fat, do not have the expected high LDL cholesterol levels or the resultant high rates of CVD (Bjerregaard et al., 1997). Likewise, polymorphisms in apolipoprotein E, a carrier protein important to liver metabolism of LDL, result in different levels of LDL and cardiovascular risk in people who eat similar diets (Miltiadous et al., 2005). A more detailed discussion of both biological and behavioral traits is provided in the following section.
The inclusion of measurable intermediate phenotypes will assist investigators in the exploration of the relationship among gene-environment interactions, risk behaviors, and health. This may involve incorporating more extensive assessments of biologically based dimensions of personality and temperament and/or incorporating laboratory-based measures of risk behavior propensity (e.g., the rewarding value of nicotine or high-fat foods). Animal and human laboratory models can be performed in parallel to test the effects of genetic factors and environmental influences on intermediate phenotype measures (Blendy et al., 2005). Using genetic animal models and human genetic association studies to stratify populations, the genetic effects on risk behaviors can be measured in the presence and absence of key social environmental cues and stressors.
However, it is not only through risk behaviors like smoking, poor eating habits and obesity, or low exercise levels that gene-environment interactions influence health. Another key pathway that is just as important involves effects of gene-environment interactions on biological characteristics involving neuroendocrine, autonomic, cardiovascular, metabolic, inflammatory, and hemostatic functions. There are several examples in the recent literature that illustrate these gene-environment interaction effects on biomarkers.
The Lys198Asn polymorphism of the Endothelin-1 gene moderates the impact of both obesity and socioeconomic status on systolic blood pressure reactivity to an acute environmental stressor in African American and Caucasian young adults (Treiber et al., 2003). The G308A polymorphism of the TNFα gene moderates the impact of chronic environmental stress, as measured by vital exhaustion levels, on plasma levels of C-reactive protein, a potent risk factor for CVD (Jeanmonod et al., 2004). The extensively studied promoter polymorphism of the serotonin transporter gene (5HTTLPR) moderates the impact of acute mental stress on blood pressure (Williams et al., 2001), an effect that has been cited as one potential mechanism that could be mediating the reported association between the 5HTTLPR long allele and increased risk of myocardial infarction (Fumeron et al., 2002).