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Exogenous ketones are unlikely to be ketogenic per se, and may inhibit ketogenesis, however, the rapid and substantial elevation of BOHB offers potential to mitigate effects of keto-induction, and thus, could play a role in improving adherence to a ketogenic diet. There has, however, been little research performed on the application of MCTs to classic ketogenic diets and whether, if applied, they would; (a) improve time to NK, (b) result in significantly higher levels of BOHB, and (c) significantly reduce symptoms of keto-induction. Modified MCT ketogenic diets do not significantly hasten the induction of NK over a classic ketogenic diet with a minimum of three parts lipid to one part non-lipid, but they do allow NK to occur in diets containing greater amounts of non-lipid macronutrients. Except for MCTs, there is limited research on the ketogenic potential of nutritional supplements, especially in human subjects. At a dosage of 395 mg/kg bodyweight, KE increased BOHB in healthy volunteers from 0.2 mmol/L (±0.02) at baseline to 3.3 mmol/L (±0.2) one hour later (Stubbs et al., 2015a), and from 0.16 mmol/L (±0.02) at baseline to 3.16 mmol/L (±0.14) (Stubbs et al., 2015b) The same dose has been used to determine the effect on ketonaemia of KE taken with or without a meal. Clarke et al. (2012) detected no R-1,3-butanediol in the plasma of participants taking a ketone monoester supplement, except at the highest dosage of 714 mg/kg body weight, at which dose plasma R-1,3-butanediol was detectable at a level of ≤ 1.0 mmol/L and was undetectable 4 h later. In a 12-month study, a classic ketogenic diet resulted in higher levels of BOHB (and acetoacetate) over all time periods (three, six, and 12 months) but this was only statistically significant at three and six months (p Neal et al., 2009). Huttenlocher first observed higher BOHB levels in children with epilepsy aged 2–9 years, at up to one month on an MCT ketogenic diet, and marginally lower after this time, when compared to a classic ketogenic diet, although these differences were not significant (Huttenlocher, 1976). MCTs also increase BOHB when calorically dose-matched to either LCTs or carbohydrate in single feeding and non-ketogenic diet studies (Decombaz et al., 1983; Seaton et al., 1986; Yost & Eckel, 1989; Krotkiewski, 2001). Huttenlocher and colleagues first demonstrated that diets containing fewer calories from lipids than a ‘classic’ ketogenic diet—around 60%–75% of calories—can induce NK if they include a high proportion of medium chain triglycerides (MCTs) (Huttenlocher, Wilbourn & Signore, 1971). 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