Dying For Caffeine

It’s not the coffee, it’s everything else.

Late last year, coffee drinkers were buoyed by the release of a massive study in the New England Journal of Medicine that “did not support a positive association between coffee drinking and mortality.” In fact, the analysis by Neal D. Freedman and associates showed that even at the level of 6 or more cups per day, coffee consumption appeared to be mildly protective against diabetes, stroke, and death due to inflammatory diseases. Men who drank that much coffee had a 10% lower risk of death, and women in this category show a 15% lower death risk. Coffee, it seemed, was good for you.

Hooray for coffee—but lost in the general joy over the findings was the constant association of coffee with unhealthy behaviors like smoking, heavy alcohol, use, and consumption of red meat. And the happy coffee findings did not consider the consumption of caffeine in other forms, such as energy drinks, stay-awake pills, various foodstuffs, and even shampoos. 

One of the earliest battles over “energy drinks” was an action taken in 1911 under the new Pure Food and Drug Act—the seizure  by government agents of 40 kegs and 20 barrels of Coca-Cola syrup in Chattanooga. Led by chemist Harvey Wiley, the first administrator of the Food and Drug Administration (FDA), agents of the fledgling organization acted on the belief that the soft drink contained enough caffeine to pose a significant public health hazard. The court case went on forever. Eventually Coca-Cola cut back on caffeine content, and the charges were dropped.

Jump cut to 2012, and watch the FDA grapple with the same question a hundred years later, citing concerns about undocumented caffeine levels in so-called energy drinks in the wake of an alleged link between the caffeinated soft drinks and the death of several young people. According to Dr. Kent Sepkowitz, writing in the Journal of the American Medical Association, while only 6% of young American men consume the drinks, “in a recent survey of U.S. overseas troops, 45% reported daily use.” In 2006, more than 500 new energy drinks hit the market. By 2011, sales of energy drinks in the U.S. climbed by more than 15% to almost $9 billion.

Death by caffeine has long been a subject of morbid interest, and a recent article in the Journal of Caffeine Research  by Jack E. James of Iceland’s Reykjavik University questions these prevailing assumptions, and brings together the latest research on this perennial question, including, yes, a consideration of whether the time has come to regulate caffeine as some sort of controlled substance.

Last month, the FDA released reports that attributed a total of 18 deaths to energy drinks. Somewhere between 3 and 10 grams of coffee will kill you, especially if you are young, old, or suffer from various health problems. The generally accepted lethal dose is 10 g. The wide gap in estimates and mortality reports reflects the wide variation in caffeine’s effects.  Half the lethal dose can kill a child, and some adults have survived 10 times that amount. As I wrote in an earlier post (“Energy Drinks: What’s the Big Deal?”): “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 hearth disease or hypertension. And if you do OD on high caffeine intake, it will not be pleasant: Severe cardiac arrhythmias, palpitations, panic, mania, muscle spasms, and seizures.”

Warning signs include racing heart, abdominal pain, vomiting, and agitation. Since the average cup of coffee weighs in at about 100 milligrams, there doesn’t seem to be much to worry about in that regard. Nonetheless, the American National Poison Data System (NPDS) has more than 6,000 “case mentions” related to caffeine. One of these cases generated considerable press coverage: the death of a 14 year-old girl with an inherited connective tissue disorder. 

In his article for the Journal of Caffeine Research, James starts by noting other fatalities, including two confirmed caffeine-related deaths in New Mexico, and four in Sweden, among other long-standing historical reports. Still, not much there to wring your hands over—but James insists that data on poisonings “do not show what contributory role caffeine may have had in cases where fatal and near-fatal outcomes were deemed to have been due to other compounds also present.”

Fair enough. But here is where the argument gets interesting. “Considerably smaller amounts of caffeine,” writes James, "may be fatal under a variety of atypical though not necessarily rare circumstances.” Among these, he singles out: 1) Prior medical conditions predisposing patients toward unusual caffeine metabolism. 2) Unknown interactions and synergies with prescription, over-the-counter, and illegal drugs. 3) Physical stress and high-intensity sports. 4) Children, for whom caffeine is easily available.

James claims we don’t know enough to insist caffeine is essentially harmless, let along good for us in large doses. He compiled this eye-opening list of foods and other products that sometimes contain caffeine: ice cream, chewing gum, yogurt, breakfast cereal, cookies, flavored milk, beef jerky, cold and flu medications, weight-loss compounds, breath-freshener sprays and mints, skin lotion, lip balm, soap, shampoo, and, most notably, as a contaminant in illegal drugs. James says that the largest category of incidents with over-caffeinated young people involve “miscellaneous stimulants and street drugs…”

As for energy drinks themselves: “As a nonselective adenosine receptor antagonist, caffeine counteracts the somnogenic effects of acute alcohol intoxication, and alcohol may in turn ameliorate the anxiogenic effects of caffeine.” It’s an age-old practice: caffeine doesn’t sober up drunks, but it does keep them awake. James believes the evidence shows that the combination of caffeine and alcohol increases the risks of unprotected sex, sexual assault, drunk driving, violence, and emergency room visits.

Furthermore, “the ubiquity of caffeine is such that it has become a biologically significant contaminant of freshwater and marine systems….”

Finally, James offers a vision of a caffeine-regulated future, noting that Denmark, France, and Norway have already introduced sales restrictions on energy drinks. “Canada requires labeling in relation to the same product, advising that it should not be mixed with alcohol.” Other countries have labeled energy drinks as “high caffeine content” beverages. And Sweden regulates the number of caffeine tablets that can be purchased at one time from a drugstore.  Meanwhile, in the U.S., makers of energy drinks, unlike makers of soft drinks, do not even have to print the amount of caffeine on the label as dietary information, although this is in the process of changing. Major energy drink makers are moving to put caffeine content labels on their products, in part to shift their relationship with the FDA.

Bonus: Check HERE for the 15 most caffeinated cities in America. Sure, Seattle is first, but can you guess the others?

Graphics credit: Wikipedia

Binge Drinking in America

And the numbers are… fuzzy.

Public health officials in the UK have been wringing their hands for some time now over perceived rates of binge drinking among the populace. In a 2010 survey of 27,000 Europeans by the official polling agency of the EU, binge drinking in the UK—defined as five or more drinks in one, er, binge—clocked in at a rate of 34%, compared to an EU average of 29%. Predictably, the highest rate of UK binge drinking was found in people between the ages of 15 and 24. This still lagged well behind the Irish (44%) and the Romanians (39%). Scant comfort, perhaps, given the historical role drinking has played in those two cultures, but still, clearly, the British and the rest of the UK are above-average drinkers.

Or are they? And what about the U.S. How do we rank? For comparative purposes, we can use the “Vital Signs” survey in the United States from 2010, performed by the Centers for Disease Control and Prevention, and published in CDC’s Morbidity and Mortality Weekly Report, results of which are pictured above. Using almost the same criteria for binge drinking—five drinks at a sitting for men, four drinks for women—the study concludes that the “overall prevalence of binge drinking was 17.1%. Among binge drinkers, the frequency of binge drinking was 4.4 episodes per month, and the intensity was 7.9 drinks on occasion.”

By the CDC’s definition, the heaviest binge drinking in America takes place in the Midwest, parts of New England, D.C., and Alaska. Survey respondents with an income in excess of $75,000 were the most serious bingers (20.2%), but those making under $25,000 binged more often and had more drinks per binge than other groups, the report says. And binge drinking is about twice as prevalent among men. Binge drinking, the survey concludes, is reported by one of every six U.S. adults.

Even so, it appears that the U.S. does not have the same level of binge drinking as the UK. However, astute readers have no doubt noticed that actual binge drinkers in the U.S. were consuming almost 8 drinks per bout, well above the official mark of four or five drinks at one time. The problem is that there is no internationally agreed upon definition of binge drinking. A 2010 fact sheet from the UK’s Institute of Alcohol Studies (IAS) maintains that “drinking surveys normally define binge drinkers as men consuming at least eight, and women at least six standard units of alcohol in a single day, that is, double the maximum recommended ‘safe limit’ for men and women respectively.”

But referring to binge drinking as “high intake of alcohol in a single drinking occasion” is misleading, says IAS. The problem is biological: “Because of individual variations in, for example, body weight and alcohol tolerance, as well as factors such as speed of consumption, there is not a simple, consistent correlation between the number of units consumed, their resulting blood alcohol level and the subjective effects on the drinker.”

Furthermore, the report charges that “researchers have criticized the term ‘binge drinking’ as unclear, politically charged and therefore, unhelpful in that many (young) people do not identify themselves as binge drinkers because, despite exceeding the number of drinks officially used to define bingeing, they drink at a slow enough pace to avoid getting seriously drunk.”

There you have it. As currently defined and measured, binge drinking is a relatively useless metric for assessing a population’s alcohol habits. “The different definitions employed need to be taken into account in understanding surveys of drinking behavior and calculations of how many binge drinkers there are in the population,” as the UK report wisely puts it. Take the above chart with a few grains of salt.

Photo Credit: CDC

How Many Calories in Your Daily Alcohol?

Booze as food.

Everywhere we turn, the news is packed with stories about the nation’s obesity epidemic. But one little-discussed fact about our daily calorie count is that Americans consume an average of 100 calories each day from alcohol, according to new numbers from the U.S. National Center for Health Statistics (NCHS).

The center, which is part of the Centers for Disease Control and Prevention, said that on a daily basis, about 33 % of men and 18% of women consume alcohol calories daily. Men, who drink more than women, account for 150 daily calories, on average. Women consume a little over 50 calories in the form of alcohol, or roughly half a glass of wine. Predictably, the hardest-drinking cohort was men aged 20-39, who accounted for about 175 calories on daily average.

That may not sound like much—and it is generally within the normal moderation guidelines of one drink per day for women and two drinks for men. However, among members of the study group, about one in five men, and 6% of the women, consumed more than 300 alcohol calories daily—three drinks or more. Considering that the average daily per capita calorie consumption was about 2,500 calories in 2008, according to USDA estimates, this category of drinker can easily end up downing 15% or more of the daily caloric intake in the form of alcohol. The report notes that government dietary guidelines for “solid fats and added sugars”—the  broad category into which alcohol falls—should represent “no more than 5%-15% of calories,” no matter what the overall level of calorie intake.

“A lot of people don’t think about the calories in the alcoholic beverages,” Cynthia Ogden, one of the researchers, told USA Today. “It’s not a diet soda.” Even a shooter of hard liquor, hold the mixer, will run 50-90 calories.  A 12-oz Coke and a 12-oz beer both contain about 150 calories. “We’ve been focusing on sugar-sweetened beverages. This is something new,” said Ogden in an AP article, prompting the unnamed AP writer to ask: “Should New York officials now start cracking down on tall-boy beers and monster margaritas?”

But the Distilled Spirits Council, the lobbying group for hard liquor, saw the silver lining in the research: “The overwhelming majority of adults drink moderately.”

Nonetheless, nutrition policy director Margo Wootan of the Center for Science in the Public Interest told AP she was disappointed that the Obama administration plans to exempt alcoholic drinks from upcoming federal rules mandating calorie labeling on restaurant menus. Customers will be able to see the number of calories in a flavored ice tea drink, but not the calorie count for a Long Island Iced Tea, with easily four times as many calories.

The NCHS Data Brief also found that “no significant differences were observed in average calories per day from alcoholic beverages consumed by non-Hispanic white, non-Hispanic black, and Hispanic persons.” In addition, those in the highest income category drank more than those whose income was at or below the poverty line. Men preferred beer, and women preferred wine.

The study was based on data from the National Health and Nutrition Examination Survey for 2007-2010. Researchers collected data through in-home interviews and at a mobile examination center. The researchers oversampled population subgroups to obtain reliable estimates of nutritional measures in those cohorts.

Graphics Credit: http://www.mslimalicious.com/

Praising Marijuana Prohibition

The view from the White House.

As regular readers of Addiction Inbox will know, I am on record as favoring some form of decriminalization for marijuana. But I also write regularly about the difficulties of marijuana addiction and withdrawal. And I have been critical of the operational strategies employed by the medical marijuana movement in the several states in which it now operates. What I have not done, to date, is offer up the official view of a drug policy analyst from the Obama administration who straightforwardly favors a continuation of the legal prohibition against marijuana. 

One of the architects of the current federal resistance to marijuana legalization is Kevin Sabet, an assistant professor and the director of the Drug Policy Institute at the University of Florida College of Medicine. Sabet served from 2009 to 2011 in the Obama Administration as Senior Advisor for the White House Office of National Drug Control Policy (ONDCP) under Drug Czar Gil Kerlikowske, and was influential in shaping federal marijuana policy. Sabet consults with governments and NGOs on a wide range of drug policy prevention issues, and recently debated legalization advocate Ethan Nadelmann on CNN. He is also a regular columnist for thefix.com  and Huffington Post. He agreed to participate in a frank and lengthy 5-question interview with Addiction Inbox. (Be sure to check out the comments below).

1. In his new book, Too High to Fail, journalist Doug Fine argues that "the Drug War is as unconscionably wrong for America as segregation or DDT." Would you comment on this sweeping condemnation?

First, I think it is interesting to note that only people who want to condemn all of our current drug policies use the term "drug war." No one in serious policy circles uses that term anymore, and that is because it is woefully inadequate and vague as a way to describe a whole slew of policies designed to both reduce drug prevalence and drug consequences. I think his comparison is clumsy and unfair. Do some drug policies hurt disadvantaged groups? Of course they do. Is it a moral imperative to fix those policies, learn from our past mistakes and make our policies better? Of course it is. There's no reason to think that those policies can't be changed—in the White House in 2009, for example, we drastically reduced the penalty for crack cocaine. But what makes Mr. Fine's comparison even more wrong-headed and backwards is that we know that if we scale-up—not eliminate, as he would—the policies we know do work in reducing drug use and its consequences, all communities in America would benefit. A handful include:

(a) community-based prevention that not only focuses on stopping drug use among school kids, but in changing bad local laws and ordinances that promote underage drinking, smoking, and marijuana use (so-called "environmental policies");

(b) early intervention and detection of drug use in health settings;

(c) evidence-based treatment, including methadone and buprenorphine, as well as 12-step programs;

(d) recovery-based policies that don't penalize people for past drug use and instead facilitate recovery;

(e) law enforcement based on credible threats and modest sanctions.

2. The Drug War is an industry—the DEA alone has a budget of 2 1/2 billion and employs almost 10,000 people. If we add in profits from the private prison industry, and the money-laundering banks, the money is staggering. Wouldn't it make sense to recoup those historical costs by legalizing and taxing marijuana?

That phrase assumes two things: (a) criminal justice and regulation costs would be drastically reduced, or eliminated, with marijuana legalization; and (b) the underground market would be eliminated with marijuana legalization. Both of those assumptions are huge leaps that don't stand up to our experience with our already two legal drugs—alcohol and tobacco.

First, we know that legalization means more consumption. More consumption means more regulation. Today we have liquor laws, laws against drinking and driving, laws against public drunkenness, etc. With regards to legal alcohol, we make 2.6 million arrests every year for the violation of those laws. Meanwhile, we arrest a million fewer times for illegal drugs (1.6 million/year). Legal alcohol costs us money with regards to crime and regulation. I think that is a big consideration in this whole debate that we rarely hear about. So that means we'd have to have more prisons, more police, and more regulation costs under legalization—especially since few people are in prison or jail solely for marijuana use.

And I'm not so sure the underground market would be eliminated with marijuana legalization. Especially if it is taxed heavily, the incentive for the underground market—having been painstakingly established for decades by multinational corporate structures (cartels)—is very little. We'll still need a black market for underage marijuana, for marijuana to be sold to repeat offenders, etc. I just don't see the cartels throwing up their hands and saying "OK, it's legalized. We're out of the game now. Let's get into the ice cream business."

3. A "Pax Cannabis" would require rescheduling marijuana at the federal level, with an overt recognition that marijuana has some redeeming medical value. What's the argument for maintaining cannabis as a Schedule 1 drug along with heroin, a drug with which it has almost nothing in common? Could you comment on the upcoming U.S. Appeals Court consideration of medical marijuana?

Rescheduling marijuana is one of the biggest red herrings I can think of in this debate. If rescheduled tomorrow, it would do nothing to allow marijuana to be sold legally. Rather, it would be a huge symbolic victory for marijuana advocates -- but it would be wholly wrong on the science. Placing a drug in schedule 1 simply means the drug has no medical use and a high potential for abuse. It has nothing to do with the other drugs in that category (e.g. heroin). If it were a drug, a telephone would also need to be in Schedule 1 - I'm addicted to my cell phone and I know it has no medical use. That doesn't mean a phone is as dangerous as a syringe of heroin.  Today, cocaine is Schedule 2 because it has some very limited hospital use. Can a 21-year-old kid with no medical knowledge sell cocaine from a "dispensary" called "Happy Clinic" legally? Of course not, though that is what is happening [with marijuana] in California.

In order to be used for medical use, a specific product needs to be approved by FDA. Marijuana's specific product, so far, is Marinol, a Schedule 3 drug which has been approved by FDA and is used by people throughout the world. Crude, raw marijuana is not a specific product. The best way I can put it is this: We don't smoke opium to get the effects of morphine, so why do we think we need to smoke marijuana to get its potential medical effects? We have non-inhaled medications that are approved and we have others on the way. For a lot more on this, you can check out an article I wrote for Join Together. I think the District court opinion will rest on the science and agree with the Department of Health and Human Services that raw, crude marijuana is not medicine.

4. Alaska decriminalized marijuana in 1975, and only recriminalized after lengthy pressure from the Reagan administration. Isn't cultivation of this flowering weed for personal use the most obvious and straightforward solution?

The Reagan Administration could have cared less about Alaska, frankly. Alaska recriminalized because voters there wanted that to happen. They didn't like the effect of decriminalization on their state. That said, I don't think many people are in favor—and I am not—of locking up people smoking small amounts of marijuana. That isn't happening anywhere. One notable exception is New York City where they impose 24-hour detentions for public use and selling as part of their broken windows approach to crime control.

Indeed, in the 1970s, twelve states formally decriminalized marijuana. This meant that persons found to have a small amount of marijuana were not subject to jail time, but rather they would receive a civil penalty, such as a fine. The discussion in the United States is highly complex because even in jurisdictions without a formal decriminalization law, persons are rarely jailed for possessing small amounts of cannabis. A rigorous government analyses of who is in jail or prison for marijuana found that less than 0.7% of all state inmates were behind bars for marijuana possession only (with many of them pleading down from more serious crimes).[1] Other independent research has shown that the risk of arrest for each “joint,” or cannabis cigarette, smoked is about 1 arrest for every 12,000 joints.[2] This probably explains the fact that the literature on early decriminalization effects on use has been mixed. Some studies found no increase in use in the so-called “depenalization” states, whereas others found a positive relationship between greater use and formal changes in the law.[3]

The more recent discussion about state-level legalization may provide more insights. Two RAND Corporation reports concluded that legalization would result in lower cannabis prices, and thus increases in use (though by how much is highly uncertain), and that “legalizing cannabis in California would not dramatically reduce the drug revenues collected by Mexican drug trafficking organizations from sales to the United States.”[4]

5. Marijuana advocates don't like to hear it, but pot is addictive for some users. Where do you stand on this controversial issue?

Science tells us that marijuana is addictive—about 1 in 11 people who ever smoke marijuana are addicted; but if you start in adolescence that number climbs to 1 in 6. That's not anyone's opinion but rather the result of rigorous scientific research done by the National Institutes of Health and confirmed by other international scientific bodies. Is marijuana as addictive as tobacco cigarettes? No. The addiction rate for tobacco is about 1 in 3; for heroin it is lower, about 1 in 4. Users who try to quit experience withdrawal symptoms that include irritability, anxiety, insomnia, appetite disturbance, and depression.

A United States study that dissected the National Longitudinal Alcohol Epidemiologic Survey (conducted from 1991 to 1992 with 42,862 participants) and the National Epidemiologic Survey on Alcohol and Related Conditions (conducted from 2001 through 2002 with more than 43,000 participants) found that the number of cannabis users stayed the same while the number dependent on the drug rose 20 percent ­ from 2.2 million to 3 million.[5]Authors speculated that higher potency marijuana may have been to blame for this increase. As I've heard said many times by experienced tokers, "this isn't your Grandfather's Woodstock Weed."

[1] “Substance Abuse and Treatment, State and Federal Prisoners, 1997.” BJS Special Report, January 1999, NCJ 172871. http://www.ojp.usdoj.gov/bjs/pub/pdf/satsfp97.pdf

[2] Beau Kilmer, Jonathan P. Caulkins, Rosalie Liccardo Pacula, Robert J. MacCoun, Peter H. Reuter, Altered State? Assessing How Cannabis Legalization in California Could Influence Cannabis Consumption and Public Budgets, RAND, 2010.

[3] For a discussion see MacCoun, R., Pacula, R. L., Reuter, P., Chriqui, J., Harris, K. (2009). Do citizens know whether they live in a decriminalization state? State cannabis laws and perceptions. Review of Law & Economics, 5(1), 347-371.

[4] Beau Kilmer, Jonathan P. Caulkins, Rosalie Liccardo Pacula, Robert J. MacCoun, Peter H. Reuter, Altered State? Assessing How Cannabis Legalization in California Could Influence Cannabis Consumption and Public Budgets, RAND, 2010. And see Kilmer, Beau , Jonathan P. Caulkins, Brittany M. Bond and Peter H. Reuter. Reducing Drug Trafficking Revenues and Violence in Mexico: Would Legalizing Cannabis in California Help?.Santa Monica, CA: RAND Corporation, 2010. http://www.rand.org/pubs/occasional_papers/OP325. Also available in print form.

[5] ]Compton, W., Grant, B., Colliver, J., Glantz, M., Stinson, F. Prevalence of Cannabis Use Disorders in the United States: 1991-1992 and 2001-2002Journal of the American Medical Association.. 291:2114-2121.

Photo Credit:http://article.wn.com/

The Truth About Weight Loss Surgery and Alcohol

Bariatrics and booze don’t always mix.

For many people with obesity, bariatric surgery has proven to be a lifesaver. But for a subset of post-operative patients, the price for losing five pounds every time you step on the scale turns out to be an increased appetite for alcohol.

In a study of almost 2,000 patients who underwent surgery for severe obesity, the patients had either gastric bypass surgery (RYGB) in which a portion of the stomach and small intestine are removed, or gastric banding, a process by which an adjustable “lap band” is tightened around the entrance to the stomach. Those who opted for gastric bypass showed an increase in alcohol consumption two years after surgery, according to a recent study by Wendy C. King and coworkers in the Journal of the American Medical Association.

The notion that weight loss surgery, known as bariatric surgery, was related to increased use of alcohol had been an anecdotal staple among patients with obesity for years. Oprah Winfrey based one of her daytime television shows on the rumor back in 2006. Dr. King and a diverse group of associates concluded last month at the American Society for Metabolic and Bariatric Surgery annual meeting that “a significantly higher prevalence of alcohol use disorder” was associated with the second year following gastric bypass surgery. (During the first postoperative year, patients are strongly advised not to drink at all.)

Moreover, some of the patients who showed high-risk alcohol intake had not been problem drinkers before surgery. Some had not been drinkers at all. But the effects of gastric bypass, coupled with permission to drink a year after surgery, lead to an increase in alcohol abuse and alcoholism. While the overall increase was relatively modest, patients who had gastric bypass surgery were twice as likely to drink heavily than patients who underwent the lap band procedure.

“It’s a great study,” says Dr. Stephanie Sogg, staff psychologist at the Massachusetts General Hospital Weight Center and assistant professor in the Department of Psychiatry at Harvard Medical School, who was not associated with the study group. In an interview for this article, Sogg called the distinction between surgeries “an extremely important finding. They saw changes in alcohol use patterns with gastric bypass, but not with gastric banding. That’s exactly what we would expect.”

The findings make biochemical sense: “Gastric bypass surgery bypasses a part of the stomach that secretes alcohol dehydrogenase,”—a primary enzyme of alcohol metabolization, says Sogg. “And in gastric bypass, the alcohol is not coming into contact with the first part of the intestine, the duodenum. That’s going to cause some changes in the way the body processes alcohol that aren’t true of gastric banding. If this were a case of people who are addicted to food having to change their eating and thus becoming addicted to alcohol, we would expect to see the same changes whether the person had gastric bypass or gastric banding.”

It would be natural to assume that people with prior drinking problems would have the most trouble with alcohol control postoperatively. But things are rarely that simple in medicine. “Previous alcohol history sets up people for risk of relapse, but there’s a significant subset of people having trouble with alcohol who never drank at all,” says Dr. Sogg. “That’s where the real story is.”

Dr. David B. Sarwer, associate professor of psychology and director of clinical services for the Center for Weight and Eating Disorders at the University of Pennsylvania, called the King study “the most definitive evidence to date on the prevalence of alcohol use disorders in persons who undergo bariatric surgery.” In an email exchange, Sarwer said: “Individuals with a history of alcohol or substance abuse are informed that the stress of the dietary and behavioral requirements of bariatric surgery, like all major life stressors, could threaten their sobriety or abstinence. However, we simply do not know enough about the use of alcohol and other substances after surgery to predict this with a great degree of certainty.”

Dr. Sogg agrees. For the bariatric surgery population, the pharmacokinetics of alcohol changes. They become more sensitized to its effects—a little now goes a long way. The main problem, she says, is that “we’re not good yet at predicting exactly whom it’s going to happen to.”

But she has some thoughts about vulnerable subsets. “Some people with obesity have poor coping skills,” she says. “And now alcohol is so much more potent and reinforcing for them that alcohol becomes the coping strategy. When this biological change with alcohol happens, they may be the ones who are at higher risk of responding to that change by developing problems with alcohol.”

Warning patients about alcohol risks of weigh-loss surgery is becoming more common, says Dr. Sogg. “It doesn't change my decision-making about whether somebody should or shouldn't have surgery. But we can evaluate people's coping skills before surgery and point out to them that it is important for them to develop other ways of dealing with negative emotions besides eating." 

She also thinks that “people who have a history of actually becoming abstinent after drug or alcohol dependence may be better equipped for surgery. They will be less likely to put themselves in the path of alcohol use, and they have experience at making major successful long-term behavior changes. Basically, we should not consider past encounters with substance abuse as contraindications for surgery. But we should be carefully evaluating whether people are currently using substances at the time of surgery.”

In the end, she said, “I tell every one of my patients before surgery that they need to be aware of the risks of problem drinking after surgery, monitor their alcohol intake, and come back to us immediately at the first sign of any concerns about their drinking.”

King WC, Chen JY, Mitchell JE, Kalarchian MA, Steffen KJ, Engel SG, Courcoulas AP, Pories WJ, & Yanovski SZ (2012). Prevalence of Alcohol Use Disorders Before and After Bariatric SurgeryAlcohol Use Disorders and Bariatric Surgery. JAMA : the journal of the American Medical Association, 1-10 PMID: 22710289

 Photo credit: http://www.treatment4addiction.com/

Random Notes from the College on Problems of Drug Dependence

Opening day addresses at the annual meeting.

(These are notes on research in progress, not findings written in stone).

--NIDA director Nora Volkow talked up buspirone (Buspar) as a treatment for cocaine addiction, and referred to favorable results on buspirone for cocaine self-administration in monkeys in a large clinical trial. Also, different vaccine strategies are in the works, including different pharmacological approaches to blocking specific dopamine transporter molecules.

--Edward Sellers of DL Global Partners, a drug research consulting firm, emphasized the importance of enzyme variations in smoking. Variants of the CYP2A6 enzyme of metabolization allow us to identify “slow metabolizers” who respond well to placebo or nicotine patch therapy, and other smokers who don’t.

--Sherry McKee of the Yale University School of Medicine reminded everyone that cigarette smokers—even very light smoking “chippers”— are far more likely to have concurrent drinking problems than non-smokers. Smoking helps drinkers drink more and longer. To demonstrate such “potentiated reinforcement,” she showed a delightful video of her child eating cookies, then craving a glass of milk, then succumbing to another round of cookie consumption…

--Jack Henningfield of Pinney Associates, and former NIDA research chief, said that the reason the National Institute on Alcohol Abuse and Alcoholism (NIAAA) became an agency focused on “one molecule” is because Senator Harold Hughes, recovering alcoholic from Iowa, and Bill W., co-founder of Alcoholics Anonymous, wanted it that way.

--David Penetar of Harvard Medical School and McLean Hospital added more evidence of the link between alcohol and cigarettes, noting that “90 per cent of smokers drink,” and that smokers are three times as likely to be alcoholics than non-smokers. He pointed to research documenting a disturbing “increased desire to drink” when wearing a nicotine patch. With a patch, subjects reported feeling the effects of alcohol sooner and longer.

Photo Credit: http://www.thejournalshop.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/

A Few Words About Glutamate

Meet another major player in the biology of addiction.

The workhorse neurotransmitter glutamate, made from glutamine, the brain’s most abundant amino acid, has always been a tempting target for new drug development. Drugs that play off receptors for glutamate are already available, and more are in the pipeline. Drug companies have been working on new glutamate-modulating antianxiety drugs, and a glutamate-active drug called acamprosate, which works by occupying sites on glutamate (NMDA) receptors, has found limited use as a drug for alcohol withdrawal after dozens of clinical trials.

Glutamine detoxifies ammonia and combats hypoglycemia, among other things. It is also involved in carrying messages to brain regions involved with memory and learning. An excess of glutamine can cause neural damage and cell death, and it is a prime culprit in ALS, known as Lou Gehrig’s disease. In sodium salt form, as pictured---> it is monosodium glutamate, a potent food additive. About half of the brain’s neurons are glutamate-generating neurons. Glutamate receptors are dense in the prefrontal cortex, indicating an involvement with higher thought processes like reasoning and risk assessment. Drugs that boost glutamate levels in the brain can cause seizures. Glutamate does most of the damage when people have strokes.

The receptor for glutamate is called the N-methyl-D-aspartate (NMDA) receptor. Unfortunately, NMDA antagonists, which might have proven to be potent anti-craving drugs, cannot be used because they induce psychosis. (Dissociative drugs like PCP and ketamine are glutamate antagonists.) Dextromethorphan, the compound found in cough medicines like Robitussin and Romilar, is also a weak glutamate inhibitor. In overdose, it can induce psychotic states similar to those produced by PCP and ketamine. Ely Lilly and others have looked into glutamate-modulating antianxiety drugs, which might also serve as effective anti-craving medications for abstinent drug and alcohol addicts.

As Jason Socrates Bardi at the Scripps Research Institute writes: "Consumption of even small amounts of alcohol increases the amount of dopamine in the nucleus accumbens area of the brain—one of the so-called ‘reward centers.’ However, it is most likely that the GABA and glutamate receptors in some of the reward centers of the basal forebrain—particularly the nucleus accumbens and the amygdala—create a system of positive reinforcement.”

Glutamate receptors, then, are the “hidden” receptors that compliment dopamine and serotonin to produce the classic “buzz” of alcohol, and to varying degrees, other addictive drugs as well. Glutamate receptors in the hippocampus may also be involved in the memory of the buzz.


Writing in The Scientist in 2002, Tom Hollon made the argument that “glutamate's role in cocaine dependence is even more central than dopamine's.” Knockout mice lacking the glutamate receptor mGluR5, engineered at GlaxoSmithKline, proved indifferent to cocaine in a study published in Nature.

In an article for Neuropsychology in 2009, Peter Kalivas of the Medical University of South Carolina and coworkers further refined the notion of glutamine-related addictive triggers: "Cortico-striatal glutamate transmission has been implicated in both the initiation and expression of addiction related behaviors, such as locomotor sensitization and drug-seeking," Kalivas writes. "While glutamate transmission onto dopamine cells in the ventral tegmental area undergoes transient plasticity important for establishing addiction-related behaviors, glutamatergic plasticity in the nucleus accumbens is critical for the expression of these behaviors."

The same year, in Nature Reviews: Neuroscience, Kalivas laid out his “glutamate homeostasis hypothesis of addiction.”

A failure of the prefrontal cortex to control drug-seeking behaviors can be linked to an enduring imbalance between synaptic and non-synaptic glutamate, termed glutamate homeostasis. The imbalance in glutamate homeostasis engenders changes in neuroplasticity that impair communication between the prefrontal cortex and the nucleus accumbens. Some of these pathological changes are amenable to new glutamate- and neuroplasticity-based pharmacotherapies for treating addiction.

This kind of research has at least a chance of leading in the direction of additional candidates for anti-craving drugs, without which many addicts are never going to successfully treat their disease.


Graphics credit: http://cnunitedasia.en.made-in-china.com/

The Strange and Secret Keeley Cure for Addiction

“Drunkenness is a disease and I can cure it.”

In America in the late 1800s, curing alcoholism was a serious business—and for Dr. Leslie Keeley, a very lucrative one. Dozens of clinics and cures already existed, and some treatment centers had even experimented with franchising. For the late 19th Century alcoholic in search of treatment, what most of them had on offer was either outright patent medicine fraud, or else well intentioned if ultimately misguided “opium” cures. None of them, writes William L. White in Slaying the Dragon, “was more famous, more geographically dispersed, more widely utilized, and more controversial than Leslie Keeley’s Double Chloride of Gold Cure for the treatment of alcoholism, drug addiction, and the tobacco habit.”

The Irish-born Dr. Keeley served as a surgeon in the Civil War, and, as family lore would have it, started a treatment program for alcoholism in a Union hospital during the war. We do know that in 1879, he opened the first Keeley Institute in Dwight, Illinois, south of Chicago. His sales pitches were colorful and varied, but boiled down to this pledge: “Drunkenness is a disease and I can cure it.” He could cure it with a secret, specific formula, injected four times daily, about which all he would hint publically was that it contained, as one of its ingredients, gold. This was not so outlandish as it may seem. Gold, silver, strychnine, and other potentially poisonous ingredients were already employed in dozens of standard medicines—and, in many cases, still are. But everything else about Dr. Keeley’s magic elixir was as secret as the ingredients in Coke.

Nonetheless, something seemed to be working. He claimed an outlandish 95% success rate, bolstered by legions of enthusiastic followers who formed proto-AA groups with the catchy title of Bi-Chloride of Gold Clubs, better known as the Keeley Leagues. And Keeley himself employed the largest collection of formerly addicted doctors in the known world. There were no counselors at Keeley clinics. There were enough doctors on staff to go around, even though an estimated total of half a million alcoholics and other addicts eventually took the Keeley Cure.

Treatment consisted of the infamous injections, a liquid cordial every two hours, and, according to White, the following modalities: “daily rest, nutrition, mutual sharing, and alternative diversions worked to improve the patient’s physical and psychological health.” We can assume, from this regimen, that some alcoholics and addicts probably improved, regardless of what was in the medicine. And there was the frequent suggestion that, really, it was probably best not to ask too many questions about what was in the medicine, anyway.

“The atmosphere was informal and friendly at the clinics,” White writes, “with a marked absence of the bars and restraints that were typical in most inebriate asylums of the period.” There were, of course, some very vocal detractors. Dr. T. D. Crothers, a leader in the inebriate asylum movement, said: “There is no gold cure for inebriety. There are no facts to show that gold has any value in this disease. All the assertions and statements concerning gold as a remedy are delusions, and will not bear the test of critical examination.”  Perhaps not. But success was success, and soon, the marketplace saw the introduction of Dr. Haines Golden Remedy, the Geneva Gold Cure, the Boston Bichloride of Gold Company, and many other knockoffs. (Keeley proclaimed that his Double Chloride of Gold cured all forms of inebriety by “speeding up the restoration of poisoned cells to their pre-poisoned condition.”)

From 1892 through 1900, the Keeley Company pulled in almost $3 million, including mail-order business. There was a Keeley Day at the 1893 World’s Fair in Chicago. Here is an excerpt from the pamphlet, “To the Keeley Graduate,” given to every patient who completed treatment:

You are now numbered among thousands of men and women who have broken the shackles of alcohol and drug addictions by the Keeley method of treatment. Your cure will be as permanent as your life, you will never have any craving for alcohol or other sedative drugs as long as you live, unless you create it by returning to their use, thus re-poisoning your nerve cells.

But by 1900, the bloom was off the Keeley miracle, as insiders fought for financial control, and congressional investigators looked into the affairs of Keeley League president Andrew J. Smith.

Of course, if Keeley had really possessed a specific, replicable formula that took away the craving for alcohol, it would have been monstrously unethical to hold it a secret. And he was constantly accused of using harmful ingredients, such as codeine, strychnine, and cocaine in his magic injections.

Keeley wouldn’t say. And neither did any of his heirs or business partners. The only thing most court records agree on is that the injection didn’t contain any gold—too many possible side effects. According to the testimony of Keeley’s original business partner, “The only patient who ever received Keeley medicine that actually had gold in it almost died.”

The secret ingredient was probably atropine—a powerful compound belonging to a very weird family of plant drugs known collectively as “anticholinergenic deliriants.”  Atropine is the active ingredient in Belladonna, aka Deadly Nightshade. Along with mandrake, henbane, and jimsonweed, the so-called Belladonna alkaloids are among the primary hallucinatory ingredients found in many a witch’s and sorcerer’s brew throughout the ages. Belladonna can cause terrifying hallucinations, feelings of flight or paralysis, blurred vision, impaired motor control, and other side effects usually experienced as highly unpleasant. It was likely Belladonna, not LSD, that served as the basic rocket fuel for the Manson’s family’s horrific activities, according to some accounts. More mundanely, atropine is familiar to armed forces personnel in the form of a self-injection device for serious wounds. Atropine has the ability to speed up a slowing or overworked heart. In ancient times, it was used as an anesthetic for surgery. Atropine is also a poison. (Scopolamine, used medically for motion sickness, is another.)

But one person’s unpleasant side effect is another’s chemical cure. Did the Keeley concoction just terrify the bejesus out of addicts, as some sort of ad hoc version of aversive therapy, or did it sedate his patients into a semi-catatonic, immobile haze, in which they could pass 3 weeks of detox in relative comfort, or at least immobility and minimal disruption? Probably both, depending on drug dosage, drug combination, and patient metabolism. There were widespread reports of Keeley patients who allegedly died or went insane.

“The pulp image of Dr. Leslie Keeley—that of the country physician who had stumbled onto a revolutionary cure for the inebriety problem that had stumped the best medical scientists,” was key to his success, White believes. “Keeley introduced an approach that carried an aura of scientific truth and all the emotional support and intensity of a revival meeting.”

“The likely ingredients of the Double Chloride of Gold remedy and tonics—alcohol, atropine, strychnia, apomorphine —did aid detoxification,” White concludes. And the graduation pamphlet went on to emphasize the importance of “sustaining the new Keeley habits: regular patterns of sleep, regular and balanced meals, regular consumption of water, abstinence from tobacco and caffeinated drinks, healthy recreation, and care in the selection of personal associates.”

If you skip the atropine injections, that series of admonitions remains the bedrock of drug and alcohol treatment programs everywhere.

Photo Credit: http://www.blairhistory.com/

7 Myths the Alcohol Industry Wants You to Believe

Staying on message in the liquor biz. 

“Our national drug is alcohol,” wrote William S. Burroughs. “We tend to regard the use of any other drug with special horror.” This emotional loophole in the psyche has been skillfully manipulated by the alcohol and tobacco industries ever since modern advertising was invented.

 Recently, the European Alcohol Policy Alliance, known as EuroCare, put together a brochure addressing the common messages the liquor industry attempts to drive home through its heavy spending on advertising. The messages are not just designed to sell product, but also to influence alcohol policy at the political level as well. (Eurocare is a network of more than 50 voluntary non-governmental organizations working on the prevention and reduction of alcohol-related harm in 20 European countries.) According to the group, the “industry”—the alcohol and tobacco companies—“has traditionally worked closely together, sharing information and concerns about regulation. They have used similar arguments to defend their products in order to prevent or delay restrictions being placed on them (Bond, et al. 2010).”

EuroCare offers this introduction: “The intention of this brochure is to inform professionals about the attempts made by the alcohol industry to influence alcohol policy globally and to subsequently arm them against the industry’s methods to prevent effective policies from being made…. For politicians and health experts it is important that they reveal to the public the subversive messaging of the alcohol industry and do not fall prey to the industry’s half-truths—or worse—outright lies.”

Message 1: Consuming alcohol is normal, common, healthy, and very responsible.

Explanation: To bring this message home, alcohol advertisements nearly always associate alcohol consumption with health, sportsmanship, physical beauty, romanticism, having friends and leisure activities.

I note here that it’s left to the social service agencies and non-profits to attempt to convey the opposite side of the coin: a dramatically heightened risk for health problems, traffic fatalities, domestic violence, loss of job, loss of marriage, suicide—you name it.

Message 2: The damage done by alcohol is caused by a small group of deviants who cannot handle alcohol.

Explanation: Indeed, the message of the industry is that ordinary citizens drink responsibly and that ‘bad’ citizens drink irresponsibly and are the cause of any and all problems associated with high alcohol consumption.

This one is insidious and unscientific. There is no evidence that alcoholics are “bad people,” or simply unwilling to stop engaging in bad behavior. For the industry, irresponsible drinkers are a major revenue source—the dream customer— even though alcohol manufacturers continue to insist that their advertising is primarily about driving home the message of responsible alcohol consumption and brand choice.

Message 3: Normal adult non-drinkers do not, in fact, exist.

Explanation: Only children under 16 years of age, pregnant women and motorists are recognized by the industry as non-drinkers.

My personal favorite, this one. The existence of non-drinkers is seen by the industry as a threat. Accordingly, they have subtly reinforced the message that moderate drinking is not only normal, but also good for you. Never mind that the real profits come from excessive drinking and pricing strategies that encourage it. Estimates vary, but recent studies  at UCLA show that “the top 5% of drinkers account for 42%of the nation’s total alcohol consumption.” If 5% of all drinkers account for nearly half of total alcohol sales, it would be folly for the alcohol industry to get serious about encouraging moderation. It’s not too far off the mark to say that the alcohol industry’s quarterly statements hinge on the success they have in encouraging alcoholics to believe that everything’s okay, everybody drinks that way. The message becomes clearer: Drinking is mandatory—unless you’re a deviant.

Message 4: Ignore the fact that alcohol is a harmful and addictive chemical substance (ethanol) for the body.

Explanation: The industry does not draw attention to the fact that alcohol (ethanol) is a detrimental, toxic, carcinogenic and addictive substance that is foreign to the body.

Naturally, pointing out the neuroscientific parallels between alcoholism and heroin addiction is not part of the message. Alcohol is a hard drug—ask any addiction expert. Alcoholism can kill you quick. But so far, the labeling mania that struck opponents of Big Tobacco has not played out in a major way in the battle against deceptive alcohol advertising.

Message 5: Alcohol problems can only be solved when all parties work together.

Explanation: Good, effective policies to combat alcohol consumption would require a higher excise-duty, no marketing or sponsoring, an increase in the drinking age to 18, a prohibition of the illegitimate sale of alcohol, and an increase, through a campaign, in the public’s awareness of the damages that alcohol can cause (Babor et al, 2010; WHO, 2009).

Obviously, these bullet points are not high on the alcohol industry’s agenda.

Message 6: "Alcohol marketing is not harmful. It is simply intended to assist the consumer in selecting a certain product or brand."

Explanation: Meanwhile, research has indisputably demonstrated that alcohol advertisements are both attractive to young people and stimulate their drinking behavior (Anderson et al., 2009: Science Group of the Alcohol and Health Forum; 2009). Yet the industry continues to flatly and publicly deny that advertising stimulates alcohol consumption (Bond et al; 2009).

Stuffed with attractive young people meeting and mating over alcohol, it seems fair to suggest that alcohol ads had better stimulate increased drinking, i.e., a boost in quarterly sales, or else the industry is wasting a lot of money fighting over pieces of a pie that isn’t getting any bigger. These days, slow growth is no growth.


Message 7: “Education about responsible use is the best method to protect society from alcohol problems.”

Explanation: Effective measures such as a higher alcohol excise-duty, establishing minimum prices, higher age limits and advertisement restrictions can reduce alcohol related harm and will therefore decrease the profits of the industry (Babor, 2003; Babor, 2010). The industry therefore does its best to persuade governments, politicians, and policy makers that the above mentioned measures would have no effect, are only symbolic in nature or are illegitimate.

A truly great dodge, because the strategy being advertised sounds so imminently sensible. Who could be against the promotion of responsible alcohol use? Irresponsible zealots and deviants, that’s who. Why should all of us happy drinkers be made to suffer for the sins of a few rotten apples?

Indeed, all of the messages, overtly or covertly, send the same signal: You should drink more. It’s good for you.

Photo Credit: http://www.frankwbaker.com

What Does Harm Reduction Mean?

A rift in the addiction treatment community over abstinence.

What is harm reduction? How does it differ from the approaches traditionally associated with drug recovery and rehab?

Originally, I became interested in harm reduction because its advocates were highlighting the folly of prison terms over treatment for drug addicts—a sentiment with which I wholeheartedly agree. Also, the various harm reduction organizations worldwide were fastened tenaciously to the issue of clean needle exchanges as a means of reducing HIV transmission—another approach I heartily support. And at its core, harm reduction has always been about reducing the number of deaths by drug overdose. At its essence, harm reduction is sensible and necessary, given the failures of the drug war, and the inability to make a significant dent in addiction statistics by traditional socioeconomic approaches.

Harm reduction, as formally defined by Harm Reduction International, concerns itself with “policies, programs and practices that aim primarily to reduce the adverse health, social and economic consequences of the use of legal and illegal psychoactive drugs without necessarily reducing drug consumption. Harm reduction benefits people who use drugs, their families, and the community.” It’s a hopeful mission statement. But reducing harm without necessarily reducing drug consumption? What does that mean, exactly?

Lately, activists in the harm reduction movement have been leaning hard on the notion that abstinence is just so much humbug; an archaic admonition that need not be automatically imposed on addicts. Who said addicts have to become abstinent for the rest of their lives? Are we forever hostage to the religious zealotry of the Cambridge Group and it’s successor, Alcoholics Anonymous? If an alcoholic drinks one drink less today than yesterday, or a junkie shoots up a bit less junk today than yesterday, that is harm reduction in action.

But now that harm reduction has become intimately associated with the abstinence debate, egged on by activists like Stanton Peele and Jack Trimpey, the ground underneath the movement has shifted. Many harm reductionists are becoming wary, and sometimes completely hostile, to the notion of addiction as a disease syndrome with a distinct, lifelong, and incurable timeline beyond the reach of notions like “Rational” or “Smart” recovery. “Your best thinking got you here,” AA likes to say, reminding alcoholics that “being smart” or feeling full of “will power” often have less to do with recovery than one might suppose.

But in order to free themselves of the need for abstinence, extreme harm reductionists often deny that addiction is in any meaningful way a medical disorder. This has created a rift in the treatment community, and complicated the mission of recovery programs based on abstinence. Kenneth Anderson, a harm reduction advocate and the author of How to Change Your Drinking, framed it this way for me in an email exchange: “The more alcohol related problems you have, the more you need to practice harm reduction by planning safe drinking strategies, until you resolve your alcohol related problems by quitting or developing a non-problematic drinking pattern.” Like many harm reductionists, Anderson is no fan of Alcoholics Anonymous. One of the book’s sections is headed: “Everything You Always Wanted to Know About Alcohol—But you got told to go to AA and not ask.”

Anderson said that the National Institute on Alcohol Abuse and Alcoholism (NIAAA) “tells us that about half of people who overcome alcohol dependence do so by quitting, the other half overcome it by cutting back.” If even the nation’s premier scientific agency for researching alcoholism doesn’t seem so sure about whether alcoholics need to strive for abstinence, why should abstinence be a stated goal at the outset of treatment at all? Said Anderson: "When abstinence is forced on people against their will, it often backfires and leads to more drug or alcohol use."
 
A few weeks ago, on Denise Krochta’s excellent podcast, Addicted to Addicts, I suggested that part of the argument over abstinence vs. controlled drinking stemmed from a confused bundling of “problem drinkers” and “alcoholics”—a move that the National Institute on Alcohol Abuse and Alcoholism, whose very name is a testimony to the institute’s fundamental ambivalence, has been championing lately. This has helped harm reductionists center the battle precisely where the definitions are fuzziest: at the point on the spectrum where “problem drinking” becomes “alcoholism.” Nonetheless, by focusing on this imprecise edge, harm reductionists make a legitimate point: Culture and environment are major influences on the course of heavy drinking.

“I do not use the word alcoholism [in the book], because it has no scientific definition in the current day and is not found in the DSM IV” Anderson told me. “Although there is some heritability of alcohol dependence, it is a great error to overlook the importance of environmental factors. Alcohol dependence is not located on a single gene--currently there are dozens of genes implicated in alcohol dependence.” And he’s right. These are legitimate caveats that apply to many of the disease models of addiction now at play in the scientific community.

The counter-argument here is that genuine alcoholics do not have, and cannot develop, a “non-problematic drinking pattern,” any more than a serious diabetic is likely to develop a non-problematic sugar doughnut strategy. What alcoholic hasn’t tried controlled drinking? Again and again? And failed? Where are the legions of former drunk-tank alcoholics who have rationally transformed themselves into social drinkers?

These are some of the terms of the current debate in the addiction recovery community. But we do a disservice by concentrating solely on points of departure. The harm reduction movement, at street level, has some very sound contributions to make regarding addiction and public policy. Anderson, in his book, drives home the overlooked but essential point that there is no one-size-fits-all treatment for destructive drinking:

• “Harm reduction never forces people to change in ways which they do not choose for themselves.”
• “Harm reduction recognizes that each of us is a unique human being different from all others.”
• “Harm reduction recognizes the need for ‘different strokes for different folks.’”
• “Harm reduction supports every positive change.”

I fervently hope that 12-Step Groups and Harm Reduction Groups can work their way toward a rapprochement. And so does Kenneth Anderson. But what stands in the way of this is, I fear, is the disease model of addiction—and medical addiction researchers aren’t likely to turn their backs on that premise any time soon. Still, we cannot say what future research will reveal. And I agree with harm reductionists that the best attitude we can bring to the subject of addiction and recovery is open-mindedness, and a willingness to treat each case as unique, in order to forestall “metabolic chauvinism.”

Graphics Credit: http://hamsnetwork.org 

FROM THE ARCHIVES: Sex, Drugs, and… Sex

Pharmaceuticals and sexual performance.

[Originally posted 9/5/10]

The search for aphrodisiacs is an ancient, if not always venerable, human pursuit. Named for Aphrodite, the Greek goddess of love, aphrodisiacs are compounds that have the reputation, real or imagined, of increasing sexual desire, pleasure, and potency. It’s safe to say that rhinoceros horn or tiger penis—various forms of sympathetic magic—just don’t reliably do the trick.

Writing in Hormones and Behavior, a group of Canadian behavioral neurobiologists recently concluded that “substantial clinical and epidemiological literatures suggest that [stimulants and depressants] either inhibit sexual responding or can be ‘prosexual’ in certain situations, thereby increasing the potential of risky sexual activity and the spread of sexually transmitted diseases.”

In other words, recreational drugs either sex you up, or they decrease your sex drive. And they either do or do not lead to risky sexual behavior among young people.

Not too promising a start. Nonetheless, JG Pfaus and coworkers at Concordia University’s Center for Studies in Behavioral Neurobiology examined more than 100 studies based on animal models, and teased out some commonalities:

Stimulants are, well, stimulating. Cocaine “facilitated penile erection” in male rats, while acute caffeine consumption amped up the sexual behavior of both male and female test animals. As for depressants, small amounts of alcohol decreased inhibitory tendencies in rats, while a high level “disrupted sexual performance.” Alcohol “increases rodent sexual motivation” but impairs specific parameters of sexual performance. 

Yes, well, Shakespeare said it best. Macbeth proclaims at one point that alcohol “provokes the desire but it takes away the performance.”  As with mice, so with men and women. In animal studies, low doses of alcohol increase sexual desire, moderate doses intensify those effects, and a high dose extinguishes the impulse altogether. Male rodents, too, are subject to Brewer’s Droop.

With the opiates, the story is much the same. In a National Institute on Drug Abuse (NIDA) study, the title of which--“Methadone reduces sexual performance and sexual motivation in the male Syrian golden hamster”--remains a classic, researchers found that after a dose of methadone, the critters were definitely disinclined to copulate. In general, systemic morphine inhibits sexual behavior in rats, mice, dogs, even donkeys. Animals don’t want to do it on opiates. Females stop engaging in “proceptive pacing and solicitation.”

And naturally, you’re wondering about the sex lives of castrated Japanese quail. Researchers managed to get them copulating again with the opioid antagonist naloxone. (Testosterone implants also work.)

Although it sometimes seems laughable, there is a good argument to be made for the use of animals for modeling certain aspects of human sexual behavior. Stripped of cultural and complex social overlays, animal studies afford an opportunity to focus relentlessly on the biological. But enough for now on the fascinating topic of rats having sex on drugs.

In studies of men and women, Pfaus found that alcohol “dose-dependently delayed ejaculation, reduced the intensity of orgasm, and decreased both physiological and subjective measures of sexual arousal. Nearly identical effects were observed in women, although alcohol increased, rather than decreased, their subjective levels of sexual arousal.” The nastiest example of alcohol’s effect on sex may be the blood vessel and nerve damage, sometimes permanent, known as chronic alcohol impotence. Alcohol damage can disrupt communication between the pituitary gland and the genitals—and that can’t be a good thing. Heavy smoking also reduces circulation to the blood vessels in the genitals.  Heavy smokers and drinkers often report impotence or continuing sexually disinterest even when they have been sober and smokeless for a while.

Alcohol’s effect on sexual performance is no secret, of course. But Pfaus also concludes that, in general, “drug use debilitates sexual responding in the majority of situations.”

He means the whole pantheon, the entire roster of usual suspects: Why would drugs like cocaine, marijuana, amphetamine and oxycontin all have an overall negative effect on sexuality? Do hashish and cocaine, common “love potions” found in classical literature, boost sexual ardor, or do they have the opposite effect?

The following is a mix of anecdotal data and clinical reporting related to common addictive drugs and other “drugs of abuse.”

LSD/Magic Mushrooms/Ecstasy/other Psychedelics: Some users report increased sexual awareness and sensitivity, but heavier doses tend to discourage sexual activity.

Marijuana/Hashish: Heightened sensory experiences can enhance sexual experiences, while heavier cannabis use can lower libido.

Cocaine: Equivocal. Users often report increased arousal and ease of orgasm. However, exactly the opposite effect is known to occur in heavy regular users.

Heroin/Oxycontin/other Opiates: Lowered libido and difficulty achieving orgasm are the norms. Yet even in this rather clear-cut case, there is no unanimity of opinion or experience. The familiar pattern is in evidence--a little bit might temporarily add some oomph to your sex drive. Heavier use is likely to lay a thick blanket across your libido.

Heroin is a strange case: In a 2003 study of women in methadone maintenance treatment programs, published in Addictive Behaviors, several different themes emerged: “Some women believe that drugs, particularly heroin, increase their sexual performance, libido, and pleasure, but for others, drugs, particularly crack cocaine, inhibit their sexual performance and desire. Many of the women believe that crack cocaine and heroin enhance a man’s sexual desire, performance, and pleasure. However, other women deem that these drugs are responsible for their partner’s abusive and coercive behavior.” The effect of drugs on rates of sexual violence varies. Differential effects can be found in every aspect of the effect of drugs on sexual behavior, for the same reason that individuals vary in their response to these drugs. Metabolisms are not all the same.

Amphetamine: The stimulant rush can amp up sexual encounters; heavy use leads to desensitization and difficulty achieving orgasm. Intense but sometimes rather psychologically detached sex sessions can lead to everything from genital chafing to the classic “fuck knot” of tangled hair sometimes produced by a prolonged bout of missionary-position intercourse.

If the usual roster of recreational drugs cannot be counted on to perform as aphrodisiacs, there are always efforts underway to identify “prosexual” drugs and natural sex-enhancing nutrients. Among the contenders:

Bromocriptine (Parlodel): This drug is used to treat pituitary tumors and Parkinson’s disease. It reduces prolactin, which is associated with age-related impotency in men. However, the dosage level required for the effect can cause unpleasant side effects.

Gamma-hydroxybutyrate (GHB): This one has been abused in the U.S. for its euphoric, sedative, and anabolic (body building) effects. It triggers the release of growth hormone from the pituitary. Not recommended. Combining GHB with alcohol sometimes leads to nausea and breathing problems.

DHEA: Big hopes were recently riding on this hormone. Sorry to say, Pfaus reports that in aging males, DHEA “had only transient effects in a well-controlled, double-blind study.” Women had some promising hormonal news in the early going: “Mixed estrogen/androgen replacement to postmenopausal women improved measures of sexual desire, satisfaction, and frequency of sexual activity, compared with treatment with estrogen alone.”

Yohimbe: Operating on a different receptor, this plant drug, long considered an aphrodisiac, pulls norepinephrine into the picture, at least in men. Yohimbine is an adrenoceptor agonist that fairly reliably turns on male rat mounting behavior and is reputed to be an effective sexual enhancer for some men.

Deprenyl (Seliginine): A dopamine booster, which also acts as a weird MAO inhibitor and is used for Parkinson’s and depression, l-deprenyl has a reputation as a so-called smart drug, and is popular with life extension enthusiasts. It also markedly improves the sex lives of older rats.  Another one with side effects to beware of.

There are also reports that L-dopa, used in patients with Parkinson’s disease, increases sexual interest in the elderly. (But L-dopa has a number of undesirable side effects, too.) Apomorphine, a dopamine receptor agonist, increases the “likelihood of spontaneous erections.” 

In animal models, a variety of dopamine-active drugs generally have positive effects on the sexual behavior of rodents.  As might be expected, drugs that block or reduce dopamine transmission also reduce sexual displays in animals. Our friend Drosophila melanogaster, the common fruit fly, doesn’t get in the mood when it is dopamine-depleted, a state that can be reversed with L-dopa. Give a virgin male rat a good dose of D-amphetamine and it is off to the races, its surge of sexual excitement cause by dopamine release in the nucleus accumbens. In women, “the ability of estrogen to stimulate dopamine release and to augment dopamine release and behavior in response to amphetamine has been well established,” according to James G. Pfaus and Barry J. Everitt in “The Psychopharmacology of Sexual Behavior.” But the specific mechanism by which this happens has not been identified.

 Other scientists have also managed to sexually stimulate rats with extracts of Turmera diffusa (Damina), Pfaffia paniculata (Brazilian ginseng), and Eurycoma longfolia Jak (Catuaba).

As for serotonin, Pfaus and Everitt find “minimal methodologically-sound evidence on the effects on human sexuality of manipulating the serotoninergic system.” So serotonin appears not to have much to do with sexual activity directly. In fact, it can have a negative effect, as users of SSRI antidepressants like Prozac have discovered. The common symptom in this case is difficulty achieving orgasm.  Serotonin at 5-HT receptors inhibits sexual impulses in women as well as men.

In the end, Pfaus maintains that the best way to get male rats back in action after a strenuous day of copulation is “a combination of the nonspecific dopamine receptor agonist apomorphine and the adrenergic receptor antagonist yohimbine.”

Pfaus, J., Wilkins, M., DiPietro, N., Benibgui, M., Toledano, R., Rowe, A., & Couch, M. (2010). Inhibitory and disinhibitory effects of psychomotor stimulants and depressants on the sexual behavior of male and female rats Hormones and Behavior, 58 (1), 163-176 DOI: 10.1016/j.yhbeh.2009.10.004

Photo Credit: http://www.aphrodisiacs.org.uk/