By Anastasiia Gryshyna
Many of us have heard a common debate between the fields of biology and sociology. Are human traits, behavior, and personality influenced by nature, or by nurture? Before we dive deep into this debate, let’s define these two terms.
Nature refers to a person’s genetic makeup. In other words, this is something that is passed down to you from your parents. An example of nature could be a genetic disorder that one or both of your parents had a gene for. Remember that a gene is a block of code in your DNA that dictates what traits you will have. Nurture, on the other hand, refers to the environmental factors that can influence your genetic “fate” by affecting which specific genes are activated or suppressed. The effect of nurture can be seen when looking at identical twins who were separated at birth. These studies, demonstrate that, even with the same genetic makeup, twins can develop different traits and habits based on the environment they were raised in (Guo, 2005; Honeycutt, 2019).
The core pillar of the classic “nature vs. nurture” debate is the idea that genes cannot be changed, and therefore, the genes you are born with will determine the personality, behavior, or even diseases you might develop. Empiricists who cling to the preeminence of the environmental contribution, on the other hand, believe that a person’s traits are primarily determined by their social interactions, experiences, foods consumed, chemicals exposed to, and so on. But what if it does not have to be one or the other? The notion that genetic expression is “set in stone” was debunked when the field of epigenetics was discovered in 1942 by an embryologist Conrad Waddington who introduced the concept of genotype and phenotype interaction (Deichmann, 2016). The term epigenetics makes use of the Greek prefix epi, meaning “over” or “on top of”, so epigenetics literally means something that lies on top of the DNA that that can influence how your genes lead to the traits you have (Ogren & Lombroso, 2008). Epigenetics is a field centered around how our genes interact with the environment to change the expression, or activation, of specific regions of our DNA. This allows scientists to understand why those genetically identical twins separated at birth can grow up to have different personalities and traits.
Epigenetics is a field centered around how our genes interact with the environment to change the expression, or activation, of specific regions of our DNA
But, how does epigenetics work? As mentioned earlier, we are born with a specific set of genes that make up our DNA. Genes have a unique code that can make specific proteins in your body perform certain tasks or bodily functions. And although it might seem like epigenetics would change the genes in your DNA, in reality, it is the expression of these proteins that is affected. A great example of epigenetics is the development of an embryo. We know that every cell in our body has the same DNA, but how do the different types of cells throughout the body know to differentiate into a heart cell or a brain cell? Cell differentiation is possible due to chemical signals released during embryonic development. These signals cause the recruitment of specific regulatory molecules that are able to increase or decrease gene expression to give a cell its particular identity. If expression is enhanced for a combination of genes specific to a brain cell, we will get a brain cell without any change to the genetic code (Ravi & Kannan, 2013)!
The “micro-environmental” changes are not the only ones that can affect your development. The effect of epigenetics on the development of the central nervous system (CNS) is especially prominent in people who were exposed to adverse childhood events, such as abuse (Kuhlman et al., 2015). Exposure to childhood abuse is linked to higher rates of alcoholism, drug abuse, mood disorders, and suicide attempts in adulthood compared to individuals without any exposure to childhood abuse (Felitti et al., 1998). Consequently, epigenetics has been explored to better understand these negative outcomes. One of the epigenetic changes in people who experienced traumatic childhood events is the disruption of a network of structures in the brain that are particularly important in modulation of cognitive, immune, and behavioral responses to stress, called the hypothalamic-pituitary-adrenal (HPA) axis (Aguilera, G. , 2011). Dysregulation of these structures is characterized by an abnormal response to stressful situations and has been associated wit increased depression, anxiety, and suicidal risk (Berardelli et al., 2020). One explanation for HPA axis dysregulation could be epigenetic changes that ultimately result in lower expression (or lower activation) of genes that encode glucocorticoid receptors (Turecki & Meaney, 2016). These receptors are activated by glucocorticoid hormones during stress to maintain homeostasis (or a stable state), so they are very important in stress regulation (Bauer et al., 1999). Indeed, decreased expression of glucocorticoid receptors was found in people who were exposed to childhood abuse and died by suicide, indicating a potential link between childhood abuse and the dysregulation of the HPA axis as a result of epigenetic changes (McGowan et al., 2009).
…exposure to stressors during early life can have a significant impact on the mental and physical health of an individual
These examples show that the brain is highly sensitive to its environment during development, and exposure to stressors during early life can have a significant impact on the mental and physical health of an individual. There is also evidence from rodent studies that a mother’s exposure to stress during pregnancy can lead to epigenetic changes in the developing fetus that correspond with the development of neurological and psychiatric conditions in humans (Zucchi et al., 2013). Additionally, prenatal stress has been associated with disrupted expression of key stress components, like the glucocorticoid receptors and corticotropin-releasing hormone (CRH) (previously known as corticotropin-releasing factor (CRF)), in male mice (Mueller & Bale, 2008). CRH is a hormone that’s associated with stress mediation and also stimulates the release of glucocorticoid hormone (Weninger et al., 1999). One of the many studies investigating the relationship of CRH and stress has shown that infusion of CRH into the rodent brain causes stress-like behaviors, indicating the importance of this hormone in stress-mediation as well as the relationship between CRH and glucocorticoid hormone (Weninger et al., 1999; Jeanneteau et al, 2012).
Epigenetics is an emerging field, and many scientists are leveraging new knowledge about epigenetics to create novel therapeutics or develop better diagnostic techniques. For example, some studies have shown that inhibition of epigenetic changes using specific molecules could potentially treat brain cancer (Mack et al., 2016). This is possible because many cancers are associated with overactive expression, which could be linked to epigenetic factors. So, an intuitive way of overcoming this problem is to block the expression of overactive genes using epigenetic inhibitors. Cancer is not the only disease that has been linked to epigenetic changes. In people suffering from PTSD, epigenetics has been linked to long-term memory formation, specifically for memories associated with a traumatic event. Therapeutic interventions using epigenetics, may also help those suffering from PTSD by preventing the strengthening of those fearful memories (Kwapis & Wood, 2014).
More and more research demonstrates that nature and nurture act together, and that the interaction of your genetics with the environment is what makes you unique. Exploring these epigenetic interactions may give us a better understanding of what it is that makes you one of a kind.
Written by Anastasiia Gryshyna
Edited by Justin McMahon, Lupita Valencia, and Zoe Dobler
Aguilera, G. (2011). HPA axis responsiveness to stress: implications for healthy aging. Experimental gerontology, 46(2-3), 90-95.
Bauer, A., Tronche, F., Wessely, O., Kellendonk, C., Reichardt, H. M., Steinlein, P., Schütz, G., & Beug, H. (1999). The glucocorticoid receptor is required for stress erythropoiesis. Genes & Development, 13(22), 2996-3002.
Berardelli, I., Serafini, G., Cortese, N., Fiaschè, F., O’connor, R. C., & Pompili, M. (2020). The involvement of hypothalamus–pituitary–adrenal (HPA) axis in suicide risk. Brain sciences, 10(9), 653. https://doi.org/10.3390/brainsci10090653
Deichmann, U. (2016). Epigenetics: The origins and evolution of a fashionable topic. Developmental biology, 416(1), 249-254.
Felitti, V. J., Anda, R. F., Nordenberg, D., Williamson, D. F., Spitz, A. M., Edwards, V., & Marks, J. S. (1998). Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults: The Adverse Childhood Experiences (ACE) study. American Journal of Preventive Medicine, 14(4), 245-258. https://doi.org/10.1016/s0749-3797(98)00017-8
Guo, G. (2005). Twin studies: what can they tell us about nature and nurture? Contexts, 4(3), 43-47. https://doi.org/10.1525/ctx.2005.4.3.43
Honeycutt, H. (2019). Nature and nurture as an enduring tension in the history of psychology. Oxford Research Encyclopedia of Psychology. https://doi.org/10.1093/acrefore/9780190236557.013.518
Jeanneteau, F. D., Lambert, W. M., Ismaili, N., Bath, K. G., Lee, F. S., Garabedian, M. J., & Chao, M. V. (2012). BDNF and glucocorticoids regulate corticotrophin-releasing hormone (CRH) homeostasis in the hypothalamus. Proceedings of the National Academy of Sciences, 109(4), 1305-1310.
Kuhlman, K. R., Vargas, I., Geiss, E. G., & Lopez‐Duran, N. L. (2015). Age of trauma onset and HPA axis dysregulation among trauma‐exposed youth. Journal of Traumatic Stress, 28(6), 572-579. https://doi.org/10.1002/jts.22054
Kwapis, J. L., & Wood, M. A. (2014). Epigenetic mechanisms in fear conditioning: implications for treating post-traumatic stress disorder. Trends in Neurosciences, 37(12), 706-720.
Mack, S. C., Hubert, C. G., Miller, T. E., Taylor, M. D., & Rich, J. N. (2016). An epigenetic gateway to brain tumor cell identity. Nature Neuroscience, 19(1), 10-19. https://doi.org/10.1038/nn.4190
McGowan, P. O., Sasaki, A., D’alessio, A. C., Dymov, S., Labonté, B., Szyf, M., … & Meaney, M. J. (2009). Epigenetic regulation of the glucocorticoid receptor in human brain associates with childhood abuse. Nature Neuroscience, 12(3), 342-348.
Mueller, B. R., & Bale, T. L. (2008). Sex-specific programming of offspring emotionality after stress early in pregnancy. Journal of Neuroscience, 28(36), 9055-9065. https://doi.org/10.1523/JNEUROSCI.1424-08.2008
Ogren, M. P., & Lombroso, P. J. (2008). Epigenetics: behavioral influences on gene function, part I. Maternal behavior permanently affects adult behavior in offspring. Journal of the American Academy of Child & Adolescent Psychiatry, 47(3), 240-244.
Ravi, B., & Kannan, M. (2013). Epigenetics in the nervous system: an overview of its essential role. Indian Journal of Human Genetics, 19(4), 384. https://doi.org/10.4103/0971-6866.124357
Slominski, A. (2009). On the role of the corticotropin‐releasing hormone signalling system in the aetiology of inflammatory skin disorders. British Journal of Dermatology, 160(2), 229-232.
Turecki, G., & Meaney, M. J. (2016). Effects of the social environment and stress on glucocorticoid receptor gene methylation: A systematic review. Biological Psychiatry, 79(2), 87-96. https://doi.org/10.1016/j.biopsych.2014.11.022
Weninger, S. C., Dunn, A. J., Muglia, L. J., Dikkes, P., Miczek, K. A., Swiergiel, A. H., Berridge, C. W., & Majzoub, J. A. (1999). Stress-induced behaviors require the corticotropin-releasing hormone (CRH) receptor, but not CRH. Proceedings of the National Academy of Sciences, 96(14), 8283-8288. https://doi.org/10.1073/pnas.96.14.8283
Zucchi, F. C. R., Yao, Y., Ward, I. D., Ilnytskyy, Y., Olson, D. M., Benzies, K., Kovalchuk, I., Kovalchuk, O., & Metz, G. A. S. (2013). Maternal stress induces epigenetic signatures of psychiatric and neurological diseases in the offspring. PLoS One, 8(2), e56967. https://doi.org/10.1371/journal.pone.0056967