Stress and Cancer (Final Project Draft)
Stress is something we all experience, with significant doses administered daily – and sometimes even hourly. In the appropriate quantity and at the right time, stress helps us meet deadlines and respond efficiently to changes in schedules. Too much stress, however, can lead to detrimental effects on the physical biology of a person; perhaps the most serious of these effects is cancer. Through understanding stress and cancer separately, I’m able to thoroughly explore their relationship and learn how stress causes and/or affects the group of cancerous diseases.
To begin, it is helpful to develop a working definition of what stress actually is. Physician Hans Selye, the “father of stress,” first coined the term in the mid-twentieth century through experiments with lab rats. After injecting rats with harmful substances to temporarily disable specific organs, Selye observed side-effects not directly caused by the disabled organs. What he found, rather, was an indirect reaction to the substances; the rats behaved differently from what the side-effects should have caused (Selye). The reactions were based on psychological responses that in turn led to other biological responses.
Selye developed a theory for the rats’ responses called the General Adaptation Syndrome. The theory is made up of three stages: “1) the alarm reaction, 2) the stage of resistance, and 3) the stage of exhaustion” (Selye). The “totality” of changes observed to have taken place during General Adaption Syndrome – as both positive and negative stress – is what Selye considered to be an accurate measurement of the amount of stress as a reaction. In other words, the magnitude of difference between the body’s natural state of readiness, or homeostasis, and the stage along the General Adaption Syndrome is what Selye considered to be an accurate measurement of stress.
Selye also discovered the initial impact stress has on the body and noted that “…stress causes certain changes in the structure and chemical composition of the body…” (Selye). Although these biological changes are not direct reactions to other biological factors, they are the result of the stress coping mechanisms. He accurately paved the way for future research in this area and properly identified how “the nervous system and endocrine (or hormonal) system play particularly important parts in maintaining resistance during stress” (Selye). Richard Contrada and Andrew Baum are two such researchers who took Selye’s findings a step further in their Handbook of Stress Science: Biology, Psychology, and Health. Selye’s theories have since been confirmed and the Hypothalamo-Pituitary-Adrenal Axis has been identified as the key biological center for stress (Contrada).
But this paper doesn’t focus on stress; it focuses on the relationship between stress and cancer. Contrada and Baum write that although there is “considerable anecdotal and ‘circumstantial’ evidence” that stress can lead to the actual induction of cancer, this specific aspect of the relationship has not been “convincingly demonstrated in human populations” (Contrada 412). Contrada argues glucocorticoids and stress networks are important factors to consider when studying the relationship between stress and cancer, and we’ll focus on these later. Heritable characteristics, social factors, shared environments, and other psychological variables play key roles in the development of cancer (Contrada). These factors complicate cancer studies and make the relationship much more difficult to distinguish.
Myrthala Moreno-Smith writes in Impact of Stress on Cancer Metastasis that although Stress Science is still a relatively new field with “only limited evidence for the role of these behavioral factors in cancer initiation,” recent studies have shed new light on the relationship. A new theory has since been introduced in attempt to explain the complex relationship “between psychosocial factors, specifically chronic stress, and cancer progression” (Moreno-Smith). Contrary to what scientists thought years ago, the “strongest links to cancer progression” are not stressful events, but prolonged exposure to moods of depression or hopelessness. Strong social support, for example, has been shown to link cancer patients with improved prognoses and greater chances for survival (Moreno-Smith).
The release of dopamine in the brain during high-stress situations is a significant contributing factor; this is regulated by the nervous and hormonal systems, as Seyle originally proposed. In areas where cancer induction is most likely, neuroendocrine mediators control cellular function. In the ovary, for example, the body responds to stress by increasing levels of catecholamine, which can actually aid in the formation of precystic follicles. And inline with Contrada’s research, glucocorticoids, or “a class of steroid hormones that bind to the GC receptor” play a key role in bridging the gap between stress and cancer (Moreno-Smith). GC receptors help modulate “immune activity and inflammatory responses” (Moreno-Smith).
Perumana Sudhakaran, however, argues that “contrary to community beliefs, there has been no evident association between stress and… cancer risk in large prospective cohort studies,” which contrasts with Moreno-Smith’s admittedly minimal evidence (Sudhakaran 156). This also contrasts heavily with the research of Contrada and Baum in their Handbook of Stress Science. Sudhakaran claims stress is “thought to be more influential in the progression and recurrence of cancer than its initial onset” (Sudhakaran). In other words, Stress has more of an impact on developed cancers than it does the disease’s actual induction, although the sources Sudhakaran references in forming this claim date back to the late-1990s and early-2000s.
“Experimental research in animals… has found that stress contributes to the initiation, growth, and metastasis of select tumors” (Sudhakaran). More importantly, stress in humans has been shown to affect “key pathogenic processes in cancer, such as antiviral defenses, DNA repair, and cellular aging” (Sudhakaran). Again, stress has more of an impact on cancer after it is developed. Sudhakaran points out that one study found strong evidence that “those whose mental health had suffered due to the stress of the Chinese social revolution” showed greater instances of cancer than others. This trend, however, is based solely on correlation with no explanation for causation. Sudhakaran actually debunks the theory as well: with a rise in workplace stress over the past 40 years, we should also see a rise in number of cancer diagnoses, and that workers in highly developed countries where workplace stress is often higher should be of higher risk for the disease. “Nearly 70 percent of the cancer deaths occur in low and middle income countries,” however, suggesting the theory is inaccurate (Sudharakan).
In conclusion, a strong relationship between stress and cancer definitely does exist. Sources conflict when considering whether or not stress can actually cause cancer; trends obviously exist, though studies have not been able to explicitly show any causation here. All sources, however, point to a definite causative trend between stress and cancer development through changes in the hormonal and nervous systems. These systems’ responses to stress can facilitate cancerous cells and promote tumorous growth, whereas social support has been shown to improve overall prognosis.
Contrada, Richard, and Andrew Baum. The Handbook of Stress Science: Biology,
Psychology, and Health. Springer, 2011. Print.
Moreno-Smith, Myrthala. “Impact of Stress on Cancer Metastasis.” Future Oncol 6.12
(2010): 1863-881. PMC. Web. 3 Nov. 2015. <http://www.ncbi.nlm.nih.gov/pmc/
Selye, Hans. The Stress of Life. New York: McGraw-Hill, 1956. Print.
Sudhakaran, Perumana. Perspectives in Cancer Prevention – Translational Cancer
Research. New Delhi: Springer, 2014. Print.