Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By Bradley E. Alger, Ph.D. Cannabis, derived from a plant and one of the oldest known drugs, has remained a source of controversy throughout its history. From debates on its medicinal value and legalization to concerns about dependency and schizophrenia, cannabis (marijuana, pot, hashish, bhang, etc.) is a hot button for politicians and pundits alike. Fundamental to understanding these discussions is how cannabis affects the mind and body, as well as the body’s cells and systems. How can something that stimulates appetite also be great for relieving pain, nausea, seizures, and anxiety? Whether its leaves and buds are smoked, baked into pastries, processed into pills, or steeped as tea and sipped, cannabis affects us in ways that are sometimes hard to define. Not only are its many facets an intrinsically fascinating topic, but because they touch on so many parts of the brain and the body, their medical, ethical, and legal ramifications are vast. The intercellular signaling molecules, their receptors, and synthetic and degradative enzymes from which cannabis gets its powers had been in place for millions of years by the time humans began burning the plants and inhaling the smoke. Despite records going back 4,700 years that document medicinal uses of cannabis, no one knew how it worked until 1964. That was when Yechiel Gaoni and Raphael Mechoulam1 reported that the main active component of cannabis is tetrahydrocannabinol (THC). THC, referred to as a “cannabinoid” (like the dozens of other unique constituents of cannabis), acts on the brain by muscling in on the intrinsic neuronal signaling system, mimicking a key natural player, and basically hijacking it for reasons best known to the plants. Since the time when exogenous cannabinoids revealed their existence, the entire natural complex came to be called the “endogenous cannabinoid system,” or “endocannabinoid system” (ECS). Copyright 2013 The Dana Foundation
Keyword: Drug Abuse
Link ID: 18874 - Posted: 11.06.2013
The generic anticonvulsant medication gabapentin shows promise as an effective treatment for alcohol dependence, based on the results of a 150-patient clinical trial of the medication. Conducted by scientists supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health, the study found that alcohol dependent patients using gabapentin were more likely to stop drinking or refrain from heavy drinking than those taking placebo. Gabapentin is already widely prescribed to treat pain conditions and epilepsy. “Gabapentin adds to the list of existing medications that have shown promise in treating alcohol dependence,” said Kenneth R. Warren, Ph.D., acting director of the NIAAA. “We will continue to pursue research to expand the menu of treatment options available for alcoholism in the hopes of reaching more people.” A report of the study, led by Barbara J. Mason, Ph.D., of The Scripps Research Institute (TSRI) in La Jolla, Calif., appears in the Nov. 4, 2013 edition of JAMA Internal Medicine. Dr. Mason and her colleagues randomly assigned alcohol dependent patients to receive a moderate or high dose of gabapentin (900 milligrams or 1,800 milligrams) or a placebo. Over the 12-week treatment, patients receiving the 1,800-milligram dose were twice as likely to refrain from heavy drinking (45 percent vs. 23 percent) and four times as likely to stop drinking altogether (17 percent vs. 4 percent), compared to placebo. Participants receiving gabapentin also reported improved sleep and mood and fewer alcohol cravings. The medication appeared to be well tolerated with few side effects.
Keyword: Drug Abuse
Link ID: 18873 - Posted: 11.05.2013
By JANE E. BRODY Marijuana has been used medically, recreationally and spiritually for about 5,000 years. Known botanically as cannabis, it has been called a “crude drug”: marijuana contains more than 400 chemicals from 18 chemical families. More than 2,000 compounds are released when it is smoked, and as with tobacco, there are dangers in smoking it. Medical marijuana clinics operate in 20 states and the District of Columbia, and its recreational use is now legal in Colorado and Washington. A Gallup poll conducted last month found that 58 percent of Americans support the legalization of marijuana. Yet researchers have been able to do relatively little to test its most promising ingredients for biological activity, safety and side effects. The main reason is marijuana’s classification by Congress in 1970 as an illegal Schedule I drug, defined as having a potential for abuse and addiction and no medical value. American scientists seeking clarification of marijuana’s medical usefulness have long been stymied by this draconian classification, usually reserved for street drugs like heroin with a high potential for abuse. Dr. J. Michael Bostwick, a psychiatrist at the Mayo Clinic in Rochester, Minn., said the classification was primarily political and ignored more than 40 years of scientific research, which has shown that cellular receptors for marijuana’s active ingredients are present throughout the body. Natural substances called cannabinoids bind to them to influence a wide range of body processes. In a lengthy report entitled “Blurred Boundaries: The Therapeutics and Politics of Medical Marijuana,” published last year in Mayo Clinic Proceedings, Dr. Bostwick noted that the so-called endocannabinoid system has an impact on the “autonomic nervous system, immune system, gastrointestinal tract, reproductive system, cardiovascular system and endocrine network.” Copyright 2013 The New York Times Company
By Lindsey Konkel and Environmental Health News Insecticides commonly used in households may be associated with behavior problems in children, according to a new study by researchers in Quebec. The study is one of the first to investigate potential human health effects of pyrethroids, which are used in more than 3,500 commercial products, including flea bombs and roach sprays. The findings raise some questions about the safety of the compounds, which have replaced other insecticides with known risks to children’s brain development. Exposure to pyrethroids, which kill insects by interfering with their nervous systems, is widespread because they are used inside homes and schools, in municipal mosquito control and on farms. In the study, the urine of 779 Canadian children between the ages of 6 and 11 was tested, and their parents answered questions about each child’s behavior. Ninety-seven percent of the children had traces of pyrethroid breakdown products in their urine, and 91 percent had traces of organophosphates, another class of pesticides. A 10-fold increase in urinary levels of one pyrethroid breakdown product, cis-DCCA, was associated with a doubling in the odds of a child scoring high for parent-reported behavioral problems, such as inattention and hyperactivity. Another breakdown product, trans-DCCA, was also associated with more behavior problems, although the association was not statistically significant, meaning the finding could be due to chance. The breakdown product, trans- and cis-DCCA, is specific to certain pyrethroids – namely permethrin, cypermethrin and cyfluthrin. © 2013 Scientific American
by Bethany Brookshire In pharmacology research, it seems like one test is never enough. If you want to test a new antidepressant, reviewers (and good logic) often demand that you use more than one test. A locomotor assay to see whether the new drug depresses or increases how much a mouse moves. A forced swim test or tail suspension test to see how it stacks up against other, known antidepressants. Does it increase swimming? Or climbing? Does it decrease immobility more or less than known antidepressants? You may want to use a chronic mild stress test, which exposes mice over a long period of time to things like mild cold, noise or light to induce stress. Does chronic exposure to your new antidepressant relieve the stress like other antidepressants do? What about responses to things like chronic bullying by other mice? Does it work then? You don’t necessarily need to run all of these tests, but you usually do need to run more than one. After all, what if the drug decreases immobility in a forced swim test, like other antidepressants, but it also makes them race around the room … because it’s cocaine? These are the kind of questions that pharmacologists end up asking. Often, to find new, potential antidepressants, for example, we end up matching them against other, known antidepressants in a series of these tests. If the drug performs well in all of them, doesn’t decrease locomotor activity but keeps the mice swimming and stops them from looking stressed after bullying, we might have something new. © Society for Science & the Public 2000 - 2013.
Melissa Dahl TODAY You know smoking doesn’t do any favors for your face – or your lungs, or your heart, or just about any other part of your body, for that matter! – but a new study of twins hints at the ways the habit makes you look older than you really are. In what is perhaps the best detail of the study, researchers used the annual Twins Days Festival in Twinsburg, Ohio (the "Largest Annual Gathering of Twins in the World!") to round up the 79 identical pairs they include in the report. A panel of three plastic surgery residents compared the faces of the twins, one of which had been smoking for at least five years longer than the other. They identified a few major areas of accelerated aging in the faces of the smoking twins: The smokers' upper eyelids drooped while the lower lids sagged, and they had more wrinkles around the mouth. The smokers were also more likely to have jowls, according to the study, which was published today in the journal Plastic and Reconstructive Surgery. Smoking reduces oxygen to the skin, which also decreases blood circulation, and that can result in weathered, wrinkled, older-looking skin, explains Dr. Bahman Guyuron, a plastic surgeon in Cleveland, Ohio, and the lead author of the study. The logic of research like this and others like it is this: If threats of cancer, heart and lung disease, or the dangers of second- and third-hand smoke aren’t enough to get people to stop smoking, or to never start in the first place, then why not try appealing to people’s vanity? (The same tactic has been used in an attempt to warn young people away from tanning.)
Keyword: Drug Abuse
Link ID: 18851 - Posted: 10.30.2013
By ADAM NAGOURNEY and RICK LYMAN LOS ANGELES — In the heart of Northern California’s marijuana growing region, the sheriff’s office is inundated each fall with complaints about the stench of marijuana plots or the latest expropriation of public land by growers. Its tranquil communities have been altered by the emergence of a wealthy class of marijuana entrepreneurs, while nearly 500 miles away in Los Angeles, officials have struggled to regulate an explosion of medical marijuana shops. But at a time when polls show widening public support for legalization — recreational marijuana is about to become legal in Colorado and Washington, and voter initiatives are in the pipeline in at least three other states — California’s 17-year experience as the first state to legalize medical marijuana offers surprising lessons, experts say. Warnings voiced against partial legalization — of civic disorder, increased lawlessness and a drastic rise in other drug use — have proved unfounded. Instead, research suggests both that marijuana has become an alcohol substitute for younger people here and in other states that have legalized medical marijuana, and that while driving under the influence of any intoxicant is dangerous, driving after smoking marijuana is less dangerous than after drinking alcohol. Although marijuana is legal here only for medical use, it is widely available. There is no evidence that its use by teenagers has risen since the 1996 legalization, though it is an open question whether outright legalization would make the drug that much easier for young people to get, and thus contribute to increased use. And though Los Angeles has struggled to regulate marijuana dispensaries, with neighborhoods upset at their sheer number, the threat of unsavory street traffic and the stigma of marijuana shops on the corner, communities that imposed early and strict regulations on their operations have not experienced such disruption. © 2013 The New York Times Company
Keyword: Drug Abuse
Link ID: 18840 - Posted: 10.28.2013
By HELENE STAPINSKI IN an office of the American Museum of Natural History, a team of scientists, artists and multimedia experts were discussing what had poisoned Skippy, a cute Jack Russell terrier that had keeled over sick in his virtual backyard. Was it the chocolate he found in the garbage can? Did a snake, or a black widow spider, bite him? Or was a poisonous cane toad to blame? Skippy is just one of many victims in the museum’s show, “The Power of Poison,” opening Nov. 16, to which the staff was busy applying finishing touches. Using iPads, visitors can examine the circumstances surrounding Skippy’s fictional poisoning and, controlling their experience individually, take a crack at solving the mystery. But because the museum is popular with small children, Skippy does not die. Instead, his animated eyes turn into Xs, he runs erratically around the yard, he drools and he vomits a bit. Eventually, though, Skippy rallies to full health. “We were not going to make this a scary show,” said the exhibit’s curator, Dr. Mark Siddall. “Instead you walk out saying, ‘Wow. That was cool.’ ” Dr. Siddall spent two hours enthusiastically discussing poison and its properties at the museum recently, walking through some of the show’s highlights. The exhibit, which takes a look at poison’s role in nature, myth, medicine and human history, examines killer caterpillars, zombie ants and deadly vipers. It also looks at the possible victims, like the heavily slumbering Snow White. Plus the age-old question of what killed Cleopatra. Was it an asp, or something else? And while we’re at it, was Napoleon really poisoned with arsenic? © 2013 The New York Times Company
Link ID: 18837 - Posted: 10.26.2013
by Tina Hesman Saey BOSTON — A variant in a gene involved in breaking down chemicals in smoke triples a smoker’s risk of multiple sclerosis, a study shows. Smoking increases by 30 to 50 percent a person’s risk of multiple sclerosis, a disease in which the immune system attacks a waxy coating around nerve cells. Scientists don’t know exactly how smoking contributes to the disease. Farren Briggs of the University of California, Berkeley and his colleagues searched DNA of thousands of people in Northern California, Norway and Sweden for genetic variants associated with both smoking and multiple sclerosis. The team found hundreds of variants in three genes involved in breaking down chemicals found in smoke, Briggs said October 24 at the annual meeting of the American Society of Human Genetics. In particular, people who smoke and who have two copies of a variant in the NAT1 gene have a risk of getting MS that is three times higher than that of smokers without the variant. For nonsmokers, the variant doesn’t increase MS risk. Citations F.B.S. Briggs et al. NAT1 in an important genetic effect modifier of tobacco smoke exposure in multiple sclerosis susceptibility in 5,453 individuals. American Society of Human Genetics annual meeting, Boston, October 24, 2013. Further Reading N. Seppa. Old drug may have new trick. Science News. Vol. 184, November 2, 2013, p. 16. N. Seppa. Black women may have highest multiple sclerosis rates. Science News. Vol. 183, June 15, 2013, p. 15. © Society for Science & the Public 2000 - 2013
Doug Greene, WVIT and NBC News staff NBC News Oreos are as addictive as cocaine, at least for lab rats, and just like us, they like the creamy center best. Eating the sugary treats activates more neurons in the brain’s “pleasure center” than drugs such as cocaine, the team at Connecticut College found. “Our research supports the theory that high-fat/ high-sugar foods stimulate the brain in the same way that drugs do,” neuroscience assistant professor Joseph Schroeder says. “That may be one reason people have trouble staying away from them and it may be contributing to the obesity epidemic.” Schroeder’s neuroscience students put hungry rats into a maze. On one side went rice cakes. “Just like humans, rats don’t seem to get much pleasure out of eating them,” Schroeder said. On the other side went Oreos. Then the rats got the option of hanging out where they liked. They compared the results to a different test. In that on, rats on one side if the maze got an injection of saline while those on the other side got injections of cocaine or morphine. Rats seems to like the cookies about as much as they liked the addictive drugs. When allowed to wander freely, they’d congregate on the Oreo side for about as much time as they would on the drug side. Oh, and just like most people - the rats eat the creamy center first.
by Simon Makin A drug similar to ketamine has been shown to work as an antidepressant, without the psychosis-like side effects associated with the party drug. In 2000, ketamine was seen to alleviate depression almost immediately in people for whom other treatments had failed. Larger clinical trials have since corroborated the findings. The drawback is that ketamine can cause hallucinations and other psychotic symptoms, making it unsuitable for use as a treatment. These effects also make it difficult to conduct randomised, placebo-controlled trials – the gold standard in clinical medicine – as it is obvious which participants have been given the drug. This meant that there was a possibility that the beneficial effects seen in previous trials were inflated. So a team led by Gerard Sanacora of Yale University and Mike Quirk of pharmaceutical firm AstraZeneca looked for an alternative compound. They decided to test lanicemine, a drug originally developed to treat epilepsy that targets the same brain receptors as ketamine. The team gave 152 people with moderate-to-severe depression and a history of poor response to antidepressants either lanicemine or a placebo three times a week, for three weeks. They were allowed to continue taking any medications they were already on. Before and after the trial the participants' level of depression was rated on a 60-point scale. After three weeks, those taking lanicemine were less depressed by an average of 13.5 points – 5.5 points better than those who took the placebo. The improvement was still statistically significant up to two weeks after the treatment ended. Dizziness was the only common side effect. © Copyright Reed Business Information Ltd.
By Larry Greenemeier The leaves of the herb kratom (Mitragyna speciosa), a native of Southeast Asia in the coffee family, are used to relieve pain and improve mood as an opiate substitute and stimulant. The herb is also combined with cough syrup to make a popular beverage in Thailand called “4x100.” Because of its psychoactive properties, however, kratom is illegal in Thailand, Australia, Myanmar (Burma) and Malaysia. The U.S. Drug Enforcement Administration lists kratom as a “drug of concern” because of its abuse potential, stating it has no legitimate medical use. The state of Indiana has banned kratom consumption outright. Now, looking to control its population’s growing dependence on methamphetamines, Thailand is attempting to legalize kratom, which it had originally banned 70 years ago. At the same time, researchers are studying kratom’s ability to help wean addicts from much stronger drugs, such as heroin and cocaine. Studies show that a compound found in the plant could even serve as the basis for an alternative to methadone in treating addictions to opioids. The moves are just the latest step in kratom’s strange journey from home-brewed stimulant to illegal painkiller to, possibly, a withdrawal-free treatment for opioid abuse. With kratom’s legal status under review in Thailand and U.S. researchers delving into the substance’s potential to help drug addicts, Scientific American spoke with Edward Boyer, a professor of emergency medicine and director of medical toxicology at the University of Massachusetts Medical School. Boyer has worked with Chris McCurdy, a University of Mississippi professor of medicinal chemistry and pharmacology, and others for the past several years to better understand whether kratom use should be stigmatized or celebrated. © 2013 Scientific American
Keyword: Drug Abuse
Link ID: 18726 - Posted: 10.01.2013
Selectively bred strains of laboratory rats that either prefer or avoid alcohol have been a mainstay of alcohol research for decades. So-called alcohol-preferring rats voluntarily consume much greater amounts of alcohol than do non-preferring rats. Scientists at the National Institutes of Health now report that a specific gene plays an important role in the alcohol-consuming tendencies of both types of rats. “This study advances our understanding of the genetics and neurobiology of alcohol consumption in an important animal model of human alcoholism,” says Kenneth R. Warren, Ph.D., acting director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of NIH. As reported online in the Proceedings of the National Academy of Sciences, a diverse team of scientists, led by David Goldman, M.D., chief of NIAAA’s Laboratory of Neurogenetics, used exome sequencing, an approach that comprehensively analyzes the DNA that encodes proteins. They found a severely dysfunctional form of the gene for a brain signaling molecule called metabotropic glutamate receptor 2 (Grm2), known as a stop codon, in alcohol-preferring rats but not in non-preferring rats. The researchers then demonstrated that drugs and genetic changes that block Grm2 increased alcohol consumption in normal rats and mice. “We’ve long known that genes play an important role in alcoholism,” says Dr. Goldman. “However, the genes and genetic variants that cause alcoholism have remained largely unknown. This first discovery of a gene accounting for alcohol preference in a mammalian model illustrates that genomic analysis of a model organism is a powerful approach for a complex disease such as alcoholism.”
The Conservative government is launching a $1.3-billion free market in medical marijuana on Tuesday, eventually providing an expected 450,000 Canadians with quality weed. Health Canada is phasing out an older system on Monday that mostly relied on small-scale, homegrown medical marijuana of varying quality, often diverted illegally to the black market. In its place, large indoor marijuana farms certified by the RCMP and health inspectors will produce, package and distribute a range of standardized weed, all of it sold for whatever price the market will bear. The first sales are expected in the next few weeks, delivered directly by secure courier. "We're fairly confident that we'll have a healthy commercial industry in time," Sophie Galarneau, a senior official with the department, said in an interview. "It's a whole other ball game." The sanctioned birth of large-scale, free-market marijuana production comes as the Conservatives pillory Liberal Leader Justin Trudeau's campaign to legalize recreational marijuana. Health Canada is placing no limits on the number of these new capital-intensive facilities, which will have mandatory vaults and security systems. Private-dwelling production will be banned. Imports from places such as the Netherlands will be allowed. Already 156 firms have applied for lucrative producer and distributor status since June, with the first two receiving licences just last week. © CBC 2013
By JOHN SCHWARTZ Candace Pert, a neuroscientist who helped discover a fundamental element of brain chemistry as a graduate student and went on to become a major proponent of alternative medicine, died on Sept. 12 at her home in Potomac, Md. She was 67. The cause was cardiac arrest, said her sister, Deane Beebe. Dr. Pert was working at the Johns Hopkins University School of Medicine in the 1970s when a team she was on found one of the most sought-after objects in brain research: the receptor in the brain that opiates like morphine fit into, like a key in a lock, allowing the drug’s effects to work. The discovery of the opioid receptor would, in 1978, earn the coveted Albert Lasker Award, often a precursor to the Nobel Prize. The award went to Solomon H. Snyder, who headed the lab. Neither Dr. Pert nor any of the other lab assistants was cited. Such omissions are common in the world of science; the graduate student in the lab rarely gets credit beyond being the first name on the papers describing the research. But Dr. Pert did something unusual: she protested, sending a letter to the head of the foundation that awards the prize, saying she had “played a key role in initiating the research and following it up” and was “angry and upset to be excluded.” Her letter caused a sensation in the field. Some saw her exclusion as an example of the burdens and barriers women face in science careers. In a 1979 article about Dr. Pert in the The Washington Post, Dr. Snyder, who had lauded Dr. Pert’s contributions in his Lasker acceptance speech, argued that “that’s the way the game is played,” adding that today’s graduate students will be tomorrow’s lab chiefs, and that “when they have students, it will be the same.” © 2013 The New York Times Company
Keyword: Pain & Touch
Link ID: 18685 - Posted: 09.21.2013
By Stuart McMillen A classic experiment into drug addiction science. Would rats choose to take drugs if given a stimulating environment and social company?
Keyword: Drug Abuse
Link ID: 18669 - Posted: 09.19.2013
By Sarah Amandolare Decades of research and billions of dollars go into developing and marketing drugs. Here's the life span of a typical brain drug—Cymbalta, a popular antidepressant Tuberculosis researchers discover that a drug that treats infections, called iproniazid, also boosts patients' mood. They learn that iproniazid slows the breakdown of three chemicals in the brain— serotonin, norepinephrine and dopamine. These molecules take center stage in the next two decades, as scientists search for antidepressants. 1974 Eli Lilly researchers develop fluoxetine (Prozac), the first selective serotonin reuptake inhibitor. Fluoxetine thwarts the absorption, or “reuptake,” of serotonin. This boosts levels of the chemical in the pockets of space between neurons. Prozac does not hit drugstore shelves until 1988. 1980s Scientists start tinkering with the reuptake of norepinephrine and dopamine, which, in addition to elevating mood, can relieve muscle and joint pain. They dub this new class of antidepressants serotonin-norepinephrine reuptake inhibitors (SNRIs). At Eli Lilly, scientists begin developing an SNRI with a special focus on norepinephrine. One of their molecules becomes known as duloxetine, later branded Cymbalta. 1986 © 2013 Scientific American
Link ID: 18660 - Posted: 09.18.2013
By JOHN TIERNEY Long before he brought people into his laboratory at Columbia University to smoke crack cocaine, Carl Hart saw its effects firsthand. Growing up in poverty, he watched relatives become crack addicts, living in squalor and stealing from their mothers. Childhood friends ended up in prisons and morgues. Carl Hart, an associate professor of psychology at Columbia, arranged experiments in which drug addicts were offered a choice between a dose of the drug or cash or vouchers. When the dose was smaller, addicts often chose cash or vouchers instead. Those addicts seemed enslaved by crack, like the laboratory rats that couldn’t stop pressing the lever for cocaine even as they were starving to death. The cocaine was providing such powerful dopamine stimulation to the brain’s reward center that the addicts couldn’t resist taking another hit. At least, that was how it looked to Dr. Hart when he started his research career in the 1990s. Like other scientists, he hoped to find a neurological cure to addiction, some mechanism for blocking that dopamine activity in the brain so that people wouldn’t succumb to the otherwise irresistible craving for cocaine, heroin and other powerfully addictive drugs. But then, when he began studying addicts, he saw that drugs weren’t so irresistible after all. “Eighty to 90 percent of people who use crack and methamphetamine don’t get addicted,” said Dr. Hart, an associate professor of psychology. “And the small number who do become addicted are nothing like the popular caricatures.” © 2013 The New York Times Company
Keyword: Drug Abuse
Link ID: 18655 - Posted: 09.17.2013
By Gary Stix New types of drugs for schizophrenia, depression and other psychiatric disorders are few and far between—and a number of companies have scaled back or dropped development of this class of pharmaceuticals. One exception stands out. Ketamine, the anesthetic and illegal club drug, is now being repurposed as the first rapid-acting antidepressant drug and has been lauded as possibly the biggest advance in the treatment of depression in 50 years. A few trials by large pharma outfits are now underway on a new, purportedly improved and, of course, more profitable variant of ketamine, which in its current generic drug form does not make pharmaceutical marketing departments salivate. Some physicians have decided they simply can’t wait for the lengthy protocols of the drug approval process to be sorted out. They have read about experimental trials in which a low-dose, slow-infusion of ketamine seems to produce what no Prozac-like pill can achieve, lifting the black cloud in hours, not weeks. With nothing to offer desperate, sometimes suicidal patients, physicians have decided against waiting for an expensive, ketamine lookalike to arrive and have started writing scripts for the plain, vanilla generic version that has been used for decades as an anesthetic. Ketamine, it seems, has captivated a bunch of white coats with the same grassroots energy that has propelled the medical marijuana movement. © 2013 Scientific American
By Scicurious Effective treatments for drug addiction have been hard to come by. There’s behavioral interventions, methadone maintenance for heroin users, nicotine patches for smokers, antabuse for acoholics, but while all of these are effective in a minority of users, they aren’t effective in all. Many require repeat behaviors that are difficult for addicts. As examples: getting to the methadone center every day can be difficult if you have bad transportation. Alcoholics often need to go to AA meetings several times a week if not several times a day. Antabuse make you feel like crap when you drink…and all you have to do is NOT take it. Nicotine patches don’t tend to scratch the smoking itch in the same way. In the case of cocaine, where is there no drug intervention option at all, when you have someone who is in serious danger of overdose, you need something to take away the effects of the cocaine. Something to work immediately. Enter the idea of a vaccine against cocaine. For those used to thinking about vaccines as things that fight chicken pox and whooping cough, the idea of a vaccine against a drug can seem a little foreign. But it’s a concept that’s been in development for some time. Not so much in the context of vaccinating against potential cocaine use, but as a way to help people get off the drug. But the question still remains: will it work? The idea is to use a vaccine made of a drug that is very close to cocaine (norcocaine), combined with an inactivated virus. The presence of the virus causes the body’s immune system to try and fight it off, creating antibodies to different parts of the molecule, both the cocaine part and the virus part. The antibodies serve as a signal for other immune cells to come along and gobble up the cocaine. After the original vaccine is gone, the antibodies stay circulating in your blood, ready to attack is they see the cocaine signal again. © 2013 Scientific American