The ketogenic diet is not a benign, holistic, or natural treatment for epilepsy; as with any serious medical therapy, complications may result. These are generally less severe and less frequent than with anticonvulsant medication or surgery. Common but easily treatable short-term side effects include constipation, low-grade acidosis, and hypoglycaemia if an initial fast is undertaken. Raised levels of lipids in the blood affect up to 60% of children and cholesterol levels may increase by around 30%. This can be treated by changes to the fat content of the diet, such as from saturated fats towards polyunsaturated fats, and if persistent, by lowering the ketogenic ratio. Supplements are necessary to counter the dietary deficiency of many micronutrients.
During the 1920s and 1930s, when the only anticonvulsant drugs were the sedative bromides (discovered 1857) and phenobarbital (1912), the ketogenic diet was widely used and studied. This changed in 1938 when H. Houston Merritt, Jr. and Tracy Putnam discovered phenytoin (Dilantin), and the focus of research shifted to discovering new drugs. With the introduction of sodium valproate in the 1970s, drugs were available to neurologists that were effective across a broad range of epileptic syndromes and seizure types. The use of the ketogenic diet, by this time restricted to difficult cases such as Lennox–Gastaut syndrome, declined further.
The word diet first appeared in English in the 13th century. Its original meaning was the same as in modern English, “habitually taken food and drink.” But diet was used in another sense too in the Middle and early modern English periods to mean “way of living.” This is, in fact, the original meaning of diet’s Greek ancestor diaita, which is derived from the verb diaitasthan, meaning “to lead one’s life.” In Greek, diaita, had already come to be used more specifically for a way of living prescribed by a physician, a diet, or other regimen.