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.
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You may also have to moderate protein intake somewhat, as high protein intake (greater than 2.0g/kg/d) may make it more difficult to maintain ketosis. However, eating too little protein may also present health issues such as poor muscle development, increased hunger, and lack of essential amino acids. That is why we recommend a moderate level of protein intake, defined as 1.2-1.7g/kg/d. See our protein guide.
What’s the catch? The ketogenic state has been linked to increasing satiety hormones and decreasing hunger hormones — well-researched during the initial phase. But once you’re off the keto diet after 30 days, the appetite-suppressing hormones will increase significantly from your baseline. Meaning that you’re likely to feel physically hungrier than you did before you started all of this dieting nonsense.
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^ Jump up to: a b c d e f g h i j k l m n o p q r s Kossoff EH, Zupec-Kania BA, Amark PE, Ballaban-Gil KR, Bergqvist AG, Blackford R, et al. Optimal clinical management of children receiving the ketogenic diet: recommendations of the International Ketogenic Diet Study Group. Epilepsia. 2009 Feb;50(2):304–17. doi:10.1111/j.1528-1167.2008.01765.x. PMID 18823325