Epilepsy is one of the most common neurological disorders after stroke, and affects around 50 million people worldwide. It is diagnosed in a person having recurrent, unprovoked seizures. These occur when cortical neurons fire excessively, hypersynchronously, or both, leading to temporary disruption of normal brain function. This might affect, for example, the muscles, the senses, consciousness, or a combination. A seizure can be focal (confined to one part of the brain) or generalised (spread widely throughout the brain and leading to a loss of consciousness). Epilepsy can occur for a variety of reasons; some forms have been classified into epileptic syndromes, most of which begin in childhood. Epilepsy is considered refractory (not yielding to treatment) when two or three anticonvulsant drugs have failed to control it. About 60% of patients achieve control of their epilepsy with the first drug they use, whereas around 30% do not achieve control with drugs. When drugs fail, other options include epilepsy surgery, vagus nerve stimulation, and the ketogenic diet.
I believe this is a disservice to those, like me, with a history of eating disorder. It has made experimenting with IF unnecessarily stressful. Despite my worry about what might happen (reading all these baseless cautions), I went ahead and experimented. In my experience, contrary to this “expert advice”, IF has been the most profoundly effective intervention I’ve experienced for my bulemia.
It has totally regulated my appetite and normalised my relationship with food. My obsessive thoughts have completely subsided, my black and white thinking around food has gone, and I no longer binge! This is amazing. For the first time in my adult life I feel like I know what it is like to have a normal relatinoship with food. I eat when I eat, a range of healthy whole foods and occasional less healthy foods. In normal amounts. In manageable amounts. And when my meal is over, I stop! Normal for others, a seeming impossibility for me (and, I’m guessing, others with eating disorders).
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.
Another difference between older and newer studies is that the type of patients treated with the ketogenic diet has changed over time. When first developed and used, the ketogenic diet was not a treatment of last resort; in contrast, the children in modern studies have already tried and failed a number of anticonvulsant drugs, so may be assumed to have more difficult-to-treat epilepsy. Early and modern studies also differ because the treatment protocol has changed. In older protocols, the diet was initiated with a prolonged fast, designed to lose 5–10% body weight, and heavily restricted the calorie intake. Concerns over child health and growth led to a relaxation of the diet's restrictions. Fluid restriction was once a feature of the diet, but this led to increased risk of constipation and kidney stones, and is no longer considered beneficial.
Initial human studies that compared fasting every other day to eating less every day showed that both worked about equally for weight loss, though people struggled with the fasting days. So I had written off IF as no better or worse than simply eating less, only far more uncomfortable. My advice was to just stick with the sensible, plant-based, Mediterranean-style diet.