Authors: Santos HO, Howell S, Earnest CP, Teixeira FJ
PMID: 31707063 DOI: 10.1016/j.pcad.2019.11.001
In recent years, health professionals and laypersons have disseminated misinformation regarding the consumption of coconut oil. Those encouraging the supplementation of coconut oil argue that it provides health benefits and protective cardiovascular effects. Our article examines the effects of coconut oil intake on the cardiometabolic profile by exploring various lipid indices, as well as potential non-lipid effects, such as weight loss. The majority of randomized controlled trials show that coconut oil intake or its supplementation increases low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDLC), and total cholesterol when compared with other vegetable oils. Lauric acid, a medium-chain fatty acid and the main constituent of coconut oil, increases LDL-C and HDL-C concentrations, since it plays a main role as a substrate for apolipoprotein (apo)A1 and apoB synthesis, which are the key molecules in HDL-C and LDL-C particles, respectively.Despite some findings demonstrating an increase in HDL-C, definitive long-term clinical trials are imperative to ascertain whether this effect is clinically relevant. In addition, coconut oil intake has failed as a weight loss strategy and should not be considered as a supplementation strategy to increase satiety and/or thermogenesis.If one desires to include coconut oil in the diet, then we suggest that it should be limited and encompassed within the current recommendations of SFA intake, which are up to 10% of total caloric intake.
Keywords: Coconut oil; Cocos nucifera; HDL; Lauric acid; Lipids.