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By Brian Handwerk In the U.S., legal hurdles have long hampered research into marijuana. But as more states approve medical and even recreational marijuana, scientific inquiries have spiked, especially studies aimed at finding out what exactly is in today's weed—and what it does to our bodies. In Colorado, which made marijuana legal in November 2012, the latest results show that the pot lining store shelves is much more potent than the weed of 30 years ago. But the boost in power comes at a cost—modern marijuana mostly lacks the components touted as beneficial by medical marijuana advocates, and it is often contaminated with fungi, pesticides and heavy metals. “There's a stereotype, a hippy kind of mentality, that leads people to assume that growers are using natural cultivation methods and growing organically," says Andy LaFrate, founder of Charas Scientific, one of eight Colorado labs certified to test cannabis. "That's not necessarily the case at all." LaFrate presented his results this week at a meeting of the American Chemical Society (ACS) in Denver. LaFrate says he's been surprised at just how strong most of today's marijuana has become. His group has tested more than 600 strains of marijuana from dozens of producers. Potency tests, the only ones Colorado currently requires, looked at tetrahydrocannabinol (THC), the psychoactive compound that produces the plant's famous high. They found that modern weed contains THC levels of 18 to 30 percent—double to triple the levels that were common in buds from the 1980s. That's because growers have cross-bred plants over the years to create more powerful strains, which today tout colorful names like Bruce Banner, Skunkberry and Blue Cookies.

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: 20712 - Posted: 03.24.2015

By John Horgan In 1990 The New York Times published a front-page article by Lawrence Altman, a reporter with a medical degree, announcing that scientists had discovered “a link between alcoholism and a specific gene.” The evidence for the "feel-good gene," which supposedly reduces anxiety, is flimsy, just like the evidence linking specific genes to high intelligence, violent aggression, homosexuality, bipolar disorder and countless other complex human traits and ailments. That was merely one in a string of reports in which the Times and other major media hyped what turned out to be erroneous claims linking complex traits and disorders—from homosexuality and high intelligence to schizophrenia and bipolar disorder—to specific genes. I thought those days were over, and that scientists and the media have learned to doubt extremely reductionist genetic accounts of complex traits and behaviors. I was wrong. Last Sunday, the “Opinion” section of the Times published an essay, “The Feel-Good Gene,” which states: “For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide–the so-called bliss molecule and our natural marijuana–in our brains. In short, some people are prone to be less anxious simply because they won the genetic sweepstakes and randomly got a genetic mutation that has nothing at all to do with strength of character.” This article, like the one touting the alcoholism gene 25 years ago, was written by a physician, Richard Friedman, professor of psychiatry at Weill Cornell Medical College. I emphasize this fact because scientific hype is often blamed on supposedly ignorant journalists like me rather than on physicians and other so-called experts. © 2015 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: 20689 - Posted: 03.14.2015

By Maggie Fox Teenagers who use marijuana heavily grow up to have poor memories and also have brain abnormalities, a new study shows. The study cannot say which came first — the brain structure differences or the pot use. But it suggests there could be long-term effects of heavy marijuana use. A team at Northwestern University looked at 97 volunteers with and without mental illness. The dope smokers said they'd used marijuana daily starting at age 16 or 17, and said they had not used other drugs. The daily marijuana users had an abnormally shaped hippocampus and performed about 18 percent more poorly on long-term memory tasks, the researchers reported in the journal Hippocampus. The hippocampus is a part of the brain used in storing long-term memory. "The memory processes that appear to be affected by cannabis are ones that we use every day to solve common problems and to sustain our relationships with friends and family," said Dr. John Csernansky, who worked on the study. Previous research by the same Northwestern team showed heavy pot smokers had poor short-term and working memory and abnormally shaped brain structures including the striatum, globus pallidus and thalamus. "It is possible that the abnormal brain structures reveal a pre-existing vulnerability to marijuana abuse," Matthew Smith, who led the study, said in a statement.

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: 20687 - Posted: 03.14.2015

|By Anne Skomorowsky On a Saturday night last month, 12 students at Wesleyan University in Connecticut were poisoned by “Molly,” a hallucinogenic drug they had taken to enhance a campus party. Ambulances and helicopters transported the stricken to nearby hospitals, some in critical condition. Molly—the street name for the amphetamine MDMA—can cause extremely high fevers, liver failure, muscle breakdown, and cardiac arrest. Given the risks associated with Molly, why would anybody take it? The obvious answer—to get high—is only partly true. Like many drugs of abuse, Molly causes euphoria. But Molly is remarkable for its “prosocial” effects. Molly makes users feel friendly, loving, and strongly connected to one another. Molly is most commonly used in settings where communion with others is highly valued, such as raves, music festivals, and college parties. Recently, psychiatrists have taken an interest in its potential to enhance psychotherapy; this has led to new research into the mechanisms by which MDMA makes people feel closer. It appears that MDMA works by shifting the user’s attention towards positive experiences while minimizing the impact of negative feelings. To investigate this, a 2012 study by Cedric Hysek and colleagues used the Reading the Mind in the Eyes Test (RMET), which was developed to evaluate people with autism. In the RMET, participants are shown 36 pictures of the eye region of faces. Their task is to describe what the person in the picture is feeling. Volunteers taking MDMA, under carefully controlled conditions, improved in their recognition of positive emotions; but their performance in recognizing negative emotions declined. In other words, they incorrectly attributed positive or neutral feelings to images that were actually negative in emotional tone. They mistook negative and threat-related images for friendly ones. © 2015 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: 20678 - Posted: 03.12.2015

By RICHARD A. FRIEDMAN CHANCES are that everyone on this planet has experienced anxiety, that distinct sense of unease and foreboding. Most of us probably assume that anxiety always has a psychological trigger. Yet clinicians have long known that there are plenty of people who experience anxiety in the absence of any danger or stress and haven’t a clue why they feel distressed. Despite years of psychotherapy, many experience little or no relief. It’s as if they suffer from a mental state that has no psychological origin or meaning, a notion that would seem heretical to many therapists, particularly psychoanalysts. Recent neuroscience research explains why, in part, this may be the case. For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide — the so-called bliss molecule and our own natural marijuana — in our brains. In short, some people are prone to be less anxious simply because they won the genetic sweepstakes and randomly got a genetic mutation that has nothing at all to do with strength of character. About 20 percent of adult Americans have this mutation. Those who do may also be less likely to become addicted to marijuana and, possibly, other drugs — presumably because they don’t need the calming effects that marijuana provides. One patient of mine, a man in his late 40s, came to see me because he was depressed and lethargic. He told me at our first meeting that he had been using cannabis almost daily for at least the past 15 years. “It became a way of life,” he explained. “Things are more interesting, and I can tolerate disappointments without getting too upset.” © 2015 The New York Times Company

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 4: The Chemistry 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: 20666 - Posted: 03.09.2015

Zoe Cormier Data from population surveys in the United States challenge public fears that psychedelic drugs such as LSD can lead to psychosis and other mental-health conditions and to increased risk of suicide, two studies have found1, 2. In the first study, clinical psychologists Pål-Ørjan Johansen and Teri Suzanne Krebs, both at the Norwegian University of Science and Technology in Trondheim, scoured data from the US National Survey on Drug Use and Health (NSDUH), an annual random sample of the general population, and analysed answers from more than 135,000 people who took part in surveys from 2008 to 2011. Of those, 14% described themselves as having used at any point in their lives any of the three ‘classic’ psychedelics: LSD, psilocybin (the active ingredient in so-called magic mushrooms) and mescaline (found in the peyote and San Pedro cacti). The researchers found that individuals in this group were not at increased risk of developing 11 indicators of mental-health problems such as schizophrenia, psychosis, depression, anxiety disorders and suicide attempts. Their paper appears in the March issue of the Journal of Psychopharmacology1. The findings are likely to raise eyebrows. Fears that psychedelics can lead to psychosis date to the 1960s, with widespread reports of “acid casualties” in the mainstream news. But Krebs says that because psychotic disorders are relatively prevalent, affecting about one in 50 people, correlations can often be mistaken for causations. “Psychedelics are psychologically intense, and many people will blame anything that happens for the rest of their lives on a psychedelic experience.” © 2015 Nature Publishing Group,

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20655 - Posted: 03.05.2015

by Michael Slezak If you want to counteract the effects of getting drunk, a big dose of the so-called "cuddle-chemical" oxytocin might be the answer. Oxytocin has important roles in sexual behaviour and social bonding, and has previously been investigated as a way to help wean alcoholics off drink. While studying this effect in rats, Michael Bowen from the University of Sydney noticed something strange. Rats that had been given oxytocin didn't seem to get drunk. "Those that had the oxytocin were up and moving about as if they hadn't had any alcohol at all, whereas the ones that didn't have oxytocin were quite heavily sedated," Bowen says. This effect was confirmed in a second experiment, in which half the rats were given an injection of oxytocin straight into the brain, at a level about 150,000 times what would normally be found there. They were then given alcohol, after which researchers tested their motor control and reaction times. Oxytocin seemed to completely counteract the effects of the booze – even when a rat had consumed what would be equivalent to about one and a half bottles of wine in humans. "The rats that had received oxytocin, as well as the alcohol, were virtually indistinguishable from the rats that hadn't received any alcohol at all," says Bowen. This could be thanks to the brain's GABA receptors, where alcohol is thought to exert its intoxicating effects. Bowen's team found that oxytocin was binding to two parts of these receptors, blocking alcohol from getting there. "It was actually preventing alcohol affecting these sites in the brain that make you intoxicated." © Copyright Reed Business Information Ltd

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: Hormones and Sex
Link ID: 20604 - Posted: 02.24.2015

Charles F. Zorumski It is indeed possible for a person to get intoxicated and not remember what she or he did. This state is called a “blackout” or, more precisely, a “memory blackout.” During a blackout a person is intoxicated but awake and interacting with the environment in seemingly meaningful ways, such as holding a conversation or driving a car. After the period of intoxication, usually the next day, the person has no or, at best, vague recall for events that occurred while inebriated. At times, being in this state can have disastrous consequences, such as waking up in an unknown or unsafe place, losing personal possessions or participating in risky behaviors. On the neural level, a blackout is a period of anterograde amnesia. That is, a person's ability to form new memories becomes impaired. Although a person does not lose previously learned information, he or she may also find it more difficult to recall certain facts while intoxicated. Yet once a person sobers up, his or her memory and ability to learn new information are not permanently affected. How alcohol, or ethanol, produces a memory blackout is not completely understood. It is clear, however, that alcohol can impair a process in brain cells called long-term potentiation (LTP), a cellular mechanism thought to underlie memory formation, particularly in the hippocampus. © 2015 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: 20603 - Posted: 02.24.2015

A dozen university students have been treated at Connecticut hospitals after overdosing on "Molly" or MDMA, a popular synthetic party drug. Police are investigating after the overdoses were reported late Sunday on the campus of Wesleyan University in Middletown, Connecticut. By Monday, eight remained in hospital and two were in critical condition. It was unclear whether the students had been together or where the drugs had come from. Middletown Police Chief William McKenna said that their "first and foremost goal is to obtain information on the batch of Molly that was distributed to the students on the campus," adding, "this information is critical in ensuring the recovery of those students affected." A pure and more powerful form of MDMA often sold as "Molly" can cause liver, kidney, cardiovascular failure, or death. In a campus-wide statement, Wesleyan president Michael S Roth urged students to "please, please stay away from illegal substances, the use of which can put you in extreme danger. One mistake can change your life forever". Dean Michael Whaley, vice president of student affairs at Wesleyan University, sent a letter to the school body on Sunday recommending students to check on their friends. Ten of the 12 people were Wesleyan students. In 2013, Molly-related deaths and illnesses forced the Electric Zoo Festival in New York to shut down early after two young people died and four were confined to hospital.

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: 20602 - Posted: 02.24.2015

|By Roni Jacobson Several pharmaceutical drugs promise to help addicts quit, and many people embrace the ease of popping a pill. Yet research continues to show that although medication can help, support networks and therapy targeting the underlying behaviors are still the best available ways to kick addiction over the long term. In addition, some of these medications come with scary side effects—hundreds of people have reportedly committed suicide while on the smoking-cessation drug Chantix, for example. Read on for short profiles of the addiction drugs currently on the market, as well as a few compounds that may hit shelves soon. © 2015 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: 20601 - Posted: 02.24.2015

Boer Deng Smoking marijuana may stoke a yearning for crisps, but understanding how it affects hunger is relevant not just to those who indulge in it. The drug has yielded a ripe target for scientists who seek to stimulate or suppress appetite: the receptor CB1, found in cells throughout the body. When activated by the anti-nausea drug dronabinol — which is also a component of marijuana (Cannabis sativa) — CB1 prompts the release of hunger-promoting hormones1. And suppressing its activity is thought to aid in weight loss2. But the mechanism by which the receptor kills or kindles appetite is not entirely understood. Now neuroscientist Tamas Horvath, of Yale University in New Haven, and colleagues report in Nature that nerve cells called pro-opiomelanocortin (POMC) neurons play a key role in this process3. POMC had generally been thought to promote satiation, but Horvath's team found that POMC neurons in the brain release not just a hunger-suppressing hormone, but also one that promotes appetite. Which hormone is secreted is regulated by a protein in the cells' mitochondria, structures that regulate energy levels. When the CB1 receptor is activated, this mitochondrial protein induces POMC to switch from secreting the substance that suppresses gorging to one that encourages it. The finding is intriguing, says Uberto Pagotto, a neuroscientist at the University of Bologna who has studied cannabinoids for many years. “It gives us a different starting point to look at CB1 receptors and the mitochondria,” he says. © 2015 Nature Publishing Group

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: 20592 - Posted: 02.18.2015

By Abigail Zuger, M.D. I had intended to discuss President Obama’s plans for personalized precision medicine with my patient Barbara last week, but she missed her appointment. Or, more accurately, she arrived two hours late, made the usual giant fuss at the reception desk and had to be rescheduled. I was disappointed. Barbara has some insight into the vortex of her own complications, and I thought she might help organize my thoughts. Mr. Obama announced last month that his new budget included $215 million toward the creation of a national databank of medical information, intended to associate specific gene patterns with various diseases and to predict what genetic, lifestyle and environmental factors correlate with successful treatment. Once all those relationships are clarified, the path will open to drugs or other interventions that firm up the good links and interrupt the bad ones. This step up the scientific ladder of medicine has many advocates. Researchers who sequence the genome are enthusiastic, as are those with a financial interest in the technology. Also celebrating are doctors and patients in the cancer community, where genetic data already informs some treatment choices and where the initial thrust of the initiative and much of its funding will be directed. Skeptics point out that genetic medicine, for all its promise, has delivered relatively few clinical benefits. And straightforward analyses of lifestyle and environment effects on health may occasionally lead to clear-cut advice (don’t smoke), but more often sow confusion, as anyone curious about the best way to lose weight or the optimal quantity of dietary salt knows. Without Barbara’s presence, I was left to ponder her medical record, a 20-year saga that might be titled “Genes, Lifestyle and Environment.” and published as a cautionary tale. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 20590 - Posted: 02.18.2015

By Lizzie Wade SAN JOSE, CALIFORNIA—Humans have been using cannabis for more than 5000 years. So why don’t scientists know more about it? Three experts gathered here at the annual meeting of AAAS (which publishes Science) to discuss what scientists and doctors know about the drug and what they still need to learn. “By the end of this session, you’ll know more about cannabis than your physician does,” said Mark Ware, a family physician at the McGill University Health Center in Montreal, Canada, who organized the talk. How does marijuana work? Our brains are primed to respond to marijuana, because “there are chemicals in our own bodies that act like THC [the psychoactive ingredient in pot]” and other compounds in cannabis called cannabinoids, explained Roger Pertwee, a neuropharmacologist at the University of Aberdeen in the United Kingdom who has studied cannabinoids since the 1960s. Cannabinoids produced by our bodies or ingested through marijuana use react with a series of receptors in our brains called the endocannabinoid system, which is involved in appetite, mood, memory, and pain sensation. Scientists have discovered 104 cannabinoids so far, but “the pharmacology of most of them has yet to be investigated,” Pertwee said. What are the known medical uses of marijuana? Marijuana has been used for decades to stimulate appetite and treat nausea and vomiting, especially in patients undergoing chemotherapy. Its success in easing the symptoms of multiple sclerosis patients led to the development of Sativex, a drug manufactured by GW Pharmaceuticals that includes THC and cannabidiol (CBD), a cannabinoid that isn’t psychoactive. © 2015 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 20582 - Posted: 02.16.2015

Smoking potent cannabis was linked to 24% of new psychosis cases analysed in a study by King's College London. The research suggests the risk of psychosis is three times higher for users of potent "skunk-like" cannabis than for non-users. The study of 780 people was carried out by KCL's Institute of Psychiatry, Psychology and Neuroscience. A Home Office spokesman said the report underlines the reasons why cannabis is illegal. Scientists found the risk of psychosis was five times higher for those who use it every day compared with non-users. They also concluded the use of hash, a milder form of the drug, was not associated with increased risk of psychosis. Psychosis refers to delusions or hallucinations that can be present in certain psychiatric conditions such as schizophrenia and bipolar disorder. "Compared with those who had never tried cannabis, users of high potency skunk-like cannabis had a threefold increase in risk of psychosis,' said Dr Marta Di Forti, lead author on the research. She added: "The results show that psychosis risk in cannabis users depends on both the frequency of use and cannabis potency." Dr Di Forti told BBC Radio 4's Today programme that the availability of skunk-like cannabis was becoming more widespread. "In London, it's very difficult to find anything else," she said. "There were lots of reports from police across the UK saying we have become a great producer of skunk. And not only do we use it locally but we export, so this is a Made in England product." Someone suffering from psychosis would often be "extremely paranoid and become very suspicious" about the people around them, she added. She has called for "a clear public message" to cannabis users, comparable to medical advice on alcohol and tobacco. © 2015 BBC

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20581 - Posted: 02.16.2015

By DENISE GRADY However bad you thought smoking was, it’s even worse. A new study adds at least five diseases and 60,000 deaths a year to the toll taken by tobacco in the United States. Before the study, smoking was already blamed for nearly half a million deaths a year in this country from 21 diseases, including 12 types of cancer. The new findings are based on health data from nearly a million people who were followed for 10 years. In addition to the well-known hazards of lung cancer, artery disease, heart attacks, chronic lung disease and stroke, the researchers found that smoking was linked to significantly increased risks of infection, kidney disease, intestinal disease caused by inadequate blood flow, and heart and lung ailments not previously attributed to tobacco. Even though people are already barraged with messages about the dangers of smoking, researchers say it is important to let the public know that there is yet more bad news. “The smoking epidemic is still ongoing, and there is a need to evaluate how smoking is hurting us as a society, to support clinicians and policy making in public health,” said Brian D. Carter, an epidemiologist at the American Cancer Society and the first author of an article about the study, which appears in The New England Journal of Medicine. “It’s not a done story.” In an editorial accompanying the article, Dr. Graham A. Colditz, from Washington University School of Medicine in St. Louis, said the new findings showed that officials in the United States had substantially underestimated the effect smoking has on public health. He said smokers, particularly those who depend on Medicaid, had not been receiving enough help to quit. © 2015 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: 20569 - Posted: 02.13.2015

By Michelle Roberts Health editor, BBC News online Women trying for a baby and those in the first three months of pregnancy should not drink any alcohol, updated UK guidelines say. The Royal College of Obstetricians and Gynaecologists (RCOG) had previously said a couple of glasses of wine a week was acceptable. It now says abstinence is the only way to be certain that the baby is not harmed. There is no proven safe amount that women can drink during pregnancy. The updated advice now chimes with guidelines from the National Institute for Health and Care Excellence (NICE). In the US, experts say there is no safe time to drink during pregnancy. But the RCOG highlights around the time of conception and the first three months of pregnancy as the most risky. Drinking alcohol may affect the unborn baby as some will pass through the placenta. Around conception and during the first three months, it may increase the chance of miscarriage, says the RCOG. After this time, women are advised to not drink more than one to two units, more than once or twice a week, it says. Drinking more than this could affect the development of the baby, in particular the way the baby's brain develops and the way the baby grows in the womb, which can lead to foetal growth restriction and increase the risk of stillbirth and premature labour, says the advice. © 2015 BBC

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20568 - Posted: 02.13.2015

Research suggests that only 20–30% of drug users actually descend into addiction — defined as the persistent seeking and taking of drugs even in the face of dire personal consequences. Why are some people who use drugs able to do so without turning into addicts, while others continue to abuse, even when the repercussions range from jail time to serious health problems? In a comprehensive review in the European Journal of Neuroscience, Barry Everitt outlines the neural correlates and learning-based processes associated with the transition from drug use, to abuse, to addiction. Drug seeking begins as a goal-directed behavior, with an action (finding and taking drugs) leading to a particular outcome (the drug high). This type of associative learning is mediated by the dorsomedial region of the striatum, the area of the brain that is associated with reward processing, which functions primarily through the neurotransmitter dopamine. In this kind of learning, devaluing the outcome (by decreasing the potency of the drug, for example) tends to decrease the pursuit of the action. When the high is not what it used to be, the motivation to continue seeking it out decreases. However, in long-term abusers, this devalued outcome does not reduce the action — indeed, researchers have found that in cases of chronic drug use, a parallel associative learning process eventually comes to the fore. This process is one of stimulus–response; the conditioned stimuli in this case are the various environmental cues — the sight of the powdery white stuff, the smell of burning aluminum foil — that users associate with getting high and that compel them to seek out drugs. © Association for Psychological Science

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: 20506 - Posted: 01.22.2015

It is now one hundred years since drugs were first banned - and all through this long century of waging war on drugs, we have been told a story about addiction, by our teachers, and by our governments. This story is so deeply ingrained in our minds that we take it for granted. It seems obvious. It seems manifestly true. Until I set off three and a half years ago on a 30,000-mile journey for my book 'Chasing The Scream - The First And Last Days of the War on Drugs' to figure out what is really driving the drug war, I believed it too. But what I learned on the road is that almost everything we have been told about addiction is wrong - and there is a very different story waiting for us, if only we are ready to hear it. If we truly absorb this new story, we will have to change a lot more than the drug war. We will have to change ourselves. I learned it from an extraordinary mixture of people I met on my travels. From the surviving friends of Billie Holiday, who helped me to learn how the founder of the war on drugs stalked and helped to kill her. From a Jewish doctor who was smuggled out of the Budapest ghetto as a baby, only to unlock the secrets of addiction as a grown man. From a transsexual crack dealer in Brooklyn who was conceived when his mother, a crack-addict, was raped by his father, an NYPD officer. From a man who was kept at the bottom of a well for two years by a torturing dictatorship, only to emerge to be elected President of Uruguay and to begin the last days of the war on drugs. ©2015 TheHuffingtonPost.com, Inc.

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: 20505 - Posted: 01.22.2015

By Consumer Reports The headlines about coffee’s impact on your health seem to change as quickly as the time it takes to drink a cup. Should you savor every drop or try to cut down? Here’s what we know right now: It may lengthen your life. True, coffee drinkers are more likely than nondrinkers to smoke, eat red meat, skimp on exercise and have other life-shortening habits, according to a large 2012 study published in the New England Journal of Medicine. But even after adjusting for such factors, they found that people age 50 to 71 who drank at least one cup of coffee per day had a lower risk than nondrinkers of dying from diabetes, heart disease or other health problems when followed for more than a decade. That may be due to beneficial compounds in coffee such as antioxidants — which might ward off disease — and not caffeine. Decaf drinkers had the same results. It may make you happier. Coffee is not just a pick-me-up; it also has been linked to a lower risk of depression. In a study led by the Harvard School of Public Health that tracked 50,000 women for 10 years, those who drank four or more cups of caffeinated coffee per day were 20 percent less likely to develop depression than nondrinkers. Another study found that adults who drank two to four cups of caffeinated coffee were about half as likely to attempt suicide as decaf drinkers or abstainers. The researchers speculated that long-term coffee drinking may boost the production of “feel good” hormones such as dopamine. It contains many good-for-you chemicals.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20494 - Posted: 01.20.2015

By Susan Svrluga Edwin Chapman’s secretary handed him a pile of prescription slips, and the doctor’s pen moved quickly across them: “Buprenorphine/naloxone.” “Buprenorphine/naloxone.” “Buprenorphine/naloxone.” His waiting room was full of heroin-addicted patients there to refill their generic prescriptions for Suboxone, a drug that helps keep their relentless cravings at bay and now outpaces methadone as a treatment. Chapman is an internist, a cardiologist. This drug has transformed his D.C. medical practice — now more than half of his patients are there to seek it, addicts edging out elderly ladies with arthritis and diabetes. And the drug, he believes, has transformed lives. He wishes more people could get it. Yet even as heroin use surges in the United States, destroying neighborhoods and families — drug overdoses kill more people than any other kind of accident — both addicts and doctors say there are barriers that keep some from the treatment they desperately need. “In the past we’ve kind of run away from these patients, put them in methadone clinics, places no one can see them,” said Chapman, who estimates that two-thirds of his heroin-addicted patients tested positive for hepatitis C and more than one in 10 for HIV. “We need to reverse that. Put them in primary care. We need to be taking care of sick folks, not running away from them.

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: 20480 - Posted: 01.14.2015