|Absinthism: fictitious 19th century syndrome|
Animal experiments with wormwood extract
It has to be stressed again that clinical reports of these days were more or less only descriptive or speculative, as causal connections between absinthe and thujone and the above-mentioned symptoms could never reliably be
proven. However, experimental studies were performed on animals to prove that wormwood was the causing agent of absinthism, especially the seizures. All these studies were carried out using so-called "essence d'absinthe" (pharmaceutical wormwood extracts) or pure etheric oil of wormwood, however, often only the term "absinthe" was used for these extracts. Even in current history books the terms "absinthe" and "essence d'absinthe" are misleadingly used as synonymous .
|Table 2: Comparative table between symptoms of absinthism and alcoholism according to animal experiments of Amory (1868) .|
|Absinthism (Injection of pure wormwood extract (0.8â4.5 g)||Alcoholism (Injection of alcohol (0.8â5 g) into the stomach of into the stomach of different animals) different animals)|
|Animal perfectly well for fifteen minutes, at the least after the ingestion; with the exception of a few muscular twichings and a slight uneasiness.|
Muscular agitation, commencing in the anterior portion of the body.
Epileptiform convulsions and rigidity, resulting in a rapid death. No apparent lesion, except, perhaps a slight cerebral congestion, showing the cause of death to be intoxication of the poison.
| In a very few minutes symptoms of inebriation resulting in torpor. |
Paralysis, commencing in posterior extremities, and then extending to the anterior.
Paralysis of both posterior and anterior extremities in succession. No convulsions. Stupor, coma, resolution and a gradual death.
Lesions of the brain and of the alimentary canal; gastritis and enteritis might have supervened, had the animals lived long enough for their development.
If injected in pure form, wormwood extracts and alcohol showed distinctly different symptoms (Table 2). These results were generalized and transferred to humans who drank high concentrations of alcohol in combination with low concentrations of wormwood extract. In further experiments, guinea pigs â among other small animals â were placed in the presence of wormwood essence, while the control guinea pig was "shut up with a saucer of pure alcohol." In contrast to the animal breathing alcohol, which was reported to have simply become drunk, the guinea pig inhaling the vapors of wormwood experienced initial excitement and subsequently seizures [43 ].
These experiments and deductions of Magnan et al. were criticized as early as 1869, when The Lancet commented upon the inadequacy of the evidence produced in order to prove that absinthism was different in its nature from chronic alcoholism. The sleeplessness, the tremor, the hallucinations, the paralysis, and even the seizures, were described to be well-known symptoms of simple alcoholic excess. The effect of inhalation of concentrated wormwood fumes was seen as not transferable to the effect of very small, continuous oral doses . In Great Britain, the hostility against Magnans experiments led so far that the Royal Society for the Prevention of Cruelty to Animals prosecuted three English doctors for assisting Magnan in 1874 in demonstrating that intravenous injection of wormwood extracts into a dog induced epilepsy. The prosecution failed as Magnan had discreetly returned to France .
Further investigations were undertaken to determine the origin of the fits in wormwood epilepsy by Boyce . For this purpose, numerous lesions were made both in the brain and spinal cord of cats, and wormwood administered immediately or after a lapse of days or weeks. It was found that wormwood, acting upon the bulbo-spinal centers (including the cerebellum) alone, could produce a series of "clonic fits", differing from the cortical in the slower rhythm of the contractions. In experiments of Ott upon rabbits those results were disputed as no "spinal" but only "cortical convulsions" were determined, which raises the question if the crude techniques of the 19th century were suitable at all to determine the physiological origin of epilepsy [ 50 ].
In the noteworthy work of Ossipow, the problem of different wormwood extracts to achieve epilepsy in animals was discussed for the first time . The failure of some researchers to replicate the experiments of Magnan was explained by misunderstandings between "absinthe", "essence d'absinthe", and "extrait d'absinthe". Ossipow stressed that only the "essence d'absinthe" (alcohol-free wormwood oil) and not the ready-to-drink alcoholic beverage (in France called "extrait d'absinthe") is usable to trigger seizures in animals.
Further studies were conducted by Cunningham [52 ] and Lesieur . The only consistent conclusion that can be drawn from all these animal experiments is that wormwood oil but not absinthe is a potent agent to cause seizures in animals.
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