In Allan Ramsay’s portrait of King George III we see a confident, powerful ruler, with no hint of the illness that would beset him later in life. Reigning during the turbulent period of the American Revolution, the “mad” King George was plagued by episodic symptoms that lasted until his death at the age of 81. At the time, royal physicians had little ability to diagnosis or aid their suffering king. Modern medical interpretations of his condition suggest the king had porphyria, an abnormality of the blood that can lead to toxic effects on nerves and the brain. Others have argued that his illnesses were more likely psychiatric, with bipolar disorder one considered theory.
George III is best known to Americans as the king whose army the colonists fought during the Revolutionary War. In Britain, he is perhaps remembered most as the “mad” king who lost the American colonies. King George III certainly suffered from many ailments, including a series of attacks, during his long reign (from 1760 to 1820), most of which at the time were undiagnosed. His first major attack, consisting of severe pains in the stomach, occurred in 1788, continuing over a period of months and resulting in weakness of the limbs and eventually delirium. These problems recurred in 1801 and 1804, and finally again in 1810. The last bout of illness left the king incapacitated, prompting his son the Prince of Wales to take over as regent in 1811. Fortunately for modern scholars, George’s physicians kept detailed accounts of the king’s illnesses and symptoms. Using these notes and other references as their sources, Ida Macaline and Richard Hunter published an article in the 1960s arguing that King George III did not have a primary psychiatric problem. Rather, they argued he suffered from porphyria. However, in more recent scholarship, Timothy Peters and Allan Beveridge posit that the king’s bouts of illness were episodes of recurrent mania, and possibly bipolar disorder.
Allan Ramsay painted this portrait of George III when the king was in his prime. We see him in his finest regalia, dressed in a gold suit with an ermine cloak. Ramsay was appointed the Principal Painter in Ordinary to George III in 1761, completing this portrait shortly thereafter. Many of the portraits painted by Ramsay were used as royal gifts, given to ambassadors and politicians. The full-length portrait shows the king standing (as opposed to seated on a throne or only shown from the waist-up), a pose popularized in the seventeenth century by Diego Velázquez with his portraits of the Spanish King Philip IV and by Anthony van Dyck’s portraits of King Charles I in England.
Porphyria is a collection of genetic disorders stemming from abnormalities in the biochemical pathway that produces heme, the iron containing portion of hemoglobin in the blood. This leads to elevations in the blood levels of other molecules (porphyrins) that usually exist only in small quantities. These abnormally high levels of substances can cause many different symptoms in the skin and the nervous system often in the form of severe attacks with normal periods in-between. Abdominal pain is very common in an attack but given all of the different causes of abdominal pain, porphyria is an exceedingly rare explanation. Patients with porphyria have been known to be incorrectly diagnosed with appendicitis and then undergo an appendectomy only to find that the appendix is normal and healthy. Involvement of the nervous system can be in the brain (confusion, seizures) or the nerves (pain, weakness, constipation, racing pulse). The classic way to make the diagnosis is to leave a patient’s urine sample exposed to light—it may take on a red or brown color. More modern methods involve testing of the blood, urine, and/or feces. Genetic testing is also possible. Treatment is aimed at preventing the attacks.
Macalpine, Ida and Richard Hunter. “Porphyria and King George III.” Scientific American (1969): 38-49.
Peters, Timothy J. and Allan Beveridge. “The madness of King George III: a psychiatric re-assessment.” History of Psychiatry Vol. 21, No. 1 (2010): 20-37.