(Lin, et. al. 2016). As the SCN1A gene is read in the nucleus of the cell, a transcript is created that travels outside of the nucleus and is eventually translated into the protein that becomes the sodium ion channel. Several factors can affect how quickly or efficiently the transcript is read. The authors found that GAPDH, an enzyme involved in the breakdown of glucose, decreases the reading of that SCN1A transcript by binding to a specific site on the transcript. The ketones produced in the ketogenic diet may weaken GAPDH’s binding to the transcript, potentially leading to increased expression of SCN1A, which may help explain the anticonvulsant effects of the ketogenic diet.

Lin, G.W., et. al. (2016). GAPDH-mediated posttranscriptional regulations of sodium channel SCN1A and SCN3A genes under seizure and ketogenic diet conditions. Neuropharmacology. Nov 2;113(Pt A);480-489. doi: 10.1016/j.neuropharm.2016.11.002. https://www.ncbi.nlm.nih.gov/pubmed/27816501