Thursday, May 28, 2015

The Illness of Vincent Van Gogh. Porphyria? From the Wilfred Niels Arnold Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, KA, USA

This Is Lengthy but a well read and documented case.  
A must read!

The Illness of Vincent van Gogh
Wilfred Niels Arnold
Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, KA, USA
ABSTRACT
Vincent van Gogh (1853–1890) was a wonderfully accomplished artist whose work is now widely
appreciated. He created a great number of masterpiece paintings and drawings in just one decade devoted to art. His productivity is even more remarkable when considered in the context of his debilitating illness. He
suffered from medical crises that were devastating, but in the intervening periods he was both lucid and creative. He left a profound, soul-searching description of his jagged life in his correspondence, which provides the basis for the present analysis. An inherited metabolic disease, acute intermittent porphyria, accounts for all of the signs and symptoms of van Gogh’s underlying illness. On this 150th anniversary of the birth of Vincent van Gogh it is appropriate to revisit the subject and to analyze the lack of organized skepticism in the popular media about other diagnoses.

Vincent van Gogh was born in the presbytery of
the Dutch Reformed Church of Zundert, in the
southern region of The Netherlands, at 11:00 am
on March 30, 1853. The obstetrician did not have
far to run – the office of Dr. Cornelis van
Ginneken was right next door. There were no
problems on that day. They would tumble out
later. An eventful life was underway and it would
last just thirty-seven years and four months.
Today, van Gogh is on everybody’s list of
outstanding artists and in every catalog of creative
people. He continues to find an appreciative
audience of young and old, novice to connoisseur,
all untrammeled by differences in cultural
background or artistic education. It was not
always so, at the time of his suicide in 1890
the accomplishments of Vincent were acknowledged
by only a small cadre of friends and
followers. No more than a handful of critics
had put pen to paper. Formal recognition during
his life was restricted to exchanges of paintings
with other artists, gifts to friends and doctors,
acceptance of canvases toward financial obligations,
three sets of commissions, a drawing sold
in The Hague, a few items sold in Paris, a selfportrait
sold to a London dealer in 1888, and
one sale from an influential Les Vingt exhibition
(1890) in Brussels.1 He died still writing of
hopes for future recognition, but indeed it was
a deep disappointment for an artist who had
been confident enough to follow the precedents
of Michelangelo Buonarroti, Raphael Santi, and
Journal of the History of the Neurosciences
2004, Vol. 13, No. 1, pp. 22–43
Address correspondence to:Wilfred Niels Arnold, Department of Biochemistry and Molecular Biology, University
of Kansas Medical Center, Kansas City, KA 66160-7421, USA. Tel.: þ1-913-588-7056. Fax: þ1-913-588-7440.
E-mail: warnold@kumc.edu
1The sale of van Gogh’s artwork during his lifetime was obviously meager, but this list should replace the popular
misunderstanding that Vincent ‘‘sold only one painting.’’
10.1080/09647040490885475$16.00 # Taylor & Francis Ltd.
Rembrandt van Rijn by using his first name
alone for professional purposes.2
Posthumous praise for his creations roused
attention but surely it has been the complementary
interest in extraordinary aspects of the person,
especially his underlying illness, that has
made Vincent van Gogh a household name. His
jagged life was marked by early years of uncertainty,
interludes of luckless love affairs,
wrenching episodes of self-mutilation, and crises
of debilitating illness. Creative people who have
shaken the world a bit are generally surrounded
by popular contemplations about their physical
and mental health. And in the visual arts the
individual who makes the advance is all too often
suspected of some individual abnormality, as if
there were a need to invent an exotic explanation
for the novelty. But in the case of van Gogh there
were certainly enough unusual episodes to raise
the question of mental derangement even during
his lifetime. Given the extraordinary influence of
the man on succeeding generations there are
ample justifications for serious studies on whether
medical problems affected his life or his artwork.3
THE PROBLEM
Superficial interest and comment on van Gogh’s
illness grew with every exhibition of his work. It
became an industry with its own history. As a
result, the typical newspaper article or exhibition
essay declared that there were one hundred and
one diagnoses on van Gogh’s illness!4 Six or
seven examples were proffered, all embraced with
equal weight by the reporter and without the
benefit of a word of evaluation. Hopes of finding
a better perspective in journal articles and books
have not always been filled because the majority
of the authors promoted pet ideas with selective
inclusion of what they believed to be supporting
data. I believe, axiomatically, that any reasonable
working hypothesismust address all of the medical
information; this includes family history and the
artist’s lifestyle, as well as the underlying illness.
The interaction between congenital disease and
exacerbation factors is central to our argument.
After Dr. Loretta Loftus and I published our
working hypothesis of acute intermittent porphyria
for Vincent and discussed the differential
diagnosis (Loftus & Arnold, 1991) we were
surprised to find that some critics, who did not
offer any assessment of the facts we presented,
were quick to respond with undocumented personal
preferences in newspaper stories or letters-tothe-
editor. Their epistles promoted alternatives
that they claimed were ‘‘more easily understood’’
or ‘‘more common disease entities,’’ as if poor
Vincent should become a poster-boy for the disease
currently in vogue for creative people. Some
made passing comparisons with other famous
persons but usually without data on any of them.
In some quarters the same weight was given to an
opinion as to a well-referenced analysis.
A large section of my subsequent book (Arnold,
1992) was devoted to van Gogh’s underlying illness.
Therein I produced tables of Vincent’s own
references (from his letters) organized by particular
medical signs and symptoms, thus offering
future scholars the benefit and convenience of a
concordance. In the chapter ‘‘Other Hypotheses’’ I
started with the assumption that all the authors
were sincere but found that only a few advanced
the field. It was also apparent tome that so many of
those suggestions were loosely conceived and
poorly documented, but they landed in the literature
and in some cases had been widely quoted and
requoted (errors to the third degree) without benefit
of common sense. A blatant example is the silly
claim of digitalis poisoning as a cause of van
Gogh’s underlying illness.
Art historians and others were quick to remark
upon van Gogh’s occasional ‘‘high yellow’’ palette.
This was hardly a revelation because the
artist himself had written about his exaggerated
use of yellow pigments and had coined the phrase.
Vincent’s fondness for yellow can be gauged from
his letters in the 1887–1890 period wherein he
mentions the yellow of his surroundings more
2The paintings he signed (a small fraction of the total)
were simply inscribed Vincent. I will use Vincent, van
Gogh, and Vincent van Gogh interchangeably.
3Some commentators, mostly from the art history
ranks, have denied the necessity to explore these
questions. The possible reasons are analyzed later.
4I have encountered no more than a dozen serious
proposals, but within each category there have been
numerous renditions and rediscoveries.
THE ILLNESS OF VINCENT VAN GOGH 23
than any other color (Arnold, 1992). But Lee
(1981) was bold enough to propose that van Gogh
suffered from a xanthopsia, wherein the patient
has a reversible view of the world as if through a
yellow filter, and that Vincent had been overexposed
to digitalis, as a decoction of the foxglove
plant. There is no doubt that too much
digitalis will have this effect; the observation
dates from the original dissertation (Withering,
1785); but there is no evidence that van Gogh ever
took the drug, and artistic preference is still the
best working hypothesis for the high yellow
canvases (Arnold & Loftus, 1991). Also, and
more important in the present context, it is absurd
to include digitalis poisoning in lists of possibilities
to explain all his neurologic and psychotic
problems that culminated in suicide.
The goal of the present review is fourfold: to
evaluate our current understanding of van Gogh’s
illness; to analyze some of the cultural and social
aspects that impinge on (and interfere with) this
field of van Gogh scholarship; to recommend a
higher level of organized skepticism; and to
promote the operational concept that the canons
of proof associated with the hard sciences should
also be applied to biography.
THE IMPORTANCE OF THE LETTERS
Theo van Gogh (1857–1891), who provided the
emotional and financial supports for his brother’s
final decade, had realized the value of Vincent’s
correspondence as a rich source of artistic and
human interest. But he died the next year after
Vincent’s suicide, and it took Theo’s widow,
Johanna van Gogh-Bonger (1862–1925), another
twenty-four years to decipher, translate, and
arrange the letters before the first reasonable
compilation appeared. In the preface, Johanna
gave an additional reason, ‘‘It would have been
an injustice to Vincent to create interest in his
personality ere the work to which he gave his life
was recognized and appreciated as it deserved.’’
(van Gogh-Bonger, 1978, xiii)
The decision by Johanna van Gogh-Bonger to
publish in English was based on her insightful
anticipation of a world-wide audience for both
Vincent the man and the huge amount of artwork
that she inherited. She was well versed in the
language and was also assisted in English phrasing
and idiom by Helen Apel Johnson (Johnson,
1934). For many years the only edition of the
letters that approached completeness was in
English, and that had a profound effect upon the
history of van Gogh scholarship.
Vincent’s namesake nephew, V.W. van
Gogh (1890–1978), identified as ‘‘Vincent the
Engineer,’’ followed his mother in the activities
of preserving the art work of his Uncle and organizing
the copious correspondence, for which he
anticipated the research potential by stating in his
introduction that, ‘‘the letters . . . are the only genuine
source of details on his [Vincent’s] life’’ (van
Gogh, 1978, xi). During our 1990 conversation, Dr.
Albert Lubin, professor of psychiatry and a van
Gogh commentator (Lubin, 1972), made a special
point about Vincent’s nephew being very much the
‘‘amateur psychologist’’ and a supporter of this
type of enquiry. Unfortunately, in my opinion,
Vincent the Engineer also endorsed some of the
more mystical interpretations of the artist’s life.5
The three volumes of letters, memoirs, and
editorial comments (van Gogh, 1978) are an
important social, medical, cultural, and literary
compilation. The descriptions of illness by the
patient himself are central to our subject.6 In this
review all references from The Complete Letters
5Dr. Humberto Nagera, another psychiatrist with direct
contact, recently spoke to me about the Engineer being
at odds with Paul-Louis Gachet (1873–1962), the son
of Dr. Paul-Ferdinand Gachet (1828–1909). The father
was Vincent’s last attending physician. Paul-Louis
was a seventeen-year-old eyewitness commentator on
Vincent’s final months in Auvers-sur-Oise, whereas the
Engineer had to rely on information that was at best
second-hand. One wonders whether the enmity of van
Gogh’s nephew for young Gachet encouraged a splinter
group that found fault with Dr. Gachet’s management of
Vincent’s case and later criticized the whole Gachet
family for exploitation of his art legacy. Their argument
remains unconvincing and flies in the face of the
generous donations (in 1949, 1951, and 1954) of van
Gogh paintings to the state by Paul-Louis Gachet and
his sister Marguerite (1869–1949).
6Most van Gogh commentators will not argue in public
about the necessity of reading The Complete Letters,
but it is no small undertaking (1,809 pages in all) and
one may wonder how many have.
24 WILFRED NIELS ARNOLD
will be noted, parenthetically, by letter numbers
as they appear in the English edition of 1978.
They overshadow the brief notes and register
entries (Tralbaut, 1981) that have survived attending
physicians in The Hague (unidentified
hospital-doctors), Eindhoven (Dr. Van der Loo),
Antwerp (Dr. Cavenaille), Paris (Drs. Rivet and
Gruby), Arles (Drs. Rey and Urpar), St. Re´my
(Dr. Peyron), and Auvers (Dr. Gachet). It seems
inconceivable that Dr. Paul Gachet (1828–1909)
kept no records, yet no journal or diary of patient
visitations has been forthcoming from his office in
the home at Auvers-sur-Oise.7 Biographical notes
on all of the above physicians, as well as the
influence of the home-remedies of Francois-
Vincent Raspail (1794–1878), have been published
(Arnold, 1992).
MEDICAL SUMMARY
Vincent’s ailment was characterized by episodes
of acute mental derangement and disability which
were separated by intervals of lucidity and creativity.
Moreover, attending physicians, family,
friends, and the artist himself were all surprised
and encouraged by the rapidity of the recoveries
after each crisis (van Gogh-Bonger, 1978). His
serious illness developed late in the third decade,
as evidenced by his concern with ‘‘the possibility
that [my] family might take steps to deprive me of
the management of my affairs and put me under
guardianship’’ (letter 204). There was a family
history of mental illness (Lubin, 1972; Tralbaut,
1981; Arnold, 1992). His underlying complaint
was characterized by frequent gastrointestinal
problems (letters 448, 530, B4, etc.), and at least
one bout of constipation that required medical
intervention (Tralbaut, 1981, pp. 177-8). The
condition caused fits with hallucinations, both
auditory and visual, (letters 592, W11, etc.) and
evoked partial seizures (Tralbaut, 1981, p. 276).
Periods of incapacitating depression and physical
discomfort were severe and grave enough to
provoke self-mutilation and eventual suicide
(van Gogh-Bonger, 1978). Some of his bouts of
sickness may have been associated with fever
(letter 206) and sexual impotence (letter 506).
His ailment was exacerbated by overwork (letter
173), malnutrition and fasting (letters 440, 571),
environmental exposure (letter B15), excessive
ingestion of alcoholic beverages (letter 581,
etc.), especially absinthe (letter A16), and a proclivity
for camphor and other terpenes (Arnold,
1988). The symptoms were palliated during institutionalization
with better diet, alcohol restriction
(letters 595, 599), and administration of bromide
therapy (letter 574). In spite of their severity he
did not experience any permanent, functional
disability after any attack (Lubin, 1972; Tralbaut,
1981; Arnold, 1992). The reader is referred to
Arnold (1992) for a much fuller treatment. In the
paragraphs that follow I shall emphasize and
explain specific aspects of van Gogh’s illness that
are central to our working hypothesis and also
dismissive of so many other hypotheses from the
past.
AGE OF ONSET
In 1882, Vincent entered the city hospital at
Brouwersgracht (a section of The Hague, in The
Netherlands) with a gonorrheal infection, for an
anticipated stay of no more than 14 days (letter
206). However, the hospital register (Tralbaut,
1981) indicated that Vincent was admitted June
7 and was not discharged until July 1 (a total of 25
days). To the surprise of his doctors, things took a
turn for the worse after about 14 days, and
Vincent complained by letter on June 22, of a
‘‘dreadful weakness’’ and wondered ‘‘if there had
been some complication that would make things
worse’’ (letter 208). He was moved to a new ward.
The symptoms were only briefly described by
Vincent but it extended his stay in the hospital
for another 11 days. Was it a complication or a
paroxysm?
7Son and daughter maintained the residence after the
doctor’s death in 1909, and they were renowned for the
care with which they preserved their father’s medical
instruments and memorabilia. They had no children and
were survived by distant relatives. Rumor has it that
somewhere along the way all of Dr. Gachet’s records
were intentionally destroyed ‘‘to protect the privacy of
his patients.’’ His views survive only in the form of
interesting anecdotes, and indirect reports with poor
documentation of time or place.
THE ILLNESS OF VINCENT VAN GOGH 25
There was a bizarre supplement. Van Gogh
claimed that the attending physicians were willing
to attest to his sanity (letter 206) if it were
challenged again by his father. This statement is
startling at first encounter but information taken
from other letters indicates that his father had
considered having him committed to an asylum in
1880 and again in 1881 (Arnold, 1992; letter 204;
and letter 158 as amended by Hulsker, 1990). The
hospitalization in The Hague took place when van
Gogh was 29 years old. First indications of
neuroses and psychoses occurred at age 27
(according to his father’s assessment). First
expression of serious mental problems thus
occurred late in the third decade of Vincent’s life.
SIX MAJOR CRISES
The last two years of van Gogh’s life included six
well-documented medical crises with serious
mental problems. The period under discussion,
October 1888 to July 1890, is shown in Figure 1,
which depicts calendar months (center line),
sequential locations (bottom line), and the crises
(stippled rectangles above the time line). Van
Gogh’s suicide is marked with a Roman cross.
The utility and power of the graphical presentation
derive from the multiplicity of facts
depicted and, in addition, from the visual summary
(the Gesta¨lt). Thus we can see that the
durations of the crises are variable (days, weeks,
or months) and there is no discernible trend (the
succeeding crises neither shorten nor lengthen in
a regular manner). The five periods between
major attacks show neither consistency nor trend.
Their lengths were 38, 148, 116, 21, and 26 days.
The range is large; the mean happens to be 70
days (standard deviation¼58 days).
Vincent was a patient (voluntary inmate) at
Saint Paul de Mausole Asylum at St. Re´my for
just over a year (May 8, 1889 to May 16, 1890),
although the initial plan had been for only three
months. The attending physician, Dr. The´ophile
Peyron (1827–1895), made occasional, spare
notations in the register. Towards the end he wrote
that ‘‘the patient [van Gogh] . . . experienced during
his stay in this institution several [medical]
attacks with a duration of two weeks to a month.’’
In reality, during the St. Re´my period with Dr.
Peyron, the durations were 45, 7, 7, and 65 days in
chronological order. The discrepancy suggests
that Dr. Peyron was writing from memory, at
some distance from the events. Van Gogh himself
had not kept accurate records.
In letter 631 Vincent wrote to brother Theo,
‘‘I pointed out to [Dr. Peyron] that such
attacks . . . have always been followed by three
or four months [i.e. 90–120 days] of complete
quiet. I want to take advantage of this period to
move [from St. Re´my to Auvers]’’ The actual
numbers were 70 58 days (see above). His last
crisis at St. Re´my ended April 29, 1890. It is
remarkable that a safe period of three months
(Vincent’s intuitive but unsupported prediction)
would literally terminate on July 29, 1890! The
suicidal act (possibly inspired by an impending
crisis) was committed on July 27.
Each crisis had an abrupt onset and, at the end
of days or weeks, a swift resolution. In some cases
the artist even used words with the following
implications ‘‘one day fine – the next day, down
with sickness’’ and ‘‘yesterday I was too sick to
write – today I pick up the pen.’’ It is worth
Fig. 1. Time course of six major crises suffered by Vincent van Gogh. Details are given in the text.
26 WILFRED NIELS ARNOLD
recalling how desperate the early prognosis
about the December 1888 crisis had been. After
Augustine Roulin (1852–1930) visited the hospital
at Arles on the 27th, Vincent had increasing
neurologic problems. The following day her husband
Joseph Roulin (1841–1903) was unable to
see him because van Gogh was suffering from
aphasia. And then, on the last day of December, to
the pleasant surprise of doctors and friends, the
patient made a recovery so rapid and complete that
Rev. Salles could report that he found him ‘‘calm,
in a state which revealed nothing abnormal’’ (van
Gogh-Bonger, 1978, xlvi). By the first week of
January Vincent was moving around the hospital
and conversing freely with Roulin and others, and
even cautioning Theo not to alarm his mother and
sister Wil. unduly (letter 569). On January 7, he
returned to his home in Arles (made famous by his
painting ‘‘The Yellow House’’) and that day
declared to his mother and sister that ‘‘there is a
chance that there will be nothing the matter with
me for a long time to come’’ (letter 569a).
The periods between major attacks were
remarkably normal. The lucidity with which the
patient comprehended and wrote letters, discussed
his condition with physicians, weighed
the possibilities for the future, and maintained
the quality of his art work, are all evident. From
all indications (van Gogh, 1978; Tralbaut, 1981;
Pickvance, 1984, 1986; Arnold, 1992), Vincent
did not write letters and did not paint during
crises. Unfortunately, this did not prevent future
romantics (see for example Schnier, 1950;
Navratil, 1959) from seeing disease in his art
work!
Potential precipitants of eight crises are
summarized in Table 1; documentation will be
provided later.
The course of van Gogh’s illness is very
instructive in approaching a retrospective diagnosis.
The features are a guide to a working
hypothesis that can then be either strengthened
or challenged by further data. Hence any reasonable
suggestion must first accommodate the
kinetics and time course of van Gogh’s illness,
and I would encourage organized skepticism in
examining how poorly the observed data fit with
ideas from the past. For example, we may ask
whether a proposed medical entity usually presents
with rapid (of the order of twenty-four
hours) onsets and resolutions, or does the patient
with the syndrome under discussion tend to drift
through days or weeks into a debilitating episode
and then later slowly emerge? Are the intervening
periods marked by complete lucidity and impressive
productivity or is there an indication of a
cumulative neurological deficit and a mounting
struggle to perform? Are the observed periods of
Table 1. Precipitating Factors According to Arnold (1992).
Date of crisis Location Precipitants
1880 The Borinage (Belgium) Fasting or general neglect of nutrition are
possibilitiesa
June 1882 The Hague (Holland) Gonorrheal infectionb
December 1888 Arles (France) Alcohol (especially absinthe)
February 1889 Arles (France) Camphor, fasting, alcohol (especially absinthe)
July–August 1889 St. Re´my (France) Alcohol (especially absinthe) consumed in Arles
during a social visit
December 1889 St. Re´my (France) Exposure to turpentinec
January 1890 St. Re´my (France) Alcohol (especially absinthe) consumed in Arles
during a social visit
February–April 1890 St. Re´my (France) Alcohol (especially absinthe) consumed in Arles
during a social visit. This crisis actually started
in Arles
Note. aPoorly documented, but related to the concerns of van Gogh’s father.
bWe refer to the ‘‘complication’’ that followed the primary infection.
cExpression of a pica (Arnold, 1988) for terpenes and terpenoid compounds: camphor, pinene (in turpentine),
thujone etc. from absinthe.
THE ILLNESS OF VINCENT VAN GOGH 27
pronounced illness for van Gogh compatible with
a candidate disease, or would one expect minutes
or hours – months or years? With any of these
other proposals, would attacks be precipitated by
seemingly unrelated factors such as fasting,
microbial infection or xenobiotics? All the while
we must bear in mind that Vincent’s organized
care during the medical crises of the last two years
was practically limited to bed rest, one prescribed
drug (potassium bromide), good nutrition, and
restriction of alcoholic beverages. During van
Gogh’s hospitalizations the attending doctors,
nuns, and other attendants were essentially
engaged in sympathetic nursing and patient-protection,
in response to observation and concern.
THE ROLE OF ABSINTHE
Artists painted and poets personified; men and
women embraced the ritual of presentation as
well as the appearance, taste, and excitement of
the liqueur called absinthe. Some of the most
creative people of the nineteenth century were
included. The aesthetics of absinthe drinking
contributed to its popularity. Nevertheless, one
looks beyond ethanol to the mood-altering chemicals
that were unique to this alcoholic beverage
in order to rationalize the volumes consumed in
some quarters (Arnold, 1989). There was a fifteen-
fold per capita increase in France from 1875
to 1913, when the national annual consumption
attained a massive 9.7 million U.S. gallons.
Whenever you have this many people imbibing
a particular beverage, there must be more to it
than poetry and attractive colors. In the department
of Bouches-du-Rhoˆne, which includes van
Gogh’s southern venues of Arles and St. Re´my,
the annual consumption was an impressive 2.45
liters per head, which was more than four times
the national average (Schmidt, 1915).
VINCENT VAN GOGH
AND THE INDIVIDUAL RESPONSE
Some years ago, while perusing the letters of
Vincent van Gogh, I was intrigued by the chemical
connection between absinthe constituents
(such as the toxic compound called thujone) and
some other terpenoid compounds in his life.
These exposures involved Vincent’s use of massive
amounts of camphor to combat insomnia, an
attempt to drink essence of turpentine (pinene),
and references to his nibbling at oil colors (mixed
with turpentine). The possibility of an interaction
became more compelling when I read Sollmann
(1948) on thujone and camphor, wherein he
remarked that the convulsions induced in experimental
animals are antagonized by bromide,
while the threshold is lowered by nicotine. While
institutionalized in Arles, van Gogh’s crises were
ameliorated by taking bromides and decreasing
smoking. Accordingly I suggested that van Gogh
had developed an affinity or a pica for terpenes,
the documented examples being thujone, camphor,
and pinene (Arnold, 1988).8 This would
help to explain some of the strangest of van
Gogh’s acts during his last two years – his
attempts to eat his paints and to drink turpentine
and kerosene – which were previously regarded
as absurdities and unrelated.
The response to any drug or xenobiotic
depends upon a variety of factors not least of
which the nutritional status of the subject. For
example, an increased toxicity of camphor and
related compounds is noted during fasting and is
attributed to a compromise in glucuronic acid
formation (Sollmann, 1948).9 Infections and unerlying
illness also play critical roles in determining
the individual’s response to drugs.
There are several indications in his letters and
in painted objects that Vincent developed an
‘‘affinity’’ for absinthe. He painted The Night
Cafe on the spot, staying up three nights in a
row and sleeping during the day (letter 533). It is
tempting to speculate that he had a glass or two
during the execution of this painting; he certainly
had access, and the landlord was apparently
pleased with the whole event. Apart from the
8Pica comes from the Latin for magpie, a bird who
carries away odd objects. In medical terminology it
refers to compulsive eating of non-nutritive substances
and has been ascribed to various disorders including
malnutrition.
9Camphor is secreted in the urine as hydroxycamphor
glucuronide.
28 WILFRED NIELS ARNOLD
possibility of this special case, we do not imply
that van Gogh painted while intoxicated.
There has been much discussion on the amount
of absinthe (and other alcoholic beverages) consumed
by Vincent in Paris, Arles, St. Re´my, and
Auvers. At one extreme we have Jan Hulsker who
steadfastly maintained that ‘‘Vincent was not a
drinker’’ (Hulsker, 1990). In an earlier publication
(Arnold, 1988) I described a pastel by Toulouse-
Lautrec and mentioned that it depicts Vincent
‘‘partaking of a glass’’ of absinthe. Hulsker
(1990, pp. 401–404) objected to ‘‘partaking’’
and insisted on the static message that Vincent
only sits before the glass. That Toulouse-Lautrec
chose to depict Vincent with a glass of absinthe
suggests to me that it was a common enough
circumstance, and that Vincent drank absinthe.
We feel that van Gogh was not in the habit of
simply decorating his table ‘‘with a glass of
absinthe in front of him’’ as Hulsker would have
it (Hulsker, 1990, p. 322). That commentator
maintains the isolated position that there is no
evidence that van Gogh was fond of absinthe, and
he also denies all the statements and anecdotes
about his drinking problem. Alas, Hulsker defeats
his own hypothesis in several places, not least of
which when he suggests that Vincent’s lack of
recall of the ear-cutting episode was ‘‘because
drinking had caused him to black out’’ (Hulsker,
1990, p. 322).
At the other extreme we have those reporters
with a list who would include absinthe abuse as a
free-standing explanation for all of Vincent’s
problems. Other commentators, who had been
told that their initial hypotheses didn’t accommodate
all of van Gogh’s signs and symptoms,
subsequently invoked absinthe as a rider. I provided
a concordance on Vincent’s references to
alcohol, including letters in which he expressed
fear of becoming an alcoholic (Arnold, 1992,
p. 79).
Paul Gauguin (1848–1903) lived with van
Gogh during the two months running up to
Vincent’s first crisis in Arles. Anecdotes suggest
that Gauguin consumed at least as much absinthe
as van Gogh, but he did not exhibit the same
medical problems. If so many were drinking
absinthe, why did his neighbors (letter 579)
regard Vincent’s behavior as so bizarre? The
explanation that has escaped most reviewers is
that Vincent was abnormally sensitive to absinthe,
even in the amounts associated with social drinking,
because of his congenital illness. Absinthe is
but one factor in the ‘‘environmental’’ impact on
Vincent’s underlying illness; it also comes under
the category of ‘‘lifestyle.’’ Hemphill (1961)
deserves much credit for being the first to consider
absinthe as an external chemical influence
on van Gogh. Vincent himself seemed to be
approaching this idea when he wrote, ‘‘it seemed
to be caused more by some outside influence than
by something within myself’’ (letter 605). Loftus
and Arnold are convinced that it was the underlying
illness of acute intermittent porphyria
that made Vincent so sensitive to absinthe and
malnutrition.
ACUTE INTERMITTENT
PORPHYRIA (AIP)10
AIP is one member of a class of metabolic
abnormalities, the porphyrias, which are characterized
by the excessive production of porphyrins, or
related compounds (Waldenstro¨m, 1957; Kappas
et al., 1989). Individuals who suffer from these
diseases are prone to excrete elevated concentrations
of these same compounds in their urine and
feces. The abnormal excretion per se is of no
intrinsic medical import but it is a reflection of
elevated concentrations circulating within the
body, and therein lies the potential for cutaneous
photosensitivity (due to porphyrins), neurological
abnormalities (due to porphyrin precursors), or
both. In the case of AIP, all of the symptoms are
neurological and the specific, overly-produced
compounds are d-aminolevulinic acid and porphobilinogen.
These are intermediates in the metabolic
pathway to porphyrins, which in turn are used in
the biosynthesis of the heme of hemoglobin, and
other heme-containing proteins. ‘‘Acute’’ refers to
the rapid onset, and abrupt cessation, of expressed
symptoms. (The underlying cause of AIP is present
from birth, so in that sense it is chronic.)
10Please consult my book (Arnold, 1992) for a much
fuller discussion of acute intermittent porphyria. Only
the most salient primary references will be given here.
THE ILLNESS OF VINCENT VAN GOGH 29
‘‘Intermittent’’ refers to the periodicity, which is
typical, and emphasizes the distinct periods of
normalcy which intercede between the episodes
of illness.
Symptoms rarely occur before puberty; the
peak decade for onset of symptoms is from age
20 to 29 (somewhat later for males than females)
but the disease sometimes remains latent throughout
a lifetime (Waldenstro¨m, 1957). Tabulations
of the most common hallmarks emphasize
abdominal pain and other gastrointestinal complaints,
symptoms referable to the peripheral and
central nervous systems, and signs of autonomic
neuropathy including tachycardia and hypertension.
Porphyria-induced hypertension can cause
early-onset renal failure (Laiwah et al., 1983).
Bladder dysfunction may result in urinary retention
(Laiwah et al., 1983; Kappas et al., 1989).
Effects on optic nerves or the occipital lobes have
been documented for AIP cases (Ridley, 1969).
Sexual impotence (Kappas et al., 1989) has occasionally
been reported. Premonitory symptoms
include restlessness and irritability; attacks develop
rapidly; resolution may occur in days or sometimes
weeks, in an unpredictable fashion. Seizures do not
always attend severe crises, but when they domany
antiseizure drugs, with the notable exception of
bromides, may adversely affect the outcome
(Bonkovsky et al., 1980; Moore, 1980).
The unpredictable nature of the disease with
respect to both onset of crises and outcome makes
an acute attack of AIP particularly treacherous. It
can be one of the most terrifying experiences
imaginable. Patients can become almost completely
paralyzed in severe cases. They are unable to
breathe, swallow or communicate properly, yet
remain conscious for some time, all the while
suffering pain, being aware of their plight, and
wondering if it will ever end. The most common
cause of death from AIP is respiratory paralysis.
Most importantly, the expression of neurological
and other symptoms depends upon lifestyle
and exposure to precipitating factors. Early examples
of AIP were revealed as a response to new
drugs; initially the hypnotic Sulfonal (2,2-bis
(ethyl sulfonyl) propane), later barbiturates; and
subsequently many other drugs, alcohol, and
sundry organic compounds (Moore, 1980). Some
steroid metabolites precipitate attacks, and endogenous
changes may account for some crises at
puberty and the earlier onset with females. Other
exacerbating factors include infections and malnutrition
(Kappas et al., 1989). Low-carbohydrate
and low-protein diets are especially detrimental
(Welland et al., 1964) and fasting can precipitate
an attack of porphyria (Knudsen et al., 1967). A
study in Scotland indicated an association between
smoking (nicotine is metabolized via cytochrome
P450) and the induction of repeated attacks in
patients already diagnosed with AIP (Lip et al.,
1991). Even an excess of coffee may be a problem
because caffeine is also porphyrogenic (Moore,
1980).
VINCENT VAN GOGH AND AIP
All of the hallmarks of Vincent’s illness can be
accommodated within this overview of AIP. The
most important and well documented are the
gastrointestinal complaints, neurological disturbances,
age of onset, jagged time course, and the
exacerbations caused by inadequate nutrition and
absinthe abuse. Other aspects such as sore throats,
eye problems, fevers, a bout of aphasia in the
Arles hospital, and impotence, have other possible
causes but are all compatible with underlying
AIP. Van Gogh’s smoking habit may have contributed
to recurrent attacks. Vincent’s urinary
tract infection in The Hague may have precipitated
an AIP crisis leading to the ‘‘complication’’
and extended hospitalization at that time. It is also
possible that his urinary retention recorded at that
time was exacerbated by an AIP attack.
Arnold (1988) suggested that van Gogh’s fondness
for absinthe developed into a pica for terpenes,
the documented examples being thujone,
camphor, and pinene. It is worth noting that 1,8
cineole, a constituent of crude camphor and
wormwood oils, is a proven precipitating agent
for AIP (Bickers et al., 1975). Van Gogh used
reckless doses of camphor oil against insomnia
(letter 570) and absinthe contained a variety of
essential oils including wormwood. Bonkovsky
and Arnold have shown that camphor, thujone,
and pinene are porphyrogenic (Bonkovsky
et al., 1992). The combination of overexposure
to camphor, absinthe abuse, and fasting or
30 WILFRED NIELS ARNOLD
malnutrition would be injurious for anyone, but
devastating for someone with AIP.
Loftus and Arnold (1991) believe that all
recorded signs and symptoms of Vincent’s illness
can be accommodated by acute intermittent porphyria.
Arnold (1992) presented cases of AIP from
the 20th century that had analogies to the illnesses
of Vincent, Theo, and their sister Wil. (1862–
1941). It behooves proponents of other hypotheses
to provide similar case histories, complemented
with the diagnostic insights ofmodernmedicine, to
either support or damage their alternatives.
THE BIOCHEMICAL LESION IN AIP
Almost any cell in the human body can engage in
synthesis of heme because it is not only vital to
hemoglobin but also for the cytochromes involved
in so many aspects of metabolism. The biochemical
pathway to heme consists of eight enzymes
and an exquisite control mechanism. A partial
deficiency (about half of normal) of enzyme
(catalyst) number three (porphobilinogen deaminase)
in this sequence is the underlying cause for
the manifold derangements of the AIP patient
under crisis. The organ of primary concern for
this inherited disease is the liver, where two thirds
of the heme that is produced is incorporated into
the various types of cytochrome P450. An even
larger proportion attains during the induction of
P450’s, which attends the liver’s encounter with
xenobiotics. The AIP patient has a vulnerable
heme pathway. The neurological problems associated
with medical attacks are a consequence of
upsetment of the heme pathway and the toxic
accumulation of two intermediate compounds, daminolevulinc
acid (ALA) and porphobilinogen.
Because porphobilinogen deaminase is not ratelimiting
to the overall pathway, 50% of normal is
sufficient for unstressed AIP patients. This explains
the lack of symptoms for latent AIP patients and
the intervening periods of normalcy for patients
who have experienced periods of sickness. It is the
first enzyme in the pathway, ALA synthetase, that
is normally rate-limiting. Therein lies the major
control feature because heme (the end product of
the pathway) causes both a repression and an
inhibition of ALA synthetase. When the heme
concentration of liver cells is depleted, the effective
amount of ALA synthetase may be increased
over ten-fold. Under those circumstances the
‘‘partial road block’’ at enzyme number three for
AIP patients is felt, and toxic levels of the preceding
compounds are produced.
Ingested compounds that are metabolized via
cytochrome P450’s in the liver deplete the heme
pool and induce the synthesis of ALA synthetase.
These include alcohol, many drugs, and many
xenobiotics (Moore, 1980). The van Gogh terpenes
(camphor, thujone and pinene) can be added to that
growing list (Bonkovsky et al., 1992). On the
other hand, synthesis of ALA synthetase can be
decreased by high glucose intake, thus helping to
explain the ameliorating effect of a high carbohydrate
diet on AIP attacks and the adverse effect of
malnutrition or fasting (Kappas et al., 1989).
More extensive discussions of the heme pathway
are given elsewhere (Kappas et al., 1989;
Arnold, 1992) and further pursuit of the biochemistry
is not appropriate to this review. However, I
would like to offer an hydraulic model of the
control mechanism to assist the non-chemical
reader. The diagram on the left of Figure 2 represents
each intermediate compound (a,b,c . . . heme)
as a solution in a cylinder being acted upon by an
enzyme (exit tube) as it passes on to the next
vessel. The AIP patient has about half the normal
amount of the third enzyme (exit partly closed by
the bold arrow). But the overall flow is steady
thanks to regulation of the first enzyme (the float
mechanism senses the level of the heme pool). The
diagram on the right depicts the consequence of
depleting the heme pool (pulling the plug): the
activity of the first enzyme increases greatly
(increased drop-size in the model) and now the
partial block at the third enzyme (in the AIP
patient) comes into play. Compounds c and d
accumulate and will spill-out (X).
Only under a crisis does the AIP patient excrete
large amounts of d-aminolevulinic acid (compound
c) and porphobilinogen (compound d) in the urine.
Even then the freshly voided urine is of normal
color, but with time these compounds polymerize
to form porphobilin which imparts a brown or red
(the color of porphyry) pigmentation to aged
specimens. The final color is influenced by concentration,
pH, light, oxygen and temperature.
THE ILLNESS OF VINCENT VAN GOGH 31
The propitious availability of a porphyric urine
sample together with the low-tech ‘‘windowsill
test’’ can be very instructive in the diagnosis of AIP.
Urine which has aged internally due to bladder
dysfunction may already be discolored when
released with a catheter, although the color is
sometimes mistaken for urinary tract bleeding. In
contradistinction to the claim that ‘‘port wine
urine’’ is the faithful telltale sign of AIP, it is
worth emphasizing that many 20th century carriers
with documented medical attacks have never
remarked upon abnormally colored urine because
it was either not saved or not aged. Dark or red
urine is not mentioned in the published van Gogh
letters but this really does no damage to the AIP
hypothesis.11
Barker and Estes (1912) were the first to note
that AIP runs in families. The extensive studies of
Waldenstro¨m (1937) in Sweden firmly established
the inherited nature of the disease. The disease
follows an autosomal dominant pattern of inheritance;
if one parent is a carrier then on the average
50% of the children will bear the defective gene
(Kappas et al., 1989). However, the penetrance is
variable, so that in some families only a fraction
of the carriers actually express signs and symptoms
of the disease (Gates, 1946).
Vincent’s mother died at 88, having led a
seemingly healthy life. His father, the Reverend
Theodorus van Gogh, died at 63; his studies
for the church had been interrupted by serious
illness; he was judged not to have been in
very good health most of his life (Tralbaut,
1981). It is believed that he died from a stroke
and, because hypertension is present in over
half of AIP patients (Goldberg, 1985), this
underlying disease would be one of many possibilities
compatible with that cause of death. Of
Vincent’s parents the father may be the more
likely (obligate) carrier of AIP, but this is little
more than an educated guess. He led a careful
and balanced life in his ‘‘post in the wilderness’’
(Tralbaut, 1981) and may have avoided the
Fig. 2. An hydraulic model for the control mechanism in the heme pathway. Details are given in the text.
11Critics of the AIP hypothesis for Vincent have
occasionally pretended that this was a serious deficiency.
It is negative evidence at best but can be
rationalized. Vincent’s accommodations were often
primitive by today’s standards; for example, the
‘‘Yellow House’’ in Arles had no toilet and he used
the facilities at the hotel next door (letter 480). He
relieved himself in the field while painting. Moreover,
even if he encountered reddish urine he may well have
attributed it to blood, given his experiences with
catheters and bougies at The Hague (letter 209).
32 WILFRED NIELS ARNOLD
precipitating factors that affected three of his six
children.
There were numerous exchanges between the
brothers concerning their ‘‘nervous’’ problems. It
is not clear whether Theo’s serious illness at age
19 was related to the expression of AIP-like
symptoms, but certainly by December 1886 (age
29) according to his future brother-in-law,
Andries Bonger, he had ‘‘serious nervous complaints,
so bad that he could not move’’ (Hulsker,
1990, p. 455). Theo seems to have been in reasonable
health at the time of Vincent’s funeral. But
two months thereafter Theo suffered further leg
pains and also hallucinations (partly in response
to an unspecified medicament for his cough),
became very irritable and occasionally violent,
muttered with difficulty in mixed languages,
experienced urine retention, and was totally
unconscious with a barely detected pulse before
he died (aged 34) (Rewald, 1986, p. 69; Hulsker,
1990, p. 455). Leg pains, mental illness, and
paralysis would all support a diagnosis of AIP,
and the violent reaction to a new drug and renal
failure would be in accord with AIP (Arnold,
1992). On the other hand the reversibility of the
leg pains does not support the diagnosis of neurosyphilis
offered by Dr. Frederik van Eeden.12
Vincent’s youngest sister, Wil., spent the latter
half of her 79 years in an asylum for psychiatric
cases. She may also have suffered from AIP,
although the lack of further documentation makes
her case much more speculative. The youngest
brother, Cor, died at 33 in South Africa from an
accident while feverish; it may have been a
suicide. Again, the medical history is scant. His
other sisters, Elizabeth and Anna, lived 77 and 75
years respectively, without any indication of medical
crises (Arnold, 1992).
Loftus and Arnold (1991) and Arnold (1992)
discussed the differential diagnosis of Vincent van
Gogh in favor of acute intermittent porphyria. We
hoped that the facts would speak for themselves
and that informed readers would have no difficulty
in rejecting other hypotheses.13 In the decade
that followed there was no new hypothesis,
but we encountered ongoing competition from
several old ones, whose authors were occasionally
quite vocal via the popular media. It is beyond the
scope of this review to look back on more than a
selection of these.
VINCENT AND EPILEPSY?
Epilepsy is defined as a paroxysmal (sudden and
recurring) transient disturbance in brain function
that is manifested by episodic impairment or loss
of consciousness, abnormal motor phenomena,
psychic or sensory disturbances, or perturbation
of the autonomic nervous system. The derivation
of the word is Greek; it means seizure. Accordingly,
the term epileptic seizures is redundant, but
common parlance. Another basic term is convulsion,
which means a violent involuntary contraction,
or series of contractions, of the normally
voluntary muscles. Niedermeyer (1983) emphasized
that epilepsy is not a disease but rather an
abnormal reaction of the brain due to numerous
causes. Several diseases and conditions are complicated
by seizures and convulsions. They may
accompany withdrawal from alcohol or barbiturates
and attend uremia. Other acute illnesses
which present with seizures include hyponatremia,
thyrotoxicosis, the acute porphyrias, and
hypoglycemia. Lead and arsenic are the most
frequently encountered metallic intoxications
which cause convulsions.
Tonic-clonic convulsions were not described
by Vincent or his doctors, so grand mal seizures
have never received much diagnostic support.
Petit mal or absence seizures (a brief lapse in
12Theo died at Willem Arntsz Stichting, near Utrecht,
on January 25, 1891. The local diagnosis was
neurosyphilis. This item was discovered 100 years
later by Dr. A. Pietersma, Archief Dienst Gemeente,
Utrecht.
13‘‘Informed readers’’ turned out to be a bigger
assumption than anticipated. A fatuous example came
from an East-Coast psychiatrist who wondered if the
subsequent lack of reference to our work ‘‘is related to
it being published in The British Medical Journal, a
journal that is not widely read in the U.S. and your main
thesis being published in a monograph’’ (private
correspondence).
THE ILLNESS OF VINCENT VAN GOGH 33
consciousness usually no longer than twenty
seconds) are certainly not indicated. Thus the
classical sorts of epilepsy, which were well understood
in Vincent’s time, were hardly indicated.
For this reason I agree with Tralbaut (1981) that
Dr. Peyron’s unqualified diagnosis of ‘‘epilepsy’’
in the St. Re´my register was based upon the
patient’s preconceived, ill-informed view.14
If indeed Drs. Rey and Urpar (Arles), and
Peyron (St. Re´my) were convinced that Vincent
van Gogh had some sort of epilepsy, then why
wasn’t he treated for it?15 Admittedly the available
therapy was meager, but Vincent was not even
treated symptomatically at St. Re´my, and no advice
along those lines was passed on to Paris when
Vincent departed. Contrast Vincent’s casewith that
of Fyodor Dostoevsky (1821–1881) who wrote, on
June 17, 1863, ‘‘I go to Paris and Berlin . . . only for
consultation of specialists (Trousseau in Paris,
Romberg in Berlin) for my epilepsy’’ (Voskuil,
1983, p. 665). If they really thought he had epilepsy,
it is curious indeed that Vincent, a quarter of
a century later, was not referred to an epilepsy
specialist at Montpellier or Paris!
As early as the 1870’s, Hughlings Jackson had
described certain hallucinations with seizures that
he related to a pathologic condition of the temporal
lobe (Jackson, 1931). Later, so-called ‘‘psychomotor’’
seizures were well described (Gibbs
et al., 1937). In the 1950’s the anatomical adjective
‘‘temporal lobe’’ was again preferred, even
though some other parts of the brain were sometimes
involved (Penfield & Jasper, 1954). Today,
these are all lumped under complex partial seizures
(Gastaut, 1970). Dr. Edgar Leroy, who
worked at St. Re´my Asylum, albeit many years
after van Gogh’s sojourn, and Dr. Victor Doiteau
considered that Vincent was epileptic but found
no evidence of aura or frank convulsions and
suggested temporal lobe epilepsy (Doiteau &
Leroy, 1928). See also Vinchon (1960).
A diagnosis of temporal lobe epilepsy might
explain Vincent’s hallucinations, the episodic
nature of his illness, and the interictal periods of
normalcy. However, the usual duration of minutes
or hours that attends the various forms of complex
partial seizures does not fit the days and weeks of
Vincent’s crises. More importantly, epilepsy does
not accommodate the numerous gastrointestinal
complaints. Likewise, some of the factors which
exacerbated his illness such as malnutrition and
fasting are not noted for inducing temporal lobe
epilepsy.
Drug therapy in the 1880’s was limited, but
Vincent’s fits and confusion (letter W11) seem to
have been controlled in Arles by bromide (letter
574), which would be indicated for absinthe intoxication
or acute intermittent porphyria, but not for
temporal lobe epilepsy. Bromides are effective
against grand mal and simple partial seizures but
not for complex partial seizures (Hemphill, 1961;
Niedermeyer, 1983). Monroe (1978, 1992) noted
that the limbic system is exquisitely sensitive to
stress and external toxins including alcohol, and he
remarked on Vincent’s affinity for absinthe. This
was rediscovered by Blumer (2002), who was
adroit in avoiding all the data on van Gogh that
did not fit temporal lobe epilepsy.
MANIC-DEPRESSIVE ILLNESS
(BIPOLAR AFFECTIVE DISORDER)?
The assumption made by some commentators that
manic-depressive psychosis was unknown in
Vincent’s day is incorrect. Falret (1854) had
described so-called ‘‘circular’’ insanity in which
mania and melancholia alternated at regular intervals.
Note that the term melancholia was still
used, but the meaning was by then approaching
a modern definition of depression.16 The same 14Tralbaut felt that the doctors at Arles and St. Re´my
were sympathetic to van Gogh’s suffering but not
particularly interested in taking a complete medical
history. My impression is that they were completely
baffled by Vincent’s illness.
15Claims (Gastaut, 1956) that Felix Rey (a young intern
still in training) was ahead of his time, and that his
friend Aussoliel was a local expert on ‘‘masked
epilepsy,’’ are not convincing.
16The first good description of a relationship between
mania and melancholia came from the Englishman
ThomasWillis (1621–1675), who mentioned that ‘‘one
can change into the other . . . this cyclic disorder is like a
burning object, one that can produce smoke or flame’’
(Willis, 1672; Finger, 2000).
34 WILFRED NIELS ARNOLD
year, Baillarger (1854) also wrote about these two
states, and also included an intercalated period of
normalcy as an integral part of the syndrome. It
should be mentioned in passing that Dr. Paul
Gachet attended lectures by both Falret and
Baillarger.17 A protracted dispute over priority
ensued, although it would seem that Baillarger’s
‘‘double-form’’ disease was closer to our present
concept (Kra¨pelin, 1921) of manic-depressive
psychosis or bipolar disorder.
The French Academy of Medicine had major
meetings on the subject starting in 1880. How
well it was recognized, received, or dealt with in
Arles and St. Re´my in 1889 and 1890 is an open
question, especially as to the intent of Drs. Urpar
and Peyron when they used the term acute mania.
I am inclined to think that they were referring to
the December 1888 events in and around the earcutting
incident and Vincent’s first hospitalization,
and then the complaints of neighbors about
Vincent’s drinking sprees which led to his readmission
to the Arles hospital in 1889. If that is
true then it was ‘‘old fashioned’’ mania a la
Pinel.18 By 1900 mania had assumed its present
psychiatric meaning of a mood disorder characterized
by expansiveness, elation, agitation,
hyperexcitability, hyperactivity, and increased
speed of thought and speech (flight of ideas).
Up until the beginning of the 19th century, the
prime meaning of melancholia was intensity of
idea, the image of the mind being strongly fixed
on, and frequently returning to, a single set of
ideas, to an extent that was deemed unhealthy.
The connotation of sadness was not always present,
and many forms of behavior that have little
relationship (from our perspective) were included
in the general class of melancholia. Not surprisingly
there was even a ‘‘productive melancholia’’
that today might be more akin to intense, creative,
concentrated thinking directed at a particular
problem, while excluding all day-to-day distractions
(monomania). Thus melancholia moved
through monomania to depression and it is
difficult to gauge how far Dr. Peyron had
progressed.19
Perry was probably the first to discuss manicdepressive
psychosis as a diagnosis for Vincent
van Gogh; her expression was ‘‘cyclothymic personality
with episodes of depression and mania’’
(Perry, 1947, p. 171). In the opinion of Hemphill,
‘‘van Gogh was a manic-depressive who developed
confusional episodes and fits in the last two
years of his life due to the toxic action of thujone,
the active agent of absinthe’’ (Hemphill, 1961,
p. 1084). Hemphill’s contribution was twofold;
he was the first to correctly refer to Vincent’s
‘‘epilepsy’’ as a disorder rather than a disease, and
he stressed the evidence for a toxic psychosis. He
supposed that the gastrointestinal complaints
came from the absinthe abuse alone, whereas
Arnold and Loftus stress van Gogh’s sensitivity
to absinthe (and other xenobiotics) due to the
underlying disease of acute intermittent porphyria.
Other writers have marched Vincent down
the bipolar trail but have discovered nothing new
since Hemphill (1961).
Manic depressive illness is widely diagnosed
today and a significant part of the pharmaceutical
industry is devoted to discovering further chemical
assists for the sufferers. These patients are
rarely aware of their states and ordinarily do not
check themselves into hospitals. Their disorders
do not have acute onsets and offsets and the time
course of van Gogh’s illness certainly does not fit
that syndrome. However, it is common enough
for artists and museum patrons to know, or
think they know, something about the syndrome
and someone in their immediate circle who has
it. Proponents of this working hypothesis exploit
this statistical swell even though they should
be arguing about the illness of just a single
individual, Vincent van Gogh.
17The title of Dr. Gachet’s thesis was E ´ tude sur la
Me´lancolie (Gachet, 1858). The work was written in
1858, in the middle of this transition period in
terminology. His thesis was really a compendium of
principles for moral treatment of the insane, spiced with
a philosophical vitalism that he encountered at the
Montpellier Medical School (Fabbri, 1966).
18In Pinel’s book (1818), mania was a disorder of one or
more faculties with sad, gay, extravagant or raging
affect, but always included blind aggression.
19The´ophile Peyron (1827–1895) made his first medical
career in the navy and then settled in Marseille as
an oculist. His appointment as director at the asylum
of St. Re´my may have been a semi-retirement position,
as Vincent hinted (letter 593).
THE ILLNESS OF VINCENT VAN GOGH 35
A course of regular cycling between mania and
depression, which is popularly held, is rarely
observed (Sarwer-Foner, 1966). On the average
there are nine to ten depressive episodes for every
manic event. A histogram of overall frequency
versus age-of-onset for manic-depressive patients
[n¼898] peaked with the 15–19 year group, and
was closely followed by the 20–24 year group
(Goodwin & Jamison, 1990). Notwithstanding
considerable searching, biochemical and genetic
markers for bipolar affective disorder have yet to
be found.
It has been widely observed that many creative
people had illnesses that were serious, debilitating,
and sometimes limiting to their productivity.
The majority opinion is that these men and
women were successful in spite of illness, and
not because of it. It is also true that many creative
people enjoyed robust and healthy lives.20 During
the 18th and 19th centuries there lived an unfortunate
philosophy relating the fevers of tuberculosis
to activities on a higher plane. This romantic
notion has now fallen by the wayside, but during
the last twenty-five years manic depressive psychosis
has popped up and down as a fashionable
disease of association with creativity.
Andreasen (1987) evaluated 30 faculty members,
over a 15-year period, at an American
university workshop for creative writing. She
claimed that the writers had a substantially higher
rate of mental illness compared with 30 control
subjects matched on sociodemographic grounds.
A higher rate of affective disorders, especially
manic depressive psychosis, was reported for the
so-called creative group as well as their firstdegree
relatives. Jamison (1989) reported that
38% of a British group consisting of 39 writers
and 8 artists, which she deemed outstanding, had
sought treatment for some form of affective disorder,
especially manic depressive psychosis,
compared with lifetime prevalence rates in that
nation of about 6%. Her attempts to link hypomanic
episodes and seasonal mood swings with
productivity were unconvincing. Rothenberg
(1990) criticized both the Adreasen study and
the Jamison follow-up on the grounds that little
consideration was given to the subjects’ reasons
for participating in the studies, and the criteria for
judging them creative were left unexplained.
Furthermore, Andreason’s self-reliance on evaluation
of relative mental health was potentially
biased because the subjects and controls were
already known to her. And Jamison built her case
on the subjects’ own reports of seeking medical
treatment.
Goodwin and Jamison (1990) came up with a
list of people they judged to have been creative
together with an indication (opinion) that they
suffered from manic depressive illness. The cautious
message from all of this should be that such
a debilitating condition is still compatible with
creativity, but in some circles there has been an
inference of causality.21 For example, Jamison’s
book on manic depressive illness and the artistic
temperament (Jamison, 1993) certainly leaves the
reader with the indication that the creative are
more susceptible to manic depressive illness than
the normal run of people, and the impression that
a sort of Faustian bargain is at play.
SCHIZOPHRENIA?
Progressive changes in content and style have
been observed in the work of artists who are
deemed to have schizophrenia (Prinzhorn,
1972). The reverse – namely to see the psychosis
in unknown artists by looking at their work – is
obviously more difficult, but not sufficiently
daunting to inhibit the proponents of schizophrenia
for Vincent van Gogh. Such was the approach
of Jaspers (1922), who is still quoted under this
heading.
Vincent had hallucinations, and he also had at
least one episode of paranoia when he thought
that neighbors were trying to poison him in Arles,
but these are not specific for schizophrenia.
The progressive deterioration of the untreated 20There have been some futile attempts at constructing
ratios. My friend Don Goodwin accused them of
playing a ‘‘floating’’ game – as they found more
candidates to be healthy they would add others to the
numerator by sticking them with illness labels.
21There is also some overlap here with Dr. Gachet’s
thesis list of outstanding individuals who suffered from
melancholia (Gachet, 1858, pp. 9–22).
36 WILFRED NIELS ARNOLD
schizophrenic is lacking in van Gogh. Perry
remarked that ‘‘[Vincent] did notwithdraw from
the world; he was cast out because of his
behavior’’ (Perry, 1947, p. 162). The schizophrenic
has a decrease in affect whereas Vincent’s
letters and pictures were surcharged with emotion.
Hemphill (1961) saw no sign of schizophrenia
in the artist and emphasized that there was
never any fantasy formation, and that his letters
were lucid and logical. There is no case for
schizophrenia (Arnold, 1992).
NEUROSYPHILIS?
Syphilis can be acquired either congenitally or,
most often, by sexual contact with an infected
individual. The primary stage is remarkably free
of systemic signs, the patient is entirely well and
usually free of fever but, at about 1–12 weeks
after contact, 50% of females and 70% of males
develop a primary lesion (chancre) at the site of
infection by the spirochete Treponema pallidum.
In the secondary stage, at 2–12 weeks after the
primary stage, a skin rash appears. Constitutional
symptoms that may accompany secondary syphilis
include fever, weight loss, malaise, and anorexia.
There follows an asymptomatic latent stage
that may last decades. About 30% of untreated
patients go on to develop tertiary lesions, but
clinical disease occurs in only half of these cases;
this fraction is 15% overall. About 80% of the
tertiary lesions affect the cardiovascular system,
10% are chronic focal inflammations (gummas) in
the liver and other sites, and up to 10% involve the
central nervous system (neurosyphilis), i.e. 1.5%
overall (Robbins, 1957).
The major clinical categories of symptomatic
neurosyphilis are meningovascular and parenchymatous
syphilis. The latter includes tabes dorsalis,
characterized by degeneration of the posterior
columns of the spinal cord and posterior spinal
roots. The interval from infection to expression of
symptoms is about 27 years. Another form of
parenchymatous syphilis, general paresis of the
insane, is associated with direct invasion of
T. pallidum into the brain. For unknown reasons
the syndrome is more common in males. The
average interval from infection to onset of general
paresis is 20 years. The course of the untreated
disease is inexorably progressive (Goodman &
Karakuis, 1988).
Neither the gamut of his symptoms nor the
time course of his crises fits neurosyphilis.
Vincent was treated for gonorrhea in The Hague
in mid-1882 at age 29. He may have had a
recurrence in Antwerp in 1885-86, at age 32.
Even if he had contracted syphilis in The Hague,
the major crises in Arles (age 35) would have
been extraordinarily early for the onset of neurosyphilis,
and his lengthy remissions from illness
also negate the possibility. Mercury treatments
were used at Arles and St. Re´my for syphilis, but
Doiteau and Leroy (1928) found no indication
that Vincent received mercury.
LEAD POISONING
About one-third of patients with excessive exposure
to lead suffer colicky, abdominal pain.
Fatigue, joint pains, headache, and irritability
are also quite common. Impotence, constipation,
vomiting, diarrhea have all been observed to some
extent. Subtle effects on personality, memory, and
learning ability are frequently associated with
chronic lead poisoning. However, seizures and
confusional states are less common, especially in
adults (Dagg et al., 1965; Ellenhorn & Barceloux,
1988).
Lead may be the oldest recognized chemical
toxin; reports of occupational lead poisoning date
to ancient Greece, and toxic levels have been
found in Egyptian mummies. Artisans of leadglazed
pottery and stained glass were particularly
susceptible to intoxication until better conditions
were adopted in the workplace. The ingestion of
paints containing lead pigments has, even in
recent times, presented a serious health hazard
for children. Artists and craftsmen were exposed
in the past because of their habit of wetting
brushes orally and their accidental ingestion of
lead-containing pigments from their tools and
hands.
Lead has an affinity for functional sulfhydryl
groups in enzymes generally and a particularly
sensitive example is d-aminolevulinic acid dehydratase.
This is enzyme number two in the heme
THE ILLNESS OF VINCENT VAN GOGH 37
biosynthetic pathway and its inhibition accounts
for excessive excretion of d-aminolevulinic acid
in the urine of lead-intoxicated patients. The last
enzyme in the pathway, ferrochelatase, which
catalyzes the incorporation of iron into protoporphyrin
to form heme, is also inhibited by lead and
this also contributes to the observed anemia
(Ettenhorn & Barceloux, 1988). The excessive
production of d-aminolevulinic acid in lead poisoning
is similar to that found in acute intermittent
porphyria, but note that porphobilinogen does
not accumulate in lead poisoning. The similarity
in neurological symptoms between AIP and lead
poisoning may be referable to d-aminolevulinic
acid.
Abdominal pain, constipation, vomiting, paralysis,
or paresis are very common in both AIP and
lead poisoning. Neuropsychiatric symptoms are
sometimes observed with lead intoxication, but
much less frequently than in acute intermittent
porphyria (Sassa, 1978). There was no chelation
therapy for lead poisoning in Vincent’s time, and if
his ingestion of lead salts (from his pigments) had
been chronic, then the time course of such an illness
would have been relentless and not episodic, as is
well documented for van Gogh.
ALCOHOLISM
The extent of Vincent’s drinking is difficult to
define, but we do know that he admitted to
excesses. It is assumed that the hospital in Arles
and the asylum at St. Re´my endeavored to restrict
alcohol consumption; how successful they were is
open to question; we do know that Theo paid a
little extra at St. Re´my so that his brother could
have wine with meals. I am convinced that Vincent
engaged in ‘‘social’’ drinking when he visited
friends in Arles, but this was for a relatively short
time of a day or so. The time course of his illness,
and the duration of some of the crises in the
asylum, do not fit alcohol withdrawal syndrome
per se.22 I believe it was more of a sensitivity to
alcoholic beverages than an extraordinary dose.
Alcohol is a an exacerbating factor for acute
intermittent porphyria. Alcoholism and lead poisoning
are reasonable suggestions but not standalone
syndromes for van Gogh – it is even less
likely that the medical problems of Theo and
sister Wil. would find much accommodation here.
ME´NIE`RE’S DISEASE
In 1861, Prosper Me´nie`re published several
papers relating his observations on afflictions of
the inner ear which caused nausea, vomiting, and
vertigo. The disease was subsequently named
after him and is characterized by hearing loss,
vertigo, and tinnitus (ringing in the ears), and is
usually unilateral (Harker & McCabe, 1980).
During an attack of vertigo the patient is completely
oriented to his surroundings and has no
neurologic deficit such as paresthesia, diplopia,
loss of consciousness, weakness, or paralysis.
Sounds are distorted in the affected ear and are
perceived as ‘‘tinny.’’ Loud sounds are intolerable
or even painful, and hearing acuity gradually
declines.
Yasuda (1979) wondered in print, ‘‘Was van
Gogh suffering from Me´nie`re’s disease?’’ The
twelve page article was published in Japanese,
but contains a full two pages of introduction and
summary in English, more than enough to grasp
the author’s thrust. Those speculations received
little support twenty years ago, because the diagnosis
of Me´nie`re’s disease was based on a limited
selection of symptoms. This dubious diagnosis
was a sincere attempt, but it received little attention
subsequently, except to be recorded in the
most comprehensive bibliographies.
The Journal of the American Medical Association,
during the week of the centenary of Vincent
van Gogh’s death, declared that, ‘‘Van Gogh had
Me´nie`re’s disease and not epilepsy’’ (Arenberg
et al., 1990). It was wrong on both counts; there is
no case for Me´nie`re’s disease and epilepsy was no
longer even the diagnosis of merit. A Colorado
ear specialist and his colleagues had rediscovered
Yasuda’s hypothesis and rewrote it as a definitive
diagnosis. Their conclusion was based on a limited
selection of symptoms, the pretense that
22Alcoholic seizures (rum fits) and delirium tremens
occur after a heavy drinking bout. It is the signs that
attend withdrawal that have some overlap with
Vincent’s illness.
38 WILFRED NIELS ARNOLD
epilepsy was the only viable alternative, and their
propensity for construing certain complaints as
hallmarks of the ear disease. Thus van Gogh’s
gastrointestinal problems were taken to be strictly
nausea and vomiting, several references to hearing
voices were relegated to tinnitus, and the
psychosis that was grave enough to cause selfmutilation
and eventual suicide was underplayed.
Their claim that van Gogh severed the lower half
of his left ear to relieve tinnitus must surely strike
readers, if not the editors of JAMA, as misplaced
surgery.23
TOKENS
There are many other working hypotheses by
authors who are distinguished more by their
conviction than common sense. Call-in talk shows
on the radio are frequently their birthplace.
Shortly after the publication of my book I encountered
‘‘borderline personality disorder’’ for van
Gogh, which may be the exemplar for this type of
offering. I thought that the title was enough to
give the concept away but, to my astonishment,
literature searches now turn it up in the form of
published papers. The ‘‘replacement child’’ sentiment
is another one in the same vein.24 I would
continue to encourage organized skepticism as the
first test.
THE CHARM OF THE PAST
There is an informal group that is keen to applaud
the diagnostic skills of Vincent’s attending physicians.
‘‘The old guys had it right after all’’ is
their banner. In their sea of indecision (sincere or
deliberately compounded) this affords an island
of safe haven blessed with nostalgia.25
Some have said that Dr. Rey (Arles) was
brilliant and insightful. Their circular argument
goes as follows: Rey embraced ‘‘epilepsy’’ without
evidence of a full-fledged case; the commentators
believe temporal lobe epilepsy (described
many years later) is an attractive possibility;
therefore they say Rey was ahead of his time. I
join those who have judged Dr. Peyron as naive
and trained in the wrong specialty, yet others have
embraced as gospel his terse statements in the St.
Re´my register. Tralbaut (1981) felt that the physicians
of the south were overly influenced by the
police reports in Arles, and by the patient’s own
statements about a family history of epilepsy on
his mother’s side. If so, then the circle was indeed
completed when Vincent wrote to Theo, ‘‘as far as
I can make out, the doctor here [Dr. Peyron] is
inclined to consider what I have had [was] some
sort of epileptic attack’’ (letter 591).
Theo van Gogh died in a mental institution in
Den Dolder on January 25, 1891. Some of their
medical records were released to Dutch newspapers
in 1990, by a local archivist. The story,
which covered the 38 days from Theo’s move out
of Paris to Den Dolder until his death, ends
dramatically, ‘‘the final diagnosis was dementia
paralytica [general paresis, a form of neurosyphilis].’’
At last the answer was out! Perhaps
Vincent had the same thing?26
Dementia paralytica was described by Bayle,
as early as 1822. Quincke is credited with introducing
the lumbar puncture procedure together
23I have only one pleasant memory of this fiasco. While
in Brisbane, Australia, as a guest for their van Gogh art
exhibition in 1994, I was taken by a friend I have known
since primary school to a beer garden. There he insisted
on introducing me to everybody, eventually including a
fellow in short pants and a singlet who was bouncing
from table to table selling lottery tickets. ‘‘Dr. Arnold is
here for the big van Gogh affair, he is going to lecture
tomorrow on van Gogh’s illness.’’ We were both
surprised by the smile of hidden wisdom and, ‘‘I know
mate, it’s Me´nie`re’s disease, my uncle had it.’’ Alas, the
misplaced power of immediate experience – others
have seen this in connection with manic depressive
illness.
24The facts do not support the thesis (Arnold, 1995).
However, it is even more bizarre to read that this sort of
thing has been projected in some quarters as the crux of
van Gogh’s underlying illness.
25In another setting the same group would supposedly be
happy enough to acknowledge the laboratory developments
that have advanced 20th century medicine.
26For reasons that still escape me the art politicians of
Holland act as if the label of syphilis for the van Gogh
brothers carries less social stigma than say alcoholism,
let alone an inherited metabolic disease. Is this a
misplaced attempt to ‘‘protect’’ the van Gogh family?
THE ILLNESS OF VINCENT VAN GOGH 39
with examination of the cerebral spinal fluid for
spirochetes, in 1892. Today, a definitive diagnosis
would be based on serology of the cerebral spinal
fluid, but this technology was not available until
well into the twentieth century. General paresis
was overly diagnosed in the nineteenth century.
The psychiatric and neurological symptoms
recorded from Theo’s case are far from definitive.
An autopsy examination could have provided
confirming evidence but apparently was not performed.
In any event, the time course of Theo’s
illness makes the case for neurosyphilis highly
unlikely (Arnold, 1992).
Dr. Paul Gachet also inherited his share of
golden admiration. His ideas about Vincent’s
illness are supposed to have included ‘‘turpentine
poisoning and the effects of too intense sun
on a Nordic brain’’ (Beer, 1935, p. 40). I have
not been able to confirm the attribution to Dr.
Gachet but I assume some verbal anecdote that
slipped into the van Gogh literature. Vincent
himself remarked upon being ‘‘dazed with the
sun’’ (letter 512) that ‘‘beats down on one’s
head . . . [and] makes one crazy’’ (letter B15).
Vincent may have been a bit reckless in his
exposure but there was certainly more to his
illness than heatstroke. The time course and the
rest of the symptomatology cannot be accommodated
under this heading.27
Rey, Peyron, and Gachet did their best to
protect and rehabilitate the artist during those
demanding two years. My observations within
this section are not intended to disparage the
van Gogh physicians but rather to make an appeal
for placing their relative merits in perspective.
They had the advantage of being there, but they
were without benefit of the biochemical tools that
we now take for granted.
RESISTANCE FROM ART
HISTORIANS, CURATORS, DEALERS,
AND THE STATE MUSEUMS
The art world harbors some people who deny any
interest in van Gogh’s underlying illness. This position,
albeit at odds with the public, takes various
forms.Thus a catalog essaymay either skip over the
subject or be content with ‘‘he died by his own hand
in 1890.’’ During themonths of one blockbuster exhibition
the museum’s education department managed
to dodge a public lecture onVincent’smedical
problems in favor of one recounting the provenance
on the painting that fetched the best price at auction.
Moreover, the vehemence with which so many
art curators and dealers resist scientific enquiry
suggests an unwholesome desire to maintain the
mystique in order to protect the art.28 They do an
injustice by assuming that the ‘‘consumer’’ of art
needs ‘‘protection.’’ On the contrary, I believe that
an explanation of Vincent’s underlying illness and
the role of the environmentwill enhance rather than
diminish genuine interest in van Gogh’s creations.
The commercial interests of dealers and the
ambitions of museums with regard to van Gogh
foster the titillating connection between creativity
and madness. Even if they are privately persuaded
otherwise, they are reluctant to change something
that they think is ‘‘working.’’ Newspaper and television
journalists are reluctant to engage them on
that turf and surely that is part of the reason for
perpetuating the lengthy lists of possible van Gogh
illnesses. They want to keep the subject vague in
order to maintain the mythology.
CONCLUDING REMARKS
The house of Dr. Paul Gachet in Auvers-sur-Oise
was recently opened to the public to coincide with
27I do not mean to defeat the message of this section but
consider the following from an AIP expert, ‘‘exposure
to oil-based paints and solvents will, in some
porphyrics, produce symptomatology including psychosis,
colic, seizures, and neuropathy. Very rarely in
acute porphyria, extreme exposure to sunlight may
provoke an attack’’ (Peters, 1986). Bonkovsky and I
showed that pinene (turpentine) is porphyrogenic – but
sunlight! Was the good Doctor Gachet blessed?
28A curator at the Boston Museum of Fine arts once told
me that he could not understand why anyone was
interested in van Gogh’s illness. I ventured that at least it
had something to do with his premature demise. No
response, so I volunteered that Picasso and Matisse could
have been contemporaries with Vincent if he had enjoyed
a predicted lifespan of about 66 years – how wonderful it
would have been to have those three guys in the same
room? ‘‘Van Gogh painted lots of pictures anyway.’’
40 WILFRED NIELS ARNOLD
the 150th anniversary of the birth of his most
famous patient. Willem van Gogh, a greatgrandnephew
of Vincent van Gogh, was in the crowd
and he said he was touched to be present (New
York Times, April 1, 2003). For those of us
interested in round numbers it is also a propitious
time to review the medical problems of the artist.
A careful review of data from the artist’s letters
and other contemporary sources indicates that
Vincent suffered from an inherited disorder manifested
by severe and manifold neurological problems,
ranging from gastrointestinal pains to fits
with hallucinations. His condition was exacerbated
by his modus vivendi, which was marked by
inadequate nutrition, abuse of alcoholic beverages,
chronic smoking, environmental exposure, and the
development of an abnormal affinity (pica) for
terpenes. The intermittent nature of his illness,
the sudden onset of crises, and the rapid return to
normalcy after each episode, are all notable. The
gamut of symptoms is best explained by a toxic
psychosis. Within that category, the disease entity
which most closely fits all of the data is acute
intermittent porphyria [AIP], which was adopted
by Loftus and Arnold (1991) and Arnold (1992) as
a working hypothesis for Vincent’s underlying illness.
This retrospective diagnosis has been compared
and contrasted with other suggestions in the
literature. The first case was described in a Dutch
medical journal (Stokvis, 1889). AIP was not
understood in Vincent’s time; even today it tends
to be under-diagnosed. I am convinced that a toxic
psychosis such as acute intermittent porphyria
remains the best working hypothesis.
Vincent van Gogh was not a ‘‘mad’’ artist, but
rather an exceptional man who suffered from an
inherited disease. He was wonderfully creative
because of intelligence, talent, and hard work. He
was a genius in spite of his illness – not because of
it. This reality enhances wholesome admiration for
van Gogh’s creations.
REFERENCES
Andreasen NC (1987): Creativity and mental illness:
prevalence rates in writers and their first-degree
relatives. Amer J Psychiat 144: 1288–1292.
Andreasen NC, Glick ID (1988): Bipolar affective
disorder and creativity: implications and
clinical management. Comp Psychiat 29:
207–217.
Arenberg IK, Countryman LF, Bernstein LH,
Shambaugh GE (1990): Van Gogh had
Me´nie`re’s disease and not epilepsy. JAMA 264:
491–493.
Arnold WN (1988): Vincent van Gogh and the thujone
connection. JAMA 260: 3042–304.
Arnold WN (1989): Absinthe. Sci Am 260: 112–117.
Arnold WN (1992): Vincent van Gogh: Chemicals,
Crises, and Creativity. Boston, Basel & Berlin,
Birkha¨user.
ArnoldWN(1995): Vincent van Gogh’s birthday. Pharos
Alpha Omega Alpha Hon Med Soc 58: 28–32.
Arnold WN, Loftus LS (1991): Xanthopsia and van
Gogh’s yellow palette. Eye 5: 503–510.
Baillarger JGF (1854): De la folie a` double-forme. Ann
Med Psychol 6: 367–391.
Barker LF, Estes WL (1912): Family hematoporphyrinuria
in association with chronic gastroduodenal
dilation, peculiar fits and acute polyneuritis: a
preliminary report. JAMA 59: 718-719.
Beer J (1935): Essai sur les rapports de l’art et de la
maladie de Vincent van Gogh. (The`se, Doctorat en
Me´decine), Strasbourg: Elie Mazel.
Bickers DR, Miller L, Kappas A (1975): Exacerbation of
hereditary hepatic porphyria by surreptitious ingestion
of an unusual provocative agent, a mouthwash
preparation. N Engl J Med 292: 1115-1116.
Blumer D (2002): The illness of Vincent van Gogh. Am
J Psychiatry 159: 519–526.
Bonkovsky HL, Cable EE, Cablew JW, Donohue SE,
White EC, Greene YJ, Lambrecht RW, Srivastava
KK, Arnold WN (1992): Porphyrogenic properties
of the terpenes – camphor, pinene, and thujone;
with a note on the illness of Vincent van Gogh.
Biochem Pharmacol 43: 2359–2368.
Bonkovsky HL, Sinclair PR, Emery S, Sinclair JF
(1980): Seizure management in acute hepatic
porphyria: risks of valproate and clonazepam.
Neurology 30: 588–592.
Dagg JH, Goldberg A, Lochhead A, Smith JA (1965):
The relationship of lead poisoning to acute intermittent
porphyria. Quart J Med 34: 163–175.
Doiteau V, Leroy E (1928): La Folie de Vincent van
Gogh. Paris, Æsculape.
Ellenhorn MJ, Barceloux DG (1988): Medical Toxicology.
New York, Elsevier.
Fabbri R Jr (1966): Dr. Paul-Ferdinand Gachet: Vincent
van Gogh’s last physician. Trans Stud Coll Physicians
Phila 33: 202–208.
Falret JP (1854): Me´moire sur la folie circulaire. Bull
Acad Natl Med 19: 382–415.
Finger S (2000): Minds Behind the Brain: A History of
the Pioneers and Their Discoveries, New York,
Oxford University Press.
THE ILLNESS OF VINCENT VAN GOGH 41
Gachet PF (1858): E ´ tude sur la Me´lancolie.
Montpellier, Montpellier Me´dical.
Gastaut H (1956): La maladie de Vincent van Gogh
envisage´e a` la lumie`re des conceptions nouvelles sur
l’e´pilepsie psychomotrice. Ann Med Psychol 1:
196–238.
Gastaut H (1970): Clinical and electroencephalographical
classification of epileptic seizures. Epilepsia
11: 102–113.
Gates RR (1946): Human Genetics. New York,
Macmillan.
Gibbs FA, Gibbs EL, Lennox WG (1937): Epilepsy:
a paroxysmal cerebral dysrhythmia. Brain 60:
377–388.
Goldberg A (1985): Molecular genetics of acute
intermittent porphyria. BMJ 291: 499-500.
Goodman LJ, Karakusis PH (1988): Neurosyphilis.
In: Vinken PJ, Bruyn GW, Klawans HL, eds.,
Handbook of Clinical Neurology. Amsterdam,
Elsevier, Vol. 52, Chapter 18.
Goodwin FK, Jamison KR (1990): Manic-Depressive
Illness. New York, Oxford University Press.
Harker LA, McCabe BF (1980): Meniere’s disease
and other peripheral labyrinthine disorders. In:
Paparella MM, Shumrick DA, eds., Otolaryngology,
2nd edition, chapter 41. Philadelphia, WB
Saunders.
Hemphill RE (1961): The illness of Vincent van Gogh.
Proc Roy Soc Med 54: 1083–1088.
Hulsker J (1990): Vincent and Theo van Gogh: A Dual
Biography. Ann Arbor, Fuller Publications.
Jackson JH (1931): Selected Writings of John
Hughlings Jackson. London, Hodder & Stoughton.
Jamison KR (1993): Touched With Fire: Manic
Depressive Illness and the Artistic Temperament.
New York, Free Press: Maxwell Macmillan.
Jaspers K (1922): Strindberg und van Gogh. Leipzig,
Ernst Bircher.
Johnson HA (1934): No madman. Art Digest 8: 11.
Kappas A, Sassa S, Galbraith RA, Nordmann Y (1989):
The porphyrias. In: Scriver CR, Beaudet AL, Sly
WS, Valle D, eds., The Metabolic Basis of Inherited
Disease. New York, McGraw-Hill, 6th edition,
pp. 1305–1365.
Knudsen KB, Sparberg M, Lecocq F (1967): Porphyria
precipitated by fasting. New Engl J Med 277:
350-351.
Kra¨epelin E (1921): Manic-depressive Insanity and
Paranoia (Translated by RM Barclay). Edinburgh,
Livingstone, 8th edition.
Laiwah AACY, Mactier R, McColl KEL, Moore MR,
Goldberg A (1983): Early-onset chronic renal
failure as a complication of acute intermittent
porphyria. Quart J Med 52: 92–98.
Lee TC (1981): Van Gogh’s vision: digitalis intoxication?
JAMA 245: 727–729.
Lip GYH, McColl KEL, Goldberg A, Moore MR
(1991): Smoking and recurrent attacks of acute
intermittent porphyria. BMJ 302: 507.
Loftus LS, Arnold WN (1991): Vincent van Gogh’s
illness: acute intermittent porphyria. BMJ 303:
1589–1591.
Lubin AJ (1972): Stranger on the Earth; A Psychological
Biography of Vincent van Gogh. New York,
Holt, Rinehart Winston.
Monroe RR (1978): The episodic psychoses of Vincent
van Gogh. J Nerv Ment Dis 166: 480–488.
Monroe RR (1992): Creative Brainstorms. New York,
Irvington.
Moore MR (1980): International review of drugs in
acute porphyria. Int J Biochem 12: 1089–1097.
Navratil L (1959): Vincent van Gogh: his disease
assessed in the light of his paintings. CIBA Found
Symp 7: 210–216.
Niedermeyer E (1983): Epilepsy Guide. Diagnosis and
Treatment of Epileptic Seizure Disorders. Baltimore
& Munich, Urban & Schwarzenberg.
Penfield W, Jasper H (1954): Epilepsy and the
Functional Anatomy of the Brain. Boston, Little,
Brown and Co.
Perry I (1947): Vincent van Gogh’s illness: a case
record. Bull Hist Med 21: 146–172.
Peters HA (1986): Acute Hepatic Porphyria. In: Johnson
RT, ed., Current Therapy in Neurologic Disease
1985-1986. New York, BC Decker, pp. 317–321.
Pickvance R (1984): Van Gogh in Arles. New York,
Harry N. Abrams Inc.
Pickvance R (1986): Van Gogh in Saint-Re´my and
Auvers. New York, Harry N. Abrams Inc.
Pinel P (1818): Nosographie Philosophique ou la
Me´thode de l’Analyse Applique´e a la Me´dicine.
Paris, Brosson, 6th edition.
Prinzhorn H (1972): Artistry of the Mentally Ill
(Translated by E von Brockdorff). New York,
Heidelberg, Berlin, Springer-Verlag. (Original German
version: Prinzhorn H. 1922. Bildnerei der
Geisteskranken. Berlin: Verlag Julius Springer.)
Rewald J (1986): Theo van Gogh as an art dealer.
In: Gordon I, Weitzenhoffer F, eds., Studies in
Postimpressionism. New York, Harry Abrams Inc,
pp. 7–115.
Ridley A (1969): The neuropathy of acute intermittent
porphyria. Quart J Med 38: 307–333.
Robbins SL (1957): Textbook of Pathology With
Clinical Applications. Philadelphia & London,
WB Saunders Co.
Rothenberg A (1990): Creativity and Madness, New
Findings and old Stereotypes. Baltimore and
London, The Johns Hopkins University Press.
Sarwer-FonerGJ (1988): The course ofmanic-depressive
(bipolar) illness. In: Georgotas A, Cancro R, eds.,
Depression andMania.NewYork, Elsevier, chapter 4.
42 WILFRED NIELS ARNOLD
Sassa S (1978): Toxic effects of lead, with particular
reference to porphyrin and heme metabolism. In: De
Matteis F, Aldridge WN, eds., Heme and Hemoproteins.
Berlin, Springer-Verlag.
Schmidt H (1915): l’Absinthe. l’Alie´nation mentale et
la criminalite´. Rapport fait au nom de la commission
d’hygie`ne publique de la chambre des de´pute´s.
Annales d’Hygiene Publique et de Me´dicine Le´gale
23: 121–133.
SchnThe Illness of Vincent van Gogh
Wilfred Niels Arnold
Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, KA, USA
ABSTRACT
Vincent van Gogh (1853–1890) was a wonderfully accomplished artist whose work is now widely
appreciated. He created a great number of masterpiece paintings and drawings in just one decade devoted to
art. His productivity is even more remarkable when considered in the context of his debilitating illness. He
suffered from medical crises that were devastating, but in the intervening periods he was both lucid and
creative. He left a profound, soul-searching description of his jagged life in his correspondence, which
provides the basis for the present analysis. An inherited metabolic disease, acute intermittent porphyria,
accounts for all of the signs and symptoms of van Gogh’s underlying illness. On this 150th anniversary of the
birth of Vincent van Gogh it is appropriate to revisit the subject and to analyze the lack of organized
skepticism in the popular media about other diagnoses.
Keywords: Vincent van Gogh, inherited disease, acute intermittent porphyria, medical crises, absinthe, alcohol,
thujone, camphor, pinene
Vincent van Gogh was born in the presbytery of
the Dutch Reformed Church of Zundert, in the
southern region of The Netherlands, at 11:00 am
on March 30, 1853. The obstetrician did not have
far to run – the office of Dr. Cornelis van
Ginneken was right next door. There were no
problems on that day. They would tumble out
later. An eventful life was underway and it would
last just thirty-seven years and four months.
Today, van Gogh is on everybody’s list of
outstanding artists and in every catalog of creative
people. He continues to find an appreciative
audience of young and old, novice to connoisseur,
all untrammeled by differences in cultural
background or artistic education. It was not
always so, at the time of his suicide in 1890
the accomplishments of Vincent were acknowledged
by only a small cadre of friends and
followers. No more than a handful of critics
had put pen to paper. Formal recognition during
his life was restricted to exchanges of paintings
with other artists, gifts to friends and doctors,
acceptance of canvases toward financial obligations,
three sets of commissions, a drawing sold
in The Hague, a few items sold in Paris, a selfportrait
sold to a London dealer in 1888, and
one sale from an influential Les Vingt exhibition
(1890) in Brussels.1 He died still writing of
hopes for future recognition, but indeed it was
a deep disappointment for an artist who had
been confident enough to follow the precedents
of Michelangelo Buonarroti, Raphael Santi, and
Journal of the History of the Neurosciences
2004, Vol. 13, No. 1, pp. 22–43
Address correspondence to:Wilfred Niels Arnold, Department of Biochemistry and Molecular Biology, University
of Kansas Medical Center, Kansas City, KA 66160-7421, USA. Tel.: þ1-913-588-7056. Fax: þ1-913-588-7440.
E-mail: warnold@kumc.edu
1The sale of van Gogh’s artwork during his lifetime was obviously meager, but this list should replace the popular
misunderstanding that Vincent ‘‘sold only one painting.’’
10.1080/09647040490885475$16.00 # Taylor & Francis Ltd.
Rembrandt van Rijn by using his first name
alone for professional purposes.2
Posthumous praise for his creations roused
attention but surely it has been the complementary
interest in extraordinary aspects of the person,
especially his underlying illness, that has
made Vincent van Gogh a household name. His
jagged life was marked by early years of uncertainty,
interludes of luckless love affairs,
wrenching episodes of self-mutilation, and crises
of debilitating illness. Creative people who have
shaken the world a bit are generally surrounded
by popular contemplations about their physical
and mental health. And in the visual arts the
individual who makes the advance is all too often
suspected of some individual abnormality, as if
there were a need to invent an exotic explanation
for the novelty. But in the case of van Gogh there
were certainly enough unusual episodes to raise
the question of mental derangement even during
his lifetime. Given the extraordinary influence of
the man on succeeding generations there are
ample justifications for serious studies on whether
medical problems affected his life or his artwork.3
THE PROBLEM
Superficial interest and comment on van Gogh’s
illness grew with every exhibition of his work. It
became an industry with its own history. As a
result, the typical newspaper article or exhibition
essay declared that there were one hundred and
one diagnoses on van Gogh’s illness!4 Six or
seven examples were proffered, all embraced with
equal weight by the reporter and without the
benefit of a word of evaluation. Hopes of finding
a better perspective in journal articles and books
have not always been filled because the majority
of the authors promoted pet ideas with selective
inclusion of what they believed to be supporting
data. I believe, axiomatically, that any reasonable
working hypothesismust address all of the medical
information; this includes family history and the
artist’s lifestyle, as well as the underlying illness.
The interaction between congenital disease and
exacerbation factors is central to our argument.
After Dr. Loretta Loftus and I published our
working hypothesis of acute intermittent porphyria
for Vincent and discussed the differential
diagnosis (Loftus & Arnold, 1991) we were
surprised to find that some critics, who did not
offer any assessment of the facts we presented,
were quick to respond with undocumented personal
preferences in newspaper stories or letters-tothe-
editor. Their epistles promoted alternatives
that they claimed were ‘‘more easily understood’’
or ‘‘more common disease entities,’’ as if poor
Vincent should become a poster-boy for the disease
currently in vogue for creative people. Some
made passing comparisons with other famous
persons but usually without data on any of them.
In some quarters the same weight was given to an
opinion as to a well-referenced analysis.
A large section of my subsequent book (Arnold,
1992) was devoted to van Gogh’s underlying illness.
Therein I produced tables of Vincent’s own
references (from his letters) organized by particular
medical signs and symptoms, thus offering
future scholars the benefit and convenience of a
concordance. In the chapter ‘‘Other Hypotheses’’ I
started with the assumption that all the authors
were sincere but found that only a few advanced
the field. It was also apparent tome that so many of
those suggestions were loosely conceived and
poorly documented, but they landed in the literature
and in some cases had been widely quoted and
requoted (errors to the third degree) without benefit
of common sense. A blatant example is the silly
claim of digitalis poisoning as a cause of van
Gogh’s underlying illness.
Art historians and others were quick to remark
upon van Gogh’s occasional ‘‘high yellow’’ palette.
This was hardly a revelation because the
artist himself had written about his exaggerated
use of yellow pigments and had coined the phrase.
Vincent’s fondness for yellow can be gauged from
his letters in the 1887–1890 period wherein he
mentions the yellow of his surroundings more
2The paintings he signed (a small fraction of the total)
were simply inscribed Vincent. I will use Vincent, van
Gogh, and Vincent van Gogh interchangeably.
3Some commentators, mostly from the art history
ranks, have denied the necessity to explore these
questions. The possible reasons are analyzed later.
4I have encountered no more than a dozen serious
proposals, but within each category there have been
numerous renditions and rediscoveries.
THE ILLNESS OF VINCENT VAN GOGH 23
than any other color (Arnold, 1992). But Lee
(1981) was bold enough to propose that van Gogh
suffered from a xanthopsia, wherein the patient
has a reversible view of the world as if through a
yellow filter, and that Vincent had been overexposed
to digitalis, as a decoction of the foxglove
plant. There is no doubt that too much
digitalis will have this effect; the observation
dates from the original dissertation (Withering,
1785); but there is no evidence that van Gogh ever
took the drug, and artistic preference is still the
best working hypothesis for the high yellow
canvases (Arnold & Loftus, 1991). Also, and
more important in the present context, it is absurd
to include digitalis poisoning in lists of possibilities
to explain all his neurologic and psychotic
problems that culminated in suicide.
The goal of the present review is fourfold: to
evaluate our current understanding of van Gogh’s
illness; to analyze some of the cultural and social
aspects that impinge on (and interfere with) this
field of van Gogh scholarship; to recommend a
higher level of organized skepticism; and to
promote the operational concept that the canons
of proof associated with the hard sciences should
also be applied to biography.
THE IMPORTANCE OF THE LETTERS
Theo van Gogh (1857–1891), who provided the
emotional and financial supports for his brother’s
final decade, had realized the value of Vincent’s
correspondence as a rich source of artistic and
human interest. But he died the next year after
Vincent’s suicide, and it took Theo’s widow,
Johanna van Gogh-Bonger (1862–1925), another
twenty-four years to decipher, translate, and
arrange the letters before the first reasonable
compilation appeared. In the preface, Johanna
gave an additional reason, ‘‘It would have been
an injustice to Vincent to create interest in his
personality ere the work to which he gave his life
was recognized and appreciated as it deserved.’’
(van Gogh-Bonger, 1978, xiii)
The decision by Johanna van Gogh-Bonger to
publish in English was based on her insightful
anticipation of a world-wide audience for both
Vincent the man and the huge amount of artwork
that she inherited. She was well versed in the
language and was also assisted in English phrasing
and idiom by Helen Apel Johnson (Johnson,
1934). For many years the only edition of the
letters that approached completeness was in
English, and that had a profound effect upon the
history of van Gogh scholarship.
Vincent’s namesake nephew, V.W. van
Gogh (1890–1978), identified as ‘‘Vincent the
Engineer,’’ followed his mother in the activities
of preserving the art work of his Uncle and organizing
the copious correspondence, for which he
anticipated the research potential by stating in his
introduction that, ‘‘the letters . . . are the only genuine
source of details on his [Vincent’s] life’’ (van
Gogh, 1978, xi). During our 1990 conversation, Dr.
Albert Lubin, professor of psychiatry and a van
Gogh commentator (Lubin, 1972), made a special
point about Vincent’s nephew being very much the
‘‘amateur psychologist’’ and a supporter of this
type of enquiry. Unfortunately, in my opinion,
Vincent the Engineer also endorsed some of the
more mystical interpretations of the artist’s life.5
The three volumes of letters, memoirs, and
editorial comments (van Gogh, 1978) are an
important social, medical, cultural, and literary
compilation. The descriptions of illness by the
patient himself are central to our subject.6 In this
review all references from The Complete Letters
5Dr. Humberto Nagera, another psychiatrist with direct
contact, recently spoke to me about the Engineer being
at odds with Paul-Louis Gachet (1873–1962), the son
of Dr. Paul-Ferdinand Gachet (1828–1909). The father
was Vincent’s last attending physician. Paul-Louis
was a seventeen-year-old eyewitness commentator on
Vincent’s final months in Auvers-sur-Oise, whereas the
Engineer had to rely on information that was at best
second-hand. One wonders whether the enmity of van
Gogh’s nephew for young Gachet encouraged a splinter
group that found fault with Dr. Gachet’s management of
Vincent’s case and later criticized the whole Gachet
family for exploitation of his art legacy. Their argument
remains unconvincing and flies in the face of the
generous donations (in 1949, 1951, and 1954) of van
Gogh paintings to the state by Paul-Louis Gachet and
his sister Marguerite (1869–1949).
6Most van Gogh commentators will not argue in public
about the necessity of reading The Complete Letters,
but it is no small undertaking (1,809 pages in all) and
one may wonder how many have.
24 WILFRED NIELS ARNOLD
will be noted, parenthetically, by letter numbers
as they appear in the English edition of 1978.
They overshadow the brief notes and register
entries (Tralbaut, 1981) that have survived attending
physicians in The Hague (unidentified
hospital-doctors), Eindhoven (Dr. Van der Loo),
Antwerp (Dr. Cavenaille), Paris (Drs. Rivet and
Gruby), Arles (Drs. Rey and Urpar), St. Re´my
(Dr. Peyron), and Auvers (Dr. Gachet). It seems
inconceivable that Dr. Paul Gachet (1828–1909)
kept no records, yet no journal or diary of patient
visitations has been forthcoming from his office in
the home at Auvers-sur-Oise.7 Biographical notes
on all of the above physicians, as well as the
influence of the home-remedies of Francois-
Vincent Raspail (1794–1878), have been published
(Arnold, 1992).
MEDICAL SUMMARY
Vincent’s ailment was characterized by episodes
of acute mental derangement and disability which
were separated by intervals of lucidity and creativity.
Moreover, attending physicians, family,
friends, and the artist himself were all surprised
and encouraged by the rapidity of the recoveries
after each crisis (van Gogh-Bonger, 1978). His
serious illness developed late in the third decade,
as evidenced by his concern with ‘‘the possibility
that [my] family might take steps to deprive me of
the management of my affairs and put me under
guardianship’’ (letter 204). There was a family
history of mental illness (Lubin, 1972; Tralbaut,
1981; Arnold, 1992). His underlying complaint
was characterized by frequent gastrointestinal
problems (letters 448, 530, B4, etc.), and at least
one bout of constipation that required medical
intervention (Tralbaut, 1981, pp. 177-8). The
condition caused fits with hallucinations, both
auditory and visual, (letters 592, W11, etc.) and
evoked partial seizures (Tralbaut, 1981, p. 276).
Periods of incapacitating depression and physical
discomfort were severe and grave enough to
provoke self-mutilation and eventual suicide
(van Gogh-Bonger, 1978). Some of his bouts of
sickness may have been associated with fever
(letter 206) and sexual impotence (letter 506).
His ailment was exacerbated by overwork (letter
173), malnutrition and fasting (letters 440, 571),
environmental exposure (letter B15), excessive
ingestion of alcoholic beverages (letter 581,
etc.), especially absinthe (letter A16), and a proclivity
for camphor and other terpenes (Arnold,
1988). The symptoms were palliated during institutionalization
with better diet, alcohol restriction
(letters 595, 599), and administration of bromide
therapy (letter 574). In spite of their severity he
did not experience any permanent, functional
disability after any attack (Lubin, 1972; Tralbaut,
1981; Arnold, 1992). The reader is referred to
Arnold (1992) for a much fuller treatment. In the
paragraphs that follow I shall emphasize and
explain specific aspects of van Gogh’s illness that
are central to our working hypothesis and also
dismissive of so many other hypotheses from the
past.
AGE OF ONSET
In 1882, Vincent entered the city hospital at
Brouwersgracht (a section of The Hague, in The
Netherlands) with a gonorrheal infection, for an
anticipated stay of no more than 14 days (letter
206). However, the hospital register (Tralbaut,
1981) indicated that Vincent was admitted June
7 and was not discharged until July 1 (a total of 25
days). To the surprise of his doctors, things took a
turn for the worse after about 14 days, and
Vincent complained by letter on June 22, of a
‘‘dreadful weakness’’ and wondered ‘‘if there had
been some complication that would make things
worse’’ (letter 208). He was moved to a new ward.
The symptoms were only briefly described by
Vincent but it extended his stay in the hospital
for another 11 days. Was it a complication or a
paroxysm?
7Son and daughter maintained the residence after the
doctor’s death in 1909, and they were renowned for the
care with which they preserved their father’s medical
instruments and memorabilia. They had no children and
were survived by distant relatives. Rumor has it that
somewhere along the way all of Dr. Gachet’s records
were intentionally destroyed ‘‘to protect the privacy of
his patients.’’ His views survive only in the form of
interesting anecdotes, and indirect reports with poor
documentation of time or place.
THE ILLNESS OF VINCENT VAN GOGH 25
There was a bizarre supplement. Van Gogh
claimed that the attending physicians were willing
to attest to his sanity (letter 206) if it were
challenged again by his father. This statement is
startling at first encounter but information taken
from other letters indicates that his father had
considered having him committed to an asylum in
1880 and again in 1881 (Arnold, 1992; letter 204;
and letter 158 as amended by Hulsker, 1990). The
hospitalization in The Hague took place when van
Gogh was 29 years old. First indications of
neuroses and psychoses occurred at age 27
(according to his father’s assessment). First
expression of serious mental problems thus
occurred late in the third decade of Vincent’s life.
SIX MAJOR CRISES
The last two years of van Gogh’s life included six
well-documented medical crises with serious
mental problems. The period under discussion,
October 1888 to July 1890, is shown in Figure 1,
which depicts calendar months (center line),
sequential locations (bottom line), and the crises
(stippled rectangles above the time line). Van
Gogh’s suicide is marked with a Roman cross.
The utility and power of the graphical presentation
derive from the multiplicity of facts
depicted and, in addition, from the visual summary
(the Gesta¨lt). Thus we can see that the
durations of the crises are variable (days, weeks,
or months) and there is no discernible trend (the
succeeding crises neither shorten nor lengthen in
a regular manner). The five periods between
major attacks show neither consistency nor trend.
Their lengths were 38, 148, 116, 21, and 26 days.
The range is large; the mean happens to be 70
days (standard deviation¼58 days).
Vincent was a patient (voluntary inmate) at
Saint Paul de Mausole Asylum at St. Re´my for
just over a year (May 8, 1889 to May 16, 1890),
although the initial plan had been for only three
months. The attending physician, Dr. The´ophile
Peyron (1827–1895), made occasional, spare
notations in the register. Towards the end he wrote
that ‘‘the patient [van Gogh] . . . experienced during
his stay in this institution several [medical]
attacks with a duration of two weeks to a month.’’
In reality, during the St. Re´my period with Dr.
Peyron, the durations were 45, 7, 7, and 65 days in
chronological order. The discrepancy suggests
that Dr. Peyron was writing from memory, at
some distance from the events. Van Gogh himself
had not kept accurate records.
In letter 631 Vincent wrote to brother Theo,
‘‘I pointed out to [Dr. Peyron] that such
attacks . . . have always been followed by three
or four months [i.e. 90–120 days] of complete
quiet. I want to take advantage of this period to
move [from St. Re´my to Auvers]’’ The actual
numbers were 70 58 days (see above). His last
crisis at St. Re´my ended April 29, 1890. It is
remarkable that a safe period of three months
(Vincent’s intuitive but unsupported prediction)
would literally terminate on July 29, 1890! The
suicidal act (possibly inspired by an impending
crisis) was committed on July 27.
Each crisis had an abrupt onset and, at the end
of days or weeks, a swift resolution. In some cases
the artist even used words with the following
implications ‘‘one day fine – the next day, down
with sickness’’ and ‘‘yesterday I was too sick to
write – today I pick up the pen.’’ It is worth
Fig. 1. Time course of six major crises suffered by Vincent van Gogh. Details are given in the text.
26 WILFRED NIELS ARNOLD
recalling how desperate the early prognosis
about the December 1888 crisis had been. After
Augustine Roulin (1852–1930) visited the hospital
at Arles on the 27th, Vincent had increasing
neurologic problems. The following day her husband
Joseph Roulin (1841–1903) was unable to
see him because van Gogh was suffering from
aphasia. And then, on the last day of December, to
the pleasant surprise of doctors and friends, the
patient made a recovery so rapid and complete that
Rev. Salles could report that he found him ‘‘calm,
in a state which revealed nothing abnormal’’ (van
Gogh-Bonger, 1978, xlvi). By the first week of
January Vincent was moving around the hospital
and conversing freely with Roulin and others, and
even cautioning Theo not to alarm his mother and
sister Wil. unduly (letter 569). On January 7, he
returned to his home in Arles (made famous by his
painting ‘‘The Yellow House’’) and that day
declared to his mother and sister that ‘‘there is a
chance that there will be nothing the matter with
me for a long time to come’’ (letter 569a).
The periods between major attacks were
remarkably normal. The lucidity with which the
patient comprehended and wrote letters, discussed
his condition with physicians, weighed
the possibilities for the future, and maintained
the quality of his art work, are all evident. From
all indications (van Gogh, 1978; Tralbaut, 1981;
Pickvance, 1984, 1986; Arnold, 1992), Vincent
did not write letters and did not paint during
crises. Unfortunately, this did not prevent future
romantics (see for example Schnier, 1950;
Navratil, 1959) from seeing disease in his art
work!
Potential precipitants of eight crises are
summarized in Table 1; documentation will be
provided later.
The course of van Gogh’s illness is very
instructive in approaching a retrospective diagnosis.
The features are a guide to a working
hypothesis that can then be either strengthened
or challenged by further data. Hence any reasonable
suggestion must first accommodate the
kinetics and time course of van Gogh’s illness,
and I would encourage organized skepticism in
examining how poorly the observed data fit with
ideas from the past. For example, we may ask
whether a proposed medical entity usually presents
with rapid (of the order of twenty-four
hours) onsets and resolutions, or does the patient
with the syndrome under discussion tend to drift
through days or weeks into a debilitating episode
and then later slowly emerge? Are the intervening
periods marked by complete lucidity and impressive
productivity or is there an indication of a
cumulative neurological deficit and a mounting
struggle to perform? Are the observed periods of
Table 1. Precipitating Factors According to Arnold (1992).
Date of crisis Location Precipitants
1880 The Borinage (Belgium) Fasting or general neglect of nutrition are
possibilitiesa
June 1882 The Hague (Holland) Gonorrheal infectionb
December 1888 Arles (France) Alcohol (especially absinthe)
February 1889 Arles (France) Camphor, fasting, alcohol (especially absinthe)
July–August 1889 St. Re´my (France) Alcohol (especially absinthe) consumed in Arles
during a social visit
December 1889 St. Re´my (France) Exposure to turpentinec
January 1890 St. Re´my (France) Alcohol (especially absinthe) consumed in Arles
during a social visit
February–April 1890 St. Re´my (France) Alcohol (especially absinthe) consumed in Arles
during a social visit. This crisis actually started
in Arles
Note. aPoorly documented, but related to the concerns of van Gogh’s father.
bWe refer to the ‘‘complication’’ that followed the primary infection.
cExpression of a pica (Arnold, 1988) for terpenes and terpenoid compounds: camphor, pinene (in turpentine),
thujone etc. from absinthe.
THE ILLNESS OF VINCENT VAN GOGH 27
pronounced illness for van Gogh compatible with
a candidate disease, or would one expect minutes
or hours – months or years? With any of these
other proposals, would attacks be precipitated by
seemingly unrelated factors such as fasting,
microbial infection or xenobiotics? All the while
we must bear in mind that Vincent’s organized
care during the medical crises of the last two years
was practically limited to bed rest, one prescribed
drug (potassium bromide), good nutrition, and
restriction of alcoholic beverages. During van
Gogh’s hospitalizations the attending doctors,
nuns, and other attendants were essentially
engaged in sympathetic nursing and patient-protection,
in response to observation and concern.
THE ROLE OF ABSINTHE
Artists painted and poets personified; men and
women embraced the ritual of presentation as
well as the appearance, taste, and excitement of
the liqueur called absinthe. Some of the most
creative people of the nineteenth century were
included. The aesthetics of absinthe drinking
contributed to its popularity. Nevertheless, one
looks beyond ethanol to the mood-altering chemicals
that were unique to this alcoholic beverage
in order to rationalize the volumes consumed in
some quarters (Arnold, 1989). There was a fifteen-
fold per capita increase in France from 1875
to 1913, when the national annual consumption
attained a massive 9.7 million U.S. gallons.
Whenever you have this many people imbibing
a particular beverage, there must be more to it
than poetry and attractive colors. In the department
of Bouches-du-Rhoˆne, which includes van
Gogh’s southern venues of Arles and St. Re´my,
the annual consumption was an impressive 2.45
liters per head, which was more than four times
the national average (Schmidt, 1915).
VINCENT VAN GOGH
AND THE INDIVIDUAL RESPONSE
Some years ago, while perusing the letters of
Vincent van Gogh, I was intrigued by the chemical
connection between absinthe constituents
(such as the toxic compound called thujone) and
some other terpenoid compounds in his life.
These exposures involved Vincent’s use of massive
amounts of camphor to combat insomnia, an
attempt to drink essence of turpentine (pinene),
and references to his nibbling at oil colors (mixed
with turpentine). The possibility of an interaction
became more compelling when I read Sollmann
(1948) on thujone and camphor, wherein he
remarked that the convulsions induced in experimental
animals are antagonized by bromide,
while the threshold is lowered by nicotine. While
institutionalized in Arles, van Gogh’s crises were
ameliorated by taking bromides and decreasing
smoking. Accordingly I suggested that van Gogh
had developed an affinity or a pica for terpenes,
the documented examples being thujone, camphor,
and pinene (Arnold, 1988).8 This would
help to explain some of the strangest of van
Gogh’s acts during his last two years – his
attempts to eat his paints and to drink turpentine
and kerosene – which were previously regarded
as absurdities and unrelated.
The response to any drug or xenobiotic
depends upon a variety of factors not least of
which the nutritional status of the subject. For
example, an increased toxicity of camphor and
related compounds is noted during fasting and is
attributed to a compromise in glucuronic acid
formation (Sollmann, 1948).9 Infections and unerlying
illness also play critical roles in determining
the individual’s response to drugs.
There are several indications in his letters and
in painted objects that Vincent developed an
‘‘affinity’’ for absinthe. He painted The Night
Cafe on the spot, staying up three nights in a
row and sleeping during the day (letter 533). It is
tempting to speculate that he had a glass or two
during the execution of this painting; he certainly
had access, and the landlord was apparently
pleased with the whole event. Apart from the
8Pica comes from the Latin for magpie, a bird who
carries away odd objects. In medical terminology it
refers to compulsive eating of non-nutritive substances
and has been ascribed to various disorders including
malnutrition.
9Camphor is secreted in the urine as hydroxycamphor
glucuronide.
28 WILFRED NIELS ARNOLD
possibility of this special case, we do not imply
that van Gogh painted while intoxicated.
There has been much discussion on the amount
of absinthe (and other alcoholic beverages) consumed
by Vincent in Paris, Arles, St. Re´my, and
Auvers. At one extreme we have Jan Hulsker who
steadfastly maintained that ‘‘Vincent was not a
drinker’’ (Hulsker, 1990). In an earlier publication
(Arnold, 1988) I described a pastel by Toulouse-
Lautrec and mentioned that it depicts Vincent
‘‘partaking of a glass’’ of absinthe. Hulsker
(1990, pp. 401–404) objected to ‘‘partaking’’
and insisted on the static message that Vincent
only sits before the glass. That Toulouse-Lautrec
chose to depict Vincent with a glass of absinthe
suggests to me that it was a common enough
circumstance, and that Vincent drank absinthe.
We feel that van Gogh was not in the habit of
simply decorating his table ‘‘with a glass of
absinthe in front of him’’ as Hulsker would have
it (Hulsker, 1990, p. 322). That commentator
maintains the isolated position that there is no
evidence that van Gogh was fond of absinthe, and
he also denies all the statements and anecdotes
about his drinking problem. Alas, Hulsker defeats
his own hypothesis in several places, not least of
which when he suggests that Vincent’s lack of
recall of the ear-cutting episode was ‘‘because
drinking had caused him to black out’’ (Hulsker,
1990, p. 322).
At the other extreme we have those reporters
with a list who would include absinthe abuse as a
free-standing explanation for all of Vincent’s
problems. Other commentators, who had been
told that their initial hypotheses didn’t accommodate
all of van Gogh’s signs and symptoms,
subsequently invoked absinthe as a rider. I provided
a concordance on Vincent’s references to
alcohol, including letters in which he expressed
fear of becoming an alcoholic (Arnold, 1992,
p. 79).
Paul Gauguin (1848–1903) lived with van
Gogh during the two months running up to
Vincent’s first crisis in Arles. Anecdotes suggest
that Gauguin consumed at least as much absinthe
as van Gogh, but he did not exhibit the same
medical problems. If so many were drinking
absinthe, why did his neighbors (letter 579)
regard Vincent’s behavior as so bizarre? The
explanation that has escaped most reviewers is
that Vincent was abnormally sensitive to absinthe,
even in the amounts associated with social drinking,
because of his congenital illness. Absinthe is
but one factor in the ‘‘environmental’’ impact on
Vincent’s underlying illness; it also comes under
the category of ‘‘lifestyle.’’ Hemphill (1961)
deserves much credit for being the first to consider
absinthe as an external chemical influence
on van Gogh. Vincent himself seemed to be
approaching this idea when he wrote, ‘‘it seemed
to be caused more by some outside influence than
by something within myself’’ (letter 605). Loftus
and Arnold are convinced that it was the underlying
illness of acute intermittent porphyria
that made Vincent so sensitive to absinthe and
malnutrition.
ACUTE INTERMITTENT
PORPHYRIA (AIP)10
AIP is one member of a class of metabolic
abnormalities, the porphyrias, which are characterized
by the excessive production of porphyrins, or
related compounds (Waldenstro¨m, 1957; Kappas
et al., 1989). Individuals who suffer from these
diseases are prone to excrete elevated concentrations
of these same compounds in their urine and
feces. The abnormal excretion per se is of no
intrinsic medical import but it is a reflection of
elevated concentrations circulating within the
body, and therein lies the potential for cutaneous
photosensitivity (due to porphyrins), neurological
abnormalities (due to porphyrin precursors), or
both. In the case of AIP, all of the symptoms are
neurological and the specific, overly-produced
compounds are d-aminolevulinic acid and porphobilinogen.
These are intermediates in the metabolic
pathway to porphyrins, which in turn are used in
the biosynthesis of the heme of hemoglobin, and
other heme-containing proteins. ‘‘Acute’’ refers to
the rapid onset, and abrupt cessation, of expressed
symptoms. (The underlying cause of AIP is present
from birth, so in that sense it is chronic.)
10Please consult my book (Arnold, 1992) for a much
fuller discussion of acute intermittent porphyria. Only
the most salient primary references will be given here.
THE ILLNESS OF VINCENT VAN GOGH 29
‘‘Intermittent’’ refers to the periodicity, which is
typical, and emphasizes the distinct periods of
normalcy which intercede between the episodes
of illness.
Symptoms rarely occur before puberty; the
peak decade for onset of symptoms is from age
20 to 29 (somewhat later for males than females)
but the disease sometimes remains latent throughout
a lifetime (Waldenstro¨m, 1957). Tabulations
of the most common hallmarks emphasize
abdominal pain and other gastrointestinal complaints,
symptoms referable to the peripheral and
central nervous systems, and signs of autonomic
neuropathy including tachycardia and hypertension.
Porphyria-induced hypertension can cause
early-onset renal failure (Laiwah et al., 1983).
Bladder dysfunction may result in urinary retention
(Laiwah et al., 1983; Kappas et al., 1989).
Effects on optic nerves or the occipital lobes have
been documented for AIP cases (Ridley, 1969).
Sexual impotence (Kappas et al., 1989) has occasionally
been reported. Premonitory symptoms
include restlessness and irritability; attacks develop
rapidly; resolution may occur in days or sometimes
weeks, in an unpredictable fashion. Seizures do not
always attend severe crises, but when they domany
antiseizure drugs, with the notable exception of
bromides, may adversely affect the outcome
(Bonkovsky et al., 1980; Moore, 1980).
The unpredictable nature of the disease with
respect to both onset of crises and outcome makes
an acute attack of AIP particularly treacherous. It
can be one of the most terrifying experiences
imaginable. Patients can become almost completely
paralyzed in severe cases. They are unable to
breathe, swallow or communicate properly, yet
remain conscious for some time, all the while
suffering pain, being aware of their plight, and
wondering if it will ever end. The most common
cause of death from AIP is respiratory paralysis.
Most importantly, the expression of neurological
and other symptoms depends upon lifestyle
and exposure to precipitating factors. Early examples
of AIP were revealed as a response to new
drugs; initially the hypnotic Sulfonal (2,2-bis
(ethyl sulfonyl) propane), later barbiturates; and
subsequently many other drugs, alcohol, and
sundry organic compounds (Moore, 1980). Some
steroid metabolites precipitate attacks, and endogenous
changes may account for some crises at
puberty and the earlier onset with females. Other
exacerbating factors include infections and malnutrition
(Kappas et al., 1989). Low-carbohydrate
and low-protein diets are especially detrimental
(Welland et al., 1964) and fasting can precipitate
an attack of porphyria (Knudsen et al., 1967). A
study in Scotland indicated an association between
smoking (nicotine is metabolized via cytochrome
P450) and the induction of repeated attacks in
patients already diagnosed with AIP (Lip et al.,
1991). Even an excess of coffee may be a problem
because caffeine is also porphyrogenic (Moore,
1980).
VINCENT VAN GOGH AND AIP
All of the hallmarks of Vincent’s illness can be
accommodated within this overview of AIP. The
most important and well documented are the
gastrointestinal complaints, neurological disturbances,
age of onset, jagged time course, and the
exacerbations caused by inadequate nutrition and
absinthe abuse. Other aspects such as sore throats,
eye problems, fevers, a bout of aphasia in the
Arles hospital, and impotence, have other possible
causes but are all compatible with underlying
AIP. Van Gogh’s smoking habit may have contributed
to recurrent attacks. Vincent’s urinary
tract infection in The Hague may have precipitated
an AIP crisis leading to the ‘‘complication’’
and extended hospitalization at that time. It is also
possible that his urinary retention recorded at that
time was exacerbated by an AIP attack.
Arnold (1988) suggested that van Gogh’s fondness
for absinthe developed into a pica for terpenes,
the documented examples being thujone,
camphor, and pinene. It is worth noting that 1,8
cineole, a constituent of crude camphor and
wormwood oils, is a proven precipitating agent
for AIP (Bickers et al., 1975). Van Gogh used
reckless doses of camphor oil against insomnia
(letter 570) and absinthe contained a variety of
essential oils including wormwood. Bonkovsky
and Arnold have shown that camphor, thujone,
and pinene are porphyrogenic (Bonkovsky
et al., 1992). The combination of overexposure
to camphor, absinthe abuse, and fasting or
30 WILFRED NIELS ARNOLD
malnutrition would be injurious for anyone, but
devastating for someone with AIP.
Loftus and Arnold (1991) believe that all
recorded signs and symptoms of Vincent’s illness
can be accommodated by acute intermittent porphyria.
Arnold (1992) presented cases of AIP from
the 20th century that had analogies to the illnesses
of Vincent, Theo, and their sister Wil. (1862–
1941). It behooves proponents of other hypotheses
to provide similar case histories, complemented
with the diagnostic insights ofmodernmedicine, to
either support or damage their alternatives.
THE BIOCHEMICAL LESION IN AIP
Almost any cell in the human body can engage in
synthesis of heme because it is not only vital to
hemoglobin but also for the cytochromes involved
in so many aspects of metabolism. The biochemical
pathway to heme consists of eight enzymes
and an exquisite control mechanism. A partial
deficiency (about half of normal) of enzyme
(catalyst) number three (porphobilinogen deaminase)
in this sequence is the underlying cause for
the manifold derangements of the AIP patient
under crisis. The organ of primary concern for
this inherited disease is the liver, where two thirds
of the heme that is produced is incorporated into
the various types of cytochrome P450. An even
larger proportion attains during the induction of
P450’s, which attends the liver’s encounter with
xenobiotics. The AIP patient has a vulnerable
heme pathway. The neurological problems associated
with medical attacks are a consequence of
upsetment of the heme pathway and the toxic
accumulation of two intermediate compounds, daminolevulinc
acid (ALA) and porphobilinogen.
Because porphobilinogen deaminase is not ratelimiting
to the overall pathway, 50% of normal is
sufficient for unstressed AIP patients. This explains
the lack of symptoms for latent AIP patients and
the intervening periods of normalcy for patients
who have experienced periods of sickness. It is the
first enzyme in the pathway, ALA synthetase, that
is normally rate-limiting. Therein lies the major
control feature because heme (the end product of
the pathway) causes both a repression and an
inhibition of ALA synthetase. When the heme
concentration of liver cells is depleted, the effective
amount of ALA synthetase may be increased
over ten-fold. Under those circumstances the
‘‘partial road block’’ at enzyme number three for
AIP patients is felt, and toxic levels of the preceding
compounds are produced.
Ingested compounds that are metabolized via
cytochrome P450’s in the liver deplete the heme
pool and induce the synthesis of ALA synthetase.
These include alcohol, many drugs, and many
xenobiotics (Moore, 1980). The van Gogh terpenes
(camphor, thujone and pinene) can be added to that
growing list (Bonkovsky et al., 1992). On the
other hand, synthesis of ALA synthetase can be
decreased by high glucose intake, thus helping to
explain the ameliorating effect of a high carbohydrate
diet on AIP attacks and the adverse effect of
malnutrition or fasting (Kappas et al., 1989).
More extensive discussions of the heme pathway
are given elsewhere (Kappas et al., 1989;
Arnold, 1992) and further pursuit of the biochemistry
is not appropriate to this review. However, I
would like to offer an hydraulic model of the
control mechanism to assist the non-chemical
reader. The diagram on the left of Figure 2 represents
each intermediate compound (a,b,c . . . heme)
as a solution in a cylinder being acted upon by an
enzyme (exit tube) as it passes on to the next
vessel. The AIP patient has about half the normal
amount of the third enzyme (exit partly closed by
the bold arrow). But the overall flow is steady
thanks to regulation of the first enzyme (the float
mechanism senses the level of the heme pool). The
diagram on the right depicts the consequence of
depleting the heme pool (pulling the plug): the
activity of the first enzyme increases greatly
(increased drop-size in the model) and now the
partial block at the third enzyme (in the AIP
patient) comes into play. Compounds c and d
accumulate and will spill-out (X).
Only under a crisis does the AIP patient excrete
large amounts of d-aminolevulinic acid (compound
c) and porphobilinogen (compound d) in the urine.
Even then the freshly voided urine is of normal
color, but with time these compounds polymerize
to form porphobilin which imparts a brown or red
(the color of porphyry) pigmentation to aged
specimens. The final color is influenced by concentration,
pH, light, oxygen and temperature.
THE ILLNESS OF VINCENT VAN GOGH 31
The propitious availability of a porphyric urine
sample together with the low-tech ‘‘windowsill
test’’ can be very instructive in the diagnosis of AIP.
Urine which has aged internally due to bladder
dysfunction may already be discolored when
released with a catheter, although the color is
sometimes mistaken for urinary tract bleeding. In
contradistinction to the claim that ‘‘port wine
urine’’ is the faithful telltale sign of AIP, it is
worth emphasizing that many 20th century carriers
with documented medical attacks have never
remarked upon abnormally colored urine because
it was either not saved or not aged. Dark or red
urine is not mentioned in the published van Gogh
letters but this really does no damage to the AIP
hypothesis.11
Barker and Estes (1912) were the first to note
that AIP runs in families. The extensive studies of
Waldenstro¨m (1937) in Sweden firmly established
the inherited nature of the disease. The disease
follows an autosomal dominant pattern of inheritance;
if one parent is a carrier then on the average
50% of the children will bear the defective gene
(Kappas et al., 1989). However, the penetrance is
variable, so that in some families only a fraction
of the carriers actually express signs and symptoms
of the disease (Gates, 1946).
Vincent’s mother died at 88, having led a
seemingly healthy life. His father, the Reverend
Theodorus van Gogh, died at 63; his studies
for the church had been interrupted by serious
illness; he was judged not to have been in
very good health most of his life (Tralbaut,
1981). It is believed that he died from a stroke
and, because hypertension is present in over
half of AIP patients (Goldberg, 1985), this
underlying disease would be one of many possibilities
compatible with that cause of death. Of
Vincent’s parents the father may be the more
likely (obligate) carrier of AIP, but this is little
more than an educated guess. He led a careful
and balanced life in his ‘‘post in the wilderness’’
(Tralbaut, 1981) and may have avoided the
Fig. 2. An hydraulic model for the control mechanism in the heme pathway. Details are given in the text.
11Critics of the AIP hypothesis for Vincent have
occasionally pretended that this was a serious deficiency.
It is negative evidence at best but can be
rationalized. Vincent’s accommodations were often
primitive by today’s standards; for example, the
‘‘Yellow House’’ in Arles had no toilet and he used
the facilities at the hotel next door (letter 480). He
relieved himself in the field while painting. Moreover,
even if he encountered reddish urine he may well have
attributed it to blood, given his experiences with
catheters and bougies at The Hague (letter 209).
32 WILFRED NIELS ARNOLD
precipitating factors that affected three of his six
children.
There were numerous exchanges between the
brothers concerning their ‘‘nervous’’ problems. It
is not clear whether Theo’s serious illness at age
19 was related to the expression of AIP-like
symptoms, but certainly by December 1886 (age
29) according to his future brother-in-law,
Andries Bonger, he had ‘‘serious nervous complaints,
so bad that he could not move’’ (Hulsker,
1990, p. 455). Theo seems to have been in reasonable
health at the time of Vincent’s funeral. But
two months thereafter Theo suffered further leg
pains and also hallucinations (partly in response
to an unspecified medicament for his cough),
became very irritable and occasionally violent,
muttered with difficulty in mixed languages,
experienced urine retention, and was totally
unconscious with a barely detected pulse before
he died (aged 34) (Rewald, 1986, p. 69; Hulsker,
1990, p. 455). Leg pains, mental illness, and
paralysis would all support a diagnosis of AIP,
and the violent reaction to a new drug and renal
failure would be in accord with AIP (Arnold,
1992). On the other hand the reversibility of the
leg pains does not support the diagnosis of neurosyphilis
offered by Dr. Frederik van Eeden.12
Vincent’s youngest sister, Wil., spent the latter
half of her 79 years in an asylum for psychiatric
cases. She may also have suffered from AIP,
although the lack of further documentation makes
her case much more speculative. The youngest
brother, Cor, died at 33 in South Africa from an
accident while feverish; it may have been a
suicide. Again, the medical history is scant. His
other sisters, Elizabeth and Anna, lived 77 and 75
years respectively, without any indication of medical
crises (Arnold, 1992).
Loftus and Arnold (1991) and Arnold (1992)
discussed the differential diagnosis of Vincent van
Gogh in favor of acute intermittent porphyria. We
hoped that the facts would speak for themselves
and that informed readers would have no difficulty
in rejecting other hypotheses.13 In the decade
that followed there was no new hypothesis,
but we encountered ongoing competition from
several old ones, whose authors were occasionally
quite vocal via the popular media. It is beyond the
scope of this review to look back on more than a
selection of these.
VINCENT AND EPILEPSY?
Epilepsy is defined as a paroxysmal (sudden and
recurring) transient disturbance in brain function
that is manifested by episodic impairment or loss
of consciousness, abnormal motor phenomena,
psychic or sensory disturbances, or perturbation
of the autonomic nervous system. The derivation
of the word is Greek; it means seizure. Accordingly,
the term epileptic seizures is redundant, but
common parlance. Another basic term is convulsion,
which means a violent involuntary contraction,
or series of contractions, of the normally
voluntary muscles. Niedermeyer (1983) emphasized
that epilepsy is not a disease but rather an
abnormal reaction of the brain due to numerous
causes. Several diseases and conditions are complicated
by seizures and convulsions. They may
accompany withdrawal from alcohol or barbiturates
and attend uremia. Other acute illnesses
which present with seizures include hyponatremia,
thyrotoxicosis, the acute porphyrias, and
hypoglycemia. Lead and arsenic are the most
frequently encountered metallic intoxications
which cause convulsions.
Tonic-clonic convulsions were not described
by Vincent or his doctors, so grand mal seizures
have never received much diagnostic support.
Petit mal or absence seizures (a brief lapse in
12Theo died at Willem Arntsz Stichting, near Utrecht,
on January 25, 1891. The local diagnosis was
neurosyphilis. This item was discovered 100 years
later by Dr. A. Pietersma, Archief Dienst Gemeente,
Utrecht.
13‘‘Informed readers’’ turned out to be a bigger
assumption than anticipated. A fatuous example came
from an East-Coast psychiatrist who wondered if the
subsequent lack of reference to our work ‘‘is related to
it being published in The British Medical Journal, a
journal that is not widely read in the U.S. and your main
thesis being published in a monograph’’ (private
correspondence).
THE ILLNESS OF VINCENT VAN GOGH 33
consciousness usually no longer than twenty
seconds) are certainly not indicated. Thus the
classical sorts of epilepsy, which were well understood
in Vincent’s time, were hardly indicated.
For this reason I agree with Tralbaut (1981) that
Dr. Peyron’s unqualified diagnosis of ‘‘epilepsy’’
in the St. Re´my register was based upon the
patient’s preconceived, ill-informed view.14
If indeed Drs. Rey and Urpar (Arles), and
Peyron (St. Re´my) were convinced that Vincent
van Gogh had some sort of epilepsy, then why
wasn’t he treated for it?15 Admittedly the available
therapy was meager, but Vincent was not even
treated symptomatically at St. Re´my, and no advice
along those lines was passed on to Paris when
Vincent departed. Contrast Vincent’s casewith that
of Fyodor Dostoevsky (1821–1881) who wrote, on
June 17, 1863, ‘‘I go to Paris and Berlin . . . only for
consultation of specialists (Trousseau in Paris,
Romberg in Berlin) for my epilepsy’’ (Voskuil,
1983, p. 665). If they really thought he had epilepsy,
it is curious indeed that Vincent, a quarter of
a century later, was not referred to an epilepsy
specialist at Montpellier or Paris!
As early as the 1870’s, Hughlings Jackson had
described certain hallucinations with seizures that
he related to a pathologic condition of the temporal
lobe (Jackson, 1931). Later, so-called ‘‘psychomotor’’
seizures were well described (Gibbs
et al., 1937). In the 1950’s the anatomical adjective
‘‘temporal lobe’’ was again preferred, even
though some other parts of the brain were sometimes
involved (Penfield & Jasper, 1954). Today,
these are all lumped under complex partial seizures
(Gastaut, 1970). Dr. Edgar Leroy, who
worked at St. Re´my Asylum, albeit many years
after van Gogh’s sojourn, and Dr. Victor Doiteau
considered that Vincent was epileptic but found
no evidence of aura or frank convulsions and
suggested temporal lobe epilepsy (Doiteau &
Leroy, 1928). See also Vinchon (1960).
A diagnosis of temporal lobe epilepsy might
explain Vincent’s hallucinations, the episodic
nature of his illness, and the interictal periods of
normalcy. However, the usual duration of minutes
or hours that attends the various forms of complex
partial seizures does not fit the days and weeks of
Vincent’s crises. More importantly, epilepsy does
not accommodate the numerous gastrointestinal
complaints. Likewise, some of the factors which
exacerbated his illness such as malnutrition and
fasting are not noted for inducing temporal lobe
epilepsy.
Drug therapy in the 1880’s was limited, but
Vincent’s fits and confusion (letter W11) seem to
have been controlled in Arles by bromide (letter
574), which would be indicated for absinthe intoxication
or acute intermittent porphyria, but not for
temporal lobe epilepsy. Bromides are effective
against grand mal and simple partial seizures but
not for complex partial seizures (Hemphill, 1961;
Niedermeyer, 1983). Monroe (1978, 1992) noted
that the limbic system is exquisitely sensitive to
stress and external toxins including alcohol, and he
remarked on Vincent’s affinity for absinthe. This
was rediscovered by Blumer (2002), who was
adroit in avoiding all the data on van Gogh that
did not fit temporal lobe epilepsy.
MANIC-DEPRESSIVE ILLNESS
(BIPOLAR AFFECTIVE DISORDER)?
The assumption made by some commentators that
manic-depressive psychosis was unknown in
Vincent’s day is incorrect. Falret (1854) had
described so-called ‘‘circular’’ insanity in which
mania and melancholia alternated at regular intervals.
Note that the term melancholia was still
used, but the meaning was by then approaching
a modern definition of depression.16 The same 14Tralbaut felt that the doctors at Arles and St. Re´my
were sympathetic to van Gogh’s suffering but not
particularly interested in taking a complete medical
history. My impression is that they were completely
baffled by Vincent’s illness.
15Claims (Gastaut, 1956) that Felix Rey (a young intern
still in training) was ahead of his time, and that his
friend Aussoliel was a local expert on ‘‘masked
epilepsy,’’ are not convincing.
16The first good description of a relationship between
mania and melancholia came from the Englishman
ThomasWillis (1621–1675), who mentioned that ‘‘one
can change into the other . . . this cyclic disorder is like a
burning object, one that can produce smoke or flame’’
(Willis, 1672; Finger, 2000).
34 WILFRED NIELS ARNOLD
year, Baillarger (1854) also wrote about these two
states, and also included an intercalated period of
normalcy as an integral part of the syndrome. It
should be mentioned in passing that Dr. Paul
Gachet attended lectures by both Falret and
Baillarger.17 A protracted dispute over priority
ensued, although it would seem that Baillarger’s
‘‘double-form’’ disease was closer to our present
concept (Kra¨pelin, 1921) of manic-depressive
psychosis or bipolar disorder.
The French Academy of Medicine had major
meetings on the subject starting in 1880. How
well it was recognized, received, or dealt with in
Arles and St. Re´my in 1889 and 1890 is an open
question, especially as to the intent of Drs. Urpar
and Peyron when they used the term acute mania.
I am inclined to think that they were referring to
the December 1888 events in and around the earcutting
incident and Vincent’s first hospitalization,
and then the complaints of neighbors about
Vincent’s drinking sprees which led to his readmission
to the Arles hospital in 1889. If that is
true then it was ‘‘old fashioned’’ mania a la
Pinel.18 By 1900 mania had assumed its present
psychiatric meaning of a mood disorder characterized
by expansiveness, elation, agitation,
hyperexcitability, hyperactivity, and increased
speed of thought and speech (flight of ideas).
Up until the beginning of the 19th century, the
prime meaning of melancholia was intensity of
idea, the image of the mind being strongly fixed
on, and frequently returning to, a single set of
ideas, to an extent that was deemed unhealthy.
The connotation of sadness was not always present,
and many forms of behavior that have little
relationship (from our perspective) were included
in the general class of melancholia. Not surprisingly
there was even a ‘‘productive melancholia’’
that today might be more akin to intense, creative,
concentrated thinking directed at a particular
problem, while excluding all day-to-day distractions
(monomania). Thus melancholia moved
through monomania to depression and it is
difficult to gauge how far Dr. Peyron had
progressed.19
Perry was probably the first to discuss manicdepressive
psychosis as a diagnosis for Vincent
van Gogh; her expression was ‘‘cyclothymic personality
with episodes of depression and mania’’
(Perry, 1947, p. 171). In the opinion of Hemphill,
‘‘van Gogh was a manic-depressive who developed
confusional episodes and fits in the last two
years of his life due to the toxic action of thujone,
the active agent of absinthe’’ (Hemphill, 1961,
p. 1084). Hemphill’s contribution was twofold;
he was the first to correctly refer to Vincent’s
‘‘epilepsy’’ as a disorder rather than a disease, and
he stressed the evidence for a toxic psychosis. He
supposed that the gastrointestinal complaints
came from the absinthe abuse alone, whereas
Arnold and Loftus stress van Gogh’s sensitivity
to absinthe (and other xenobiotics) due to the
underlying disease of acute intermittent porphyria.
Other writers have marched Vincent down
the bipolar trail but have discovered nothing new
since Hemphill (1961).
Manic depressive illness is widely diagnosed
today and a significant part of the pharmaceutical
industry is devoted to discovering further chemical
assists for the sufferers. These patients are
rarely aware of their states and ordinarily do not
check themselves into hospitals. Their disorders
do not have acute onsets and offsets and the time
course of van Gogh’s illness certainly does not fit
that syndrome. However, it is common enough
for artists and museum patrons to know, or
think they know, something about the syndrome
and someone in their immediate circle who has
it. Proponents of this working hypothesis exploit
this statistical swell even though they should
be arguing about the illness of just a single
individual, Vincent van Gogh.
17The title of Dr. Gachet’s thesis was E ´ tude sur la
Me´lancolie (Gachet, 1858). The work was written in
1858, in the middle of this transition period in
terminology. His thesis was really a compendium of
principles for moral treatment of the insane, spiced with
a philosophical vitalism that he encountered at the
Montpellier Medical School (Fabbri, 1966).
18In Pinel’s book (1818), mania was a disorder of one or
more faculties with sad, gay, extravagant or raging
affect, but always included blind aggression.
19The´ophile Peyron (1827–1895) made his first medical
career in the navy and then settled in Marseille as
an oculist. His appointment as director at the asylum
of St. Re´my may have been a semi-retirement position,
as Vincent hinted (letter 593).
THE ILLNESS OF VINCENT VAN GOGH 35
A course of regular cycling between mania and
depression, which is popularly held, is rarely
observed (Sarwer-Foner, 1966). On the average
there are nine to ten depressive episodes for every
manic event. A histogram of overall frequency
versus age-of-onset for manic-depressive patients
[n¼898] peaked with the 15–19 year group, and
was closely followed by the 20–24 year group
(Goodwin & Jamison, 1990). Notwithstanding
considerable searching, biochemical and genetic
markers for bipolar affective disorder have yet to
be found.
It has been widely observed that many creative
people had illnesses that were serious, debilitating,
and sometimes limiting to their productivity.
The majority opinion is that these men and
women were successful in spite of illness, and
not because of it. It is also true that many creative
people enjoyed robust and healthy lives.20 During
the 18th and 19th centuries there lived an unfortunate
philosophy relating the fevers of tuberculosis
to activities on a higher plane. This romantic
notion has now fallen by the wayside, but during
the last twenty-five years manic depressive psychosis
has popped up and down as a fashionable
disease of association with creativity.
Andreasen (1987) evaluated 30 faculty members,
over a 15-year period, at an American
university workshop for creative writing. She
claimed that the writers had a substantially higher
rate of mental illness compared with 30 control
subjects matched on sociodemographic grounds.
A higher rate of affective disorders, especially
manic depressive psychosis, was reported for the
so-called creative group as well as their firstdegree
relatives. Jamison (1989) reported that
38% of a British group consisting of 39 writers
and 8 artists, which she deemed outstanding, had
sought treatment for some form of affective disorder,
especially manic depressive psychosis,
compared with lifetime prevalence rates in that
nation of about 6%. Her attempts to link hypomanic
episodes and seasonal mood swings with
productivity were unconvincing. Rothenberg
(1990) criticized both the Adreasen study and
the Jamison follow-up on the grounds that little
consideration was given to the subjects’ reasons
for participating in the studies, and the criteria for
judging them creative were left unexplained.
Furthermore, Andreason’s self-reliance on evaluation
of relative mental health was potentially
biased because the subjects and controls were
already known to her. And Jamison built her case
on the subjects’ own reports of seeking medical
treatment.
Goodwin and Jamison (1990) came up with a
list of people they judged to have been creative
together with an indication (opinion) that they
suffered from manic depressive illness. The cautious
message from all of this should be that such
a debilitating condition is still compatible with
creativity, but in some circles there has been an
inference of causality.21 For example, Jamison’s
book on manic depressive illness and the artistic
temperament (Jamison, 1993) certainly leaves the
reader with the indication that the creative are
more susceptible to manic depressive illness than
the normal run of people, and the impression that
a sort of Faustian bargain is at play.
SCHIZOPHRENIA?
Progressive changes in content and style have
been observed in the work of artists who are
deemed to have schizophrenia (Prinzhorn,
1972). The reverse – namely to see the psychosis
in unknown artists by looking at their work – is
obviously more difficult, but not sufficiently
daunting to inhibit the proponents of schizophrenia
for Vincent van Gogh. Such was the approach
of Jaspers (1922), who is still quoted under this
heading.
Vincent had hallucinations, and he also had at
least one episode of paranoia when he thought
that neighbors were trying to poison him in Arles,
but these are not specific for schizophrenia.
The progressive deterioration of the untreated 20There have been some futile attempts at constructing
ratios. My friend Don Goodwin accused them of
playing a ‘‘floating’’ game – as they found more
candidates to be healthy they would add others to the
numerator by sticking them with illness labels.
21There is also some overlap here with Dr. Gachet’s
thesis list of outstanding individuals who suffered from
melancholia (Gachet, 1858, pp. 9–22).
36 WILFRED NIELS ARNOLD
schizophrenic is lacking in van Gogh. Perry
remarked that ‘‘[Vincent] did notwithdraw from
the world; he was cast out because of his
behavior’’ (Perry, 1947, p. 162). The schizophrenic
has a decrease in affect whereas Vincent’s
letters and pictures were surcharged with emotion.
Hemphill (1961) saw no sign of schizophrenia
in the artist and emphasized that there was
never any fantasy formation, and that his letters
were lucid and logical. There is no case for
schizophrenia (Arnold, 1992).
NEUROSYPHILIS?
Syphilis can be acquired either congenitally or,
most often, by sexual contact with an infected
individual. The primary stage is remarkably free
of systemic signs, the patient is entirely well and
usually free of fever but, at about 1–12 weeks
after contact, 50% of females and 70% of males
develop a primary lesion (chancre) at the site of
infection by the spirochete Treponema pallidum.
In the secondary stage, at 2–12 weeks after the
primary stage, a skin rash appears. Constitutional
symptoms that may accompany secondary syphilis
include fever, weight loss, malaise, and anorexia.
There follows an asymptomatic latent stage
that may last decades. About 30% of untreated
patients go on to develop tertiary lesions, but
clinical disease occurs in only half of these cases;
this fraction is 15% overall. About 80% of the
tertiary lesions affect the cardiovascular system,
10% are chronic focal inflammations (gummas) in
the liver and other sites, and up to 10% involve the
central nervous system (neurosyphilis), i.e. 1.5%
overall (Robbins, 1957).
The major clinical categories of symptomatic
neurosyphilis are meningovascular and parenchymatous
syphilis. The latter includes tabes dorsalis,
characterized by degeneration of the posterior
columns of the spinal cord and posterior spinal
roots. The interval from infection to expression of
symptoms is about 27 years. Another form of
parenchymatous syphilis, general paresis of the
insane, is associated with direct invasion of
T. pallidum into the brain. For unknown reasons
the syndrome is more common in males. The
average interval from infection to onset of general
paresis is 20 years. The course of the untreated
disease is inexorably progressive (Goodman &
Karakuis, 1988).
Neither the gamut of his symptoms nor the
time course of his crises fits neurosyphilis.
Vincent was treated for gonorrhea in The Hague
in mid-1882 at age 29. He may have had a
recurrence in Antwerp in 1885-86, at age 32.
Even if he had contracted syphilis in The Hague,
the major crises in Arles (age 35) would have
been extraordinarily early for the onset of neurosyphilis,
and his lengthy remissions from illness
also negate the possibility. Mercury treatments
were used at Arles and St. Re´my for syphilis, but
Doiteau and Leroy (1928) found no indication
that Vincent received mercury.
LEAD POISONING
About one-third of patients with excessive exposure
to lead suffer colicky, abdominal pain.
Fatigue, joint pains, headache, and irritability
are also quite common. Impotence, constipation,
vomiting, diarrhea have all been observed to some
extent. Subtle effects on personality, memory, and
learning ability are frequently associated with
chronic lead poisoning. However, seizures and
confusional states are less common, especially in
adults (Dagg et al., 1965; Ellenhorn & Barceloux,
1988).
Lead may be the oldest recognized chemical
toxin; reports of occupational lead poisoning date
to ancient Greece, and toxic levels have been
found in Egyptian mummies. Artisans of leadglazed
pottery and stained glass were particularly
susceptible to intoxication until better conditions
were adopted in the workplace. The ingestion of
paints containing lead pigments has, even in
recent times, presented a serious health hazard
for children. Artists and craftsmen were exposed
in the past because of their habit of wetting
brushes orally and their accidental ingestion of
lead-containing pigments from their tools and
hands.
Lead has an affinity for functional sulfhydryl
groups in enzymes generally and a particularly
sensitive example is d-aminolevulinic acid dehydratase.
This is enzyme number two in the heme
THE ILLNESS OF VINCENT VAN GOGH 37
biosynthetic pathway and its inhibition accounts
for excessive excretion of d-aminolevulinic acid
in the urine of lead-intoxicated patients. The last
enzyme in the pathway, ferrochelatase, which
catalyzes the incorporation of iron into protoporphyrin
to form heme, is also inhibited by lead and
this also contributes to the observed anemia
(Ettenhorn & Barceloux, 1988). The excessive
production of d-aminolevulinic acid in lead poisoning
is similar to that found in acute intermittent
porphyria, but note that porphobilinogen does
not accumulate in lead poisoning. The similarity
in neurological symptoms between AIP and lead
poisoning may be referable to d-aminolevulinic
acid.
Abdominal pain, constipation, vomiting, paralysis,
or paresis are very common in both AIP and
lead poisoning. Neuropsychiatric symptoms are
sometimes observed with lead intoxication, but
much less frequently than in acute intermittent
porphyria (Sassa, 1978). There was no chelation
therapy for lead poisoning in Vincent’s time, and if
his ingestion of lead salts (from his pigments) had
been chronic, then the time course of such an illness
would have been relentless and not episodic, as is
well documented for van Gogh.
ALCOHOLISM
The extent of Vincent’s drinking is difficult to
define, but we do know that he admitted to
excesses. It is assumed that the hospital in Arles
and the asylum at St. Re´my endeavored to restrict
alcohol consumption; how successful they were is
open to question; we do know that Theo paid a
little extra at St. Re´my so that his brother could
have wine with meals. I am convinced that Vincent
engaged in ‘‘social’’ drinking when he visited
friends in Arles, but this was for a relatively short
time of a day or so. The time course of his illness,
and the duration of some of the crises in the
asylum, do not fit alcohol withdrawal syndrome
per se.22 I believe it was more of a sensitivity to
alcoholic beverages than an extraordinary dose.
Alcohol is a an exacerbating factor for acute
intermittent porphyria. Alcoholism and lead poisoning
are reasonable suggestions but not standalone
syndromes for van Gogh – it is even less
likely that the medical problems of Theo and
sister Wil. would find much accommodation here.
ME´NIE`RE’S DISEASE
In 1861, Prosper Me´nie`re published several
papers relating his observations on afflictions of
the inner ear which caused nausea, vomiting, and
vertigo. The disease was subsequently named
after him and is characterized by hearing loss,
vertigo, and tinnitus (ringing in the ears), and is
usually unilateral (Harker & McCabe, 1980).
During an attack of vertigo the patient is completely
oriented to his surroundings and has no
neurologic deficit such as paresthesia, diplopia,
loss of consciousness, weakness, or paralysis.
Sounds are distorted in the affected ear and are
perceived as ‘‘tinny.’’ Loud sounds are intolerable
or even painful, and hearing acuity gradually
declines.
Yasuda (1979) wondered in print, ‘‘Was van
Gogh suffering from Me´nie`re’s disease?’’ The
twelve page article was published in Japanese,
but contains a full two pages of introduction and
summary in English, more than enough to grasp
the author’s thrust. Those speculations received
little support twenty years ago, because the diagnosis
of Me´nie`re’s disease was based on a limited
selection of symptoms. This dubious diagnosis
was a sincere attempt, but it received little attention
subsequently, except to be recorded in the
most comprehensive bibliographies.
The Journal of the American Medical Association,
during the week of the centenary of Vincent
van Gogh’s death, declared that, ‘‘Van Gogh had
Me´nie`re’s disease and not epilepsy’’ (Arenberg
et al., 1990). It was wrong on both counts; there is
no case for Me´nie`re’s disease and epilepsy was no
longer even the diagnosis of merit. A Colorado
ear specialist and his colleagues had rediscovered
Yasuda’s hypothesis and rewrote it as a definitive
diagnosis. Their conclusion was based on a limited
selection of symptoms, the pretense that
22Alcoholic seizures (rum fits) and delirium tremens
occur after a heavy drinking bout. It is the signs that
attend withdrawal that have some overlap with
Vincent’s illness.
38 WILFRED NIELS ARNOLD
epilepsy was the only viable alternative, and their
propensity for construing certain complaints as
hallmarks of the ear disease. Thus van Gogh’s
gastrointestinal problems were taken to be strictly
nausea and vomiting, several references to hearing
voices were relegated to tinnitus, and the
psychosis that was grave enough to cause selfmutilation
and eventual suicide was underplayed.
Their claim that van Gogh severed the lower half
of his left ear to relieve tinnitus must surely strike
readers, if not the editors of JAMA, as misplaced
surgery.23
TOKENS
There are many other working hypotheses by
authors who are distinguished more by their
conviction than common sense. Call-in talk shows
on the radio are frequently their birthplace.
Shortly after the publication of my book I encountered
‘‘borderline personality disorder’’ for van
Gogh, which may be the exemplar for this type of
offering. I thought that the title was enough to
give the concept away but, to my astonishment,
literature searches now turn it up in the form of
published papers. The ‘‘replacement child’’ sentiment
is another one in the same vein.24 I would
continue to encourage organized skepticism as the
first test.
THE CHARM OF THE PAST
There is an informal group that is keen to applaud
the diagnostic skills of Vincent’s attending physicians.
‘‘The old guys had it right after all’’ is
their banner. In their sea of indecision (sincere or
deliberately compounded) this affords an island
of safe haven blessed with nostalgia.25
Some have said that Dr. Rey (Arles) was
brilliant and insightful. Their circular argument
goes as follows: Rey embraced ‘‘epilepsy’’ without
evidence of a full-fledged case; the commentators
believe temporal lobe epilepsy (described
many years later) is an attractive possibility;
therefore they say Rey was ahead of his time. I
join those who have judged Dr. Peyron as naive
and trained in the wrong specialty, yet others have
embraced as gospel his terse statements in the St.
Re´my register. Tralbaut (1981) felt that the physicians
of the south were overly influenced by the
police reports in Arles, and by the patient’s own
statements about a family history of epilepsy on
his mother’s side. If so, then the circle was indeed
completed when Vincent wrote to Theo, ‘‘as far as
I can make out, the doctor here [Dr. Peyron] is
inclined to consider what I have had [was] some
sort of epileptic attack’’ (letter 591).
Theo van Gogh died in a mental institution in
Den Dolder on January 25, 1891. Some of their
medical records were released to Dutch newspapers
in 1990, by a local archivist. The story,
which covered the 38 days from Theo’s move out
of Paris to Den Dolder until his death, ends
dramatically, ‘‘the final diagnosis was dementia
paralytica [general paresis, a form of neurosyphilis].’’
At last the answer was out! Perhaps
Vincent had the same thing?26
Dementia paralytica was described by Bayle,
as early as 1822. Quincke is credited with introducing
the lumbar puncture procedure together
23I have only one pleasant memory of this fiasco. While
in Brisbane, Australia, as a guest for their van Gogh art
exhibition in 1994, I was taken by a friend I have known
since primary school to a beer garden. There he insisted
on introducing me to everybody, eventually including a
fellow in short pants and a singlet who was bouncing
from table to table selling lottery tickets. ‘‘Dr. Arnold is
here for the big van Gogh affair, he is going to lecture
tomorrow on van Gogh’s illness.’’ We were both
surprised by the smile of hidden wisdom and, ‘‘I know
mate, it’s Me´nie`re’s disease, my uncle had it.’’ Alas, the
misplaced power of immediate experience – others
have seen this in connection with manic depressive
illness.
24The facts do not support the thesis (Arnold, 1995).
However, it is even more bizarre to read that this sort of
thing has been projected in some quarters as the crux of
van Gogh’s underlying illness.
25In another setting the same group would supposedly be
happy enough to acknowledge the laboratory developments
that have advanced 20th century medicine.
26For reasons that still escape me the art politicians of
Holland act as if the label of syphilis for the van Gogh
brothers carries less social stigma than say alcoholism,
let alone an inherited metabolic disease. Is this a
misplaced attempt to ‘‘protect’’ the van Gogh family?
THE ILLNESS OF VINCENT VAN GOGH 39
with examination of the cerebral spinal fluid for
spirochetes, in 1892. Today, a definitive diagnosis
would be based on serology of the cerebral spinal
fluid, but this technology was not available until
well into the twentieth century. General paresis
was overly diagnosed in the nineteenth century.
The psychiatric and neurological symptoms
recorded from Theo’s case are far from definitive.
An autopsy examination could have provided
confirming evidence but apparently was not performed.
In any event, the time course of Theo’s
illness makes the case for neurosyphilis highly
unlikely (Arnold, 1992).
Dr. Paul Gachet also inherited his share of
golden admiration. His ideas about Vincent’s
illness are supposed to have included ‘‘turpentine
poisoning and the effects of too intense sun
on a Nordic brain’’ (Beer, 1935, p. 40). I have
not been able to confirm the attribution to Dr.
Gachet but I assume some verbal anecdote that
slipped into the van Gogh literature. Vincent
himself remarked upon being ‘‘dazed with the
sun’’ (letter 512) that ‘‘beats down on one’s
head . . . [and] makes one crazy’’ (letter B15).
Vincent may have been a bit reckless in his
exposure but there was certainly more to his
illness than heatstroke. The time course and the
rest of the symptomatology cannot be accommodated
under this heading.27
Rey, Peyron, and Gachet did their best to
protect and rehabilitate the artist during those
demanding two years. My observations within
this section are not intended to disparage the
van Gogh physicians but rather to make an appeal
for placing their relative merits in perspective.
They had the advantage of being there, but they
were without benefit of the biochemical tools that
we now take for granted.
RESISTANCE FROM ART
HISTORIANS, CURATORS, DEALERS,
AND THE STATE MUSEUMS
The art world harbors some people who deny any
interest in van Gogh’s underlying illness. This position,
albeit at odds with the public, takes various
forms.Thus a catalog essaymay either skip over the
subject or be content with ‘‘he died by his own hand
in 1890.’’ During themonths of one blockbuster exhibition
the museum’s education department managed
to dodge a public lecture onVincent’smedical
problems in favor of one recounting the provenance
on the painting that fetched the best price at auction.
Moreover, the vehemence with which so many
art curators and dealers resist scientific enquiry
suggests an unwholesome desire to maintain the
mystique in order to protect the art.28 They do an
injustice by assuming that the ‘‘consumer’’ of art
needs ‘‘protection.’’ On the contrary, I believe that
an explanation of Vincent’s underlying illness and
the role of the environmentwill enhance rather than
diminish genuine interest in van Gogh’s creations.
The commercial interests of dealers and the
ambitions of museums with regard to van Gogh
foster the titillating connection between creativity
and madness. Even if they are privately persuaded
otherwise, they are reluctant to change something
that they think is ‘‘working.’’ Newspaper and television
journalists are reluctant to engage them on
that turf and surely that is part of the reason for
perpetuating the lengthy lists of possible van Gogh
illnesses. They want to keep the subject vague in
order to maintain the mythology.
CONCLUDING REMARKS
The house of Dr. Paul Gachet in Auvers-sur-Oise
was recently opened to the public to coincide with
27I do not mean to defeat the message of this section but
consider the following from an AIP expert, ‘‘exposure
to oil-based paints and solvents will, in some
porphyrics, produce symptomatology including psychosis,
colic, seizures, and neuropathy. Very rarely in
acute porphyria, extreme exposure to sunlight may
provoke an attack’’ (Peters, 1986). Bonkovsky and I
showed that pinene (turpentine) is porphyrogenic – but
sunlight! Was the good Doctor Gachet blessed?
28A curator at the Boston Museum of Fine arts once told
me that he could not understand why anyone was
interested in van Gogh’s illness. I ventured that at least it
had something to do with his premature demise. No
response, so I volunteered that Picasso and Matisse could
have been contemporaries with Vincent if he had enjoyed
a predicted lifespan of about 66 years – how wonderful it
would have been to have those three guys in the same
room? ‘‘Van Gogh painted lots of pictures anyway.’’
40 WILFRED NIELS ARNOLD
the 150th anniversary of the birth of his most
famous patient. Willem van Gogh, a greatgrandnephew
of Vincent van Gogh, was in the crowd
and he said he was touched to be present (New
York Times, April 1, 2003). For those of us
interested in round numbers it is also a propitious
time to review the medical problems of the artist.
A careful review of data from the artist’s letters
and other contemporary sources indicates that
Vincent suffered from an inherited disorder manifested
by severe and manifold neurological problems,
ranging from gastrointestinal pains to fits
with hallucinations. His condition was exacerbated
by his modus vivendi, which was marked by
inadequate nutrition, abuse of alcoholic beverages,
chronic smoking, environmental exposure, and the
development of an abnormal affinity (pica) for
terpenes. The intermittent nature of his illness,
the sudden onset of crises, and the rapid return to
normalcy after each episode, are all notable. The
gamut of symptoms is best explained by a toxic
psychosis. Within that category, the disease entity
which most closely fits all of the data is acute
intermittent porphyria [AIP], which was adopted
by Loftus and Arnold (1991) and Arnold (1992) as
a working hypothesis for Vincent’s underlying illness.
This retrospective diagnosis has been compared
and contrasted with other suggestions in the
literature. The first case was described in a Dutch
medical journal (Stokvis, 1889). AIP was not
understood in Vincent’s time; even today it tends
to be under-diagnosed. I am convinced that a toxic
psychosis such as acute intermittent porphyria
remains the best working hypothesis.
Vincent van Gogh was not a ‘‘mad’’ artist, but
rather an exceptional man who suffered from an
inherited disease. He was wonderfully creative
because of intelligence, talent, and hard work. He
was a genius in spite of his illness – not because of
it. This reality enhances wholesome admiration for
van Gogh’s creations.
REFERENCES
Andreasen NC (1987): Creativity and mental illness:
prevalence rates in writers and their first-degree
relatives. Amer J Psychiat 144: 1288–1292.
Andreasen NC, Glick ID (1988): Bipolar affective
disorder and creativity: implications and
clinical management. Comp Psychiat 29:
207–217.
Arenberg IK, Countryman LF, Bernstein LH,
Shambaugh GE (1990): Van Gogh had
Me´nie`re’s disease and not epilepsy. JAMA 264:
491–493.
Arnold WN (1988): Vincent van Gogh and the thujone
connection. JAMA 260: 3042–304.
Arnold WN (1989): Absinthe. Sci Am 260: 112–117.
Arnold WN (1992): Vincent van Gogh: Chemicals,
Crises, and Creativity. Boston, Basel & Berlin,
Birkha¨user.
ArnoldWN(1995): Vincent van Gogh’s birthday. Pharos
Alpha Omega Alpha Hon Med Soc 58: 28–32.
Arnold WN, Loftus LS (1991): Xanthopsia and van
Gogh’s yellow palette. Eye 5: 503–510.
Baillarger JGF (1854): De la folie a` double-forme. Ann
Med Psychol 6: 367–391.
Barker LF, Estes WL (1912): Family hematoporphyrinuria
in association with chronic gastroduodenal
dilation, peculiar fits and acute polyneuritis: a
preliminary report. JAMA 59: 718-719.
Beer J (1935): Essai sur les rapports de l’art et de la
maladie de Vincent van Gogh. (The`se, Doctorat en
Me´decine), Strasbourg: Elie Mazel.
Bickers DR, Miller L, Kappas A (1975): Exacerbation of
hereditary hepatic porphyria by surreptitious ingestion
of an unusual provocative agent, a mouthwash
preparation. N Engl J Med 292: 1115-1116.
Blumer D (2002): The illness of Vincent van Gogh. Am
J Psychiatry 159: 519–526.
Bonkovsky HL, Cable EE, Cablew JW, Donohue SE,
White EC, Greene YJ, Lambrecht RW, Srivastava
KK, Arnold WN (1992): Porphyrogenic properties
of the terpenes – camphor, pinene, and thujone;
with a note on the illness of Vincent van Gogh.
Biochem Pharmacol 43: 2359–2368.
Bonkovsky HL, Sinclair PR, Emery S, Sinclair JF
(1980): Seizure management in acute hepatic
porphyria: risks of valproate and clonazepam.
Neurology 30: 588–592.
Dagg JH, Goldberg A, Lochhead A, Smith JA (1965):
The relationship of lead poisoning to acute intermittent
porphyria. Quart J Med 34: 163–175.
Doiteau V, Leroy E (1928): La Folie de Vincent van
Gogh. Paris, Æsculape.
Ellenhorn MJ, Barceloux DG (1988): Medical Toxicology.
New York, Elsevier.
Fabbri R Jr (1966): Dr. Paul-Ferdinand Gachet: Vincent
van Gogh’s last physician. Trans Stud Coll Physicians
Phila 33: 202–208.
Falret JP (1854): Me´moire sur la folie circulaire. Bull
Acad Natl Med 19: 382–415.
Finger S (2000): Minds Behind the Brain: A History of
the Pioneers and Their Discoveries, New York,
Oxford University Press.
THE ILLNESS OF VINCENT VAN GOGH 41
Gachet PF (1858): E ´ tude sur la Me´lancolie.
Montpellier, Montpellier Me´dical.
Gastaut H (1956): La maladie de Vincent van Gogh
envisage´e a` la lumie`re des conceptions nouvelles sur
l’e´pilepsie psychomotrice. Ann Med Psychol 1:
196–238.
Gastaut H (1970): Clinical and electroencephalographical
classification of epileptic seizures. Epilepsia
11: 102–113.
Gates RR (1946): Human Genetics. New York,
Macmillan.
Gibbs FA, Gibbs EL, Lennox WG (1937): Epilepsy:
a paroxysmal cerebral dysrhythmia. Brain 60:
377–388.
Goldberg A (1985): Molecular genetics of acute
intermittent porphyria. BMJ 291: 499-500.
Goodman LJ, Karakusis PH (1988): Neurosyphilis.
In: Vinken PJ, Bruyn GW, Klawans HL, eds.,
Handbook of Clinical Neurology. Amsterdam,
Elsevier, Vol. 52, Chapter 18.
Goodwin FK, Jamison KR (1990): Manic-Depressive
Illness. New York, Oxford University Press.
Harker LA, McCabe BF (1980): Meniere’s disease
and other peripheral labyrinthine disorders. In:
Paparella MM, Shumrick DA, eds., Otolaryngology,
2nd edition, chapter 41. Philadelphia, WB
Saunders.
Hemphill RE (1961): The illness of Vincent van Gogh.
Proc Roy Soc Med 54: 1083–1088.
Hulsker J (1990): Vincent and Theo van Gogh: A Dual
Biography. Ann Arbor, Fuller Publications.
Jackson JH (1931): Selected Writings of John
Hughlings Jackson. London, Hodder & Stoughton.
Jamison KR (1993): Touched With Fire: Manic
Depressive Illness and the Artistic Temperament.
New York, Free Press: Maxwell Macmillan.
Jaspers K (1922): Strindberg und van Gogh. Leipzig,
Ernst Bircher.
Johnson HA (1934): No madman. Art Digest 8: 11.
Kappas A, Sassa S, Galbraith RA, Nordmann Y (1989):
The porphyrias. In: Scriver CR, Beaudet AL, Sly
WS, Valle D, eds., The Metabolic Basis of Inherited
Disease. New York, McGraw-Hill, 6th edition,
pp. 1305–1365.
Knudsen KB, Sparberg M, Lecocq F (1967): Porphyria
precipitated by fasting. New Engl J Med 277:
350-351.
Kra¨epelin E (1921): Manic-depressive Insanity and
Paranoia (Translated by RM Barclay). Edinburgh,
Livingstone, 8th edition.
Laiwah AACY, Mactier R, McColl KEL, Moore MR,
Goldberg A (1983): Early-onset chronic renal
failure as a complication of acute intermittent
porphyria. Quart J Med 52: 92–98.
Lee TC (1981): Van Gogh’s vision: digitalis intoxication?
JAMA 245: 727–729.
Lip GYH, McColl KEL, Goldberg A, Moore MR
(1991): Smoking and recurrent attacks of acute
intermittent porphyria. BMJ 302: 507.
Loftus LS, Arnold WN (1991): Vincent van Gogh’s
illness: acute intermittent porphyria. BMJ 303:
1589–1591.
Lubin AJ (1972): Stranger on the Earth; A Psychological
Biography of Vincent van Gogh. New York,
Holt, Rinehart Winston.
Monroe RR (1978): The episodic psychoses of Vincent
van Gogh. J Nerv Ment Dis 166: 480–488.
Monroe RR (1992): Creative Brainstorms. New York,
Irvington.
Moore MR (1980): International review of drugs in
acute porphyria. Int J Biochem 12: 1089–1097.
Navratil L (1959): Vincent van Gogh: his disease
assessed in the light of his paintings. CIBA Found
Symp 7: 210–216.
Niedermeyer E (1983): Epilepsy Guide. Diagnosis and
Treatment of Epileptic Seizure Disorders. Baltimore
& Munich, Urban & Schwarzenberg.
Penfield W, Jasper H (1954): Epilepsy and the
Functional Anatomy of the Brain. Boston, Little,
Brown and Co.
Perry I (1947): Vincent van Gogh’s illness: a case
record. Bull Hist Med 21: 146–172.
Peters HA (1986): Acute Hepatic Porphyria. In: Johnson
RT, ed., Current Therapy in Neurologic Disease
1985-1986. New York, BC Decker, pp. 317–321.
Pickvance R (1984): Van Gogh in Arles. New York,
Harry N. Abrams Inc.
Pickvance R (1986): Van Gogh in Saint-Re´my and
Auvers. New York, Harry N. Abrams Inc.
Pinel P (1818): Nosographie Philosophique ou la
Me´thode de l’Analyse Applique´e a la Me´dicine.
Paris, Brosson, 6th edition.
Prinzhorn H (1972): Artistry of the Mentally Ill
(Translated by E von Brockdorff). New York,
Heidelberg, Berlin, Springer-Verlag. (Original German
version: Prinzhorn H. 1922. Bildnerei der
Geisteskranken. Berlin: Verlag Julius Springer.)
Rewald J (1986): Theo van Gogh as an art dealer.
In: Gordon I, Weitzenhoffer F, eds., Studies in
Postimpressionism. New York, Harry Abrams Inc,
pp. 7–115.
Ridley A (1969): The neuropathy of acute intermittent
porphyria. Quart J Med 38: 307–333.
Robbins SL (1957): Textbook of Pathology With
Clinical Applications. Philadelphia & London,
WB Saunders Co.
Rothenberg A (1990): Creativity and Madness, New
Findings and old Stereotypes. Baltimore and
London, The Johns Hopkins University Press.
Sarwer-FonerGJ (1988): The course ofmanic-depressive
(bipolar) illness. In: Georgotas A, Cancro R, eds.,
Depression andMania.NewYork, Elsevier, chapter 4.
42 WILFRED NIELS ARNOLD
Sassa S (1978): Toxic effects of lead, with particular
reference to porphyrin and heme metabolism. In: De
Matteis F, Aldridge WN, eds., Heme and Hemoproteins.
Berlin, Springer-Verlag.
Schmidt H (1915): l’Absinthe. l’Alie´nation mentale et
la criminalite´. Rapport fait au nom de la commission
d’hygie`ne publique de la chambre des de´pute´s.
Annales d’Hygiene Publique et de Me´dicine Le´gale
23: 121–133.
Schnier J (1950): The blazing sun: a psychological
approach to van Gogh. Am Imago 7: 143–162.
Sollmann T (1948): A Manual of Pharmacology and its
Applications to Therapeutics and Toxicology.
Philadelphia & London: WB Saunders Company,
7th edition.
Stokvis BJ (1889): Over twee zeldzame kleurstoffen in
urine van zieken. Weekblad van het Nederlandsch
Tijdschrift voor Geneeskunde 2: 409–417.
Tralbaut ME (1981): Vincent van Gogh. New York, The
Alpine Fine Arts Collection.
van Gogh VW (1978): The Complete Letters of Vincent
van Gogh Boston, New York Graphic Society, Vols.
I–III, 2nd edition.
van Gogh-Bonger (1978): Memoir of Vincent van
Gogh. In: van Gogh VW, ed., The Complete Letters
of Vincent van Gogh. Boston, New York Graphic
Society, Vol. I, 2nd edition, pp XV–LIII.
Vinchon J (1960): Diagnostic de la ‘‘folie’’ de van
Gogh. Historie de la Me´decine Communications
pre´sente´es a` Paris a` la Socie´te´ Francaise d’Histoire
de la Me´decine en 1960, pp. 23-24.
Voskuil PHA (1983): The epilepsy of Fyodor
Mikhailovitch Dostoevsky (1821–1881). Epilepsia
24: 658–667.
Waldenstro¨m J (1937): Studien ueber Porphyrie. Acta
Med Scand 82(Suppl.): 1–254.
Waldenstro¨m J (1957): The porphyrias as inborn errors
of metabolism. Am J Med 22: 758–773.
Welland FH, Hellman ES, Gaddis EM, Collins A,
Hunter GW Jr, Tschudy DP (1964): Factors
affecting the excretion of porphyrin precursors by
patients with acute intermittent porphyria. I.
The effect of diet. Metabolism 13: 232–250.
Willis T (1672): De anima brutorum: Oxonii: R. Davis.
Translated by S. Porage. In: Practice of Physick as
Two Discourses Concerning the Soul of Brutes.
London, Dring, Harper, Leigh (1683), Vol. I,
p. 188.
Withering W (1785): An Account of the Foxglove and
Some of its Medical Uses: with Practical Remarks
on Dropsy and other Diseases. Birmingham, GGJ
& J Robinson. (This book was reproduced under
the same general title, with annotations by
Aronson JK (1985): London, Oxford University
Press).
Yasuda K (1979): Was van Gogh suffering from
Me´nie`re’s disease? Otologia Fukuoka 25:
1427–1439.ier J (1950): The blazing sun: a psychological
approach to van Gogh. Am Imago 7: 143–162.
Sollmann T (1948): A Manual of Pharmacology and its
Applications to Therapeutics and Toxicology.
Philadelphia & London: WB Saunders Company,
7th edition.
Stokvis BJ (1889): Over twee zeldzame kleurstoffen in
urine van zieken. Weekblad van het Nederlandsch
Tijdschrift voor Geneeskunde 2: 409–417.
Tralbaut ME (1981): Vincent van Gogh. New York, The
Alpine Fine Arts Collection.
van Gogh VW (1978): The Complete Letters of Vincent
van Gogh Boston, New York Graphic Society, Vols.
I–III, 2nd edition.
van Gogh-Bonger (1978): Memoir of Vincent van
Gogh. In: van Gogh VW, ed., The Complete Letters
of Vincent van Gogh. Boston, New York Graphic
Society, Vol. I, 2nd edition, pp XV–LIII.
Vinchon J (1960): Diagnostic de la ‘‘folie’’ de van
Gogh. Historie de la Me´decine Communications
pre´sente´es a` Paris a` la Socie´te´ Francaise d’Histoire
de la Me´decine en 1960, pp. 23-24.
Voskuil PHA (1983): The epilepsy of Fyodor
Mikhailovitch Dostoevsky (1821–1881). Epilepsia
24: 658–667.
Waldenstro¨m J (1937): Studien ueber Porphyrie. Acta
Med Scand 82(Suppl.): 1–254.
Waldenstro¨m J (1957): The porphyrias as inborn errors
of metabolism. Am J Med 22: 758–773.
Welland FH, Hellman ES, Gaddis EM, Collins A,
Hunter GW Jr, Tschudy DP (1964): Factors
affecting the excretion of porphyrin precursors by
patients with acute intermittent porphyria. I.
The effect of diet. Metabolism 13: 232–250.
Willis T (1672): De anima brutorum: Oxonii: R. Davis.
Translated by S. Porage. In: Practice of Physick as
Two Discourses Concerning the Soul of Brutes.
London, Dring, Harper, Leigh (1683), Vol. I,
p. 188.
Withering W (1785): An Account of the Foxglove and
Some of its Medical Uses: with Practical Remarks
on Dropsy and other Diseases. Birmingham, GGJ
& J Robinson. (This book was reproduced under
the same general title, with annotations by
Aronson JK (1985): London, Oxford University
Press).
Yasuda K (1979): Was van Gogh suffering from
Me´nie`re’s disease? Otologia Fukuoka 25:
1427–1439.


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Organizations around the world unite for Porphyria links

The following organizations have websites in English The American Porphyria Foundation has a very extensive website, including a section ...