Role of Different Dietary Saturated Fatty Acids for Cardiometabolic Risk

David Iggman; Ulf Risérus


Clin Lipidology. 2011;6(2):209-223. 

In This Article

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).[48] Increased apoB levels after SFA intake also suggests an increased number of LDL particles, also associated with increased CVD risk.[49] 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[52] 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[51] and, in terms of foodstuffs, for replacing animal SFA with vegetable oils (e.g., rapeseed [canola] oil) (Figure 1).[50] Total SFA has also been associated with slight increases in adiposity in men[58] and women,[59] impaired endothelial function[60] and endothelial cell growth,[61] postprandial oxidative stress[62] 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.[64]

Figure 1.

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 [50], 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.[65] 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.[66] One suggested mechanism to explain this is the low vitamin E levels of coconut oil, compared with polyunsaturated vegetable oils.[67] Overall, compared with carbohydrate and LC SFA, results on cardiovascular risk markers are conflicting.

Figure 2.

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 [50].

Long-chain SFA

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.[50] Postprandial lipemia has been demonstrated for 14:0–18:0 but not for SC and MC SFA.[68] The effects from consumption of 18:0 on lipoproteins is neutral compared with carbohydrate, and decreases LDL-C compared with other LC SFA,[64] which has led to the suggestion that 18:0 would be preferable to 16:0 as a substitute for partially dehydrogenated vegetable oils/TFA.[69] 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%).[70] 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.[71] 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,[72] although other studies have failed to demonstrate prothrombotic effects[73] or even demonstrate beneficial effects on thrombogenic risk profiles compared with 16:0.[74] Collective evidence suggests that other LC SFA (12:0–16:0), rather than 18:0, are the major activators of clotting factor VII.[75] Then again, 18:0 has been demonstrated to induce more endothelial cell death and inflammation in humans[76] and in vitro[61] than other LC SFA and its presence in parenteral formulations has thus been questioned.[61] 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).[77]