Stress and Cancer Risk: Examining HPA Axis, Inflammation, and Epigenetic Mechanisms

By: Brian S. MH, MD (Alt. Med.)

This article responds to a case in which a woman developed breast cancer shortly after losing her job. Prior to this, she worked as a manager at an herbal tea manufacturing company, where she consumed a substantial amount of herbal tea daily. She attributed her cancer to the herbal teas she regularly consumed.

Chronic stress is likely a significant factor contributing to the development of her cancer, rather than solely the herbal tea she consumed.Research strongly supports the idea that chronic stress and its physiological impacts—particularly through dysregulation of the HPA (hypothalamic-pituitary-adrenal) axis, increased cortisol levels, inflammation, oxidative stress, and epigenetic alterations—can influence cancer risk and progression.

1. Chronic Stress and HPA-Axis Dysregulation

Chronic stress triggers prolonged activation of the HPA axis, which leads to continuous secretion of cortisol, the primary stress hormone (McEwen, 2008). High cortisol levels under chronic stress conditions can disrupt the body’s normal physiological processes. Cortisol, while anti-inflammatory in acute phases, can promote inflammation when elevated long-term due to immune system dysregulation (Chida et al., 2008). Chronic inflammation is a known risk factor for cancer because it fosters an environment conducive to DNA damage, cellular mutations, and immune evasion by cancer cells (Coussens & Werb, 2002).

In this case, prolonged stress from both job loss and the emotional strain of losing a familiar routine might have exacerbated the woman’s HPA axis dysregulation, leading to cortisol imbalance. Elevated cortisol also interferes with the body’s natural detoxification processes, which means that potential environmental toxins and cellular waste may not be efficiently cleared, creating conditions that promote oxidative stress. The accumulation of free radicals and subsequent oxidative damage can lead to cellular mutations, which increase the risk of cancerous growth (Reuter et al., 2010).

2. Increased Cortisol, Oxidative Stress, and Inflammation

Chronic stress-induced cortisol elevation also impedes normal antioxidant defenses, leading to increased oxidative stress. Studies show that cortisol and other stress hormones can contribute to cellular oxidative damage by increasing the production of reactive oxygen species (ROS) (Elenkov & Chrousos, 2002). ROS damage cellular DNA, which can induce genetic mutations that initiate cancer development.

Furthermore, inflammation from prolonged cortisol exposure can contribute to a pro-tumor environment. Inflammation is associated with angiogenesis (formation of new blood vessels) and tissue remodeling, both of which can support the growth and metastasis of tumors (Mantovani et al., 2008). This woman’s persistent emotional stress would likely increase her oxidative stress load, creating conditions conducive to DNA mutations and impaired cellular repair mechanisms.

3. Epigenetic Alterations

Chronic stress may also lead to cancer through epigenetic modifications, changes that regulate gene expression without altering the DNA sequence. Stress is known to modify DNA methylation patterns, histone acetylation, and miRNA expression—all of which can silence tumor suppressor genes or activate oncogenes (Flanagan et al., 2006). For example, studies indicate that stress-induced epigenetic changes can silence genes responsible for DNA repair, allowing mutations to accumulate unchecked (Hunter et al., 2015).

In this case, job-related stress likely induced epigenetic changes that contributed to a genetic environment favoring tumor growth. These epigenetic modifications can persist over time, leading to long-term alterations in gene expression that could initiate or accelerate cancer progression. This pathway emphasizes that chronic stress can indirectly promote cancer by “unlocking” cancer-promoting genes or suppressing protective ones, even if initial cancerous cells were already present in low numbers.

Conclusion

While herbal tea’s role in triggering cancer is unclear, the significant and well-documented effects of chronic stress on HPA axis function, inflammation, oxidative stress, and epigenetic regulation provide a plausible explanation for this woman’s development of breast cancer. The connection between stress and cancer is increasingly acknowledged, suggesting that chronic stress may be a more likely trigger for her cancer than her employer’s herbal tea products.

References

Chida, Y., Hamer, M., Wardle, J., & Steptoe, A. (2008). "Do stress-related psychosocial factors contribute to cancer incidence and survival?" Nature Clinical Practice Oncology, 5(8), pp. 466-475.

Coussens, L. M., & Werb, Z. (2002). "Inflammation and cancer." Nature, 420(6917), pp. 860-867.

Elenkov, I. J., & Chrousos, G. P. (2002). "Stress Hormones, Th1/Th2 patterns, Pro/Anti-inflammatory Cytokines and Susceptibility to Disease." Trends in Endocrinology and Metabolism, 13(4), pp. 197-204.

Flanagan, J. M., et al. (2006). "Epigenome-wide methylation profiling in cancer: new opportunities for diagnostic and therapeutic intervention." Expert Reviews in Molecular Medicine, 8(18), pp. 1-21.

Hunter, R. G., McEwen, B. S., & Pfaff, D. W. (2015). "Stress and the dynamic genome: Steroid hormones, epigenetics, and the transposome." Proceedings of the National Academy of Sciences, 112(2), pp. 6828-6833.

Mantovani, A., et al. (2008). "Cancer-related inflammation." Nature, 454(7203), pp. 436-444.

McEwen, B. S. (2008). "Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators." European Journal of Pharmacology, 583(2-3), pp. 174-185.

Reuter, S., et al. (2010). "Oxidative stress, inflammation, and cancer: How are they linked?" Free Radical Biology and Medicine, 49(11), pp. 1603-1616.

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