A Night of Serious Drinking: The Results

"A systematic review of the next‐day effects of heavy alcohol consumption on cognitive performance"

The latest scientific rundown on the ramifications of hangovers, in the journal Addiction, can be found HERE.

 

There Is No "Safe" Amount of Alcohol

 Moderate daily drinking will not improve your health.

As a growing number of addiction and alcohol consumption researchers have been pointing out, the notion of a safe and even beneficial level of daily drinking is outmoded and in error. In an article published in Lancet, researchers offer strong evidence against the theory, based on data from the Global Burden of Diseases, Injuries, and Risk Factors Study of 195 countries and territories.

 In an accompanying commentary, researchers note that the data "clearly demonstrate the substantial, and larger than previously estimated, contribution of alcohol to death, disability, and ill health, globally." Moreover, the Chief Medical Officer of the UK announced that there is “no safe level of alcohol consumption” and suggested that policies designed to decrease daily drinking should receive top priority.


(See my post from 2015 predicting the death of the "moderate drinking" meme.)

The NIAAA and Big Alcohol

Officials halt government study on moderate drinking funded by alcohol industry

The New York Times reports: “The extensive government trial was intended to settle an age-old question about alcohol and diet: Does a daily cocktail or beer really protect against heart attacks and stroke?

To find out, the National Institutes of Health gave scientists $100 million to fund a global study comparing people who drink with those who don’t. Its conclusions could have enshrined alcohol as part of a healthy diet.
As it turned out, much of the money for the study came from the alcohol industry. Earlier this year, The New York Times reported that officials at the National Institute on Alcohol Abuse and Alcoholism (NIAAA) part of the N.I.H., had solicited that funding from alcohol manufacturers, a violation of federal policy.

On Friday, an advisory panel to Dr. Francis Collins, director of the N.I.H., recommended that the trial be stopped altogether. Shortly afterward, Dr. Collins agreed.”

for the rest of the story, go HERE.

The Myth of Healthy Drinking

Another meta-study demolishes decades of wishful thinking.

Vox notes that "an impressive new meta-study involving 600,000 participants, published recently in The Lancet, suggests that levels of alcohol previously thought to be relatively harmless are linked with an earlier death. What’s more, drinking small amounts of alcohol may not carry all the long-touted protective effects on the cardiovascular system."

Readers of Addiction Inbox will not be surprised by this finding. Back in 2014, I wrote a blog post entitled "Alcohol and Your Heart: Health benefits of moderate drinking come under fire." The post referenced studies suggesting that recent findings were bringing “the hypothesized cardioprotective effect of alcohol into question.”

Also in 2014, I published a report with the headline "Single Bout of Binge Drinking Linked to Immune System Effects."

It's not at all surprising that research touting alcohol's health benefits has been heavily pushed by the alcohol industry. See my post, "Alcoholic Deception: Big Alcohol Wants a Piece of the Health Market".

In the end, the myth about the health effects of moderate drinking made its way into the public consciousness for one obvious reason: People very much wanted it to be true.

Do Alcoholic Women Want Women-Only Treatment?

It's complicated. 

In an article appearing in the June 29 edition of the journal Addiction, researchers ask women what they think about it:

"Women‐only addiction services tend to be provided on a poorly evidenced assumption that women want single‐sex treatment. We draw upon women's expectations and experiences of women‐only residential rehabilitation to stimulate debate on this issue."

Full text available HERE.

New Study Casts Doubt on Current "Despair" Models of Addiction

The recent Hari/Hart/Lewis hypothesis that addiction is not primarily metabolic or genetic, but rather the result of "despair" or "sociological conditions" or "flawed learning," takes a major hit in a new report appearing in The National Bureau of Economic Research. The study suggests that "changes in economic conditions account for less than one-tenth of the rise in drug and opioid-involved mortality rates." 

Jason Schwartz at Addiction & Recovery News does a deep dive into the flawed thinking behind the new (old?) sociological views of addiction here.

Alcohol and Cancer, Explained

"Alcohol and endogenous aldehydes damage chromosomes and mutate stem cells"

Juan I. Garaycoechea, Gerry P. Crossan, Frédéric Langevin, Lee Mulderrig, Sandra Louzada,  Fentang Yang, Guillaume Guilbaud, Naomi Park, Sophie Roerink, Serena Nik-Zainal, Michael R.
Stratton & Ketan J. Patel

    Nature doi:10.1038/nature25154

This pay-walled article, published in "Nature," presents fresh evidence that alcohol can damage chromosomes and cause mutations. If you don't have a zillion dollars to spare, The American Cancer Society has put together a layman's version of the subject here.

Here's an explainer from Britain's National Health Service. And here's an interview with one of the authors, published in "Genetic Engineering and Biotechnology News." Suffice to say that among the many health problems alcohol can cause, the one that all too often goes unmentioned, namely cancer, is not a trivial side effect.

Cancer: Alcohol’s Dirty Little Secret?

What Doctors Don’t Tell You

It is, in fact, no secret at all that alcohol causes cancer.  Rather than conferring any demonstrable metabolic benefit, alcohol is more likely to damage your health in a variety of ways. The body converts alcohol (ethanol) into acetaldehyde as part of the metabolic process, and acetaldehyde is carcinogenic in sufficient quantities. Drinkers are particularly susceptible to cancers of the head and neck, as well as the liver, breast, and bowel.

However, you wouldn’t know this if you only talked to doctors. In a commentary written for the journal Addiction, Terry Slevin and Tanya Chikritzhs of Curtin University in Perth, Australia, suggest that health professionals may be consciously or unconsciously in denial.

A 2015 survey taken in the UK demonstrated that only about 13% of the population was aware of a link between alcohol and cancer. Moreover, surveys of physicians show that “significant proportions are not aware of or resist the notion that alcohol causes cancer and do not advise their patients of the relationship. This is compounded by the fact that many physicians are reluctant to ask about patient alcohol use, particularly when drinking does not appear to have a direct impact upon their health.” (98% of medical students in a survey from Saudi Arabia, where drinking is rare, said that alcohol causes cancer.)

The authors raise the following question: Could individual alcohol use among doctors be part of the problem? Some studies have shown that physicians drink more than average, other studies conclude that they drink about the same as everybody else. As for attitudes about drinking, the authors reference a U.S. study showing that 24% of doctors admitted to having imbibed alcohol while on call. 64% reported witnessing colleagues who appeared to be under the influence of alcohol while on call.

Given that most doctors probably drink socially at about the levels one would expect of the general population, the authors point up the possibility that a form of cognitive dissonance might be behind an apparent, perhaps unconscious reluctance to discuss the alcohol/cancer link. If true, “an important source of health information for members of the public may not be communicating the alcohol-causes-cancer message consistently or effectively.”

The alcohol industry itself has always viewed the alcohol/cancer question primarily as a threat to sales. These powerful companies exhibit “a vested interest in maintaining the status quo of relative ignorance, uncertainty and denial among the general population and their trusted health advisors. In the face of this, it is time that health professionals set aside any leanings that might stem from their own drinking—good or bad—and convey unreservedly to their patients and the communities they serve that alcohol causes cancer.”

Graphics: http://www.alcoholandcancer.eu/risks/

Jack London and his Alcoholic Memoirs

Meet John Barleycorn.

In the early years of the 20th Century, writer Jack London was the equivalent of a rock star. A ruggedly good-looking sportswriter, globetrotting war correspondent, successful novelist and short story writer, London came up the hard way on the Oakland docks in California. He had his first drink at the age of 5, ran an oyster smuggling operation as a teenager, and allegedly brought the sport of surfing from Waikiki to the West Coast. At least one critic has referred to him as the Norman Mailer of the early 1900s.

In 1913, the author of the Call of the Wild published what was arguably his least successful book, John Barleycorn, a non-fiction account carrying the subtitle Alcoholic Memoirs. John Sutherland, professor of English Literature at University College in the UK, wrote in his introduction to the Oxford edition of Jack London’s book that London had pitched the book as “the bare, bald, absolute fact… of my own personal experiences in the realm of alcohol.” As Sutherland notes, “The drunk’s stigma was, however, indelible in 1913. No one of London’s public standing had ever come clean on the question of problem drinking before—at least not while at the zenith of their power and fame.”

Yet what are we to make, Sutherland asks, of London’s assertions, “three times in the first five pages, that drinker he may be, but ‘I was no hereditary alcoholic… I have no constitutional predisposition for alcohol.’”? Is this, the critic asks, “self-delusion or self-knowledge?”

After reading the book, I would have to say a little bit of both, given the limitations of medical knowledge at the time.  In London’s view, common back then, “dipsomania” was a chemical, congenital defect, much maligned and considered to be as rare as one in every several thousand drinkers. Nonetheless, several prominent London biographers have asserted that Jack London was chronically drunk-sick in his later years, ultimately dying of uremia and other complications brought on by years of excessive drinking. Writer Upton Sinclair claimed in 1915 that he had seen London wandering Oakland “dazed and disagreeably drunk.” Still others claim London’s bar bills were always modest and much of John Barleycorn is fiction. Yet London writes frankly of his morning shakes and hair-of-the-dog drinking and suicidal impulses. Describing his life in 1910, London writes: “I achieved a condition in which my body was never free from alcohol. Nor did I permit myself to be away from alcohol…. There was no time in all my waking time, that I didn’t want a drink.”

Was Jack London a Hemingway-style brawler or a hopeless alcoholic? As we have come to understand, it is sometimes possible to be both, for a while. Jack London was not writing for a medical journal, he was relating the experiences of his own life. And when the battle for universal suffrage began in earnest, London was an early an enthusiastic backer, on the grounds that if women got the vote, alcohol prohibition would surely follow, and the children of American would be saved from the wiles of John Barleycorn.

The lack of enthusiasm for the book when it was published stemmed, in part, from these built-in ambiguities. In addition, writes Sutherland, “John Barleycorn is an extended meditation on pessimism, or alcohol induced melancholy.” These days, we are more likely to refer to this condition as depression. This was not the Jack London his fans had come to know and love, even though London insisted in the book that he was “writing of the effects of alcohol on the normal, average man. I have no word to say for or about the microscopically unimportant excessivist, the dipsomaniac.”

For all the hedging, there is plenty of recognizable plain talk about the devotees of Mr. Barleycorn: “When good fortune comes, they drink. When they have no fortune, they drink to the hope of good fortune. If fortune be ill, they drink to forget it. If they meet a friend, they drink. If they quarrel with a friend and lose him, they drink…. He coarsens and grossens them, twists and malforms them out of the original goodness and fineness of their natures.”

In another passage describing the tavern life of tradesmen and laborers, he “saw men doing, drunk, what the would never dream of doing sober…. Time and again I heard the one explanation: If I hadn’t been drunk I wouldn’t a-done it.”

And as time passes, Jack London, the resolutely non-alcoholic, highly-regarded novelist, finds the terrain underneath his own feet is changing: “And the thing began so imperceptibly, that I, old intimate of John Barleycorn, never dreamed whither it was leading me…. It was at this time I became aware of waiting with expectancy for the pre-dinner cocktail. I wanted it, and I was conscious that I wanted it…. And right there John Barleycorn had me. I was beginning to drink regularly, I was beginning to drink alone.”

These developments shook up London sufficiently for him to ask himself: “Had I, a non-alcoholic, by long practice, become an alcoholic?” He has no trouble marshaling evidence for the argument: “The more I drank the more I was required to drink to get an equivalent effect…. Whenever I was in a hurry, I ordered double cocktails. It saved time.”

There were other warnings: “Where was this steady drinking leading? But trust John Barleycorn to silence such questions. ‘Come on and have a drink and I’ll tell you all about it,’ is his way.”

London concludes, before taking most of it back in later pages: “There are hundreds of thousands of men of this sort in the United States to-day, in clubs, hotels, and in their own homes—men who are never drunk, and who, though most of them will indignantly deny it, are rarely sober. And all of them fondly believe, as I fondly believed, that they are beating the game.”

And finally, this: “But a new and most diabolical complication arose: The work refused to be done without drinking. It just couldn’t be done. I had to drink in order to do it.”

In the end, let us hear from his last wife, Charmian, who made the following entry in her diary on July 1, 1912: “I know now that Jack, facing the writing of John Barleycorn, intends to drink moderately in the future, just to prove to an unbelieving public that he is the opposite of an ‘alcoholic’, that he is not afraid of being an alcoholic, and never was an alcoholic. Perhaps he is right, but I feel a trifle dashed.”

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

Another Look at Acamprosate

The most popular pharmaceutical treatment for alcoholism, explained.

(First published February 17, 2014)

“Occasionally,” reads the opening sentence of a commentary published online earlier this year in Neuropsychopharmacology, “a paper comes along that fundamentally challenges what we thought we knew about a drug mechanism.” The drug in question is acamprosate, and the mechanism of action under scrutiny is the drug’s ability to promote abstinence in alcoholics. The author of the unusual commentary is Markus Heilig, Chief of the Laboratory of Clinical and Translational Studies at the National Institute on Alcohol Abuse and Alcoholism (NIAAA).

Acamprosate, in use worldwide and currently the most widely prescribed medication for alcohol dependence in the U.S., may work by an entirely different mechanism than scientists have believed on the basis of hundreds of studies over decades. Rainer Spanagel of the Institute of Psychopharmacology at the University of Heidelberg, Germany, led a large research group in revisiting research that he and others had performed on acamprosate ten years earlier. In their article   for Neuropsychopharmacology, Spanagel and coworkers concluded that a sodium salt version of acamprosate was totally ineffective in animal models of alcohol-preferring rats.

“Surprisingly,” they write, “calcium salts produce acamprosate-like effects in three animal models…. We conclude that N-acetylhomotaurinate is a biologically inactive molecule and that the effects of acamprosate described in more than 450 published original investigations and clinical trials and 1.5 million treated patients can possibly be attributed to calcium.”

At present, the Food and Drug Administration (FDA] has approved three drugs for alcoholism— Antabuse, naltrexone, plus acamprosate in 2004. In addition, there is considerable clinical evidence behind the use of four other drugs—topiramate, baclofen, ondansetron, and varenicline. Acamprosate as marketed is the calcium salt of N-acetyl-homotaurinate, a close relative of the amino acid taurine. It has also been found effective in European studies.

What did scientists think acamprosate was doing? Various lines of research had linked acamprosate to glutamate transmission. Changes in glutamate transmission have been directly implicated in active alcoholism. A decade ago, the Spanagel group had decided that acamprosate normalized overactive glutamate systems, and hypothesized that acamprosate was modulating GABA transmission. So it became known as a “functional glutamate antagonist.”  But specific mechanisms have remained elusive ever since.

Now, as Heilig comments, “the reason it has been difficult to pin down the molecular site of acamprosate action may simply be because it does not exist. Instead, the authors propose that the activity attributed to acamprosate has all along reflected actions of the Ca++ it carries.” As the researcher paper explains it: “N-acetylhomotaurinate by itself is not an active psychotropic molecule…. We have to conclude that the proposed glutamate receptor interactions of acamprosate cannot sufficiently explain the anti-relapse action of this drug.” Further work shows that acamprosate doesn’t interact with glutamate binding sites at all.  In other words, calcium appears to be the major active ingredient in acamprosate. Animal studies using calcium chloride or calcium gluconate reduced alcohol intake in animals at rates similar to those seen in acamprosate, the researchers claim.

Subsequently, the researchers revisited the earlier clinical studies, subjected them to secondary analysis, and concluded that “in acamprosate-treated patients positive outcomes are strongly correlated with plasma Ca++ levels. No such correlation exists in placebo-treated patients.” In addition, calcium salts delivered via different carrier drugs replicated the suppression of drinking in the earlier animal findings.

Where there cues pointing toward calcium? The researchers conclude that “calcium sensitivity of the synapse is important for alcohol tolerance development, calcium given intraventricularly significantly enhances alcohol intoxication in a dose-dependent manner,” and “activity of calcium-dependent ion channels modulate alcohol drinking.”

Interestingly, in the late 50s and early 60s, there was a brief period of interest in calcium therapy for the treatment of alcoholism. In 1964, the Journal of Psychology ran an article titled “Intensive Calcium Therapy as an Initial Approach to the Psychotherapeutic Relationship in the Rehabilitation of the Compulsive Drinker.” Now it appears possible that a daily dose of acamprosate is effective for some abstinent alcoholics because it raises calcium plasma levels. Calcium supplements may be in for a round of intensive clinical testing if these findings hold up.

The authors now call for “ambitious randomized controlled clinical trials,” to directly compare “other means of the Ca++ delivery as an approach to treat alcohol addiction. Data in support of a therapeutic role of calcium would open fascinating clinical possibilities.”  Indeed it would.

Spanagel R., Vengeliene V., Jandeleit B., Fischer W.N., Grindstaff K., Zhang X., Gallop M.A., Krstew E.V., Lawrence A.J. & Kiefer F.  (2013). Acamprosate Produces Its Anti-Relapse Effects Via Calcium, Neuropsychopharmacology, 39 (4) 783-791. DOI: 10.1038/npp.2013.264

Photo Credit: http://medlibrary.org/lib/rx/meds/acamprosate-calcium-1/page/3/

Alcohol and Your Heart

Health benefits of moderate drinking come under fire.

One of those things that “everybody knows” about alcohol is that a drink or two per day is good for your heart. But maybe not as good for your heart as no drinks at all.

Joint first authors Michael V. Holmes of the Department of Epidemiology and Public Health at University College in London, and Caroline E. Dale at the London School of Hygiene & Tropical Medicine in London, recently published a multi-site meta-analysis of epidemiological studies centering on a common gene for alcohol metabolization. The report, published in the UK journal BMJ, brings “the hypothesized cardioprotective effect of alcohol into question,” according to the authors.

People who are born with a particular variant in the gene controlling for the expression of alcohol dehydrogenase, the major enzyme involved in converting alcohol into waste products, will show the familiar flush reaction when they drink. Alcohol, literally, can make many of them sick. This genetic variant, in combination with other enzymes, can be strongly protective against alcohol, and is much more commonly found among Asian populations. Roughly 40% of Japanese, Korean, and Northeastern Chinese populations show the characteristic “Asian glow” to one degree or another if they choose to drink.  (One reason why this effect isn't better known is that the condition is close to nonexistent in Westerners).

 People with this alcohol dehydrogenase deficiency, the researchers found, not only consume less alcohol, for obvious reasons, but “had lower, not higher, odds of developing coronary heart disease regardless of whether they were light, moderate, or heavy drinkers.”  Here are the conclusions in detail: “Carriers of the rs1229984 A-allele had lower levels of alcohol consumption and exhibited lower levels of blood pressure, inflammatory biomarkers, adiposity measures, and non-HDL cholesterol, and reduced odds of developing coronary heart disease, compared with non-carriers of this allele.”

The authors conclude that "reduction of alcohol consumption, even for light to moderate drinkers, is beneficial for cardiovascular health.”

How does this work? The researchers aren’t completely sure, but note that the “most widely proposed mechanism” is an increase in high-density lipoprotein (HDL) cholesterol. “Although an HDL cholesterol raising effect of alcohol has been reported in experimental studies, the small sample size and short follow-up means existing studies may be prone to bias,” thereby limiting their usefulness. Moreover, the BMJ study itself found “no overall difference between allele carriers and non-carriers in HDL concentration.”

Like most meta-studies, this one has its strengths and weaknesses. The study used a large sample size, used detailed alcohol phenotypic data, and didn't have to deal with the inherent biases of observational-type studies. On the minus side, the lack of a connection between the allele in question and HDL levels is troubling, and stroke data was lacking.

But overall, the authors believe that "social pressure in heavier drinking cultures is unlikely to override the effect of the genetic variant on alcohol consumption."

In retrospect, there have been some trouble spots along the way: A 2008 study in Current Atherosclerosis Reports concluded:

In the absence of large randomized trials of moderate alcohol consumption and heart failure, we cannot exclude residual confounding or unmeasured confounding as possible explanations for the observed relationships. Thus, for patients who do not consume any alcohol, it would be premature to recommend light-to-moderate drinking as a means to lower the risk of heart failure, given the possible risk of abuse and resulting consequences.

At present, the American Heart Association does not recommend drinking any amount of wine or other alcoholic beverages in order to gain potential health benefits.


Holmes M.V.,  L. Zuccolo,  R. J. Silverwood,  Y. Guo,  Z. Ye,  D. Prieto-Merino,  A. Dehghan,  S. Trompet,  A. Wong &  A. Cavadino &  (2014). Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data, BMJ, 349 (jul10 6) g4164-g4164. DOI: http://dx.doi.org/10.1136/bmj.g4164

Photo credit: http://qsystem.gblifesciences.com/

Gone in June

Alcohol takes a friend.

What good does it do: You write about addiction, research it, think about it, formulate new ideas about it. You try to be of service.

What good does it do: One of your best friends ever, a talented writer you have talked to and argued with and smoked with and paddled with for more than two decades, lies dead this morning of alcohol-related liver failure at 62.

What good does it do: I couldn’t save him, couldn’t turn the head of that runaway horse, not through encouragement, shame, praise, incentive, disgust, indifference, furious anger. Not through any of that.

What good does it do: His doctor, with my help, presented a program of 30-day detox and Ativan for the rough parts. He ordered the pills, never picked them up at the pharmacy. He never went back to the doctor, claiming a lack of health insurance. He never quit. He tried, like so many deluded alcoholics, to cut back on his drinking. He kept the phone number for the local AA group in a desk drawer, but never called. When his girlfriend told him it was either her or the bottle, he picked the bottle.

What good does it do: We cajoled, we watched him, we tripped over bags of empties in the basement and he didn’t care. We couldn’t save him. I couldn’t save him. I know more about alcoholism than most addiction therapists, and I couldn’t save him. I saved myself, 25 years ago, but could not save him.

What good does it do: I don’t know how to treat alcoholism, and save alcoholics, and neither do you. And if anybody tells me today, the day of my friend’s death, that alcoholism is a lifestyle choice, I promise to throw a swift right cross and knock them out on the spot.

The only possible light on the horizon is continued scientific research aimed at better elucidating the mechanisms behind addiction. Without that, one idea is about as good as another.

Tripling the Tax on Alcohol

Would it do any good?

A recent article in Slate by Reihan Salam, a sort of modest proposal on behalf of a big boost in alcohol excise taxes, caught considerable flack from free market advocates and conservative bloggers last week.

Salam says Americans agree on the fact that marijuana is not as dangerous a drug as alcohol, and that this agreement offers us an opportunity to “regulate alcohol more stringently than we regulate marijuana.” In fact, Salam argues, why not push the envelope: “Raise the alcohol tax to a point just shy of where large numbers of people will start making moonshine in their bathtubs.”

Salam tries to head off some of the usual criticisms by noting that Prohibition was an unmitigated disaster, but that “what most of us forget is that the movement for Prohibition arose because alcohol abuse actually was destroying American society in the first decades of the 20th Century," and that companies like Anheuser Busch and MillerCoors are plotting with national retail chains as you read this, scheming to make alcohol as cheap and easy to buy as humanly possible.

Salam further justifies a tripling of alcohol taxes by viewing it as a tactical offset to the efforts of liquor companies to focus on their best customers: “the small minority of people who drink the most.” Salam says that right now, it costs about two bucks per inebriated hour to get your drink on. Can we really argue that this price level is just too unsustainably high? Drug expert Mark Kleiman, Professor of Public Policy at UCLA, agrees.  In his book Marijuana Legalization: What Everyone Needs to Know, Kleiman and co-authors argue that “tripling the tax would raise the price of a drink by 20 percent and reduce the volume of drinking in about the same proportion. Most of the reduced drinking would come from heavy drinkers, both because they dominate the market in volume terms and because their consumption is more price-sensitive…."

Minnesota legislators recently passed a bill that opponents say would increase state excise taxes on alcoholic beverages to six times the current levels. Supporters of the alcohol tax say it means an extra $200 million per year to the state, at a cost to drinkers of about seven cents per drink. Or, in Salam's example: “Charging two-drink-per-day drinkers an extra $12 per month seems like a laughably small price to pay to deter binge drinking…. If you’re going to tax tanning beds and sugary soft drinks, why on earth wouldn’t you raise alcohol taxes too?”

Why wouldn’t you? Because it doesn’t accomplish what you want to accomplish, writes Michelle Minton at openmarket.org, the blog of the Competitive Enterprise Institute.  After a bit of throat clearing about the Nanny State, Minton writes that “fortunately, a society’s relationship with alcohol isn’t based solely on the price of alcohol…. Research shows that alcohol price is not an effective means of achieving lower total consumption or reducing binge drinking.” As evidence, Minton points to studies showing that Luxembourg and the Czech Republic “have both the highest priced alcohol and the highest rates of consumption in Europe.”

As for a comparison favored by Salam—New York’s anti-smoking campaign—Minton admits that the new higher cost of cigarettes cut the adult smoking rate dramatically, but points out that “New York is now the number-one market for smuggled cigarettes—which account for more than half of all cigarettes smoked in the state.” This is a powerful argument. If we triple the taxes on alcohol, do we risk a black market of dangerous home-brew bootlegger booze?

In my view, such threats are real, but they are theoretical. The current costs of alcohol in socioeconomic terms are enormous and undeniable. Tripling the alcohol tax might be asking for trouble, but we could get there in stages if Americans saw it as a desirable goal. Arguments against tax increases tend to ignore the fact that alcohol is a different kind of product, capable of addicting a significant minority of users, in addition to killing a certain percentage of drinkers outright through alcohol poisoning and traffic accidents. If we ignore the issue of drug dependence, and the health and legal costs of assorted alcohol-related mayhem, and simply lean on the fact that most people who drink use alcohol responsibly, then it gets easier to argue against increases in alcohol and cigarette taxes. Alcohol is not like other household products, and needn't be regulated like them.

How Alcoholism Causes Muscle Weakness

It’s a mitochondrial thing.

Chronic alcohol intake weakens muscles. This condition can take the form of numbness or shooting pains in arms and legs, muscle cramps, fatigue, heat intolerance, and problems urinating. In some cases it can lead to diarrhea, nausea, vomiting, spasms, muscle atrophy, and movement disorders, even chronic pain and long-term disability. Leg symptoms are the most common. Alcohol-related neuropathy of this kind generally develops over time and gradually worsens. But until recently, the mechanism behind alcoholic neuropathy has remained obscure.

As it turns out, it’s a mitochondrial thing. Mitochondria, as we all remember from 10th grade biology, are little structures known as the “power plants” of cells. They are constantly changing tubular organelles that form networks inside of cells to convert oxygen into energy used in cellular processes. But if the proper enzymes that trigger the process go missing, less energy gets produced for activities like muscle function.

Patients with certain forms of mitochondrial disease, in which mitochondria fail to self-repair, show pronounced muscle weakness as a symptom. In some cases, this is due to a mutation for a particular mitochondrial fusion protein, leading to “late onset myopathy.”

Muscle tissue repairs itself through a process known as mitochondrial fusion, through which a broken mitochondrial cell component can repair itself by fusing with healthy mitochondria and exchanging bodily fluids, so to speak. It had previously been thought that the tightly packed fibers of muscle cells might not allow for normal fusion among the mitochondrial organelles found in skeletal muscle. Not so, according to a recent paper for the Journal of Cell Biology. Principle author Gyorgy Hajnoczky in the Department of Pathology, Anatomy and Cell Biology at Philadelphia’s Thomas Jefferson University writes that the animal study shows how chronic alcohol exposure “suppresses mitochondrial fusion in muscle fibers.” The problem worsens over time due to “lesser metabolic fitness of the mitochondria, which progressively hinders calcium cycling during trains of stimulation.” What this means is that, in cases of prolonged heavy drinking, mitochondria have less “reserve capacity” for supporting calcium regulation in cells.

The researchers began with the known finding that “mitochondrial ultrastructure damage is apparent in the skeletal muscle of alcoholics, and mitochondria and their quality control are considered to be a primary target of chronic alcohol exposure.” Furthermore, “mitochondria represent a major target of alcohol and loose their normal shape upon persistent alcohol exposure.”

The study, funded by the NIAAA, demonstrated that mitochondrial fusion is the key to repair in skeletal muscle, as it is in other muscle tissue. In the study, researchers color-tagged mitochondria in the skeletal muscle of rats, and demonstrated that mitochondrial fusion occurs, and is governed by key players called mitofusin 1 fusion proteins (Mfn1). Chronic alcohol abuse interferes with this repair process. In the study, alcoholic rats showed a decrease in Mfn1 levels of up to 50 percent, while other fusion proteins were not affected.

“That alcohol can have a specific effect on this one gene involved in mitochondrial fusion suggests that other environmental factors may also alter specifically mitochondrial fusion and repair,” Hajnoczky said in a prepared statement.

The study has provided insight “into why chronic heavy drinking often saps muscle strength,” which could also “lead to new targets for medication development,” according to Dr. George Koob, head of the National Institute on Alcohol Abuse and Alcoholism (NIAAA).

Eisner V., Lenaers G. & Hajnoczky G.  Mitochondrial fusion is frequent in skeletal muscle and supports excitation-contraction coupling, The Journal of Cell Biology,    DOI: 10.1083/jcb.201312066

Photo Credit: http://mda.org

Acamprosate For Alcohol: Why the Research Might Be Wrong

Calcium may be curbing the urge to drink.

“Occasionally,” reads the opening sentence of a commentary published online last month in Neuropsychopharmacology, “a paper comes along that fundamentally challenges what we thought we knew about a drug mechanism.” The drug in question is acamprosate, and the mechanism of action under scrutiny is the drug’s ability to promote abstinence in alcoholics. The author of the unusual commentary is Markus Heilig, Chief of the Laboratory of Clinical and Translational Studies at the National Institute on Alcohol Abuse and Alcoholism (NIAAA).

Acamprosate, in use worldwide and currently the most widely prescribed medication for alcohol dependence in the U.S., may work by an entirely different mechanism than scientists have believed on the basis of hundreds of studies over decades. Rainer Spanagel of the Institute of Psychopharmacology at the University of Heidelberg, Germany, led a large research group in revisiting research that he and others had performed on acamprosate ten years earlier. In their article  for Neuropsychopharmacology, Spanagel and coworkers concluded that a sodium salt version of acamprosate was totally ineffective in animal models of alcohol-preferring rats.

“Surprisingly,” they write, “calcium salts produce acamprosate-like effects in three animal models…. We conclude that N-acetylhomotaurinate is a biologically inactive molecule and that the effects of acamprosate described in more than 450 published original investigations and clinical trials and 1.5 million treated patients can possibly be attributed to calcium.”

At present, the Food and Drug Administration (FDA] has approved three drugs for alcoholism— Antabuse, naltrexone, plus acamprosate in 2004. In addition, there is considerable clinical evidence behind the use of four other drugs—topiramate, baclofen, ondansetron, and varenicline. Acamprosate as marketed is the calcium salt of N-acetyl-homotaurinate, a close relative of the amino acid taurine. It has also been found effective in European studies.

What did scientists think acamprosate was doing? Various lines of research had linked acamprosate to glutamate transmission. Changes in glutamate transmission have been directly implicated in active alcoholism. A decade ago, the Spanagel group had decided that acamprosate normalized overactive glutamate systems, and hypothesized that acamprosate was modulating GABA transmission. So it became known as a “functional glutamate antagonist.”  But specific mechanisms have remained elusive ever since.

Now, as Heilig comments, “the reason it has been difficult to pin down the molecular site of acamprosate action may simply be because it does not exist. Instead, the authors propose that the activity attributed to acamprosate has all along reflected actions of the Ca++ it carries.” As the researcher paper explains it: “N-acetylhomotaurinate by itself is not an active psychotropic molecule…. We have to conclude that the proposed glutamate receptor interactions of acamprosate cannot sufficiently explain the anti-relapse action of this drug.” Further work shows that acamprosate doesn’t interact with glutamate binding sites at all.  In other words, calcium appears to be the major active ingredient in acamprosate. Animal studies using calcium chloride or calcium gluconate reduced alcohol intake in animals at rates similar to those seen in acamprosate, the researchers claim.

Subsequently, the researchers revisited the earlier clinical studies, subjected them to secondary analysis, and concluded that “in acamprosate-treated patients positive outcomes are strongly correlated with plasma Ca++ levels. No such correlation exists in placebo-treated patients.” In addition, calcium salts delivered via different carrier drugs replicated the suppression of drinking in the earlier animal findings. 

Where there cues pointing toward calcium? The researchers conclude that “calcium sensitivity of the synapse is important for alcohol tolerance development, calcium given intraventricularly significantly enhances alcohol intoxication in a dose-dependent manner,” and “activity of calcium-dependent ion channels modulate alcohol drinking.”

Interestingly, in the late 50s and early 60s, there was a brief period of interest in calcium therapy for the treatment of alcoholism. In 1964, the Journal of Psychology ran an article titled “Intensive Calcium Therapy as an Initial Approach to the Psychotherapeutic Relationship in the Rehabilitation of the Compulsive Drinker.” Now it appears possible that a daily dose of acamprosate is effective for some abstinent alcoholics because it raises calcium plasma levels. Calcium supplements may be in for a round of intensive clinical testing if these findings hold up.

The authors now call for “ambitious randomized controlled clinical trials,” to directly compare “other means of the Ca++ delivery as an approach to treat alcohol addiction. Data in support of a therapeutic role of calcium would open fascinating clinical possibilities.”  Indeed it would.

Spanagel R., Vengeliene V., Jandeleit B., Fischer W.N., Grindstaff K., Zhang X., Gallop M.A., Krstew E.V., Lawrence A.J. & Kiefer F.  (2013). Acamprosate Produces Its Anti-Relapse Effects Via Calcium, Neuropsychopharmacology, 39 (4) 783-791. DOI: 10.1038/npp.2013.264

Hazelden Offers Companion to the “Big Book”

New guide attempts a modest AA update.

The founders of AA published their book, Alcoholics Anonymous (The Big Book) back in 1939. The world has changed a great deal since then, so it’s not surprising that there have been periodic calls for an update. Barring an official revision, which is unlikely, Hazelden, the Minnesota treatment organization, has published an updated companion volume to the Big Book. (Narcotics Anonymous published their version of the basic text in 1962). “The core principles and practices offered in these basic texts hold strong today,” says Hazelden, “but addiction science and societal norms have changed dramatically since these books were first published decades ago.”

Hazelden’s book, Recovery Now, billed as an easy-to-follow guide to the teachings of Alcoholics Anonymous and Narcotics Anonymous, dispenses with the divisive question of medications for withdrawal straightaway. In a foreword by Dr. Marvin D. Seppala, chief medical officer at Hazelden, the doctor makes it clear: “I agree with the majority of treatment professionals who support using these meds to help with cravings when it is appropriate to do so. Addiction is a disease that calls for the best that science has to offer.” The unnamed authors of the “little green book” agree, stating that “for some mental health disorders, medications such as antidepressants are needed. These aren’t addictive chemicals and so professionals, as well as AA and NA, accept that we can take them and still be considered clean and sober (abstinent).” There are now, as well, specific Twelve Step groups for those with both addiction disorders and mental health disorders: Dual Diagnosis Anonymous and Dual Recovery Anonymous among them.

As Seppala points out in the foreword, when some alcoholics and other drug addicts hear about the research showing that addiction is similar to many other mental and physical disorders we call diseases, it reorients their thinking amid the shame, stigma, and negative emotional states associated with active addiction. For some, it opens the door to treatment.

Okay. Hazelden, Betty Ford, and many other major treatment providers are no longer fighting a rear-guard action against a host of medications, from buprenorphine to Zoloft. But two-thirds of the Big Book consists of stories of how people recognized and dealt with their sundry addictions. That’s really about it, which tracks well with AA’s core operating principle: one drunk helping another. AA believes that much of its success stems from the fact that the program is run by the members, without direct rule setting and intervention from organizations, including their own. (All statements hold for NA as well).

What else? Recovery Now takes on another sticking point for many: the fact that “the AA Big Book and other writings include traditional male-focused and religious language, like discussing God as a ‘he.’” And there is the matter of “the realities and stereotypes of the 1930s, which is why it contains a chapter titled ‘To the Wives.’” Hazelden continues the recent tradition of broadening acceptable interpretations of “higher power.” One example given is from Samantha, a young cocaine and alcohol addict: “My higher power is the energy of this group. I call her Zelda.”

The book presents some of the psychological aspects of the AA program as a sort of reverse cognitive behavioral therapy. CBT attempts to teach people how to unkink their thinking and turn harmful thoughts into helpful ones. AA attempts to convince people to first change their behavior—“fake it until you make it”—and helpful thoughts will follow.

Perhaps the genuine sea change lies in this passage, which can be contrasted with the faith and certainty with which the Big Book proclaims that AA will work for all but the most stubbornly self-centered. Even with the myriad of choices of AA groups now available, Hazelden acknowledges that “a group based on the Twelve Steps doesn’t work for all of us. Some of us have found help in recovery groups that offer alternatives to the Twelve Steps, such as SMART Recovery, Women for Sobriety, and Secular Organizations for Sobriety.”  This is a change of heart, given that groups like SMART Recovery don’t necessarily buy the idea of total abstinence, and often structure recovery as an exercise in controlled drinking. Hazelden also suggests that many of “us” have found the necessary ongoing support for recovery at churches, mental health centers, and nonreligious peer support groups.

As for anonymity, Recovery Now states: “While Twelve Step members do not reveal anything about another member of the group, any one of us may choose to go public with our own story.” Another promising development is the proliferation of Twelve Step meetings catering to specific populations—AA meetings for African Americans, Latinos, Native Americans, women, seniors, gays, and drug-specific (Cocaine Anonymous).

In the end, one of the best arguments for attendance at the AA program (free of charge) is that many addicts have “worn out our welcome” with families and friends, “and they have a hard time putting all that behind them and supporting us completely. But at most Twelve Step recovery meetings we can find the support we need.”

Dr. David Nutt on Alcohol

Rebutting industry myths.

A couple of years ago, 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. According to EuroCare, 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.”

I wrote a blog post on EuroCare’s list of alcohol untruths called “7 Myths the Alcohol Industry Wants You to Believe." Here they are:

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

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

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

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

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

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

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

Recently, I ran across a great response to these same 7 myths by Dr. David Nutt, the British psychiatrist perhaps best known in the states as the scientist who got fired a few years ago from his post on the government’s Advisory Council on the Misuse of Drugs. Nutt’s primary sin was to suggest that, on a straightforward calculation of risks and harms, horseback riding was probably a more dangerous activity than taking the drug Ecstasy. The Home Secretary at the time insisted that you couldn’t compare a legal activity to an illegal one, or something like that, and Nutt compounded his sins by suggesting that marijuana was a safer drug than alcohol. British politicians took a serious dislike to him, the more so since most of the published medical science was on his side. After the dust settled, Nutt was one of the primary founders of the Independent Scientific Committee on Drugs (ISCD), formed to offer alternative views on drugs and addiction grounded in science.

Anyway, in his book, Drugs Without the Hot Air, Nutt has his own responses to the 7 Myths, which I excerpt here:

1. Consuming Alcohol is Normal: It’s normal, so long as you have the “normal” high-activity variant of the ALDH2 enzyme. If you don’t have that form of the enzyme, Nutt reminds his readers, as many Asians and Aleuts do not, then alcohol will affect you quite non-normally through the so-called alcohol flush reaction. Moreover, many cultures and societies unfamiliar with its effects “suffer hugely when new types of alcohol appear, particularly if they are aggressively marketed.”

2. Alcohol damage is caused by a small group of deviants: According to Dr. Nutt, statistics show that “millions of people, NOT a tiny minority, suffer harm from their own alcohol consumption, or cause harm to others…. It is the everyday drinking of people who have come to see alcohol as an essential part of life rather than the luxury it used to be, that has created a spike in cancers and stomach problems, and will see liver disease match heart disease as the leading cause of death in the UK by 2020.”

3. Normal adult non-drinkers do not exist: The alcohol industry is forever reminding politicians of how unpopular alcohol restrictions are to the voting populace. “The existence of non-drinkers obviously threatens this portrayal of society, so the industry tends to dismiss them as having something wrong with them. While some teetotalers are recovering alcoholics, many others have made a positive choice not to drink.” And there are others, I would add, often referred to as “sick” teetotalers, who have quit drinking for medical reasons unrelated to alcoholism.

4. Ignore alcohol’s harm to the body: Nutt reminds us that “there is no other drug which is so damaging to so many different organ systems in the body…. Most other drugs cause damage primarily in one or two areas—heart problems from cocaine, or urinary tract problems from ketamine. Alcohol is harmful almost everywhere.”

5. Alcohol problems can be solved when everybody works together: “In practice, what the industry means by ‘working together’ is bring in voluntary codes rather than statutory regulation—solving problems through rules that the industry CHOOSES to comply with, rather than laws which they MUST comply with.”

6. Alcohol marketing is intended to assist consumers in selecting products: Specifically, 800 million British pounds every year for advertising and promotion, according to Nutt. That’s just the kind of civic-minded bunch those alcohol sellers are. The reality, of course is that “marketing communications do have a marked effect on consumption…. All this further entrenches the false division between alcohol and illegal drugs, persuades people that consuming alcohol is safe, and makes realistic discussions of the harm alcohol causes very difficult.”

7. Education about responsible use is the best approach: “It is useful for the drinks industry,” Nutt explains, “to emphasize the value of education, because it takes the focus off regulation…. There is also extensive evidence gathered by the WHO from around the world, showing that merely providing information and education without bringing in other policy measures doesn’t change people’s drinking behavior.”

As I wrote in my original post: 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.

Graphics Credit: http://www.holyrood.com/2011/04/at-what-price/

Researchers Link Alcoholism and Binge Eating Behavior

Addiction and the role of genetic overlap.

More evidence has arrived, courtesy of Washington University School of Medicine in St. Louis, demonstrating a genetic link between alcoholism and binge eating disorders.

In clinical practice, it is no secret that certain binge eaters and people with bulimia also show high rates of alcoholism. Various reasons have been suggested, but one of the obvious ones is that people prone to alcoholism are also genetically susceptible to certain kinds of eating disorders. A common set of genetic factors may convey these intertwined vulnerabilities to a subset of the population.

In order to examine the matter, Dr. Melissa Munn-Chernoff and coworkers followed the time-honored route: They studied twins, both identical and fraternal, from a database of 6,000 adult twins in Australia. Twin studies have been crucial to medical understanding of comorbid disorders and addiction. In general, while alcoholism and binge/purge disorders were seen as most likely genetic in origin, it was thought that the two disorders were transmitted in families independently. Writing in the Journal of Studies on Alcohol and Drugs, the researchers conclude that “in women, some of the genetic risk factors that influenced vulnerability to alcohol dependence also influenced vulnerability to both binge eating and compensatory behaviors [purging, laxatives, diuretics].”

Previous studies cited by the researchers have pegged the individual heritabilities of alcohol dependence (50-64 percent) and bulimia (28-83%). However, the question of genetic overlap had remained relatively underexplored. Munn-Chernoff and colleagues wanted to evaluate the links between alcohol dependence and binge eating behaviors in women. Among the study group, 6 percent of women had been dependent on alcohol at some point in their lives. As for binge eating, 13% of women had experienced problems with it. 14% of women had engaged in purging or laxative abuse.

The researchers judged the genetic correlation between the two disorders to be statistically relevant: “In women, the multivariate twin model suggested that additive genetic and nonshared environmental effects influenced alcohol dependence, binge eating, and compensatory behaviors, with heritability estimates ranging from 38% to 53%.”(For the specific statistical correlations, see the full-text article. The correlation was stronger for women than for men).

In addition, the study did not find any significant shared environmental influences contributing to covariance between alcoholism and binge behaviors.

Limitations of the study include an older age cohort (mean age 44 in women), higher alcoholism rates in the Australian sample compared with the U.S., and the possibility that other comorbidities, such as depression, might influence the association.

“It appears that some genes that influence alcohol dependence also influence binge eating in men and women,” said Melissa Munn-Chernoff, in a prepared statement. “When you go to an eating disorder treatment center, they don’t often ask questions about alcoholism. And when you go for alcoholism treatment, they don’t generally ask questions about eating disorder symptoms. If centers could be aware of that and perhaps treat both problems at the same time, that would be a big help.”

Women who abuse alcohol have it tough for any number of reasons, and this study gets at one of them: “A combination of pressures to adjust to the changing body at puberty, increased access to alcohol via peer networks, and genetic predispositions for eating disorder symptoms and alcohol problems could result in comorbid alcohol dependence and bulimia symptoms."

Munn-Chernoff M.A., Duncan A.E., Grant J.D., Wade T.D., Agrawal A., Bucholz K.K., Madden P.A.F., Martin N.G. & Heath A.C.  A twin study of alcohol dependence, binge eating, and compensatory behaviors., Journal of studies on alcohol and drugs,    PMID: 23948525

Photo credit: https://www.facebook.com/WUSTLmedicine.health?group_id=0

Building Better Baby Brains: Just Say No To FAS

Fetal Alcohol Syndrome is our most preventable form of disability.

Despite a growing focus on the hazards of prescription painkillers for newborns, drinking during pregnancy remains the nation’s leading preventable cause of birth defects and developmental disorders in children. Fetal Alcohol Spectrum Disorders (FASD) encompass a wide variety of neurobehavioral and central nervous system disabilities related to alcohol use during pregnancy, including, but not limited to, developmental delays, growth retardation speech disabilities, and poor social skills. The classic physical characteristics of FASD, such as small head size, wide-set eyes and a thin upper lip, are not always present.

September 9th is International Fetal Alcohol Spectrum Disorders Awareness Day. Kenneth Warren, acting director of the National Institute on Alcohol Abuse and Alcoholism, said in a prepared statement that “Almost 40 years have passed since we recognized that drinking during pregnancy can result in a wide range of disabilities for children, of which fetal alcohol syndrome (FAS) is the most severe. Yet up to 30 percent of women report drinking alcohol during pregnancy.”

NIAAA, in a brief history of the disorder, calls fetal alcohol syndrome the “most common known cause of mental retardation.” Tragically, the knowledge of alcohol as a teratogen responsible for birth defects was not widely recognized by the medical community in American until the 1970s, when a group of crusading physicians began reporting observations of clustered birth defects among alcoholic mothers. (French doctors were on to FAS in the 1960s). In short order, the Surgeon General issued an FAS advisory, the U.S. Congress passed laws requiring pregnancy warning labels on alcoholic beverages, and doctors began warning their pregnant patients about the hazards of heavy drinking while pregnant. Nonetheless, CDC studies have shown that 0.2 to 1.5 cases of fetal alcohol syndrome (FAS) occur for every 1,000 live births.

Not surprisingly, the NIAAA finds that the risk for teratogenic injury and the severity of injury “appear to increase with greater levels of alcohol consumption.” Facial features associated with FAS are linked to early fetal exposure, so it is possible that “an embryo may escape the injury necessary to develop the characteristic FAS face but receive sufficient injury later in development to exhibit all the FAS-associated CNS and neurobehavioral deficits.”

Organ abnormalities are also characteristic of early exposure, while growth deficits are more likely the result of alcohol exposure later in pregnancy. Binge drinking—high peak dose drinking—is especially troublesome, as it has a great negative impact than low-dose steady drinking. But no period is risk-free. Genetic and environmental factors are plausibly invoked as contributors, but nobody knows what they are at present.

The disabilities caused by FASD often linger throughout adulthood, burdening families with anguish and heavy medical costs. “The message is simple, not just on Sept. 9, but every day,” says Warren. “There is no known safe level of drinking while pregnant. Women who are, who may be, or who are trying to become pregnant, should not drink alcohol.”

Graphics Credit: http://edmontonfetalalcoholnetwork.org/

Thursday is National Alcohol Screening Day

Assess your drinking risk with this easy test.

The more you drink, the less likely you are to accurately perceive the risks of heavy drinking, according to a survey by Screening for Mental Health (SMH), a Boston-area non-profit group.  The phone survey of 1,000 adults in the U.S. indicated that 7 out of 10 respondents would consult a health care provider if they “thought they might have a problem with alcohol,” but that only 50% of responders with the highest number of at-risk drinking episodes per year said they would seek medical help.

Phone surveys can be notoriously unreliable when it comes to questions about the personal use of drugs and alcohol. However, the point being made here is clear: There are ways to screen high-risk drinkers, who aren’t always the best judge of their own behavior. For National Alcohol Screening Day on Thursday, April 11, SMH offers www.HowDoYouScore.org, where you can take a quick quiz to see how you measure up. More than a thousand community organizations, colleges, and military bases will be taking part. The screening, which is geared toward younger drinkers, is free, anonymous, and online—just the way college students like it. The event, held in April in conjunction with Alcohol Awareness Month, netted more than 40,000 online anonymous screenings last year.

In another finding from the survey, 20% of respondents said that drinking heavily is a “phase many kids go through,” which is certainly true and a suspiciously rare choice in this survey. It’s unlikely that people are eager to approve of young people drinking heavily, even as a “phase.” Nonetheless, we know that kids who begin drinking before age 15 are far more likely to drink alcoholically as adults. And at-risk drinking correlates strongly with age: Most of the mayhem is committed by men under age 35. No surprise there.

“Despite public opinion, at-risk drinking increases your chances of developing alcohol use disorders—such as alcoholism—as well as other physical and mental health problems," said Douglas G. Jacobs, M.D., associate clinical professor of psychiatry at Harvard Medical School and medical director of SMH, in a prepared statement. “In the U.S., about 18 million people have an alcohol use disorder. The screenings allow individuals to assess their drinking habits and have an opportunity to connect with local support resources.”

And while we are on the subject of, and in the month of, alcohol awareness, here are some earlier posts on ethyl alcohol and you:

7 Myths the Alcohol Industry Wants You to Believe

The Truth About Weight Loss Surgery and Alcohol

Mixing up the Medicine: What Alcohol Doesn’t Go With

Alcoholic Deception

Dude, where’s my metaconsciousness?