Polymorphisms at the APOA1/C3/A4 gene cluster and the APOE gene have been extensively studied in order to examine their potential association with plasma lipid levels, coronary heart disease risk and more recently with inter-individual variability in response to dietary therapies. Although the results have not been uniform across studies, the current research supports the concept that variation at these genes explains a significant, but still rather small, proportion of the variability in fasting and postprandial plasma lipid responses to dietary interventions. This information constitutes the initial frame to develop panels of genetic markers that could be used to predict individual responsiveness to dietary therapy for the prevention of coronary heart disease. Future progress in this complex area will come from experiments carried out using animal models, and from carefully controlled dietary protocols in humans that should include the assessment of several other candidate gene loci coding for products that play a relevant role in lipoprotein metabolism (i.e. APOB, CETP, LPL, FABP2, SRBI, ABC1 and CYP7).

Thirty-eight male volunteers participated in a double-blind cross-over trial evaluating the effect of replacing the usual sources of saturated fat in the Dutch diet (animal fats and hydrogenated oils) by palm oil, which is virtually free of cholesterol and trans-fatty acids, on serum lipids, lipoproteins and apolipoproteins. Maximum (about 70%) replacement had no significant effect on serum total cholesterol or most lipoprotein fractions, but resulted in an 11% increase in serum high-density-lipoprotein (HDL)2-cholesterol relative to the control (P2 = 0.01). The palm-oil diet also caused an 8% decrease in low-density-lipoprotein (LDL):HDL2+HDL3-cholesterol ratio (P2 = 0.02) as well as a 9% decrease in triacylglycerols in the low-density-lipoprotein fractions (P2 = 0.01). Palm oil consumption resulted in a 4% increase in serum apolipoprotein AI (P2 = 0.008) and a 4% decrease in apolipoprotein B (P2 = 0.01) relative to the control diet; the B:AI apolipoprotein ratio was decreased by 8% (P2 < 0.0001). These results were not significantly affected by the different lipoprotein E phenotypes of the volunteers. Although the observed differences were relatively modest, the present study, nonetheless, indicates that dietary palm oil, when replacing a major part of the normal fat content in a Dutch diet, may slightly reduce the lipoprotein- and apolipoprotein-associated cardiovascular risk profiles