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

机译:非自杀自我危害和自杀企图遗传流行病学的探索

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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.
机译:缺乏支持自杀企图(SA)和非自杀自我伤害(NSSH)之间区分的经验证据。虽然NSSH是SA的危险因素,但目前我们目前不知道这些行为是否位于严重程度的连续性上,或者它们是否是具有不同疾病的离散结果。我们进行了这项探索性遗传流行病学研究,进一步调查了这个问题。我们探讨了NSSH和SA之间的遗传重叠的程度,在大型丰富的表现群体(父母和儿童的AVON纵向研究; N?= 4959),利用个体级别的遗传和表型数据进行基因组的分析 - 广泛的复杂性状和多种子基风险评分(PRS)。 NSSH的单核苷酸多态性遗传性估计为13%(SE 0.07),SA为0%(SE 0.07)。在调查的特征中,NSSH与较高的IQ最强烈相关(RG?= 0.31,SE?=?0.22),NSSH和SA之间的高遗传相关性很少(RG?= ??? 0.1,SE? =?0.54),可能是由于SA的低遗传性估计。抑郁症的PRS在多项式回归中与NSSH和SA之间的分化。 SA的最佳PRS预测模型(NageLkerke R2 0.022,P≤0.001)包括ADHD,抑郁,收入,厌食症和神经质,并解释了比NSSH的最佳预测模型更具方差(Nagelkerke R2 0.010,P?< 0.001)包括ADHD,醇消耗,自闭症谱条件,抑郁症,智商,神经质和自杀性尝试。我们的研究结果表明,SA没有大型遗传组成部分,虽然NSSH和SA不是离散的结果,但两者之间似乎很少遗传重叠。相对较小的样本尺寸和导致SA的低遗传性估计是对该研究的限制。结合低遗传性估计,这意味着SA Gwass中的家庭或人口结构可能有助于检测到的信号。

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