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RESEARCH PRODUCT

Saturated fat intake and alcohol consumption modulate the association between the APOE polymorphism and risk of future coronary heart disease: a nested case-control study in the Spanish EPIC cohort

Larraitz ArriolaConcepción Moreno-iribasMaría José SánchezNúria SalaFrancesc FrancésCarlos GonzálezCarmen MartinezNerea LarrañagaOlga PortolésPablo Martínez-camblorCarmen NavarroLaudina RodríguezJosé Ramón QuirósDolores CorellaJosé María HuertaAurelio BarrricarteEsther MolinaMaría Dolores ChirlaqueEmilio Ros

subject

AdultMaleApolipoprotein Emedicine.medical_specialtyAlcohol DrinkingGenotypeEndocrinology Diabetes and MetabolismSaturated fatClinical BiochemistryPopulationCoronary DiseaseBiochemistryGastroenterologyWhite PeopleApolipoproteins ERisk FactorsInternal medicineOdds RatiomedicineHumansLongitudinal StudieseducationMolecular BiologyAllelesAgededucation.field_of_studyPolymorphism GeneticNutrition and Dieteticsbusiness.industryFatty AcidsCase-control studyCholesterol LDLOdds ratioMiddle AgedDietEuropean Prospective Investigation into Cancer and NutritionEndocrinologySpainCase-Control StudiesMultivariate AnalysisNested case-control studySaturated fatty acidRegression AnalysisFemalebusiness

description

The association is still not clear between the common APOE polymorphism and coronary heart disease (CHD) risk, nor its modulation by diet. Thus, our aim was to study the association between the APOE genotypes and incident CHD and how dietary fat and alcohol consumption modify these effects. We performed a nested case-control study in the Spanish European Prospective Investigation into Cancer and Nutrition cohort. Healthy men and women (41,440, 30-69 years) were followed up over a 10-year period, with the incident CHD cases being identified. We analyzed 534 incident CHD cases and 1123 controls. APOE, dietary intake and plasma lipids were determined at baseline. The APOE polymorphism was significantly associated with low-density lipoprotein cholesterol (LDL-C), and gene-alcohol interactions in determining LDL-C were detected. In the whole population, the E2 allele was significantly associated with a lower CHD risk than E3/E3 subjects [odds ratio (OR), 0.58; 95% confidence interval (CI), 0.38-0.89]. The E4 allele did not reach statistical significance vs. E3/E3 (OR, 1.17; 95% CI, 0.88-1.58). However, saturated fat intake modified the effect of the APOE polymorphism in determining CHD risk. When saturated fat intake was low (<10% of energy), no statistically significant association between the APOE polymorphism and CHD risk was observed (P=.682). However, with higher intake (≥10%), the polymorphism was significant (P=.005), and the differences between E2 and E4 carriers were magnified (OR for E4 vs. E2, 3.33; 95% CI, 1.61-6.90). Alcohol consumption also modified the effect of the APOE on CHD risk. In conclusion, in this Mediterranean population, the E2 allele is associated with lower CHD risk, and this association is modulated by saturated fat and alcohol consumption.

yearjournalcountryeditionlanguage
2011-05-01The Journal of Nutritional Biochemistry
https://doi.org/10.1016/j.jnutbio.2010.04.003