When Nurture Shapes Nature: The Role of Epigenetics in Inherited Trauma
By Alisha Karuvannur-Sandhu, Behavioral Neuroscience & Philosophy, 2023
The nature versus nurture debate has been a pressing controversy for centuries, from John Locke’s blank slate theory in 1690, to the twentieth century ideology of biological determinism. But what if the two are not as separate as we once thought? The rising field of epigenetics is demonstrating that nature and nurture don’t merely exist as discrete entities — they’re inherently intertwined.
Epigenetics, in short, is the study of gene expression modification. Literally defined as “above genetics,” epigenetics work to drive cell differentiation and function. Genes contain all the instructions for the cells in our body, but the epigenome determines how those instructions are actually carried out. If the genome is the hardware of our cells, then the epigenome is the software, acting in collaboration with the genome to dictate what is expressed and where. Gene expression is what distinguishes skin cells from muscle cells, glial cells from endothelial cells, and so forth. Our genes are fixed: from fertilization until death, every cell in our bodies contains the same DNA. Our epigenome, on the other hand, is fluid, constantly being molded by our environment, our experiences, our traumas. As the field continues to grow, we’re learning that epigenetics have a major impact on not only physical health, but psychological health as well. And as it turns out, the effect of trauma on epigenetics goes beyond the individual; the repercussions can span across generations. This phenomenon, where one person’s experiences alter the psychology of their progeny, has been coined the name transgenerational trauma.
The rising field of epigenetics is demonstrating that nature and nurture don’t merely exist as discrete entities — they’re inherently intertwined.
Numerous behavioral studies have exemplified that trauma can be biologically inherited. In one study conducted by Brian Dias and Kerry Ressler at Emory University, mice were conditioned to fear the smell of the chemical acetophenone. The F0 generation was placed in a chamber, where Ressler and Dias would waft the scent through. The mice would be delivered electric shocks every time the odor was introduced, leading them to associate the smell of acetophenone with pain until they exhibited a fear response to the scent even in the absence of shocks. The subsequent F1 and F2 generations demonstrated the same response when they encountered acetophenone, despite never having been directly conditioned to connect the scent to pain. This same reaction was observed in offspring conceived via in vitro fertilization, regardless of whether it was the eggs from conditioned mothers or sperm from conditioned fathers used for IVF. Ressler and Dias studied the neuroanatomy of F0 and F1 mice and found that both generations had high numbers of acetophenone–responsive olfactory sensory neurons.
The variability of the epigenome begs the question: is there a way, then, to reverse epigenetic changes caused by trauma?
There are several processes by which epigenetic markers work to modify gene expression. DNA methylation is one such process which researchers have proposed is likely linked to the inheritance of trauma. Methylation works by altering the structure of chromatin, the complex of DNA strands and histone proteins found in the cell nucleus. When methyl groups are added to the strands, it causes the chromatin to become more tightly condensed, hence repressing gene transcription by making DNA less accessible. In the acetophenone conditioning study, the mice’s sperm cells showed less methylation on genes linked to acetophenone sensing. This decreased methylation means that the mice would show greater expression of acetophenone odor-receptor genes. Still, the exact mechanism that causes odor-detection to be associated with pain remains unknown.
Of course, there are other non-biological factors that play into the concept of transgenerational trauma. Firsthand exposure to trauma likely impacts parental behavior, possibly contributing to the transmission of trauma. The jury’s still out on just how heavily epigenetic modification weighs against these social components of traumatic inheritance. Additionally, it’s a tricky issue to research — after all, the complexity of human trauma is difficult to replicate in more psychologically simplistic animal models. Nevertheless, this growing field does offer some hope for the descendants of trauma survivors. The variability of the epigenome begs the question: is there a way, then, to reverse epigenetic changes caused by trauma? As epigenetics research continues to advance, psychotherapeutic and pharmacological interventions may show promise in the treatment of inherited trauma-related dysfunction.
Nature (2013) DOI: 10.1038/nn.3594
Environ Epigenet (2018) DOI: 10.1093/eep/dvy018
Brain Sci. (2018) DOI: 10.3390/brainsci8050083
Curr Psychiatry Rep (2018) DOI: 10.1007/s11920–018–0898–7
Nature (2019) DOI: 10.1038/s41380–018–0272–5
