Abstract
BackgroundEmpirical evidence supporting the distinction between suicide attempt (SA) and non-suicidal self-harm (NSSH) is lacking. Although NSSH is a risk factor for SA, we do not currently know whether these behaviours lie on a continuum of severity, or whether they are discrete outcomes with different aetiologies. We conducted this exploratory genetic epidemiology study to investigate this issue further.MethodsWe explored the extent of genetic overlap between NSSH and SA in a large, richly-phenotyped cohort (the Avon Longitudinal Study of Parents and Children; N = 4959), utilising individual-level genetic and phenotypic data to conduct analyses of genome-wide complex traits and polygenic risk scores (PRS).ResultsThe single nucleotide polymorphism heritability of NSSH was estimated to be 13% (SE 0.07) and that of SA to be 0% (SE 0.07). Of the traits investigated, NSSH was most strongly correlated with higher IQ (rG = 0.31, SE = 0.22), there was little evidence of high genetic correlation between NSSH and SA (rG = − 0.1, SE = 0.54), likely due to the low heritability estimate for SA. The PRS for depression differentiated between those with NSSH and SA in multinomial regression. The optimal PRS prediction model for SA (Nagelkerke R2 0.022, p < 0.001) included ADHD, depression, income, anorexia and neuroticism and explained more variance than the optimal prediction model for NSSH (Nagelkerke R2 0.010, p < 0.001) which included ADHD, alcohol consumption, autism spectrum conditions, depression, IQ, neuroticism and suicide attempt.ConclusionsOur findings suggest that SA does not have a large genetic component, and that although NSSH and SA are not discrete outcomes there appears to be little genetic overlap between the two. The relatively small sample size and resulting low heritability estimate for SA was a limitation of the study. Combined with low heritability estimates, this implies that family or population structures in SA GWASs may contribute to signals detected.
Highlights
Empirical evidence supporting the distinction between suicide attempt (SA) and non-suicidal selfharm (NSSH) is lacking
Genetic correlations between NSSH, SA and related phenotypes As single nucleotide polymorphism (SNP) heritability for SA was negligible, genetic correlations were only estimated between NSSH and related
Our findings suggest that the variance captured by SNPs is small, and there was a greater proportion of common genetic variation explained for NSSH than SA
Summary
Empirical evidence supporting the distinction between suicide attempt (SA) and non-suicidal selfharm (NSSH) is lacking. NSSH is a risk factor for SA, we do not currently know whether these behaviours lie on a continuum of severity, or whether they are discrete outcomes with different aetiologies We conducted this exploratory genetic epidemiology study to investigate this issue further. Understanding the genetic basis of suicide is complicated by the broad spectrum of behaviours that fall under “suicidal behaviour”, which include self-harm with varying levels of suicidal intent as well as death by suicide Within this broad definition there is a lack of consensus as to whether self-harm without suicidal intent (referred to as ‘non suicidal self-harm’ (NSSH)) and SA lie on a continuum of increasingly severe and lethal behaviour, or whether they should be considered discrete [10, 11]. Utilising genetic data to explore relationships between risk factors and suicidal behaviour reduces the potential for confounding and allows for a more nuanced exploration of traits that may confer liability to NSSH and/or SA
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