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One of the major sources of the recurring resistance to the evidence supporting the presence of a genetic factor in the etiology of schizophrenia is the fear of therapeutic nihilism. Some colleagues believe if a genetic factor is operative, all therapeutic efforts short of genetic manipulation must be useless. Others are not so extreme in their concerns but believe such a factor would at the least negate the value of psychotherapy. It is as if the existence of a genetic factor will invalidate social intervention.
Initially, this paper will review three major lines cf evidence for the existence of a genetic factor in the etiology of schizophrenia and then place the biologic conclusion in a broader clinical perspective. The first line of evidence derives from the consanguinity studies. It was found that the relatives of individuals labeled schizophrenic showed the disorder significantly more frequently than did the general population. More importantly, there was a direct linear correlation between the degree of blood relationship and the frequency of the disorder. The closer the biologic bond the more likely was schizophrenia to be present. As is usually the case, these findings permit a variety of interpretations. An environmental explanation will fit equally well as a biologic one. It can be argued that families share more than a common genetic heritage, and the closer the biologic bond the more likely are the individuals to share similar environmental experiences.
The second line of evidence derives from the twin studies. Virtually every study has found that monozygotic twins show a significantly higher concordance rate than dizygotic twins.’ The concordance rates vary as a function of the severity of the illness in the index case and the methods used in obtaining the study population. The choice of chronically hospitalized index cases and the use of the same clinical examiner for both members yields a monozygotic concordance rate of up to 86 percent.2 The choice of