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Abstract
Background: Recent studies suggest psychotic and eating disorders can be comorbid and could have shared genetic liability. However, so far this comorbidity has been largely overlooked in the epidemiological literature.Aim: To test whether polygenic risk scores (PRS) for schizophrenia are associated with disordered eating behaviours and body mass index in the general population.
Methods: Using data from the Avon Longitudinal Study of Parents and Children and random effect logistic and linear regression models, we investigated the association between PRS for schizophrenia and self-reported disordered eating behaviours (binge-eating, purging, fasting, excessive exercise) and body mass index at 14, 16, and 18 years.
Results: Of the 6,920 children had available genetic data 4,473 (64.6%) and 5,069 (73.3%), had at least one disordered eating and one BMI outcome measurement, respectively. A standard deviation increase in PRS was associated with greater odds of having binge-eating behaviours (odds ratio: 1.36, 95% confidence interval [CI]: 1.16, 1.60, p<0.0001) and lower body mass index (coefficient: -0.03, 95% CI: -0.06, -0.01, p=0.02). We did not observe any other associations.
Conclusions: Our findings suggest the presence of shared genetic risk between schizophrenia and binge eating behaviours. Intermediate phenotypes such as impaired social cognition and irritability, previously shown to be positively correlated in this sample with schizophrenia PRS, could represent risk factors for both phenotypes. Shared genetic liability between binge-eating and schizophrenia could also explain higher rates of metabolic syndrome in individuals with schizophrenia as binge eating could be a mediator of this association in drug naïve individuals. The finding of an association between greater PRS and lower BMI, although consistent with existing epidemiological and genetic literature, requires further investigation.
Methods: Using data from the Avon Longitudinal Study of Parents and Children and random effect logistic and linear regression models, we investigated the association between PRS for schizophrenia and self-reported disordered eating behaviours (binge-eating, purging, fasting, excessive exercise) and body mass index at 14, 16, and 18 years.
Results: Of the 6,920 children had available genetic data 4,473 (64.6%) and 5,069 (73.3%), had at least one disordered eating and one BMI outcome measurement, respectively. A standard deviation increase in PRS was associated with greater odds of having binge-eating behaviours (odds ratio: 1.36, 95% confidence interval [CI]: 1.16, 1.60, p<0.0001) and lower body mass index (coefficient: -0.03, 95% CI: -0.06, -0.01, p=0.02). We did not observe any other associations.
Conclusions: Our findings suggest the presence of shared genetic risk between schizophrenia and binge eating behaviours. Intermediate phenotypes such as impaired social cognition and irritability, previously shown to be positively correlated in this sample with schizophrenia PRS, could represent risk factors for both phenotypes. Shared genetic liability between binge-eating and schizophrenia could also explain higher rates of metabolic syndrome in individuals with schizophrenia as binge eating could be a mediator of this association in drug naïve individuals. The finding of an association between greater PRS and lower BMI, although consistent with existing epidemiological and genetic literature, requires further investigation.
Original language | English |
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Pages (from-to) | 428-433 |
Number of pages | 6 |
Journal | British Journal of Psychiatry |
Volume | 215 |
Issue number | 1 |
Early online date | 6 Mar 2019 |
DOIs | |
Publication status | Published - 1 Jul 2019 |
Keywords
- ALSPAC
- eating disorders
- genetics
- schizophrenia
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