Genetics and the epidemiology of chronic diseases : a symposium, June 17-19, 1963, Ann Arbor, Michigan ... / edited by James V. Neel, Margery Shaw, William J. Schull.

Date:
1965
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Licence: Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)

Credit: Genetics and the epidemiology of chronic diseases : a symposium, June 17-19, 1963, Ann Arbor, Michigan ... / edited by James V. Neel, Margery Shaw, William J. Schull. Source: Wellcome Collection.

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    our past upon our future is the consequence of our heritage. But even casual reflection leads to the realization that this survival cannot be attributed to any one item in our genetic code; rather the influences are multiple or polygenic. It is the combination which counts. This adds to the complexity of an already complicated problem for, as Mayr (1961) points out, there is as yet no adequate analysis of a single polygenic trait in man, although they include characteristics that are particularly important to mankind. Similarly, there are few, if any, disorders whose occurrence is not the resultant of multiple convergent factors. So when the human geneticist turns to disease and disorder in the population as his basis of genetic analysis, he is promptly in epidemiology. And when he asserts the concept of multiple factors to produce an effect, he is in full cry epidemiologically. Conversely, where the epidemiologist seeks explanation for familial or other group aggregations of health or disease, he is immediately involved in genetic problems. In each case the investigator is concerned with popula¬ tion thinking (Mayr, 1961), and the beginning of formation of an epidemosis (Francis, 1959). An inherited characteristic may be brought to view only by appro¬ priate challenge. It has been repeatedly emphasized that whether a gene is harmful or useful or indifferent is commonly related to the environment in which the bearer is exposed. The genetic epidemiol¬ ogist then becomes ecologist seeking significant correlations between a group disorder and one or other stress from the great array of en¬ vironmental influences. The success of these efforts wiU obviously be related to the uniqueness of the stress and the directness of its effect, to the frequency of the basic defect and to the ease of detection of the disorder under consideration. Geographic variations may be valu¬ able but also confusing. And even if one ñnds a correlation, perhaps all he can say is, Redheads are more sensitive to heat. It is clear that this type of extensive and intensive investigation is not entered into readily, unless the problem is of major importance. Neverthe¬ less, it is the starting point for mapping the numerous genetic factors which go into determining resistance or susceptibility of a population to pathogenic stresses in the environment. In a heterogeneous popu¬ lation and a rapidly changing environment the possibilities seem infinite. The difliculty in establishing genetic correlations for certain dis¬ orders, as distinct from environmental effects, has been well recognized. Nevertheless, it is one of the basic hopes of the Community Health Study which we are conducting in Tecumseh, Michigan. Taking atherosclerosis and coronary heart disease as an example, the hypothe¬ sis is briefly this : Atherosclerosis and coronary heart disease are the result of a basic metabolic disturbance. Despite much discussion and inferential data, it is not established that coronary heart disease has a significant familial distribution nor has the weight of genetic factors 3