Effects on Cardiovascular Risk Factors
Overall SFA Intake
Animal experiments and controlled feeding studies in humans have demonstrated increases in fasting levels of TC and LDL-C after SFA consumption. Then again, when carbohydrate is replaced with SFA, TC and LDL-C are increased, but HDL-C is also increased. It should be noted that increased LDL-C is a stronger and more established risk marker for cardiovascular disease (CVD) than decreased HDL-C. In addition, increased HDL-C levels may not directly promote protection against atherosclerosis, as the inherent capacity for cholesterol efflux from macrophages is not specifically determined by HDL-C levels, and may be affected by other factors (e.g., smoking). Increased apoB levels after SFA intake also suggests an increased number of LDL particles, also associated with increased CVD risk. TGs are also decreased, at least compared with high glycemic index (GI) carbohydrates, but not compared with unsaturated fats.[50,51] Furthermore, replacing carbohydrates with SFA may decrease the number of small, dense LDL, which are considered particularly prone to oxidation and glycation.[53,54] Therefore, alternative markers have been proposed to better reflect cardiovascular risk, such as the TC:HDL-C ratio or apolipoproteins.[55–57] The greatest benefit on these markers have been demonstrated for replacing SFA with PUFA and, in terms of foodstuffs, for replacing animal SFA with vegetable oils (e.g., rapeseed [canola] oil) (Figure 1). Total SFA has also been associated with slight increases in adiposity in men and women, impaired endothelial function and endothelial cell growth, postprandial oxidative stress and inflammation.[57,63] Owing to the inter-relative nature of SFA, evidence of effects on markers of cardiometabolic risk from individual SFA is limited, although some additional knowledge has emerged since a previous review article on lipids and lipoproteins.
Predicted changes (Δ) in the serum total cholesterol:HDL-C ratio when mixed fat constituting 10% of energy in the 'average' US diet is replaced isoenergetically with a particular fat.
Adapted with permission from the American Society for Nutrition , modified to focus on fats.
Lauric Acid (12:0)
Lauric acid (12:0), present in coconut oil, palm kernel oil, dairy, and some margarines and spreads, is the most potent SFA for increasing TC and LDL-C, which has led to the assumption that tropical oils would be especially deleterious for cardiovascular health. However, 12:0 intake increases HDL-C levels to a proportionally higher degree than LDL-C, and is the only LC SFA that improves the TC:HDL-C ratio, compared with carbohydrate (Figure 2).[50,57] In rabbits, isocaloric feeding with coconut oil compared with standard chow induces atherosclerosis and markers of the metabolic syndrome, even in the absence of weight gain. In humans, consumption of a high-fat meal from coconut oil compared with PUFA reduces the anti-inflammatory properties of HDL, and a nonsignificant trend towards reduced arterial endothelial reactivity has been demonstrated postprandially. One suggested mechanism to explain this is the low vitamin E levels of coconut oil, compared with polyunsaturated vegetable oils. Overall, compared with carbohydrate and LC SFA, results on cardiovascular risk markers are conflicting.
Predicted changes (Δ) in serum total cholesterol:HDL-C ratio and in LDL-C and HDL-C concentrations when refined carbohydrates constituting 1% of energy are replaced isoenergetically with lauric acid (12:0), myristic acid (14:0), palmitic acid (16:0) or stearic acid (18:0).
*p < 0.001.
Adapted with permission from the American Society for Nutrition .
After consumption of 14:0 and 16:0, TC is increased, and LDL-C and HDL-C are increased to a nearly similar extent, when substituted for carbohydrate. The TC:HDL-C ratio is virtually unaffected (Figure 2). Of note in such comparisons is that carbohydrate quality is generally not considered and these relationships are mainly true for high-GI carbohydrate. Postprandial lipemia has been demonstrated for 14:0–18:0 but not for SC and MC SFA. The effects from consumption of 18:0 on lipoproteins is neutral compared with carbohydrate, and decreases LDL-C compared with other LC SFA, which has led to the suggestion that 18:0 would be preferable to 16:0 as a substitute for partially dehydrogenated vegetable oils/TFA. However, stearic acid has been demonstrated to increase Lp(a) levels (+10%) compared with a baseline diet high in dairy fat, although the effect was less than for TFA (+30%). A recent German cohort study demonstrated associations with weight gain for 18:0, but not for other SFA, plausibly related to the low oxidation rate of 18:0. In addition, 18:0 intake has been demonstrated to increase fibrinogen levels compared with diets high in carbohydrate, other LC SFA, TFA and 18:1n-9 after a 5-week intervention in men, although other studies have failed to demonstrate prothrombotic effects or even demonstrate beneficial effects on thrombogenic risk profiles compared with 16:0. Collective evidence suggests that other LC SFA (12:0–16:0), rather than 18:0, are the major activators of clotting factor VII. Then again, 18:0 has been demonstrated to induce more endothelial cell death and inflammation in humans and in vitro than other LC SFA and its presence in parenteral formulations has thus been questioned. Overall, it is presently unclear whether replacement of TFA is preferable with vegetable oils high in SFA (e.g., palm oil), or by fully hydrogenated oils (i.e., interesterified 16:0 or 18:0).
Clin Lipidology. 2011;6(2):209-223. © 2011 Future Medicine Ltd.