Cited by 19Epigenetics and DNA MethylationBullying, Victimization, and AggressionChild Abuse and Trauma

Associations between epigenetic aging and childhood peer victimization, depression, and suicidal ideation in adolescence and adulthood: a study of two population-based samples

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Perret, L. C., Geoffroy, M-C., Barr, E., Parnet, F., Provencal, N., Boivin, M., O’Donnell, K. J., Suderman, M. +3 more·2023·Frontiers in Cell and Developmental Biology

Abstract

Background: Prior studies indicate that peer victimization (including bullying) is associated with higher risk for depression and suicidal ideation across the life course. However, molecular mechanisms underlying these associations remain unclear. This two-cohort study proposes to test whether epigenetic aging and pace of aging, as well as a DNA methylation marker of responsive to glucocorticoids, are associated to childhood peer victimization and later depressive symptoms, or suicidal ideation. Methods: Cohort 1: Epigenome-wide DNA methylation (EPIC array) was measured in saliva collected when participants were 10.47 years (standard deviation = 0.35) in a subsample of the Quebec Longitudinal Study of Child Development (QLSCD, n = 149 participants), with self-reported peer victimization at 6–8 years, depressive symptoms (mean symptoms, and dichotomized top 30% symptoms) and suicidal ideation at 15–17 years. Cohort 2: Epigenome-wide DNA methylation (EPIC array) was measured in blood collected from participants aged 45.13 years (standard deviation = 0.37) in a subsample of the 1958 British Birth cohort (1958BBC, n = 238 participants) with information on mother-reported peer victimization at 7–11 years, self-reported depressive symptoms at 50 years, and suicidal ideation at 45 years. Five epigenetic indices were derived: three indicators of epigenetic aging [Horvath’s pan-tissue (Horvath1), Horvath’s Skin-and-Blood (Horvath2), Pediatric-Buccal-Epigenetic age (PedBE)], pace of aging (DunedinPACE), and stress response reactivity (Epistress). Results: Peer victimization was not associated with the epigenetic indices in either cohort. In the QLSCD, higher PedBE epigenetic aging and a slower pace of aging as measured by DunedinPACE predicted higher depressive symptoms scores. In contrast, neither the Horvath1, or Horvath2 epigenetic age estimates, nor the Epistress score were associated with depressive symptoms in either cohort, and none of the epigenetic indices predicted suicidal ideation. Conclusion: The findings are consistent with epigenome-wide and candidate gene studies suggesting that these epigenetic indices did not relate to peer victimization, challenging the hypothesis that cumulative epigenetic aging indices could translate vulnerability to depressive symptoms and suicidal ideation following peer victimization. Since some indices of epigenetic aging and pace of aging signaled higher risk for depressive symptoms, future studies should pursue this investigation to further evaluate the robustness and generalization of these preliminary findings.

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  • Global methylation measures are unable to capture stress-related risk.

    “Of note, global methylation measures are unable to capture stress-related risk.”

    From Exploring the neurobiological markers of suicidal behaviors in pediatric population: a narrative review (2026) · cites this paper as [63]

    The Results (page unavailable) report that childhood peer victimization was not associated with the epigenetic indices in either cohort. But the paper studied selected methylation-based indices, not global methylation measures, and found some associations with depressive symptoms. Its findings do not establish that global measures are unable to capture stress-related risk generally. (LLM, conf=0.87)

    Experimental — accuracy not yet measured
  • Such global epigenetic aging indices primarily track biological aging rather than specific stress-responsive methylation alterations.

    “These findings demonstrate that such global indices primarily track biological aging rather than specific stress-responsive methylation alterations, and underscore the need for more targeted epigenetic biomarkers reflecting cumulative psychosocial stress rather than general methylation drift (63).”

    From Exploring the neurobiological markers of suicidal behaviors in pediatric population: a narrative review (2026) · cites this paper as [63]

    The Introduction (page unavailable) says epigenetic clocks were developed to capture aging-related methylation changes and distinguishes them from the glucocorticoid-sensitive Epistress score. That supports the distinction between aging indices and a stress-responsive measure, but the Discussion does not demonstrate that the clocks primarily track aging *rather than* stress-related changes: it reports no association with peer victimization for either the clocks or Epistress. Nor does it call for targeted biomarkers of cumulative psychosocial stress instead of general methylation drift. (LLM, conf=0.84)

    Experimental — accuracy not yet measured
  • In Perret et al., although victimized youth exhibited higher rates of later depression and suicidality, broad methylation-age metrics (Horvath1/2 clocks, DunedinPACE, Epistress glucocorticoid scores) did not differ between exposed and control groups.

    “Perret et al. examined whether childhood peer victimization was reflected in established epigenetic aging indices such as the Horvath1/2 clocks, DunedinPACE, and Epistress glucocorticoid scores. Although victimized youth exhibited higher rates of later depression and suicidality, these broad methylation-age metrics did not differ between exposed and control groups (63).”

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Authors
Perret, L. C., Geoffroy, M.-C., Barr, E., Parnet, F., Provencal, N., Boivin, M., O’Donnell, K. J., Suderman, M., Power, C., Turecki, G., & Ouellet-Morin, I.
Affiliations
  • McGill University (CA)
  • Simon Fraser University (CA)
  • Université de Montréal (CA)
  • Université Laval (CA)
  • Canadian Institute for Advanced Research (CA)
  • University of Bristol (GB)
  • University College London (GB)
Venue
Frontiers in Cell and Developmental Biology
Published
2023-01-12
Volume
10
Pages
1051556-1051556
ISSN
2296-634X (ISSN-L)
OpenAlex
W4315707307
Cited by
19
References
79
Citations by year
2026: 4 · 2025: 9 · 2024: 5 · 2023: 1
FWCI
1.69
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Cell and Developmental Biology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion, cc-by)
  • eScholarship@McGill (McGill) (submittedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
American Foundation for Suicide Prevention
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
  • Social Sciences › Psychology › Social Psychology › Bullying, Victimization, and Aggression
  • Social Sciences › Psychology › Clinical Psychology › Child Abuse and Trauma
Keywords
bullying, depression, suicidal ideation, DNA methylation, pace of aging, glucocorticoid response, epigenetic age, adulthood, cumulative adversity, 1958 British birth cohort, Quebec Longitudinal Study of Child Development, blood DNA methylation

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