An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt

被引:11
作者
Russell, Abigail Emma [1 ]
Hemani, Gibran [2 ,3 ]
Jones, Hannah J. [4 ]
Ford, Tamsin [5 ]
Gunnell, David [4 ,6 ,7 ]
Heron, Jon [4 ]
Joinson, Carol [4 ]
Moran, Paul [4 ,6 ,7 ]
Relton, Caroline [2 ,3 ]
Suderman, Matthew [2 ,3 ]
Watkins, Sarah [4 ]
Mars, Becky [4 ,6 ,7 ]
机构
[1] Univ Exeter, Coll Med & Hlth, Children & Young Peoples Mental Hlth Res Collabor, Exeter, Devon, England
[2] Univ Bristol, Sch Med, MRC Integrat Epidemiol Unit, Bristol, Avon, England
[3] Univ Bristol, Sch Med, Populat Hlth Sci, Bristol, Avon, England
[4] Univ Bristol, Sch Med, Ctr Acad Mental Hlth, Populat Hlth Sci, Bristol, Avon, England
[5] Univ Cambridge, Dept Psychiat, Cambridge, England
[6] Univ Hosp Bristol NHS Fdn Trust, NIHR Biomed Res Ctr, Bristol, Avon, England
[7] Univ Bristol, Bristol, Avon, England
基金
英国惠康基金; 英国医学研究理事会;
关键词
Suicide; self-harm; non-suicidal self-injury; Genetic epidemiology; Polygenic risk scores; GENOME-WIDE ASSOCIATION; AGE-OF-ONSET; INJURY; METAANALYSIS; SEVERITY; BEHAVIOR; OUTCOMES; TRAITS; SCORES; INTENT;
D O I
10.1186/s12888-021-03216-z
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Background Empirical 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. Methods We 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). Results The 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 R-2 0.022, p < 0.001) included ADHD, depression, income, anorexia and neuroticism and explained more variance than the optimal prediction model for NSSH (Nagelkerke R-2 0.010, p < 0.001) which included ADHD, alcohol consumption, autism spectrum conditions, depression, IQ, neuroticism and suicide attempt. Conclusions Our 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.
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页数:12
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