| 11. |
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| 12. |
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| 13. |
- Arnau-Soler, A, et al.
(författare)
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Genome-wide by environment interaction studies of depressive symptoms and psychosocial stress in UK Biobank and Generation Scotland
- 2019
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Ingår i: Translational psychiatry. - : Springer Science and Business Media LLC. - 2158-3188. ; 9:1, s. 14-
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Tidskriftsartikel (refereegranskat)abstract
- Stress is associated with poorer physical and mental health. To improve our understanding of this link, we performed genome-wide association studies (GWAS) of depressive symptoms and genome-wide by environment interaction studies (GWEIS) of depressive symptoms and stressful life events (SLE) in two UK population-based cohorts (Generation Scotland and UK Biobank). No SNP was individually significant in either GWAS, but gene-based tests identified six genes associated with depressive symptoms in UK Biobank (DCC, ACSS3, DRD2, STAG1, FOXP2 and KYNU; p < 2.77 × 10−6). Two SNPs with genome-wide significant GxE effects were identified by GWEIS in Generation Scotland: rs12789145 (53-kb downstream PIWIL4; p = 4.95 × 10−9; total SLE) and rs17070072 (intronic to ZCCHC2; p = 1.46 × 10−8; dependent SLE). A third locus upstream CYLC2 (rs12000047 and rs12005200, p < 2.00 × 10−8; dependent SLE) when the joint effect of the SNP main and GxE effects was considered. GWEIS gene-based tests identified: MTNR1B with GxE effect with dependent SLE in Generation Scotland; and PHF2 with the joint effect in UK Biobank (p < 2.77 × 10−6). Polygenic risk scores (PRSs) analyses incorporating GxE effects improved the prediction of depressive symptom scores, when using weights derived from either the UK Biobank GWAS of depressive symptoms (p = 0.01) or the PGC GWAS of major depressive disorder (p = 5.91 × 10−3). Using an independent sample, PRS derived using GWEIS GxE effects provided evidence of shared aetiologies between depressive symptoms and schizotypal personality, heart disease and COPD. Further such studies are required and may result in improved treatments for depression and other stress-related conditions.
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| 14. |
- Baker, JH, et al.
(författare)
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Genetic risk factors for disordered eating in adolescent males and females
- 2009
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Ingår i: J Abnorm Psychol. - 0021-843X. ; 118:3, s. 576-86
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Tidskriftsartikel (refereegranskat)abstract
- The etiologic role of genetic and environmental factors on disordered eating was examined in a sample of 15- to 17-year-old female-female, male-male, and opposite-sex twin pairs. Also assessed was whether a single factor is underlying 3 facets (body dissatisfaction, drive for thinness, bulimia) of disordered eating, including the possible importance of sex differences. Univariate model-fitting analyses indicated that genetic factors are more important for girls and environment more important for boys for body dissatisfaction and drive for thinness. A multivariate common factor analysis indicated that a single factor accounted for the association among these 3 facets of disordered eating in both sexes. However, only 50% of the genetic risk for this factor is shared between the sexes.
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| 15. |
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| 16. |
- Baker, JH, et al.
(författare)
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Intrauterine testosterone exposure and risk for disordered eating
- 2009
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Ingår i: The British journal of psychiatry : the journal of mental science. - : Royal College of Psychiatrists. - 1472-1465. ; 194:4, s. 375-376
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Tidskriftsartikel (refereegranskat)abstract
- Previous research has suggested that prenatal testosterone exposure masculinises disordered eating by comparing opposite- and same-gender twins. The objective of the current study is to replicate this finding using a sample of 439 identical and 213 fraternal females, 461 identical and 344 fraternal males, and 361 males and 371 females from opposite-gender twin pairs. Disordered eating was compared across twin types using the Eating Disorder Inventory–2. Inconsistent with previous findings, a main effect of co-twin gender was not found. Our results raise questions about the validity of prior evidence of the impact of prenatal testosterone exposure on patterns of disordered eating.
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| 17. |
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| 19. |
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| 20. |
- Bigdeli, TB, et al.
(författare)
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Genetic effects influencing risk for major depressive disorder in China and Europe
- 2017
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Ingår i: Translational psychiatry. - : Springer Science and Business Media LLC. - 2158-3188. ; 7:3, s. e1074-
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Tidskriftsartikel (refereegranskat)abstract
- Major depressive disorder (MDD) is a common, complex psychiatric disorder and a leading cause of disability worldwide. Despite twin studies indicating its modest heritability (~30–40%), extensive heterogeneity and a complex genetic architecture have complicated efforts to detect associated genetic risk variants. We combined single-nucleotide polymorphism (SNP) summary statistics from the CONVERGE and PGC studies of MDD, representing 10 502 Chinese (5282 cases and 5220 controls) and 18 663 European (9447 cases and 9215 controls) subjects. We determined the fraction of SNPs displaying consistent directions of effect, assessed the significance of polygenic risk scores and estimated the genetic correlation of MDD across ancestries. Subsequent trans-ancestry meta-analyses combined SNP-level evidence of association. Sign tests and polygenic score profiling weakly support an overlap of SNP effects between East Asian and European populations. We estimated the trans-ancestry genetic correlation of lifetime MDD as 0.33; female-only and recurrent MDD yielded estimates of 0.40 and 0.41, respectively. Common variants downstream of GPHN achieved genome-wide significance by Bayesian trans-ancestry meta-analysis (rs9323497; log10 Bayes Factor=8.08) but failed to replicate in an independent European sample (P=0.911). Gene-set enrichment analyses indicate enrichment of genes involved in neuronal development and axonal trafficking. We successfully demonstrate a partially shared polygenic basis of MDD in East Asian and European populations. Taken together, these findings support a complex etiology for MDD and possible population differences in predisposing genetic factors, with important implications for future genetic studies.
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