Question: Is the buzz from absinthe really any different from plain liquor?
Researched and written by Owen
Emlen for "Ask
Erowid", Erowid.org.
Edited by another Erowid contributor and volunteer (spoon).
While some people don't report feeling a different high from absinthe, the presence
of Thujone from Wormwood in many Absinthe preparations may alter the effects of
alcohol.
Wormwood oil (and therefore, Absinthe) contains both alpha- and beta-Thujone.
Beta-Thujone is less toxic and less potent than alpha-Thujone, and the pharmacodynamics
of both substances appear to be similar. Therefore, as the more toxic constituent
of Absinthe, alpha-Thujone is the focus of the majority of current research.
In an article discussing alpha-Thujone's mechanism of action, Hold, Sirisoma, Ikeda,
and Narahasha (2000) found that alpha-Thujone was a modulator of the GABA-A receptor
chloride channel. Under normal conditions, GABA binds to a postsynaptic neuron
and allows chloride to enter the cell body. The influx of chloride causes
hyper-polarization, or a "calming" effect on the neuron. Alpha-Thujone
blocks this influx of chloride into the postsynaptic neuron, resulting in the "calming"
inhibitory signals being blocked. This reduction in GABA-mediated inhibition
results in excitation, which is why alpha-Thujone is classified as a convulsant
and lowers seizure threshold.
Intra-peritoneal (IP) injections of 45mg/kg alpha-Thujone resulted in 50% mortality
in mice. Death occurred by convulsion, which began approximately two minutes
after injection at doses between 30-45mg/kg. Mice administered higher doses
died more quickly, and all mice administered 60mg/kg of alpha-Thujone died within
a minute after injection due to tonic convulsion. However, most mice pretreated
with either diazepam or Phenobarbital (which both modulate GABA-A, allowing more
chloride to enter the neuron) survived alpha-Thujone injection at doses as high
as 100mg/kg. Mice bred to be resistant to picrotoxinin (another drug which
blocks GABA chloride channels) were also resistant to alpha-Thujone poisoning, further
indicating that the two substances work in similar ways.
The blocking of the usual GABA-A mediated inhibitory effects of alcohol may be the
reason why Absinthe drinkers may be more talkative, appear less inebriated, and
may drink more alcohol than usual, unintentionally. This can lead to dangerously
high blood alcohol levels.
In other words, the alcohol and Thujone may work against each other on the GABA-A
receptor, reducing some specific effects of alcohol intoxication.
The less-potent metabolites of alpha-Thujone are active as well, and may remain
in the body for longer periods of time. It may be possible that residual activity
by alpha-Thujone metabolites, in combination with alcohol withdrawal symptoms, could
lead to seizures and possibly add to the mystique of absinthe in inducing both madness
and bouts of creativity when consumed in large quantities over a long period of
time.
After completing their research with mice, Hold et al. (2000) conclude that "Current
low levels of alpha- and beta-Thujone in absinthe are of
much less toxicological concern than the ethanol content" (Hold, Sirisoma,
Ikeda, & Narahasha, 2000, p. 3831). However, the likelihood of drinking
more alcohol than normally would be consumed may be a major risk factor associated
with Absinthe consumption.
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Reference: Hold KM, Sirisoma NS, Ikeda T, Narahashi T, Casida JE. "Alpha-thujone
(the active component of absinthe): gamma-aminobutyric acid type A receptor modulation
and metabolic detoxification." Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):3826-31.
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