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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). Interestingly, vinegar is commonly prescribed as a ‘free food’ in ketogenic diet trials (Rother, 2007; Perez-Guisado & Munoz-Serrano, 2011; Nebeling & Lerner, 1995), and may provide an under-recognized stimulus for ketogenesis. Higher leucine (and isoleucine) concentrations result from a ketogenic diet and are related to reduced glutamate-to-GABA ratio and this might explain some of the anti-seizure activity of a ketogenic diet in epilepsy (Roy et al., 2015). There is a paucity of studies on time to NK and mitigation of symptoms of keto-induction an as data related to the effects of various supplements on time to induction of ketosis and on symptoms of keto-induction are limited, and there is a lack of homogeneity between study objectives, outcomes, and measures, a narrative review style was chosen. This paper reviews the available scientific literature relevant to improvements in time to ketosis and symptoms of keto-induction, resulting from these nutritional supplements. Several studies have described adverse effects during ketogenic diets but to our knowledge, no studies have specifically described symptoms of keto-induction in the short time between commencing a ketogenic diet and the achievement of NK. Ketogenic diets are now commonly applied, for a range of desired outcomes, and with differing definitions of what constitutes a ketogenic diet. 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