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Vinegar has been demonstrated to improve postprandial insulin sensitivity in healthy and diabetic people and improve glycaemic responses to meals (Johnston, Kim & Buller, 2004; Liljeberg & Björck, 1998; Brighenti et al., 1995). The highest quantities of short-chain fatty acids have been observed in portal blood, followed by hepatic, and far less in peripheral blood (Cummings et al., 1987). Those short-chain fatty acids that escape metabolism by epithelial cells are, therefore, primarily absorbed via the hepatic portal vein and do not require ‘bundling’ with micelles and chylomicrons for absorption (Kuksis, 2000). It is generally accepted that chain length affects the relative deposition of fatty acids into either lymph or the portal vein (Mu & Høy, 2004). Short chain fatty acids, especially butyric acid, are used extensively as a fuel substrate by intestinal epithelial cells (Wong et al., 2006). Studies in mice have shown that while ingested L-leucine can reduce seizure activity similarly to a KD, it does not independently increase blood levels of BOHB (Hartman et al., 2015). Leucine can also be degraded in rat astroglial cells to the ketone bodies, including BOHB, and when released by these cells, used by neighbouring neurones as a fuel substrate (Bixel & Hamprecht, 1995). Progression of fasting increases the conversion of leucine to ketone bodies and peripheral tissue is catabolised to provide leucine for ketogenesis (Kulaylat et al., 1988). There appears to be a high affinity of kidney cells for ketogenesis from leucine (Noda & Ichihara, 1976). 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. 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