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Complementary Alternative Cardiovascular Medicine

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76 <strong>Alternative</strong> <strong>Cardiovascular</strong> <strong>Medicine</strong><br />

amount of dietary cholesterol. The original equations developed by Keys<br />

et al. (5) and Hegsted et al. (6), reported by both in 1965, and more<br />

recently by Mensink and Katan (7), Hegsted et al. (8), and Clarke et al.<br />

(9), demonstrated that saturated fat was hypercholesterolemic, whereas<br />

PUFA lowered blood cholesterol levels. Saturated fat was twice as potent<br />

in raising blood cholesterol levels as PUFA was in lowering them. Specifically,<br />

the blood cholesterol predictive equations demonstrated that for<br />

each 1% increase in saturated fatty acids (SFAs), blood cholesterol<br />

increased 1.5 to 2.7 mg/dL. The investigators reported that MUFA had<br />

a neutral effect and that dietary cholesterol raised the blood cholesterol<br />

level but less so than saturated fat. A summary of the effect of SFA on<br />

LDL cholesterol is shown in Fig. 1.<br />

TRANS FATTY ACIDS<br />

Trans fatty acids are unsaturated fatty acids with one or more double<br />

bonds in the trans configuration. The resulting extended fatty acid chain<br />

is similar to saturated fat. Several epidemiologic studies have reported<br />

a positive relationship between trans fatty acid intake and both incidence<br />

of CHD and risk factors for CHD, notably lipids and lipoproteins (10–12).<br />

Numerous early controlled feeding studies reported that hydrogenated<br />

fats elicited a blood cholesterol response that was intermediate to<br />

that observed for unhydrogenated oils and saturated fats (reviewed in<br />

ref. 13). More recently, studies have been conducted to evaluate the<br />

plasma lipid and lipoprotein effects of trans fatty acids. These studies<br />

have consistently shown that trans fatty acids increase plasma total and<br />

LDL cholesterol relative to unsaturated fatty acids (14–16). Trans fatty<br />

acids elicit comparable cholesterol-raising effects vs SFA. In addition,<br />

trans fatty acids do not increase high-density lipoprotein (HDL) cholesterol<br />

as does SFA (17), resulting in a lower HDL cholesterol and a<br />

worsening of the LDL:HDL ratio which, in turn, increases CHD risk (see<br />

Fig. 2) (18).<br />

DIETARY CHOLESTEROL<br />

Numerous controlled clinical studies have shown a positive linear association<br />

between dietary cholesterol and LDL cholesterol. Consequently,<br />

because of an increase in LDL cholesterol, there is an increase in CHD risk.<br />

However, the LDL cholesterol-raising effect of dietary cholesterol is less<br />

than that of SFA. An increase of 100 mg/d of dietary cholesterol is predicted<br />

to result in a 0.5 to 1 mmol/L increase in total serum cholesterol,<br />

resulting in a 1% to 2% increase in CHD risk (see Fig. 3) (1).

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