Freud and his Drug Demons

Cocaine addiction and psychoanalysis.

That Sigmund Freud was a cocaine abuser for some portion of his professional life is by now well known. Reading An Anatomy of Addiction by Howard Markel, M.D., which chronicles the careers of Freud and another famed cocaine abuser, Johns Hopkins surgeon William Halsted, I was struck by the many ways in which even the father of modern psychotherapy could not see the delusions, evasions and outright lies that were the byproducts of his very own disease of the body and mind: drug addiction. Markel makes the case that in several important ways Freud’s cocaine addiction was hopelessly entangled with, and partially responsible for, his theorizing about the workings of the mind.

In 1884, Freud published his book, On Coca, a treatise on the wonders of cocaine. To his fiance, he wrote: “I have other hopes and intentions about [cocaine]. I take very small doses of it regularly against depression and against indigestion and with the most brilliant of success.” The book, a comprehensive review of cocaine’s effects, had an “n of 1”: “I have carried out experiments and studied, in myself and others, the effect of coca on the healthy human body.”

One of the defects of On Coca was its assertion that the drug was an effective antidote to serious morphine and alcohol abuse. Most astonishingly, however, Freud “skimmed over cocaine’s most important clinical use as a local anesthetic.” That discovery was later championed by ophthalmologist Carl Koller, whom Freud never forgave, even though the mistake was Freud’s alone. It seems reasonable to suggest that a moody doctor, who happened to be treating a close friend for morphine addiction at the time, might tend to focus on cocaine’s use against depression and drug abuse. And two years later, Freud vigorously fought back against an influential American doctor’s unambiguous assertion that cocaine was addictive. The U.S. physician had written that a “doctor self-prescribing cocaine was the equivalent of the lawyer representing himself in court: each had a fool for a patient or client.”

Markel notes that it is “also telling that he does not reveal to [his fiancé] the precise amount of cocaine he was ingesting. In fact, throughout his notes during this period, Freud minimizes the amount and frequency of his cocaine dosage, using such terms as ‘a little cocaine’ or a ‘bit of cocaine,’ a tactic many substance abusers employ to avoid the disapproval or intervention of others.”

Writing in his capacity as a physician, Markel states:

In light of the physical symptoms Freud suffered during this period, in my medical opinion, there is ample evidence that he was abusing significant amounts of cocaine during the early 1890s and that he was using it in a dependent, if not outright addictive fashion. In fact, cocaine likely had a negative effect on virtually every aspect of Sigmund’s personal relationships, behavior, and health. We can make such a declarative statement because his letters to Wilhelm Fleiss tells us precisely so…. Sigmund explained that he was suffering from a Fliessian syndrome of ‘crossed reflexes’ of the nose, brain, and genitals that had led to severe migraine headaches. The excruciating pain, not surprisingly, could only be interrupted by the multiple doses of cocaine prescribed by Dr. Fliess.

It was not pretty: “From a diagnostic standpoint, Sigmund’s nasal stuffiness is intriguing… Sigmund’s need for cauterization—the placement of a hot knife against swollen, blocked nasal tissue to, literally, burn open a passage for air—in concert with his disinclination to write suggests serious cocaine abuse.” And also telling is Freud’s habit of smoking 20 or more cigars each day.

By 1894, Markel writes, “the cardiac symptoms associated with cocaine use and the severe depression and headaches after its use—similar to what Sigmund was experiencing—were finally being reported in the medical journals of the day.” And, much like an alcoholic explaining away his chronic stomach troubles, “Freud continued to search for alternative explanations for his chest pain rather than seriously contemplate cocaine’s potential role in the matter.”

For readers in need of socioenvironmental triggers for addiction, Freud had a ready supply: “risk taking, resentments, loneliness, alienation, emotional pain, traumatic family experiences, phobias, neuroses, depression, denials and secretiveness about his sexuality, a possible sexual relationship with his sister-in-law, a brief flirtation with excessive drinking, and his self-documented cocaine abuse, to name some of his demons.”

About 1896, Freud stopped discussing his use of cocaine, and more or less dropped the subject altogether. Later in life, he speculated on whether his love of cigars (which eventually killed him) had helped keep him away from the task of working out his own psychological problems. “One wonders,” writes Markel, “whether his compulsive cocaine abuse from 1884 to 1896 was one of those unexplored problems.”

From 1896 to 1900, presumably cocaine-free years, Freud suffered from “depression, cocaine urges, occasional binge drinking, sexual affairs, caustic behaviors, and emotional absence.” To Markel, this adds up to the classic portrait of a “dry drunk,” AA’s description of someone who has given up drinking and drugs, and is miserable about it, and is making everyone around them miserable as well.

Markel points to the theory promulgated by historian Peter Swales to the effect that Freud’s entire concept of the libido “is merely a mask and a symbol for cocaine; the drug, or rather its invisible ghost, haunts the whole of Freud’s writing to the very end.”

Cannabis Receptors and the Runner’s High

[First published August 4 2010]

Maybe it isn't endorphins after all.

What do long-distance running and marijuana smoking have in common? Quite possibly, more than you’d think. A growing body of research suggests that the runner’s high and the cannabis high are more similar than previously imagined.

The nature of the runner’s high is inconsistent and ephemeral, involving several key neurotransmitters and hormones, and therefore difficult to measure. Much of the evidence comes in the form of animal models. Endocannabinoids—the body’s internal cannabis—“seem to contribute to the motivational aspects of voluntary running in rodents.” Knockout mice lacking the cannabinioid CB1 receptor, it turns out, spend less time wheel running than normal mice. 

A Canadian neuroscientist who blogs as NeuroKuz suggests that “a reduction in CB1 levels could lead to less binding of endocannabinoids to receptors in brain circuits that drive motivation to exercise.” NeuroKuz speculates on why this might be the case. Physical activity and obtaining rewards are clearly linked. The fittest and fleetest obtain the most food. “A possible explanation for the runner’s high, or ‘second wind,’ a feeling of intense euphoria associated with going on a long run, is that our brains are stuck thinking that lots of exercise should be accompanied by a reward.”

In 2004, the British Journal of Sports Medicine ran a research review, “Endocannabinoids and exercise,” which seriously disputed the “endorphin hypothesis” assumed to be behind the runner’s high. To begin with, other studies have shown that exercise activates the endocannabinoid system.

“In recent years,” according to the authors, “several prominent endorphin researchers—for example, Dr Huda Akil and Dr. Solomon Snyder—have publicly criticised the hypothesis as being ‘overly simplistic,’ being ‘poorly supported by scientific evidence’, and a ‘myth perpetrated by pop culture.’” The primary problem is that the opioid system is responsible for respiratory depression, pinpoint pupils, and other effects distinctly unhelpful to runners.

The investigators wired up college students and put them to work in the gym, and found that “exercise of moderate intensity dramatically increased concentrations of anandamide in blood plasma.” The researchers break the runner’s high into four major components. Exercise, they say, “suppresses pain, induces sedation, reduces stress, and elevates mood.” Some of the parallels with the cannabis high are not hard to tease out: “Analgesia, sedation (post-exercise calm or glow), a reduction in anxiety, euphoria, and difficulties in estimating the passage of time.”

There are cannabinoid receptors in muscles, skin and the lungs. Intriguingly, the authors suggest that unlike “other rhythmic endurance activities such as swimming, running is a weight bearing sport in which the feet must absorb the ‘pounding of the pavement.’” Swimming, the authors speculate, “may not stimulate endocannabinoid release to as great an extent as running.” Moreover, “cannabinoids produce neither the respiratory depression, meiosis, or strong inhibition of gastrointestinal motility associated with opiates and opioids. This is because there are few CB1 receptors in the brainstem and, apparently, the large intestine.”

A big question remains: What about running and the “motor inhibition” characteristic of high-dose cannabis? (An inhibition that may make cannabis useful in the treatment of movement disorders like tremors or tics.) Running a marathon is not the first thing on the minds of most people after getting high on marijuana.  The paper maintains, however, that at low doses, “cannabinoids tend to produce hyperactivity,” at least in animal models. The CB1 knockout mice were abnormally inactive, due to the effect of cannabinoids on the basal ganglia. Practiced, automatic motor skills like running are controlled in part by the basal ganglia. The authors predict that “low level skills such as running, which are controlled to a higher degree by the basal ganglia than high level skills, such as basketball, hockey, or tennis, may more readily activate the endocannabinoid system.”

The authors offer other intriguing bits of evidence. Anandamide, one of the brain’s own cannabinoids, “acts as a vasodilator and products hypotension, and may thus facilitate blood flow during exercise.” In addition, “endocannabinoids and exogenous cannabinoids act as bronchodilators” and could conceivably facilitate breathing during steady exercise. The authors conclude: “Compared with the opioid analgesics, the analgesia produced by the endocannabinoid system is more consistent with exercise induced analgesia.”

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

The Zendo Project

The Zendo Project

Caffeine, Energy Drinks, and Everything Else

It's the everything else that adds up.

A couple of years ago, 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 an 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.

In 2013, the FDA released reports that attributed a total of 18 deaths to energy drinks. Somewhere between 3 and 10 grams of caffeine 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. Restrictions on the sale of powdered caffeine may follow, as a valid public health measure. “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. Last year, The Food and Drug Administration advised consumers to avoid powdered caffeine due to health risks.

Originally published March 13, 2013

Graphics: http://www.runnersworld.com

Marijuana Deconstructed

What's In Your Weed?

Australia has one of the highest rates of marijuana use in the world, but until recently, nobody could say for certain what, exactly, Australians were smoking. Researchers at the University of Sydney and the University of New South Wales recently analyzed hundreds of cannabis samples seized by Australian police, and put together comprehensive data on street-level marijuana potency across the country. They sampled police seizures and plants from crop eradication operations. The mean THC content of the samples was 14.88%, while absolute levels varied from less than 1% THC to almost 40%.  Writing in PLoS one, Wendy Swift and colleagues found that roughly ¾ of the samples contained at least 10% total THC. Half the samples contained levels of 15% or higher—“the level recommended by the Garretsen Commission as warranting classification of cannabis as a ‘hard’ drug in the Netherlands.”

In the U.S., recent studies have shown that THC levels in cannabis from 1993 averaged 3.4%, and then climbed to THC levels in 2008 of almost 9%. By 2015, marijuana with THC levels of 20% were for sale in Colorado and Washington.

CBD, or cannabidiol, another constituent of cannabis, has garnered considerable attention in the research community as well as the medical marijuana constituency due to its anti-emetic properties. Like many other cannabinoids, CBD is non-psychoactive, and acts as a muscle relaxant as well. CBD levels in the U.S. have remained consistently low over the past 20 years, at 0.3-0.4%. In the Australian study, about 90% of cannabis samples contained less than 0.1% total CBD, based on chromatographic analysis, although some of the samples had levels as high as 6%.

The Australian samples also showed relatively high amounts of CBG, another common cannabinoid. CBG, known as cannabigerol, has been investigated for its pharmacological properties by biotech labs. It is non-psychoactive but useful for inducing sleep and lowering intra-ocular pressure in cases of glaucoma.

CBC, yet another cannabinoid, also acts as a sedative, and is reported to relieve pain, while also moderating the effects of THC. The Australian investigators believe that, as with CBD, “the trend for maximizing THC production may have led to marginalization of CBC as historically, CBC has sometimes been reported to be the second or third most abundant cannabinoid.”

Is today’s potent, very high-THC marijuana a different drug entirely, compared to the marijuana consumed up until the 21st Century? And does super-grass have an adverse effect on the mental health of users? The most obvious answer is, probably not. Recent attempts to link strong pot to the emergence of psychosis have not been definitive, or even terribly convincing. (However, the evidence for adverse cognitive effects in smokers who start young is more convincing).

It’s not terribly difficult to track how ditch weed evolved into sinsemilla. It is the historical result of several trends: 1) Selective breeding of cannabis strains with high THC/low CBD profiles, 2) near-universal preference for female plants (sinsemilla), 3) the rise of controlled-environment indoor cultivation, and 4) global availability of high-end hybrid seeds for commercial growing operations. And in the Australian sample, much of the marijuana came from areas like Byron Bay, Lismore, and Tweed Heads, where the concentration of specialist cultivators is similar to that of Humboldt County, California.

The investigators admit that “there is little research systematically addressing the public health impacts of use of different strengths and types of cannabis,” such as increases in cannabis addiction and mental health problems. The strongest evidence consistent with lab research is that “CBD may prevent or inhibit the psychotogenic and memory-impairing effects of THC. While the evidence for the ameliorating effects of CBD is not universal, it is thought that consumption of high THC/low CBD cannabis may predispose users towards adverse psychiatric effects….”

The THC rates in Australia are in line with or slightly higher than average values in several other countries. Can an increase in THC potency and corresponding reduction in other key cannabinoids be the reason for a concomitant increase in users seeking treatment for marijuana dependency? Not necessarily, say the investigators. Drug courts, coupled with greater treatment opportunities, might account for the rise. And schizophrenia? “Modelling research does not indicate increases in levels of schizophrenia commensurate with increases in cannabis use.”

One significant problem with surveys of this nature is the matter of determining marijuana’s effective potency—the amount of THC actually ingested by smokers. This may vary considerably, depending upon such factors as “natural variations in the cannabinoid content of plants, the part of the plant consumed, route of administration, and user titration of dose to compensate for differing levels of THC in different smoked material.”

Wendy Swift and her coworkers call for more research on cannabis users’ preferences, “which might shed light on whether cannabis containing a more balanced mix of THC and CBD would have value in the market, as well as potentially conferring reduced risks to mental wellbeing.”


Swift W., Wong A., Li K.M., Arnold J.C. & McGregor I.S. (2013). Analysis of Cannabis Seizures in NSW, Australia: Cannabis Potency and Cannabinoid Profile., PloS one, PMID: 23894589

(First published at Addiction Inbox Sept. 3 2013)

Graphics Credit: https://budgenius.com/marijuana-testing.html

Such Stuff As Dreams Are Made On: Marijuana and Sleeping

Study sheds potential light on indica vs. sativa debate.

[Thanks to Ivan Oransky (@ivanoransky) for alerting me to this study.]

Anyone who has smoked marijuana more than a couple of times knows that cannabis can alter how you sleep. The effect of cannabis on sleep is even part of the never-ending debate over Cannabis indica vs. Cannabis sativa, the two major species of the marijuana plant. Indica smokers typically report a marijuana high that is body-intensive and often soporific, sometimes leading to the condition aptly known as “couch lock.” Whereas sativa smokers, according to marijuana lore, experience a more cerebral, energetic “head high,” with fewer somatic effects. Not surprisingly, hybrid strains incorporating the alleged characteristics of both indica and sativa strains are popular in the medical marijuana community.

Although there is no official sanction for it in the medical community, marijuana is often dispensed medically for sleep problems. One piece of common wisdom holds that the higher the THC content of marijuana, the more helpful it will be in promoting sleep and improving poor sleep. The stronger the better, in other words. Similarly, indica strains are assumed to promote sleep more than sativa strains.

In an effort to clear the air, so to speak, a group of researchers, writing in Addictive Behaviors, sought to “document naturalistic choice of particular medical cannabis types among individuals who self-report using cannabis for the treatment of sleep problems…. Little research has documented species or cannabinoid concentration preferences among individuals who use medical cannabis for particular conditions…. We also evaluated the interaction between the type of cannabis used and diagnosis of cannabis use disorder among study participants.”

The researchers recruited participants from a medical cannabis dispensary in California under procedures approved by the VA and Stanford University review boards. 163 people with a mean age of 40, who used cannabis twice a day on average, provided self-reported information on their cannabis use for the study. 81 participants reported using cannabis for the management of insomnia, and another 14 reported using cannabis to reduce nightmares. (Frequent smokers insist they dream less. THC does appear to decrease the density of REM cycles, leading to more restful, dream-free sleep, according to some studies. )

So what did they find?

—“Individuals who reported using cannabis for nightmares, compared to those who did not, preferred sativa to indica.” (Small effect.)

Indica, considered the “heavier” high, might have seemed the likely choice here.

—"Individuals who self-report using cannabis to treat symptoms of insomnia and those with greater self-reported sleep latency reported using cannabis with significantly higher concentrations of CBD.” (Large effect.)

Again, a somewhat counterintuitive finding, since it is widely believed that CBD conduces toward a more wakeful state than THC alone.

—“Individuals who used sleep medication less than once/week used cannabis with higher THC concentrations than those who used sleep medication at least once a week.” (Large effect.) “There were no differences in THC concentration as a function of self-reported sleep quality, or use for insomnia or nightmares.”

Pretty straightforward finding: THC makes you sleepy. It is not clear, however, that above a certain threshold, more THC makes you even sleepier. In fact, some researchers would consider this finding unexpected, given that high THC concentrations have been shown to have a stimulating effect.

—“Older individuals were less likely to have cannabis use disorder compared to those younger….

No surprise about the older folks, since prior studies show a decrease in the prevalence of cannabis use disorders with age.

—“Individuals who preferred sativa or primary sativa hybrid strains were less likely to have cannabis use disorder compared to those who preferred indica or primary indica hybrid strains.” (Small effect.)

If replicated, this finding could have significant implications; both in strengthening programs to reduce marijuana smoking among the very young, and it warning consumers that some evidence suggests indica strains may be more addictive than sativa strains in plants with similar THC/CBD levels and ratios.

—“Neither concentration of THC nor CBD were associated with cannabis use disorder.”

Common sense, but useful to remember. In other addictive behaviors, such as heroin and alcohol abuse, the relative strength of the drug is not the primary determinant of its addictive potential.

Caveats and design limitations: The survey relied on retrospective reports of sleep quality and pot preferences. Also lacking is an examination of additional variables such as PTSD and co-occurring substance abuse.

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/