To the Editor: Julius Caesar (100 to 44 BC) was an orator, conqueror, and political strategist, who brought Rome to the height of its glory. In recent years, many possible causes have been proposed to explain Caesar’s disease: neoplasia, hypoglycemia, and vagus nerve disease. Ultimately, the most recent and accredited hypotheses are those of the development of a neurocysticercosis1 and microstrokes.2 All of these hypotheses appear to have a good basis, starting with epilepsy, which has been considered as a practical possibility for centuries. However, the late onset of the illness discredits this hypothesis (there are no reliable resources regarding seizures that manifest at a young age). Furthermore, one must not forget the military and political position covered by Caesar, who could have benefited from advocating his illness as a manifestation of the so-called “sacred disease.” As for neurocysticercosis, this may have been contracted by Caesar during one of his military campaigns, in particular, the one in Egypt, as tapeworm cystic structures have been found to be present in an Egyptian mummy dating from around the first century BC.3 However, it is difficult for this form to placate with an inherited event (according to various sources, although not of direct descendants, even Britannicus and Caligula appeared to have suffered from nerve and epileptic syndromes). For the latter, modern scholars have suggested that mood swings, as well as epilepsy and hyperthyroidism, may have been factors. Along with these hypotheses, even strokes seem to fit the description handed down by Plutarch concerning the emperor’s illness, which he termed as the suffering from recurrent headaches, and subject to epilepsy: a description that Suetonius added to the late onset of symptoms. Nevertheless, the aforesaid symptoms, together with depression, change of mood, and nightmares (developed in the last years of his life) could be related to celiac disease (CD), even in the absence of gastroenterological disorders. Infact, it has been estimated that about 6% to 10% of the CD patients have such neurological symptoms (neuropathy, ataxia, seizure disorder, and depression) that may also fall outside of apparent gastrointestinal manifestations.4 Meanwhile, other interesting values have been reported in adults in whom there has been a headache—CD association of about 30% as against a control group with an association of only 14%.5 That is not all. This hypothesis may indeed provide an explanation regarding other aspects handed down by Plutarch, which described him as a very pale man of notable thinness, affected by alopecia. It may also provide a possible explanation for the “giddiness,” which prevented him from standing up to praise the senators. Also, neural symptoms induced by a CD could better explain the clarity and the unaltered cognitive abilities that were constantly present up until the end of his life more than the microstrokes. Just as important, it provides a possible explanation for the inheritance of the disease, placing a limit on any doubts of how a vascular complication may arise in a context characterized by a moderate Mediterranean diet, also characterized by an elevated consumption of bread and spelt. This does not resolve the controversy of Caesar’s epilepsy attacks that has lingered on for centuries, but in the face of these new observations, we can rightly include CD among the possible causes of the Emperor’s ailment.
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