ABSTRACT
This chapter focuses on common genetic variants which are associated with significant excess risk only when the individual is exposed to a 'high-risk' environment. It discusses the gene-environment interactions that have been identified in the field of coronary artery heart disease, much of the general approach is relevant to the analysis of any complex multi-factorial disorder of late onset, such as diabetes or hypertension, and probably disorders, Alzheimer's disease or even cancer. By stimulating catecholamines, smoking up-regulates hormone sensitive lipase, increasing circulating free fatty acid levels, thus causing atherogenic dyslipidaemia. The chapter discusses a significant inverse relationship between the half-life of bradykinin and both serum angiotensin converting enzyme (ACE) activity and the conversion of Ang I to Ang II, confirming that the ACE genotype influences bradykinin degradation. In the context of a cell, genes can be considered simply to code for the synthesis of proteins, which allow the maintenance of intracellular homeostasis in the face of extracellular or environmental changes.
