Advances in Genetics Nutrigenomics in Cardiovascular Medicine

Nutrigenomics represents a suitable approach to cardiovascular medicine, potentially enabling both, better prevention and treatment of cardiovascular diseases (CVD) through optimization of individuals’ dietary intakes. However, nutrigenomics is still developing its research methodology and learning from its achievements and its shortcomings. Its foundations have been laid, allowing us to validate its theoretical basis and, from there, to pursue research aimed to obtain a higher level of scientific evidence needed for its effective translation to clinical practice. This review discusses these aspects and summarizes the literature pertaining to gene-diet interactions related to intermediate and final CVD phenotypes. Despite their multifactorial complexity, CVD have been the group of diseases in which most progress has been made on the knowledge of their genetic risk factors, both in identifying candidate genes through the classic approach based on the protein function and through the recent genomewide association studies. Current knowledge regarding CVD genetic factors is summarized in several recent reviews.1–5 This has been possible due to the previous characterization of multiple intermediate phenotypes linked to those diseases, among which are plasma lipid concentrations, plasma glucose and related parameters, markers of inflammation and endothelial damage, oxidative stress, blood pressure, anthropometric measurements, and even phenotypes obtained by means of noninvasive imaging techniques such as measuring the intima-media thickness of artery walls.6,7 The relative ease of measuring these intermediate phenotypes and the specific understanding of them as risk factors has allowed many studies to be carried out aimed at identifying gene and genetic variants related to each of them and so obtaining a more detailed knowledge of the numerous genes involved in the final phenotypes of CVD (ie, coronary heart diseases, cerebrovascular diseases, and peripheral CVD). Despite the spectacular advances made over recent decades in the discovery of genes and gene variants involved in the intermediate and final phenotypes of CVD, we still have a very incomplete knowledge of all genes and genetic variants that are providing such genetic susceptibility. Moreover, in that search for genetic susceptibility, the interaction with environmental factors must be taken into account. Therefore, a genetic variant will not always present a greater risk of disease, but its effects will be modified by the environmental factors (ie, tobacco smoking, physical activity, and dietary intake) that interact with it. Among the environmental factors, diet may be the most directly involved in the genetic modulation of the different intermediate and final phenotypes of CVD. However, we still need to find out how certain dietary components may modulate the risk conferred by genetic susceptibility due to variation in one or more genes involved in the etiology of CVD. This knowledge is not only crucial for contributing to better primary prevention of CVD but also for increasing the effectiveness of the treatment once the altered phenotypes have been diagnosed. Furthermore, from the Public Health point of view, the understanding of really important gene-diet modulations could help to profile the general dietary recommendations for each population.