immediately after stress, as well as long term ones. when you suffer strong stressors in development, you can end up with changes all the way into adulthood, from cognitive deficits to predisposition to psychiatric disorders. Why is stress in development so important? During development, our brains are developing too, particularly our hippocampus. While the hippocampus is best known for its role in memory and spatial navigation, it’s also extremely important in emotional responses. Neuronal growth in the hippocampus can come from enriched environments or chronic antidepressants, and death of those neurons can come from chronic stress. Chronic stress also disrupts the hypothalamic-pituitary-adrenal axis (the HPA axis) And that’s just in adults! During development, animals are very susceptible to stress, and the hippocampus is still developing its connections. And we’re still figuring out what changes occur during early life stress and how they relate to behaviors in adulthood. © 2013 Scientific American
Related chapters from BP6e: Chapter 15: Emotions, Aggression, and Stress; Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18257 - Posted: 06.11.2013
By GRETCHEN REYNOLDS For thousands of years, coffee has been one of the two or three most popular beverages on earth. But it’s only recently that scientists are figuring out that the drink has notable health benefits. In one large-scale epidemiological study from last year, researchers primarily at the National Cancer Institute parsed health information from more than 400,000 volunteers, ages 50 to 71, who were free of major diseases at the study’s start in 1995. By 2008, more than 50,000 of the participants had died. But men who reported drinking two or three cups of coffee a day were 10 percent less likely to have died than those who didn’t drink coffee, while women drinking the same amount had 13 percent less risk of dying during the study. It’s not clear exactly what coffee had to do with their longevity, but the correlation is striking. Other recent studies have linked moderate coffee drinking — the equivalent of three or four 5-ounce cups of coffee a day or a single venti-size Starbucks — with more specific advantages: a reduction in the risk of developing Type 2 diabetes, basal cell carcinoma (the most common skin cancer), prostate cancer, oral cancer and breast cancer recurrence. Perhaps most consequential, animal experiments show that caffeine may reshape the biochemical environment inside our brains in ways that could stave off dementia. In a 2012 experiment at the University of Illinois at Urbana-Champaign, mice were briefly starved of oxygen, causing them to lose the ability to form memories. Half of the mice received a dose of caffeine that was the equivalent of several cups of coffee. After they were reoxygenated, the caffeinated mice regained their ability to form new memories 33 percent faster than the uncaffeinated. Close examination of the animals’ brain tissue showed that the caffeine disrupted the action of adenosine, a substance inside cells that usually provides energy, but can become destructive if it leaks out when the cells are injured or under stress. The escaped adenosine can jump-start a biochemical cascade leading to inflammation, which can disrupt the function of neurons, and potentially contribute to neurodegeneration or, in other words, dementia. Copyright 2013 The New York Times Company
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 18239 - Posted: 06.06.2013
By Stuart McMillen A classic experiment into drug addiction science. Would rats choose to take drugs if given a stimulating environment and social company?
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 18214 - Posted: 06.01.2013
Sally Satel From the recent announcement of President Obama's BRAIN Initiative to the Technicolor brain scans ("This is your brain on God/love/envy etc") on magazine covers all around, neuroscience has captured the public imagination like never before. Understanding the brain is of course essential to developing treatments for devastating illnesses like schizophrenia and Parkinson's. More abstract but no less compelling, the functioning of the brain is intimately tied to our sense of self, our identity, our memories and aspirations. But the excitement to explore the brain has spawned a new fixation that my colleague Scott Lilienfeld and I call neurocentrism -- the view that human behavior can be best explained by looking solely or primarily at the brain. The critical question, though, is whether this neural disruption proves that the addict's behavior is involuntary, and that he is incapable of self-control. It does not. Sometimes the neural level of explanation is appropriate. When scientists develop diagnostic tests or a medications for, say, Alzheimer's disease, they investigate the hallmarks of the condition: amyloid plaques that disrupt communication between neurons, and neurofibrillary tangles that degrade them. Other times, a neural explanation can lead us astray. In my own field of addiction psychiatry, neurocentrism is ascendant -- and not for the better. Thanks to heavy promotion by the National Institute on Drug Abuse, part of the National Institutes of Health, addiction has been labeled a "brain disease." © 2013 by The Atlantic Monthly Group.
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18213 - Posted: 06.01.2013
By Ian Chant Most people make good decisions most of the time. But when drug addiction, disease or brain injury enters the picture, rational thinking can go awry. What if the damaged brain just needed a little reminder of how it feels to choose wisely? Enter the MIMO neural prosthesis, an array of electrodes implanted in the brain that make contact with eight neuron circuits in the prefrontal cor-tex, the brain's command center for decision making. The device can both record the brain activity associated with good choices and stimulate the relevant neurons to get the brain back on track. Although the implant can listen in only on a tiny subset of the neurons in this region, the scientists who developed it, based at Wake Forest Baptist Medical Center, were surprised to discover that they could still pick up signature patterns associated with correct choices, at least in the context of a simple task. The researchers tested the neural prosthesis on monkeys that were trained to move a cursor over a picture on a computer screen to get a food reward. The implant first recorded the brain activity associated with choosing the correct picture. Then the monkeys were given cocaine, and their performance plummeted. But when the implant was switched on to send electric current to the neurons that had earlier been associated with the correct answers, the monkeys immediately started selecting the right pictures again. Some of them did an even better job than they had before receiving cocaine. © 2013 Scientific American,
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 18141 - Posted: 05.11.2013
Ella Pickover A “helpful” new drug which could help problem drinkers reduce the amount of alcohol they consume will today become available to UK patients. If dependent drinkers take the drug nalmefene and undergo counselling they can cut their consumption levels by 61 per cent, manufacturers said. The pill, also known as selincro, has been licensed for use by health officials and will be available for doctors to prescribe to their patients from today. The drug, which is to be taken once a day, has been licensed for "the reduction of alcohol consumption in adult patients with alcohol dependence without physical withdrawal symptoms and who do not require immediate detoxification". While current drugs help patients to become teetotal, nalmefene helps people with drinking problems to cut back on the amount they drink. The drug works by modulating the reward mechanism in the brain. A clinical trial into the drug helped patients cut the amount they consumed from 12.75 units a day to five units a day - a 61 per cent reduction. And patients who underwent counselling as well as taking the drug reduced their "heavy drinking days" from 23 days a month to nine days a month after undergoing the treatment for six months, researchers said. "The people who we saw in the study were not stereotypical alcoholics, most of them had families and jobs," said drug investigator Dr David Collier, of Barts and The London School of Medicine. © independent.co.uk
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18129 - Posted: 05.07.2013
Distinct patterns of brain activity are linked to greater rates of relapse among alcohol dependent patients in early recovery, a study has found. The research, supported by the National Institutes of Health, may give clues about which people in recovery from alcoholism are most likely to return to drinking. "Reducing the high rate of relapse among people treated for alcohol dependence is a fundamental research issue," said Kenneth R. Warren, Ph.D., acting director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of NIH. "Improving our understanding of the neural mechanisms that underlie relapse will help us identify susceptible individuals and could inform the development of other prevention strategies." Using brain scans, researchers found that people in recovery from alcoholism who showed hyperactivity in areas of the prefrontal cortex during a relaxing scenario were eight times as likely to relapse as those showing normal brain patterns or healthy controls. The prefrontal brain plays a role in regulating emotion, the ability to suppress urges, and decision-making. Chronic drinking may damage regions involved in self-control, affecting the ability to regulate cravings and resist relapse. Findings from the study, which was funded by NIAAA, appear online at the JAMA Psychiatry website.
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 18106 - Posted: 05.02.2013
By ABIGAIL ZUGER, M.D. Addiction swallows lives whole, and not only with overdose, illness and concentric cycles of rehab and relapse. A less onerous but still tenacious kind of post-traumatic stress disorder may develop as well, with recovered addicts and their families compulsively reliving the past in private — or, like David Sheff and his son Nic, in public. In the last five years the two have written a small library of memoirs centered on Nic’s battle with substance use, with two by Nic (now 31, and sober) and the 2008 best seller by his father, “Beautiful Boy.” Now comes “Clean,” less memoir than guide for those just entering the terrain Mr. Sheff knows so well. If the book represents a certain redundancy of subject, its likely audience — those who must watch as friends and family spiral away — cannot hear too many sympathetic reiterations of the same truths. In “Clean,” Mr. Sheff changes perspective, writing as advocate and journalist rather than distraught father. Still, his story line recreates that of “Beautiful Boy,” tracing the trajectory of addiction from cradle to rehab and beyond with the same question in mind: How does a promising cleareyed kid from a good family wind up in an inconceivable sea of trouble? His answer, bludgeoned home with the repetitive eloquence of the missionary, is entirely straightforward: The child is ill. Addiction must be considered a disease, as devoid of moral overtones as diabetes or coronary artery disease, just as amenable as they are to scientific analysis, and just as treatable with data-supported interventions, not hope, prayer or hocus-pocus. © 2013 The New York Times Company
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18098 - Posted: 04.30.2013
By Cheryl Knepper Substance abuse and dependence rarely occur in a vacuum. Today’s addict is faced with a multitude of issues that may co-exist and compromise recovery. Co-existing addictions/compulsive behaviors such as drugs and alcohol, pathological gambling, sex, food, work, internet and gaming can become chronic and progressive if left unidentified and untreated. Many of these addictions don’t only coexist, but interact, reinforce and fuse together becoming part of a package known as Addiction Interaction. The term “Addiction Interaction Disorder” was introduced by Patrick Carnes PhD in 2011. Caron Treatment Centers conducted a research study among adult patients with drug and alcohol addictions to determine what percentage may be at risk for sex and love addiction. The 485 participants were given the SAST-R (Sexual Addiction Screening Tool-Revised a 45 item forced choice (Yes/No) instrument): Carnes, Green & Carnes, 2010. The findings of this study indicated that 21 percent of individuals being treated for primary substance dependence scored at risk. Another interesting finding from the study showed a higher percentage of cannabis, cocaine and amphetamine abuse or dependence diagnosis in the individuals that scored at-risk for sexual addiction. In addition, at-risk individuals had higher percentages of mood disorder, PTSD and eating disorder diagnoses. © 2013 Scientific American
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18097 - Posted: 04.30.2013
By Nathan Seppa The tobacco and fruit mixture smoked in public hookah bars might be considerably more dangerous than its pleasant scent would suggest. An analysis of people who smoked from water pipes three times a day finds that the pipes deliver more carbon monoxide and benzene, a carcinogen, than does smoking half a pack of cigarettes daily. In an upcoming issue of Cancer Epidemiology, Biomarkers & Prevention, researchers document those and several other cancer-causing compounds that showed up in urine tests of the water-pipe smokers. The research calls into question a common assumption: that hookahs are safe. “This is a great addition to the literature,” says Thomas Eissenberg, a psychologist at Virginia Commonwealth University in Richmond. He and his colleagues had previously found toxic substances in hookah smoke. The new paper extends his findings by detecting carcinogens and other bad actors in water-pipe smokers themselves, he says. Hookah smoking goes back hundreds of years in India, the Middle East and North Africa, but it is newer in parts of Europe and North America. The substances heated in a hookah vary. In the study, researchers used pastes chosen by the participants that were 5 to 10 percent tobacco combined with honey, molasses and bits of fruit. This paste goes in the bowl of the pipe, which is covered with a perforated piece of aluminum foil and topped with a burning piece of charcoal, says study coauthor Peyton Jacob III, a research chemist at the University of California, San Francisco. © Society for Science & the Public 2000 - 2013
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18088 - Posted: 04.29.2013
by Scicurious Mmmmm beer! Just a sip is enough to prime the brain's dopamine addiction circuits, if reports of a new study are to be believed. Photograph: Johnny Green/PA It's been a long day at work, followed by a long workout. I'm tired, and all I really want is to relax with a beer. I grab one out of the fridge and take a sip. I feel better already. A new study tells us that this is due to dopamine, a neurotransmitter that plays an important role in things like motivation and reward. Drugs of abuse, such as cocaine, increase dopamine levels in areas of the brain associated with the expectation of reward, such as the ventral striatum, and this increase is part of what makes them feel so good, and do so bad. But dopamine can also signal the expectation of something that might be rewarding. This means that as we learn that some things are rewarding, like, say, beer, we begin to respond, not only to the alcohol, but to the cues that alcohol is coming: to the beer bottles, the glass, or the taste. And taste is what this study looked at. The authors took 49 male beer drinkers and divided them up into three groups: those with a family history of alcoholism, those without, and those who didn't know. They used positron emission tomography (PET) to examine how the dopamine in their brains responded to a taste of beer. The big effect? The mere taste of your favourite beer (15 millilitres – not enough to get any effects of the alcohol) produces an increase in dopamine in the ventral striatum, as well as an increased desire to … drink more beer. This suggests that a cue (the taste) produces a sign of reward expectation long before the alcohol hits your system. And the effect of the taste of beer on dopamine in the ventral striatum was larger in people who had a family history of alcohol abuse. What's not to love! It's beer! It's dopamine! It's brain scans! Of course the media got excited. © 2013 Guardian News and Media Limited
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 18053 - Posted: 04.20.2013
A study by researchers at the National Institutes of Health gives insight into changes in the reward circuitry of the brain that may provide resistance against cocaine addiction. Scientists found that strengthening signaling along a neural pathway that runs through the nucleus accumbens — a region of the brain involved in motivation, pleasure, and addiction — can reduce cocaine-seeking behavior in mice. Research suggests that about 1 in 5 people who use cocaine will become addicted, but it remains unclear why certain people are more vulnerable to drug addiction than others. “A key step in understanding addiction and advancing treatment is to identify the differences in brain connectivity between subjects that compulsively take cocaine and those who do not,” said Ken Warren, Ph.D., acting director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA). Researchers at NIAAA, part of NIH, conducted the study. “Until now, most efforts have focused on finding traits associated with vulnerability to develop compulsive cocaine use. However, identifying mechanisms that promote resilience may prove to have more therapeutic value,” said the paper’s senior author, Veronica Alvarez, Ph.D., acting chief of the Section on Neuronal Structure in the NIAAA Laboratory for Integrative Neuroscience. The study is available on the Nature Neuroscience website ahead of print. In the study, mice were conditioned to receive an intravenous dose of cocaine each time they poked their nose into a hole in their enclosure. Cocaine was then made unavailable for periods of time during the day. Some of the mice would stop seeking the drug once it was removed while others would obsessively continue to poke the hole in an effort to obtain the drug.
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 18041 - Posted: 04.16.2013
By Puneet Kollipara Rats that will go to great lengths to get a cocaine fix might blame a group of sluggish neurons. Controlling the problem may come down to a flick of a light switch: Stimulating those brain cells with lasers reduces the addicted rats’ cocaine use, researchers report in the April 4 Nature. “It's an outstanding piece of work,” says neuroscientist A.J. Robison of Michigan State University, who wasn’t involved in the study. The findings could help researchers better understand the role of neural circuitry in drug addiction in humans, he says. Scientists know that when certain neurons fire less frequently in the prelimbic cortex, a brain region that handles impulse control and reward-driven behavior, a person’s self-control can decrease. But researchers didn’t know whether using cocaine chronically could make the neurons drowsy to begin with, and whether that sluggishness could also promote drug use in spite of ill consequences. Billy Chen, then of the National Institutes of Health, and colleagues trained rats to take cocaine. The rats learned to press levers to receive a dose of drug through an IV. After about two months, researchers started giving the rats shocks roughly one-third of the time when the animals pressed the levers. Most of the rats stopped taking cocaine, but about 30 percent continued. These were compulsive cocaine users, says coauthor Antonello Bonci, a neuroscientist at the NIH’s National Institute on Drug Abuse. © Society for Science & the Public 2000 - 2013
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17991 - Posted: 04.05.2013
A new manual for mental disorders is slated to be released in May and video-game addiction experts are hoping for a new addition. The Diagnostic and Statistical Manual of Mental Disorders doesn’t currently list video-game addiction in its list of disorders, but tech-addiction expert Hilarie Cash said that needs to change. Cash runs Restart in Seattle, Wash., one of the few known internet and video game addiction rehabilitation centres in North and South America. “People’s lives completely fall apart, and there are people who die from it,” said Cash. “It’s rewarding, right? You get this pump and then it fades and you miss it and you want it back,” said Valesquez. “It’s like a cycle.” He began gaming when he got his first Nintendo. When he shifted to gaming online, he saw major success. He was even sponsored by a gaming company at age 12. “If I couldn’t play, it was like profound boredom,” he said. That’s when it turned from a hobby into a habit for Valesquez. “I was generally playing, at the very peak, six to ten hours a day,” he said. As a result, his grades slid and he began to replace his real life friends with ones that were online. “Even if you don’t want to play, you feel a responsibility to go online. It’s like a community,” said Valesquez. Cash said those are classic signs of video-game addiction. “Most people understand that gambling can become, can develop into a serious addiction, so it’s like that,” said Cash. She said the most addictive games have a social component and are competitive. © CBC 2013
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17980 - Posted: 04.02.2013
By BARRY MEIER A group of 18 doctors, researchers and public health experts jointly urged the Food and Drug Administration on Tuesday to take action on energy drinks to protect adolescents and children from the possible risks of consuming high amounts of caffeine. “There is evidence in the published scientific literature that the caffeine levels in energy drinks pose serious potential health risks,” the doctors and researchers wrote.In their letter to Dr. Margaret A. Hamburg, the F.D.A. commissioner, the group argued that energy drink makers had failed to meet the regulatory burden placed on them to show that the ingredients used in their beverages were safe, specifically where children, adolescents and young adults are concerned. As a result, the group urged the F.D.A. to restrict caffeine content in the products and to require manufacturers to include caffeine content on product labels. A similar letter was sent to the agency by the San Francisco city attorney, Dennis J. Herrera, who is one of several public officials conducting investigations of the energy-drink industry. Energy drink makers have insisted their products are safe and that their levels of caffeine, a stimulant, are on a par with other widely consumed drinks, like coffee. The F.D.A. has said that it is safe for adults to consume about 400 milligrams of caffeine daily, though many experts say that most adults can consume 600 milligrams or more of caffeine without ill effect. A 16-ounce cup of Starbucks coffee has about 330 milligrams of caffeine, an amount about twice that of some similarly sized energy drinks. © 2013 The New York Times Company
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17924 - Posted: 03.20.2013
By Scicurious We humans love us some caffeine. The mild stimulant have saved many a student, parent, and hard working adult from nodding over their desks. And it’s a natural product of plants like the coffee plant and the tea bush. But the question is, why do these plants have it in the first place? It turns out that there are two answers to that question. First, caffeine is a natural pesticide, which can paralyze and kill insects that want to chomp on the leaves, berries, or other parts of the plant. It’s good for keeping a bug off your back. But these plants also produce flowers, and these flowers need bees. So it’s somewhat surprising to realize that the coffee plant, as well as plants from the Citrus genus (yup, that means oranges), have caffeine in their nectar. After all, if caffeine is a poison to some bugs, you don’t want to be poisoning your pollinators! But it turns out that bees aren’t like other bugs, and may enjoy themselves a jolt like humans do! Whether they enjoy it or not, they certainly remember it! The authors started out by examining exactly HOW much caffeine was in the nectar of various coffee and citrus plants. And the concentrations of caffeine in the nectar could get up to that of one cup of coffee (though, obviously, in a much smaller volume total). I’m starting to wonder if there’s a “honeyed nectar” energy drink in the future. © 2013 Scientific American
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17888 - Posted: 03.11.2013
By Meghan Rosen Alcohol may give heavy drinkers more than just a buzz. It can also fuel their brains, a new study suggests. Long-term booze use boosts brain levels of acetate, an energy-rich by-product of alcohol metabolism, researchers report online March 8 in the Journal of Clinical Investigation. In the study, people who downed at least eight drinks per week also sucked more energy from acetate than their light-drinking counterparts. The extra energy may give heavy drinkers more incentive to imbibe, says study coauthor Graeme Mason of Yale University. And the caloric perk might help explain why alcohol withdrawal is so hard. “I think it's a very good hypothesis,” says biochemical geneticist Ting-Kai Li of Duke University. Scientists had suspected that heavy drinkers absorb and burn more acetate, but, he adds, “Graeme Mason showed that this is actually happening.” Acetate is best known as a chemical in vinegar. But when people drink a glass of wine or drain a can of beer, their liver breaks down the alcohol and pumps out acetate as leftovers. The bloodstream then delivers acetate throughout the body, including to the brain. Human brains typically run on sugar. But with enough acetate in the blood, Mason thought, brains might crank up their ability to burn it too. To find out if his suspicion was correct, Mason and his colleagues peered into the brains of seven heavy drinkers and seven light drinkers, who quaffed fewer than two drinks per week. © Society for Science & the Public 2000 - 2013
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of Internal States
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 17887 - Posted: 03.11.2013
By JAMES GORMAN Nothing kicks the brain into gear like a jolt of caffeine. For bees, that is. And they don’t need to stand in line for a triple soy latte. A new study shows that the naturally caffeine-laced nectar of some plants enhances the learning process for bees, so that they are more likely to return to those flowers. “The plant is using this as a drug to change a pollinator’s behavior for its own benefit,” said Geraldine Wright, a honeybee brain specialist at Newcastle University in England, who, with her colleagues, reported those findings in Science on Thursday. The research, other scientists said, not only casts a new light on the ancient evolutionary interaction between plants and pollinators, but is an intriguing confirmation of deep similarities in brain chemistry across the animal kingdom. Plants are known to go to great lengths to attract pollinators. They produce all sorts of chemicals that affect animal behavior: sugar in nectar, memorable fragrances, even substances in fruit that can act like laxatives in the service of quick seed dispersal. Lars Chittka, who studies bee behavior at Queen Mary, University of London, and wrote a commentary on the research in the same issue of Science, said that in the marketplace of plants seeking pollinators, the plants “want their customers to remain faithful,” thus the sugary nectar and distinctive scents. © 2013 The New York Times Company
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17878 - Posted: 03.09.2013




