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Estimating the heritability of reporting stressful life events captured by common genetic variants

  • R. A. Power (a1), T. Wingenbach (a1), S. Cohen-Woods (a1), R. Uher (a1) (a2), M. Y. Ng (a1), A. W. Butler (a1) (a3), M. Ising (a4), N. Craddock (a5), M. J. Owen (a5), A. Korszun (a6), L. Jones (a7), I. Jones (a6), M. Gill (a8), J. P. Rice (a9), W. Maier (a10), A. Zobel (a10), O. Mors (a11), A. Placentino (a12), M. Rietschel (a13), S. Lucae (a4), F. Holsboer (a4), E. B. Binder (a4), R. Keers (a1) (a6), F. Tozzi (a14), P. Muglia (a14) (a15) (a16), G. Breen (a1) (a17), I. W. Craig (a1), B. Müller-Myhsok (a4), J. L. Kennedy (a18) (a19), J. Strauss (a18) (a19), J. B. Vincent (a18) (a19), C. M. Lewis (a1), A. E. Farmer (a1) and P. McGuffin (a1)...

Although usually thought of as external environmental stressors, a significant heritable component has been reported for measures of stressful life events (SLEs) in twin studies.


We examined the variance in SLEs captured by common genetic variants from a genome-wide association study (GWAS) of 2578 individuals. Genome-wide complex trait analysis (GCTA) was used to estimate the phenotypic variance tagged by single nucleotide polymorphisms (SNPs). We also performed a GWAS on the number of SLEs, and looked at correlations between siblings.


A significant proportion of variance in SLEs was captured by SNPs (30%, p = 0.04). When events were divided into those considered to be dependent or independent, an equal amount of variance was explained for both. This ‘heritability’ was in part confounded by personality measures of neuroticism and psychoticism. A GWAS for the total number of SLEs revealed one SNP that reached genome-wide significance (p = 4 × 10−8), although this association was not replicated in separate samples. Using available sibling data for 744 individuals, we also found a significant positive correlation of R2 = 0.08 in SLEs (p = 0.03).


These results provide independent validation from molecular data for the heritability of reporting environmental measures, and show that this heritability is in part due to both common variants and the confounding effect of personality.

Corresponding author
*Address for correspondence: Mr R. A. Power, MRC Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, London SE5 8AF, UK. (Email:
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Psychological Medicine
  • ISSN: 0033-2917
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