|Published Scientific Papers on Thujone
Absinthe: what’s your poison?
by J. Strang, W. Arnold, T. Peters
Published in BMJ, December 1999
Though absinthe is intriguing, it is alcohol in general we should worry about
Absinthe, the emerald green liqueur associated with excess, is back in business. Having been banned in many countries in the early
20th century, its newly fashionable image, combined with global purchasing opportunities through the internet, has brought its revival.
Since 1998 several varieties of absinthe have again been available in Britain—from bars, stores, and mail order. But is absinthe a
special problem or simply part of a general concern about excessive alcohol consumption?
Originally formulated in Switzerland, absinthe became most popular in 19th century France. Between 1875 and 1913 French
consumption of the liquor increased 15-fold.
It became an icon of “la vie de bohème,” and in fin-de-siècle Paris l’heure verte (the green [cocktail] hour) was a daily event. Although
never as popular in Britain, the fashion of mixed drinks with a “spot” or “kick” of absinthe was reported in London as late as 1930.
Many creative artists had their lives touched by absinthe (Toulouse-Lautrec, Oscar Wilde, Picasso). The illness of Vincent van Gogh was
certainly exacerbated by excessive drinking of absinthe, and one of his six major crises was precipitated by drinking. Van Gogh probably
had acute intermittent porphyria—a working hypothesis compatible with the documented porphyrogenicity of the terpenoids in absinthe
as well as ethanol. His case illustrates the importance of lifestyle, underlying illness, and the individual response.
Toulouse-Lautrec mixed his absinthe with brandy, but the traditional method was to take about 30 ml of the bitter liqueur in a special
glass and to add about five volumes of cold water, trickled over a sugar cube on a slotted spoon. As the alcohol concentration drops, the
terpenoids come out of solution to form a yellow opalescence. This louche effect is retained in modern absinthe substitutes (pastis,
such as Pernod and Ricard), which are rich in anise but contain no thujone. The alcohol concentration of diluted absinthe was thus not
greater than that of other spirit based drinks.
Pointing the finger at thujone
Absinthe was classically manufactured from dried wormwood (Artemisia absinthium), anise, and fennel, which were steeped overnight
in 85% (by volume) ethanol. The next day water was added, the concoction boiled, and the distillate (alcohol plus steam distilled
terpenoids) collected. The process was completed by a further extraction of dried Roman wormwood (A pontica), hyssop, and lemon
balm and then filtration to yield a clear, green liqueur of 74% alcohol. The plant products in absinthe varied among manufacturers, the
only universal components being alcohol and wormwood essence.
Convulsions resembling epilepsy were observed in humans and induced in animals with toxic doses of absinthe. The essential oils
were first implicated, then specifically wormwood, and finally one chemical, thujone. Quantitatively speaking this is justified, though
thujyl alcohol (wormwood), as well as pinocamphone (hyssop) and fenchone (fennel), can precipitate convulsions if used in large
The thujone content of old absinthe was about 0.26 g/l (260 ppm) and 350 ppm when the thujyl alcohol from the wormwoods is
included. Currently available versions of absinthe boast of thujone inclusion—in one case at 8-9 ppm (still within the European
Commission upper limit of 10 ppm).
The acute toxic effects of thujone include epileptiform convulsions. Cases of poisoning with wormwood still occur, mostly out of
misplaced loyalty to folk remedies or sheer ignorance.
Thujone is a porphyrogenic terpenoid: it increases 5-aminolevulinic acid synthase activity and induces porphyrin production in chicken
embryonic liver cells. The livers of 19th century absinthe drinkers could easily have experienced concentrations of thujone of 20-200
mol/l, which might have presented a problem for drinkers born with a compromised heme pathway.
From the late 1850s onwards absinthe aroused medical interest and became the subject of animal experiments with either the liqueur
or oil of wormwood. A distinct condition—absinthism—stood alongside the emerging descriptions of alcoholism. Absinthism was
associated with gastrointestinal problems, acute auditory and visual hallucinations, epilepsy, brain damage, and increased risk of
psychiatric illness and suicide. French scientific warnings eventually reached the popular presses but were countered by denials from a
government interested in taxes and an industry enjoying profits. Meanwhile, consumers from all walks of life strove to convince
themselves that the risks were at least commensurate with the pleasures of absinthe’s appearance, fragrance, taste, amusing ritual,
and mistaken reputation as an aphrodisiac.
Between 1905 and 1913 Belgium, Switzerland, the United States, and Italy banned absinthe. The French government made absinthe
less available after 1915.
It was never formally banned in Spain, Portugal, the Czech Republic, or the United Kingdom, but the overall effect of substantial
international action in the first two decades of this century was to achieve something close to global prohibition.
Wider harms from alcohol
As with other early descriptions of alcohol related conditions such as “rum fits,” there is a grave danger of demonising a particular drink
and thereby missing the wider importance of alcohol related harm. Although alcoholic liver disease (maladie de foie) was initially
emphasised, the damaging effects of ethanol on all tissues in the body have been increasingly recognized over the past 50 years, and
organ damage by ethanol is now established as a relatively long term affair. A poor diet exacerbates the effects of ethanol in certain
tissues, especially the nervous system, but the view in the 1940s that such damage was due exclusively to associated malnutrition,
rather than to ethanol and its metabolites, is incorrect.
As our knowledge of multiple organ damage, neurotoxicity, and diverse psychiatric sequelae of excessive alcohol use has increased,
the possibility emerges that much of the syndrome of absinthism was actually acute alcohol intoxication, withdrawal, dependence, and
other neuropsychiatric complications—major health and social problems, but not unique to absinthe. On the other hand, the differences
between ethanol and ethanol plus thujone in the time course for onset of symptoms in experimental animals have always been
challenging. As yet we know little about the characteristics or consumption patterns of the new absinthe drinkers, and the long term
effects of thujone and other terpenoids remain unclear. Until data from properly conducted studies are available, one can only resort to
limp warnings of the potential risks from the low levels of thujone in contemporary absinthe-like products. So next time someone offers
you a drink and says “What’s your poison?” think carefully before you answer.
John Strang, Professor of the Addictions
National Addiction Centre, Institute of Psychiatry, King’s College,
London SE5 8AF
Wilfred N Arnold, Professor of Biochemistry and
University of Kansas Medical Center, Kansas City, KS 66160-7421, USA
Timothy Peters, Professor of Clinical Biochemistry
King’s College Hospital, London SE5 9PJ
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