Stress-Induced Apoptosis

By Elijah Powell

From Unsplash

Intro

Stress has become increasingly prevalent. We are exposed to stressors on a daily basis—media usage, the hyper-competitiveness of the job market, and negative social interactions can all be causes of stress. Short-term stress can be healthy and result in a boost to your immune system, cognitive performance, and more. Chronic stress, however, can be detrimental to physical and mental health, resulting in completely adverse effects. The solution is to rethink stress so we can maintain healthy levels of it and find new strategies to cope.

Keywords: hypothalamic-pituitary-adrenal axis; Cortisol; Central Nervous System; Peripheral Nervous System; Adaptive Immune Response; Innate Immune Response; Secondary Immune Response; lymphocytes; monocytes; Stressor

Stress

Stress is a biological reaction to different stressors. Your brain receives external stimuli and interprets them as stressors, activating a cascade of events that result in the activation of the hypothalamic-pituitary-adrenal axis (HPA axis). Simultaneously, the sympathetic nervous system is activated, giving you the feeling of being “antsy,” experiencing butterflies, or acute anxiety. This junction, connecting the Central and Peripheral Nervous Systems, is one of the many examples of how neurotic behaviors can be detrimental to physical well-being.

Researchers have also found that stress activates the immune response by creating pro-inflammatory environments.

An Inhibited Immune Response

In the short term, this can be advantageous. Triggering the immune response can isolate pathogens that would otherwise go undetected, strengthen anti-tumor immune responses, improve innate, secondary, and adaptive immune responses, increase cardiovascular function, enhance mental/cognitive performance, and more. However, once stress reaches chronic levels, it can have completely adverse effects. These include the inhibition of the immune response, physical and cognitive decline, the development of severe neurotic traits such as anxiety, and apoptosis, also known as programmed cell death. Apoptosis is a process of natural cell death. This process is effective when eliminating potentially cancerous or otherwise unhealthy cells and possibly preventing agglutination—the bursting of blood cells due to protein mismatches.

Cortisol-Induced Cell Death (Apoptosis)

Cortisol-induced cell death occurs due to the immune system’s activation. This can be harmful as it prevents the immune system from reacting to more detrimental issues, such as fighting disease or eliminating cancerous cells. Chronic stress has been shown to cause immunosuppression by killing healthy white blood cells, specifically lymphocytes and monocytes. This increases your susceptibility to infection and even specific cancers.

Conclusion

The prevalence of stress in our society necessitates the development of more effective coping mechanisms. Stress cannot be eliminated from our lives, nor should it be. Instead, we should learn to handle stressful situations, be able to identify when stress is healthy, and recognize when it’s not. Chronic stress can make you susceptible to certain cancers and infections by inhibiting your body’s natural defense mechanisms.

Works cited

Dhabhar F. S. (2018). The short-term stress response - Mother nature's mechanism for enhancing protection and performance under conditions of threat, challenge, and opportunity. Frontiers in neuroendocrinology, 49, 175–192. https://doi.org/10.1016/j.yfrne.2018.03.004

Dhabhar F. S. (2009). Enhancing versus suppressive effects of stress on immune function: implications for immunoprotection and immunopathology. Neuroimmunomodulation, 16(5), 300–317. https://doi.org/10.1159/000216188

Feng, X., Reini, S. A., Richards, E., Wood, C. E., & Keller-Wood, M. (2013). Cortisol stimulates proliferation and apoptosis in the late gestation fetal heart: differential effects of mineralocorticoid and glucocorticoid receptors. American journal of physiology. Regulatory, integrative and comparative physiology, 305(4), R343–R350. https://doi.org/10.1152/ajpregu.00112.2013