Dr. Wilf. Arnold was born in Brisbane, Australia, where he earned a B.Sc. at the University of Queensland. After completing an M.A. degree at UCLA and a Ph.D. (1962) at Cornell University he held various research and teaching positions before coming to the University of Kansas Medical Center (1971). He has published over one hundred papers and a two volume book in biological chemistry. Professor Arnold has also earned an international reputation for bringing the rigor of scientific research to studies of art history and history of medicine. His book, Vincent van Gogh: Chemicals, Crises, and Creativity was published in English (1992) and German (1993) editions. He wrote the lead essay for the exhibition catalog, Vincent van Gogh: his sources, genius, and influence, Art Exhibitions Australia Ltd., (1993) and presented a plenary lecture at the Sigma Xi National Forum, Science, the Arts and the Humanities: Connections and Collisions, (2001). American Chemical Society, Atlantic Seaboard Circuit Lecturer [Virginia Blue Ridge Section, Virginia Military Institute, March 21, 1994; Virginia Section, Longwood College, March 22, 1994; Hampton Roads Section, Old Dominion University, March 23, 1994; Eastern North Carolina Section, Barton College, March 24, 1994.]
The Chemistry of Vincent van Gogh
At the time of his suicide in 1890 the genius of Vincent van Gogh was acknowledged by only a small cadre of friends and followers. His jagged thirty-seven years had been marked by early uncertain¬ties, interludes of luckless love affairs, wrenching episodes of self-mutilation, crises of debilitating sickness, and periods of painful striving for lofty goals. Today, his art is universally recognized. He is on everybody’s list of outstanding artists and in every catalog of creative people. Van Gogh not only had an identifiable syndrome, based on medical signs and the time-course of his illness, but his life-style directly influenced the expression and severity of symptoms, exacerbated his condition, and provoked crises. Such well-documented yet seemingly disparate factors as overindulgence in alcohol (especially as the romantic but toxic absinthe), smoking too much, malnutrition, fasting, environmental exposure, and infections all come together and support a unifying hypothesis of acute intermittent porphyria as the artist’s underlying disease, from which two of his five siblings also suffered. In this PowerPoint presentation the portrait of Vincent van Gogh is not as a mad artist, but rather as an exceptional man who suffered from an inherited metabolic disorder. He was wonderfully creative because of intelligence, talent, and hard work. He was a genius in spite of his illness — not because of it.
Category: Biochemistry, Chemical Education, History of Chemistry, Science Café, Toxicology
King George III’s Urine and Indigo Blue
The Madness of George III was first performed at the Royal National Theatre, London, in 1991. In dramatizing the illness of King George III (1738-1820), Alan Bennett evoked sympathy, titillation, humor — all within a milieu of power struggles. Success led to a film, that was also well received in the U.S. In the final scene two attendants remark upon their King’s return to health and observe that the royal urine which had been blue is now normal. A sentence floats overhead to inform the audience that the King suffered from porphyria, as first proposed by McAlpine and Hunter. The remarkable thing for any student of porphyria is the reference to blue because porphyric urines, after aging, are associated with red, reddish-brown, or purple pigments. However, detailed reading of the literature reveals that on two occasions specimens of bluish urine were actually registered on behalf of the King by Sir Henry Halford (1766-1844). This PowerPoint presentation demonstrates the formation of blue pigment in aged urine as due to the excretion of abnormal amounts of indoxyl sulfate from the patient, the participation of bacterial cells in the collection vessel, and the eventual formation of indigo blue. I reproduced the observations of Sir Henry from 1811 using physiologically-reasonable concentrations of indoxyl sulfate; a common bacterium called Providencia stuartii; and porcelain crucibles to mimic chamber pots. Furthermore, a rational story for the historic blue urine follows from King George III’s suffering from acute intermittent porphyria, accompanied by episodes of severe constipation, as indicated in royal bulletins.
Frédéric Chopin was born near Warsaw, Poland, in 1810 but from 1831 lived mostly in France where he achieved international acclaim for his music in spite of a debilitating and life-shortening illness. He died in 1849 and an autopsy by Dr. Jean Cruveilhier supposedly confirmed tuberculosis of the lungs and larynx, together with cachexia, although written documentation was subsequently lost. Chopin’s body was interred in Père Lachaise Cemetery, Paris, except for the heart which was preserved in alcohol (cognac), sealed in a crystal urn, taken to his native Poland by his sister Ludwika, and sequestered within a pillar of the Holy Cross Church, in Warsaw. In 1987, a novel analysis of the available information led to the suggestion of cystic fibrosis as Chopin’s congenital disease. In 2006, a group of Polish biologists not only adopted this diagnosis but attempted to justify genetic analysis on a sample of Chopin’s heart, “to deepen our knowledge about the great Polish composer, but foremost to give hope and meaning to those who nowadays suffer from genetically inherited disorders.” [To suggest that discovering a famous person with the same disease would bring understanding or solace to current patients seems to me to be a specious argument.] To date, Polish authorities have refused DNA testing on the alcohol-preserved organ. This PowerPoint presentation will show that the clinical and pathological evidence for tuberculosis, a microbial disease, remains much more compelling than that for the genetic disease of cystic fibrosis and this surely adds to the societal and religious arguments that have been expressed against invasive interference with the relic.
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