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Karl Gebhardt (1897-1948) had a distinguished career as professor of sports medicine before the Second World War. He developed sports for the disabled at a specialised orthopaedic clinic at Hohenlychen and was President of the Red Cross in Germany. During the war, Gebhardt also acted as Heinrich Himmler's personal physician and was responsible for medical experimentation on prisoners in the concentration camps at Auschwitz and Ravensbrück. In his capacity as SS consultant surgeon, he treated Reinhard Heydrich (a high ranking Nazi official, also known as 'the Hangman') after an attempt was made on his life. When Heydrich died, Gebhardt was accused of failing to treat him with sulphonamides. To prove his innocence he carried out a series of experiments on Ravensbrück concentration camp prisoners, breaking their legs and infecting them with various organisms in order to prove the worthlessness of the drugs in treating gas gangrene. He also attempted to transplant the limbs from camp victims to German soldiers wounded on the Russian front. He was tried after the war and executed for these crimes in 1948. This paper explores the paradox of a gifted doctor who was also the perpetrator of inhuman crimes.

This article outlines the history of ergot of rye up to 1900. Ergot is a fungal disease that affects many grasses but is particularly damaging to rye. It occurs as the result of an infection by the parasitic organism Claviceps purpurea, which produces characteristic black spurs on the grass. When incorporated into grain, the ergot fungus can cause severe outbreaks of poisoning in humans called ergotism. There are two main clinical forms of toxicity, gangrenous and convulsive, where coma and death often supervene: the death rate for ergotism has been reported to be between 10 and 20 per cent in major outbreaks. Historical accounts note that ergot could accelerate labour, stop postpartum haemorrhage and inhibit lactation. At the end of the nineteenth century ergot was still regarded as a 'glorious chemical mess', but help would arrive in the early 1900s and the complex jigsaw would be solved.

Queen Maria de' Medici (1573-1642) died in a miserable, marasmic state. Infections, gangrene, weight loss, fatigue and respiratory problems suggest a progressive decompensation of a previously existing Type 2 diabetes. The lack of biochemical data, however, permits only circumstantial evidence of this hypothesis. The author proposes that the queen developed subclinical diabetes after the age of 45, when she became obese due to excessive eating and lack of exercise. With a clear familial predisposition, she could have become insulin resistant and chronically hyperglycaemic. The presence of an internal deviation of the left eye, visible on several late portraits, suggests a mononeuropathy of cranial nerve VI. Repeated skin infections and gangrene of the lower limbs during the last month of her life complete the clinical diagnosis. Hyperglycaemic ketosis with Kussmaul respiration without adequate treatment may have caused her death.