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It has been demonstrated by Sandstrom and colleagues that in a hypercaloric diet, there are increased BOHB levels observed with the application of MCTs that aren’t seen in a hypocaloric state (Sandström et al., 1995). When fed intravenously, MCTs increase ketogenesis when compared to both structurally similar fats (Mingrone et al., 1993) and LCTs (Jiang et al., 1993; Lai & Chen, 2000). MCTs promote ketonaemia and ketogenesis (useful to reduce the risk of night-time hypoglycaemic coma) in those with carnitine palmitoyltransferase deficiency, a rare genetic condition which inhibits the ability to produce ketone bodies from long-chain fatty acids (Bonnefont et al., 1989; Bougnères et al., 1981). Dietary MCTs are also known to promote both ketonaemia and ketogenesis in animals (Bach et al., 1977; Yeh & Zee, 1976) and humans with and without health conditions (St-Onge et al., 2003; Yajnik et al., 1997). Similar to the short-chain fatty acids and unlike long-chain triglycerides (LCTs), MCTs do not require the actions of bile, nor micellar-chylomicron mediated absorption into the lymphatics and instead are diffused directly into the hepatic portal vein and preferentially converted into bio-available ketone bodies in the liver. Both 2 g and 4 g of butyric acid were demonstrated to be more ketogenic than either 5 g of leucine, or 5 or 10 g of O-MAG (St-Pierre et al., 2017). For example, silage butyrate content has been shown to provide no significant effect on subclinical ketosis in dairy cows (Samiei et al., 2015), however, sub-clinical ketosis is higher in those receiving silage higher in butyrate content (Vicente et al., 2014). Urinary excretion of acetone (a ketone body) is increased in phloridzinised dogs and fasting rats after feeding with acetic acid (MacKay et al., 1940). Thus, they bypass the usual route of absorption (for the more common long-chain fatty acids) into the lymphatics and deposition into the bloodstream via the subclavian vein, and instead, are transported via the hepatic portal vein to the liver where they can be converted into the ketone bodies (Bugaut, 1987; Bourassa et al., 2016; Stilling et al., 2016). The authors postulated that this could be due to the ketogenic effect of leucine, but may also result from a greater availability of BCAAs (Evangeliou et al., 2009). Adverse effects resulting from a VLCKD are likely to reduce compliance and tolerability (Vining et al., 1998), and thus affect the efficacy of these diets as clinical interventions. So, while the achievement of ketosis has been described in the medical literature, there are inconsistencies in the measurement of, and definition for ketosis in these papers. Other studies have measured either tangentially or directly, the achievement of ‘ketosis’ but have not specifically identified the time at which a level of ≥0.5 mmol L−1 was achieved. The process of ketogenesis further allows coenzymes to be freed to ensure continued fatty-acid β-oxidation (Lehninger, Cox & Nelson, 2008). Ketosis refers to the production of ketone bodies, derived from fats (and some amino acids) for use as an alternative fuel in times of fasting or drastic carbohydrate restriction. This demonstrated that butyric acid is more ketogenic than either leucine or an 8-chain monoglyceride. This paper reviews the scientific literature on the effects of these methods on time-to-NK and on symptoms during the keto-induction phase. Several methods have been suggested as useful for encouraging entry into nutritional ketosis (NK) and reducing symptoms of keto-induction. 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