Unraveling Intergenerational Trauma
By Evelyn Kong
What is the relationship between memory and the self? For years, most scholars would have referenced anything from W.E.B. Du Bois’ theory of double consciousness to Émile Durkheim’s concept of collective trauma — all schools of thought that examine memory and the self in their most abstract form. Now, as a scholarly intersection of epigenetics and intergenerational trauma begins to emerge, a new spindle of knowledge is working to unravel unique insights from within the human genome.
Intergenerational trauma refers to the transfer of extreme adaptations to stressors from one generation to the next [x]. Epigenetics can be defined as the study of how one’s behavior and environmental changes can impact the function of heritable genes [x]. In a recent study published by Nature, researchers found that the phenotype for Environmental Sensitivity (ES) has a verifiable genetic basis.
While every human is bound to react differently to different environments, in this study of around 2,000 twins, researchers found that the offspring of parents who adjusted to significantly negative environmental events were inclined to inherit a higher disposition to neuroticism [x] and lower levels of extraversion.
Think of your phenotype—or physical traits as determined by your DNA—as being dormant unless “switched on.” Some are switched on at birth, but others stay inert unless triggered by external stimuli.
If you were living through an extremely traumatic event that required you to stay alert and active, your body may “switch on” a genetic chemical marker that triggers a consistent release of stimulant hormones such as adrenaline. Adrenaline works to raise your heart rate and blood pressure while also repressing your appetite and need for sleep. In a “fight-or-flight” setting, this may save your life. In an environment where your body does not need to endure such stress, if unattended to, this inclination may snowball into clinical anxiety, PTSD, insomnia, and/or various eating disorders.
Say, then, that you have a child after surviving a horrendous environmental event. Even if your child may never experience the same event(s), studies much like the ones mentioned prior have found that their inherited genetic makeup holds a higher likelihood of stating otherwise.
In 2015, Dr. Rachel Yehuda, director of Mount Sinai’s Director of the Traumatic Stress Studies Division, published a popular study that linked Holocaust exposure via FKBP5 methylation from one generation to the next. FKBP5 is a gene known to increase risk for depression and PTSD.
When blood samples of 32 Holocaust survivors and their subsequent offspring were taken, FKBP5 methylation between the two groups were found to be directly correlated. That is, while direct survivors of the Holocaust were more inclined to develop depression and PTSD, their children were born with a genetic imprint suggesting that they experienced the same stressors. This meant that from birth, they inherited an inclination to develop certain stress or anxiety disorders.
Both studies on ES and FKBP5 highlight a growing proof of concept for intergenerational trauma. As researchers continue to unravel the stories hidden within our DNA, the development of empirical scientific evidence may work to unfurl new insights into the process through which a legacy of trauma persists.
Assary, E., Zavos, H. M. S., Krapohl, E., Keers, R., & Pluess, M. (2020). Genetic architecture of Environmental Sensitivity reflects multiple heritable components: A twin study with adolescents. Molecular Psychiatry, 1–9. https://doi.org/10.1038/s41380-020-0783-8
Epigenetics. (n.d.). Genome.Gov. Retrieved October 18, 2021, from https://www.genome.gov/genetics-glossary/Epigenetics
The legacy of trauma. (n.d.). Https://Www.Apa.Org. Retrieved October 18, 2021, from https://www.apa.org/monitor/2019/02/legacy-trauma
Yehuda, R., Daskalakis, N. P., Bierer, L. M., Bader, H. N., Klengel, T., Holsboer, F., & Binder, E. B. (2016). Holocaust Exposure Induced Intergenerational Effects on FKBP5 Methylation. Biological Psychiatry, 80(5), 372–380. https://doi.org/10.1016/j.biopsych.2015.08.005