The classic nature versus nurture debate revolves around the idea that either genes or the environment make us who we are. But what if these two factors interact in a way that our experiences become embedded in our genes?
Biological embedding is a concept in medical and life sciences described in metaphor by Hertzman (2012) as “experience, ‘getting under the skin’ in ways that alter human biological and developmental processes.” Historically, this concept originated in population health upon observing that a socioeconomic gradient was correlated with the differences in health outcomes of individuals.
One of the underlying mechanisms of biological embedding is epigenetics. Meaning “on or above the genes”, this subfield of genetics focuses on the study of DNA modifications that do not involve changes in the nucleotide sequence, but affect the level at which genes are expressed or silenced, and are heritable to cellular progenies.
DNA methylation is a gene-silencing mechanism with astounding importance in the development of an organism. It refers to the addition of a methyl group at the 5’ position of cytosine in CG sequences of the DNA, known as CpG sites. Cytosine methylation is stable (due to covalent bonding) and reversible; thus, it is effective for the environmental programming of gene expression (Meaney & Szyf, 2005).
Research on animals shows that experience is associated with differences in DNA methylation. For instance, in rodents, high maternal licking and grooming of pups were associated with lower methylation at the promoter of the glucocorticoid receptor gene (Nr3c1), which is involved in stress coping response. Likewise, cross-fostering of pups from low to high maternal care reduced methylation at Nr3c1 (Weaver et al., 2004; McGowan et al., 2011). The induced DNA demethylation by maternal care increased the binding of the transcription factor NGFI-A (nerve growth factor-inducible protein A) to Nr3c1 (Weaver et al., 2004). Therefore, changes to the epigenome served as a cellular memory of that early life experience.
In humans, the social environment also induces DNA methylation changes. Past catastrophes resulted in negative metabolic and mental health outcomes in the later life of survivors. For example, a gene that plays a role in growth and metabolism was found to be hypomethylated among adults born to women who experienced famine during the Dutch Hunger Winter (Heijmans’s et al., 2008). Meanwhile, reduced methylation of the FKBP5 gene, correlated with reduced cortisol production, was observed among adult offspring of Holocaust survivors (Yehuda et al., 2016). However, it is important to note that because of the multifaceted environment that humans inhabit, it is difficult to isolate specific aspects of experience that induce epigenetic changes.
The interplay between genes and environment adds another layer of uniqueness to each individual. What previously seemed to be a competition between these two things is now viewed as a collaboration giving rise to the most elaborate gene regulatory mechanisms, revealing our genome to be etched with the traces of our life experiences.
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