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Trying to get at what the true effects of absinthe drinking in
the first three quarters of the 19th century were is typical of
trying to understand the effects of many psychoactive substances.
The ‘evidence’ presented for a particular effect is likely to be coloured by the point of view of the presenter. Thus, it may well be true that the campaign against absinthe in the late 19th century was biased by an unholy alliance of prohibitionists with the French wine industry, which was anxious to recover the market share lost during the outbreak of grape phylloxera that began in the middle of the century. For the wine growers, it was important to find grounds for attacking absinthe which did not rely on the inherent harm potential in all alcohol consumption.
It seems to be the case that the majority of those saying that absinthe is not the demon it was made out to be either have a financial interest in absinthe sales or are avid absinthe drinkers. Then there are those who want absinthe to appear to be capable of delivering a ‘legal’ high so as to sell it to people who would not consider using Cannabis sativa, marijuana, because of its status.
Both these groups want to demonstrate that absinthe today is no different from what the great artists are alleged to have drunk in France.
But, absinthe’s bad reputation dates from long before the end of the 19th century so is it possible, from this distance in time, to say if there is any truth in its alleged ability to cause hallucinations and convulsions and the condition described in the 1860s as ‘absinthe epilepsy’?
The suggestion that the effect of thujone results from its
similarity to THC comes from a letter entitled ‘Marijuana, absinthe
and the central nervous system’ (by J. Del Castillo, M. Anderson, G.
M. Rubottom, Published in Nature, January 1975). The authors started
from the point of view that absinthe and cannabis produced similar
psychological effects and hypothesised that this resulted from
similarities in the molecular structure of thujone and THC which
might result in the substances binding to the same receptors in the
central nervous system.
It should be stressed that the authors ‘propose [my italics] therefore that both thujone and THC exert their psychotomimetic effects by interacting with a common receptor in the central nervous system’ and conclude that ‘This hypothesis suggests new experimental approaches’. It must also be remembered that this was a letter and not a full scientific paper.
Nonetheless, this association between thujone and THC was seized on and, quickly, became the accepted wisdom. Note, that in ‘This And That - An Artefactual Alkaloid And Its Peptide Analogs’, published in Trends In Pharmacological Sciences 13 (9): 341-345, 1992, B. Max states ‘The literature on the pharmacology of thujone is, to put it bluntly, second rate’ so there was little work going on to challenge this position. (No public abstract available.)
The rapid uptake of this erroneous view may say something about the debate on cannabis. ‘Everybody knows’ that 19th century absinthe was a very dangerous substance so demonstrating that this was because it behaved like cannabis might help to reinforce the message on the alleged harm caused by cannabis.
It may, also, have to do with companies projecting the image of cannabis onto their versions of absinthe. Logan Distribution, Inc. on its website repeats the claimed similarity between thujone and THC and goes on to state that the absinthe it offers, in the USA, is ‘as strong as the legitimate Absinthes of the 19th century’. That claim is worthy of further examination.
The true nature of the action of thujone was given in a 2000 paper entitled ‘α-Thujone: γ-Aminobutyric acid type A (GABA-A) receptor modulation and metabolic detoxification’. This says that thujone can greatly disrupt the nervous system and damage the brain’s self-control mechanism producing epileptiform convulsions, hallucinations and delirium. But, did mid-19th century absinthe contain enough thujone to produce these effects?
As with any substance, the quantity consumed must be expected to
have a bearing on the effect produced. The claimed effects of 19th
century absinthe depend on the perception that it had much higher
thujone levels than modern versions.
Professor Wilfred N. Arnold, in his book “Vincent Van Gogh: Chemicals, Crises and Creativity'', quotes a typical thujone level in 19th century absinthe of 260 mg/l. Professor Arnold told Theodore A. Breaux, one of the authors of the next paper, that this figure was arrived at by calculation and not by analysing any absinthe. These postulated levels have been challenged, most recently in ‘Chemical Composition of Vintage Preban Absinthe with Special Reference to Thujone, Fenchone, Pinocamphone, Methanol, Copper, and Antimony Concentrations’ by Dirk W. Lachenmeier, David Nathan-Maister, Theodore A. Breaux, Eva-Maria Sohnius, Kerstin Schoeberl, and Thomas Kuballa, published in the Journal of Agricultural and Food Chemistry in May, 2008. In March 2009, the same authors published a short article seeking to answer the criticism that thujone deteriorates with time so their results could not be taken as indicating the original strength of the samples. They say that whilst thujone is degraded by exposure to UV light, the green bottles in which absinthe was stored prevent this action.
It should be pointed out, for the sake of being open, that two of the authors have a financial interest in sales of absinthe though Ted Breaux has assured me that at the time he had no commercial interest in absinthe though, as a result of his work, he created Lucid Absinthe. Also, all the ‘preban’, that is pre-1915, samples tested dated from 1895 at the earliest. Vincent Van Gogh, said to be one of the most prominent absinthe drinkers though Martin Gayford's 2006 book 'The Yellow House' suggests that Van Gogh did not drink anything in large quantities and drank wine and brandy as well as absinthe, died in 1890. By the last decade of the century, grape phylloxera, first seen in France in 1863, had caused considerable damage to the French wine industry and it is possible that absinthe makers revised their formulations to encourage more wine drinkers to sample the spirit.
It is believed that Professor Arnold based his work on recipes found in Pierre Duplais’s 1855 book whose title translates as ‘A Treatise On The Manufacture And Distillation Of Alcoholic Liquors’. This might explain the difference between Professor Arnold’s thujone levels and those found in turn of the century products.
Reports talking about these results speak of the European Union lifting its ban on absinthe without stating that the thujone levels are required to be below 10mg/l. Again, it seems, modern day suppliers of absinthe are seeking to demonstrate that their wares are ‘the real thing’ by claiming similar levels of thujone to 19th century versions.
As recently as December 2007, writing in Scientific American,
Professor Arnold said that thujone ‘can cause hallucinations,
convulsions and permanent damage to the nervous system’.
Lachenmeier et al, however, try and suggest that absinthe is no more harmful that any other strong alcohol and that it is the alcohol which is capable of causing harm and not the thujone or other herb extracts used in the drink.
There is some suggestion that deliberate adulteration or accidental contamination might have resulted in the production of absinthes which did cause the effects ascribed to thujone but it is also said that many of the effects seen were simply those of acute alcoholism. Ted Breaux has confirmed that there was no standard for absinthe (even today only Switzerland has a legally binding definition of 'absinthe') and says 'buying cheap absinthe in 19th century France was akin to buying cheap vodka in Russia'.
The term ‘absinthe epilepsy’ appears to have been coined by Dr Magnan who, in the 1860s, had some 250 absinthe abusers in his care and based his new term both on his observations of these patients and by experimentation on animals. In 1895, the Royal Society published a paper detailing experiments on cats to determine the progress of absinthe epilepsy. In a paper delivered to a conference on eugenics in 1912, Dr. Magnan describes in detail the attacks suffered by absinthe abusers and says ‘it is exactly like an attack of epilepsy’. Of course, Dr. Magnan had a financial interest in boosting the numbers of people receiving treatment in his clinic and this may have coloured his evaluation of the effects of drinking absinthe.
There is no dispute about the harm which can be caused by the oil of Wormwood extracted from Artemisia absinthium which contains high concentrations of thujone but it seems unlikely that there was sufficient thujone, even in crudely produced absinthe, to carry those effects into absinthe drunk in ‘normal’ quantities. As far as I am aware no-one has ever produced alcohol free absinthe in order to study the effects of the wormwood separate from the alcohol.
Readers may have noticed that many of the issues surrounding the true effects of absinthe, (Is the mechanism properly understood? Is contamination or adulteration a factor? Do those proposing a particular theory have a prejudice towards that view? Is quantity a determining cause of harm? Are the financial interests of businesses driving the debate in a particular direction?) are similar to those inherent in the debate over the true nature of cannabis.