Dude, where’s my metaconsciousness?

“Lost in the sauce.”

I have to admit I was taken with the opening sentence of this 2009 study published in Psychological Sciences: “Alcohol consumption alters consciousness in ways that make drinking both alluring and hazardous.”

Indeed it does. There’s no improving on that direct statement about the basic paradox presented by booze: Like so many pleasures, it is both seductive and dangerous. I was further intrigued by the prospects held out by the abstract, which promised “a rigorous examination of the effects of alcohol on experiential consciousness and metaconsciousness.” After all, we have come a long ways from the 50s, when alcohol was seen in Freudian terms, as a way of releasing tension, steam-engine style.

The study, by Michael A. Sayette and Erik D. Reichle of the University of Pittsburgh in Santa Barbara, along with Jonathan Schooler of the University of California at Santa Barbara, walks us through the salient recent theories, including the alcohol-myopia theory that gained a foothold in the 90s. In this theory, alcohol “reduces processing capacity so that a great proportion of this capacity has to be devoted to the demands of immediate, ongoing activity.” Like remaining upright, or inserting a key in the lock of a door. It also means that alcohol consciousness is precarious. The pissed-off office worker who comes home to drink may relieve his worries “if he is distracted by television, but he may ‘cry in his beer’ if no such distraction is available.”

One of the alluring and hazardous affects of alcohol is its tendency to cause what the study authors meticulously refer to scientifically as: zoning out. That is to say, episodes of mind wandering.

Enjoy drinking while you read? Listen to this: “Participants who drank alcohol were mind-wandering without awareness of doing so about 25% of the time that they were engaged in the reading task. This frequency was more than double that for participants in the placebo condition.”

The study—“Lost in the Sauce: The Effects of Alcohol on Mind Wandering?”—investigated “the effect of alcohol on both the occurrence of mind wandering and the capacity to notice that one’s mind has wandered.” The psychologists gathered 50 men between 21 and 35, put them in a lab, and then split them into a control group and test group. The participants entered the “drink-mixing room where a research was waiting with a tray containing a chilled vodka bottle, a bottle of chilled cranberry-juice cocktail (Ocean Spray), a glass, a graduate cylinder, and a beaker.”

Participants are never in short supply for this kind of clinical study. For half the group, the bottle contained 100-proof Smirnoff. The placebo group got flattened tonic water in a glass pre-slimed with vodka, and were later given fake blood-alcohol test results to further the illusion that they’d had a little alcohol. The drinking participants achieved a mean blood alcohol level of 0.067. Participants in the placebo group received a bogus reading of 0.045, which is the “highest credible reading for deceived participants.”

How did the researchers know if the drinkers were zoning out? They asked. But first, they set them to work reading the first five chapters of War and Peace on a computer. The experimenters asked each participant if they had read War and Peace, in whole or in part, before the experiment, and “all indicated that they had not.” (Men aged 21 to 35, recall.) Their task was to read the first 34 pages of the book, or read for 30 minutes, whichever came first. Before starting, the researchers drilled them on the technical description of zoning out: “At some point during reading, you realize that you have no idea what you just read.”

That’s it in a nutshell, and as we all know, you don’t have to be drunk to experience that effect—but it helps. We have all been witness to the drunk who “loses the thread” of his or her monologue and heads off in another linguistic direction altogether, without apparently noticing the shift. The researchers asked participants to hit a special key, helpfully marked “ZO,” when they noticed during reading that they had zoned out. And they used an additional probe measure, interrupting the readers with a tone and asking them if their mind was wandering or concentrated on the text at that moment. At the end of the session, both groups took a 20-question true/false test on what they had read.

So, what were the differences? Both the placebo group and the drinking group spend about the same amount of time reading, and scored roughly the same on the reading comprehension test. No significant differences in reading rates or immediate retention. And when the researchers compared the first, self-reported measure of mind wandering, the two groups were also “similar in the frequency with which they caught themselves zoning out.”

The big difference showed up when researchers compared the frequency of mind wandering as measured by the arbitrary prompts. In that case, the drinkers zoned out twice as often, but were less likely to catch themselves at it. What the drinkers appeared to be sacrificing was a significant degree of meta-awareness, the act of “thinking about thinking.”

So, when they got probed, what were the drinkers thinking about instead of War and Peace? According to the authors, “alcohol seemed to particularly increase distraction related to sensory states, such as hunger, thirst, and other consummatory motives.” One might be tempted to call them “mammalian motives,” in the sense that alcohol intoxication sometimes reduces drinkers to back-brain, lower-order, fight-or-flight responses not highly compatible with meta-cognition.

This is not exactly a groundbreaking study, it’s fair to say. But it does point up the fact that only a few ounces of alcohol can induce episodes of mind wandering which are not detected by the drinker—mini-blackouts, in a manner of speaking.

Although a reduction in working memory capacity is part of the answer, it is not the whole story. What else fuels this “alcohol myopia” is unclear, but the authors suggest that their findings represent the first practical demonstration that “alcohol disrupts individuals’ meta-awareness of the current contents of thought.” Or, as a heavy drinker might be prone to put it, “Now where was I?”

Graphics Credit: http://www.pnas.org/

“Addiction Fiction”

Coming-of-Age Drug Novels

Call it “addiction fiction.” In the past few years we have seen a blossoming of this genre, where the private eye goes to 12-Step meetings, and one day your sponsor may just save your life by gunning down a rival in the street. Or, where the wise-beyond-their-years prep school drug addicts engage in Brett Easton Ellis-style sex and ennui.

Fiction readers of a certain age will recall that this is not a new thing under the sun. From Junky to The Man With the Golden Arm, from Naked Lunch to Less Than Zero, drug novels have always been with us. Addiction fiction has two distinct subgenres: addicts with money, and addicts without money. For obvious reasons, the latter genre is the prevailing one—Trainspotting and Requiem for a Dream come to mind. But the wealthy end of the spectrum is not without representation. Consider The Basketball Diaries, or Bright Lights, Big City.

As an example of the first type of book, the one where the addict has no money, we have Spoonful, by first-time author Chris Mendius. As for the upscale second type, there is the recently released novel, No Alternative,  by William Dickerson, a budding film director with an MFA. I would judge both authors to be well south of the age of 40, making both of them pure examples of Generation X. 

Ah, the 90s. As time passes, it seems clear that the death of Kurt Cobain has been added to the touchstones of American youth culture, in a tradition going back to the 60s. Where were you when Kennedy died? When Lennon died? When Cobain died? This last question matters, since Nirvana and Cobain are threaded thematically through both of these new novels. As Chris Willman wrote at Stop the Presses: “April 5 is to many contemporary rock fans what November 22 is to older baby boomers: the day you can almost certainly remember where you were or what you were doing when you heard that ___ died. That's not to say that Kurt Cobain's suicide represented a loss of national innocence in the same way that JFK's assassination did. For one thing, Cobain's whole life and career already symbolized lost innocence, long before he died.”

In Generation X drug novels, lost innocence isn’t lost—there was never any innocence in the first place.

Michael, the narrator of Spoonful, is the kind of drug addict with no money. Michael is forthright, if not one to probe the philosophical ironies of his condition: “Nobody ever says, ‘When I grow up, I want to be a junkie.’” End of story. Well, the beginning, really. In this well-written junky novel, author Chris Mendius brings his tragic characters to life in a manner that calls to mind Hubert Selby, Jr.’s stark New York classics of addiction without redemption.

Set in Chicago’s Wicker Park area, young Michael and his pal Sal find their way to heroin in a hurry. They also quickly learn the flip side of the illness—the sickness of withdrawal, “like having a debilitating combination of food poisoning and the flu, with periodic muscle cramps.” No matter. “Once we made it through all that, we decided to stay off dope. A month passed with no discernible improvement in our lives and we promptly resumed getting high.”

It’s heroin he craves. Michael is no fan of cocaine: “You’re up all night, running your mouth, jaw twitching, nose burning. You might want to fuck but you can’t. All you can do is keep going. Before you know it, the birds are chirping and the garbage trucks are rolling. You’re out hundreds of dollars and for what?” And they scoff at pharmaceutical efforts at non-addictive synthetic opiates, “engineered to not let anyone feel a moment of undeserved pleasure.” One character likens kicking methadone to “getting your skin pulled off with pliers.”

The debate over freely distributing the drug naloxone as an anti-OD safety measure is referred to obliquely: “That’s the thing with smack. It’s a fine line between the time of your life and the end of your life…. More often than not, the difference between life and death was having someone there to revive you or call somebody who could.”

Mendius is good at drawing a picture of the addict’s endless grind: “Finding the ways and means to score is a twenty-four-seven gig. You might get lucky and hit it big now and then but you’re always looking ahead. Plotting. Planning. No matter how much you get or how close the scrape, you always gotta keep at it. Day in and day out.”

Michael never quits for long, and when he is off heroin, he buries himself in marijuana and booze. There is no redemptive ending. He walks off into the sunset.

From seedy Chicago to the upper reaches of Westchester, New York. Like Spoonful, No Alternative by William Dickerson features characters whose collective memory goes back no farther than the 80s. Which sucked, as we all know, and as Thomas, the narrator, never tires of telling us. Thomas and his friends are drug and alcohol abusers with money. The drugs of choice are prescription medications, not heroin or cocaine, for these products of Fordham Prep. 

It is 1994, and the grunge youth of Yonkers, the children of Vietnam vets and hippies, are rootless and confused. “There was no clear-cut path beckoning them. No modus operandi.” It was a generation, Dickerson writes, that “earned a label that was just about as vague as their sense of what to do with their lives: Generation X.” In this version, not much has changed since the crack-crazy L.A. 80s of Brett Easton Ellis. The names and the drugs have been altered, but otherwise the trappings are indistinguishable: high disposable income and excessive ennui.

Thomas supports his crazy little sister Bridget, who becomes a white rapper named Bri Da B. His sister’s drug of choice is cutting herself: “She was determined to be in control. If she was going to bleed, it was going to be a decision, it was going to be controlled, and she was going to bleed everywhere, not just from the abyss between her legs. If pain was to be a constant, might as well get used to it and build up a tolerance.”

No Alternative is readable enough, but it does not carry the campy forward motion of other rich-kid addiction books. It is more measured, dry, and there is an odd hitch in the narration, which is resolved, rather shakily, at the end, with a big Reveal that distracts the reader from the central relationships in the story.

So, two early novels, by promising young writers, about drugs and what they do to you. It will be interesting to find out what becomes of these authors, and what manner of new work they get up to in the future. The story never ends where you think it does.

Ivan Oransky on the Disease Model at TEDMED 2012

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.”

From Their Mouth to Your Ear: Researchers Talk Drugs

A collection of five-question interviews.

I’ll be away from the Addiction Inbox office this week, attending the big TEDMED health and medicine powwow in Washington, D.C.

In the meantime, here’s a summation (with links) of the interviews I’ve been doing recently in the “five-question interview” series. I’ve been very lucky to nab some state-of-the-art thinkers, working at the top of their fields, from psychiatry to pharmacology to neuroscience.

See below for the story thus far:



David Kroll, former Professor and Chair of Pharmaceutical Science at North Carolina Central University in Durham, is now Science Communications Director for the Nature Research Center at the North Carolina Museum of Natural Sciences.

“The attraction to users was, until recently, that Huffman cannabis compounds (prefixed with "JWH-" for his initials) could not be detected in urine by routine drug testing. Hence, incense products containing these compounds have been called ‘probationer's weed.’" MORE

Vaughan Bell is a Senior Research Fellow at the Institute of Psychiatry, King’s College, London. He is also honorary professor at the Universidad de Antioquia in Medellín, Colombia.

"I was very struck by the appearance of classic Kluver form constants [after taking ayahuasca], geometric patterns that are probably caused by the drug affecting the visual neurons that deal with basic perceptual process (e.g. line detection)." MORE

Jon Simons, a cognitive neuroscientist, is a lecturer in the Department of Experimental Psychology at the University of Cambridge, UK, and principal investigator at the University’s Memory Laboratory.

“If you’re at a party and happen to drunkenly strike up conversation with Angelina Jolie (or Brad Pitt, if you prefer) and, bowled over by your charm and witty repartee, she tells you her phone number, you may well not remember it when you wake up sober the next morning. However, the evidence suggests that you would have a better chance of recalling the number if you got drunk again." MORE

Bankole Johnson is professor and chairman of the University of Virginia’s Department of Psychiatry and Neurobehavioral Sciences.

“With growing and clear acceptance of the neurobiological underpinnings of addiction, our work on pharmacogenetics promises to provide effective medications—such as ondansetron—that we can deliver to an individual likely to be a high responder, based on his or her genetic make up." MORE

Michael Farrell is the director of the National Drug and Alcohol Research Centre (NDARC) at the University of New South Wales in Sydney, Australia. Before that, he was Professor of Addiction Psychiatry at the Institute of Psychiatry at Kings College, London.

“The near complete absence of methadone or buprenorphine treatment in American prisons is hard to understand, when you see what a great contribution US research and treatment with methadone and buprenorphine has had globally. Now there are over 300,000 people on methadone in China as part of HIV and AIDS prevention." MORE

Deni Carise is a clinical psychologist who serves as senior vice president and chief clinical officer at Phoenix House, a leading U.S. non-profit drug treatment organization with more than 100 programs in 10 states.

“Those in recovery see the disease of alcoholism or addiction as a moral obligation to get well. If you know you have this disease and the only way to keep it under control is not to use alcohol or drugs, then that’s what you have to do." MORE


Keith Laws is professor of cognitive neuropsychology and head of research in the School of Psychology at the University of Hertfordshire, UK.

"Some may tolerate 100s or even 1000s of E tablets, but for others far fewer may lead to memory problems. We can predict that 3 in 4 users will develop memory problems, but not which 3 or after how many tablets." MORE

photo credit: http://www.startawritingbusiness.co.uk

Interview with Cognitive Neuropsychologist Keith Laws

LSD, E, CBT, and “Mind-Pops.”

Our latest participant in the “Five Question Interview” series is Dr. Keith Laws, professor of cognitive neuropsychology and head of research in the School of Psychology at the University of Hertfordshire, UK. Dr. Laws holds a Ph.D. from the Department of Experimental Psychology at the University of Cambridge, and is the author of Category-Specificity: Evidence for Modularity of Mind. He has written extensively on cognitive deficits resulting from certain types of neurological injury, and has won several awards for his research on cognitive functioning in schizophrenia. He also maintains an active interest in the challenges of functional brain imaging. Professor Laws is frequently quoted in the British media, and is the author of more than 100 peer-reviewed articles. He is a Chartered Psychologist and an Associate Fellow of the British Psychological Society. And recently, Professor Laws became a blogger, launching the LawsNeuroBlog. He maintains a web homepage, and is virtually unbeatable in the category of obscure British rock trivia.

1. LSD is back in the news, with a rehash of several old studies on acid and alcoholism. A lot of people would like to revive research interest in LSD, MDMA, magic mushrooms, and other psychedelics. What’s your view?

Keith Laws: Yes, “re-hash” is an appropriate phrase—we are witnessing a rebranding of “counter-culture” as “over-the-counter-culture.” The history of LSD research is frequently retold as if grand therapeutic advances were halted because hostile governments criminalised LSD. The bottom-line, however, is that most studies of the 50s and 60s produced little worthy of further scientific pursuit. The recent meta-analysis of 60s studies examining whether LSD reduces “alcohol misuse” is a case in point.

That meta-analysis consisted of 6 trials—none of which produced a significant effect, but their total pooled effect suggested some impact on alcohol misuse. In my recent post on this study, I highlighted a series of points, including: how it is likely that further negative studies have been gathering dust in the file drawers of researchers over the years; how some samples consisted of people with serious comorbid mental health and neurological problems (schizophrenia, epilepsy, organic brain disorder, low IQ); and crucially, how the authors made the totally unfounded assumption that anyone dropping-out of the studies had relapsed into drinking. This had a large and disproportionate impact on the control samples in those studies—as many more dropped out from control groups. Combined with the lack of significant effects in any one study, doubts exist about relying on these data as a justification for starting large-scale trials of LSD for alcoholism. We should certainly skeptically regard statements by some, such as Professor David Nutt, that LSD is “as good as anything we’ve got for treating alcoholism.”

2. Tell us about your research interest in the effect of Ecstasy (MDMA) on memory.

Keith Laws: First, I think its crucial not to confuse E and MDMA. Studies of MDMA in humans are few, and mostly examine acute effects via self-report. The vast majority of studies though, including our work, examine the residual effects of street-E in abstinent users i.e. taking largely unknown compounds mixed with varying degrees of MDMA. For me, the real public health issue relates to street-E since most people outside of the lab rarely get to consume pure MDMA.

In 2007 we meta-analysed 26 studies that had examined memory on standardized tests in over 600 ecstasy users and 600 non-users and found significant long and short-term verbal memory impairments in 75% of users. Intriguingly, E was unrelated to visual memory problems; however those who also smoked cannabis did display significant visual memory impairment. A key finding of ours was that the lifetime number of E tablets consumed was unrelated to the degree of memory impairment. This led to a host of misrepresentations in the media and amongst E users who saw it as license to take as many Es as they want. I view this finding, however in a much starker light—taking E is akin to playing Russian Roulette with your memory. Some may tolerate 100s or even 1000s of E tablets, but for others far fewer may lead to memory problems—we can predict that 3 in 4 users will develop memory problems, but not which 3 or after how many tablets. Of course, ecstasy (like Cannabis) is often advocated as a safe-ish drug because it rarely kills. Indeed, metrics of drug harm developed in the UK emphasise physical and social harm, but fail to explicitly acknowledge the cognitive problems associated with E and other recreational drugs. Given that as many as 500,000 young people in the UK use E each week and 75% are affected, then that’s 375,000 young people developing significant verbal memory problems!

3. You’re not convinced by the findings of a recent study of magic mushrooms, where the researchers documented an overall decrease in brain activity. What else could account for this effect?

Keith Laws: Well, the surprising thing about the Carhart-Harris et. al. psilocybin study was the general pattern of brain deactivation, which contrasts with the findings of activation in others such as Vollenweider and colleagues in Switzerland who find increased activation. The decreased activation especially in the medial prefrontal cortex (mPFC) and the posterior cingulate cortex (PCC) were curious and reminded me of the similar deactivation in these areas linked both to anxiety and to the anticipation of unpleasant events. It occurred to me that the prospect of tripping in a scanner may be quite anxiety provoking, and several features of the study led to me to think this may have been the case. First the order of testing was always the same - participants received the placebo scan always before the psilocybin scan and so, could always anticipate the trip— potentially heightening anxious anticipation in that condition. Second, Carhart-Harris et. al. measured “anxiety” and “fear of losing one’s mind” and both multiplied many fold in the psilocybin condition. Interestingly and subsequently, Vollenweider and colleagues pooled date from 23 studies and found that experimental settings involving scanning most strongly predicted unpleasant and/or anxious reactions to psilocybin - converging directly on my suspicion. Although nobody would deny that hallucinogens such as psilocybin impact brain function - the question is which parts reflect the “trip” and which parts reflect “anxiety about the trip”?

4. You have also looked at the matter of using cognitive behavioral therapy for various kinds of mental disorders. How does CBT measure up, in your opinion? Is it useful for addiction?

Keith Laws: Yes, unlike any other country, the UK endorses using CBT to treat psychotic symptoms and to prevent relapse in schizophrenia. Indeed, “NICE” (the National Institute of Clinical Excellence), which decide which treatments are made available to UK patients, suggest that we offer CBT to “all people with schizophrenia”. Anyway, we meta-analysed the data for whether CBT reduces symptomatology or prevents relapse and came to the conclusion that the evidence supports neither. Crucially, CBT only appeared to “work” when the therapists were not blind at outcome assessment i.e. they knew to which group the patient was assigned (CBT or control)! The irony is that CBT therapists sing the mantra of evidence-based practice!

In terms of the use of CBT in people with substance abuse problems, it produces a small impact on abstinence with opiates, stimulants and cocaine, but has little or impact on alcohol use; and as one might expect, these effects disappear across time. Some evidence also suggests that women respond better to CBT than men. Perhaps the most intriguing finding in this area is that CBT has had much greater success in reducing cannabis use, with up to 80% showing significant reduction in use.

5. What else have you been investigating recently? What are you excited about?

Keith Laws: Over the past 3 years or so I have been doing more work with individuals suffering from the obsessive compulsive syndrome of disorders i.e. OCD, Body Dysmorphic Disorder, Trichotillomania, Schizo-Obsessive disorder, Tourette’s, and Perfectionism. Our work is looking at phenotypes that might be expressed through this range of disorders and in their first-degree unaffected relatives. 

Other things we are working on include what we call “Mind-Pops”—those little thoughts, words, images, or tunes that suddenly pop into your mind at unexpected times and are totally unrelated to your current activity—described long ago by novelists such as Marcel Proust and Vladimir Nabokov.  We have just published a paper showing that verbal hallucinations, the core symptom of schizophrenia, may be related to the mind-pop phenomenon that almost everybody experiences, but just manifests itself in a different way.

MDMA Likes It Hot

X and ambient air temperature.

One of the enduring mysteries about MDMA, the popular amphetamine derivative known as Ecstasy, or X, is the relationship between the drug and ambient air temperature. Why are raves hot, sweaty, and full of loud music and flashing lights? Because “human subjects report a higher euphoric state when taking the drug in sensory rich environments,” according to researchers. So there’s a reason for all those glow sticks and speaker stacks. But is it something inherent in the mechanism of the drug—or simply the overheated party atmosphere combined with vigorous dancing—that can sometimes raise a ravers’ body temperature to dangerous levels?

Drug researchers have known for some time that Ecstasy and high temperature are somehow interlinked. Animal studies have produced strong evidence that a heated environment can cause an increase in MDMA-stimulated serotonin 5-HT response. Many ravers take steps to prevent hyperthermia, or overheating, by regularly drinking water and coming off the dance floor at regular intervals. Most people have heard of hypothermia, a condition in which body temperature drops to dangerously low levels. But hyperthermia can be just as deadly, and it is a common emergency room complaint in MDMA admissions. 

In animal models, rats on MDMA (they like it enough to self-administer) show significantly elevated responses to serotonin in the nucleus accumbens at high room temperatures. What does that mean? What goes up must come down: It opens the door to possible serotonin depletion, which can cause dysfunctions in mood and cognition. Researchers at the University of Texas in Austin have found that in rodents, “the magnitude of the hyperthermic response has been tightly correlated with MDMA-induced 5-HT depletion in various brain regions.” The question they pose is whether “elevated ambient temperatures, such as those encountered in rave venues, can exacerbate MDMA-induced temperature-increasing effects and the likelihood of adverse drug effects.” (Cocaine has temperature-related effects as well. When the ambient air temperature is higher than 75 degrees F, accidental cocaine overdoses increase.)

Ecstasy boosts dopamine as well. The Texas researchers suggest that “the combined enhancement of 5-HT and dopamine may contribute to MDMA’s unique effects on thermoregulation.” They also found that core temperature responses appeared to be “experience-dependent,” meaning that rats didn’t show significantly elevated core temperatures in warm rooms until after they had rolled with MDMA at least ten times. And the worse it gets, the worse it gets, according to the report, published in European Neuropsychopharmacology: “Our results suggest that a heated environment facilitates MDMA-induced disruption of homeostatic thermoregulatory responses, but that repeated exposure to MDMA may also disrupt thermoregulation regardless of ambient temperature.”

So, while all that sweaty dancing amps up the perceptual effects of Ecstasy, it isn’t necessarily implicated in overheating. To simulate a nightclub full of X-ed out ravers, investigators at the Scripps Research Institute tested rats on MDMA while the animals exercised on activity wheels.  Writing in Pharmacology Biochemistry and Behavior, the researchers found that “wheel activity did not modify the hyperthermia produced…. These results suggest that nightclub dancing in the human Ecstasy consumer may not be a significant factor in medical emergencies.”

Bottom line: Although we have a reasonable idea of how it works in animals, we don’t really know how much of that knowledge applies to humans in rave settings. Research aimed at teasing out the specifics of temperature-related responses to MDMA is ongoing. And it does matter. Frequent heat-induced responses could lead to prolonged 5-HT depletion, which is suspected of causing an escalation of drug intake in experienced Ecstasy users. And frequent, escalating use of MDMA is implicated in a long roster of potential cognitive impairments. 

Photo Credit: http://electricchildren.com

The Mysteries of the Blunt

Why do so many smokers combine tobacco with marijuana?

People who smoke a combination of tobacco and marijuana, a common practice overseas for years, and increasingly popular here in the form of “blunts,” may be reacting to some unidentified mechanism that links the two drugs. Researchers believe such smokers would be well advised to consider giving up both drugs at once, rather than one at a time, according to an upcoming study in the journal Addiction.

Clinical trials of adults with cannabis use disorders suggest that “approximately 50% are current tobacco smokers,” according to the report, which was authored by Arpana Agrawal and Michael T. Lynskey of Washington University School of Medicine, and Alan J. Budney of the University of Arkansas for Medical Sciences.  “As many cannabis users smoke a mixture of cannabis and tobacco or chase cannabis use with tobacco, and as conditioned cues associated with smoking both substances may trigger use of either substance,” the researchers conclude, “a simultaneous cessation approach with cannabis and tobacco may be most beneficial.”

A blunt is simply a marijuana cigar, with the wrapping paper made of tobacco and the majority of loose tobacco removed and replaced with marijuana. In Europe, smokers commonly mix the two substances together and roll the combination into a single joint, the precise ratio of cannabis and nicotine varying with the desires of the user. “There is accumulating evidence that some mechanisms linking cannabis and tobacco use are distinct from those contributing to co-occurring use of drugs in general,” the investigators say. Or, as psychiatry postdoc Erica Peters of Yale put it in a press release, “There’s something about tobacco use that seems to worsen marijuana use in some way.” The researchers believe that this “something” involved may be a genetic predisposition. In addition to an overall genetic proclivity for addiction, do dual smokers inherit a specific propensity for smoked substances? We don’t know—but evidence is weak and contradictory so far.

Wouldn’t it be easier to quit just one drug, using the other as a crutch? The researchers don’t think so, and here’s why: In the few studies available, for every dually addicted participant who reported greater aggression, anger, and irritability with simultaneous cessation, “comparable numbers of participants rated withdrawal associated with dual abstinence as less severe than withdrawal from either drug alone.” So, for dual abusers, some of them may have better luck if they quit marijuana and cigarettes at the same time. The authors suggest that “absence of smoking cues when abstaining from both substances may reduce withdrawal severity in some individuals.” In other words, revisiting the route of administration, a.k.a. smoking, may trigger cravings for the drug you’re trying to quit. This form of “respiratory adaption” may work in other ways. For instance, the authors note that, “in addition to flavorants, cigarettes typically contain compounds (e.g. salicylates) that have anti-inflammatory and anesthetic effects which may facilitate cannabis inhalation.”

Studies of teens diagnosed with cannabis use disorder have shown that continued tobacco used is associated with a poor cannabis abstention rate. But there are fewer studies suggesting the reverse—that cigarette smokers fair poorly in quitting if they persist in cannabis use. No one really knows, and dual users will have to find out for themselves which categories seems to best suit them when it comes time to deal with quitting.

We will pass up the opportunity to examine the genetic research in detail. Suffice to say that while marijuana addiction probably has a genetic component like other addictions, genetic studies have not identified any gene variants as strong candidates thus far. The case is stronger for cigarettes, but to date no genetic mechanisms have been uncovered that definitively show a neurobiological pathway that directly connects the two addictions.

There are all sorts of environmental factors too, of course. Peer influences are often cited, but those influences often seem tautological: Drug-using teens are members of the drug-using teens group. Tobacco users report earlier opportunities to use cannabis, which might have an effect, if anybody knew how and why it happens.

Further complicating matters is the fact that withdrawal from nicotine and withdrawal from marijuana share a number of similarities.  The researchers state that “similar withdrawal syndromes, with many symptoms in common, may have important treatment implications.” As the authors sum it up, cannabis withdrawal consists of “anger, aggression or irritability, nervousness or anxiety, sleep difficulties, decreased appetite or weight loss, psychomotor agitation or restlessness, depressed mood, and less commonly, physical symptoms such as stomach pain and shakes/tremors.” Others complain of night sweats and temperature sensitivity.

And the symptoms of nicotine withdrawal? In essence, the same. The difference, say the authors, is that cannabis withdrawal tends to produce more irritability and decreased appetite, while tobacco withdrawal brings on an appetite increase and more immediate, sustained craving. Otherwise, the similarities far outnumber the differences.

None of this, however, has been reflected in the structure of treatment programs: “Emerging evidence suggests that dual abstinence may predict better cessation outcomes, yet empirically researched treatments tailored for co-occurring use are lacking.”

The truth is, we don’t really know for certain why many smokers prefer to consume tobacco and marijuana in combination. But we do know several reasons why it’s not a good idea. Many of the health-related harms are similar, and presumably cumulative: chronic bronchitis, wheezing, morning sputum, coughing—smokers know the drill. Another study cited by the authors found that dual smokers reported smoking as many cigarettes as those who only smoked tobacco. All of this can lead to “considerable elevation in odds of respiratory distress indicators and reduced lung functioning in those who used both.” However, there is no strong link at present between marijuana smoking and lung cancer.

Some researchers believe that receptor cross-talk allows cannabis to modify receptors for nicotine, or vice versa. Genes involved in drug metabolism might somehow predispose a subset of addicts to prefer smoking. But at present, there are no solid genetic or environmental influences consistent enough to account for a specific linkage between marijuana addiction and nicotine addiction, or a specific genetic proclivity for smoking as a means of drug administration.

Agrawal, A., Budney, A., & Lynskey, M. (2012). The Co-occurring Use and Misuse of Cannabis and Tobacco: A Review Addiction DOI: 10.1111/j.1360-0443.2012.03837.x

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