What It Means to Say Alcoholism is Genetic

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."

Gateway to Absurdity

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

Review: Memoirs of an Addicted Brain

“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/

What's in That X Pill, Ravers?

Ecstasy comes loaded with other drugs. 

 I'm not a huge fan of infographics, mostly because they tend to overpromise and are often marred by factual errors. But this one sticks to basics, and reminds kids that pure MDMA is not the play here. Familiar with dibenzylpiperazine? How about 5-MEO-DIPT? Good old methamphetamine you know—but do you want your Ecstasy, itself an amphetamine spinoff, springloaded with an extra dose of it? Scroll down for pictures of "dirty rolls."

 Via Recovery Connection
View More Addiction Related Infographics

Addiction Doctors Pick Top Ten Journal Articles

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/

A Drug For Marijuana Withdrawal?

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 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/

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/