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?

Marijuana and Strokes: Medical Reality or Scare Story?

Heavy tokers may be at higher risk, but alcohol is the hidden confounder.

Young people don’t suffer from strokes, as a rule. And when they do, at least half the time there is no obvious cardiovascular explanation. So it’s not surprising that drugs are often invoked as the culprit.

A New Zealand study earlier this year once again raised the specter of a possible link between stroke and marijuana smoking. As reported by Maia Szalavitz at Time Healthland, the confounding issue, as is typical of such studies, is the coexisting use of other drugs, like alcohol and cigarettes. As Szalavitz writes:

The stroke study, which incorporated preliminary data, is the first trial of its kind to study a possible connection between marijuana use and stroke. It included 160 patients aged 18 to 55 who had suffered a stroke connected to a blood clot in the brain, and who agreed to have their urine tested for marijuana within 72 hours of the stroke.  These results were compared to those from 160 controls who had not had a stroke but came to the hospital for other reasons. They were matched on age, gender and ethnic background, all of which can also affect the risk for this type of stroke. About 16% of the stroke patients showed traces of marijuana in their urine, compared to 8% of those in the control group, suggesting a doubling of the risk of stroke.

However, because of nicotine and other confounding variables, that study was considered inconclusive. In an earlier study published in Stroke, the journal of the American Heart Association, Valerie Wolff and colleagues from the University of Strasbourg in France searched the medical literature and found 59 cases of stroke in which cannabis could be considered a cardiovascular risk factor. The investigators used only cases that had been confirmed by neuroimaging. The researchers focused on cases where a stroke had occurred while smoking marijuana, or within a half hour after the last joint or bong hit.

But proving a cause and effect relationship is tricky. Assuming, for now, that all of the strokes in question were not caused or compounded by alcohol or drugs other than marijuana, the French scientists postulated several mechanisms that could conceivably account for a cannabis-related ischemic stroke (a stroke caused by obstruction of a blood vessel). These include orthostatic hypotension, altered cerebral vasomotor function, major swings in blood pressure, and cardiac arrhythmias. However, the only solid commonality in cannabis-related strokes was that the users were more likely to be heavy smokers.

In the 50 strokes the researchers were able to confirm by cerebral imaging, the patterns in some patients were similar to those observed in a syndrome called reversible cerebral vasoconstriction syndrome (RCVS). RCVS  is marked by severe headaches, strokes, and brain edema, but symptoms typically resolve in a few months.  “Reversibility of the vasoconstriction within 12 weeks is a key point of this syndrome,” the authors write. “The long duration of stenosis [blockage] argues in favor of a drug-induced immunoallergic vasculitis rather than vasospasm. Our point of view is that this disorder may be considered as a variant of RCVS,” rather than as a garden-variety ischemic stroke triggered by excessive use of cannabis.

According to the French study, “The most frequently presented characteristics of cannabis users who experienced a stroke are young male chronic tobacco and cannabis abusers who have had an unusual high consumption of cannabis and alcohol before stroke.” The most convincing mechanism to explain ischemic strokes in young people, the researchers say, is “reversible cerebral angiopathy involving several arteries, associated with cannabis consumption in association with tobacco and alcohol use.”

And there you have it. Smoke weed, and you appear to have a slight risk of suffering stroke, which, under age 50, is an extremely uncommon medical event.  Add tobacco, and the stroke risk goes up. Add alcohol, and the stroke risk ratchets even higher. By itself, marijuana appears to be a minor factor in strokes—but it appears likely that pot is indeed the culprit at least some of the time.

“Cannabis-related stroke is not a myth,” the scientists conclude, “and a likely mechanism of stroke in most cannabis users is the presence of reversible multifocal intracranial stenosis (MIS) induced by this drug. The reality of the relationship between cannabis and stroke is, however, complex, because other confounding factors have to be considered (ie, lifestyle and genetic factors).”

Wolff V., Armspach J.P., Lauer V., Rouyer O., Bataillard M., Marescaux C. & Geny B. (2013). Cannabis-related Stroke: Myth or Reality?, Stroke, 44 (2) 558-563. DOI: 10.1161/STROKEAHA.112.671347

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

Smokers’ Genes: Evidence From a 4-Decade Study

How adolescent risk becomes adult addiction.

 Pediatricians have often remarked upon it: Give one adolescent his first cigarette, and he will cough and choke and swear never to try another one. Give a cigarette to a different young person, and she is off to the races, becoming a heavily dependent smoker, often for the rest of her life. We have strong evidence that this difference in reaction to nicotine is, at least in part, a genetic phenomenon.

But so what? Is there any practical use to which such knowledge can be put? As it turns out, the answer may be yes. People with the appropriate gene variations on chromosomes 15 and 19 move very quickly from the first cigarette to heavy use of 20 or more cigarettes per day, and have more difficulty quitting, according to a new report published in JAMA Psychiatry. From a public health point of view, these findings add a strong genetic rationale to early smoking prevention efforts— especially programs that attempt to “disrupt the developmental progression of smoking behavior” by means of higher prices and aggressive enforcement of age restrictions on smoking.

What the researchers found were small but identifiable differences that separated people with these genetic variations from other smokers. The gene clusters in question “provide information about smoking risks that cannot be ascertained from a family history, including information about risk for cessation failure,” according to authors Daniel W. Belsky, Avshalom Caspi, and colleagues at the University of North Carolina and Duke University.

The group looked at three prominent genome-wide association studies of adult smoking to see if the results could be applied to “the developmental progression of smoking behavior.” They used the data from the genome work to analyze the results of a 38-year prospective study of 1,037 New Zealanders, known as the Dunedin Study. A total of 405 cohort members in this study ended up as daily smokers, and only 20% of the daily smokers ever achieved cessation, defined as a year or more of continual abstinence.

The researchers came up with a multilocus genetic risk score (GRS) based on single-nucleotide polymorphisms associated with smoking behaviors. Previous meta-analyses had identified several suspects, specifically a region of chromosome 15 containing the CHRNA5-CHRNA3-CHRNB4 gene cluster, and a region of chromosome 19 containing the gene CYP2A6. These two clusters were already strong candidate genes for the development of smoking behaviors. For purpose of the study, the GRS was calculated by adding up the alleles associated with higher smoking quantity. The genetic risk score did not pertain to smoking initiation, but rather to the number of cigarette smoked per day.

When the researchers applied these genetic findings to the Dunedin population cohort, representing ages 11 to 38, they found that an unfortunate combination of gene types seemed to be pushing some smokers toward heavy smoking at an early age. Individuals with a high GRS score “progressed more rapidly to heavy smoking and nicotine dependence, were more likely to become persistent heavy smokers and persistently nicotine dependent, and had more difficulty quitting,” according to the study. However, these effects took hold only when young smokers “progressed rapidly from smoking initiation to heavy smoking during adolescence.” The variations found on chromosomes 15 and 19 influence adult smoking “through a pathway mediated by adolescent progression from smoking initiation to heavy smoking.”

Curiously, the group of people who had the lowest Genetic Risk Scores were not people who had never smoked, but rather people who smoked casually and occasionally—the legendary “chippers,” who can take or leave cigarettes, sometimes have one late at night, or a couple at parties, without ever falling victim to nicotine addiction. These “light but persistent smokers” were accounted for “with the theory that the genetic risks captured in our score influence response to nicotine, not the propensity to initiate smoking.”

Naturally, the study has limitations. Everyone in the Dunedin Study was of European descent, and the life histories ended at age 38. Nor did the study take smoking bans or different ages into account. The study cries out for replication, and hopefully that won’t be long in coming.

Could information of this sort be used to identify high-risk young people for targeted prevention programs? That is the implied promise of such research, but no, probably not. The gene associations are not so dramatic as to cause youngsters with the “bad” alleles to inevitably become chain smokers, nor do the right set of genes confer protection against smoking. It’s not that simple. However, the study is definitely one more reason to push aggressive smoking prevention efforts aimed at adolescents.


Belsky D.W.  Polygenic Risk and the Developmental Progression to Heavy, Persistent Smoking and Nicotine DependenceEvidence From a 4-Decade Longitudinal StudyDevelopmental Progression of Smoking Behavior, JAMA Psychiatry,   1. DOI: 10.1001/jamapsychiatry.2013.736

Graphics Credit: http://cigarettezoom.com/

More Hard Facts About Addiction Treatment

“Yes, we take your insurance.”

Recent reportage, such as Anne Fletcher’s book, Inside Rehab, has documented the mediocre application of vague and questionable procedures in many of the nation’s addiction rehab centers. You would not think the addiction treatment industry had much polish left to lose, but now comes a devastating analysis of a treatment industry at “an ethics crossroads,” according to Alison Knopf’s 3-part series in Addiction Professional. Knopf deconstructs the problems inherent in America’s uniquely problematic for-profit treatment industry, and documents a variety of abuses. We are not talking about Medicaid, Medicare, or Block Grants here. Private sector dollars, Knopf reaffirms, do not “guarantee that the treatment is evidence-based, worth the money, and likely to produce a good outcome.” Even Hazelden, it turns out, is prepared to offer you “equine therapy,” otherwise known as horseback riding.

Knopf, who is editor of Alcoholism and Drug Abuse Weekly, was specifically looking at private programs, paid for by insurance companies or by patients themselves. Who is in charge of enforcing specific standards of business practice when it comes to private drug and alcohol rehabs? Does the federal government have some manner of regulatory control? According to a physician with the Substance Abuse and Mental Health Services Administration (SAMHSA), the feds rely on the states to do the regulating. And according to state officials, the states look to the federal agencies for regulatory guidance.

All too often, the states routinely license but do not effectively monitor treatment facilities, or give useful consumer advice. Florida state officials do not even know, with any certainty, exactly how many treatment centers are in operation statewide. And even if state monitoring programs were effective and aggressively applied, “just because something is legal doesn’t mean it’s ethical,” said the SAMHSA official.

“We see this as a pivotal time for the treatment field as we have come to know it,” said Gary Enos, editor of Addiction Professional, in an email exchange with Addiction Inbox. Enos said that “the Affordable Care Act (ACA) will move addiction treatment more into the mainstream of healthcare, and this will mean that treatment centers' referral and insurance practices will come under more scrutiny than ever before.”

 Among the questionable practices documented by Knopf:

—Paying bounties and giving gifts to interventionists in return for client referrals.

Under Medicare, paying interventionists for referrals is banned. “In the private sector,” says a California treatment official, “it’s not illegal. But it is unethical.” According to treatment lobbyist Carol McDaid, “kickbacks happen all the time. Treatment centers that are doing this will do so at their own peril in the future,” she told Knopf.

—Giving assurances that treatment will be covered by insurance even though only a portion of the cost is likely to be covered.

Under the Affordable Care Act (ACA), says the SAMHSA official, “We are trying to position people to know more about their benefit package. And the industry has to be more straightforward about what the package will cover.” John Schwarzlose, CEO of the Betty Ford Center, told Knopf that “it’s very hard for ethical treatment providers to compete against insurance bait-and-switch,” when patients are told their insurance is good—but aren’t told that the coverage ends after 7 days, or that the daily maximum payout doesn’t meet the daily facility charges.

—Billing patients directly for proprietary nutrient supplements, brain scans, and other unproven treatment modalities.

“Equine therapy, Jacuzzi therapy, those are nice things, and maybe they help with the process of engagement,” said one therapist. “But people need to recognize that these ancillaries aren’t the essence of getting sober.”

—Engaging in dubious Internet marketing schemes.

You see them on the Internet: dozens and dozens of addiction and rehab referral sites. They list private services in various states, and look, on the surface, like legitimate information resources for people in need. As the owner of a blog about drugs and addiction, I hear from them constantly, asking me for links. “Family members and patients frequently have no way of knowing that a treatment program was really a call center they got to by Googling ‘rehab,’ writes Knopf, “and that the call center gets paid for referring patients to the actual treatment center. They don’t know that a program that promises to ‘work with’ health insurance knows full well the insurance will cover only a few days at the facility, and the rest will have to be paid out of pocket.” She points to a 2011 Wired magazine article, which said the Internet marketing cost of key words like “rehab” and “recovery” can be stratospheric. But “by spending that money—not necessarily providing good service—treatment provides can come out on top on searches. It’s the new marketing to the desperate.”

The group with the most to lose from revelations of this nature is the National Association of Addiction Treatment Providers (NAATP), the association representing both private and non-profit rehab programs. The Betty Ford Center has discontinued its membership in NAATP, a move that reflects the turmoil of the industry today. “It’s crazy that we have treatment centers inviting interventionists and other referents on a cruise, and then giving everyone an iPad,” Schwarzlose said.

As one man who lost his son to an overdose said: “I don’t get it. There’s the American Cancer Society, but I look for drugs and alcohol and I can’t find anything. There’s no National Association for Addictive Disease. How can this be?”

The investigative series will be featured in Addiction Professional’s March/April print issue. Enos believes that “influential treatment leaders are more interested than ever to see this debate aired more publically,” and says that the online publication of Knopf’s articles for the magazine has sparked “a great deal of discussion in treatment centers and on social media, including comments about other questionable practices that harm the field’s reputation.”

Drug News in Brief

Short takes on matters various.

Taking Aim at Pot—Researchers have recently made clinical efforts to test three drugs that might help during marijuana withdrawal to keep pot abstainers on the straight and narrow. Researchers at Columbia University, led by Margaret Haney, have been testing a synthetic THC compound called nabilone. The drug is designed to address sleep and appetite problems during withdrawal.  Whether it is any better tolerated by users than Marinol, Uncle Sam’s widely unpopular version of synthetic THC, remains to be seen. This approach can be viewed rather like methadone or buprenorphine substitution therapy. Meanwhile, work goes on with lofexidine, a drug sometimes used in combination with naltrexone for opiate detoxification. A 2008 study in Psychopharmacology showed a modest improvement over placebo when lofexidine was used for marijuana abstinence, but it worked much better when combined with, yes, synthetic THC. Finally, velafaxine, better known as the antidepressant Effexor, was used in a randomized, double-blind, placebo controlled trial of marijuana-dependent outpatients recently published in Addiction. Not only did velafaxine fail to help the patients with their cannabis dependence, but in fact “may lead to an increase in cannabis use.”

Smoking is Bad to the Bone—The Journal of Adolescent Health reports that cigarette smoking dramatically impacts the rate of bone density growth in teenage girls. Young women may be smoking their way toward a future of osteoporosis, the loss of bone density that often plagues older women. “This age group is when you should gain about 50 percent of your bone accrual,” reports study author Lorah Dorn at Cincinnati Children’s Hospital Medical Center, in Science News. A 2001 study of adult smokers found that smoking increased the risk of hip fracture by 31% in women. In addition, at the recent annual meeting of the American Academy of Orthopedic Surgeons, researchers reported on a study of 6,779 patients undergoing treatment for spinal disorders with severe pain. Those who quit smoking during treatment reported greater pain improvement than patients who didn't stop smoking. 

Dr. Google Will See You Now—Researchers are starting to data-mine the Internet to identify unanticipated side effects and interactions between prescription drugs. According to an article in Science by Sean Treacy, one study in 2011 data-mined reports to the FDA from doctors, nurses, and patients, and “uncovered a hidden drug interaction: When taken together the antidepressant paroxetine and the cholesterol suppressant pravastatin can cause hyperglycemia, or high blood sugar.”  Bioinformatics researcher Nigam Shah of Stanford told the magazine that “if a lot of people are concerned about a symptom, that in itself is valuable information.”

Fetal Health—Scientists have traced out a molecular signaling pathway that appears to play a crucial role in the development of fetal alcohol spectrum disorders (FASD). According to the researchers, whose study was published in the Proceedings of the National Academy of Sciences, “ethanol may cause FASD in part by decreasing the adhesion of the developmentally critical L1 cell adhesion molecule through interactions with an alcohol binding pocket on the extracellular domain.” In English, it means that the research points to strong candidate genes, therefore identifying a specific locus of action for future drugs designed to block alcohol neurotoxicity in the womb. A group led by Michael Charness at Harvard Medical School did the work, building on previous studies that identified the alcohol sensitivity of L1 adhesion molecules. “Prenatal alcohol exposure is the leading preventable cause of birth defects and developmental disorders in the United States,” according to perennial Acting NIAAA Director Kenneth Warren, in an NIH news release.

Photo Credit:  http://jimbaker.wordpress.com/

Big Tobacco Easily Evades “Light” Cigarette Ban

Color coding allows smokers to easily identify their former brands.

The tobacco industry has once again made a mockery of the Food and Drug Administration’s attempts to ban ‘light” cigarettes from the marketplace, by simply eliminated the objectionable wording and substituting an easily-decoded color scheme. In a brochure prepared for cigarette retailers marked “For trade use only: not to be shown or distributed to customers,” tobacco giant Philip Morris wrote that “some cigarettes and smokeless packaging is changing, but the product remains the same.”

Research done at Harvard demonstrates "the continued attempts of the industry to avoid reasonable regulation of tobacco products,” said Hillel Alpert, co-author of a new study on light cigarettes, in a prepared statement. The Family Smoking Prevention and Tobacco Control Act (FSPTCA) of 2009 highlights the banning of light cigarettes as a critical mission, since cigarettes marketed in this way are in fact no safer than regular cigarettes. What makes a cigarette Light or Ultra-light is a series of tiny holes drilled through the filter (See earlier post). This “filter ventilation” was calibrated to the descriptors: Ultra-lights had more holes drilled in the filter than Lights. Studies have demonstrated conclusively that such filter schemes do not make smoking safer or cut down on related diseases. A 2001 report from the National Cancer Institute documented how smokers were compensating for the ventilation holes by smoking more cigarettes, smoking them more intensely, or by blocking the filter holes with fingers or lips.

In a study for Tobacco Control, Gregory Connolly and Hillel Alpert of the Harvard School of Public Health documented the process. In 2010, Philip Morris sent manuals to retailers detailing how they were to deal with the new sales situation. Philip Morris made clear that “current pack descriptors such as light, ultra-light and mild will be removed from all packages.” All well and good. However, the Philip Morris material also specified how a series of new package names were to be doled out. Marlboro Light became Marlboro Gold. Marlboro Mild morphed into Marlboro Blue. And Marlboro Ultra-light reemerged as Marlboro Silver.

When the researchers commissioned a large public survey to document the state of affairs one year after the official “light” ban, they found that “88%-91% of smokers found it either ‘somewhat easy’ or ‘very easy’ to identify their usual brand of cigarettes by the banned descriptor names, Lights, Mediums or Ultra-Lights.” Sales figures for these brands in the first two quarters of 2010 were essentially unchanged, the authors report. They conclude that “the majority of smokers of brands in all categories correctly identified their brands’ pack color.”

The lesson here may well be that countries like Australia and the UK are on the right track: Plain packaging may be best. If lawmakers allow “misleading numbers, the use of colors, imagery, brand extensions, and other devices that contribute to deception” in place of words, nothing has really changed. “The findings of the present research strongly suggest that tobacco manufacturers have evaded one of the most important provisions of the FSPTCA for protecting the public health from the leading cause of preventable death and disease,” the authors conclude.

In a press release, co-author Gregory Connolly, director of the Center for Global Tobacco Control at Harvard, explained that the industry “was found guilty by a federal court in 2006 for deceptively promoting ‘light’ cigarettes as safer after countless smokers who switched to lights died prematurely, thinking they had reduced their health risks.”

Connolly G.N. & Alpert H.R. (2013). Has the tobacco industry evaded the FDA's ban on 'Light' cigarette descriptors?, Tobacco Control, PMID: 23485704

Photo Credit:http://www.mydiscountcigarette.net

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