Ordovas Jose M, Corella Dolores
Nutrition and Genomics Laboratory, JM USDA HNRCA at Tufts University, 711 Washington Street, Boston, MA 02111, USA.
Curr Cardiol Rep. 2005 Nov;7(6):480-6. doi: 10.1007/s11886-005-0067-6.
Cardiovascular diseases (CVD) result from complex interactions between genetic and environmental factors. The evidence supports that gene-environment interactions modulate plasma lipid concentrations and potentially CVD risk. The findings from studies examining gene-diet interactions and lipid metabolism have been promising. Several loci (eg, APOA1, APOE, LIPC) are providing proof of concept for the application of genetics in the context of personalized nutrition for CVD prevention. The spectrum of candidate genes has been expanding to incorporate those involved in intracellular lipid metabolism (eg, iPPARs, CYP7A1). However, the practical application of these findings is not ready for prime time. There is a compelling need for replication using a higher level of scientific evidence. Moreover, we need to evolve from the simple scenarios examined nowadays (ie, one single dietary component, SNP, and risk factor) to more realistic situations involving multiple interactions. In summary, there is need for both large population studies and well-standardized intervention studies.
心血管疾病（CVD）是由遗传和环境因素之间的复杂相互作用导致的。有证据支持基因 - 环境相互作用可调节血浆脂质浓度，并潜在地影响心血管疾病风险。研究基因 - 饮食相互作用与脂质代谢的研究结果很有前景。几个基因座（如APOA1、APOE、LIPC）为遗传学在心血管疾病预防的个性化营养背景下的应用提供了概念验证。候选基因的范围一直在扩大，纳入了那些参与细胞内脂质代谢的基因（如iPPARs、CYP7A1）。然而，这些发现的实际应用尚未成熟。迫切需要采用更高水平的科学证据进行重复验证。此外，我们需要从目前所研究的简单情况（即单一饮食成分、单核苷酸多态性和风险因素）转向涉及多种相互作用的更现实情况。总之，既需要大规模人群研究，也需要标准化良好的干预研究。
