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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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 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 BP7e: Chapter 4: The Chemistry 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 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 BP7e: Chapter 4: The Chemistry 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 BP7e: Chapter 4: The Chemistry 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 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 BP7e: Chapter 4: The Chemistry 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 BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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 BP7e: Chapter 4: The Chemistry 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

By MICHAEL MOSS On the evening of April 8, 1999, a long line of Town Cars and taxis pulled up to the Minneapolis headquarters of Pillsbury and discharged 11 men who controlled America’s largest food companies. Nestlé was in attendance, as were Kraft and Nabisco, General Mills and Procter & Gamble, Coca-Cola and Mars. Rivals any other day, the C.E.O.’s and company presidents had come together for a rare, private meeting. On the agenda was one item: the emerging obesity epidemic and how to deal with it. While the atmosphere was cordial, the men assembled were hardly friends. Their stature was defined by their skill in fighting one another for what they called “stomach share” — the amount of digestive space that any one company’s brand can grab from the competition. James Behnke, a 55-year-old executive at Pillsbury, greeted the men as they arrived. He was anxious but also hopeful about the plan that he and a few other food-company executives had devised to engage the C.E.O.’s on America’s growing weight problem. “We were very concerned, and rightfully so, that obesity was becoming a major issue,” Behnke recalled. “People were starting to talk about sugar taxes, and there was a lot of pressure on food companies.” Getting the company chiefs in the same room to talk about anything, much less a sensitive issue like this, was a tricky business, so Behnke and his fellow organizers had scripted the meeting carefully, honing the message to its barest essentials. “C.E.O.’s in the food industry are typically not technical guys, and they’re uncomfortable going to meetings where technical people talk in technical terms about technical things,” Behnke said. “They don’t want to be embarrassed. They don’t want to make commitments. They want to maintain their aloofness and autonomy.” A chemist by training with a doctoral degree in food science, Behnke became Pillsbury’s chief technical officer in 1979 and was instrumental in creating a long line of hit products, including microwaveable popcorn. He deeply admired Pillsbury but in recent years had grown troubled by pictures of obese children suffering from diabetes and the earliest signs of hypertension and heart disease. In the months leading up to the C.E.O. meeting, he was engaged in conversation with a group of food-science experts who were painting an increasingly grim picture of the public’s ability to cope with the industry’s formulations — from the body’s fragile controls on overeating to the hidden power of some processed foods to make people feel hungrier still. It was time, he and a handful of others felt, to warn the C.E.O.’s that their companies may have gone too far in creating and marketing products that posed the greatest health concerns. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17843 - Posted: 02.25.2013

By Erin Wayman BOSTON — The taste for alcohol may be an ancient craving. The ability to metabolize ethanol — the alcohol in beer, wine and spirits — might have originated in the common ancestor of chimpanzees, gorillas and humans roughly 10 million years ago, perhaps when this ancestor became more terrestrial and started eating fruits fermenting on the ground. Chemist Steven Benner of the Foundation for Applied Molecular Evolution in Gainesville, Fla., reached that conclusion by “resurrecting” the alcohol-metabolizing enzymes of extinct primates. Benner and his colleagues estimated the enzymes’ genetic code, built the enzymes in the lab and then analyzed how they work to understand how they changed over time. “It’s like a courtroom re-enactment,” said biochemist Romas Kazlauskas of the University of Minnesota in Minneapolis. Benner “can re-enact what happened in evolution.” Benner proposed the idea February 15 at the annual meeting of the American Association for the Advancement of Science. Today, humans rely on an enzyme called alcohol dehydrogenase 4, or ADH4, to break down ethanol. The enzyme is common throughout the esophagus, stomach and intestines, and is the first alcohol-metabolizing enzyme that comes into contact with what a person drinks. Among primates, not all ADH4s are the same — some can’t effectively metabolize ethanol. © Society for Science & the Public 2000 - 2013

Related chapters from BP7e: Chapter 4: The Chemistry 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: 17819 - Posted: 02.19.2013

By JANE E. BRODY The title of a recent report on smoking and health might well have paraphrased the popular ad campaign for Virginia Slims, introduced in 1968 by Philip Morris and aimed at young professional women: “You’ve come a long way, baby.” Today that slogan should include: “…toward a shorter life.” Ten years shorter, in fact. The new report is one of two rather shocking analyses of the hazards of smoking and the benefits of quitting published last month in The New England Journal of Medicine. The data show that “women who smoke like men die like men who smoke,” Dr. Steven A. Schroeder, a professor of health and health care at the University of California, San Francisco, wrote in an accompanying editorial. That was not always the case. Half a century ago, the risk of death from lung cancer among men who smoked was five times higher than that among women smokers. But by the first decade of this century, that risk had equalized: for both men and women who smoked, the risk of death from lung cancer was 25 times greater than for nonsmokers, Dr. Michael J. Thun of the American Cancer Society and his colleagues reported. Today, women who smoke are even more likely than men who smoke to die of lung cancer. According to a second study in the same journal, women smokers face a 17.8 times greater risk of dying of lung cancer than women who do not smoke; men who smoke are at 14.6 times greater risk to die of lung cancer than men who don’t. Women who smoke now face a risk of death from lung cancer that is 50 percent higher than the estimates reported in the 1980s, according to Dr. Prabhat Jha of the Center for Global Health Research in Toronto and his colleagues. After controlling for age, body weight, education level and alcohol use, the new analysis found something else: men and women who continue to smoke die on average 10 years sooner than those who never smoked. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: Hormones and Sex
Link ID: 17817 - Posted: 02.18.2013

By Melinda Wenner Moyer On the night of my 32nd birthday, my husband and I enjoyed a delicious dinner while on vacation in Orvieto, Italy. To complement my pasta, I drank a single glass of red wine, my first since learning I was pregnant four months earlier. Even now my indulgence that evening inspires periodic pangs of guilt: Did I stunt my son's potential by sipping that Sangiovese? Nobody questions the notion that heavy drinking during pregnancy is harmful. It can cause facial abnormalities, central nervous system problems and stunted growth. But evidence regarding the effects of light or occasional drinking is mixed. In five epidemiological studies published in 2012, medical psychologist Erik Mortensen of the University of Copenhagen and his colleagues found that five-year-old children born to women who had one to four drinks a week during pregnancy displayed no deficits in general intelligence, attention or other types of higher-order thinking. On the other hand, in 2011 psychiatrist Nancy Day of the University of Pittsburgh and her colleagues reported that teens born to women who averaged more than one drink a week during pregnancy were twice as likely as those born to nondrinkers to have conduct disorder, a condition characterized by theft, deceit or violence. The truth is hard to discern because research on the issue is fraught with problems. The ideal type of experiment is not ethical: scientists cannot randomly assign one group of women to drink during pregnancy and compare the outcome with those instructed to abstain. As a result, they must compare what happens to women who choose to drink during pregnancy with those who do not, and these women often differ in important ways. All things considered, having an occasional drink during those nine months—say, one or two a week—probably poses little, if any, harm. Still, some experts warn, light or sporadic drinking may have effects we do not know how to measure. © 2013 Scientific American

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 17801 - Posted: 02.14.2013