Learning from The Past

While his art is now highly renowned and eulogized, Vincent Willem Van Gogh spent his lifetime in considerable obscurity, fraught with numerous unprofitable endeavors, misfortunes and various illnesses leading up to his ultimate suicide at the age of 37. Years of extensive research into the possible ailments that plagued Van Gogh near the end of his life have revealed several factors that could have contributed to both his physical symptoms as well as the art style of his paintings.

Seizures

Much of Van Gogh’s neuropsychiatric symptoms, most notably his episodes of seizures, began around the time of his move to the city of Arles in southern France. While the pathology of his seizures has been most famously described by Henri Gastaut (1) as a form of temporal lobe epilepsy, the cause of his disorder remains uncertain. While it is reasonable to point to his poor diet and excessive alcohol consumption as the primary factor for his symptoms, a look into Van Gogh’s substance abuse indicates the possibility of several other causes for his convulsions.

Absinthe

Dr. Hemphill (1961) was the first psychiatrist to link absinthe to Van Gogh’s illness (2). Absinthe is an alcoholic drink that became largely popular around the time of Van Gogh’s move to Paris. Traditionally, it comprises anise, fennel, wormwood and various herbs that undergo distillation. However, it is perhaps most popularly known for its supposed hallucinogenic properties, attributable to the chemical component Thujone. While the oil of wormwood is also known to have some convulsant properties (3), the majority of seizures that occur from consumption of absinthe are likely due to the toxic properties of Thujone. In the year 2000, it was revealed that Thujone possesses the ability to block the γ-aminobutyric acid type A (GABA A) receptor chloride channel (4). GABA works in the human body as a neurotransmitter that inhibits brain cell firing. Binding of GABA to its target receptor causes the influx of Chloride ions into cells, thereby producing inhibitory effects that most commonly cause sedation. Whereas anticonvulsant, sedative and anesthetic medication commonly stimulate the GABA receptor, Thujone antagonizes its effects, resulting in the increased excitation of brain cells that predisposes the body to seizures. Hemphill 1961 noted that, not only was Van Gogh’s consumption of absinthe excessive even by normal standards at the time, he was, in fact, more sensitive to its detrimental effects. To add further insult to injury, the continued use of absinthe during this time caused Van Gogh to develop pica. Pica, usually the consequence of a nutritional disorder, causes individuals to crave the consumption of items that are not considered a source of nutrition (e.g. stones, dirt, hair, paint, etc). The phenomenon usually occurs as a result of need-determined behavior secondary to malnutrition (5). Van Gogh’s pica involved a specific predilection toward consuming ‘turpene’ chemicals such as camphor and turpentine oils.
Camphor

Wilfred Niels Arnold, a biochemist who analyzed the mental health and lifestyle of Vincent Van Gogh (6), connected several of Van Gogh’s odd habits to substance use. While he was hospitalized for having cut off his ear in 1888, the artist suffered from insomnia. In an effort to ameliorate his symptoms, reports suggest that he frequently placed camphor under his pillow to help him fall asleep. In addition to this, as described above, he also routinely ingested the substance as a consequence of his pica disorder. Although originally extracted from the barks of the Cinnamomum camphora tree, camphor is now produced only synthetically from components in turpentine and is found in non-prescription products such as lip balms, skin coolers (Vicks VapoRub) and various creams for muscle aches. During Van Gogh’s time, the substance was likely procured in an oil-based form that he both ingested and used topically. The mechanism of toxicity of camphor is unknown, but it has been associated with depression of the Central Nervous System, producing signs and symptoms such as confusion, hyperreflexia, headache, agitation and seizure. (7)
Turpentine

With his increasing psychosis and advanced disease, Van Gogh’s odd consumption habits eventually extended to turpentine oils in the year 1889. Primarily attributed to his pica, Van Gogh was noted to drink the essence of turpentine as well as chew on his oil colors. Turpentine oils, produced by distilling the resin obtained from trees (mainly pine trees), are comprised of chemicals known as turpenes, most notably pinene. Inhalation of large quantities or ingestion of the compound has been shown to produce convulsions, gastric irritation, dizziness, agitation, cyanosis, coma and even death in patients. (8)

Vision Changes

Speculation exists surrounding the influence of drugs on Van Gogh’s vision. Though most authors now believe this to be a mostly unfounded connection, the predominant use of yellow (Figure 1) coupled with halo-like patterns (Figure 2) observed in some of Van Gogh’s later works have often been attributed to toxicity from digitalis.

While researchers believe there to be very little evidence of digitalis use in Van Gogh’s life, the association, at the very least, provides a useful mnemonic for medical students to familiarize themselves with the vision changes related to digitalis toxicity.

Digitalis

Digitalis is a cardiac glycoside that primarily acts on the cardiac myocyte by inhibiting the Na+/K+ ATPase pump (outlined in Figure 3). Under normal conditions, this pump acts to exchange intracellular Na+ for K+. Therefore, blocking its activity results in an accumulation of intracellular Na+, which then allows the adjacent Na+/Ca2+ exchange channel to use the excess intracellular Na+ to bring in more Ca2+, resulting in a net increase in intracellular Ca2+ which acts as an inotrope for the cardiac cells.

Digitalis is said to purport its effects on vision through a similar mechanism. In this case, acting on Na+/K+ ATPase channels in the retina results in changes to the arrangement of rods and cones, thereby propagating the symptoms of ‘Xanthopsia’- a term used to describe a distortion in color perception with a tendency toward visualizing colored halos.

The presumption that Van Gogh was exposed to digitalis arose from the fact that, during those times, digitalis (extracted from the plant species, known commonly as the foxglove) may have been used to treat epilepsy. In fact, a plant resembling the foxglove was noted in Van Gogh’s portrait of his psychiatrist (Figure 4).

Worsening Mental State

Finally, great debate exists surrounding the cause for Van Gogh’s worsening mental state during the last years of his life. While everything from malnutrition to Acute Intermittent Porphyria has been implicated in the development of his cognitive decline, an interesting toxicological cause that may have been, at least in part, a culprit for his condition is lead poisoning.

Lead Poisoning

The prevalence of lead-based paints in those times, coupled with Van Gogh’s peculiar consumption of oils and paint (pica), suggests both inhalation and ingestion as possible routes of lead exposure for Van Gogh. While exposure does not necessarily confirm poisoning in this case, some of Van Gogh’s evident neuropsychiatric decline does match the psychotic features associated with lead poisoning (also referred to as ‘Saturnism’). An outline of common manifestations of lead poisoning is mapped below (Figure 5)

Conclusion

Since most of the information obtained on Van Gogh’s illness is extracted from unreliable accounts and excerpts of letters he wrote toward the end of his life, any causal association, toxicological or otherwise, would ultimately be pure conjecture. At the very least, however, the relations outlined above provide an educational insight into the possibilities and mechanisms by which the substances prevalent in Van Gogh’s lifestyle could, in part, be contributory to his tendencies and even his psychiatric disease.

References and Further Reading

Gastaut H: La maladie de Vincent van Gogh envisagée a la lumière des conceptions nouvelles sur l épilepsie psychomotrice. Ann Méd Psychol (Paris) 1956; 114:196–238
Hemphill RE (1961): The illness of Vincent van Gogh. Proc Roy Soc Med 54: 1083–1088
Simonetti G. Simon & Schuster’s Guide to Herbs and Spices. New York: Simon & Schuster; 1990. pp. 261–262
Hold K M, Sirisoma S I, Ikeda T, Narahashi T, Casida J E. Proc Natl Acad Sci USA. Alpha-thujone (the active component of absinthe): gamma-aminobutyric acid type A receptor modulation and metabolic detoxification. 2000;97:3826–3831
Richter CP. Self-selection of diets. Essays in Biology. Berkeley, CA: University of California Press; 1943
Vincent van Gogh: chemicals, crises, and creativity, Author: Wilfred Niels Arnold, Published by Birkhäuser, 1992
Phelan WJ, 3rd. Camphor poisoning: over-the-counter dangers. Pediatrics 1976; 57:428–431, Klingensmith WR. Poisoning by camphor. J Am Med Assoc 1934; 102:2182–2183
Pande TK, Pani S, Hiran S, Rao VVB, Shah H, Vishwanathan KA (1994) Turpentine poisoning: a case report. Forensic Sci Int 65: 47–49

Cite this article as: Mohammad Anzal Rehman, UAE, "Learning from The Past," in International Emergency Medicine Education Project, August 7, 2019, https://iem-student.org/2019/08/07/learning-from-the-past/, date accessed: December 2, 2023