The inherent complexities of gene–environment interactions

The article outlines the complexities of gene–environment interactions in the determination of human disease, especially as they relate to aging, and stresses the importance of continuing such studies, in spite of their inherent difficulties. First, a capsule review of the literature pertaining to studies of gene–environment interactions is presented, and designs and methodologies used to detect these interactions are briefly discussed. Second, research questions and problems that can be addressed as outcomes of gene–environment interaction studies are exemplified. Third, a number of illustrative examples of gene–environment interactions are presented. Fourth, various types of gene–environment interactions are briefly discussed. Fifth, concluding remarks are offered, and possibilities of studying gene–environment interaction within social and biological research on aging are outlined. ‘‘The majority of potters do not die of bronchitis. It is quite possible that if we really understood the causation of this disease, we should find that only a fraction of potters are of a constitution that rendered them liable to it.’’ (Haldane, 1938, p. 102) W ITH this thought, Haldane (1938) captured the essenceof what is now referred to as ‘‘gene–environment interaction.’ ’ When stating that only a percentage of all potters exposed to occupational dust develop bronchitis, Haldane referred to instances in which the combined effect of genetic and environmental risks or protective factors is substantially greater than that anticipated from a simple sum of their independent effects. Today, there are several distinct branches of medical science that address the issue of gene–environment interaction (Shostak, 2003). Specifically, this interaction is central to the fields o