Apolipoprotein E Polymorphism Predicts Death From Coronary Heart Disease in a Longitudinal Study of Elderly Finnish Men

Abstract

Allelic variation in the apoE gene is a statistically significant predictor of CHD death in these samples of elderly Finnish men.

Should animal fats be back on the table? A critical review of the human health effects of animal fat

“…Carriers of the e4 allele have a 40% increased risk and homozygotes for this allele have approximately double the risk of CHD compared with the APOE e3 homozygotes in Western countries (Menzel et al 1983;Song et al 2004;Mooijaart et al 2006). While it may be coincidental that the age-adjusted death rates for CHD in East Finland and Crete were very similar to the frequencies of homozygotes for APOE e4 in these two cohorts, APOE genotype has been shown to affect CHD in the East and West Finland populations of the Seven Countries study (Stengard et al 1995). The response of APOE e4 to SFA versus MUFA is significantly different to the response of APOE e3, with SFA-dominated fats resulting in a substantially elevated LDL-C profile for this allele (Moreno et al 2009;Egert et al 2012).…”

“…The overall ration also had low levels of linoleic acid as a proportion of calories and a low ratio of n-6 to n-3 FA (Keys and Kimura 1970;Keys et al 1970). First, the West Finland cohort had the same median TSC value as the East Finland cohort (Keys et al 1970;Stengard et al 1995) but had only a third the rate of age adjusted CHD compared with the East Finland cohort. Furthermore, West Finland had a higher average TSC than the Zutphen (Netherlands) or US Railroad cohorts, and the same or more SFA as a proportion of calories than either of those, but less CHD than either Zutphen or US Railroad.…”

Apolipoprotein E Polymorphism and Stroke in a Population From Eastern Turkey

“…A less robust cytoskeleton, oxidative damage, increased edema, and poor mobilization of cholesterol and lipids are all putative mechanisms by which apo E could affect acute stroke. Studies-to-date have produced apparently conflicting results on the influence of APOE alleles on predisposition to ischemic stroke Strittmatter et al, 1993;Davignon et al, 1998;Stengard et al, 1995;Kokubo et al, 2000;Margaglione et al, 1998;Kessler et al, 1997). In small case-control or cross-sectional studies, e2 (Couderc et al, 1993), e4 (PedroBotet et al, 1992), or both alleles (Kuusisto et al, 1995) have been significantly overrepresented, while others have found no influence of APOE polymorphisms (Coria et al, 1995;Basun et al, 1996;Mahieux et al, 1990).…”

“…It is also associated with higher total serum cholesterol and LDL cholesterol levels (Davignon et al, 1998), atherosclerosis, and ischemic heart disease (Stengard et al, 1995).…”

Calpain-10 (NIDDM1) as a Susceptibility Gene for Common Type 2 Diabetes

“…According to the common disease common variant hypothesis, major alleles can be disease susceptibility alleles, represented by PPARγ (Pro12Ala) for type 2 diabetes [20]; minor alleles as susceptibility alleles are represented by ApoE (ε4<ε3) for coronary artery diseases [21] or Alzheimer's disease [22] and the calpain-10 gene (SNP-44 C<T) for type 2 diabetes [6,7]. For the latter two genes, the major allele may have originally been beneficial by reducing the risk of common metabolic syndromes but become detrimental relatively recently.…”