According to McGuffin et al. (1995), at the beginning of this century schizophrenia was already considered to have a genetic component. However, this was disputed during the 1960s by the word of R.D. Laing and others, who considered schizophrenia as primarily environmental, and as representing an adaptive response to a crazy-making culture. In looking carefully at the research, however, the current consensus is that there is clearly a genetic component to schizophrenia, although the exact method of transmission has not been identified. The intent in the following pages is to explore some of the research, looking at problems, methods, and future directions, along with the current state of knowledge.
There are many problems associated with the study of schizophrenia, not the least of which it appears to be a complex syndrome that actually includes more than one disease. Clinical observation has supported the possibility that there are several different symptom "dimensions," each of which may result from a different pathophysiologic process. Pharmacologic investigation, genetic research, brain imaging, and other types of studies have indicated that schizophrenia cannot be associated with any one cause (Flaum, 1996).
This makes it difficult to study and obtain results that are definitive. For example, simply in looking at genetic research, it is apparent that the disorder is probably genetically complex and non-Mendelian (Harrison and Geddes, 1996). In other words, it cannot be traced as directly heritable in the same way that other disorders are.
As a consequence, one of the major methods used in genetic research has some important limitations. Linkage studies, which are common in genetic research, are limited in detecting genes of small effect. Thus, studies may show that there is no apparent linkage between a particular gene or chromosome site, but this does not definitively prove that there is no involvement at that ...