What’s your earliest memory? Can you remember everything that happened between the ages of three to five? No? Me neither. Despite the gaps in your memory, your body—specifically your DNA—knows what happened to you. It shouldn’t be surprising that DNA has such a good memory. After all, it stores genetic information tracing back thousands of years. This of course prompts several questions, namely the following; how does DNA store my memories and how does that affect me?
Let’s start from the beginning. Epigenetics encompasses all heritable changes in gene activity that do not stem from a change in DNA sequences (Moore et al, 2013). DNA methylation introduces a particularly salient new epigenetic mechanism for gene regulation and cell differentiation. The key to DNA methylation lies within the special enzymes that modify the cytosine DNA base by adding a methyl group (Moore et al, 2013; Suelves, 2016). Interestingly, cell differentiation is partly driven by differing levels of DNA methylation. An overall increase in DNA methylation occurs during the differentiation process, while a decrease in it at cell-specific loci helps define cellular identity (Suelves et al, 2016). Additionally, the progressive decrease in overall DNA methylation can contribute to physiological aging and the development of cancer (Suelves et al, 2016). Overall, these altered cytosines play key roles in human development and health issues (Moore et al, 2013).
This brings us to the second question: how does my DNA’s photographic memory affect me? Well, it turns out that choices such as diet, drinking, exercise, illness, and environmental conditions can all have an impact on genomic stability and gene-specific DNA methylation (Lim et al, 2012). So while you might not remember what happened as a kid, your DNA may already be internalizing those experiences. The Avon Longitudinal Study of Parents and Children patiently waited for years so they could specifically study how childhood experiences affect epigenetic markers in adolescence. A cohort of 13,988 children with due dates between April 1991 and 1992 were monitored for exposure to childhood adversity from birth to the age of eleven. Using changes in DNA methylation at the age of fifteen, researchers investigated whether the timing of adversity has epigenetic consequences across childhood and adolescence (Lussier et al, 2023).
Each mother reported whether their child faced any of the following seven types of childhood adversity; caregiver physical or emotional abuse, sexual or physical abuse, maternal psychopathology, one-adult households, family instability, and neighborhood disadvantage as well as the timing that the adversity was present. Out of the 13,988 children, 609-665 showed signs of both adversity and a decrease in DNA methylation at 15 years old (Lussier et al, 2023).
Within this sample from the original cohort, further DNA analysis identified twenty-two loci that showed significant associations between exposure to adversity and altered DNA methylation at the age of 15 (Lussier et al, 2023). Of the loci identified to be associated with decreased DNA methylation, the highest percent of loci were correlated with growing up in one-adult households (Lussier et al, 2023). None of the identified loci indicated that adversity may alter DNA methylation at birth or the age of seven, but instead only emerged in adolescence (Lussier et al, 2023).
Researchers concluded that the ages between three and five years old are when children are vulnerable to adversity and the consequences of this adversity may biologically embed itself and later manifest itself in adolescence (Lussier et al, 2023). Additionally, the adversity-associated decrease in DNA methylation is correlated to have effects on the central nervous system (Lussier et al, 2023). Of course, it’s great timing that the altered DNA methylation becomes an issue during puberty. Especially since it’s associated with poor self-esteem and increased depressive symptoms.
What’s the upside? There has to be a silver lining or else this article is just a doomsday proclamation. The ability to finally trace health complications back to epigenetic mechanisms due to latent childhood trauma provides an important piece of the puzzle of understanding complex diseases. However, the puzzle is far from solved. The cohort in this study was predominantly of European descent and further research into how the complexities of race factor into DNA methylation and childhood adversity is the next step in this journey.
Literature Cited:
Lim , U., & Song, M. (2012). Dietary and Lifestyle Factors of DNA Methylation. In Cancer Epigenetics (Vol. 863, pp. 359–376). Humana Press.
Lussier, A. A., Zhu, Y., Smith B. J., Cerutti J., Fisher J., Melton P. E., Wood N. M., Cohen-Woods S., Huang R., Mitchell C., et al. (2023). Association between the timing of childhood adversity and epigenetic patterns across childhood and adolescence: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC) prospective cohort. Lancet Child Adolesc Health. 7(8), 532-43. https://doi.org/10.1016/S2352-4642(23)00127-X
Moore, L. D., Le, T., & Fan, G. (2013). DNA methylation and its basic function. Neuropsychopharmacology, 38(1), 23–38. https://doi.org/10.1038/npp.2012.112
Suelves, M., Carrió, E., Núñez-Álvarez, Y., & Peinado, M. A. (2016). DNA methylation dynamics in cellular commitment and differentiation. Briefings in Functional Genomics, elw017. https://doi.org/10.1093/bfgp/elw017