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- Hunjan, AK, et al.
(författare)
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Association between polygenic propensity for psychiatric disorders and nutrient intake
- 2021
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Ingår i: Communications biology. - : Springer Science and Business Media LLC. - 2399-3642. ; 4:1, s. 965-
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Tidskriftsartikel (refereegranskat)abstract
- Despite the observed associations between psychiatric disorders and nutrient intake, genetic studies are limited. We examined whether polygenic scores for psychiatric disorders are associated with nutrient intake in UK Biobank (N = 163,619) using linear mixed models. We found polygenic scores for attention-deficit/hyperactivity disorder, bipolar disorder, and schizophrenia showed the highest number of associations, while a polygenic score for autism spectrum disorder showed no association. The relatively weaker obsessive-compulsive disorder polygenic score showed the greatest effect sizes suggesting its association with diet traits may become more apparent with larger genome-wide analyses. A higher alcohol dependence polygenic score was associated with higher alcohol intake and individuals with higher persistent thinness polygenic scores reported their food to weigh less, both independent of socioeconomic status. Our findings suggest that polygenic propensity for a psychiatric disorder is associated with dietary behaviour. Note, nutrient intake was self-reported and findings must therefore be interpreted mindfully.
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- Hunjan, AK, et al.
(författare)
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No Evidence for Passive Gene-Environment Correlation or the Influence of Genetic Risk for Psychiatric Disorders on Adult Body Composition via the Adoption Design
- 2021
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Ingår i: Behavior genetics. - : Springer Science and Business Media LLC. - 1573-3297 .- 0001-8244. ; 51:1, s. 58-67
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Tidskriftsartikel (refereegranskat)abstract
- The relationship between genetic and environmental risk is complex and for many traits, estimates of genetic effects may be inflated by passive gene-environment correlation. This arises because biological offspring inherit both their genotypes and rearing environment from their parents. We tested for passive gene-environment correlation in adult body composition traits using the ‘natural experiment’ of childhood adoption, which removes passive gene-environment correlation within families. Specifically, we compared 6165 adoptees with propensity score matched non-adoptees in the UK Biobank. We also tested whether passive gene-environment correlation inflates the association between psychiatric genetic risk and body composition. We found no evidence for inflation of heritability or polygenic scores in non-adoptees compared to adoptees for a range of body composition traits. Furthermore, polygenic risk scores for anorexia nervosa, attention-deficit/hyperactivity disorder and schizophrenia did not differ in their influence on body composition traits in adoptees and non-adoptees. These findings suggest that passive gene-environment correlation does not inflate genetic effects for body composition, or the influence of psychiatric disorder genetic risk on body composition. Our design does not look at passive gene-environment correlation in childhood, and does not test for ‘pure’ environmental effects or the effects of active and evocative gene-environment correlations, where child genetics directly influences home environment. However, these findings suggest that genetic influences identified for body composition in this adult sample are direct, and not confounded by the family environment provided by biological relatives.
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