Saturday, October 31, 2015

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 fiancĂ©] 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.”

Monday, October 12, 2015

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.”