I was reviewing multiple choice questions for an answer bank, and the answer to the rate of schizophrenia among monozygotic twins was given as 50%. I thought this is not that high. So I went had a look a the data.
In 2003, Sullivan and Kendler performed a meta analysis. They found.
Seven of the 12 studies and the meta-analytic summary estimate(rMZ = 0.92; 95% confidence interval [CI], 0.91-0.94; and rDZ = 0.52; 95% CI, 0.48-0.56) lie between lines depicting extreme cases in which a trait is entirely due to additive genetic effects (100% a2) or entirely due to common environmental effects (100% c2), suggesting the presence of both additive genetic and common environmental effects in the etiology of schizophrenia.
For additive genetic effects, the point estimates from all but 2 studies are in excess of 50%. The 95% CIs for the estimates are often large because of the relatively small sample sizes of the individual studies. The meta-analytic summary for additive genetic variance in liability to schizophrenia was estimated at 81% (95% CI, 73%-90%).
A more recent paper looked at psychotic experiences (PE) rather than diagnosis in a large twin database. They note
This was the first time, to our knowledge, that individual PE assessed dimensionally in adolescence have been examined for genetic and environmental contributions. More than 5000 twins were assessed on 6 spectra of PE. We found that PE in adolescence were moderately heritable, with paranoia and parent-rated negative symptoms showing the highest heritability and hallucinations showing the lowest. Nonshared environmental influences played an important role in their etiology. Shared environmental influences were only significant for hallucinations and negative symptoms. This is consistent with previous research, which has shown a number of environmental risk factors for psychosis that may be specific to the individual, such as stressful life events, cannabis use, and childhood trauma.- The low heritability estimate for hallucinations is consistent with emerging research indicating the significance of early trauma in their occurrence. Indeed, the heritability estimates argue for a renewed interest in the contribution of the environment to risk of PE.
The most recent data comes from Denmark, where all cases are recorded in a national database. They note:
The AE models estimated that the additive genetic effects accounted for 78.9% and 73.3% of the variance in liability to SZ and SZ spectrum disorders, respectively, while environmental effects accounted for 21.1% and 26.7% of the variance of the two diagnostic categories (Table 3).
For comparison with previous studies, the data for both SZ and SZ spectrum disorder were analyzed without consideration for censoring. When analyzing these data, a reduced twin sample consisting of n = 19,539 twin pairs born between 1951 and 1981 compared with twin pairs born between 1951 and 2000 in the adjusted analysis was included to ensure a minimum follow-up of 30 years. The results can be seen in Supplemental Tables S1 and S2. The analyses resulted in lower probandwise concordance rates for MZ twins (0.33) and heritability estimates (SZ = 75.5%; SZ spectrum disorder = 69.5%).
My recommendation to the group who run the exam bank is to delete the question. The rate of concordance among monozygotic twins if one has Schizophrenia or a schizophrenic spectrum disorder varies markedly between studies. The larger, less selected studies may have lower rates: the volunteer bias for such studies may include families with genetic loading, or the studies relying on official diagnoses may underestimate the rate due to variations in coding driven by a clinician’s wish to avoid a stigmatising diagnosis.
It is better to note our limitations than be overconfident