Genetic epidemiology can contribute as greatly to the understanding of major chronic and degenerative diseases as classical genetics has to the understanding of inborn errors of metabolism and as classical epidemiology has to the understanding of diseases of environmental origin. Through increasing knowledge of genetic-environmental interactions, genetic epidemiology has potential for expanding the horizons of fields such as nutrition and for contributing to the development of new directions in medical and public health policy.
Public health programs were developed originally to deal with diseases of environmental origin-infectious diseases, nutritional deficiency diseases, dental caries-to which all individuals in the population are susceptible. Individual variability in susceptibility to these diseases was recognized but much of this variability, like the diseases themselves, was considered to be of environmental origin with only a small component of genetic origin. As genetic variability among most biological characteristics of a healthy population follows a Gaussian distribution, such differences were dealt with statistically assuming a basically uniform population.
Even after it was recognized that inborn errors of metabolism resulted from specific genetic defects, and that individuals with such defects represented unique populations that lay outside the predicted Gaussian distribution, public health programs continued to be based mainly on the concept of individual variability within a single population. This is readily understandable because carriers of the defective gene for an autosomal recessive condition with an incidence of 1/1O,OOO, who might represent close to 2% of the population [Motulsky, 19871 do not develop an identifiable disease. The traditional public health approach, in which it is assumed that all members of the population are equally susceptible (within the limits of the normal distribution) and that general public health measures can prevent the disease in the