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

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 dif...

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Autores principales: Russell, Abigail Emma, Hemani, Gibran, Jones, Hannah J, Ford, Tamsin, Gunnell, David, Heron, Jon, Joinson, Carol, Moran, Paul, Relton, Caroline, Suderman, Matthew, Watkins, Sarah, Mars, Becky
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8066869/
https://www.ncbi.nlm.nih.gov/pubmed/33892675
http://dx.doi.org/10.1186/s12888-021-03216-z
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author Russell, Abigail Emma
Hemani, Gibran
Jones, Hannah J
Ford, Tamsin
Gunnell, David
Heron, Jon
Joinson, Carol
Moran, Paul
Relton, Caroline
Suderman, Matthew
Watkins, Sarah
Mars, Becky
author_facet Russell, Abigail Emma
Hemani, Gibran
Jones, Hannah J
Ford, Tamsin
Gunnell, David
Heron, Jon
Joinson, Carol
Moran, Paul
Relton, Caroline
Suderman, Matthew
Watkins, Sarah
Mars, Becky
author_sort Russell, Abigail Emma
collection PubMed
description 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. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12888-021-03216-z.
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spelling pubmed-80668692021-04-26 An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt Russell, Abigail Emma Hemani, Gibran Jones, Hannah J Ford, Tamsin Gunnell, David Heron, Jon Joinson, Carol Moran, Paul Relton, Caroline Suderman, Matthew Watkins, Sarah Mars, Becky BMC Psychiatry Research Article 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. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12888-021-03216-z. BioMed Central 2021-04-23 /pmc/articles/PMC8066869/ /pubmed/33892675 http://dx.doi.org/10.1186/s12888-021-03216-z Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Russell, Abigail Emma
Hemani, Gibran
Jones, Hannah J
Ford, Tamsin
Gunnell, David
Heron, Jon
Joinson, Carol
Moran, Paul
Relton, Caroline
Suderman, Matthew
Watkins, Sarah
Mars, Becky
An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt
title An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt
title_full An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt
title_fullStr An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt
title_full_unstemmed An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt
title_short An exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt
title_sort exploration of the genetic epidemiology of non-suicidal self-harm and suicide attempt
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8066869/
https://www.ncbi.nlm.nih.gov/pubmed/33892675
http://dx.doi.org/10.1186/s12888-021-03216-z
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