Schizophrenia has a high heritability in the range of 60-80%. This is a highly robust and well-replicated finding of psychiatric genetics, with convergence of estimates from studies using many different methods and populations. Heritability is a population-level statistic. It refers to the degree of variation in a trait in a population that is due to genetic variation between individuals in that population. I believe it is legitimate to debate how to best interpret the concept, to ask what heritability says about genetic risk at the individual level, and whether it is sufficient for us to characterize the condition as being a “genetic disorder” (and indeed, I have discussed these issue in a previous post). There is nonetheless broad scientific agreement that high heritability indicates a major role for genetic risk factors. The genetic factors are nonspecific, they are not determinative, they are not sufficient, their expression can only be understood in the context of gene-environment interactions, but they are substantial and they exist. To dispute this is to place oneself far outside the scientific consensus and on the fringes of scientific respectability (View Highlight)
Twin studies repeatedly show that identical twins are at high risk of developing schizophrenia, anywhere from 15% to 50% (compared to ~1% risk in the general population and 3-20% in non-identical twins). At present, genetic influence remains the most viable and plausible explanation of this increased risk in identical twins. (View Highlight)
Even if genetic factors confer a greater risk than environmental factors, it would still be reasonable to develop treatments that target environmental factors. The existence of genetic risk factors doesn’t preclude environmental interventions from having a large therapeutic effect. Furthermore, genetic risk (even if it is greater than environmental risk) doesn’t preclude full recovery from the condition in question. It is one thing to recognize that people mistakenly interpret genetic risk as implying that the condition is fixed and permanent and to suggest that we need to be mindful of connotations; it’s entirely another thing to accept that these false connotations are true and to actively foster the view that hope and recovery depend on a rejection of the existence of genetic risk. (View Highlight)