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Paternal age at childbirth and eating disorders in offspring

  • K. N. Javaras (a1), M. E. Rickert (a2), L. M. Thornton (a1), C. M. Peat (a1) (a3), J. H. Baker (a1), A. Birgegård (a4), C. Norring (a4), M. Landén (a5), C. Almqvist (a5) (a6), H. Larsson (a5), P. Lichtenstein (a5), C. M. Bulik (a1) (a5) (a7) and B. M. D'Onofrio (a2)...



Advanced paternal age at childbirth is associated with psychiatric disorders in offspring, including schizophrenia, bipolar disorder and autism. However, few studies have investigated paternal age's relationship with eating disorders in offspring. In a large, population-based cohort, we examined the association between paternal age and offspring eating disorders, and whether that association remains after adjustment for potential confounders (e.g. parental education level) that may be related to late/early selection into fatherhood and to eating disorder incidence.


Data for 2 276 809 individuals born in Sweden 1979–2001 were extracted from Swedish population and healthcare registers. The authors used Cox proportional hazards models to examine the effect of paternal age on the first incidence of healthcare-recorded anorexia nervosa (AN) and all eating disorders (AED) occurring 1987–2009. Models were adjusted for sex, birth order, maternal age at childbirth, and maternal and paternal covariates including country of birth, highest education level, and lifetime psychiatric and criminal history.


Even after adjustment for covariates including maternal age, advanced paternal age was associated with increased risk, and younger paternal age with decreased risk, of AN and AED. For example, the fully adjusted hazard ratio for the 45+ years (v. the 25–29 years) paternal age category was 1.32 [95% confidence interval (CI) 1.14–1.53] for AN and 1.26 (95% CI 1.13–1.40) for AED.


In this large, population-based cohort, paternal age at childbirth was positively associated with eating disorders in offspring, even after adjustment for potential confounders. Future research should further explore potential explanations for the association, including de novo mutations in the paternal germline.


Corresponding author

*Address for correspondence: C. M. Bulik, Department of Psychiatry, University of North Carolina at Chapel Hill, 101 Manning Drive CB #7160, Chapel Hill, NC 27599-7160, USA. (Email:


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