ABSTRACT
Common complex human diseases result from a combination of genetics, environment, and the interactions between the two. Although genome-wide association studies (GWAS) have produced many clues regarding the genetic contributions to the pathogenesis of complex human disease, the genetic risk factors identied so far only explain a small proportion of disease risks (Altshuler, Daly, and Lander 2008; Lusis, Attie, and Reue 2008). Environmental factors are also a signicant contributor for human diseases. Air pollution, for example, has been shown to increase risks of lung, heart, and possibly liver disease, and many studies have shown that stress contributes to heart disease. It is also well accepted that diet is one of the main factors contributing to the current obesity pandemic and its associated health consequences, such as cardiovascular diseases and diabetes. High-fat diets increase the risk of breast, colon, prostate, and possibly pancreatic and ovarian cancers, and 30%–40% of cancers have been directly linked to dietary factors (Glade 1999). Diet not only contributes to diseases directly, but also interacts with other risk factors by inuencing metabolic pathways, homeostasis, and the ow of genetic information from gene expression to protein synthesis and degradation. A systems biology approach, which gives a comprehensive and holistic view of how diet contributes to complex human diseases and disease prevention, is needed to understand these complex interactions.
