Proceedings of the Nutrition Society

Research Article

ApoE genotype, cardiovascular risk and responsiveness to dietary fat manipulation

Symposium on ‘Molecular basis for diseases’

on 3–6 July 2006, The Summer Meeting of the Nutrition Society, was held at the Aberdeen Exhibition and Conference Centre, Aberdeen.

A. M. Minihanea1 c1, L. Jofre-Monsenya2, E. Olano-Martina1 and G. Rimbacha2

a1 Hugh Sinclair Unit of Human Nutrition, School of Chemistry, Food Biosciences and Pharmacy, University of Reading, Reading RG6 6AP, UK

a2 Institute of Human Nutrition and Food Science, Christian Albrechts University, Hermann-Rodewald-Strasse 6, 24098 Kiel, Germany

Abstract

Cardiovascular risk is determined by the complex interactions between genetic and environmental factors. The apoE genotype represents the most-widely-studied single nucleotide polymorphism in relation to CVD risk, with >3600 publications cited in PubMed. Although originally described as a mediator of lipoprotein metabolism, the lipoprotein-independent functions of apoE are being increasingly recognised, with limited data available on the potential impact of genotype on these metabolic processes. Furthermore, although meta-analyses suggest that apoE4 carriers may have a 40–50% increased CVD risk, the associations reported in individual studies are highly heterogeneous and it is recognised that environmental factors such as smoking status and dietary fat composition influence genotype–phenotype associations. However, information is often derived from observational studies or small intervention trials in which retrospective genotyping of the cohort results in small group sizes in the rarer E2 and E4 subgroups. Either larger well-standardised intervention trials or smaller trials with prospective recruitment according to apoE genotype are needed to fully establish the impact of diet on genotype–CVD associations and to establish the potential of dietary strategies such as reduced total fat, saturated fat, or increased antioxidant intakes to counteract the increased CVD burden in apoE4 carriers.

Correspondence:

c1 *Corresponding author: Dr Anne M. Minihane, fax +44 118 9310080, email a.m.minihane@reading.ac.uk