The quest for cardiovascular health in the genomic era: nutrigenetics and plasma lipoproteins.
Nutrigenetics and nutrigenomics are promising multidisciplinary fields that focus on studying the interactions between nutritional factors, genetic factors and health outcomes. Their goal is to achieve more efficient individual dietary intervention strategies aimed at preventing disease, improving quality of life and achieving healthy aging. Our studies, and those of many other investigators, using population-based and intervention studies have found evidence for interactions between dietary factors, genetic variants and biochemical markers of CVD. Now, the characterization of individuals who may respond better to one type of dietary recommendation than another can be begun. Thus, a low-fat low-cholesterol strategy may be particularly efficacious in lowering the plasma cholesterol levels of those subjects carrying the apoE4 allele at the APOE gene. HDL-cholesterol (HDL-C) levels are also modulated by dietary, behavioural and genetic factors. It has been reported that the effect of PUFA intake on HDL-C concentrations is modulated by an APOA1 genetic polymorphism. Thus, subjects carrying the A allele at the -75 G/A polymorphism show an increase in HDL-C with increased intakes of PUFA, whereas those homozygotes for the more common G allele have the expected lowering of HDL-C levels with increased intake of PUFA. Variability at the hepatic lipase gene is also associated with interactions between intake of fat and HDL-C concentrations that could shed some light on the different abilities of certain ethnic groups to adapt to new nutritional environments. This knowledge should lead to successful dietary recommendations partly based on genetic factors that may help to reduce cardiovascular risk more efficiently than the current universal recommendations.
Ordovas
Jose M
JM
Nutrition and Genomics Laboratory, JM-USDA-Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA. jordov01@tufts.edu
D016632:Apolipoprotein A-I / Q000235:genetics; D053327:Apolipoprotein E4; D001057:Apolipoproteins E / Q000235:genetics; D002318:Cardiovascular Diseases / Q000209:etiology / Q000235:genetics / Q000517:prevention & control; D003924:Diabetes Mellitus, Type 2; D023281:Genomics; D006293:Health Promotion; D006801:Humans; D007333:Insulin Resistance; D008074:Lipoproteins / Q000097:blood*; D009747:Nutritional Physiological Phenomena; D009765:Obesity; D011110:Polymorphism, Genetic; D012307:Risk Factors
D016632:Apolipoprotein A-I; D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D008074:Lipoproteins