The Green Fairies: What Absinthe and Cannabis Have in Common

By Charlie Tetiyevsky on September 29, 2017

Absinthe, that famous anise-flavored green alcohol, has a storied past, not least in part for having caught favor among creatives and intellectuals of the 19th and early 20th centuries. People have been mystified by the drink for centuries, and its modern return has brought a resurgence of curiosity about its hallucinogenic—and possibly dangerous—qualities. Modern research, however, has shown that its psychoactive properties have been greatly overstated and question the validity of early claims about absinthe’s dangers.

Stories about the horrors of absinthe ran the gamut, like Vincent Van Gogh’s morbid tale: He’d supposedly been addicted to the drink and became increasingly psychotic before shooting himself. Van Gogh’s clear case of mental illness either wasn’t as glamorous a story, or, more likely, didn’t fit in with the early 19th century imperative to demonize and ban the drink. The term “absinthism” came about to describe the poisoning that had resulted from absinthe use, including hallucinations and seizures—qualities also present, of course, in common chronic alcoholism.

Absinthism was the center of fin de siècle backlash against the drink, with claims that it was a new, different form of addiction than alcoholism. Murders and violence were blamed on absinthe specifically, and the medical community pursued research that helped to perpetuate fear among the populace. They blamed an “increase in insanity and other serious medical problems” specifically on the drink. In a move backed by winemakers and teetotalers both, absinthe was banned from the United States in 1912. France, eventually concerned about “a weakening of military power in the light of absinthe abuse” among soldiers, banned the substance in 1915. So too did Belgium, Switzerland, Italy and Germany.

Researchers at the time performed studies on animals using pure wormwood oil and varying classes and clarities of absinthe. Pre-ban absinthe often contained two types of wormwood, a type of wild daisy similar to chamomile and often relatively rich in the terpene thujone. There are, of course, still a number of factors that ultimately decide how much thujone and wormwood make their way into the drink. 

There are three grades of pre-ban absinthe: absinthe suisse, the purest form of the drink with 68 to 72 percent alcohol by volume (abv); absinthe demi-fine, which had 50 to 68 percent abv; and absinthe ordinaire, containing 45 to 50 percent abv. While the others were distilled with ethyl alcohol, absinthe suisse’s maceration and steam distillation process created a pure herbal distillate containing wormwood and other plants like sage, spinach and tansy. Absinthe makers in different countries tended to have their own preferred herbal blends: The Czech added peppermint, the Swiss added melissa, hyssop or angelica root alongside their own specific Swiss alpine wormwood, and the French added coriander. Cheap imitators began to pop up as absinthe gained popularity, with drinks that contained any number of unsavory ingredients used to match absinthe’s taste and characteristic light chartreuse color (which real absinthe simply got from the chlorophyll in wormwood and spinach). Some unscrupulous brewers went as far as to include the carcinogenic compound aniline green and highly toxic methanol. 

Studies done by researchers at the turn of the century used any number of these varying substances to test reactions on animals, ranging from proper absinthe to pure wormwood oil alone. 

True too is that the maceration and distillation of wormwood oil meant that not all of the thujone contained in the original herbal mix made its way into the end product, and so testing with wormwood oil itself would create a vastly different result from testing with the resulting thujone levels. “Even at the highest concentrations found in any of the samples tested,” explains Liquers de France, “the effects of the alcohol would far outweigh those of the thujone.”

A study done in Germany in 2006 explained that early researchers did indeed not control for ethanol content and therefore also did not necessarily distinguish the reaction of animals to this amount of alcohol compared to thujone. This is not to mention that thujone levels, like other terpenes (including those in cannabis), differ depending on where the wormwood is grown. Thujone wasn’t detectable, for example, in wormwood from the Pyrenees or Tuscany, and was more predominant when grown in the lower zones of the Swiss alpines versus at high altitudes.

Researchers became distracted from studying alcoholism itself with their belief that they’d solved the problem by eliminating absinthism. The doctors, unsurprisingly, referred callously to alcoholics as “idiotic… degenerate and deformed” rather than individuals with a disease. They were glad to make do with “solving” the problem of epileptogenic and hallucinogenic absinthe when they were really more likely facing one of alcoholism. Naturally, the problem wasn’t solved with the absinthe bans and led to American alcohol prohibition in full.

Researchers, however blundering their attempts at studies were, may have inadvertently made an accurate point about thujone that hadn’t been discovered until recently. It is not necessarily present within absinthe in enough quantities to cause any harm—modern European Union beverage laws established in the 1990s that re-legalized the drink put the cap on thujone content at 35 mg per liter. But it does operate on some of the brain’s receptors as an antagonist, which means that it blocks the sites where a certain amino acid would be taken in—which does affect one of the brain’s mechanisms of managing seizures. The inhibited amino acid is GABA, a neurotransmitter—meaning that it jumps from cell to cell as a “chemical messenger,” transmitting nerve signals between neurons, or nerve cells, in the brain. It is one of the “most abundant neurotransmitters in the central nervous system… especially in the cerebral cortex, which is where thinking occurs and sensations are interpreted.” 

Neurotransmitters like GABA click into place in spaces called receptors, after which they generally make the neuron they’ve docked in send “an electrical impulse” across a synapse, which is the pathway between neurons. GABA, though, is “a neurotransmitter in the central nervous system [that works to] inhibit nerve transmission in the brain, calming nervous activity.” GABA is essentially a “chemical messenger” that “blocks nerve impulses” and tells cells not to fire off, making it a crucial component of preventing anxiety, muscle tension, insomnia, short temper, IBS, migraines, addiction, depression, allergies and, yes, seizures. The mechanism of GABA-function dysregulation mirrors how an imbalance of serotonin can lead to unstable and depressed moods.

The amino acid GABA is being sold in vitamin stores all over as a supposed cure for these symptoms. But only supplements like L-Theanine (a metabolite of GABA—that is, what it breaks down into) have been shown to capable of crossing the blood-brain barrier and helping with these ailments. Taking GABA itself won’t do anything for them because it can’t get from the bloodstream into the brain.

Relatively recently studies popped up comparing tetrahydrocannabinol (THC) to thujone, with the hypothesis that thujone also acted on cannabinoid receptors. This was disproven in 1999. While THC, like GABA, is a central nervous system depressant, it’s also a GABA agonist and inhibitor, meaning that THC keeps GABA from being released and then binds to the locations in which GABA should be instead.

Cannabidiol (CBD), another cannabinoid found in marijuana, is a different story. CBD seems to work on GABA receptors like anxiety medications and anticonvulsants known as benzodiazepines (e.g., Xanax or Klonopin), though on different sites in the receptor than those drugs. When studied, researchers found that CBD interacted with GABA in a positive way, enhancing its ability to bind with the receptor instead of blocking it. This “may be relevant to the anticonvulsant and anxiolytic effects of [CBD].” CBD has the opposite effect on GABA than THC, which might have to do with why it inhibits the psychoactive nature of THC.

Research suggests a couple of things about cannabis consumption, including that consumers might be advised to take an L-Theanine supplement or something else to increase their GABA production and uptake. But even with the supplement, the real solution may lie in limiting THC levels in recreational and medical cannabis and encouraging the production of midis with high CBD levels instead of the current trend of pushing for higher THC strains. 

It’s undoubtable that THC, like thujone, affects GABA levels and uptake in the brain and so the key here, if you’re not using a high-CBD/low-THC or CBD-only strain, is moderation. As Oscar Wilde said about absinthe, “After the first glass you see things as you wish they were. After the second, you see things as they are not. Finally you see things as they really are, and that is the most horrible thing in the world.”

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