The Genetic Epidemiology of Schizophrenia in a Finnish Twin Cohort

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Abstract
THAT GENETIC factors are involved in the etiology of schizophrenia is no longer a matter of controversy.1 Less certain is the nature and extent of the genetic contribution to liability. Previous twin studies have reported estimates of broad heritability ranging from 0.41 to 0.87.2-5 In all but one6 of these studies, heritability estimates were calculated using information from exclusively index twin pairs (ie, one or both co-twins affected), by either subtracting from one the ratio of the probandwise concordance rates in dizygotic (DZ) and monozygotic (MZ) pairs or multiplying by 2 the difference between the correlations in liability7 in MZ and DZ pairs using a literature-derived estimate of the population base rate. Estimates using the first approach are limited in that concordance rates are proportions that do not derive their meaning from a genetic liability model and ignore critical information on pairs concordant for nonaffection.2 Estimates using the second approach are limited in that the population base rate is assumed to be known without error, resulting in an underestimation of confidence intervals,8 and assumed to be representative of the base rate in twins, the truth of which can only be determined empirically. A limitation of both approaches is that there is no direct statistical test of whether additive and dominance genetic effects contribute to liability.