Sample Research Paper On Stress And Cancer

Psychology

Introduction
The human body is an intricately interlinked organism. Every system of the body has a role to play in the well being of the other. The most prevalent disease of the modern age is cancer, and there has been considerable effort to determine the causes of cancer. Substantial research in this regard point to stress being one of the leading causes of cancer.

The Impact of Stress on Cancer

Cancer, medically called ‘tumorigenesis’ (Thaker, Lutgendorf, & Sood, 2007, p.430) occurs when cells in the body orient themselves for malignant growth. Such cells show ‘self-sufficiency in growth signals’, are ‘insensitive to anti-growth signals’ and have ‘limitless replicative potential’ (Thaker, Lutgendorf, & Sood, 2007, p.430). Once a particular set of cells become malignant, the malignancy can spread to other set of cells in different organs due to ‘crosstalk’ between the affected cells and their surrounding ‘tissues’ and ‘micro-environments’(Thaker, Lutgendorf, & Sood, 2007, p.430).
Current research is focusing on the role of ‘neuropeptides’ and ‘neurotransmitters’ in the occurrence of cancer. Researchers have observed that cancerous cells require nutrients and the diffusion of oxygen to proliferate malignantly. In this aspect, stress-related hormones act as inhibitors or stimulants to cancerous growth depending upon the type of hormone and the type of cancer. It has been established that ‘-agnostic isoproproterenol’(Thaker, Lutgendorf, & Sood, 2007, p.431), a byproduct of stress, promotes ovarian cancer cells to spread. Stress hormones have also been seen to facilitate cancerous cells to migrate along tissue surfaces and spread. ‘Norepinephrine’ and ‘epinephrine’ (Thaker, Lutgendorf, & Sood, 2007, p.431), byproducts of physiological stress, act as facilitators in ovarian and colon cancer.
Cell death, called ‘apoptosis’, is critical for a human body to remain healthy. In the normal course, cells should die and new ones take their place. Apoptosis of cervical and lung cells is stymied by ‘glucocorticoids’(Thaker, Lutgendorf, & Sood, 2007, p.431), a byproduct of stress. Once cervical and lung cells stop dying, they result in the malignant growth of cancer.
Solid cancer tumors grow beyond 1-2 mm of diameter through a process called ‘angiogenesis’(Thaker, Lutgendorf, & Sood, 2007, p.431). Angiogenesis is facilitated by the presence of chemicals that are grouped as ‘vascular endothelial growth factors (VEGF)’ (Thaker, Lutgendorf, & Sood, 2007, p.431). Scientists have observed that VEGF is found in lower levels when social support is evident. Lack of social support, therefore, is surmised to be causing stress that leads to excess amounts of VEGF in the system, which in turn promotes the growth of cancerous tumors (Thaker, Lutgendorf, & Sood, 2007).
Researchers have assessed the impact of the effect of -hormones in promoting cancer. Using -blockers that inhibit the incidence of -hormones, researchers have found that the resultant cancerous growth has been limited. In a study on colon cancer patients, researchers have observed that those patients who took -blockers showed a greater resistance to cancerous growth. This has reinforced the assessment that -hormones released during stressful situations enhance the proliferation of cancerous growth. (Thaker, Lutgendorf, & Sood, 2007).
Researchers have delved into the subtypes of stress and depression that result in cancer. In a study on colon cancer, researchers have observed that ‘melancholy’, ‘depressed moods’, ‘sleeplessness’, ‘cognitive depression’ and ‘anhedonia’(schizophrenia) are different types of depression, causing different types of colon cancer. Researchers have accordingly propagated different treatment protocols depending upon the type of depression that promotes cancer Sharpley, Bitsika & Christie, 2013).
With growing realization of stress having a role to play in promoting cancerous growth, a number of experiments have been conducted to see if reduction of stress would mitigate the growth of malignant cancer cells. In a study, 89 cancer patients were initially assessed for their mood state, and then made to practise home meditation for 1.5 hours a day over seven weeks. After six months, the patients once again underwent the test to assess their mood and stress levels. It was observed that the mood of the patients was better and their stress levels had reduced. Follow up checks on cancerous growth showed that the patients who had followed the meditation protocol now displayed lower levels of malignancy. Thus, the experiment proved that meditation to reduce stress could have a positive role in mitigating the growth of cancer (Carlson, Ursuliak, Goodey, Angen & Speca, 2000).

Conclusion

The realization of the effects of stress on cancer is growing with every day. While the exact chemical sequences of how the neurotransmitters of the brain impact on cancerous cells are still opaque, enough experiments have reinforced the overall cause and effect linkage between stress and cancer. Researchers have also observed that stress causes different physiological manifestations, each of which has a different role to play in cancer. Thus, medications and treatments are devised to tackle different manifestations of stress in different manners. The role of stress reduction through meditation has been observed to cause a reduction in hormones that promote malignant growth. Thus, meditation and other measures to reduce stress in daily life are acknowledged to mitigate the risk of cancer and reduce malignant growth where cancer exists.
In the overall interest of society, it is therefore necessary to take steps to reduce the levels of stress in daily life. Proactive measures of stress alleviation would help organizations and individuals in the long run to remain healthy and productive in the long run and avoid the debilitating costs to society incurred with the onset of cancer.

References

Carlson, L.E., Ursuliak, Z., Goodey, E., Angen, M., & Speca, M. (2000). The effects of a mindfulness meditation-based stress reduction program on mood and symptoms of stress in cancer outpatients: 6 month follow-up. Support Care Cancer 9: 112-123. DOI 10.1007/s005200000206. Retrieved March 21, 2015, from http://link.springer.com/article/10.1007/s005200000206#page-1
Sharpley, C.F., Bitsika, V., & Christie, D.R.H. (2013). The incidence and causes of different subtypes of depression in prostrate cancer patients: Implications for cancer cure. European Journal of Cancer Care 22: 815-823. DOI: 10.1111/ecc.12090. Retrieved March 21, 2015, from EBSCOHost. AN 91699113.
Thaker, P.H., Lutgendorf, S.K., & Sood, A.K. (2007). The neuroendocrine impact of chronic stress on cancer. Cell Cycle 6/4: 430-433. DOI: 10.4161/cc.6.4.3829. Retrieved March 21, 2015, from http://www.tandfonline.com/doi/pdf/10.4161/cc.6.4.3829