Abstract
Research in the genetics of human behavioral disorders* confronts a complex of problems from the moment of its inception. First of all, how does one go about doing this research when one obviously has no leverage on the implicated genes per se? One cannot engage in the traditional forms of experimental breeding, so that one has no control at all over the breeding of his sample population; and that is as it should be. No matter which behavioral disorder one studies, it is apparent from the outsetand always has beenthat its distribution in families follows no Mendelian pattern. What are we talking about, then, when we talk about the genetics of such disorders? The truth is that much of psychiatric genetics has been devoted to explaining awaynot explainingthe non-Mendelian distributions found. Initially, there was a predilection for positing such factors as reduced penetrance and varying manifestation in homozygotes and heterozygotes, depending on whether one's own preference was for a of dominance or recessiveness. Such theories? are based, in turn, on empirical statistical distributions that are fallibly determined and that vary appreciably from sample to sample and from study to study. In more recent times, the tendency has been to turn away from such theorizing and either to postulate a simple, additive, polygenic system to explain away the non-Mendelian distributions or to speculate that such disorders are genetically heterogeneous, i.e., that there are a number of different major single-genes at different loci that can lead to the same type of disorder. It is a simple matter for any investigator to choose to believe one kind of rather than another, and the fact is that the variety and abundance of theories that have been proposed in the past fifty years constitute an eloquent testimonial to the fact that we have been offered articles of faith and fancy rather than hard substance on which to develop a genetic theory of human behavioral disorders.
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