An epigenetic candidate–gene association study of parental styles in suicide attempters with substance use disorders

Author:

Chrétienneau Clara123ORCID,Spindola Leticia M.45,Vorspan Florence123,Lagerberg Trine Vik6,Marie‐Claire Cynthia23,Bellivier Frank123,Mouly Stéphane78,Laplanche Jean‐Louis23,Bloch Vanessa239,Le Hellard Stéphanie45,Icick Romain123ORCID

Affiliation:

1. Département Universitaire de Psychiatrie et de Médecine Addictologique, GHU APHP. Nord Assistance Publique – Hôpitaux de Paris Paris France

2. INSERM UMR‐S 1144, Optimisation Thérapeutique en Neurospsychopharmacologie, OTeN Université Paris Cité Paris France

3. FHU NOR‐SUD Network of Research in Substance Use Disorders Paris France

4. NORMENT, Department of Clinical Science University of Bergen Bergen Norway

5. Dr. Einar Martens Research Group for Biological Psychiatry, Department of Medical Genetics Haukeland University Hospital Bergen Norway

6. Division of Mental Health and Addiction  Department of Psychology, Faculty of Social Sciences Oslo University Hospital | University of Oslo, Oslo, Norway Oslo Norway

7. Department of Internal Medicine Lariboisière Hospital, Assistance Publique‐Hôpitaux de Paris Paris France

8. Université Paris Cité Paris France

9. Pharmacie Hospitalière Assistance Publique – Hôpitaux de Paris, GHU APHP. Nord Paris France

Abstract

AbstractSuicide attempts (SA) are prevalent in substance use disorders (SUD). Epigenetic mechanisms may play a pivotal role in the molecular mechanisms of environmental effects eliciting suicidal behaviour in this population. Hypothalamic–pituitary–adrenal axis (HPA), oxytocin and neurotrophin pathways have been consistently involved in SA, yet , their interplay with childhood adversity remains unclear, particularly in SUD. In 24 outpatients with SUDs, we examined the relation between three parental dysfunctional styles and history of SA with methylation of 32 genes from these pathways, eventually analysing 823 methylation sites. Extensive phenotypic characterization was obtained using a semi‐structured interview. Parental style was patient‐reported using the Measure of Parental Style (MOPS) questionnaire, analysed with and without imputation of missing items. Linear regressions were performed to adjust for possible confounders, followed by multiple testing correction. We describe both differentially methylated probes (DMPs) and regions (DMRs) for each set of analyses (with and without imputation of MOPS items). Without imputation, five DMRs in OXTR, CRH and NTF3 significantly interacted with MOPS father abuse to increase the risk for lifetime SA, thus covering the three pathways. After imputation of missing MOPS items, two other DMPs from FKBP5 and SOCS3 significantly interacted with each of the three father styles to increase the risk for SA. Although our findings must be interpreted with caution due to small sample size, they suggest implications of stress reactivity genes in the suicidal risk of SUD patients and highlight the significance of father dysfunction as a potential marker of childhood adversity in SUD patients.

Publisher

Wiley

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