Background: Coconut oil contains 6% C8, 7% C10 (C8+C10 range of 8-15%), 51% C12 (lauric acid) (range of 45-78%), 21% C14 (myristic acid), and 9% C16 (palmitic acid). Consuming more than 2 tablespoons of coconut oil is frowned upon by health authorities and lipid and nutrition researchers and MDs, because of the high amount of potentially LDL (“bad”) cholesterol-raising C12 (lauric acid), C14 (myristic acid), and C16 (palmitic acid). Coconut oil is not a strongly ketogenic fat, and the C12, C14, and C16 (unlike C6-C10) accumulate mostly in adipose tissue (fat stores) like other long chain fatty acids.
In early textbooks, C12, a major component of coconut oil, was considered to be a long chain fatty acid (LCFA). In some more recent text books C12 (lauric acid), perhaps guided by commercial interests and publications, has been considered a MCFA. Biologically, C12 behaves more like a LCFA, in its extent of incorporation into adipose tissues (fat stores), ability to increase LDL (bad) cholesterol in high amounts, and lack of ketogenicity (Cunnane 2015; Pierotti et al. 2015; St-Pierre et al. 2015). This contradicts what the Coconut Board and its affiliates, and those with a vested interest, may indicate. Moreover, despite the plethora of internet claims and some scientific literature, the so-called “anti-microbial” properties of lauric acid and lauric acid bound to glycerol, have not been demonstrated in vivo (in living people). Lauric acid as a free acid or as a monoglyceride does have food preservative microbial-killing properties and microbial killing properties in vitro (in the test tube). With the recognition that many microbes are good for us, it is a vast over-simplification to speak of “anti-microbial” properties of a fatty acid (or any natural substance): in what form of the fatty acid; in what dose; based on what evidence; what organisms are killed and which are spared; how many organisms are killed; and is the amount of killing biologically meaningful, etc.???