Absinthe: what's your poison?

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.¹ 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 1930.²

Many creative artists had their lives touched by absinthe (Toulouse-Lautrec, Oscar Wilde, Picasso).³ The illness of Vincent van Gogh was certainly exacerbated by excessive drinking of absinthe,⁴ and one of his six major crises was precipitated by drinking.³ Van Gogh probably had acute intermittent porphyria—a working hypothesis⁵ compatible with the documented porphyrogenicity of the terpenoids in absinthe as well as ethanol.⁶ 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.⁷ 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 enough amounts.³ The thujone content of old absinthe was about 0.26 g/l (260 ppm)⁸ and 350 ppm when the thujyl alcohol from the wormwoods is included.³ 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 ppm⁹).

The acute toxic effects of thujone include epileptiform convulsions.⁴ Cases of poisoning with wormwood still occur, mostly out of misplaced loyalty to folk remedies or sheer ignorance.¹⁰ Thujone is a porphyrogenic terpenoid: it increases 5-aminolevulinic acid synthase activity and induces porphyrin production in chicken embryonic liver cells.⁶ The livers of 19th century absinthe drinkers could easily have experienced concentrations of thujone of 20-200 μmol/l,⁶ 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.⁷,¹¹ A distinct condition—absinthism—stood alongside the emerging descriptions of alcoholism.¹² Absinthism was associated with gastrointestinal problems, acute auditory and visual hallucinations, epilepsy, brain damage, and increased risk of psychiatric illness and suicide.¹² 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 1915.¹ 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 recognised over the past 50 years,¹³ 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.