Addictions News Review - 11:18 AM 6/6/2012
http://forpn.blogspot.com/2012/06/addictions-news-review-1118-am-662012_06.html
The D.S.M. Gets Addiction Right - NYTimes.com
via addiction - Google News on 6/5/12
The DSM Gets Addiction Right
New York Times WHEN we say that someone is “addicted” to a behavior like gambling or eating or playing video games, what does that mean? Are such compulsions really akin to dependencies like drug and alcohol addiction — or is that just loose talk |
Op-Ed Contributor
The D.S.M. Gets Addiction Right
By HOWARD MARKEL
Published: June 5, 2012
Ann Arbor, Mich.
WHEN we say that someone is “addicted” to a behavior like gambling or eating or playing video games, what does that mean? Are such compulsions really akin to dependencies like drug and alcohol addiction — or is that just loose talk?
This question arose recently after the committee writing the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (D.S.M.), the standard reference work for psychiatric illnesses, announced updated definitions of substance abuse and addiction, including a new category of “behavioral addictions.” At the moment, the only disorder featured in this new category is pathological gambling, but the suggestion is that other behavioral disorders will be added in due course. Internet addiction, for instance, was initially considered for inclusion but was relegated to an appendix (as was sex addiction) pending further research.
Skeptics worry that such broad criteria for addiction will pathologize normal (if bad) behavior and lead to overdiagnosis and overtreatment. Allen J. Frances, a professor of psychiatry and behavioral sciences at Duke University who has worked on the D.S.M., has said that the new definitions amount to “the medicalization of everyday behavior” and will create “false epidemics.” Health insurance companies are fretting that the new diagnostic criteria may cost the health care system hundreds of millions of dollars annually, as addiction diagnoses multiply.
There is always potential for misuse when diagnostic criteria are expanded. But on the key scientific point, the D.S.M.’s critics are wrong. As anyone familiar with the history of the diagnosis of addiction can tell you, the D.S.M.’s changes accurately reflect our evolving understanding of what it means to be an addict.
The concept of addiction has been changing and expanding for centuries. Initially, it wasn’t even a medical notion. In ancient Rome, “addiction” referred to a legal dependency: the bond of slavery that lenders imposed upon delinquent debtors. From the second century A.D. well into the 1800s, “addiction” described a disposition toward any number of obsessive behaviors, like excessive reading and writing or slavish devotion to a hobby. The term often implied a weakness of character or a moral failing.
“Addiction” entered the medical lexicon only in the late 19th century, as a result of the over-prescription of opium and morphine by physicians. Here, the concept of addiction came to include the notion of an exogenous substance taken into the body. Starting in the early 20th century, another key factor in diagnosing addiction was the occurrence of physical withdrawal symptoms upon quitting the substance in question.
This definition of addiction was not always carefully applied (it took years for alcohol and nicotine to be classified as addictive, despite their fitting the bill), nor did it turn out to be accurate. Consider marijuana: in the 1980s, when I was training to become a doctor, marijuana was considered not to be addictive because the smoker rarely developed physical symptoms upon stopping. We now know that for some users marijuana can be terribly addictive, but because clearance of the drug from the body’s fat cells takes weeks (instead of hours or days), physical withdrawal rarely occurs, though psychological withdrawal certainly can.
Accordingly, most doctors have accepted changes to the definition of addiction, but many still maintain that only those people who compulsively consume an exogenous substance can be called addicts. Over the past several decades, however, a burgeoning body of scientific evidence has indicated that an exogenous substance is less important to addiction than is the disease process that the substance triggers in the brain — a process that disrupts the brain’s anatomical structure, chemical messaging system and other mechanisms responsible for governing thoughts and actions.
For example, since the early 1990s, the neuropsychologists Kent C. Berridge and Terry E. Robinson at the University of Michigan have studied the neurotransmitter dopamine, which gives rise to feelings of craving. They have found that when you repeatedly take a substance like cocaine, your dopamine system becomes hyper-responsive, making the drug extremely difficult for the addicted brain to ignore. Though the drug itself plays a crucial role in starting this process, the changes in the brain persist long after an addict goes through withdrawal: drug-using cues and memories continue to elicit cravings even in addicts who have abstained for years.
Furthermore, a team of scientists led by Nora Volkow at the National Institute on Drug Abuse have used positron emission tomography (PET) scans to show that even when cocaine addicts merely watch videos of people using cocaine, dopamine levels increase in the part of their brains associated with habit and learning. Dr. Volkow’s group and other scientists have used PET scans and functional magnetic resonance imaging to demonstrate similar dopamine receptor derangements in the brains of drug addicts, compulsive gamblers and overeaters who are markedly obese.
The conclusion to draw here is that though substances like cocaine are very effective at triggering changes in the brain that lead to addictive behavior and urges, they are not the only possible triggers: just about any deeply pleasurable activity — sex, eating, Internet use — has the potential to become addictive and destructive.
Disease definitions change over time because of new scientific evidence. This is what has happened with addiction. We should embrace the new D.S.M. criteria and attack all the substances and behaviors that inspire addiction with effective therapies and support.
Howard Markel, a physician and a professor of the history of medicine at the University of Michigan, is the author of “An Anatomy of Addiction: Sigmund Freud, William Halsted, and the Miracle Drug Cocaine.”
One woman’s journal.
From Insanity to Serenity, by Tommi Lloyd
Excerpts:
"I was born in 1963 in Toronto, Canada, to a family struggling long before I arrived. My dad was an alcoholic, born in Wales in 1921. His father and namesake was also an alcoholic who died at age 28…. My oldest sibling and only brother, Harry, entered a treatment centre at age 36 and has been sober for more than 20 years…. My Uncle Griff died from alcoholism when I was 10 years old…. There were no reprieves by which we spent a day or two in a sober environment. Dad drank from morning until night…. Christmas, Thanksgiving, and Easter—these were some of the worst days of the year…. Santa started leaving a carton of cigarettes next to my stocking at Christmas and I thought it was great.
"I yearned for some quality time before his drinking took center stage for the day… he drank from the minute he got up to the minute he passed out. At the height of his addiction, he was drinking more than 40 ounces of vodka a day…. There were many times when I would walk into the bedroom and see him guzzling the vodka straight from the bottle. It made me feel physical ill and utterly helpless.
"I too, am an alcoholic. In addition to alcohol, my teenage love of marijuana turned into a 30-year affair…. I have two nephews who are addicted to marijuana…. Rather than being sloppy drunks, my nephews opted for the mellow alternative that’s not addictive, (so we like to think) and you can pay for your habit by selling it to your friends.
"By age 11 I tried drinking for the first time…. I recall Susie telling us we could try drinking, but it had to be done quickly so as not to get caught. We poured some very strong rum and cokes and I guzzled mine down by holding my nose with my free hand…. As soon as I lay down on my bed the room started spinning and it wasn’t long before I was throwing up. Mom fussed over me, concluding I had the flu and I recall feeling both happy and guilty at the same time. I loved the attention but felt badly for the cause of my illness. I didn’t drink again for a few years….
"There is nothing more validating for me as a mother than to know I’m an inspiration to my children. I could not have asked for a better gift. This is what sobriety and a renewed spiritual life has brought my children and me…. Intellectually, I recognize how my childhood experiences and the disease of alcoholism molded a lot of my behavior and have been the root of much of my struggle with self-esteem. But self-knowledge does not change our circumstances, action does."
It’s getting harder to interpret genetics studies, and that’s a good thing.
Reporting the results of published studies concerned with genetic risk factors has always been a tricky proposition. Beyond the inevitable, and too often ideological nature/nurture split, there has been an unfortunate history of false positives in the rush to make news with a “gene for” alcoholism or schizophrenia or belief in God.
But single gene theories are mostly a thing of the past, and results tend to be broader and more tentative, as befits the state of our knowledge about genes and
risk in a post-epigenetic landscape. Nonetheless, there’s no denying that genes play a strong role in all kinds of behaviors and processes. A large group of U.S. tobacco researchers went looking for associations between genetic risk factors and the ability to stop smoking successfully, and published their results in the American Journal of Psychiatry. The group came down strongly in favor of the proposition that genetic variations in the chromosome 15q25 region help dictate who manages to quit smoking and who does not.
The genetic variants in question are for nicotine receptors, and are called CHRNA5-CHRNA3-CHRNB4. They compose a “high-risk haplotype” that Li-Shiun Chen and coworkers believe to be involved in the ability to quit. (A haplotype is a combination of DNA sequences on a chromosome that are transmitted as a unit). People with these genetic variants “quit later than those at low genetic risk; this difference was manifested as a 2-year delay in median quit age.” However, this association tended to wash out at very high levels of smoking. Nonetheless, “pharmacological cessation treatment significantly increased the likelihood of abstinence in individuals with the high-risk haplotype,” compared to the low-risk group.
The suspicious haplotypes did not reliably predict tobacco abstinence across all groups that were studied. And any pharmacological treatment at all vastly increases abstinence rates, compared to placebo, while those who smoke the fewest cigarettes per day have the best shot at abstinence no matter what. In one sense, all the study is saying is that anti-craving drugs are more likely to be effective in smokers “who are biologically predisposed to have difficulty quitting.” Other smokers may not need them at all as a quitting aid—which is very much as common sense would have it. But further research in this area may allow medical workers to genetically identify smokers who will definitely require a pharmacological booster shot to overcome their crippling addiction.
In brief, the study says that success in quitting may be directly modulated by certain types of genetic variation among smokers. And genetic variations influencing quitting success may be different from gene variants controlling for “severity of nicotine dependence” (how many cigarettes you smoke), and whether you get addicted in the first place. It is all very complicated. But it’s the sort of thing that gives researchers hope when they contemplate deploying forms of personalized medicine in addiction treatment.
Study limitations abound. The work looked at only one genetic locus, while the success of smoking cessation might depend on multiple gene sites. The placebo arm was relatively small, and the smoking reports were obtained through a combination of biochemical confirmation and self-reporting.
Baker, T. (2012). Interplay of Genetic Risk Factors (CHRNA5-CHRNA3-CHRNB4) and Cessation Treatments in Smoking Cessation Success American Journal of Psychiatry DOI: 10.1176/appi.ajp.2012.11101545
Graphics Credit: (Li-Shiun Chen)
Researchers get good results with gabapentin.
Marijuana, as researchers and pundits never tire of pointing out, is the most widely used illegal drug in the world, by a serious margin. And while the argument still rages, for some years now drug researchers have been migrating to the camp that sees marijuana as an addictive drug for a minority of people who exhibit a propensity for addiction. The scientific literature supporting the contention of marijuana as addictive for some users is robust and growing, as is the body of anecdotal evidence. It’s also clear that in many countries, cultures, and subcultures, combining cannabis with tobacco is a common practice that increases health risks all around.
Ongoing work at the Scripps Research Institute’s Pearson Center for Alcoholism and Addiction Research in La Jolla, California, has focused in part on the lack of FDA-approved medical therapies for treating marijuana addiction. Barbara J. Mason andcoworkers at Scripps have reported preliminary success in a 12-week, double-blind, placebo-controlled pilot study with 50 treatment-seeking volunteers, using the anti-seizure drug gabapentin. Gabapentin, sold as Neurontin, pops up as a possible treatment for various forms of pain and anxiety, and sharp-eyed readers will recall that gabapentin was one of the ingredients in the now-defunct addiction drug Prometa.
Marijuana addiction numbers are hard to come by, and often inflated, since many small-time pot offenders end up in mandatory treatment programs, where they tend to be classified as marijuana addicts, whether or not that is objectively the case. Nonetheless, there are plenty of people seeking treatment on their own for cannabis dependence. For people strongly addicted to pot, the problems are very real, and withdrawal and abstinence pose serious challenges. People for whom marijuana poses no addictive threat should bear this in mind, the way casual drinkers bear in mind the existence of alcoholism in others.
The study, published recently in Neuropsychopharmacology, says that “activation of brain stress circuitry caused by chronic heavy marijuana use” can lead to withdrawal symptoms that persist “for weeks or even months, as in the case of marijuana craving and sleep disturbances.” A variety of existing medications have been tested in recent years, including buspirone, an anti-anxiety medication; Serzone, an antidepressant; and Wellbutrin, an antidepressant commonly used for smoking cessation. None of these treatments has shown any effect on cannabis use or withdrawal, according to Mason.
Gabapentin, as the name suggests, was modeled after the neurotransmitter GABA, and works via a transporter protein to raise GABA levels. Effective only for partial-onset seizures, common side effects include drowsiness, dizziness, and possible weight gain. It is a popular anti-epileptic drug, because it is relatively safe, with a low side-effect profile, compared to many of the medications in its class. For the same reasons, it is a common treatment for neuropathic pain. In addition to neuralgia, it has found some use as a migraine preventative.
Gabapentin normalizes GABA activation caused by corticotrophin-releasing factor, or CRF. CRF is a major player in the brain’s stress responses. As it turns out, withdrawal from both cannabis and alcohol ramp up anxiety levels by increasing CRF release in the amygdala, animal studies have shown. “Gabapentin had a significant effect in decreasing marijuana use over the course of treatment, relative to placebo,” the authors report. In addition, gabapentin produced “significant reductions in both the acute symptoms of withdrawal as well as in the more commonly persistent symptoms involving mood, craving, and sleep.”
As a bonus, the researchers discovered that “overall improvement in performance across cognitive measures was significantly greater for gabapentin-treated subjects compared with those receiving placebo.” Gabapentin was associated with improvement in “tasks related to neurocognitive executive functioning”—things like attention, concentration, visual-motor functioning, and inhibition. Counseling alone, represented by the placebo group, “resulted in less effective treatment of cannabis use and withdrawal, and no improvement in executive function.”
As in the case of Chantix for cigarette cessation, a treatment, which now requires additional caveats about possible suicidal ideation, researchers looking for a treatment for drug withdrawal, must weigh the benefits of pharmacological treatment against the possible side effects of the treatment itself. Does gabapentin for marijuana withdrawal pass the “Do No Harm” test? According to Mason, it does. “Gabapentin was well tolerated and without significant side effects” in the admittedly small trial study. The two groups did not differ in the number of adverse medical events reported in the first two weeks, when dropout rates due to side effects are highest in these kinds of studies. The investigators were not relying solely on self-reporting, either. They used urine drug screens, and verified that only 3% of the study sample tested positive for other drugs.
In short, the authors report that gabapentin reduced cannabis use and eased withdrawal with an acceptable safety profile and no signs of dependence. Gabapentin, the authors conclude, “may offer the most promising treatment for cannabis withdrawal and dependence studied to date.” Further clinical research is needed, of course, but the positive results of this proof-of-concept study should make funding a bit easier.
Mason, B., Crean, R., Goodell, V., Light, J., Quello, S., Shadan, F., Buffkins, K., Kyle, M., Adusumalli, M., Begovic, A., & Rao, S. (2012). A Proof-of-Concept Randomized Controlled Study of Gabapentin: Effects on Cannabis Use, Withdrawal and Executive Function Deficits in Cannabis-Dependent Adults Neuropsychopharmacology DOI: 10.1038/npp.2012.14
Photo Credit: http://pep3799.hubpages.com/
[From time to time, I reprint earlier posts that have remained perennial favorites at Addiction Inbox. This one originally ran on August 4, 2010.]
What do long-distance running and marijuana smoking have in common? Quite possibly, more than you’d think. A growing body of research suggests that the runner’s high and the cannabis high are more similar than previously imagined.
What we think about when we think about “disease.”
It’s a safe bet that the number of M.D.s who have made a mid-career switch to journalism is rather small. And when Dr. Ivan Oransky did it, he didn’t go in for half measures. The former online editor of Scientific American, and the former deputy editor of The Scientist, Oransky now serves as Executive Editor of Reuters Health. He teaches medical journalism at New York University, where he also holds an appointment as clinical assistant professor of medicine—while maintaining three, yes three, separate blogs. He is well known for two innovative blogs known as Retraction Watch and Embargo Watch. And he recently kicked off a personal blog, the Oransky Journal.
So clearly, he’s a very lazy man. Nonetheless, he found time to give a very popular talk on the shortcomings of the disease model of medicine at last week’s TEDMED conference in Washington, D.C. And he found additional time to grant me an interview afterwards, with some interesting thoughts on how the mania for medicalization could affect addiction treatment.
Speaking at the Kennedy Center for the Performing Arts, Oransky compared patients in the nation’s current medical system to baseball coach Billy Beane, a once-promising player who washed out in the minors and was recently portrayed by Brad Pitt in the movie Moneyball. “Our medical system is just as bad at predicting what’s happening to patients as baseball scouts were at predicting what would happen to Billy Beane,” Oransky told the audience of 1,500.
“Every day, thousands of people across the country are diagnosed with pre-conditions,” he said. “We hear about pre-hypertension, we hear about pre-dementia and pre-anxiety. We also refer to sub-clinical conditions, like sub-clinical hardening of the arteries. One of my favorites is called sub-clinical acne. If you look up their website as I did, you’ll see that they say this is the easiest acne to treat. You don’t have any pustules or inflammation—you don’t actually have acne. I have a name for preconditions—I call them preposterous.”
Every year, according to Oransky, “we are spending more than two trillion dollars on health care," and yet more than 100,000 people a year are dying from complications of the treatments they're getting, rather than from the conditions that are being treated. [Revised 4-15]. And most patient advocacy groups eventually learn to “expand the number of people who are eligible for a given treatment” for fundraising purposes, he said.
As evidence of this trend toward medicalization, Oransky pointed to the novel notion of a “previvor.” According to FORCE, the cancer research advocacy group that coined the term: "A previvor is a survivor of a predisposition to cancer.” The term is used to describe someone who, for example, has a genetic risk for breast cancer, but has not been diagnosed with the disease. “Previvor was coined in 2000 after a challenge from a community member who said she ‘needed a label,’” according to the group’s web site.
We are all previvors of some disorder, Oransky argues. In the spirit of giving everyone a precondition, Oransky coined the term “pre-death.” What is pre-death? “Every single one of you has it,” Oransky told the audience, “because you have the risk factor for it, which is being alive."
Using his favorite metaphor—baseball—Oransky explained the secret of Billy Beane’s revolutionary success as a coach: “The secret wasn’t to swing at every pitch, like the sluggers do. You had to find the guys who liked to walk, because getting on base by a walk is just as good. And in our health care system, we need to figure out, ‘is that really a good pitch, or do we need to let it go by, and not swing at everything?’ We all need to keep in mind that in medicine, sometimes less is more.”
After his talk, I asked Oransky how the theme of medicalization might apply to the disease of addiction. Medicalization, he said, is a matter of “taking advantage of people, manipulating them so they can’t make informed decisions.” In the case of addiction treatment, Oransky pointed to the “proliferation of ads for treatment in beautiful places. It’s all selling and self-diagnosis. They’re selling you on the fact that you need to be treated.” He also pointedly referred to the practice of “medical astro-turfing,” where a supposedly grass roots effort by patients or advocates is “usurped by interest group pressure.” Sometimes that usurpation is patently obvious, is in the case of many advocacy groups set in motion and funded by pharmaceutical companies or the liquor industry.
Sometimes, of course, you do need to be treated. And Oransky notes that in health areas such as addiction and mental illness—disorders where social stigma remains high, compared to, say, a blood infection—there are “fewer pressures to medicalize.” And possibly, too few pressures to medicalize. “There’s no quick and easy test, no MRI where you can point to the place in the brain that lights up and say, “you are an alcoholic.” The science of addiction, which has been moving by fits and starts into the medical mainstream, has a long way to go, compared with many other disease categories. And it has left a gap through which medical workers and treatment staff can march, chanting, “I have a system,” Oransky says.
Perhaps, then, the study of addiction to alcohol and other drugs requires both more medicalization of the research kind, and less of the “precondition” or “sub-clinical” kind. As for the second kind, Oransky believes we are already medicalizing binge drinking in a counterproductive way. In addition, “there are always attempts to widen the market. Look at how obesity has been made to overlap with addiction.” As for medications being used to combat craving among addicts in treatment, Oransky noted the tendency to “repurpose” drugs on the basis of soft data. “They took wellbutrin, an antidepressant that didn’t work very well, and offered it for smoking cessation. So I would want to see data that is really robust” before treating addicts with such medications.
On the other hand, Oransky noted, “We don’t have to worry about malaria, we don’t need to medicalize tuberculosis. But do diseases that have a strong stigma, like addiction, actually benefit from medicalization? If we find out that they do, than we should do it.”
There’s something else Oransky believes is overdue for true medicalization: “The social determinants of health care—poverty, the way we build our suburban environments. Concentrate on stuff that we know kills people. Medicalize that.”
In the end, he said, “we need to use marketing strategies to effectively get treatment to the people who need it, not to the people who don’t.”
State law criminalizes “gateway sexual activity.”
It’s the gateway to hell and perdition, that’s what it is. It doesn’t necessarily lead to drugs but it will drag you in the direction of Ess Eee Exx. And while sex is probably not addictive in the traditional sense, it is always and inevitably very bad when unaccompanied by marriage and the procreative urge.
Like anthropology’s search for the “missing link,” or the physicist’s search for a “unified field theory,” psychologists and social workers have spent decades hunting for the mythical gateway drug. This is the drug that, when used regularly, will head you reliably down the path of full-blown addiction. The findings of addiction medicine now make the identification of any kind of universal gateway drug an antique pursuit. Every addict finds his or her own gateway, and pushes through. If any drugs qualify as gateway drugs in a broad sense, it would have to be alcohol and tobacco, simply on the basis of ready availability.
But a gateway for full-blown recreational teenage sex—did you ever think about that? One might have thought the legislators would answer, yes, it’s called puberty, and move on. But no. The Tennessee legislature, led by Rep. Jim Gotto (R), managed to push through a bill “allowing parents to sue teachers and other outside parties for ‘promoting or condoning gateway sexual activity’ by students.”
Interestingly, the bill apparently fails to define such activity in concrete terms. Evidently, Rep. Gotto has attempted to outlaw “first base.” Or, as TPMMuckraker put it, “other things.” Gateway sexual activity is defined, according to what I shall dub the bill’s "money" sentence, “sexual conduct encouraging an individual to engage in a non-abstinent behavior.” Okay, then. Earnest glances, hair tossing, hand holding—all potentially actionable, should any sex ed teachers be caught “promoting” such activities.
And not without reason: According to data released last month by the National Center for Health Statistics, the states with the highest teen birth rate in 2010 include Tennessee, which ranked 10th worst with 43.2 births per 1,000 teenage girls. And according to a 2009 risk behavior study in Memphis City, 61 percent of high school students have had sex, along with 27 percent of middle school students, putting Memphis City, and by extension Tennessee, considerably above the national average.
Apparently, the real target here is Planned Parenthood, which has been known to provide sex education information in Tennessee schools, and which would be facing fines and penalties under the new law. The bill calls for abstinence-only instruction.
Photo Credit: http://cbcpforlife.com/?p=4277
Smoked marijuana reduced spasticity in a small trial of MS patients.
The leading wedge of the medical marijuana movement has traditionally been centered on pot as medicine for the effects of chemotherapy, for the treatment of glaucoma, and for certain kinds of neuropathic pain. From there, the evidence for conditions treatable with marijuana quickly becomes either anecdotal or based on limited studies. But pharmacologists have always been intrigued by the notion of treating certain neurologic conditions with cannabis. Sativex, which is sprayed under the tongue as a cannabis mist, has been approved for use against multiple sclerosis, or MS, in Canada, the UK, and some European countries. (In the U.S., parent company GW Pharma is seeking FDA approval for the use of Sativex to treat cancer pain).
There is accumulating evidence that cannabinoid receptors may be involved in controlling spasticity, and that anandamide, the brain’s endogenous form of cannabis, is a specific antispasticity agent.
Additional evidence that researchers may be on to something appeared recently in the Canadian Medical Association Journal. Dr. Jody Corey-Bloom and coworkers at the University of California in San Diego conducted a small, placebo-controlled trial with adult patients suffering from poorly controlled spasticity. Thirty participants were randomly divided into two groups. Those in the first group were given a daily joint, and those in the second group received “identical placebo cigarettes.” After three days, the investigators found that smoked marijuana resulted in a reduction in treatment-resistant spasticity, compared to placebo.
Clearly, it’s hard for a study of this sort to be truly blind: Participants, one presumes, had little trouble distinguishing the medicine from the placebo. And in fact, an appendix to the study shows this to be true: “Seventeen participants correctly guessed their treatment phase for all six visits… For the remaining participants, cannabis was correctly guessed on 33/35 visits.” This raises the question of various kinds of self-selection bias and expectancy effects, and the study authors themselves write that the results “might not be generalizable to patients who are cannabis-naïve.” On the other hand, cannabis-naïve patients were in the minority. The average age of the participants was 50, and fully 80% of them admitted to previous “recreational experience” with cannabis. (I don’t have a good Baby Boomer joke for the occasion, but if I did, this is where it would go).
I asked Dr. Corey-Bloom about this potential problem in an email exchange: “The primary outcome measure was the Ashworth Spasticity Scale, which is an objective measure, carried out by an independent rater,” she wrote. “Their job was just to come in and feel the tone around each joint (elbow, hip, knee), rate it, and leave. That's why we think it was so important to have an objective measure, rather than just self-report.”
With all this in mind, the study found that “smoking cannabis reduced patient scores on the modified Ashworth scale by an average of 2.74 points.” The authors conclude: “We saw a beneficial effect of smoked cannabis on treatment-resistant spasticity and pain associated with multiple sclerosis among our participants.”
Other studies have found similar declines in spasticity from cannabinoids, but have tended not to use marijuana in smokable form.
Corey-Bloom, J., Wolfson, T., Gamst, A., Jin, S., Marcotte, T., Bentley, H., & Gouaux, B. (2012). Smoked cannabis for spasticity in multiple sclerosis: a randomized, placebo-controlled trial Canadian Medical Association Journal DOI: 10.1503/cmaj.110837
Photo Credit: http://blog.amsvans.com/
Review of The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition.
Part I
It’s easy to think of cigarettes, and the machinations of the tobacco industry, as “old news.” But in his revealing 737-page book, The Golden Holocaust, based on 70 million pages of documents from the tobacco industry, Stanford professor Robert N. Proctor demonstrates otherwise. He demonstrates how Big Tobacco invented freebasing. He shows how they colluded in misleading the public about “safe” alternatives like filters, “low-tar,” and “ultra-lights.” We discover in Lorillard’s archives an explanation of menthol’s appeal to African Americans: It is all part of a desire by “negroes” to mask a “genetic body odor.” Radioactive isotopes were isolated in cigarette smoke, and evidence of the find was published, as early as 1953. He reveals that the secret ingredient in Kent’s “micronite filter” was asbestos. And he charges that the “corruption of science” lies behind the industry’s drive to continue its deadly trade. “Collaboration with the tobacco industry,” writes Proctor, “is one of the most deadly abuses of scholarly integrity in modern history.”
Half of all cigarette smokers will die from smoking—about a billion people this century, if present trends continue. In the U.S., this translates into roughly two jumbo jets crashing, killing everyone onboard, once daily. Cigarettes kill more people than bullets. The world smokes 6 trillion of them each year. (The Chinese alone account for about 2 trillion). Some people believe that tobacco represents a problem (more or less) solved, at least in the developed West.
All of this represents a continuing triumph for the tobacco industry. The aiders and abettors of tobacco love to portray the tobacco story as “old news.” But as Stanford Professor Robert M. Proctor writes in The Golden Holocaust, his exhaustive history of tobacco science and industry: “Global warming denialists cut their teeth on tobacco tactics, fighting science with science, creating doubt, fostering ignorance.”
Checking in at 737 pages, The Golden Holocaust is nobody’s idea of a light read, and at times its organization seems clear only to the author. But what a treasure trove of buried facts and misleading science Proctor has uncovered, thanks to more than 70 million pages of industry documents now online (http://legacy.library.ucsf.edu) as part of the Master Settlement Agreement of 1998. Once the material was finally digitized and available online, scholars like Proctor could employ full-text optical character recognition for detailed searchability. Ironically, this surreal blizzard of documentation was meant to obscure meaningful facts, not make them readily available, but tobacco executives seem not to have factored in digital technology when they turned over the material.
The single most important technological breakthrough in the history of the modern cigarette was flue-curing, which lowers the pH of tobacco smoke enough to make it inhalable. The reason few people inhale cigars, and very few used to inhale cigarettes, is that without some help, burning tobacco has a pH too high for comfortable inhalation. It makes you cough. But flue-curing lowered pH levels, allowing for a “milder,” less alkaline smoke that even women and children could tolerate.
World War I legitimized cigarettes in a major way. Per capita consumption in the U.S. almost tripled from 1914 to 1919, which Proctor considers “one of the most rapid increases in smoking ever recorded.” After World War II, the Marshall Plan shipped a staggering $1 billion worth of tobacco and other “food-related items.” (The U.S. Senator who blustered the loudest for big postwar tobacco shipments to Europe was A. Willis Robertson of Virginia, the father of televangelist Pat Robertson.)
The military, as we know, has historically been gung-ho on cigarettes. And Proctor claims that “the front shirt pocket that now adorns the dress of virtually every American male, for example, was born from an effort to make a place to park your cigarette pack.” In addition, cigarette makers spent a great deal of time and effort convincing automakers and airline manufacturers to put ashtrays into the cars and planes they sold. Ashtrays were built into seats in movie theaters, barbershops, and lecture halls. There was even an ashtray built into the U.S. military’s anti-Soviet SAGE computer in the 50s.
In the early 50s, research by Ernest Wynder in the U.S. and Angel Roffo in Argentina produced the first strong evidence that tobacco tars caused cancer in mice. Roffo in particular seemed convinced that tobacco caused lung cancer, that it was the tar rather than the nicotine, and that the main culprits were the aromatic hydrocarbons such as benzpyrene. Curiously enough, it was influential members of Germany’s Third Reich in the 40s who first took the possibility of a link seriously. Hans Reiter, a powerful figure in public health in Germany, said in a 1941 speech that smoking had been linked to human lung cancers through “painstaking observations of individual cases.”
In the December 1953 issue of Cancer Research, Wynder, et al. published a paper demonstrating that “tars extracted from tobacco smoke could induce cancers when painted on the skins of mice.” As it turns out, the tobacco industry already knew it. Executives had funded their own research, while keeping a close eye on outside academic studies, and had been doing so since at least the 30s. In fact, French doctors had been referring to cancers des fumeurs, or smokers’ cancers, since the mid-1800s. All of which knocks the first leg out from under the tobacco industry’s classic position: We didn’t know any stuff about cancer hazards until well into the 1950s.
Only weeks after the Wynder paper was published, tobacco execs went into full conspiracy mode during a series of meetings at the Plaza Hotel in New York, “where the denialist campaign was set in motion.” American Tobacco Company President Paul Hahn issued a press release that came to be known as the “Frank Statement” of 1954. Proctor calls it the “magna carta of the American’s industry’s conspiracy to deny any evidence of tobacco harms.” How, Proctor asks, did science get shackled to the odious enterprise of exonerating cigarettes? The secret was not so much in outright suppression of science, though there was plenty of that: In one memorable action known as the “Mouse House Massacre,” R.J. Reynolds abruptly shut down their internal animal research lab and laid off 26 scientists overnight, after the researchers began obtaining unwelcome results about tobacco smoke. But the true genius of the industry “was rather in using even ‘good’ science, narrowly defined, as a distraction, something to hold up to say, in effect: See how responsible we are?”
Entities like the Council for Tobacco Research engaged in decoy research of this kind. As one tobacco company admitted, “Research must go on and on.”
A good deal of the industry’s research in the 50s and 60s was in fact geared toward reverse engineering competitors’ successes. Consider Marlboro. Every cigarette manufacturer want to know: How did they do it? What was the secret to Marlboro’s success?
As it turns out, they did it by increasing nicotine’s kick. And they accomplished that, in essence, by means of freebasing, a process invented by the cigarette industry. Adding ammonia or some other alkaline compound transforms a molecule of nicotine from its bound salt version to its “free” base, which volatilizes much more easily, providing low-pH smoke easily absorbed by body tissue. And there you have the secret: “The freebasing of cocaine hydrochloride into ‘crack’ is based on a similar chemistry: the cocaine alkaloid is far more potent in its free base form than as a salt, so bicarbonate is used to transform cocaine hydrochloride into chemically pure crack cocaine.” Once other cigarette makers figured out the formula, they too began experimenting with the advantages of an “enhanced alkaline environment.”
(End of Part I)
Photo Credit: http://theloungeisback.wordpress.com/
A review of The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition
Part II
The famous Surgeon General’s Report of 1964, officially warning Americans about the dangers of smoking, and publicizing the cancer connection, is typically seen as a triumphal moment in American medical history. But according to Stanford history professor Robert Proctor in his book, The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition, the report was “flawed in a number of interesting respects.” [The author, above, with paraphernalia] For one thing, members of the advisory committee consulting on the report, many of them congressman friendly to the tobacco cause, succeeded in their attempts to have smoking referred to as a “habit” rather than as addiction—a shameful Orwellian turn that went uncorrected for 25 years.
Meanwhile, the industry continued to fund new institutes, and continued to give out research grants for “red herring” research. As an example, the highest-ranking officer of the American Heart Association received money from one of the industry’s fraudulent research arms.
As late as the early 80s, most smokers believed they suffered from a bad habit, rather than an addiction—even though a majority of them wished they didn’t smoke. That is an odd kind of consumer “choice.” Cigarette makers have spent millions to perpetuate this myth. Proctor views tobacco industry executives and lawyers as a unique form of disease vector, spreading the pernicious health consequences of smoking across the globe.
The 2008 World Health Organization (WHO) Report on the Global Tobacco Epidemic fleshes out this metaphor, suggesting that all epidemics have a means of contagion, “a vector that spreads disease and death. For the tobacco epidemic, the vector is not a virus, bacterium or other microorganisms—it is an industry and its business strategy.”
In an email exchange, I asked Professor Proctor to expand on this notion of a disease vector:
“We tend to divide "communicable" from "non-communicable" diseases,” Proctor told me, “when the reality is that many "non-communicable" diseases are in fact spread by communications.”
Examples? “Through ignorance and propaganda, for example, which can spread like a virus,” Proctor wrote. “We don't count the anthropogenic communications, oddly enough, even though these can be just as dangerous, and just as deadly. And just as preventable--by changing our exposure environments.”
In a recent article for Tobacco Control, Proctor laid out how the calculus of the disease vector plays out. We know, for example, that smoking will cause roughly 6 million deaths in 2015. And about a third of those will be from lung cancer. We know that 25 acres of tobacco plants will result in about 10 lung cancer deaths per year, starting 20 or 30 years down the road. Here’s a sick equivalence: “A 40 ft container of the sort shipped overseas or trucked by highway houses 10 million cigarettes, which means that each container will cause about 10 deaths.” Proctor works out the numbers for the value of a human life:
“Cigarette companies make about a penny in profit for every cigarette sold, or about $10,000 for every million cigarettes purchased. Since there is one death for every million cigarettes sold (or smoked), a tobacco manufacturer will make about $10,000 for every death caused by their products…. The value of a human life to a cigarette manufacturer is therefore about $10,000.”
Proctor has even produced a “factories of death” chart, illustrating that arguably the world’s most lethal production plant is Philip Morris’s Richmond cigarette facility, which churned out 146 billion cigarettes in 2010, which adds up to about 146,000 deaths per year.
By 1964, researchers at Harvard had already identified the presence of radioactivity in the form of polonium 210 in cigarette smoke, and the cry went up for safety. As for the notion of safer cigarettes, Proctor says all cigarette filters function the same way—“basically like drinking through a somewhat thinner straw.” He goes even further, arguing that “filters have reduced smoke particle size, producing cancers deeper in the lungs, making them harder to identify and harder to treat.” (Scientists determined that the radiation source was the newer “superphosphate” fertilizers being used heavily on tobacco plants.)
Next came mandated “tar and nicotine numbers,” which turned out to be misleading measures obtained from smoking robots. Then, “an opportunity presented itself to game the system, as we find in the brilliant trick of ventilation.” Manufacturers pricked tiny holes in the paper near the mouthpiece of cigarettes brands like Carlton and True, which consumers got around by covering the holes with fingers or with “lipping” behavior. “Low tars were a fraud, just as “lights” would be,” Proctor writes. Smokers just smoked harder, or differently, or more frequently. In 1983, pharmacologist Neal Benowitz at UCSF broke the official news in the New England Journal of Medicine: Smokers got just as much nicotine, whether they smoked high-, low-, filtered, unfiltered, regular, light, or ultra-light. The industry itself had known this for more than 20 years. “Nicotine in the actual rod was rarely allowed to drop below about 10 milligrams per cigarette,” Proctor asserts, “and no cigarette was ever commercially successful with much less than this amount.” (A Philip Morris psychologist compared nicotine-free cigarettes to “sex without orgasm.”)
Indeed, almost every design modification put in place by tobacco companies over the past century, from flue-curing to filters, has served to make cigarettes deadlier than before. “Talk of ‘safer cigarettes’ is rather like talking about safer terrorism, or safer smallpox, or safer forms of drowning,” Proctor concludes.
And the industry testing continues. The point of tobacco-sponsored research is not simply to discredit an individual researcher’s work, but to create an aggregate bias in the pattern of research—a lot of “noise” in the signal. In other words, “you basically fund lots of research to dispute a hazard, then cite this same research to say that lots of scholars dispute it.” We are told about “mucociliary escalators,” which dredge the tar up and out of smokers’ lungs. We learn that “a rabbit will scream if nicotine is introduced into the eye.” We read excerpts from anguished letters to tobacco companies: “Do you suppose if I continue to smoke Camel Ultra Light Cigarettes and I should develop cancer it will be ‘Ultra Light Cancer?’”
Proctor brings us up to date: Harm reduction, he writes, has become the industry’s new mantra. “The companies now want us to believe that less hazardous products can be and are being made and marketed.” Proctor thinks harm reduction “may end up causing even greater harm” if products touted as “safer” make smokers less likely to quit. As for public health campaigns, “consumers are encouraged to stop consuming,” Proctor writes, “but producers are never discouraged from producing.” Or, as Louis Pasteur once wrote: “When meditating over a disease, I never think of finding a remedy for it, but, instead, a means of preventing it.”
So, what comes next? A glimpse of the future may already be here, in the form of cinnamon- and mint-flavored Camel Orbs, “which look like Tic Tac candy and contain about a milligram of nicotine in a highly freebased form.”
As for the industry’s success in corrupting scientists and academics through various means, the story is just as bad as you think it is: “It would take many thousands of pages to chronicle the full extent of Big Tobacco’s penetration of academia; the scale of such collaborations is simply too vast. From 1995 to 2007 alone, University of California researchers received at least 108 awards totaling $37 million from tobacco manufacturers….”
Part II of III.
Photo Credit: http://theloungeisback.wordpress.com/
A review of The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition
Part III
Academic collaborations come in many flavors. Just because the money is corporate doesn’t mean the studies that are funded are flawed by definition. But the cigarette industry’s academic philanthropy set new records for hubris, writes Robert Proctor, professor of history at Stanford University, in his new book, The Golden Holocaust. Duke University and Bowman Gray School of Medicine, both in North Carolina, are named for tobacco magnates.
Harvard has a long and dubious history of tobacco largesse. Harvard’s Tobacco and Health Research Program kicked off in 1972 with a generous tobacco grant from the Tobacco Institute, who dreamed up the program in the first place. “The Harvard project made the industry look good and so was handsomely endowed, absorbing $7 million over an eight-year period.” Also in 1972, Harvard anthropologist Carl Seltzer testified for the industry in numerous public hearings, stating: “We do not know whether or not there is a causal relationship between smoking and heart disease.” In 2002, Harvard’s School of Public Health declared it would no longer undertake research sponsored by the cigarette industry. Many universities had already gone cold turkey, and after Harvard, bans were put in place by the Karolinska Institute, Johns Hopkins University, Emory University, and many others.
Proctor informs us that “Washington University in St. Louis has been another big sponge for tobacco money." In 1971, the university set a new world record for an industry grant to a single institution, and “millions more were eventually funneled into the School of Medicine, turning it into a hotbed of cigarette-friendly activism.” The irony of taking money from Big Tobacco to fund research on lung cancer is not lost on Proctor. A good deal of the research was aimed away from tobacco and toward possible causes like viruses. “The goal was clearly more than cancer cures,” he writes. “The industry also hoped to generate good PR and academic allies.” The industry was able to garner sympathetic headlines, like “Helping in Fight against Cancer,” in the St. Louis Globe-Democrat.
The other academic hotbed thoroughly penetrated by Big Tobacco was UCLA, according to Proctor. “Tobacco collaborators at UCLA have attracted their fair share of criticism from public health advocates, and for understandable reasons.” The university picked up its own multimillion-dollar grant from cigarette makers for the Program on Tobacco and Health in 1974, and that wasn’t the first tobacco money the university had taken. “As with all such projects,” Proctor writes, “industry lawyers… played a key role in the decision to fund—with the companies also conceding that the decision ‘should be based more on public relations than on purely scientific grounds.’” The end came in 2007, when “UCLA’s dance with the devil” garnered a ton of unwanted press. Reports showed that UCLA had taken more than $6 million from Philip Morris for research “to compare how children’s brains and monkey brains react to nicotine.”
Proctor admits that singling out Harvard, Washington University and UCLA is somewhat misleading, “given that scholars throughout the world have gorged themselves on tobacco money. Indeed it may well be the rare institution that has NOT at one time or another dipped into this pot.”
Including Stanford, where Proctor teaches. Plenty of Stanford researchers have undertaken contract work and served as expert witnesses for the industry right in Proctor’s own backyard, where “at least eighteen faculty members have received monies (in the form of sponsored research) from the Council for Tobacco Research, with at least two of these—Judith Swain and Hugh McDevitt from the medical school—serving on its Scientific Advisory Board. Stanford pharmacologists were assisting the industry with its diethylene glycol studies as early as the 1930s…”
In the conclusion to his densely researched but surprisingly readable work, Proctor returns to the controlling irony of the book: “Our bizarre starting point is the well-stocked shelf of cigarettes, to which we respond by begging people not to purchase them.” He presents the dream of a world in which cigarettes have been abolished. To do so, he admits, would require a leap. “If phasing out tobacco seems out of reach, this is only because our imaginations are impoverished.” And he has scant patience for the “Prohibition failed” argument. It failed, he says, because people like to drink. “Tobacco presents us with a very different situation. Nicotine is not a recreational drug. Most people who smoke wish they didn’t, and most smokers (90 percent) regret ever having started.”
Graphics Credit: http://www.prwatch.org/node/7004
The sons of Red Bull are sporting record concentrations of caffeine.
via addiction - Google News on 6/5/12
The DSM Gets Addiction Right
New York Times WHEN we say that someone is “addicted” to a behavior like gambling or eating or playing video games, what does that mean? Are such compulsions really akin to dependencies like drug and alcohol addiction — or is that just loose talk? Pope Benedict knows that this is the age of addictionCatholic Herald Online (blog) all 2 news articles » |
via addiction - Google News on 6/4/12
 The Atlantic |
Can These 6 Questions Tell You If You're Clinically Addicted to Facebook?
The Atlantic By Brian Fung In a society awash with digital media, concerns about addiction are natural. But are they unfounded? American medical discourse is chock full of addictions these days. There's video game addiction. Porn addiction. Gambling addiction. Are you addicted to Facebook?WTOP Addicted To Facebook? Answer These 6 Questions To Find Out!The Frisky all 4 news articles » |
via Addiction Inbox by Dirk Hanson on 4/29/12
A screen for problem gambling, medications for insomniac alcoholics, and more.
A group of addiction doctors presented a Top Ten List of peer-reviewed articles from 2011 at the American Society of Addiction Medicine’s Annual Medical-Scientific Conference in Richmond, VA. Dr. Michael Weaver presented the findings, noting that the list was “reached by consensus, and articles were selected not only for their quality but also to represent different areas of addiction medicine.” Dr. Weaver stressed that “not all published studies were done really well, and some may not apply to the patients treated by a particular clinician.”
According to Dr. Edward Nunes, with the Department of Psychiatry at Columbia University, the journal articles provide a "nice mixture on epidemiology and clinical outcome or clinical trials research,” which represent “the type of evidence most relevant to patient care."
Thanks to Catharine Zivkovic (@ccziv) for drawing attention to this list. The summaries are my own. Disclaimer: In some cases, these brief summaries are based solely on a reading of the journal abstracts.
1.
Hsueh-Han Yeh, M.S. et al. (2011). Five-Year Trajectories of Long-Term Benzodiazepine Use by Adolescents: Patient, Provider, and Medication Factors. Psychiatric Services 62(8): 900–907.
A Taiwanese study analyzing benzodiazepine prescription records came up with a simple solution: “Prescribers can reduce the risk of long-term use by assessing whether pediatric patients have received benzodiazepines from multiple doctors for various medical conditions.” Huh. Who’d have thought of that one, eh? But for various reasons, such checks, and the open records required to make them possible, are the exception rather than the rule in current health care systems. The study group found that for long-term users under 21, defined as anyone in receipt of a benzodiazepine prescription for 31 or more days in a calendar year, one in four patients fell into the categories of “accelerating or chronic users.” Specifically, “A history of psychosis or epilepsy, prescription by providers from multiple specialties, and receipt of benzodiazepines with a long half-life or mixed indications significantly increased one's risk of becoming a chronic or accelerating user.”
2.
McBride, O, and Cheng, Hui G. (2011) Exploring the emergence of alcohol use disorder symptoms in the two years after onset of drinking: findings from the National Surveys on Drug Use and Health. Addiction 106(3): 555-563.
This study looked for clinical features of alcohol dependence and socially maladaptive drinking patterns during the first 24 months of alcohol use, based on stats from the 2004-2007 National Surveys on Drug Use and Health (NSDUH). Result: New alcohol users “frequently experienced problems relating to self-reported tolerance, spending a great deal of time recovering from the effects of alcohol and unsuccessful attempts at cutting down on drinking. The likelihood of experiencing the clinical features increased steadily in the first 9 months after use, but appeared to plateau or only gradually increase thereafter.” The researchers suggest there may be a window of opportunity during the 2nd year of drinking.
3.
Volberg, Rachel A., et al. (2011) A Quick and Simple Screening Method for Pathological and Problem Gamblers in Addiction Programs and Practices. The American Journal on Addictions. 20(3): 220-227.
Doctors, as these researchers point out, don’t often screen their patients for pathological gambling. To combat this, the investigators offer health professionals brief computer screenings they have developed for use in identifying problem gambling. “Given the high rates of comorbidity, routine and accurate identification of gambling-related problems among individuals seeking help for substance abuse and related disorders is important.”
4.
Alford, Daniel. P., et al. (2011). Collaborative Care of Opioid-Addicted Patients in Primary Care Using Buprenorphine: Five-Year Experience. Archives of Internal Medicine 171(5):425-431.
Buprenorphine remains an underused but often effective treatment for opiate addiction, the authors of this study maintain. The cohort being studied was a group of addicted patients under the dual care of general physicians and nurse care managers. “Of patients remaining in treatment at 12 months, 154 of 169 (91.1%) were no longer using illicit opioids or cocaine based on urine drug test results,” the investigators report. However, dropout rates were high. The researchers did find that the nurse-doctor model was workable: “Collaborative care with nurse care managers in an urban primary care practice is an alternative and successful treatment method for most patients with opioid addiction that makes effective use of time for physicians who prescribe buprenorphine.”
5.
Kolla, B.P., et. al. (2011) Pharmacological Treatment of Insomnia in Alcohol Recovery: A Systematic Review. Alcohol and Alcoholism 46: 578-585.
In this Mayo Clinic review of drugs used for sleep problems in alcohol recovery, the authors combed through more than 1,200 articles and reported that, of all the old and new drugs being used, an old and rarely used medication—trazadone—improved sleep measures as reliably as anything else that was tested. Gabapentin got good but equivocal marks due to questions about testing and inclusion criteria. Topiramate and carbamazepine helped in some cases. Furthermore, “in single, small, mostly open-label studies, quetiapine, triazolam, ritanserin, bright light and magnesium have shown efficacy, while chlormethiazole, scopolamine and melperone showed no difference or worsening. Conclusion: Trazodone has the most data suggesting efficacy.”
6.
Bohnert, A.S., et. al. (2011). Association between opioid prescribing patterns and opioid overdose-related deaths. Journal of the American Medical Association 305: 1315-1321.
Accidental prescription overdose deaths are on the rise, and this group of university researchers in Ann Arbor and Indianapolis thinks it may have something to do with how the dosing instructions are usually worded. They set out to investigate “the association of maximum prescribed daily opioid dose and dosing schedule (“as needed,” regularly scheduled, or both) with risk of opioid overdose death among patients with cancer, chronic pain, acute pain, and substance use disorders.” They found from VHA hospital records that “the frequency of fatal overdose over the study period among individuals treated with opioids was estimated to be 0.04%.” The risk for overdose was directly related to the “maximum prescribed daily dose of opioid medication.” And patients who stuck with regular dosages, or took opioids “as needed,” were not at any elevated risk for overdose. Another obvious but frequently overlooked conclusion: “Among patients receiving opioid prescriptions for pain, higher opioid doses were associated with increased risk of opioid overdose death.”
7.
Allsop, D.J. et al. (2011). The Cannabis Withdrawal Scale development: patterns and predictors of cannabis withdrawal and distress. Drug and Alcohol Dependence 19(1-2):123-9.
Rates of treatment for marijuana abuse and addiction are increasing, say these Australian authors, along with relapse rates. They have devised a Cannabis Withdrawal Scale that measures such withdrawal effects as associated distress, strange dreams, trouble sleeping, and angry outbursts—common manifestations of withdrawal from weed. The scientists maintain that their “Cannabis Withdrawal Scale can be used as a diagnostic instrument in clinical and research settings where regular monitoring of withdrawal symptoms is required.”
8.
West, R., et al. (2011) Placebo-Controlled Trial of Cytisine for Smoking Cessation. New England Journal of Medicine 365: 1193-1200.
This important study assessed the effectiveness of the drug cytisine in smoking cessation programs, and a potential star was born. In a single-center, randomized, double-blind, placebo-controlled trial, the journal paper concluded that “cytisine was more effective than placebo for smoking cessation. The lower price of cytisine as compared with that of other pharmacotherapies for smoking cessation may make it an affordable treatment to advance smoking cessation globally.”
9.
Elkashef A., et al. (2011) Topiramate for the treatment of methamphetamine addiction: a multi-center placebo-controlled trial. Addiction Published online 12/16.
Conducted at eight medical centers across the U.S., this study found that for most of the 140 methamphetamine-dependent adults under scrutiny, use of topiramate produced “abstinence from methamphetamine during weeks 6-12.” That’s the good news. Unfortunately, “secondary outcomes included use reduction versus baseline, as well as psychosocial variables… topiramate did not increase abstinence from methamphetamine during weeks 6-12.” That’s the bad news. And here’s the silver lining, as far as the investigators are concerned: “Topiramate does not appear to promote abstinence in methamphetamine users but can reduce the amount taken and reduce relapse rates in those who are already abstinent.”
10.
Levina. A., et al. (2011). Molecular Mechanism for a Gateway Drug: Epigenetic Changes Initiated by Nicotine Prime Gene Expression by Cocaine. Science Translation Medicine 3(107) 107-109.
There really is s a gateway drug. In fact, there are two of them in our culture. Almost every potential addict starts out with alcohol or cigarettes or both. Because they are legal and easily available. So is cocaine and marijuana, once you get the hang of it, but in the beginning, and all around us, it’s booze and cigs. The amazing premise of this final study is this: “Pretreatment of mice with nicotine increased the response to cocaine, as assessed by addiction-related behaviors and synaptic plasticity in the striatum, a brain region critical for addiction-related reward.” Nicotine primes subjects for cocaine addiction, in effect. “These results from mice prompted an analysis of epidemiological data, which indicated that most cocaine users initiate cocaine use after the onset of smoking and while actively still smoking, and that initiating cocaine use after smoking increases the risk of becoming dependent on cocaine, consistent with our data from mice. If our findings in mice apply to humans, a decrease in smoking rates in young people would be expected to lead to a decrease in cocaine addiction.”
Photo Credit: www.flickr.com/
via addiction - Google News on 6/4/12
 Forbes |
The Straight Dope on What Bath Salts Do to Your Brain and Why They're Dangerous
Forbes Bath salts are dangerous for chiefly two reasons, and neither have anything to do with addiction or hallucinations. The first reason is dosage, and the second is sleep deprivation. Before addressing each of those in more detail, let's quickly go over ... and more » |
via NIDA News on 3/20/12
The structure of the kappa-opioid receptor with bound antagonist JDTic is shown resting in a poppy flower, the source of opium. Image by Yekaterina Kadyshevskaya, PSI:Biology GPCR Network, The Scripps Research Institute.
Scientists are now one step closer to developing anti-addiction medications, thanks to new research that provides a better understanding of the properties of the only member of the opioid receptor family whose activation counteracts the rewarding effects of addictive drugs.
via ASAM President's Blog on 3/27/12
ASAM Acting President Dr. Stuart Gitlow writes about reaching consensus on the use of medical marijuana and asks for public input
via Journal of Addiction Medicine - Featured Articles - Featured Articles by Crean, Rebecca D.; Tapert, Susan F.; Minassian, Arpi; MacDonald, Kai; Crane, Natania A.; Mason, Barbara J. on 2/11/11
This case describes the clinical course of a cannabis-dependent individual entering a 12-week abstinence-based research program. The case illustrates the effects of chronic, heavy cannabis use on executive functions at 3 time points: (1) 12 hours of abstinence; (2) 4 weeks of abstinence; and (3) 12 weeks of abstinence. It is followed by discussions by 2 clinical psychologists and a psychiatrist. The findings described here have important clinical implications, because executive functions have a vital role in treatment participation and in sustaining recovery. It should be of particular interest to clinicians who work with people with cannabis use disorders.
via addiction - Google News on 6/6/12
 Nanaimo Daily News |
Addicted newborns 'national emergency'
Windsor Star Dr. Pradeep Merchant - seen here through an empty incubator in the neonatal unit at the Ottawa Civic Hospital - has seen a dramatic increase in the number of babies born to women addicted to prescription drugs such as OxyContin. More babies born addicted to painkillersVancouver Sun More babies being born hooked on prescription painkillersOttawa Citizen all 16 news articles » |
via addiction - Google Blog Search by Turtle on 6/5/12
The University of Texas' Waggoner Center For Alcohol and Addiction Research received a $3.3 million dollar grant from the National Institute on Alcohol Abuse and Alcohol in hopes to develop a drug to treat alcoholism.
via Journal of Addiction Medicine - Most Popular Articles by Calcaterra, Susan; Blatchford, Patrick; Friedmann, Peter D.; Binswanger, Ingrid A. on 5/31/12
Objectives: Psychostimulants are highly addictive and their use is increasing. Little is known about psychostimulant-related deaths. This study identified characteristics, risk factors, and contributing substances reported upon death among former prison inmates who died from a psychostimulant-related death. Methods: This retrospective cohort study of released inmates from 1999 to 2003 (N = 30,237) linked data from the Washington State Department of Corrections with the National Death Index. We examined characteristics of individuals who died with psychostimulants listed among their causes of death. These were categorized into 3 groups: (1) noncocaine psychostimulants, (2) cocaine only, and (3) all psychostimulants. Cox proportional hazards regression determined risk factors for death in each group, and the risk of death in the first 2 weeks after release from prison Results: Of the 443 inmates who died, 25 (6%) had noncocaine psychostimulants listed among their causes of death. Six of these 25 deaths had both noncocaine psychostimulants and cocaine listed among their causes-of-death. Most of the former inmates who died with noncocaine psychostimulants were male (n = 21, 84%) and non-Hispanic white (88%, n = 22). Cocaine only was listed among the causes-of-death for 49 former inmates; most were male (n = 35, 71%) and non-Hispanic white (n = 27, 55%). Longer length of incarceration was associated with a reduced risk of death from any psychostimulant use (hazard ratio = 0.76, confidence interval = 0.63–0.920 for each additional year of incarceration) and from use of noncocaine psychostimulants (hazard ratio = 0.42, 95% CI = 0.22–0.80). Risk of death was highest during the first 2 weeks postrelease for cocaine only–related deaths (incidence mortality ratio = 1224.0, confidence interval = 583–1865). Conclusions: Former prisoners have a significant risk of death from psychostimulants, especially within the first 2 weeks postrelease.
via Addiction Inbox by Dirk Hanson on 5/8/12
One woman’s journal.
From Insanity to Serenity, by Tommi Lloyd
Excerpts:
"I was born in 1963 in Toronto, Canada, to a family struggling long before I arrived. My dad was an alcoholic, born in Wales in 1921. His father and namesake was also an alcoholic who died at age 28…. My oldest sibling and only brother, Harry, entered a treatment centre at age 36 and has been sober for more than 20 years…. My Uncle Griff died from alcoholism when I was 10 years old…. There were no reprieves by which we spent a day or two in a sober environment. Dad drank from morning until night…. Christmas, Thanksgiving, and Easter—these were some of the worst days of the year…. Santa started leaving a carton of cigarettes next to my stocking at Christmas and I thought it was great.
"I yearned for some quality time before his drinking took center stage for the day… he drank from the minute he got up to the minute he passed out. At the height of his addiction, he was drinking more than 40 ounces of vodka a day…. There were many times when I would walk into the bedroom and see him guzzling the vodka straight from the bottle. It made me feel physical ill and utterly helpless.
"I too, am an alcoholic. In addition to alcohol, my teenage love of marijuana turned into a 30-year affair…. I have two nephews who are addicted to marijuana…. Rather than being sloppy drunks, my nephews opted for the mellow alternative that’s not addictive, (so we like to think) and you can pay for your habit by selling it to your friends.
"By age 11 I tried drinking for the first time…. I recall Susie telling us we could try drinking, but it had to be done quickly so as not to get caught. We poured some very strong rum and cokes and I guzzled mine down by holding my nose with my free hand…. As soon as I lay down on my bed the room started spinning and it wasn’t long before I was throwing up. Mom fussed over me, concluding I had the flu and I recall feeling both happy and guilty at the same time. I loved the attention but felt badly for the cause of my illness. I didn’t drink again for a few years….
"There is nothing more validating for me as a mother than to know I’m an inspiration to my children. I could not have asked for a better gift. This is what sobriety and a renewed spiritual life has brought my children and me…. Intellectually, I recognize how my childhood experiences and the disease of alcoholism molded a lot of my behavior and have been the root of much of my struggle with self-esteem. But self-knowledge does not change our circumstances, action does."
via Addiction Inbox by Dirk Hanson on 6/4/12
It’s getting harder to interpret genetics studies, and that’s a good thing.
Reporting the results of published studies concerned with genetic risk factors has always been a tricky proposition. Beyond the inevitable, and too often ideological nature/nurture split, there has been an unfortunate history of false positives in the rush to make news with a “gene for” alcoholism or schizophrenia or belief in God.
But single gene theories are mostly a thing of the past, and results tend to be broader and more tentative, as befits the state of our knowledge about genes and
risk in a post-epigenetic landscape. Nonetheless, there’s no denying that genes play a strong role in all kinds of behaviors and processes. A large group of U.S. tobacco researchers went looking for associations between genetic risk factors and the ability to stop smoking successfully, and published their results in the American Journal of Psychiatry. The group came down strongly in favor of the proposition that genetic variations in the chromosome 15q25 region help dictate who manages to quit smoking and who does not. The genetic variants in question are for nicotine receptors, and are called CHRNA5-CHRNA3-CHRNB4. They compose a “high-risk haplotype” that Li-Shiun Chen and coworkers believe to be involved in the ability to quit. (A haplotype is a combination of DNA sequences on a chromosome that are transmitted as a unit). People with these genetic variants “quit later than those at low genetic risk; this difference was manifested as a 2-year delay in median quit age.” However, this association tended to wash out at very high levels of smoking. Nonetheless, “pharmacological cessation treatment significantly increased the likelihood of abstinence in individuals with the high-risk haplotype,” compared to the low-risk group.
The suspicious haplotypes did not reliably predict tobacco abstinence across all groups that were studied. And any pharmacological treatment at all vastly increases abstinence rates, compared to placebo, while those who smoke the fewest cigarettes per day have the best shot at abstinence no matter what. In one sense, all the study is saying is that anti-craving drugs are more likely to be effective in smokers “who are biologically predisposed to have difficulty quitting.” Other smokers may not need them at all as a quitting aid—which is very much as common sense would have it. But further research in this area may allow medical workers to genetically identify smokers who will definitely require a pharmacological booster shot to overcome their crippling addiction.
In brief, the study says that success in quitting may be directly modulated by certain types of genetic variation among smokers. And genetic variations influencing quitting success may be different from gene variants controlling for “severity of nicotine dependence” (how many cigarettes you smoke), and whether you get addicted in the first place. It is all very complicated. But it’s the sort of thing that gives researchers hope when they contemplate deploying forms of personalized medicine in addiction treatment.
Study limitations abound. The work looked at only one genetic locus, while the success of smoking cessation might depend on multiple gene sites. The placebo arm was relatively small, and the smoking reports were obtained through a combination of biochemical confirmation and self-reporting.
Baker, T. (2012). Interplay of Genetic Risk Factors (CHRNA5-CHRNA3-CHRNB4) and Cessation Treatments in Smoking Cessation Success American Journal of Psychiatry DOI: 10.1176/appi.ajp.2012.11101545
Graphics Credit: (Li-Shiun Chen)
via Addiction Inbox by Dirk Hanson on 4/25/12
Marijuana, as researchers and pundits never tire of pointing out, is the most widely used illegal drug in the world, by a serious margin. And while the argument still rages, for some years now drug researchers have been migrating to the camp that sees marijuana as an addictive drug for a minority of people who exhibit a propensity for addiction. The scientific literature supporting the contention of marijuana as addictive for some users is robust and growing, as is the body of anecdotal evidence. It’s also clear that in many countries, cultures, and subcultures, combining cannabis with tobacco is a common practice that increases health risks all around.
Ongoing work at the Scripps Research Institute’s Pearson Center for Alcoholism and Addiction Research in La Jolla, California, has focused in part on the lack of FDA-approved medical therapies for treating marijuana addiction. Barbara J. Mason and
coworkers at Scripps have reported preliminary success in a 12-week, double-blind, placebo-controlled pilot study with 50 treatment-seeking volunteers, using the anti-seizure drug gabapentin. Gabapentin, sold as Neurontin, pops up as a possible treatment for various forms of pain and anxiety, and sharp-eyed readers will recall that gabapentin was one of the ingredients in the now-defunct addiction drug Prometa.Marijuana addiction numbers are hard to come by, and often inflated, since many small-time pot offenders end up in mandatory treatment programs, where they tend to be classified as marijuana addicts, whether or not that is objectively the case. Nonetheless, there are plenty of people seeking treatment on their own for cannabis dependence. For people strongly addicted to pot, the problems are very real, and withdrawal and abstinence pose serious challenges. People for whom marijuana poses no addictive threat should bear this in mind, the way casual drinkers bear in mind the existence of alcoholism in others.
The study, published recently in Neuropsychopharmacology, says that “activation of brain stress circuitry caused by chronic heavy marijuana use” can lead to withdrawal symptoms that persist “for weeks or even months, as in the case of marijuana craving and sleep disturbances.” A variety of existing medications have been tested in recent years, including buspirone, an anti-anxiety medication; Serzone, an antidepressant; and Wellbutrin, an antidepressant commonly used for smoking cessation. None of these treatments has shown any effect on cannabis use or withdrawal, according to Mason.
Gabapentin, as the name suggests, was modeled after the neurotransmitter GABA, and works via a transporter protein to raise GABA levels. Effective only for partial-onset seizures, common side effects include drowsiness, dizziness, and possible weight gain. It is a popular anti-epileptic drug, because it is relatively safe, with a low side-effect profile, compared to many of the medications in its class. For the same reasons, it is a common treatment for neuropathic pain. In addition to neuralgia, it has found some use as a migraine preventative.
Gabapentin normalizes GABA activation caused by corticotrophin-releasing factor, or CRF. CRF is a major player in the brain’s stress responses. As it turns out, withdrawal from both cannabis and alcohol ramp up anxiety levels by increasing CRF release in the amygdala, animal studies have shown. “Gabapentin had a significant effect in decreasing marijuana use over the course of treatment, relative to placebo,” the authors report. In addition, gabapentin produced “significant reductions in both the acute symptoms of withdrawal as well as in the more commonly persistent symptoms involving mood, craving, and sleep.”
As a bonus, the researchers discovered that “overall improvement in performance across cognitive measures was significantly greater for gabapentin-treated subjects compared with those receiving placebo.” Gabapentin was associated with improvement in “tasks related to neurocognitive executive functioning”—things like attention, concentration, visual-motor functioning, and inhibition. Counseling alone, represented by the placebo group, “resulted in less effective treatment of cannabis use and withdrawal, and no improvement in executive function.”
As in the case of Chantix for cigarette cessation, a treatment, which now requires additional caveats about possible suicidal ideation, researchers looking for a treatment for drug withdrawal, must weigh the benefits of pharmacological treatment against the possible side effects of the treatment itself. Does gabapentin for marijuana withdrawal pass the “Do No Harm” test? According to Mason, it does. “Gabapentin was well tolerated and without significant side effects” in the admittedly small trial study. The two groups did not differ in the number of adverse medical events reported in the first two weeks, when dropout rates due to side effects are highest in these kinds of studies. The investigators were not relying solely on self-reporting, either. They used urine drug screens, and verified that only 3% of the study sample tested positive for other drugs.
In short, the authors report that gabapentin reduced cannabis use and eased withdrawal with an acceptable safety profile and no signs of dependence. Gabapentin, the authors conclude, “may offer the most promising treatment for cannabis withdrawal and dependence studied to date.” Further clinical research is needed, of course, but the positive results of this proof-of-concept study should make funding a bit easier.
Mason, B., Crean, R., Goodell, V., Light, J., Quello, S., Shadan, F., Buffkins, K., Kyle, M., Adusumalli, M., Begovic, A., & Rao, S. (2012). A Proof-of-Concept Randomized Controlled Study of Gabapentin: Effects on Cannabis Use, Withdrawal and Executive Function Deficits in Cannabis-Dependent Adults Neuropsychopharmacology DOI: 10.1038/npp.2012.14
Photo Credit: http://pep3799.hubpages.com/
via Addiction Inbox by Dirk Hanson on 3/18/12
“A potentially life-threatening situation.”
Earlier this month, state officials became alarmed by a cluster of puzzling health problems that had suddenly popped up in Casper, Wyoming, population 55,000. Three young people had been hospitalized with kidney injuries, and dozens of others were allegedly suffering from vomiting and back pain after smoking or snorting an herbal product sold as “blueberry spice.” The Poison Review reported that the outbreak was presently under investigation by state medical officials. “At this point we are viewing use of this drug as a potentially life-threatening situation,” said Tracy Murphy, Wyoming state epidemiologist.
It is beginning to look like acute kidney injury from the newer synthetic drugs may be a genuine threat. And if that wasn’t bad enough, continuing research has implicated MDMA, better known as Ecstasy, as another potential source of kidney damage. Recreational druggies, forewarned is forearmed.
Bath salts first. In the Wyoming case, while the drug in question may have been one of the synthetic marijuana products marketed as Spice, it’s entirely possible that the drug in question was actually one or more of the new synthetic stimulants called bath salts. (Quality control and truth in packaging are not part of this industry). The American Journal of Kidney Diseases recently published a report titled “Recurrent Acute Kidney Injury Following Bath Salts Intoxication.” It features a case history that Yale researchers believe to be “the first report of recurrent acute kidney injury associated with repeated bath salts intoxication.” The most common causes for emergency room admissions due to bath salts—primarily the drugs MDPV and mephedrone—are agitation, hallucinations, and tachycardia, the authors report. But the case report of a 26-year old man showed recurrent kidney injury after using bath salts. The authors speculate that the damage resulted from “severe renal vasospasm induced by these vasoactive substances.” (A vasoactive substance can constrict or dilate blood vessels.)
American Journal of Kidney Diseases recently published a report titled “Recurrent Acute Kidney Injury Following Bath Salts Intoxication.” It features a case history that Yale researchers believe to be “the first report of recurrent acute kidney injury associated with repeated bath salts intoxication.” The most common causes for emergency room admissions due to bath salts—primarily the drugs MDPV and mephedrone—are agitation, hallucinations, and tachycardia, the authors report. But the case report of a 26-year old man showed recurrent kidney injury after using bath salts. The authors speculate that the damage resulted from “severe renal vasospasm induced by these vasoactive substances.” (A vasoactive substance can constrict or dilate blood vessels.)
A possible secondary mechanism of action for kidney damage among bath salt users is rhabdomyolysis—a breakdown of muscle fibers that releases muscle fiber contents into the bloodstream, causing severe kidney damage. Heavy alcohol and drug use, especially cocaine, are also known risk factors for this condition. The complicating factor here is that rhabdomyolysis has also been described in cases of MDMA intoxication, and here we arrived at the second part of the story.
In 2008, the Clinical Journal of the American Society of Nephrology published “The Agony of Ecstasy: MDMA and the Kidney.” In this study, Garland A. Campbell and Mitchell H. Rosner of the University of Virginia Department of Medicine found that “Ecstasy has been associated with acute kidney injury that is most commonly secondary to nontraumatic rhabdomyolysis but also has been reported in the setting of drug-induced liver failure and drug-induced vasculitis.”
Chemically, MDMA is another amphetamine spinoff, like mephedrone and other bath salts. Many people take this club drug regularly without apparent harm, whereas others seem to be acutely sensitive and can experience serious toxicity, possibly due to genetic variance in the breakdown enzyme CYP2D6. The authors trace the first case report of acute kidney injury due to Ecstasy back to 1992, but “because most of these data are accrued from case reports, the absolute incidence of this complication cannot be determined.”
Campbell and Rosner believe that nontraumatic rhabdomyolysis is a likely culprit in many cases, and speculate that the condition is “greatly compounded by the ambient temperature, which in crowded rave parties is usually elevated.” If a physician suspects rhabdomyolysis in an Ecstasy user, “aggressive cooling measures should be undertaken to lower the patient’s core temperature to levels that will lessen further muscle and end-organ injury.” This complication can have far-reaching effects: The authors note the case history of “transplant graft loss of both kidneys obtained from a donor with a history of recent Ecstasy use.”
In addition, there may be undocumented risks to the liver as well. An earlier study by Andreu et. al. claims that “up to 31% of all drug toxicity-related acute hepatic failure is due to MDMA… Patients with severe acute hepatic failure secondary to ecstasy use often survive with supportive care and have successfully undergone liver transplantation.”
But the picture is far from clear: “Unfortunately, no case reports of acute kidney injury secondary to ecstasy have had renal biopsies performed to allow for further elucidation…” And attributing firm causation is difficult, due to the fact that MDMA users often use other drugs in combination, some of which, like cocaine, can cause kidney problem all by themselves.
A study by Harold Kalant of the University of Toronto’s Addiction Research Foundation, published in the Canadian Medical Association Journal, proposed that “dantrolene, which is a drug used to stop the intense muscle contractures in malignant hyperthermia, should also be useful in the hyperthermic type of MDMA toxicity. Numerous cases have now been treated in this way, some with rapid and dramatic results even when the clinical picture suggested the likelihood of a fatal outcome.”
Adebamiro, A., and Perazella, M. (2012). Recurrent Acute Kidney Injury Following Bath Salts Intoxication American Journal of Kidney Diseases, 59 (2), 273-275 DOI: 10.1053/j.ajkd.2011.10.012
Graphics Credit: http://trialx.com
via Journal of Addiction Medicine - Featured Articles - Featured Articles by Rose, Mark E.; Grant, Jon E. on 5/26/10
Blackouts from acute alcohol ingestion are defined as the inability to recall events that occurred during a drinking episode and are highly prevalent in both alcoholic and nonalcoholic populations. This article reviews the clinical manifestations, epidemiology, risk factors, cognitive impairment, and neurobiology associated with alcohol-induced blackout, with special emphasis on the neurochemical and neurophysiological basis, and gender differences. Two types of blackout have been identified: en bloc, or complete inability to recall events during a time period, and fragmentary, where memory loss is incomplete. The rapidity of rise in blood alcohol concentration is the most robust predictor of blackout. Alcohol impairs different brain functions at different rates, and cognitive and memory performance are differentially impaired by ascending versus descending blood alcohol concentration. Cognitive and memory impairment occurs before motor impairment, possibly explaining how a drinker appearing fully functional can have little subsequent memory. Blackouts are caused by breakdown in the transfer of short-term memory into long-term storage and subsequent retrieval primarily through dose-dependent disruption of hippocampal CA1 pyramidal cell activity. The exact mechanism is believed to involve potentiation of gamma-aminobutyric acid-alpha-mediated inhibition and interference with excitatory hippocampal N-methyl-d-aspartate receptor activation, resulting in decreased long-term potentiation. Another possible mechanism involves disrupted septohippocampal theta rhythm activity because of enhanced medial septal area gamma-aminobutyric acid-ergic neurotransmission. Women are more susceptible to blackouts and undergo a slower recovery from cognitive impairment than men, due in part to the effect of gender differences in pharmacokinetics and body composition on alcohol bioavailability. (C) 2010 American Society of Addiction Medicine
via Journal of Addiction Medicine - Featured Articles - Featured Articles by Topf, Jocelyn L.; Yip, Sarah W.; Potenza, Marc N. on 9/1/09
Pathologic gambling (PG) is categorized as an impulse control disorder. Phenomenologic, neurobiologic, and pharmacologic data suggest similarities in the pathophysiologies of substance use disorders and PG. Both behavioral and pharmacologic approaches, including those that have been empirically validated for substance use disorders, have shown promise in the treatment of PG. Findings from biologic studies of PG are reviewed, and treatment approaches based on controlled studies are summarized. (C) 2009 American Society of Addiction Medicine
via Journal of Addiction Medicine - Most Popular Articles by Carnes, Patrick J.; Green, Bradley A.; Merlo, Lisa J.; Polles, Alexis; Carnes, Stefanie; Gold, Mark S. on 2/29/12
Sexual addiction is estimated to afflict up to 3% to 6% of the population. However, many clinicians lack clear criteria for detecting potential cases. Objectives: The present studies were conducted to assess the effectiveness of a brief sexual addiction screening instrument (ie, PATHOS Questionnaire) to correctly classify patients being treated for sex addiction and healthy volunteers. Methods: In study 1, a 6-item questionnaire, which utilizes the mnemonic “PATHOS,” was examined in regard to sensitivity and specificity using a sample combining patients being treated for sex addiction and healthy volunteers (970 men/80.2% patients; 938 women/63.8% patients). In study 2, a cross-validation sample of 672 men (93% patients) and 241 women (35.3% patients) completed the PATHOS screener. Results: Results of receiver operating characteristics analyses in study 1 demonstrated that the PATHOS captured 92.6% of the area under the curve and achieved 88.3% sensitivity and 81.6% specificity for classifying the male sample (n = 963) as patients and healthy subjects using a cutoff score of 3. Similarly, the PATHOS captured 90.2% of the area under the curve and, with a cutoff of 3, achieved 80.9% sensitivity and 87.2% specificity for the female sample (n = 808). In study 2, results of receiver operating characteristics analyses indicated that the PATHOS captured 85.1% of the area under the curve, with sensitivity of 70.7% and specificity of 86.9% for men (cutoff of 3). For women, the PATHOS captured 80.9% of the area under the curve and achieved 69.7% sensitivity and 85.1% specificity with the cutoff of 3. Conclusions: These studies provide support for the use of the PATHOS as a screening instrument to detect potential sexual addiction cases in clinical settings.
via Journal of Addiction Medicine - Most Popular Articles by Wolitzky-Taylor, Kate; Operskalski, Joachim T.; Ries, Richard; Craske, Michelle G.; Roy-Byrne, Peter on 11/30/11
Anxiety disorders commonly occur among those with substance use disorders. This article reviews the literature describing the prevalence and patterns of this comorbidity in epidemiological and clinical samples and theoretical models explaining this comorbidity, and reviews the effects of anxiety disorders on substance use outcomes and data from clinical trials that target comorbid anxiety disorders to examine the effects of treating anxiety disorders on substance use outcomes. Next, this review outlines evidence-based pharmacological and psychological treatments for anxiety disorders and provides treatment recommendations for those treating this comorbid population. Finally, a discussion of treatment-delivery issues is presented to address the important issues that arise when treating anxiety disorders in typical addictions-treatment settings.
via NIDA News on 9/22/10
Twelve scientific teams in more than a dozen states will receive National Institutes of Health (NIH) grants to study effective ways to prevent and treat HIV/AIDS among people in the criminal justice system. The grants, announced today, will be awarded primarily by the National Institute on Drug Abuse (NIDA), with additional support from the National Institute of Mental Health (NIMH) and the National Institute of Allergy and Infectious Diseases (NIAID), all components of NIH. The research will take place over a five-year period.
via NIDA News on 8/14/10
A regulatory protein best known for its role in a rare genetic brain disorder also may play a critical role in cocaine addiction, according to a recent study in rats, funded by the National Institute on Drug Abuse (NIDA), a component of the National Institutes of Health. The study was published today in the journal Nature Neuroscience.
via NIDA News on 7/6/10
A specific and remarkably small fragment of RNA appears to protect rats against cocaine addiction - and may also protect humans, according to a recent study funded by the National Institute on Drug Abuse (NIDA), a component of the National Institutes of Health. The study was published today in the journal Nature.
via NIDA News on 3/27/10
Some of the same brain mechanisms that fuel drug addiction in humans accompany the emergence of compulsive eating behaviors and the development of obesity in animals, according to research funded by the National Institute on Drug Abuse (NIDA), a component of the National Institutes of Health.
via NIDA News on 5/19/10
WHAT: The National Institute on Drug Abuse (NIDA), a component of the National Institutes of Health, will present a special research track at the American Psychiatric Association's (APA's) 163rd annual meeting in New Orleans from May 22-26.
via NIDA News on 3/14/10
Normal individuals who scored high on a measure of impulsive/antisocial traits display a hypersensitive brain reward system, according to a brain imaging study by researchers at Vanderbilt University. The findings provide the first evidence of differences in the brain’s reward system that may underlie vulnerability to what’s typically referred to as psychopathy. The study in the current issue of the journal Nature Neuroscience was funded by the National Institute on Drug Abuse (NIDA), a component of the National Institutes of Health.
via NIDA News on 1/6/10
Researchers have identified a key epigenetic mechanism in the brain that helps explain cocaine's addictiveness, according to research funded by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health.
via Journal of Addiction Medicine - Featured Articles - Featured Articles by Norcross, John C.; Koocher, Gerald P.; Fala, Natalie C.; Wexler, Harry K. on 10/15/10
Evidence-based practice promotes those research-supported treatments that have proven effective, but it rarely identifies discredited treatments that are to be avoided. We sought to establish a professional consensus on discredited addiction treatments using Delphi methodology. A panel of 75 experts participated in a 2-stage study, reporting familiarity with 65 treatments and rating these on a continuum from "not at all discredited" to "certainly discredited." We report their composite opinions and significant differences that occurred as a function of the panelists' theoretical orientation. The results require careful interpretation, but do offer a cogent first step in identifying a professional consensus of discredited treatments for addictions. (C) 2010 American Society of Addiction Medicine
via Journal of Addiction Medicine - Featured Articles - Featured Articles by Terplan, Mishka; Smith, Erica J.; Kozloski, Michael J.; Pollack, Harold A. on 10/15/10
Objectives: To describe trends in court-mandated treatment in pregnancy. In particular, to determine whether pregnant women who enter treatment via the criminal justice system differ from women who enter voluntarily. Methods: Data were obtained from the Treatment Episode Data Set, an administrative data set that captures admissions to federally funded treatment centers in the United States. Demographic and treatment-related measures were examined among pregnant women comparing referral source and stratified by year of admission to assess trends over time. Results: Throughout the study period, the proportion of pregnant women entering substance abuse treatment via the criminal justice system increased more rapidly than the increase observed among men or nonpregnant women reaching 30.9% by 2005. Compared with voluntary admissions, admissions originating in the criminal justice system were more likely to be white, young, and employed. The primary substances compelling court-mandated treatment for pregnant women were alcohol and cocaine in 1994, and by 2005 it had shifted to amphetamine and marijuana. Conclusion: The increase in criminal justice referrals parallels the growth of drug courts. The demographic characteristics of the pregnant referrals, however, suggest the presence of gaps in both screening and treatment in pregnancy. (C) 2010 American Society of Addiction Medicine
via NIDA News on 3/20/12
Scientists are now one step closer to developing anti-addiction medications, thanks to new research that provides a better understanding of the properties of the only member of the opioid receptor family whose activation counteracts the rewarding effects of addictive drugs.
via Journal of Addiction Medicine - Featured Articles - Editor's Picks by Gearhardt, Ashley N.; Corbin, William R.; Brownell, Kelly D. on 9/12/09
The evidence for food's addictive properties is steadily growing. In addition to clinical and evolutionary plausibility, the possibility of addiction to food is supported by animal model research and increasingly by research with humans. Much as classic drugs of abuse "hijack" the brain, accumulating evidence with food suggests a similar impact, but with weaker effects. Although neurobiological evidence for food addiction is compelling, dependence as conceptualized with respect to alcohol and other drugs of abuse is fundamentally a behavioral disorder. Thus, we review the current state of food addiction research in the context of each of the diagnostic criterion for dependence (ie, tolerance, withdrawal, loss of control) and briefly explore other relevant addiction topics such as expectancies, reinforcement, and incentive salience. There is substantial evidence that some people lose control over their food consumption, suffer from repeated failed attempts to reduce their intake, and are unable to abstain from certain types of food or reduce consumption in the face of negative consequences. Although there is some evidence for other dependence criterion, further research is needed to examine tolerance and withdrawal to high-fat sweets, time spent in obtaining, using, and recovering from excess food consumption and the degree to which important activities are given up due to overconsumption. As science continues forward and both the public and elected leaders become aware that food may trigger an addictive process, this information will likely be used to inform policy. Thus, researchers need to carefully consider the implications of their work and the way in which the results may be interpreted. (C) 2009 American Society of Addiction Medicine
via Twitter / NIAAAnews on 5/30/12
NIAAAnews: Alcohol and drug problems would be categorized differently in revised manual: http://t.co/HucbazCK
via addiction - Google News on 6/4/12
UT researchers hope to create drug to treat alcohol addiction
The Horn University of Texas researchers are looking at how alcohol affects brain receptors and gene expression in hopes of treating alcohol addiction. University of Texas researchers are looking at how alcohol affects brain receptors and gene expression in ... |
via addiction - Google News on 6/4/12
A Holistic Approach to Health in Early Recovery: Withdrawal and Insomnia
Huffington Post These days, we all know someone affected by addiction. If it's not something we ourselves grapple with, then it's a friend, sibling, or parent. If you're lucky enough to not be personally affected by the disease of addiction, you need look no further ... |
via addiction - Google Blog Search by Stanton Peele on 6/2/12
How far have we come in treating addiction in five decades? By Stanton Peele...
via addiction - Google News on 6/4/12
Addiction grips Afghan women, children
Tucson Citizen The mundane nature of the work and long hours are made tolerable by drugs that make addicts of mothers and children. Kunduz province, population 800000, has more than 30000 drug addicts, according to the Kunduz Drug Treatment Center. and more » |
via addiction - Google Blog Search by unknown on 6/5/12
The Patient Protection and Affordable Care Act (ACA), known far and wide as “Obamacare,” will create greater access to drug and alcohol treatment if it passes.
via ASAM President's Blog on 1/17/12
1/17/2012 1:22 PM The New York Times reported last week that nicotine gum and skin patches face new doubt. T...
via Journal of Addiction Medicine - Featured Articles - Editor's Picks by Saitz, Richard; Larson, Mary Jo; LaBelle, Colleen; Richardson, Jessica; Samet, Jeffrey H. on 9/12/09
Chronic disease (care) management (CDM) is a patient-centered model of care that involves longitudinal care delivery; integrated, and coordinated primary medical and specialty care; patient and clinician education; explicit evidence-based care plans; and expert care availability. The model, incorporating mental health and specialty addiction care, holds promise for improving care for patients with substance dependence who often receive no care or fragmented ineffective care. We describe a CDM model for substance dependence and discuss a conceptual framework, the extensive current evidence for component elements, and a promising strategy to reorganize primary and specialty health care to facilitate access for people with substance dependence. The CDM model goes beyond integrated case management by a professional, colocation of services, and integrated medical and addiction care-elements that individually can improve outcomes. Supporting evidence is presented that: 1) substance dependence is a chronic disease requiring longitudinal care, although most patients with addictions receive no treatment (eg, detoxification only) or short-term interventions, and 2) for other chronic diseases requiring longitudinal care (eg, diabetes, congestive heart failure), CDM has been proven effective. (C) 2008 American Society of Addiction Medicine
via Addiction Inbox by Dirk Hanson on 3/16/12
Back when acid was legal.
After last week’s blitz of coverage concerning studies done in the 60s on the use of LSD for the treatment of alcoholism, I thought it would be useful to provide a bit of background; some pertinent psychedelic history to help put this information in perspective:
It may come as a surprise to many people that throughout the 60s, there were LSD clinics operating in England and Europe. European LSD therapists tended to use very low doses as an adjunct to traditional psychoanalytic techniques. But North American researchers took a different, bolder approach. When “psychedelic” therapy began to catch on in Canada and the United States, therapists typically gave patients only one or two sessions at very high doses. These early efforts were aimed at producing spontaneous breakthroughs or recoveries in alcoholics through some manner of religious epiphany or inner conversion experience. The only other quasi-medical approach of the day, the Schick Treatment Center’s brand of “aversion therapy,” was not seen to produce very compelling long-term recovery rates, and subsequently fell out of favor. In this light, the early successes with LSD therapy, sometimes claimed to be in the 50-75 per cent range, looked noteworthy indeed. However, the design and criteria of the LSD/alcoholism studies varied so widely that it has never been possible to draw definitive conclusions about the work that was done, except to say that LSD therapy seemed to be strikingly effective for certain alcoholics. Some patients were claiming that two or three trips on LSD were worth years of conventional psychotherapy—a claim not heard again until the advent of Prozac thirty years later.
“I’ve taken lysergic acid several times, and have collected considerable information about it,” Bill Wilson, the co-founder of Alcoholics Anonymous, disclosed in a private letter written in 1958. “At the moment, it can only be used for research purposes. It would certainly be a huge misfortune if it ever got loose in the general public without a careful preparation as to what the drug is and what the meaning of its effects may be.” Like many others, Wilson was excited by LSD’s potential as a treatment for chronic alcoholism. Even Hollywood was hip to the new therapy. Cary Grant, among others, took LSD under psychiatric supervision and pronounced it immensely helpful as a tool for psychological insight. Andre Previn, Jack Nicholson, and James Coburn agreed. (It could be argued that the human potential movement began here).
No drug this powerful and strange, if American history was any guide, could remain legal for long. Unlike their colleagues in the intelligence agencies, politicians and law enforcement officers didn’t know about Mongolian shamans and their fly agaric mushrooms; about European witches and their use of psychoactive plant drugs like nightshade and henbane; about Persian sheiks with their cannabis water pipes; Latin American brujos with their magic vines.
But for the CIA, the big fish was always LSD.
What interested the Central Intelligence Agency about LSD was its apparent ability to produce the symptoms of acute psychosis. Operation ARTICHOKE was designed to ferret out LSD’s usefulness as an instrument of psychological torture, and as a possible means of destabilizing enemy forces by means of aerosol sprays or contaminated water supplies. (The drug’s overwhelming potency made such parts-per-billion fantasies a possibility.)
The agency knew where to turn for a secure American source of supply. Eli Lilly and Co., the giant drug manufacturer, was already involved in LSD research on behalf of the U.S. government. The trouble was that LSD was expensive, and all roads led to Sandoz Laboratories in Switzerland. Organic LSD had to be painstakingly extracted from ergot, a fungus that grows in kernels of rye. Eventually, Sandoz and Eli Lilly successfully synthesized LSD in their own laboratories. With the advent of a reliable domestic supplier of synthetic LSD, the CIA under Allen Dulles was assured of a steady source for experimental purposes.
When LSD did not pan out as a reliable agent of interrogation, CIA investigators turned their attention to its purported ability to mimic acute psychosis—its “psychomimetic” aspect—which researchers were praising as a new avenue toward a biological understanding of schizophrenia. The CIA funneled grant money for LSD research into the academic and commercial R&D world through a host of conduits. Various experiments with non-consenting subjects—typically military or prison personnel—showed that LSD could sometimes break down established patterns of thought, creating a “twilight zone” during which the mind was more susceptible to various forms of psychological coercion and control. Perhaps, under the influence of LSD, prisoners could be transformed into counter-espionage agents. It also occurred to the CIA that the same drug could be used on their own agents for the same purposes. Numerous CIA agents took LSD trips in order to familiarize them with acid’s Alice-in-Wonderland terrain. Some of these unusual experiments were captured on film for use in military training videos.
One place where ARTICHOKE research took place was the Addiction Research Centre at the Public Health Service Hospital in Lexington, Kentucky—the same hospital that specialized in the treatment of hardcore heroin addicts. Lexington was part hospital and part penitentiary, which made it perfect for human experimentation. The addict/inmates of Lexington were sometimes given LSD without their consent, a practice also conducted at the federal prison in Atlanta, and at the Bordentown Reformatory in New Jersey.
In 1953, then-CIA director Allen Dulles authorized Operation MK-ULTRA, which superseded earlier clandestine drug investigations. Under the direction of Dr. Sidney Gottlieb, a chemist, the government began slipping LSD and other psychoactive drugs to unwitting military personnel. During a work retreat in Maryland that year, technicians from both the Army and the CIA were dosed without their knowledge, and were later told that they had ingested a mind-altering drug. Dr. Frank Olson, a civilian biochemist involved in research on biological warfare, wandered away from the gathering in a confused state, and committed suicide a few days later by leaping to his death from an upper floor of the Statler Hilton in New York City. The truth about Olson’s death was kept secret from his family, and from the rest of the nation, for more than twenty years. In 1966, LSD was added to the federal schedule of controlled substances, in the same category as heroin and amphetamine. Simple possession became a felony. The Feds had turned off the spigot, and the research came to a halt. Federal drug enforcement agents began showing up at the homes and offices of well-known West Coast therapists, demanding the surrender of all stockpiles of LSD-25. The original acid elite was being hounded, harassed, and threatened in a rancid atmosphere of pharmaceutical McCarthyism. Aldous Huxley, Humphrey Osmond, even father figure Albert Hoffman, all viewed these American developments with dismay. The carefully refined parameters and preparations, the attention to set and setting, the concerns over dosage, had gone out the window, replaced by a massive, uncontrolled experiment in the streets. Small wonder, then, that the circus atmosphere of the Haight-Ashbury “Summer of Love” in 1967 seemed so badly timed. Countercultural figures were extolling the virtues of LSD for the masses—not just for research, not just for therapy, not as part of some ancient religious ritual—but also just for the freewheeling American hell of it. What could be more democratic than the act of liberating the most powerful mind-altering drug known to man?
It is at least conceivable that researchers and clinicians eventually would have backed away from LSD anyway, on the grounds that the drug’s effects were simply too weird and unpredictable to conform to the rigorous dictates of clinical studies. Nonetheless, researchers had been given a glimpse down a long, strange tunnel, before federal authorities put an end to the research.
Graphics Credit: http://news.sky.com
via addiction - Google Blog Search by seanmeshorer on 6/5/12
Whitney is hardly the only person to struggle with addiction. From the very famous to the utterly anonymous, no area of our society is immune, no set of life circumstances insulate us. The questions are: what are the underlying ...
via addiction - Google Blog Search by Lisa Frederiksen on 6/5/12
I was struck by Jonathan Haidt's essay appearing in the June 1, 2012, issue of The Week, titled,
via addiction - Google News on 6/4/12
 USA TODAY |
Afghan women, children held in addiction's grip
USA TODAY The mundane nature of the work and long hours are made tolerable by drugs that make addicts of mothers and children. Kunduz province, population 800000, has more than 30000 drug addicts, according to the Kunduz Drug Treatment Center. and more » |
via Journal of Addiction Medicine - Featured Articles - Editor's Picks by Cowan, Alan on 9/12/09
The historical background leading to the current use of buprenorphine as an analgesic and its role in the management of opioid dependence is summarized. The popular description of buprenorphine as a "partial agonist" is discussed in relation to efficacy in animal models of antinociception and clinical analgesia. The latest information on the respiratory depressant effects of buprenorphine and its N-dealkylated metabolite (norbuprenorphine) is presented. New data on the buprenorphine withdrawal syndrome in rats are described. (C) 2007 American Society of Addiction Medicine
via Journal of Addiction Medicine - Featured Articles - Editor's Picks by Littleton, John M. on 9/12/09
Acamprosate, in combination with psychosocial therapy, has been shown to be clinically effective in maintaining abstinence in alcohol dependence. Current research suggests that its mechanism of action involves functional antagonism of the ionotropic glutamate N-methyl-d-aspartate (NMDA) receptor. However, direct interactions between acamprosate and the NMDA receptor are weak, and recent findings suggest that acamprosate may modulate NMDA receptors via regulatory polyamine sites, or that it may act directly on metabotropic glutamate receptors. All of these mechanisms are novel for the treatment of alcohol dependence and have far-reaching implications for understanding relapse, as well as for the discovery of drugs with greater efficacy. Understanding the mechanism of action of acamprosate may be an important stimulus for change in the perception and treatment of alcohol dependence. (C) 2007 American Society of Addiction Medicine
via addiction - Google News on 6/4/12
The Atlantic |
Can These 6 Questions Tell You If You're Clinically Addicted to Facebook?
The Atlantic By Brian Fung In a society awash with digital media, concerns about addiction are natural. But are they unfounded? American medical discourse is chock full of addictions these days. There's video game addiction. Porn addiction. Gambling addiction. Are you addicted to Facebook?WTOP Addicted To Facebook? Answer These 6 Questions To Find Out!The Frisky all 4 news articles » |
via ASAM President's Blog on 3/27/12
ASAM Acting President Dr. Stuart Gitlow writes about reaching consensus on the use of medical marijuana and asks for public input
via NIDA News on 12/13/10
WASHINGTON -- Fueled by increases in marijuana use, the rate of eighth-graders saying they have used an illicit drug in the past year jumped to 16 percent, up from last year's 14.5 percent, with daily marijuana use up in all grades surveyed, according to the 2010 Monitoring the Future Survey (MTF). For 12th-graders, declines in cigarette use accompanied by recent increases in marijuana use have put marijuana ahead of cigarette smoking by some measures. In 2010, 21.4 percent of high school seniors used marijuana in the past 30 days, while 19.2 percent smoked cigarettes.
via NIDA News on 11/1/11
A landmark study in mice identifies a biological mechanism that could help explain how tobacco products could act as gateway drugs, increasing a person’s future likelihood of abusing cocaine and perhaps other drugs as well, according to the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health. The study is the first to show that nicotine might prime the brain to enhance the behavioral effects of cocaine.
via Journal of Addiction Medicine - Most Popular Articles by Reece, Albert S. on 2/29/12
Objective: There is considerable recent interest in immunostimulation caused by opiates, but, although there is intense interest in this process within the central nervous system particularly in connection with the pathways underlying chronic pain, few studies set out to define the course of clinical markers of this process in the systemic circulation or over the temporal span of the life course. Methods: For this reason, we have compared clinical pathology results from 1747 opiate substance use disorder with 6450 non–substance use disorder patients taken from our clinical pathology database. All continuous data were transformed to their natural logarithm to improve normality assumptions. Results: Globulins, erythrocyte sedimentation rate, white cell count, lymphocytes, monocytes, and platelets were all high in substance use disorder (P ≤ 0.01). These variables, C-reactive protein, high-sensitivity C-reactive protein, and neutrophils were all high at multiple regression when corrected for age (P < 0.0001) in both sexes (P ≤ 0.01). There were significant interactions between age and addictive status for C-reactive protein, high-sensitivity C-reactive protein, erythrocyte sedimentation rate, globulins, white cell count, and lymphocytes and monocytes (P < 0.01). Conclusions: These results are consistent with immunostimulation affecting soluble and cellular elements of the blood both in relative terms and after correction for age. They are consistent with other data showing diffuse and generalized immunostimulation like the high-risk polyclonal immunosenescent gammopathy seen in the very elderly known as “inflamm-aging” that carries an uncommonly poor prognosis for longevity. As such, it merits further detailed investigation.
via Journal of Addiction Medicine - Most Popular Articles by el-Guebaly, Nady on 2/29/12
Objective: To review the evolution of the paradigm of recovery in addiction and its implications. Method: A systematic literature review was conducted using the MEDLINE and PsychInfo databases over the past 10 years and key references from the retrieved literature. Findings: The historical evolution of the concept of recovery has been shaped by several driving forces, including consumer experience, the need to better define our treatment outcome and parallel elaboration of the concepts of health, quality of life, and chronic disorders. Similarities and differences with the concept of “recovery” in mental health and other biomedical fields are identified. The empirical basis is growing in support of various proposed attributions and features of recovery along with the temporal benchmarks involved. The various forms of recovery, such as “natural,” “transformational,” or “medication-assisted,” describe a choice of pathways to a common goal. The management implications are far-reaching and call for system shifts from acute stabilization to sustained recovery, including the growth of alternative institutions, and roles complementary to mutual help. Tools for the sustenance of recovery, including educational kits, recovery workbooks, and e-recovery initiatives, are developing. Conclusions: Although first-person accounts of recovery abound, a more systematic empirical investigation of the concept has just begun, including demographic and cultural differences. Management implications are derived from the experience with other “mainstream” chronic disorders with treatment providing stabilization and initiation of recovery and a range of long-term resources becoming available to sustain it.
via Journal of Addiction Medicine - Most Popular Articles by Castaldi, Silvana; Gelatti, Umberto; Orizio, Grazia; Hartung, Uwe; Moreno-Londono, Ana Maria; Nobile, Marta; Schulz, Peter J. on 5/31/12
This study assesses the use of cognitive enhancement medication among university students in Northern Italy. It was conducted as a cross-sectional analysis on the basis of a paper-and-pencil survey of 77 undergraduate students attending courses in the Faculty of Medicine of the University of Milan, Milano, Italy. Although the share of students who have taken cognitive enhancement medication themselves in the past is still small (16%), the use of these drugs is rather common and freely communicated in some social circles. Enhancing the ability to study outside of the class was students' primary motive for use. Students who think that there is no or an acceptable risk involved in cognitive enhancement medication are more likely to take drugs and dietary supplements than those who perceive the risk as high.
via Journal of Addiction Medicine - Most Popular Articles by Keshtkar, Abbasali; Majdzadeh, Reza; Nedjat, Saharnaz; Gholipour, Mahin; Badakhshan, Abbas; Qorbani, Mostafa; Vakili, Mohammadali; Salari, Hadi on 5/31/12
Objectives: This study was conducted to estimate the prevalence and the associated factors of high-risk sexual behaviors among drug abusers referred to a methadone clinic in Gorgan, the capital of Golestan province in the northeast of Iran, to help health care decision makers on designing interventional programs. Methods: In this cross-sectional study, 400 drug abusers referred to our methadone clinic were evaluated for high-risk sexual behavior. A logistic regression model was fitted for the association between independent variables and high-risk sexual behavior. Results: Approximately a quarter of patients (25.5%) had high-risk sexual behavior among which 47% had not used a condom in their last sexual contact. Drug abusers who had poor economic status had a lower chance of high-risk sexual behavior than those with good economic status (adjusted odds ratio [AOR] = 0.35, 95% confidence interval [CI] = 0.13–0.96). Also, 1-year increase in age reduced the chance by 6% (AOR = 0.94, 95% CI = 0.91–0.98). Heroin abusers, compared with opium abusers, had a duplicated chance of having high-risk sex (AOR = 2.11, 95% CI = 1.12–3.96). Conclusion: According to this study, high-risk sexual behavior in the drug abusers referred to methadone clinic was associated with younger age, good economic status, and heroin addiction. Hence, in interventional planning, more attention should be paid to young drug abusers, patients with good economic status, and heroin addicts as well.
via Addiction Inbox by Dirk Hanson on 3/9/12
Maybe it isn't endorphins after all.
[From time to time, I reprint earlier posts that have remained perennial favorites at Addiction Inbox. This one originally ran on August 4, 2010.]
What do long-distance running and marijuana smoking have in common? Quite possibly, more than you’d think. A growing body of research suggests that the runner’s high and the cannabis high are more similar than previously imagined.
The nature of the runner’s high is inconsistent and ephemeral, involving several key neurotransmitters and hormones, and therefore difficult to measure. Much of the evidence comes in the form of animal models. Endocannabinoids—the body’s internal cannabis—“seem to contribute to the motivational aspects of voluntary running in rodents.” Knockout mice lacking the cannabinioid CB1 receptor, it turns out, spend less time wheel running than normal mice.
A Canadian neuroscientist who blogs as NeuroKuz suggests that “a reduction in CB1 levels could lead to less binding of endocannabinoids to receptors in brain circuits that drive motivation to exercise.” NeuroKuz speculates on why this might be the case. Physical activity and obtaining rewards are clearly linked. The fittest and fleetest obtain the most food. “A possible explanation for the runner’s high, or ‘second wind,’ a feeling of intense euphoria associated with going on a long run, is that our brains are stuck thinking that lots of exercise should be accompanied by a reward.”
In 2004, the British Journal of Sports Medicine ran a research review, “Endocannabinoids and exercise,” which seriously disputed the “endorphin hypothesis” assumed to be behind the runner’s high. To begin with, other studies have shown that exercise activates the endocannabinoid system.
“In recent years,” according to the authors, “several prominent endorphin researchers—for example, Dr Huda Akil and Dr. Solomon Snyder—have publicly criticised the hypothesis as being ‘overly simplistic,’ being ‘poorly supported by scientific evidence’, and a ‘myth perpetrated by pop culture.’” The primary problem is that the opioid system is responsible for respiratory depression, pinpoint pupils, and other effects distinctly unhelpful to runners.
The investigators wired up college students and put them to work in the gym, and found that “exercise of moderate intensity dramatically increased concentrations of anandamide in blood plasma.” The researchers break the runner’s high into four major components. Exercise, they say, “suppresses pain, induces sedation, reduces stress, and elevates mood.” Some of the parallels with the cannabis high are not hard to tease out: “Analgesia, sedation (post-exercise calm or glow), a reduction in anxiety, euphoria, and difficulties in estimating the passage of time.”
There are cannabinoid receptors in muscles, skin and the lungs. Intriguingly, the authors suggest that unlike “other rhythmic endurance activities such as swimming, running is a weight bearing sport in which the feet must absorb the ‘pounding of the pavement.’” Swimming, the authors speculate, “may not stimulate endocannabinoid release to as great an extent as running.” Moreover, “cannabinoids produce neither the respiratory depression, meiosis, or strong inhibition of gastrointestinal motility associated with opiates and opioids. This is because there are few CB1 receptors in the brainstem and, apparently, the large intestine.”
A big question remains: What about running and the “motor inhibition” characteristic of high-dose cannabis? (An inhibition that may make cannabis useful in the treatment of movement disorders like tremors or tics.) Running a marathon is not the first thing on the minds of most people after getting high on marijuana. The paper maintains, however, that at low doses, “cannabinoids tend to produce hyperactivity,” at least in animal models. The CB1 knockout mice were abnormally inactive, due to the effect of cannabinoids on the basal ganglia. Practiced, automatic motor skills like running are controlled in part by the basal ganglia. The authors predict that “low level skills such as running, which are controlled to a higher degree by the basal ganglia than high level skills, such as basketball, hockey, or tennis, may more readily activate the endocannabinoid system.”
The authors offer other intriguing bits of evidence. Anandamide, one of the brain’s own cannabinoids, “acts as a vasodilator and products hypotension, and may thus facilitate blood flow during exercise.” In addition, “endocannabinoids and exogenous cannabinoids act as bronchodilators” and could conceivably facilitate breathing during steady exercise. The authors conclude: “Compared with the opioid analgesics, the analgesia produced by the endocannabinoid system is more consistent with exercise induced analgesia.”
Photo Credit: http://www.madetorun.com/
via Addiction Inbox by Dirk Hanson on 4/15/12
What we think about when we think about “disease.”
It’s a safe bet that the number of M.D.s who have made a mid-career switch to journalism is rather small. And when Dr. Ivan Oransky did it, he didn’t go in for half measures. The former online editor of Scientific American, and the former deputy editor of The Scientist, Oransky now serves as Executive Editor of Reuters Health. He teaches medical journalism at New York University, where he also holds an appointment as clinical assistant professor of medicine—while maintaining three, yes three, separate blogs. He is well known for two innovative blogs known as Retraction Watch and Embargo Watch. And he recently kicked off a personal blog, the Oransky Journal.
So clearly, he’s a very lazy man. Nonetheless, he found time to give a very popular talk on the shortcomings of the disease model of medicine at last week’s TEDMED conference in Washington, D.C. And he found additional time to grant me an interview afterwards, with some interesting thoughts on how the mania for medicalization could affect addiction treatment.
Speaking at the Kennedy Center for the Performing Arts, Oransky compared patients in the nation’s current medical system to baseball coach Billy Beane, a once-promising player who washed out in the minors and was recently portrayed by Brad Pitt in the movie Moneyball. “Our medical system is just as bad at predicting what’s happening to patients as baseball scouts were at predicting what would happen to Billy Beane,” Oransky told the audience of 1,500.
“Every day, thousands of people across the country are diagnosed with pre-conditions,” he said. “We hear about pre-hypertension, we hear about pre-dementia and pre-anxiety. We also refer to sub-clinical conditions, like sub-clinical hardening of the arteries. One of my favorites is called sub-clinical acne. If you look up their website as I did, you’ll see that they say this is the easiest acne to treat. You don’t have any pustules or inflammation—you don’t actually have acne. I have a name for preconditions—I call them preposterous.”
Every year, according to Oransky, “we are spending more than two trillion dollars on health care," and yet more than 100,000 people a year are dying from complications of the treatments they're getting, rather than from the conditions that are being treated. [Revised 4-15]. And most patient advocacy groups eventually learn to “expand the number of people who are eligible for a given treatment” for fundraising purposes, he said.
As evidence of this trend toward medicalization, Oransky pointed to the novel notion of a “previvor.” According to FORCE, the cancer research advocacy group that coined the term: "A previvor is a survivor of a predisposition to cancer.” The term is used to describe someone who, for example, has a genetic risk for breast cancer, but has not been diagnosed with the disease. “Previvor was coined in 2000 after a challenge from a community member who said she ‘needed a label,’” according to the group’s web site.
We are all previvors of some disorder, Oransky argues. In the spirit of giving everyone a precondition, Oransky coined the term “pre-death.” What is pre-death? “Every single one of you has it,” Oransky told the audience, “because you have the risk factor for it, which is being alive."
Using his favorite metaphor—baseball—Oransky explained the secret of Billy Beane’s revolutionary success as a coach: “The secret wasn’t to swing at every pitch, like the sluggers do. You had to find the guys who liked to walk, because getting on base by a walk is just as good. And in our health care system, we need to figure out, ‘is that really a good pitch, or do we need to let it go by, and not swing at everything?’ We all need to keep in mind that in medicine, sometimes less is more.”
After his talk, I asked Oransky how the theme of medicalization might apply to the disease of addiction. Medicalization, he said, is a matter of “taking advantage of people, manipulating them so they can’t make informed decisions.” In the case of addiction treatment, Oransky pointed to the “proliferation of ads for treatment in beautiful places. It’s all selling and self-diagnosis. They’re selling you on the fact that you need to be treated.” He also pointedly referred to the practice of “medical astro-turfing,” where a supposedly grass roots effort by patients or advocates is “usurped by interest group pressure.” Sometimes that usurpation is patently obvious, is in the case of many advocacy groups set in motion and funded by pharmaceutical companies or the liquor industry.
Sometimes, of course, you do need to be treated. And Oransky notes that in health areas such as addiction and mental illness—disorders where social stigma remains high, compared to, say, a blood infection—there are “fewer pressures to medicalize.” And possibly, too few pressures to medicalize. “There’s no quick and easy test, no MRI where you can point to the place in the brain that lights up and say, “you are an alcoholic.” The science of addiction, which has been moving by fits and starts into the medical mainstream, has a long way to go, compared with many other disease categories. And it has left a gap through which medical workers and treatment staff can march, chanting, “I have a system,” Oransky says.
Perhaps, then, the study of addiction to alcohol and other drugs requires both more medicalization of the research kind, and less of the “precondition” or “sub-clinical” kind. As for the second kind, Oransky believes we are already medicalizing binge drinking in a counterproductive way. In addition, “there are always attempts to widen the market. Look at how obesity has been made to overlap with addiction.” As for medications being used to combat craving among addicts in treatment, Oransky noted the tendency to “repurpose” drugs on the basis of soft data. “They took wellbutrin, an antidepressant that didn’t work very well, and offered it for smoking cessation. So I would want to see data that is really robust” before treating addicts with such medications.
On the other hand, Oransky noted, “We don’t have to worry about malaria, we don’t need to medicalize tuberculosis. But do diseases that have a strong stigma, like addiction, actually benefit from medicalization? If we find out that they do, than we should do it.”
There’s something else Oransky believes is overdue for true medicalization: “The social determinants of health care—poverty, the way we build our suburban environments. Concentrate on stuff that we know kills people. Medicalize that.”
In the end, he said, “we need to use marketing strategies to effectively get treatment to the people who need it, not to the people who don’t.”
via addiction - Google Blog Search by admin on 6/6/12
If you can sense the change of intensity that people have in the way they conduct their daily activities nowadays, I'm sure that you will notice that if those people fail to manage and balance their stress of their daily activities, it can lead to terrible ...
via Journal of Addiction Medicine - Featured Articles - Featured Articles by Canfield, Marta C.; Keller, Craig E.; Frydrych, Lynne M.; Ashrafioun, Lisham; Purdy, Christopher H.; Blondell, Richard D. on 5/26/10
Objective: This study was designed to assess nonmedical prescription opioid use among a sample of opioid dependent participants. Methods: A cross-sectional survey was conducted with a convenience sample of patients hospitalized for medical management of opioid withdrawal. We collected data related to participant demographics, socioeconomic characteristics, the age of first opioid use, types of opioids preferred, and routes of administration. We also asked participants to describe how they first began using opioids and how their use progressed over time. Results: Among the 75 participants, the mean age was 32 years (SD: +/-11, range: 18-70 years), 49 (65%) were men, 58 (77%) considered themselves to be "white," 55 (74%) had a high school diploma or equivalent, and 39 (52%) were unemployed. All of these participants considered themselves to be "addicted." Thirty-one (41%) felt that their addiction began with "legitimate prescriptions," 24 (32%) with diverted prescription medications, and 20 (27%) with "street drugs" from illicit sources; however, 69 (92%) had reported purchasing opioids "off the street" at some point in time. Thirty-seven (49%) considered heroin to be their current preferred drug, and 43 (57%) had used drugs intravenously. Conclusions: We found that many treatment-seeking opioid-dependent patients first began using licit prescription drugs before obtaining opioids from illicit sources. Later, they purchased heroin, which they would come to prefer, because it was less expensive and more effective than prescription drugs. (C) 2010 American Society of Addiction Medicine
via ASAM President's Blog on 2/28/12
If you were a patient, who would you trust with your treatment? In his latest blog post, ASAM Acting President Dr. Stuart Gitlow asks what level of training and qualifications are necessary to treat chronic medical illnesses. The answer is not so simple.
via ASAM President's Blog on 3/13/12
3/13/2012 1:27 PM For many years, it has been clear that there are insufficient physician specialists to meet the medical needs of the population with addiction. Making matters worse are the physicians prescribing excessive quantities of controlled subs...
via Addiction Inbox by Dirk Hanson on 5/4/12
“I’m a drug addict turned neuroscientist.”
What’s it like to swallow 400 milligrams of dextromethorphan hydrobromide, better known as Romilar cough syrup? “Flashes of perception go by like clumps of scenery on either side, while you float along with the slow, irresistible momentum of a dream.” Marc Lewis, a former addict, now a practicing neuroscientist, further muses: “But what was Romilar? It sounded like an ancient kingdom. Would this dark elixir take me to some faraway place? Would it take me into another land? Would it be hard to come back?”
In Memoirs of an Addicted Brain: A Neuroscientist Examines his Former Life on Drugs, Dr. Marc Lewis follows his description of his gateway Romilar drug experience with the neurological basics of the matter: “The problem is that the NMDA receptors in my brain are now clogged with dextromethorphan molecules! The glutamate isn’t getting through. The receptor neurons aren’t firing, or they’re not firing fast enough…. Drugs like DM, ketamine, PCP, angel dust, and those most damaging of substances, glue and gasoline, are called dissociatives, because they do exactly what drugs are supposed to do: they dissociate feeling from reality, meaning from sense—and that’s all they do.”
Speaking of the self-reinforcing cycle “through which calamities of the mind arise from vulnerabilities of the brain,” Lewis argues that dissociatives only produce an absence. As a friend of his puts it with regard to another popular dissociative, “Nitrous oxide doesn’t give you consciousness. It takes it away.” And then, the friend adds: “Just bonk yourself on the head with a baseball bat if you want to lose consciousness.”
Lewis ultimately turns to opioids. “The emotional circuitry of the ventral striatum seems to derive its power from an intimate discourse between opioid liking and dopamine wanting.” In the end, this partnership does more than produce pleasure. It also, Lewis points out, “gets us to work for things.” And by doing that, addictive drugs demonstrate “the fundamental chemistry of learning which really means learning what feels good and how to get more of it. Yet there’s a downside: the slippery slope, the repetition compulsion, that constitutes addiction. In other words, addiction may be a form of learning gone bad. For me, this neurochemical sleight of hand promises much more pain than pleasure in the years to come.”
Lewis does a good job of capturing the feeling of existential despair brought on by uncontrolled addiction: “Contemptible. That’s what I was. Unbelievably stupid, unbelievably irresponsible: selfish, selfish, selfish! But that wasn’t quite it. What described me, what this inner voice accused me of, wasn’t exactly selfish, not exactly weak, but some meridian of self-blame that included both, and also, dirty, disgusting… maybe just BAD.”
How did heroin feel? “I feel relief from that pervasive hiss of wrongness. Every emotional wound, every bruise, every ache in my psyche, the background noise of angst itself, is soaked with a balm of unbelievable potency. There is a ringing stillness. The sense of impending harm, of danger, of attack, both from within and without, is washed away.”
And Lewis provides a memorable summation of the reward system, as dopamine streams from the ventral tegmental area to its targets, “the ventral striatum, where behavior is charged, focused, and released; the orbitofrontal cortex, where it infuses cells devoted to the value of this drug; and the amygdala, whose synapses provide a meeting place for the two most important components of associative memory, imagery and emotion.” In fact, “dopamine-powered desperation can change the brain forever, because its message of intense wanting narrows the field of synaptic change, focusing it like a powerful microscope on one particular reward. Whether in the service of food or heroin, love or gambling, dopamine forms a rut, a line of footprints in the neural flesh.”
And, of course, Lewis relapses, and eventually ends his addictive years in an amphetamine-induced psychosis, committing serial burglaries to fund his habit. “You’d think that getting busted, put on probation, kicked out of graduate school, and enduring a kind of infamy that was agonizing to experience and difficult to hide—all of that, an the need to start life over again—would be enough to get me to stop. It wasn’t.”
Not then, anyway. But Lewis has been clean now for 30 years. “Nobody likes an addict,” he writes. “Not even other addicts.”
If drugs are such feel-good engines, what goes wrong? Something big. “Because when drugs (or booze, sex, or gambling) are nowhere to be found, when the horizon is empty of their promise, the humming motor of the orbitofrontal cortex sputters to a halt. Orbitofrontal cells go dormant and dopamine just stops. Like a religious fundamentalist, the addict’s brain has only two stable states: rapture and disinterest. Addictive drugs convert the brain to recognize only one face of God, to thrill to only one suitor.” The addict’s world narrows. Dopamine becomes “specialized, stilted, inaccessible through the ordinary pleasures and pursuits of life, but gushing suddenly when anything associated with the drug comes into awareness…. I wish this were just an exercise in biological reductionism, or neuro-scientific chauvinism, but it’s not. It’s the way things really work.”
Photo Credit: http://ebookstore.sony.com/
via Addiction Inbox by Dirk Hanson on 5/7/12
State law criminalizes “gateway sexual activity.”
It’s the gateway to hell and perdition, that’s what it is. It doesn’t necessarily lead to drugs but it will drag you in the direction of Ess Eee Exx. And while sex is probably not addictive in the traditional sense, it is always and inevitably very bad when unaccompanied by marriage and the procreative urge.
Like anthropology’s search for the “missing link,” or the physicist’s search for a “unified field theory,” psychologists and social workers have spent decades hunting for the mythical gateway drug. This is the drug that, when used regularly, will head you reliably down the path of full-blown addiction. The findings of addiction medicine now make the identification of any kind of universal gateway drug an antique pursuit. Every addict finds his or her own gateway, and pushes through. If any drugs qualify as gateway drugs in a broad sense, it would have to be alcohol and tobacco, simply on the basis of ready availability.
But a gateway for full-blown recreational teenage sex—did you ever think about that? One might have thought the legislators would answer, yes, it’s called puberty, and move on. But no. The Tennessee legislature, led by Rep. Jim Gotto (R), managed to push through a bill “allowing parents to sue teachers and other outside parties for ‘promoting or condoning gateway sexual activity’ by students.”
Interestingly, the bill apparently fails to define such activity in concrete terms. Evidently, Rep. Gotto has attempted to outlaw “first base.” Or, as TPMMuckraker put it, “other things.” Gateway sexual activity is defined, according to what I shall dub the bill’s "money" sentence, “sexual conduct encouraging an individual to engage in a non-abstinent behavior.” Okay, then. Earnest glances, hair tossing, hand holding—all potentially actionable, should any sex ed teachers be caught “promoting” such activities.
And not without reason: According to data released last month by the National Center for Health Statistics, the states with the highest teen birth rate in 2010 include Tennessee, which ranked 10th worst with 43.2 births per 1,000 teenage girls. And according to a 2009 risk behavior study in Memphis City, 61 percent of high school students have had sex, along with 27 percent of middle school students, putting Memphis City, and by extension Tennessee, considerably above the national average.
Apparently, the real target here is Planned Parenthood, which has been known to provide sex education information in Tennessee schools, and which would be facing fines and penalties under the new law. The bill calls for abstinence-only instruction.
Photo Credit: http://cbcpforlife.com/?p=4277
via Addiction Inbox by Dirk Hanson on 5/16/12
Smoked marijuana reduced spasticity in a small trial of MS patients.
The leading wedge of the medical marijuana movement has traditionally been centered on pot as medicine for the effects of chemotherapy, for the treatment of glaucoma, and for certain kinds of neuropathic pain. From there, the evidence for conditions treatable with marijuana quickly becomes either anecdotal or based on limited studies. But pharmacologists have always been intrigued by the notion of treating certain neurologic conditions with cannabis. Sativex, which is sprayed under the tongue as a cannabis mist, has been approved for use against multiple sclerosis, or MS, in Canada, the UK, and some European countries. (In the U.S., parent company GW Pharma is seeking FDA approval for the use of Sativex to treat cancer pain).
There is accumulating evidence that cannabinoid receptors may be involved in controlling spasticity, and that anandamide, the brain’s endogenous form of cannabis, is a specific antispasticity agent.
Additional evidence that researchers may be on to something appeared recently in the Canadian Medical Association Journal. Dr. Jody Corey-Bloom and coworkers at
the University of California in San Diego conducted a small, placebo-controlled trial with adult patients suffering from poorly controlled spasticity. Thirty participants were randomly divided into two groups. Those in the first group were given a daily joint, and those in the second group received “identical placebo cigarettes.” After three days, the investigators found that smoked marijuana resulted in a reduction in treatment-resistant spasticity, compared to placebo. Clearly, it’s hard for a study of this sort to be truly blind: Participants, one presumes, had little trouble distinguishing the medicine from the placebo. And in fact, an appendix to the study shows this to be true: “Seventeen participants correctly guessed their treatment phase for all six visits… For the remaining participants, cannabis was correctly guessed on 33/35 visits.” This raises the question of various kinds of self-selection bias and expectancy effects, and the study authors themselves write that the results “might not be generalizable to patients who are cannabis-naïve.” On the other hand, cannabis-naïve patients were in the minority. The average age of the participants was 50, and fully 80% of them admitted to previous “recreational experience” with cannabis. (I don’t have a good Baby Boomer joke for the occasion, but if I did, this is where it would go).
I asked Dr. Corey-Bloom about this potential problem in an email exchange: “The primary outcome measure was the Ashworth Spasticity Scale, which is an objective measure, carried out by an independent rater,” she wrote. “Their job was just to come in and feel the tone around each joint (elbow, hip, knee), rate it, and leave. That's why we think it was so important to have an objective measure, rather than just self-report.”
With all this in mind, the study found that “smoking cannabis reduced patient scores on the modified Ashworth scale by an average of 2.74 points.” The authors conclude: “We saw a beneficial effect of smoked cannabis on treatment-resistant spasticity and pain associated with multiple sclerosis among our participants.”
Other studies have found similar declines in spasticity from cannabinoids, but have tended not to use marijuana in smokable form.
Corey-Bloom, J., Wolfson, T., Gamst, A., Jin, S., Marcotte, T., Bentley, H., & Gouaux, B. (2012). Smoked cannabis for spasticity in multiple sclerosis: a randomized, placebo-controlled trial Canadian Medical Association Journal DOI: 10.1503/cmaj.110837
Photo Credit: http://blog.amsvans.com/
via ASAM President's Blog on 5/22/12
In the latest post of President’s Blog, ASAM Acting President Dr. Stuart Gitlow asks why addiction medications like buprenorphine have dosage and patient limits. These medications are reasonably safe, nearly impossible to overdose on and have a lower street value than other narcotics, in comparison to dozens of opioids and sedative-hypnotics that can be prescribed without any apparent limitations.
via Addiction Inbox by Dirk Hanson on 5/23/12
Review of The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition.
Part I
It’s easy to think of cigarettes, and the machinations of the tobacco industry, as “old news.” But in his revealing 737-page book, The Golden Holocaust, based on 70 million pages of documents from the tobacco industry, Stanford professor Robert N. Proctor demonstrates otherwise. He demonstrates how Big Tobacco invented freebasing. He shows how they colluded in misleading the public about “safe” alternatives like filters, “low-tar,” and “ultra-lights.” We discover in Lorillard’s archives an explanation of menthol’s appeal to African Americans: It is all part of a desire by “negroes” to mask a “genetic body odor.” Radioactive isotopes were isolated in cigarette smoke, and evidence of the find was published, as early as 1953. He reveals that the secret ingredient in Kent’s “micronite filter” was asbestos. And he charges that the “corruption of science” lies behind the industry’s drive to continue its deadly trade. “Collaboration with the tobacco industry,” writes Proctor, “is one of the most deadly abuses of scholarly integrity in modern history.”
Half of all cigarette smokers will die from smoking—about a billion people this century, if present trends continue. In the U.S., this translates into roughly two jumbo jets crashing, killing everyone onboard, once daily. Cigarettes kill more people than bullets. The world smokes 6 trillion of them each year. (The Chinese alone account for about 2 trillion). Some people believe that tobacco represents a problem (more or less) solved, at least in the developed West.
All of this represents a continuing triumph for the tobacco industry. The aiders and abettors of tobacco love to portray the tobacco story as “old news.” But as Stanford Professor Robert M. Proctor writes in The Golden Holocaust, his exhaustive history of tobacco science and industry: “Global warming denialists cut their teeth on tobacco tactics, fighting science with science, creating doubt, fostering ignorance.”
Checking in at 737 pages, The Golden Holocaust is nobody’s idea of a light read, and at times its organization seems clear only to the author. But what a treasure trove of buried facts and misleading science Proctor has uncovered, thanks to more than 70 million pages of industry documents now online (http://legacy.library.ucsf.edu) as part of the Master Settlement Agreement of 1998. Once the material was finally digitized and available online, scholars like Proctor could employ full-text optical character recognition for detailed searchability. Ironically, this surreal blizzard of documentation was meant to obscure meaningful facts, not make them readily available, but tobacco executives seem not to have factored in digital technology when they turned over the material.
The single most important technological breakthrough in the history of the modern cigarette was flue-curing, which lowers the pH of tobacco smoke enough to make it inhalable. The reason few people inhale cigars, and very few used to inhale cigarettes, is that without some help, burning tobacco has a pH too high for comfortable inhalation. It makes you cough. But flue-curing lowered pH levels, allowing for a “milder,” less alkaline smoke that even women and children could tolerate.
World War I legitimized cigarettes in a major way. Per capita consumption in the U.S. almost tripled from 1914 to 1919, which Proctor considers “one of the most rapid increases in smoking ever recorded.” After World War II, the Marshall Plan shipped a staggering $1 billion worth of tobacco and other “food-related items.” (The U.S. Senator who blustered the loudest for big postwar tobacco shipments to Europe was A. Willis Robertson of Virginia, the father of televangelist Pat Robertson.)
The military, as we know, has historically been gung-ho on cigarettes. And Proctor claims that “the front shirt pocket that now adorns the dress of virtually every American male, for example, was born from an effort to make a place to park your cigarette pack.” In addition, cigarette makers spent a great deal of time and effort convincing automakers and airline manufacturers to put ashtrays into the cars and planes they sold. Ashtrays were built into seats in movie theaters, barbershops, and lecture halls. There was even an ashtray built into the U.S. military’s anti-Soviet SAGE computer in the 50s.
In the early 50s, research by Ernest Wynder in the U.S. and Angel Roffo in Argentina produced the first strong evidence that tobacco tars caused cancer in mice. Roffo in particular seemed convinced that tobacco caused lung cancer, that it was the tar rather than the nicotine, and that the main culprits were the aromatic hydrocarbons such as benzpyrene. Curiously enough, it was influential members of Germany’s Third Reich in the 40s who first took the possibility of a link seriously. Hans Reiter, a powerful figure in public health in Germany, said in a 1941 speech that smoking had been linked to human lung cancers through “painstaking observations of individual cases.”
In the December 1953 issue of Cancer Research, Wynder, et al. published a paper demonstrating that “tars extracted from tobacco smoke could induce cancers when painted on the skins of mice.” As it turns out, the tobacco industry already knew it. Executives had funded their own research, while keeping a close eye on outside academic studies, and had been doing so since at least the 30s. In fact, French doctors had been referring to cancers des fumeurs, or smokers’ cancers, since the mid-1800s. All of which knocks the first leg out from under the tobacco industry’s classic position: We didn’t know any stuff about cancer hazards until well into the 1950s.
Only weeks after the Wynder paper was published, tobacco execs went into full conspiracy mode during a series of meetings at the Plaza Hotel in New York, “where the denialist campaign was set in motion.” American Tobacco Company President Paul Hahn issued a press release that came to be known as the “Frank Statement” of 1954. Proctor calls it the “magna carta of the American’s industry’s conspiracy to deny any evidence of tobacco harms.” How, Proctor asks, did science get shackled to the odious enterprise of exonerating cigarettes? The secret was not so much in outright suppression of science, though there was plenty of that: In one memorable action known as the “Mouse House Massacre,” R.J. Reynolds abruptly shut down their internal animal research lab and laid off 26 scientists overnight, after the researchers began obtaining unwelcome results about tobacco smoke. But the true genius of the industry “was rather in using even ‘good’ science, narrowly defined, as a distraction, something to hold up to say, in effect: See how responsible we are?”
Entities like the Council for Tobacco Research engaged in decoy research of this kind. As one tobacco company admitted, “Research must go on and on.”
A good deal of the industry’s research in the 50s and 60s was in fact geared toward reverse engineering competitors’ successes. Consider Marlboro. Every cigarette manufacturer want to know: How did they do it? What was the secret to Marlboro’s success?
As it turns out, they did it by increasing nicotine’s kick. And they accomplished that, in essence, by means of freebasing, a process invented by the cigarette industry. Adding ammonia or some other alkaline compound transforms a molecule of nicotine from its bound salt version to its “free” base, which volatilizes much more easily, providing low-pH smoke easily absorbed by body tissue. And there you have the secret: “The freebasing of cocaine hydrochloride into ‘crack’ is based on a similar chemistry: the cocaine alkaloid is far more potent in its free base form than as a salt, so bicarbonate is used to transform cocaine hydrochloride into chemically pure crack cocaine.” Once other cigarette makers figured out the formula, they too began experimenting with the advantages of an “enhanced alkaline environment.”
(End of Part I)
Photo Credit: http://theloungeisback.wordpress.com/
via Addiction Inbox by Dirk Hanson on 5/26/12
A review of The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition
Part II
The famous Surgeon General’s Report of 1964, officially warning Americans about the dangers of smoking, and publicizing the cancer connection, is typically seen as a triumphal moment in American medical history. But according to Stanford history professor Robert Proctor in his book, The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition, the report was “flawed in a number of interesting respects.” [The author, above, with paraphernalia] For one thing, members of the advisory committee consulting on the report, many of them congressman friendly to the tobacco cause, succeeded in their attempts to have smoking referred to as a “habit” rather than as addiction—a shameful Orwellian turn that went uncorrected for 25 years.
Meanwhile, the industry continued to fund new institutes, and continued to give out research grants for “red herring” research. As an example, the highest-ranking officer of the American Heart Association received money from one of the industry’s fraudulent research arms.
As late as the early 80s, most smokers believed they suffered from a bad habit, rather than an addiction—even though a majority of them wished they didn’t smoke. That is an odd kind of consumer “choice.” Cigarette makers have spent millions to perpetuate this myth. Proctor views tobacco industry executives and lawyers as a unique form of disease vector, spreading the pernicious health consequences of smoking across the globe.
The 2008 World Health Organization (WHO) Report on the Global Tobacco Epidemic fleshes out this metaphor, suggesting that all epidemics have a means of contagion, “a vector that spreads disease and death. For the tobacco epidemic, the vector is not a virus, bacterium or other microorganisms—it is an industry and its business strategy.”
In an email exchange, I asked Professor Proctor to expand on this notion of a disease vector:
“We tend to divide "communicable" from "non-communicable" diseases,” Proctor told me, “when the reality is that many "non-communicable" diseases are in fact spread by communications.”
Examples? “Through ignorance and propaganda, for example, which can spread like a virus,” Proctor wrote. “We don't count the anthropogenic communications, oddly enough, even though these can be just as dangerous, and just as deadly. And just as preventable--by changing our exposure environments.”
In a recent article for Tobacco Control, Proctor laid out how the calculus of the disease vector plays out. We know, for example, that smoking will cause roughly 6 million deaths in 2015. And about a third of those will be from lung cancer. We know that 25 acres of tobacco plants will result in about 10 lung cancer deaths per year, starting 20 or 30 years down the road. Here’s a sick equivalence: “A 40 ft container of the sort shipped overseas or trucked by highway houses 10 million cigarettes, which means that each container will cause about 10 deaths.” Proctor works out the numbers for the value of a human life:
“Cigarette companies make about a penny in profit for every cigarette sold, or about $10,000 for every million cigarettes purchased. Since there is one death for every million cigarettes sold (or smoked), a tobacco manufacturer will make about $10,000 for every death caused by their products…. The value of a human life to a cigarette manufacturer is therefore about $10,000.”
Proctor has even produced a “factories of death” chart, illustrating that arguably the world’s most lethal production plant is Philip Morris’s Richmond cigarette facility, which churned out 146 billion cigarettes in 2010, which adds up to about 146,000 deaths per year.
By 1964, researchers at Harvard had already identified the presence of radioactivity in the form of polonium 210 in cigarette smoke, and the cry went up for safety. As for the notion of safer cigarettes, Proctor says all cigarette filters function the same way—“basically like drinking through a somewhat thinner straw.” He goes even further, arguing that “filters have reduced smoke particle size, producing cancers deeper in the lungs, making them harder to identify and harder to treat.” (Scientists determined that the radiation source was the newer “superphosphate” fertilizers being used heavily on tobacco plants.)
Next came mandated “tar and nicotine numbers,” which turned out to be misleading measures obtained from smoking robots. Then, “an opportunity presented itself to game the system, as we find in the brilliant trick of ventilation.” Manufacturers pricked tiny holes in the paper near the mouthpiece of cigarettes brands like Carlton and True, which consumers got around by covering the holes with fingers or with “lipping” behavior. “Low tars were a fraud, just as “lights” would be,” Proctor writes. Smokers just smoked harder, or differently, or more frequently. In 1983, pharmacologist Neal Benowitz at UCSF broke the official news in the New England Journal of Medicine: Smokers got just as much nicotine, whether they smoked high-, low-, filtered, unfiltered, regular, light, or ultra-light. The industry itself had known this for more than 20 years. “Nicotine in the actual rod was rarely allowed to drop below about 10 milligrams per cigarette,” Proctor asserts, “and no cigarette was ever commercially successful with much less than this amount.” (A Philip Morris psychologist compared nicotine-free cigarettes to “sex without orgasm.”)
Indeed, almost every design modification put in place by tobacco companies over the past century, from flue-curing to filters, has served to make cigarettes deadlier than before. “Talk of ‘safer cigarettes’ is rather like talking about safer terrorism, or safer smallpox, or safer forms of drowning,” Proctor concludes.
And the industry testing continues. The point of tobacco-sponsored research is not simply to discredit an individual researcher’s work, but to create an aggregate bias in the pattern of research—a lot of “noise” in the signal. In other words, “you basically fund lots of research to dispute a hazard, then cite this same research to say that lots of scholars dispute it.” We are told about “mucociliary escalators,” which dredge the tar up and out of smokers’ lungs. We learn that “a rabbit will scream if nicotine is introduced into the eye.” We read excerpts from anguished letters to tobacco companies: “Do you suppose if I continue to smoke Camel Ultra Light Cigarettes and I should develop cancer it will be ‘Ultra Light Cancer?’”
Proctor brings us up to date: Harm reduction, he writes, has become the industry’s new mantra. “The companies now want us to believe that less hazardous products can be and are being made and marketed.” Proctor thinks harm reduction “may end up causing even greater harm” if products touted as “safer” make smokers less likely to quit. As for public health campaigns, “consumers are encouraged to stop consuming,” Proctor writes, “but producers are never discouraged from producing.” Or, as Louis Pasteur once wrote: “When meditating over a disease, I never think of finding a remedy for it, but, instead, a means of preventing it.”
So, what comes next? A glimpse of the future may already be here, in the form of cinnamon- and mint-flavored Camel Orbs, “which look like Tic Tac candy and contain about a milligram of nicotine in a highly freebased form.”
As for the industry’s success in corrupting scientists and academics through various means, the story is just as bad as you think it is: “It would take many thousands of pages to chronicle the full extent of Big Tobacco’s penetration of academia; the scale of such collaborations is simply too vast. From 1995 to 2007 alone, University of California researchers received at least 108 awards totaling $37 million from tobacco manufacturers….”
Part II of III.
Photo Credit: http://theloungeisback.wordpress.com/
via Addiction Inbox by Dirk Hanson on 5/30/12
A review of The Golden Holocaust: Origins of the Cigarette Catastrophe and the Case for Abolition
Part III
Academic collaborations come in many flavors. Just because the money is corporate doesn’t mean the studies that are funded are flawed by definition. But the cigarette industry’s academic philanthropy set new records for hubris, writes Robert Proctor, professor of history at Stanford University, in his new book, The Golden Holocaust. Duke University and Bowman Gray School of Medicine, both in North Carolina, are named for tobacco magnates.
Harvard has a long and dubious history of tobacco largesse. Harvard’s Tobacco and Health Research Program kicked off in 1972 with a generous tobacco grant from the Tobacco Institute, who dreamed up the program in the first place. “The Harvard project made the industry look good and so was handsomely endowed, absorbing $7 million over an eight-year period.” Also in 1972, Harvard anthropologist Carl Seltzer testified for the industry in numerous public hearings, stating: “We do not know whether or not there is a causal relationship between smoking and heart disease.” In 2002, Harvard’s School of Public Health declared it would no longer undertake research sponsored by the cigarette industry. Many universities had already gone cold turkey, and after Harvard, bans were put in place by the Karolinska Institute, Johns Hopkins University, Emory University, and many others.
Proctor informs us that “Washington University in St. Louis has been another big sponge for tobacco money." In 1971, the university set a new world record for an industry grant to a single institution, and “millions more were eventually funneled into the School of Medicine, turning it into a hotbed of cigarette-friendly activism.” The irony of taking money from Big Tobacco to fund research on lung cancer is not lost on Proctor. A good deal of the research was aimed away from tobacco and toward possible causes like viruses. “The goal was clearly more than cancer cures,” he writes. “The industry also hoped to generate good PR and academic allies.” The industry was able to garner sympathetic headlines, like “Helping in Fight against Cancer,” in the St. Louis Globe-Democrat.
The other academic hotbed thoroughly penetrated by Big Tobacco was UCLA, according to Proctor. “Tobacco collaborators at UCLA have attracted their fair share of criticism from public health advocates, and for understandable reasons.” The university picked up its own multimillion-dollar grant from cigarette makers for the Program on Tobacco and Health in 1974, and that wasn’t the first tobacco money the university had taken. “As with all such projects,” Proctor writes, “industry lawyers… played a key role in the decision to fund—with the companies also conceding that the decision ‘should be based more on public relations than on purely scientific grounds.’” The end came in 2007, when “UCLA’s dance with the devil” garnered a ton of unwanted press. Reports showed that UCLA had taken more than $6 million from Philip Morris for research “to compare how children’s brains and monkey brains react to nicotine.”
Proctor admits that singling out Harvard, Washington University and UCLA is somewhat misleading, “given that scholars throughout the world have gorged themselves on tobacco money. Indeed it may well be the rare institution that has NOT at one time or another dipped into this pot.”
Including Stanford, where Proctor teaches. Plenty of Stanford researchers have undertaken contract work and served as expert witnesses for the industry right in Proctor’s own backyard, where “at least eighteen faculty members have received monies (in the form of sponsored research) from the Council for Tobacco Research, with at least two of these—Judith Swain and Hugh McDevitt from the medical school—serving on its Scientific Advisory Board. Stanford pharmacologists were assisting the industry with its diethylene glycol studies as early as the 1930s…”
In the conclusion to his densely researched but surprisingly readable work, Proctor returns to the controlling irony of the book: “Our bizarre starting point is the well-stocked shelf of cigarettes, to which we respond by begging people not to purchase them.” He presents the dream of a world in which cigarettes have been abolished. To do so, he admits, would require a leap. “If phasing out tobacco seems out of reach, this is only because our imaginations are impoverished.” And he has scant patience for the “Prohibition failed” argument. It failed, he says, because people like to drink. “Tobacco presents us with a very different situation. Nicotine is not a recreational drug. Most people who smoke wish they didn’t, and most smokers (90 percent) regret ever having started.”
Graphics Credit: http://www.prwatch.org/node/7004
via Journal of Addiction Medicine - Featured Articles - Editor's Picks by Helmbrecht, Gary D.; Thiagarajah, Siva on 9/12/09
In this article, we will review the prevalence of addiction disorders in pregnancy and the impact that it has on perinatal morbidity and mortality. We will then review effective screening techniques and propose a management scheme for achieving short-term abstinence leading to the ultimate goal of long-term recovery. The various medical and obstetric complications unique to this patient population will be discussed as well as the specific adverse effects of substance abuse on placentation and the developing fetus. Finally, medications proven efficacious in the treatment of addiction disorders will be reviewed in the context of their use in the pregnant population. (C) 2008 American Society of Addiction Medicine
via addiction - Google Blog Search by Paige on 6/5/12
We often talk and read about the “up” side of Facebook—its global reach, exponential growth and the unparalleled advantages of using it as a networking and marketing tool. Yet, as the law of polarity would have it, with every ...
via addiction - Google News on 6/5/12
Q & A With Addiction Specialist About Spice
Patch.com How many patients would you say have been treated for Spice addictions and how has that increased/decreased over the past few years? It has definitely increased on both our substance abuse unit as well as our child adolescent unit. and more » |
via addiction - Google News on 6/5/12
 USA TODAY |
Getting help for K2 addicts
MyFox Detroit Whether it's bath salts, K2 or Spice, the question is where do you turn for help once you realize your loved one is addicted to it. Whether it's bath salts, K2 or Spice, the question is where do you turn for help once you realize your loved one is ... Macomb County father describes struggle with son's K2 addictionWDIV Detroit Efforts to ban synthetic marijuana prove to be difficultDetroit Free Press Phony drug stealing real livesExaminer.com Tucson Citizen all 85 news articles » |
via addiction - Google News on 6/5/12
 ABC News |
Recovering from a 'bath salt' addiction
KOKI FOX 23 A former meth addict who bought bath salts for a legal fix knows it's being sold. "I think it's doing business with the people they've been dealing with and it definitly is underground,” said the woman who didn't want to reveal her identity. 'Bath salts' drug behind Miami face-eating attack could be banned in CanadaNational Post SPECIAL INVESTIGATION: DEADLY TRUTH ABOUT MIAMI CANNIBAL MADMANThe National Enquirer 'Bath salts' plan wins applause in NSCBC.ca Staunton News Leader -The Epoch Times -CTV.ca all 251 news articles » |
via Twitter / NIAAAnews on 5/23/12
NIAAAnews: The NIAAA website has been completely redesigned! It features a modern look, easier navigation, and improved content: http://t.co/zukajlri
via NIDA News on 12/8/11
The National Institute on Drug Abuse (NIDA) will hold a press conference on Wednesday, December 14, to announce the results of its 2011 Monitoring the Future survey. The survey, funded by NIDA—part of the National Institutes of Health—tracks annual drug abuse trends of 8th, 10th, and 12th-grade students, including attitudes and perceived risk of specific illicit drugs. It is one of three major polling instruments the Department of Health and Human Services uses to monitor the nation's substance abuse patterns.
via NIDA News on 1/16/12
A new resource, Seeking Drug Abuse Treatment: Know What to Ask, will help individuals and families struggling with addiction ask the right questions before choosing a drug treatment program. It was developed by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health, and is available to the public free online or in hard copy through NIDA’s DrugPubs service (see information below).
via NIDA News on 12/13/11
Cigarette and alcohol use by eighth, 10th and 12th-graders are at their lowest point since the Monitoring the Future (MTF) survey began polling teenagers in 1975, according to this year's survey results. However, this positive news is tempered by a slowing rate of decline in teen smoking as well as continued high rates of abuse of other tobacco products (e.g., hookahs, small cigars, smokeless tobacco), marijuana and prescription drugs.
via NIDA News on 2/20/12
A new, easy-to-read website on drug abuse designed for adults with a low reading literacy level (eighth grade or below) was launched today by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health. The site, which provides plain language information on neuroscience, drug abuse prevention and treatment, is also a resource for adult literacy educators. It has a simple design with a large default text size, motion graphic videos and other features that make it easy to read and use.
via Journal of Addiction Medicine - Most Popular Articles by Meyer, Marjorie; Benvenuto, Anna; Howard, Diantha; Johnston, Anne; Plante, Dawn; Metayer, Jerilyn; Mandell, Todd on 5/31/12
Background: The goal of this study was to determine whether improved access to medication assisted therapy in the general population, with improved coordination of ancillary services for pregnant women, improved perinatal outcomes in a nonurban area. Methods: The cohort of women treated for opioid dependence during pregnancy with medication-assisted therapy and delivered at a single institution between 2000 and 2006 were retrospectively identified (n = 149 women; n = 151 neonates). Access to opioid agonist therapy for the general population was determined as the combined number of available treatment positions for medication-assisted therapy. Treatment during pregnancy (interim substitution therapy vs opioid treatment program) and pregnancy outcomes were noted from chart review. The primary outcome of trend of prenatal care indices and newborn birth weight over time was determined by Kendall's tau. Results: As access to treatment in the general population expanded from 2000 to 2006, the number of women receiving treatment increased, the proportion of women receiving interim substitution therapy decreased (P < 0.001), gestational age at the initiation of treatment decreased (P < 0.001), and the proportion of women receiving treatment before pregnancy increased (P < 0.001). Infants delivered to mothers in a treatment program had improved birth weight z score compared with those receiving interim substitution therapy (P = 0.007). The proportion of infants discharged to the care of the mother and remaining in maternal care at 1 year improved both over time (P = 0.03; P = 0.004) and with treatment within a treatment program (P < 0.001; P = 0.004). Conclusions: Improved access to opioid agonist treatment programs for the general population in nonurban areas improves perinatal outcome and retention of maternal guardianship.
via Journal of Addiction Medicine - Most Popular Articles by Kelly, Sharon M.; Schwartz, Robert P.; O'Grady, Kevin E.; Gandhi, Devang; Jaffe, Jerome H. on 5/31/12
Objective: Human immunodeficiency virus (HIV)-risk behaviors were examined at 4- and 12-month follow-up for 230 newly admitted methadone patients randomly assigned to receive either methadone only (n = 99) or methadone with drug abuse counseling (n = 131) in the first 4 months of treatment. Methods: The AIDS Risk Assessment was administered at baseline (treatment entry) and at 4- and 12-month follow-up. Linear mixed model analysis examined changes in HIV drug- and sex-risk behaviors over the 12 months in the total sample, drug-risk behaviors in the subsample that reported injecting drugs at baseline (n = 110), and sex-risk behaviors in the subsample that reported engaging in unprotected sex at baseline (n = 130). Results: Significant decreases over time were found in the frequencies of injecting, injecting with other injectors, and sharing cooker, cotton, or rinse water in the total sample and the injector subsample (P < 0.05). Decreases were also found in the frequencies of having sex without a condom either with someone who was not a spouse or primary partner or while high (P < 0.05) in the total sample and the frequencies of having sex without a condom and having sex without a condom while high in the unprotected-sex subsample (P < 0.05). No significant treatment group main effects or Treatment Group × Time interaction effects were found in any of the HIV-risk behaviors in the total sample or either subsample (P > 0.05). Conclusions: During the first 12 months of treatment, providing drug abuse counseling with methadone compared with providing methadone alone was not associated with significant changes in HIV-risk behaviors for methadone maintenance patients.
via Journal of Addiction Medicine - Featured Articles - Featured Articles by Arria, Amelia M.; Caldeira, Kimberly M.; Kasperski, Sarah J.; O'Grady, Kevin E.; Vincent, Kathryn B.; Griffiths, Roland R.; Wish, Eric D. on 5/26/10
Objectives: This longitudinal study examined the prevalence and correlates of energy drink use among college students, and investigated its possible prospective associations with subsequent drug use, including nonmedical prescription drug use. Methods: Participants were 1060 undergraduates from a large, public university who completed 3 annual interviews, beginning in their first year of college. Use of energy drinks, other caffeinated products, tobacco, alcohol, and other illicit and prescription drugs were assessed, as well as demographic and personality characteristics. Results: Annual weighted prevalence of energy drink use was 22.6%wt and 36.5%wt in the second and third year of college, respectively. Compared with energy drink nonusers, energy drink users had heavier alcohol consumption patterns, and were more likely to have used other drugs, both concurrently and in the preceding assessment. Regression analyses revealed that Year 2 energy drink use was significantly associated with Year 3 nonmedical use of prescription stimulants and prescription analgesics, but not with other Year 3 drug use, holding constant demographics, prior drug use, and other factors. Conclusions: A substantial and rapidly growing proportion of college students use energy drinks. Energy drink users tend to have greater involvement in alcohol and other drug use and higher levels of sensation seeking, relative to nonusers of energy drinks. Prospectively, energy drink use has a unique relationship with nonmedical use of prescription stimulants and analgesics. More research is needed regarding the health risks associated with energy drink use in young adults, including their possible role in the development of substance use problems. (C) 2010 American Society of Addiction Medicine
via ASAM President's Blog on 4/10/12
ASAM Acting President Dr. Stuart Gitlow writes what attending Med-Sci means to him and invites all to come join the learning and interact with colleagues at the conference.
via ASAM Headlines on 5/17/12
5/17/2012 3:36 PM National Council on Alcoholism and Drug Dependence, Inc. (NCADD) and its National Network of Affiliates declared May 14-May 20 as a week of awareness for the dangerous effects of consuming alcohol and drugs during pregnancy.
via Addiction Inbox by Dirk Hanson on 3/11/12
Celebrate your sentience March 12-18.
Gather ‘round, children, and the Dana Foundation will tell you an amazing tale about… the You Man Brain…
Well, that is, the HUMAN brain—and the many ways of increasing understanding and awareness of this little three-pound marvel. Officially the brainchild of the Dana Alliance for Brain Initiatives in New York and the European Dana Alliance for the Brain, “Brain Awareness Week (BAW) is the global campaign to increase public awareness of the progress and benefits of brain research,” according to the BAW website.
Founded in 1996, Brain Awareness Week is designed to unite partner organizations around the world “in a week-long celebration of the brain.” Partners include universities, hospitals, schools, government agencies, and service organizations. Partner organizations come up with creative and innovative community activities to educate people of all ages “about the brain and the promise of brain research.” For example, on Wednesday the Dana Alliance is sponsoring a “brain bee” at The Rockefeller University in New York City, where students from 21 area high schools will go head-to-head on their knowledge of neuroscience.
To see the full list of partnerships, from 41 countries, go HERE. For a list of events planned for the week, take a look HERE. Events include open houses at neuroscience laboratories, special brain exhibitions at museums, displays and lectures at community centers, and workshops in the classroom.
If you’re feeling cocky, you can test your brain with several challenges at http://www.testmybrain.org/
Sadly, none of this hoopla will necessarily solve certain perennial brain conundrums, such as:
--If you can’t change your mind, how do you know you have one?
--Is that hole in a man’s penis really there to get oxygen to his brain?
--How can we believe that the brain is the most important organ, when the brain is the organ telling us that?
And finally, the one that keeps me awake at night:
-- How did the scarecrow know he didn't have a brain?
via addiction - Google Blog Search by Damian Thompson on 6/6/12
Benedict XVI is the first pontiff of the age of addiction – and he knows it. In almost all his speeches to young people he mentions illegal drugs: not just to condemn their use, but also to acknowledge their seductiveness.
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The sons of Red Bull are sporting record concentrations of caffeine.
Are energy drinks capable of pushing some people into caffeine-induced psychotic states? Some medical researchers think so, under the right set of conditions.
Red Bull, for all its iconic ferocity, is pretty tame, weighing in at approximately half a cup of coffee. Drinks like Monster Energy and Full Throttle push it up to 100-150, or the equivalent of a full cuppa joe, according to USDA figures at Talk About Coffee. That doesn’t sound so bad—unless you’re ten years old. A little caffeine might put you on task, but an overdose can leave you scattered and anxious—or worse. If you cut your teeth on Coke and Pepsi, then two or three energy drinks can deliver an order-of-magnitude overdose by comparison.
Readers are entitled to ask: Are you serious? Can’t we just ignore the inevitable view-this-with-alarm development in normal kid culture, and move on?
My interest began when I ran across a 2009 case report in CNS Spectrums, describing an apparent example of “caffeine-induced delusions and paranoia” in a very heavy coffee drinking farmer. “Convinced of a plot against him,” the psychologists write, “he installed surveillance cameras in his house and on his farm…. He became so preoccupied with the alleged plot that he neglected the business of the farm…. and he had his children taken from him because of unsanitary living conditions.”
The patient was not known to be a drinker, reporting less than a case of beer annually. He had shown no prior history of psychotic behaviors. But for the past 
seven years, he had been consuming about 36 cups of coffee per day, according to his account. Take that number of cups times 125 milligrams, let’s say, for a daily total of 4500 milligrams. At that level, he should be suffering from panic and anxiety disorders, according to caffeine toxicity reports, and he would be advised to call the Poison Control Center. And that certainly seems to have been the case. “At presentation,” the authors write, “the patient reported drinking 1 gallon of coffee/day.”
seven years, he had been consuming about 36 cups of coffee per day, according to his account. Take that number of cups times 125 milligrams, let’s say, for a daily total of 4500 milligrams. At that level, he should be suffering from panic and anxiety disorders, according to caffeine toxicity reports, and he would be advised to call the Poison Control Center. And that certainly seems to have been the case. “At presentation,” the authors write, “the patient reported drinking 1 gallon of coffee/day.”
On the one hand, the idea of caffeine causing a state resembling chronic psychosis is the stuff of sitcoms. On the other hand, metabolisms do vary, and the precise manner in which coffee stimulates adenosine receptors can lead to anxiety, aggression, agitation, and other conditions. Could caffeine, in an aberrant metabolism, break over into full-blown psychosis? At the Caffeine Web, where psychiatrists and toxicologists duke it out over all things caffeinated, Sidney Kay of the Institute of Legal Medicine writes: “Coffee overindulgence is overlooked many times because the bizarre symptoms may resemble and masquerade as an organic or mental disease.” Symptoms, he explains, can include "restlessness, silliness, elation, euphoria, confusion, disorientation, excitation, and even violent behavior with wild, manic screaming, kicking and biting, progressing to semi-stupor.”
That doesn’t sound so good. In “Energy drinks: What is all the hype?” Mandy Rath examines the question in a recent issue of the Journal of the American Academy of Health Practitioners.
Selling energy drinks to kids from 6 to 19 years old is a $3.5 billion annual industry,Rath asserts. And while “most energy drinks consumed in moderation do not pose a huge health risk,” more and more youngsters are putting away higher and higher doses of caffeine. At the level of several cans of Coke, or a few cups of strong coffee or, an energy drink or three, students can expect to experience improved reaction times, increased aerobic endurance, and less sleepiness behind the wheel. Most people can handle up to 300 mg of caffeine in a concentrated blast. Certainly a better bargain, overall, than three or four beers.
But first of all, you don’t need high-priced, caffeine-packed superdrinks to achieve that effect. A milligram of caffeine is a milligram of caffeine. But wait, what about the nifty additives in Full Throttle and Monster and Rockstar? The taurine and… stuff. Taurine is an amino acid found in lots of foods. Good for you in the abstract. Manufacturers also commonly add sugar (excess calories), ginseng (at very low levels), and bitter orange (structurally similar to norepinephrine). However, the truly interesting addition is guarana, a botanical product from South America. When guarana breaks down, it’s principal byproduct is, yes, caffeine. Guarana seeds contain twice the caffeine found in coffee beans. Three to five grams of guarana provide 250 mg of caffeine. Energy drink manufacturers don’t add that caffeine to the total on the label because—oh wait, that’s right, because makers of energy drinks, unlike makers of soft drinks, don’t have to print the amount of caffeine as dietary information. And on an ounce-for-pound basis, kids are getting a lot more caffeine with the new drinks than the older, labeled ones.
All of this increases the chances of caffeine intoxication. Rath writes that researchers have identified caffeine-related increases among children in hypertension, insomnia, motor tics, irritability, and headaches. Chronic caffeine intoxication results in “anxiety, emotional disturbances, and chronic abdominal pain.” Not to mention cardiac arrhythmia, seizures, and mania.
So what have we learned, kids? Energy drinks are safe—if you don’t guzzle several of them in a row, or substitute them for dinner, or have diabetes, or an ulcer, or happen to be pregnant, or are suffering from heart disease or hypertension. And if you do OD on high-caffeine drinks, it will not be pleasant: Severe palpitations, panic, mania, muscle spasms, etc. Somebody might even want to take you to the emergency room. Coaches and teachers need to keep a better eye out for caffeine intoxication.
Note: There is a “caffeine calculator” available at the Caffeine Awareness website, designed to determined whether you are a coffee addict. I can by no means swear to its scientific accuracy, but, based on my own, distinctly non-young person daily intake, the test told me that my consumption was likely to manifest itself as “high irritability, moodiness & personality disorders.” Can I blame it all on those endless cokes we had as kids? Growing up in the Baby Boom suburbs, we all drank carbonated caffeine beverages instead of water. Nothing much has changed except the caffeine levels.
Rath, M. (2012). Energy drinks: What is all the hype? The dangers of energy drink consumption Journal of the American Academy of Nurse Practitioners, 24 (2), 70-76 DOI: 10.1111/j.1745-7599.2011.00689.x
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via ASAM Headlines on 5/30/12
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Tammerlin Drummond: Technology addiction a global social disease
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 Minnesota Public Radio |
Boogaard's addiction: Street sale of prescription drugs
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Mothers battling addiction
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