a1 Department of Psychiatry, Institute of Psychiatry, King's College London, UK
a2 Centre for Health Equity Studies (CHESS), Stockholms Universitet/Karolinska Institutet, Stockholm, Sweden
a3 London School of Hygiene and Tropical Medicine (LSHTM), London, UK
Background Schizophrenic patients have fewer offspring than the general population but it is unclear whether (i) this persists for more than one generation, (ii) the reduced fertility is compensated by increased fertility in unaffected relatives, (iii) sociodemographic factors confound or interact with the association, and (iv) patients with affective psychosis have a similar fertility disadvantage. This study measured biological fitness over two generations in patients with schizophrenia or affective psychosis, and their unaffected siblings.
Method We conducted a historical cohort study using a Swedish birth cohort of 12 168 individuals born 1915–1929 and followed up until 2002. We compared biological fitness over two generations in patients with schizophrenia (n=58) or affective psychosis (n=153), and their unaffected siblings, with the population, adjusting for a range of sociodemographic variables from throughout the lifespan.
Results Patients with schizophrenia had fewer children [fertility ratio (FR) 0.42, 95% confidence interval (CI) 0.29–0.61] and grandchildren (FR 0.51, 95% CI 0.33–0.80) than the population. Some of this reduction was related to lower marriage rates in schizophrenic patients. The unaffected siblings of schizophrenic patients showed no evidence of any compensatory increase in fitness, but there was a trend towards enhanced fertility among the offspring of schizophrenia patients. Patients with affective psychosis and their relatives did not differ from the general population on any fertility measure.
Conclusions Schizophrenia, but not affective psychosis, is associated with reduced biological fertility; this disadvantage is partly explained by marital status and persists into the second generation.
(Received July 11 2008)
(Revised December 19 2008)
(Accepted January 15 2009)
(Online publication March 06 2009)
c1 Address for correspondence: Dr J. H. MacCabe, B.Sc., MBBS, MRCPsych, M.Sc., Ph.D., Clinical Lecturer in Psychiatry, Department of Psychiatry, Institute of Psychiatry, King's College London, De Crespigny Park, London SE5 8AF, UK. (Email: email@example.com)