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Laura Sanders Kratom, an herbal supplement available at vape shops and online stores, has been linked to 91 deaths over 18 months from July 2016 to December 2017, according to a report by the U.S. Centers for Disease Control and Prevention. Those deaths made up less than 1 percent of the 27,338 overdose fatalities analyzed for the report, released online on April 12. Although small, the numbers point to increasing numbers of people using the plant to combat pain, depression and even opioid addiction. Interest in, and exposure to, kratom is apparently rising. “We’d see about 10 cases a year, and now we’re seeing hundreds,” says toxicologist Henry Spiller of the Central Ohio Poison Center in Columbus. Here, scientists weigh in on what’s known and unknown about the herbal supplement. What is kratom, and why are people using it? The supplement is mashed leaves from the tropical tree Mitragyna speciosa, a coffee cousin that grows in the warm, wet forests of Southeast Asia. Pulverized leaves create a green powder that can be dissolved in tea, packed into pill capsules or extracted into alcohol. Traditionally, workers chew the leaves in search of a mild stimulant effect during the day, and then drink tea to relieve pain, says pharmacologist and toxicologist Oliver Grundmann of the University of Florida in Gainesville. |© Society for Science & the Public 2000 - 2019

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26157 - Posted: 04.20.2019

By Richard A. Oppel Jr. and Serge F. Kovaleski The steep rise in the number of people suffering opioid addiction has helped spawn the widespread use of another substance: kratom, a green powdered herbal supplement that is widely available and virtually unregulated. Derived from the leaves of a tree native to Southeast Asia and sold in the United States online and in bodegas and head shops, kratom has long been used as a mood booster, energy supplement and pain reliever. It is also increasingly being used by those who swear by it as a curb for opioid addiction. Some veterans also say it helps control symptoms of post-traumatic stress. Several million Americans are now believed to use kratom. One is Andrew Turner, whose PTSD, herniated discs and movement problems affecting his face and neck were so severe after multiple deployments with the Navy that he took as many as 20 prescription medications, including opioids, daily. “I was on the path to suicide, and losing hope,” Mr. Turner said. After he began drinking kratom tea, the pain and dread diminished, he said. “It was a night-and-day difference.” But the authorities warn that kratom can be dangerous. Reported side effects include seizures, hallucinations and symptoms of psychosis, and there have been calls from inside the Trump administration to curb its use. A new government review links kratom to nearly 100 overdose deaths. “There is no evidence to indicate that kratom is safe or effective for any medical use,” Scott Gottlieb, until recently the commissioner of the Food and Drug Administration, said last year. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26154 - Posted: 04.19.2019

By Denise Gellene Paul Greengard, an American neuroscientist whose 15-year quest to understand how brain cells communicate provided new insights into psychological diseases and earned him a Nobel Prize, and who used his entire $400,000 award to create an academic prize in memory of the mother he never knew, died on Saturday in Manhattan. He was 93. His death was confirmed by Rockefeller University, where he had worked since 1983. Dr. Greengard received the 2000 Nobel Prize in Physiology or Medicine with Dr. Arvid Carlsson of Sweden and Dr. Eric R. Kandel of the United States for independent discoveries related to the ways brain cells relay messages about movement, memory and mental states. Their discoveries offered new insights into disorders linked to errors in cell communication, such as Parkinson’s disease, schizophrenia, bipolar disorder and drug addiction. Dr. Greengard’s research described how cells react to dopamine, an important chemical messenger in the brain. His work provided the underlying science for many antipsychotic drugs, which modulate the strength of chemical signals in the brain. “Our work shows the details of how dopamine produces these effects — in other words, what’s wrong in these diseases and what can be done to correct them,” Dr. Greengard said. Dr. Greengard’s research extended from the late 1960s to the mid-1980s. For much of the period, his work was ignored. A majority of biologists believed brain cells communicated through the use of electrical signals. To them, the only thing that mattered was whether a cell fired off a signal. © 2019 The New York Times Company

Related chapters from BN8e: 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: 26139 - Posted: 04.15.2019

/ By Troy Farah Despite the ubiquity of labels and advertisements reminding those who drink to “enjoy responsibly,” millions of Americans fail to heed the warning. According to the U.S. Centers for Disease Control and Prevention, one in six adults binge drinks about four times a month. Defined as the consumption of four or more drinks within two hours for women, and five or more drinks in that timespan for men, binge drinking is associated with an array of health problems, including alcohol dependence, memory issues, and unintentional injuries. The problem is global. Alcohol is directly or indirectly responsible for more than 5 percent of all deaths worldwide — or around 3 million annually, according to the World Health Organization. At least seven cancers are linked to its use, and it is considered a causal factor in more than 200 diseases. Heavy drinking, recent research suggests, can even alter DNA, triggering more cravings. For decades, efforts to curb binge drinking and other forms of alcohol misuse have largely focused on reductions in alcohol purchases, and more vigorous enforcement of laws against underage drinking and drunk driving. But as the problem continues to rise, a growing number of scientists — many of them taking a careful, regulated approach, and some not so much — are turning their attention toward developing chemical solutions. “Replacing alcohol is going to be a very challenging thing to do,” said David Nutt, a neuropsychopharmacologist at Imperial College London. “The person that does it first is going to become very successful.” Yet Nutt is attempting to do just that. Copyright 2019 Undark

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26113 - Posted: 04.04.2019

By Jeffrey Mervis A fledgling, small-scale approach to dealing with the state’s opioid crisis paid off big last week for Oklahoma State University (OSU) when it became the surprise beneficiary of a $270 million legal settlement with Purdue Pharma. It’s the first agreement in some 1700 pending cases around the United States against Purdue, which makes the painkiller OxyContin, and other manufacturers of prescription opioids. On 26 March, the state of Oklahoma agreed to drop its suit alleging deceptive marketing practices by Purdue in exchange for a National Center for Addiction Studies and Treatment at OSU’s medical complex in Tulsa. Purdue and the Sackler family, which owns the Stamford, Connecticut–based company, will provide a $177 million endowment for the national center, along with $20 million over 5 years for naloxone and other drugs to treat opioid addiction. The state is continuing its suit against several other companies, with opening arguments set for 28 May. The windfall for the new entity, which aspires “to become the premier addiction research center in the nation,” rewards OSU’s ambition. In October 2017, it opened a modest Center for Wellness and Recovery within its medical school to train future addiction medicine physicians, study the underlying causes of addiction and pain, provide treatment to those suffering from opioid use disorder, and educate the public about the burgeoning epidemic, which claims 130 lives a day in the United States and in 2017 killed nearly 800 Oklahomans. The center now has a staff of eight and a $2.4 million budget. © 2019 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26108 - Posted: 04.03.2019

Maria Temming Synthetic opioids outlast current antidotes. A nanoparticle-based alternative could fix that. A newly developed single-dose opioid antidote lasts several days, a study in mice shows. If the results can be duplicated in humans, the treatment may one day help prevent overdoses from deadly drugs like fentanyl. Normally, a dose of the opioid antidote naloxone passes through a person’s body in about 30 minutes — far too quickly to fully counteract the effects of such synthetic opioids as fentanyl and carfentanil (SN Online: 5/1/18). These drugs, tens to thousands of times stronger than morphine, can linger in a person’s system for hours or even days (SN: 6/10/17, p. 22). That requires multiple doses of an antidote to prevent someone from overdosing. So researchers developed a new naloxone-based antidote to outlast synthetic opioids by creating nanoparticles in which naloxone molecules are tangled up with a biodegradable polymer called polylactic acid. Water and enzymes in the body slowly break down these nanosized tangles, gradually releasing naloxone. In mice, the new nanoparticle delivery system counteracted the pain-relieving effects of morphine for up to 96 hours after administering a single dose of the antidote, according to research being presented March 31 at the American Chemical Society meeting in Orlando, Fla. |© Society for Science & the Public 2000 - 2019

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26097 - Posted: 04.01.2019

Laura Sanders A few months back, a new storefront appeared in my small Oregon town. Its shelves were packed with tinctures, jars of salve, coffee beans, bath bombs — even beard oil. This motley collection shared a single star ingredient: CBD. Produced by the cannabis plant, CBD is the straitlaced cousin of marijuana’s more famous component — the THC that delivers a mind-swirling high. CBD, or cannabidiol, has no such intoxicating effects on the mind. Yet the molecule has captured people’s attention in a profound way, sold as a remedy for pain, anxiety, insomnia and other ailments — all without the high. That neighborhood shop, CBD Scientific, is far from alone in its efforts to sell people on the benefits of CBD, which is found in both marijuana and hemp, two versions of the Cannabis sativa plant. CBD is popping up in products in pet stores, coffee shops and the health and beauty sections of mainstream grocery stores. It’s even being brewed into beer. I left the shop with a $5 bottle of water infused with “5,000,000 nanograms” of CBD. So far, messages of CBD’s purported health benefits come from people trying to sell CBD products — not from scientists, says Margaret Haney, a neurobiologist who directs the Marijuana Research Laboratory at Columbia University. A gaping chasm separates the surging CBD market and the scientific evidence backing it. While there are reasons to be excited about CBD, the science just isn’t there yet, Haney says. |© Society for Science & the Public 2000 - 2019

Related chapters from BN8e: 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: The Biology of Behavioral Disorders
Link ID: 26084 - Posted: 03.27.2019

By Roni Caryn Rabin Pot brownies and other cannabis “edibles” like gummy bears that are sold online and where marijuana is legal may seem like harmless fun, but new research indicates that edibles may be more potent and potentially more dangerous than pot that is smoked or vaped. The new study analyzed thousands of cannabis-triggered emergency room visits in the greater Denver area, and found that edibles induced a disproportionate number of pot-related medical crises. Edibles were also more likely than inhaled pot to cause severe intoxication, acute psychiatric symptoms in people with no history of psychiatric illness and cardiovascular problems. Pot smokers, on the other hand, were more likely to have gastrointestinal complaints, including a vomiting condition called cannabinoid hyperemesis syndrome, and they were more likely to be hospitalized if they needed emergency care. Emergency room doctors in Colorado started noticing several years ago that “there were a lot of visits associated with edibles, even though they were not the predominant product used, and they seemed to be sicker compared to those who inhaled,” said Dr. Andrew Monte, an associate professor of medicine and the lead author of the new study, published in Annals of Internal Medicine on Monday. He also noted that the only deaths in Colorado that have been definitively attributed to cannabis involved edibles, and those deaths were surprisingly violent. In all three incidents, including a murder and a suicide in 2014 and another suicide in 2015, the pot users exhibited extremely erratic behavior after consuming edibles, according to news reports and trial testimony. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26079 - Posted: 03.26.2019

Amy Fleming ‘This is what my brain looks like,” says David Nutt, showing me an intense abstract painting by a friend of his that is sitting on the windowsill in his office. Nutt’s base at Hammersmith hospital has a cosy, lived-in feel – a stark contrast to the gleaming white laboratory he oversees as director of the neuropsychopharmacology unit at Imperial College London. Lab coats hang on a hook by the door, an ancient kettle sits in the corner and next to the painting is an unruly collection of objects that offer clues to his research interests: brain-shaped awards, an atomic model of Nutt’s invention for detecting inflammation in the brain of Alzheimer’s and Parkinson’s patients, a poster for the 1967 film LSD Flesh of Devil and two carved wooden mushrooms – the final items hinting at his role at Imperial’s psychedelic research group. All that is missing is something to do with the demon drink, to reflect Nutt’s ambitious plan to bring a safe synthetic alcohol substitute called Alcarelle to the masses. Nutt has long been developing a holy grail of molecules – also referred to as “alcosynth” – that will provide the relaxing and socially lubricating qualities of alcohol, but without the hangovers, health issues and the risk of getting paralytic. It sounds too good to be true, and when I discuss the notion with two alcohol industry experts, they independently draw parallels with plans to colonise Mars. Yet Alcarelle finding its way into bars and shops is starting to look like a possibility. Seed funding was raised in November 2018, allowing Nutt and his business partner, David Orren, to attempt to raise £20m from investors to bring Alcarelle to market. “The industry knows alcohol is a toxic substance,” says Nutt. “If it were discovered today, it would be illegal as a foodstuff. The safe limit of alcohol, if you apply food standards criteria, would be one glass of wine a year.” © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26078 - Posted: 03.26.2019

By Michelle Roberts Health editor, BBC News online Smoking potent 'skunk-like' cannabis increases your risk of serious mental illness, say researchers. They estimate around one in 10 new cases of psychosis may be associated with strong cannabis, based on their study of European cities and towns. In London and Amsterdam, where most of the cannabis that is sold is very strong, the risk could be much more, they say in The Lancet Psychiatry. Daily use of any cannabis also makes psychosis more likely, they found. Experts say people should be aware of the potential risks to health, even though the study is not definitive proof of harm. Lead researcher and psychiatrist Dr Marta Di Forti said: "If you decide to use high potency cannabis bear in mind there is this potential risk." Dr Adrian James from the Royal College of Psychiatrists said: "This is a good quality study and the results need to be taken seriously." People experiencing psychosis lose touch with reality, and may hear voices, see things that are not actually there or have delusional, confused thoughts. It is a recognised medical condition and different to getting high on a drug. There is disagreement as to what extent cannabis might cause or worsen mental health problems and many countries have gone ahead and legalised or decriminalised cannabis use. Doctors are concerned about the growing use of high potency cannabis that contains lots of the ingredient THC - the one that gives the high. Skunk-like cannabis with a THC content of 14% now makes up 94% of the drug sold on the streets of London, according to experts. © 2019 BBC

Related chapters from BN8e: 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: The Biology of Behavioral Disorders
Link ID: 26053 - Posted: 03.20.2019

By Jonathan N. Stea Cannabis is deeply misunderstood. It has been hailed as a potential hero in the fight against all ailments, including cancer and the opioid epidemic. It has also been called the devil’s lettuce, with claims that its use will lead to laziness, madness and even murder. In part, this polarization in beliefs can be explained by the complexity of cannabis. It is not helpful or accurate to think about cannabis as a single substance, but rather as a mixture of over 500 chemicals with varying combinations of dosages. Given that cannabis is essentially a chemical soup that until recently had mostly been prepared in the black marketplace, it has been difficult to draw conclusions from research about its effects. This is particularly true in the area of addiction and mental health, where many factors contribute to the muddy the picture of whether cannabis can be helpful or harmful. In recent years, it has been suggested that cannabis could be the white knight of the opioid epidemic. Indeed, recent state regulations in the United States (e.g., Illinois, New York) have explicitly approved medical cannabis as a treatment for opioid addiction. Critics of these policy decisions have argued that there is not yet enough evidence to support and promote cannabis as an effective treatment. They are correct. There have been no randomized controlled trials evaluating cannabis specifically for the treatment of opioid addiction. © 2019 Scientific American

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26043 - Posted: 03.16.2019

By Sheila Kaplan and Matt Richtel Dr. Scott Gottlieb became commissioner of the Food and Drug Administration in 2017 with an ambitious plan to reduce cigarette smoking, a habit that kills nearly half a million Americans each year, by shifting smokers to less harmful alternatives like e-cigarettes. But he was quickly embroiled in an unexpected crisis: the explosion of vaping among millions of middle and high school students, many of whom were getting addicted to nicotine. Dr. Gottlieb will depart at the end of this month, following his sudden announcement last week that he would resign, with his plans to toughen regulation of both vaping and smoking unfinished and powerful lobbying forces quietly celebrating the exit of a politically canny administrator who aggressively wielded his regulatory powers. Opponents are already swooping in, making their case to Congress and reaching out to the White House. A coalition of conservative organizations that oppose government intervention in the marketplace has harshly criticized Dr. Gottlieb’s crackdown on e-cigarettes. Retailers, including convenience store and gas station owners, are on Capitol Hill lobbying against guidelines Dr. Gottlieb proposed on Wednesday to restrict sales of most flavored e-cigarettes to separate adult-only areas and to require age verification of customers. And major tobacco companies are likely to seize on his departure to try to scuttle his long-term plans to lower nicotine levels in cigarettes to nonaddictive levels and to ban menthol cigarettes, which make up more than a third of the cigarette market and dominate sales to African-Americans. Some longtime officials inside the F.D.A. said privately that they fear these ideas could be delayed indefinitely. “There have been well-intentioned commissioners before Gottlieb,” said Jonathan Havens, a former F.D.A. tobacco lawyer now in private practice. “But they were not as good at capturing the attention of the nation, of the stakeholders. I think that momentum could very well stall on some of these products, or be lost completely.” © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26042 - Posted: 03.16.2019

By Andrew Jacobs What do these ads featuring Joe Camel, Kool-Aid Man and the maniacal mascot for Hawaiian Punch have in common? All three were created by Big Tobacco in the decades when cigarette makers, seeking to diversify their holdings, acquired some of America’s iconic beverage brands. They used their expertise in artificial flavor, coloring and marketing to heighten the products’ appeal to children. That tobacco companies once sold sugar-sweetened drinks like Tang, Capri Sun and Kool-Aid is not exactly news. But researchers combing through a vast archive of cigarette company documents at the University of California, San Francisco stumbled on something revealing: Internal correspondence showed how tobacco executives, barred from targeting children for cigarette sales, focused their marketing prowess on young people to sell sugary beverages in ways that had not been done before. The archive, known as the Truth Tobacco Industry Documents, was created as part of a settlement between major cigarette companies and states that were seeking to recoup smoking-related health care costs. The researchers published their findings on Thursday in the medical publication BMJ. Using child-tested flavors, cartoon characters, branded toys and millions of dollars in advertising, the companies cultivated loyalty to sugar-laden products that health experts said had greatly contributed to the nation’s obesity crisis. At a time of mounting childhood obesity, with nearly a third of children in the United States overweight or obese and rates of type 2 diabetes soaring among adolescents, the study’s authors said it was important to chart how companies created and marketed junk food and sugary drinks to youngsters. © 2019 The New York Times Company

Related chapters from BN8e: 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: 26036 - Posted: 03.15.2019

/ By Jonathan S. Jones Newly unsealed documents from a lawsuit by the state of Massachusetts allege that Purdue Pharma, maker of OxyContin and other addictive opioids, actively sniffed out new, sinister ways to cash in on the opioid crisis. Despite years of negative press coverage, unwanted attention from regulators, multimillion dollar fines and several major lawsuits, Purdue staff and owners sought to expand the company’s sights beyond its usual array of opioid painkillers. Purdue planned to become an “end-to-end pain provider,” by branching into the market for opioid addiction and overdose medicines, looking to peddle these medicines even while the company continued to aggressively market its addictive opioids. Internal research materials coldly explained the rationale behind this plan: “Pain treatment and addiction are naturally linked.” As thousands of Americans continue to overdose on opioids annually, Purdue’s secret marketing research predicted that sales of naloxone, the overdose reversal drug, and buprenorphine, a medicine used to treat opioid addiction, would increase exponentially. Addiction to Purdue’s opioids would thus drive the sale of the company’s opioid addiction and overdose medicines. Purdue even planned to target as customers patients already taking the company’s opioids and doctors who prescribed opioids excessively, according to the Massachusetts lawsuit filing. To keep the plan quiet, Purdue staff dubbed the scheme “Project Tango.” Copyright 2019 Undark

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26005 - Posted: 03.05.2019

Assessing the patterns of energy use and neuronal activity simultaneously in the human brain improves our understanding of how alcohol affects the brain, according to new research by scientists at the National Institutes of Health. The new approach for characterizing brain energetic patterns could also be useful for studying other neuropsychiatric diseases. A report of the findings is now online in Nature Communications. “The brain uses a lot of energy compared to other body organs, and the association between brain activity and energy utilization is an important marker of brain health,” said George F. Koob, Ph.D., director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of NIH, which funded the study. “This study introduces a new way of characterizing how brain activity is related to its consumption of glucose, which could be very useful in understanding how the brain uses energy in health and disease.” The research was led by Dr. Ehsan Shokri-Kojori and Dr. Nora D. Volkow of the NIAAA Laboratory of Neuroimaging. Dr. Volkow is also the director of the National Institute on Drug Abuse at NIH. In previous studies they and their colleagues have shown that alcohol significantly affects brain glucose metabolism, a measure of energy use, as well as regional brain activity, which is assessed through changes in blood oxygenation. “The findings from this study highlight the relevance of energetics for ensuring normal brain function and reveal how it is disrupted by excessive alcohol consumption,” says Dr. Volkow.

Related chapters from BN8e: 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: 26004 - Posted: 03.05.2019

By Roni Caryn Rabin Cannabidiol, or CBD, a nonintoxicating component of the marijuana plant, is touted as a magic bullet that eases pain, anxiety, insomnia and depression. Salves, sprays, tinctures and oils containing CBD are marketed as aphrodisiacs that boost desire; as balms for eczema, pimples and hot flashes; and even as treatments for serious diseases like diabetes and multiple sclerosis. Unlike THC, or tetrahydrocannabinol, the “psychoactive” component of the cannabis plant, CBD won’t get you “high.” But scientists know little about what it can do: Most of the information about CBD’s effects in humans is anecdotal or extrapolated from animal studies, and few rigorous trials have been conducted. “It is a kind of a new snake oil in the sense that there are a lot of claims and not so much evidence,” said Dustin Lee, an assistant professor in psychiatry and behavioral sciences at Johns Hopkins University who is planning a human trial of CBD for use in quitting smoking. The Food and Drug Administration has approved some drugs made from synthetic substances similar to THC to treat poor appetite and nausea in people with A.I.D.S. or cancer. But so far, the F.D.A. has approved only one drug containing CBD, Epidiolex, after clinical trials found it reduced seizures in children with two rare, severe forms of epilepsy. “There’s a lot of hype about everything about CBD,” said Dr. Orrin Devinsky, the director of the NYU Langone Comprehensive Epilepsy Center, who led the Epidiolex studies and went out of his way to say the drug’s effect was “not miraculous.” “There is certainly data that it has a variety of anti-inflammatory effects, but whether that translates into improving human health is unknown. Does it help people with eczema, rheumatoid arthritis or ulcerative colitis? We don’t know. There is a good theoretical basis, but the studies have not been done.” © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 10: Biological Rhythms and Sleep
Link ID: 25988 - Posted: 02.27.2019

By Tom Avril Smoking cigarettes has long been known for its ability to damage eyesight, on top of the harm it causes to the lungs, heart and other organs. But a new study suggests that smoking can impair vision far earlier than is commonly thought. Heavy smokers with an average age of 35 were markedly worse than nonsmokers at distinguishing colors as well as the contrast between different shades of gray, the study authors said. Previous research has linked smoking with macular degeneration and cataracts, which tend to occur decades later. The new results, published in Psychiatry Research, do not indicate how smoking damages perception of color and contrast. But the broad nature of the impairment suggests that it is not the result of damage to specific kinds of light-sensitive cells, such as rods or cones, said co-author Steven Silverstein, a professor of psychiatry and ophthalmology at Rutgers Robert Wood Johnson Medical School. Instead, cigarette use probably harms a more general aspect of vision biology, such as blood vessels or nerve cells. “There is probably some more widespread problem like overall blood flow in the eye that is compromised due to all the toxic chemicals in cigarettes,” said Silverstein, who collaborated with authors from the Perception, Neuroscience and Behavior Laboratory in Joao Pessoa, Brazil. © 1996-2019 The Washington Post

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Vision: From Eye to Brain
Link ID: 25985 - Posted: 02.26.2019

A genetic variant found only in people of African descent significantly increases a smoker’s preference for cigarettes containing menthol, a flavor additive. The variant of the MRGPRX4 gene is five to eight times more frequent among smokers who use menthol cigarettes than other smokers, according to an international group of researchers supported by the U.S. Food and Drug Administration and the National Institutes of Health. The multiethnic study is the first to look across all genes to identify genetic vulnerability to menthol cigarettes. The paper was published online in the journal PLOS Genetics (link is external) on Feb. 15. Menthol provides a minty taste and a cooling or soothing sensation, and plays a particularly troubling role in U.S. cigarette smoking patterns. According to the FDA, nearly 20 million people in the United States smoke menthol cigarettes, which are particularly popular among African-American smokers and teen smokers. In the U.S., 86 percent of African-American smokers use menthol cigarettes, compared to less than 30 percent of smokers of European descent. In addition, menthol cigarettes may be harder to quit than other cigarettes. Although not originally the focus of the study, researchers also uncovered clues as to how menthol may reduce the irritation and harshness of smoking cigarettes. “This study sheds light on the molecular mechanisms of how menthol interacts with the body,” said Andrew Griffith, M.D., Ph.D., scientific director and acting deputy director of NIH’s National Institute on Deafness and Other Communications Disorders (NIDCD). “These results can help inform public health strategies to lower the rates of harmful cigarette smoking among groups particularly vulnerable to using menthol cigarettes.”

Related chapters from BN8e: 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: 25969 - Posted: 02.18.2019

Terry Gross Growing up, neuroscientist Judith Grisel would take little sips of alcohol at family events, but it wasn't until she was 13 that she experienced being drunk for the first time. Everything changed. "It was so complete and so profound," she says. "I suddenly felt less anxious, less insecure, less inept to cope with the world. Suddenly I was full and OK in a way that I had never been." Grisel began chasing that feeling. Over the years, she struggled with alcohol, marijuana and cocaine. But along the way, she also became interested in the neuroscience of addiction. "I'm always interested in the mechanisms of things," she says. "And when I heard that I had a disease, I kind of felt naturally that that would have a biological basis, and I figured that I could study that biological basis and understand it and then maybe fix it." Now it has been 30 years without using drugs or alcohol for Grisel, a professor of psychology at Bucknell University, where she studies how addictive drugs work on the brain. Her new book is Never Enough: The Neuroscience and Experience of Addiction. Interview Highlights On how drug and alcohol abuse affects the brains of young people The changes in behavior that happen during adolescence are so important and lasting because the brain is forming permanent structures. So whatever you experience as an adolescent is going to have a much more impactful influence on the rest of your life trajectory than it would, say, if you did this at another time in development when your brain wasn't so prone to changing. © 2019 npr

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25958 - Posted: 02.13.2019

/ By Ronnie Cohen Dr. Samir Grover was taken aback when, early in his gastroenterology career, he saw one physician speak two times and present contradictory conclusions about the same medication. Each time, the speaker presented identical data on a drug used to treat inflammatory bowel disease. First, he recommended the pharmaceutical. A week later, he deemed it ineffective. “How could this exact same data be spun in two very different ways?” asked Grover, a professor at the University of Toronto. One fact did change — the drug manufacturer that sponsored and paid for the lecture. “Simply following clinical practice guidelines could lead doctors — even those who shun all industry gifts — to unwittingly dispense financially tainted medicine” It’s no secret that drug makers pay doctors to hype their products to other doctors. But few outside the halls of hospitals witness physicians bending a single set of facts in opposing ways. After watching similar acts of statistical wizardry throughout his nine years of medical practice, Grover set out to investigate a more sweeping question about conflicts of interest. Do they infect clinical practice guidelines? Professional societies produce thousands of these documents every year. They steer the decisions of health care professionals and insurance companies about how to prevent and treat an ever-widening range of conditions — from diabetes, hypertension, and heart disease to arthritis, hepatitis, cancer, and depression. Grover and his colleagues’ paper and a companion study recently published in JAMA Internal Medicine suggest that simply following clinical practice guidelines could lead doctors — even those who shun all industry gifts — to unwittingly dispense financially tainted medicine. More than half of the authors of guidelines examined in the two studies had financial conflicts of interest. In many cases, the doctors who wrote the guidelines were paid by the same companies that produced the drugs they recommended. In addition, a significant portion of the doctors who took pharmaceutical money failed to disclose the payments, many of which amounted to $10,000 or more. Copyright 2019 Undark

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 25930 - Posted: 02.04.2019