Degenerative diseases have likely plagued Homo sapiens for most of the species' evolutionary history (Hinkle, 1987). Their prevalence now is clearly far greater than at any previous time. One reason for this increase may be related to the fact that degenerative disease generally afflicts people over 40, a segment of human populations which has disproportionately grown in Western industrialized populations as survivorship has increased to six decades and longer (Adams & Smouse, 1985; Stini, this volume).

Finding the genetic basis for diseases such as hypertension, coronary heart disease (CHD), cancer, and non-insulin-dependent diabetes mellitus (NIDDM) has proved to be a formidable challenge. One of the main reasons for the difficulty is that many chronic diseases are denned (in general) as a pathological end point of several polygenic traits. The heritability of these diseases is thus related to the heritability of the traits for which they represent pathology, such as blood pressure, serum cholesterol, plasma glucose levels and body fat. In addition, because of the polygenic nature of these traits, environment significantly contributes to their phenotypic expression and hence also plays a major role in the development of the disease state. This discussion will focus on the conceptual and methodological problems inherent in studying the genetics of chronic disease, and how the perspective of human population biology and biological anthropology may improve our understanding of why these diseases arose and how they may be inherited.