With the increasing mass consumption of absinthe, more and more of the chronic – and most probably high-dose – absinthe consumers developed seizures, speech impairment, sleep disorder, mental prostration, auditory and visual hallucinations and finally death. This collection of symptoms gave birth to the term "absinthism;" it is unclear, however, if this syndrome ever really existed at all. Absinthism in these days was supposedly further characterized by brain damage, gastrointestinal problems, risk of psychiatric disease and even suicide [38]. Even an increased incidence of oesophageal cancer in absinthe drinkers was noticed [39]. In contrast, other authors recommended moderate doses of absinthe as a valuable remedy against depressions [40].

Both the serious and the populist medical literature of the day demonized absinthe, in many cases laying the groundwork for the anti-absinthe temperance movement. The definition of absinthism as a particular syndrome separate from alcoholism is intimately connected with the French physician Valentin Magnan. A biography of Magnan is available in a recent review article [41]. In Magnan's work about absinthism between 1864 and 1874 he described visual and auditory hallucinations accompanied by alterations in consciousness after consumption of absinthe [42,43]. Other authors described acute symptoms of absinthe, such as hallucination, restlessness, confusion, delirium and seizures [44] (Table 1). Symptomatic differences between the drinker of absinthe and the ordinary alcoholic were presented at the First International Eugenics Congress: in absinthism, the "hallucination insanity" was described to be "more active with sudden attacks of delirium, more terrifying, sometimes provoking most dangerous reactions of extreme violence"[45]. In addition, complete statistics of the central service for the admission of insane persons for the town of Paris were given. In the years 1867–1912, a number of 16,532 patients were treated for alcoholic intoxication. 70.3% of all patients were diagnosed as "chronic alcoholics," but only 1.0% of all patients were found to have symptoms of absinthism. Due to the high consumption of absinthe in Paris of that time, one questions if very severe forms of chronic alcoholism were misleadingly described as absinthism.

In a clinical report on a case of absinthe intoxication, published in the Boston Medical and Surgical Journal (today the New England Journal of Medicine) in 1868, Amory, a former pupil of Magnan, observed "pleural effusions", "epileptiform seizures" and a "reddish discoloration of the urine"[38]. The latter symptom can be interpreted – among other possible causes – as an episode of acute porphyria. It has been shown in vitro that thujone and other terpenes exhibit porphyrogenic properties. In primary chicken embryo liver cell cultures, an acute porphyria-like state was mimicked by the addition of the iron chelator desferrioxamine. Upon addition of thujone, a marked accumulation of protoporphyrin was observed. Bonkovsky et al. concluded that the tested terpenes, i.e., thujone, are porphyrinogenic and hazardous, especially to patients with underlying defects in hepatic heme synthesis [46].