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Although some AED doses were adjusted, no significant effect on plasma concentrations was seen after three months on the diet and the authors concluded it is not necessary to adjust drug doses due to pharmacokinetic interactions when starting a KD (1). The first measured plasma levels of valproic acid (VPA), lamotrigine, topiramate, clonazepam and phenobarbital in 51 children on the classical KD. Further research is needed into long-term adherence and practicality of VLCKD, but the current results are promising for weight management, lipid profiles, and insulin sensitivity. 53 This trial was limited by small sample size, short duration, and inability to extrapolate the results as the study was performed in the inpatient setting. The management of plasma glucose and modulation of insulin’s effects on lipid metabolism are important targets in the treatment of diabetes and the prevention of comorbid conditions, including systemic microvascular complications. This subsequently decreases HDL and promotes small, dense atherogenic LDL particles.55–57 Not only does hyperinsulinemia contribute to triglyceride-rich lipoprotein production, but it also stimulates hepatic de-novo lipogenesis, triglyceride synthesis, and can inhibit VLDL clearance.5,58 Furthermore, insulin plays a role in the synthesis of endogenous cholesterol, via direct diet-related activation of HMGCoA reductase. Elevated plasma triglyceride levels are correlated with a shift towards smaller, dense LDL particles via cholesterol esterification of abundant VLDL particles.46,55 In controlled amounts over short periods of time, insulin normally acts to suppress VLDL production; however, with prolonged secretion in the setting of persistent hyperglycemia, hyperinsulinemia leads to hepatic insulin resistance and an increase in triglyceride-rich VLDL particles. The positive lipid effects of VLCKD are explained by the principles and driving forces behind lipoprotein turnover. 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