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Absinthism: fictitious 19th century syndrome

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Degeneration and absinthism

A further strong argument of the anti-absinthe phalanx was grounded on the Lamarckian theories of the inheritance of diseases (Jean-Baptiste Lamarck, 1744–1829). According to these theories, any traits acquired by absinthe drinkers would be passed on to their children. The idea of degeneration was also used by Magnan to explain mental illnesses [54]. It is interesting to note that this hereditary feature was also ascribed to alcoholism.






Table 3: Summary of data about toxicology of thujone


Toxicity data  
oral LD50 in rats 192 mg/kg bw

oral LD50 in rats

500 mg/kg bw


iv LD50 in rabbits

0.031 mg/kg bw


NOEL for convulsions in rats

12.5 mg/kg bw (males)


NOEL for convulsions in rats

5 mg/kg bw (females), 10 mg/kg bw (males)


NOEL for convulsions in rats

5 mg/kg bw


TDI (based on NOEL with safety factor of 500)

10 µg/kg bw/d



2-,4-, and 7-hydroxylation


Mechanism of toxicity

GABA Type A modulation (α-thujone neurotoxicity, convulsant effects)


Mechanism of toxicity

Porphyrogenicity (determined in cultures of chick embryo liver cells)


Behavioral effects

5-HT3 receptor modulation, but no conclusive evidence for psychotropic actions of thujone


The editorial section of JAMA published the theory that a larger proportion of the children of alcoholics were more "idiotic, epileptic, neurotic, alcoholic, degenerate and deformed" than the children of healthy parentage, and total abstinence was postulated [55].

The condition of absinthism was introduced into late 19th century medicine together with the first emerging descrip tions of alcoholism [37]. Intriguingly, this fact could hold the key for the solution of the debate about whether absinthism was a clinical pattern of its own and how it should be distinguished from chronic alcoholism. As mentioned previously, due to the low solubility of etheric oils, absinthe usually contains high concentrations of ethanol, which means that there was no ingestion of thujone without ingestion of remarkably high quantities of ethanol.

Recently, in an editorial, Strang et al. raised the question of "absinthe: what's your poison?" [56]. To us, however, the question is really what happened to the symptoms of absinthism after its prohibition. Did this mysterious syndrome disappear abruptly or did these symptoms simply continue to exist among chronic alcohol abusers under the name of alcoholism, which seems to be more tolerated by society? Finally, as with so many facets of the green fairy, this issue remains controversial and perhaps will never be solved.
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