Different specific saturated fatty acids may have different effects on CHD risk. In particular, there is a growing interest in stearic acid as a substitute for TFA to give texture and solidity to foods. Metabolic studies show that lauric acid most markedly increases total and LDL cholesterol, whereas stearic acid somewhat lowers total and LDL cholesterol when it replaces carbohydrates (Fig. 1.2) (Mensink et al., 2003). However, lauric acid also has the strongest HDL raising effect, whereas stearic acid raises HDL cholesterol less than other saturated or cis-unsaturated fatty acids. The net effect is that lauric and stearic acid have less unfavourable effects on the total to HDL cholesterol ratio than myristic and palmitic acids. However, consequences of these differences for CHD risk are unclear. Saturated fatty acids tend to occur together in diets due to shared food sources, there are therefore hardly any epidemiological data for specific saturated fatty acids. Only one published study provides evidence about the effects of stearic acid and other specific saturates on CVD end-points (Hu et al., 1999). In this study, the relative risk for a 1% increase in intake of stearic acid was 1.19, which was not substantially different from the relative risks for other saturated fatty acids (Hu et al., 1999). Effects of stearic acid on risk factors other than blood lipids, such as blood clotting tendency, also do not provide a conclusive answer on whether stearic acid may have different effects on CHD risk.
As mentioned, the available studies on effects of SAFA on these risk factors are not consistent, and the clinical meaning of these effects is unclear. For example, one recent study suggests that stearic acid has less unfavourable effects on haemostatic factors than other saturates (Tholstrup et al., 2003), but others found the opposite (Baer et al., 2004; Lefevre et al., 2004). Baer et al. found that a diet with 8% of energy as stearic acid increased fibrinogen concentration, which would theoretically translate to an increased risk of CHD. This study also compared the haemostatic effects of a diet with 4% of energy as stearic acid plus 4% of energy as TFA with those of a high-carbohydrate, low-fat control diet. In this comparison, there was no effect on fibrinogen concentration. Thus, at this realistic level of intake of stearic acid, no adverse effects on fibrinogen levels would be expected. Another study in 105 healthy subjects found no differences between stearic and palmitic acids in their effects on vascular function (Sanderson et al., 2004).
Thus, metabolic studies show that different saturated fatty acids can have different effects on lipoprotein cholesterol levels. However, data on CHD risk beyond blood lipids are limited. There is no clear evidence that supports making a distinction between stearic acid and other saturated fatty acids.
The two major dietary sources of TFA are ruminant dairy and meat fat, mainly providing vaccenic acid (trans--C18:1n-7), and industrial hydrogenated vegetable oils, providing a broad range of positional trans isomers with elaidic acid (trans-C18:1n-9) being the most abundant. It has been suggested that TFA from ruminant sources may be less detrimental for health than TFA from industrial sources. The few epidemiological comparisons of ruminant and industrial TFA have investigated associations of CHD risk with relative intakes of TFA (i.e. the highest vs the lowest categories of intake), without taking differences in absolute intake in the population between ruminant and industrial TFA into account. A recent review describes the epidemiological associations of CHD risk with absolute TFA intakes (i.e. grams eaten per day) (Weggemans et al., 2004). This analysis reveals that there are no differences in CHD risk between total, ruminant, and industrial TFA for intakes up to 2.5 g/day. At higher intakes (more than 3 g/ day), total and industrial TFA were associated with CHD, but at these levels of intake there are insufficient data on ruminant TFA.
There are no human data comparing effects of ruminant versus industrial TFA on blood lipids. The metabolic studies on industrial TFA show that different mixtures of trans isomers obtained by slightly different hydrogenation procedures of different types of vegetable oils have similar adverse effects on blood lipids (Ascherio et al., 1999). This would suggest that the position of the trans double bond in the carbon chain is not an important determinant. Thus, the scarce data that are available do not support discriminating between ruminant and industrial TFA.
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