Cardiovascular disease (CVD) is the current leading cause of death in the United States, accounting for hundreds of thousands of deaths annually and disproportionately, which in turn affects marginalized communities (Gupta et al., 2025). Individual genetics and lifestyle choices such as diet, exercise, and smoking have been historically used as dominant explanations for CVD. Even though these factors are important to assess, we also need to recognize that social experiences can be biologically embedded. Chronic stressors, including racism, poverty, food insecurity, and environmental pollutants, can modify gene expression through epigenetic processes without altering the underlying DNA sequence (Aroke, 2018). A strong framework for comprehending how social contexts “get under the skin” and influence cardiovascular risk throughout life is provided by epigenetics, which is the study of heritable changes in gene expression that take place without changes in DNA sequence (Feinberg, 2018).

It is crucial to distinguish between genetics and epigenetics in order to comprehend this relationship. The DNA sequence inherited from one’s parents, which serves as the blueprint for biological development, is referred to as genetics. On the other hand, epigenetics deals with changes that control whether genes are “on” or “off.” One typical analogy used for this phenomenon is that DNA is like a computer’s hardware, while epigenetic markers are like software instructions that control how that hardware works. These alterations affect how genes are expressed but do not alter the genetic code itself. DNA methylation, histone modification, and telomere shortening are examples of important epigenetic processes. DNA methylation is the process of adding methyl groups to DNA, and this frequently results in the suppression of gene expression (Eberharter, 2002). Histone modification affects gene accessibility by changing the degree to which DNA is coiled around histone proteins (Zhang, 2020). Cellular age and prolonged stress cause telomeres, the protective caps at the ends of chromosomes, to shorten, which adds to biological deterioration.

Because the cardiovascular system reacts quickly to stress hormones, inflammation, and metabolic disturbances, it is especially vulnerable to epigenetic modifications. Prolong activation of stress-response mechanisms can disrupt lipid metabolism, increase vascular inflammation, and dysregulate blood pressure, which are all key in the development of atherosclerosis and hypertension. Repeated activation of these symptoms over time results in cumulative physiological burden, which is also known as an allostatic load (McEwen & Gianaros, 2010).

Chronic stress and allostatic load are two important pathways that connect socioeconomic factors to cardiovascular outcomes. Stress stimulates the sympathetic nervous system, which raises blood pressure and heart rate, and activates the hypothalamic-pituitary-adrenal (HPA) axis, which releases cortisol (Chu, 2024). Short-term stress reactions are adaptive, but long-term exposurecasues hypertension, endothelial dysfunction, and persistent inflammation. According to research, extended stress may change the methylation patterns in genes that control inflammatory pathways and cortisol responses, recalibrating the body’s stress response system (Hing, 2018). Poverty, employment insecurity, caregiving responsibilities, and dangerous areas are examples of social factors that lead to long-term stress exposure rather than short-term difficulties. These exposures eventually raise blood pressure, cause vascular inflammation, and raise the risk of heart attacks and strokes (McEwen & Gianaros, 2010).

One powerful long-term stressor with quantifiable biological effects is racism. In addition to institutional racism ingrained in the housing, work, and healthcare systems, experiences of discrimination, hypervigilance, and microaggressions cause long-term psychological and physical strain. Evidence reveals that racial disparities in cardiovascular outcomes are caused by social settings molded by racism rather than innate biological variations (Rollin, 2023). Research has also found evidence of increases biological aging, also referred to as “weathering,” and changed DNA methylation patterns which are linked to chronic prejudice (Geronimus et al., 2006). Chronic racial stress has also been linked to telomere shortening, which is a sign of cumulative cellular aging (Chae et al., 2020). These molecular mechanisms are consistent with epidemiological evidence that Black Americans have greater incidences of hypertension and heart disease that manifests earlier (Flack et al., 2003). Racism-related maternal stress may also affect prenatal programming, making offspring more vulnerable to CVD in later life (Liu & Glynn, 2021). Therefore, racism functions as a social determinant that uses epigenetic pathways to become biologically ingrained.

Another important channel is diet and the food surroundings. Food deserts, also known as food swamps, are prevalent in many places and are defined by the scarcity of fresh produce and the abundance of highly processed goods. Major risk factors for CVD include obesity, insulin resistance, and dyslipidemia, which are all exacerbated by diets heavy in sodium, carbohydrates, and unhealthy fats (Dina et al., 2025). Poor diet can change the expression of genes that are linked to lipid metabolism and metabolic control epigenetically. For instance, methylation alterations in genes related to insulin signaling and inflammation have been linked to high-fat diets (Keleher et al., 2018). Additionally, fetal gene expression patterns can be influenced by the mother’s diet during pregnancy; this process is referred to as developmental or fetal programming (Lee, 2015). The intergenerational effects of food disparities are demonstrated by the increased lifetime vulnerability to metabolic diseases and cardiovascular disease caused by inadequate prenatal nutrition (Shonkoff et al., 2012).

Through epigenetic pathways, environmental exposures, including lead, air pollution, and industrial pollutants, increase the risk of cardiovascular disease. Air pollution can cause systemic inflammation and oxidative stress, which can alter DNA methylation in genes that control vascular function (Rider, 2019). These procedures raise the risk of coronary artery disease, stroke, and hypertension. Due to historical redlining and zoning practices, communities of color and low-income residents are disproportionately exposed to environmental dangers, which perpetuates structural disparities in cardiovascular outcomes (Needham et al., 2015).

Additionally, epigenetics sheds light on life-course and intergenerational ramifications. Prenatal or early childhood epigenetic markings can last until adulthood and, in certain situations, be passed down across generations (Bohacek & Mansuy, 2012). Stress, malnutrition, and exposure to toxins during pregnancy can affect how the embryonic cardiovascular system develops, which places people at risk for high blood pressure and metabolic problems in the future (Cui et al., 2026). This helps explain why, even in cases when hereditary variations are negligible, cardiovascular disparities continue to exist over generations. One generation’s social circumstances can influence a subsequent generation’s biological susceptibility.

These discoveries have significant policy and public health ramifications. Going beyond individual-level advice to “eat better” or “exercise more” is necessary to address CVD. Behavior modification is crucial, but without structural changes, it is insufficient. To mitigate biologically embedded risk, policies that increase housing stability, provide access to nutritional meals, lower environmental pollution, and eliminate discriminatory systems are crucial. Investing in community-driven interventions, tackling structural racism, and screening for social determinants of health in clinical settings are essential tactics for reducing CVD inequities at their source.

In conclusion, epigenetic mechanisms can transform social experiences into biological realities. Gene expression patterns that affect inflammation, blood pressure, and metabolic regulation are altered by long-term stress, racism, food injustice, and environmental pollutants. By bridging the gap between social science and biology, epigenetics shows that cardiovascular inequities are socially created and therefore avoidable, rather than being inherent. In addition to lowering present cardiovascular risk, enhancing social and environmental conditions can change gene expression patterns for future generations, thereby promoting health equity.

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References

 Aroke, E. N., Joseph, P. V., Roy, A., Overstreet, D. S., Tollefsbol, T. O., Vance, D. E., & Goodin, B. R. (2019). Could epigenetics help explain racial disparities in chronic pain? Journal of Pain Research, 12, 701–710. https://doi.org/10.2147/JPR.S191848

Bohacek, J., & Mansuy, I. M. (2012). Epigenetic Inheritance of Disease and Disease Risk. Neuropsychopharmacology, 38(1), 220–236. https://doi.org/10.1038/npp.2012.110

Chae, D. H., Wang, Y., Martz, C. D., Slopen, N., Yip, T., Adler, N. E., Fuller-Rowell, T. E., Lin, J., Matthews, K. A., Brody, G. H., Spears, E. C., Puterman, E., & Epel, E. S. (2020). Racial discrimination and telomere shortening among African Americans: The Coronary Artery Risk Development in Young Adults (CARDIA) Study. Health Psychology, 39(3), 209–219. https://doi.org/10.1037/hea0000832

Chu, B., Marwaha, K., Ayers, D., & Sanvictores, T. (2024, May 7). Physiology, Stress Reaction. PubMed; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK541120/

Cui, S., Deng, F., Lu, M., Zhang, M., Yang, Z., Ma, Y., Fan, L., Gao, Q., & Feng, D. (2026). Maternal nutritional imbalance during pregnancy and the development of fetal-origin cardiovascular diseases. Frontiers in Nutrition, 13. https://doi.org/10.3389/fnut.2026.1717069

Dina, C., Tit, D. M., Radu, A., Bungau, G., & Radu, A.-F. (2025). Obesity, Dietary Patterns, and Cardiovascular Disease: A Narrative Review of Metabolic and Molecular Pathways. Current Issues in Molecular Biology, 47(6), 440. https://doi.org/10.3390/cimb47060440

Eberharter, A., & Becker, P. B. (2002). Histone acetylation: a switch between repressive and permissive chromatin. EMBO Reports, 3(3), 224–229. https://doi.org/10.1093/embo-reports/kvf053

Feinberg, A. P. (2018). The Key Role of Epigenetics in Human Disease Prevention and Mitigation. New England Journal of Medicine, 378(14), 1323–1334. https://doi.org/10.1056/nejmra1402513

Geronimus, A. T., Hicken, M., Keene, D., & Bound, J. (2006). “Weathering” and Age Patterns of Allostatic Load Scores Among Blacks and Whites in the United States. American Journal of Public Health, 96(5), 826–833.

https://doi.org/10.2105/ajph.2004.060749

Flack, J. M., Ferdinand, K. C., & Nasser, S. A. (2003). Epidemiology of Hypertension and Cardiovascular Disease in African Americans. The Journal of Clinical Hypertension, 5(1), 5–11. https://doi.org/10.1111/j.1524-6175.2003.02152.x

Gupta, P. S., Jetani, V., Desai, H. D., Kyada, S., Sonani, S. B., Gopi, G., Acharya, S., Trivedi, Y., Kotnani, S., & Jain, H. (2025). Widening Racial and Sociodemographic Disparities in Cardiovascular Disease Death Counts in the United States: A Comprehensive Analysis of 2018-2023 National Data. Cureus. https://doi.org/10.7759/cureus.95210

Hing, B., Braun, P., Cordner, Z. A., Ewald, E. R., Moody, L., McKane, M., Willour, V. L., Tamashiro, K. L., & Potash, J. B. (2018). Chronic social stress induces DNA methylation changes at an evolutionary conserved intergenic region in chromosome X. Epigenetics, 13(6), 627–641. https://doi.org/10.1080/15592294.2018.1486654

Keleher, M. R., Zaidi, R., Hicks, L., Shah, S., Xing, X., Li, D., Wang, T., & Cheverud, J. M. (2018). A high-fat diet alters genome-wide DNA methylation and gene expression in SM/J mice. BMC Genomics, 19(1). https://doi.org/10.1186/s12864-018-5327-0

Lee, H.-S. (2015). Impact of Maternal Diet on the Epigenome during In Utero Life and the Developmental Programming of Diseases in Childhood and Adulthood. Nutrients, 7(11), 9492–9507. https://doi.org/10.3390/nu7115467

Liu, S. R., & Glynn, L. M. (2021). The contribution of racism-related stress and adversity to disparities in birth outcomes: Evidence and research recommendations. F&S Reports, 3(2). https://doi.org/10.1016/j.xfre.2021.10.003

McEwen, B. S., & Gianaros, P. J. (2010). Central role of the brain in stress and adaptation: Links to socioeconomic status, health, and disease. Annals of the New York Academy of Sciences, 1186(1), 190–222. https://doi.org/10.1111/j.1749-6632.2009.05331.x

Needham, B. L., Smith, J. A., Zhao, W., Wang, X., Mukherjee, B., Kardia, S. L. R., Shively, C. A., Seeman, T. E., Liu, Y., & Diez Roux, A. V. (2015). Life course socioeconomic status and DNA methylation in genes related to stress reactivity and inflammation: The multi-ethnic study of atherosclerosis. Epigenetics, 10(10), 958–969. https://doi.org/10.1080/15592294.2015.1085139

Rider, C. F., & Carlsten, C. (2019). Air pollution and DNA methylation: effects of exposure in humans. Clinical Epigenetics, 11(1). https://doi.org/10.1186/s13148-019-0713-2

Rollin, F. G., Mould, K. J., & Colon Hidalgo, D. (2023). Racial disparities in cardiovascular outcomes are windows into structural racism, not genetics. Sleep Medicine, 105, 85. https://doi.org/10.1016/j.sleep.2023.03.010

Shonkoff, J., & Garner, A. (2012). The Lifelong Effects of Early Childhood Adversity and Toxic Stress. PEDIATRICS, 129(1), 232–246. https://doi.org/10.1542/peds.2011-2663

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