Is It Written In Our Genes? Epigenetic Impact of Collective Trauma

Previous findings by our group indicate that psychological factors such as trauma-impacted versus resilient family environments, and individual vulnerability versus resilience, predict both negative and positive mental health outcomes among children of trauma survivors across different populations (Bekes & Starrs, 2024; Kaur & Bekes, 2025). Earlier work also demonstrated the relevance of specific genetic polymorphisms (e.g., DRD4, 5-HTTLPR, MAOA) in determining increased sensitivity or resilience to early social environments (Lakatos et al., 2003; Gervai et al., 2007). The present study integrates these two lines of research to examine the interaction between psychosocial and genetic factors influencing vulnerability and resilience among descendants of Holocaust survivors. Data are collected from more than 300 Holocaust survivors and descendants of Holocaust survivors in Hungary, including psychological self-report measures and biological (saliva) samples. Psychological vulnerability and resilience are assessed by self-reported childhood trauma, adverse childhood experiences, trauma-impacted versus resilient family environment, as well as individual vulnerability and resilience. Genetic variables are derived from saliva samples, focusing on sensitivity- and resilience-related allelic variants. Mental health outcomes include self-reported symptoms of anxiety, depression, PTSD, and complex PTSD (C-PTSD), as well as measures of flourishing and psychological well-being. Beyond the examination of gene–environment interactions, the study also explores potential epigenetic mechanisms contributing to trauma transmission. Biological samples will be stored in a biobank to allow analyses of DNA methylation and other molecular markers. Specifically, we aim to test whether genetic and epigenetic variants confer heightened biological susceptibility to trauma, predicting vulnerability to depression, anxiety, PTSD, and C-PTSD symptoms following trauma exposure. We will also examine whether these sensitivity factors interact with parenting style and childhood adversity to predict psychological outcomes in the context of transgenerational trauma. In addition, we aim to assess whether transgenerational trauma is associated with accelerated biological aging in the second and third generations (G2, G3), and whether trauma exposure during different life stages (childhood versus adulthood) affects DNA methylation and epigenetic aging indicators differentially. This approach builds on recent evidence suggesting that trauma exposure can leave lasting epigenetic marks, particularly in stress response-related genes such as FKBP5 and NR3C1 (Yehuda et al., 2016; Bierer et al., 2020; Jawaid et al., 2018; Youssef et al., 2018). Altered methylation levels in these regions have been linked to dysregulation of the stress response system and to intergenerational differences in mental health outcomes. By integrating psychological, genetic, and epigenetic perspectives, the present study aims to clarify mechanisms of both sensitivity and resilience in the long-term effects of collective trauma. The findings will contribute to understanding individual differences in vulnerability and adaptation, and identify protective factors that promote resilience and thriving across generations. Genetic variants: Genetic sensitivity and resilience markers: presence/absence of specific gene variants known to influence environmental sensitivity, including: Dopamine D4 receptor (DRD4) gene exon 3 VNTR long (7-repeat) allele and short (4-repeat) allele) Serotonin transporter gene promoter region VNTR (5-HTTLPR): short (14-repeat) allele Monoamine oxidase A (MAOA) gene length polymorphism: low activity variant Epigenetic variants: DNA methylation levels in candidate genes related to stress response and HPA axis regulation, including FKBP5, NR3C1 (glucocorticoid receptor) genes), as well as exploratory analyses of genome-wide epigenetic variation. Epigenetic aging: calculated using established methylation-based epigenetic clocks to estimate biological age acceleration relative to chronological age