An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt.
An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt.
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DOI：
10.1186/s12888-021-03216-z
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发表时间：
2021-04-23
期刊：
影响因子：
4.4
通讯作者：
Mars B
中科院分区：
文献类型：
--
作者：
Russell AE;Hemani G;Jones HJ;Ford T;Gunnell D;Heron J;Joinson C;Moran P;Relton C;Suderman M;Watkins S;Mars B
缺乏支持自杀未遂(SA)和非自杀自残(NSSH)之间区别的经验证据。虽然NSSH是SA的一个危险因素，但我们目前不知道这些行为是否取决于严重程度的连续体，或者它们是否是具有不同病因的离散结果。我们进行了这项探索性的遗传流行病学研究，以进一步研究这一问题。我们在一个大型、表型丰富的队列(雅芳父母和孩子纵向研究；N = 4959)中探索了NSSH和SA之间的遗传重叠程度，利用个人水平的遗传和表型数据来进行全基因组复杂特征和多基因风险分数(PR)的分析。NSSH的单核苷酸多态遗传力为13%(SE 0.07)，SA的单核苷酸多态遗传度为0%(SE 0.07)。在所研究的性状中，NSSH与较高的智商(Rg = 0.31，SE = 0.22)的相关性最强，几乎没有证据表明NSSH与SA(Rg = − 0.1，SE = 0.54)之间存在较高的遗传相关性，这可能是由于SA的遗传力估计较低所致。经多项回归分析，NSSH组与SA组之间的差异有统计学意义。对SA(Nagelkerke R2 0.022，p <； 0.001)的最优预测模型包括多动症、抑郁、收入、厌食症和神经质，可解释的变异比对非SSH的最优预测模型(Nagelkerke R2 0.010，p <； 0.001)更多，后者包括多动症、饮酒、自闭症谱系状况、抑郁、智商、神经质和自杀企图。我们的发现表明，SA没有很大的遗传成分，尽管NSSH和SA不是独立的结果，但两者之间似乎几乎没有遗传重叠。相对较小的样本量和由此导致的SA的低遗传力估计是该研究的局限性。结合低遗传力估计，这意味着SA GWAS中的家族或群体结构可能对检测到的信号起作用。网上版载有补充材料，可在10.1186/s12888-021-03216-z查阅。
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. 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). 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 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. 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. The online version contains supplementary material available at 10.1186/s12888-021-03216-z.
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影响因子：
11
作者：
Davies G;Marioni RE;Liewald DC;Hill WD;Hagenaars SP;Harris SE;Ritchie SJ;Luciano M;Fawns-Ritchie C;Lyall D;Cullen B;Cox SR;Hayward C;Porteous DJ;Evans J;McIntosh AM;Gallacher J;Craddock N;Pell JP;Smith DJ;Gale CR;Deary IJ
通讯作者：
Deary IJ
影响因子：
5
作者：
Fry A;Littlejohns TJ;Sudlow C;Doherty N;Adamska L;Sprosen T;Collins R;Allen NE
通讯作者：
Allen NE
影响因子：
30.8
作者：
Bulik-Sullivan, Brendan K.;Loh, Po-Ru;Finucane, Hilary K.;Ripke, Stephan;Yang, Jian;Patterson, Nick;Daly, Mark J.;Price, Alkes L.;Neale, Benjamin M.
通讯作者：
Neale, Benjamin M.
DOI：
10.1111/jcpp.12831
发表时间：
2018-04
期刊：
Journal of child psychology and psychiatry, and allied disciplines
影响因子：
--
作者：
Cha CB;Franz PJ;M Guzmán E;Glenn CR;Kleiman EM;Nock MK
通讯作者：
Nock MK
影响因子：
168.9
作者：
Grimes, DA;Schulz, KF
通讯作者：
Schulz, KF