User:Wenwatata/sandbox

There has been increasing interest to understand how genes and nutrients interact to promote atherosclerosis. </ref> A lot of studies have focused on how plasma lipid concentrations affect such interactions under different intakes of fats and cholesterol. </ref> The polymorphism at the apolipoprotein E gene (APOE) which greatly impacts human lipoprotein metabolism has been seriously implicated in this conditions and is also been the most studied gene in this respect. </ref> A lot of evidence has suggested that variation at the APOE gene locus is associated with differences in the risk of early atherosclerosis and the development of Alzheimer disease. This is supported by evidence that carriers of the APOE 4 (E4) allele have higher LDL-cholesterol concentrations, as opposed to carriers of the APO E2 (E2) allele, who have lower LDL-cholesterol levels. However, age has been reported as a confounding factor to this disease pattern, as children and elderly subjects with the E4 allele have less negligible difference in LDL-cholesterol concentrations, while those with the E2 allele present with an antiatherogenic lipoprotein pattern, which suggests that the effect of genetic variation in APOE on plasma lipids is modifiable.