Study Links Stress to Cancer Development

If you didn’t get the memo, stress is bad. It’s just like that commercial with a talking lizard in it – everyone knows about it. People pretty much know this horrible feeling, stress, that looms over you like a curse most likely carries harmful biological effects.

At the very top of that harmful effects list sits the dreaded, cancer. Just mentioning it makes one a bit squeamish. Mostly because its hard to entertain the idea of having cancer. Stress and cancer have always been associated with one another, however, there hasn’t been solid scientific evidence tying stress to cancer development.

Related: Is Living Stress Free Truly Beneficial

There have been many anecdotal experiences that suggest stress may accelerate the growth of cancer, but the problem is that they are in fact merely anecdotal. With the help of modern research technology and advancements in modern genetic modification in animals, researchers from Wake Forest School of Medicine may have found a crucial scientific evidence linking stress to cancer development.

Behavioral stress accelerates prostate cancer development in mice

They devised two methods to test their hypothesis. In the first method, they implanted human prostate cancer cells into the mice and immediately gave the mice prostate cancer treatment. This prostate cancer treatment is currently in clinical trials. When free from stress, the drug was successful in increasing apoptosis, death rate of cells, in cancer tumors and destroyed cancer cells. It worked as intended. The researchers then subjected the mice to stress as simulated by immobilization and exposure to predator-scent. This signaled to the mice they are about to get eaten which is an extremely stressful stimuli. This triggered the release of adrenaline into the circulatory system. With the introduction of stress, the drug was unable to accelerate apoptosis and cancer cells did not die.

In the second method, genetically-modified mice with the tendency to develop prostate cancer cells were used. They found stress accelerated the development of cancer tumors in the mice. They used a current prostate cancer treatment, Bicalutamide, to treat the mice which decreased the size of the tumors. The effects of Bicalutamide, however, were inhibited when the mice were subjected to further repeated episodes of stress. In both methods, with two different prostate cancer treatments, stress inhibited the intended effects of the drug.

Extreme Stress Accelerates the Growth of Cancer

The findings in this study imply that stress accelerates the growth of cancer. Upon closer look, you will see its not just any stress. The study found that it is extreme stress that enables the release of adrenaline which accelerates cancer development and nullifies the effects of cancer treatment. Furthermore, it is repeated extreme stress. Not just the typical chronic stress, but repeated extreme stress. Basically, a person diagnosed with cancer will go through episodes of extreme stress because they feel like their life is in danger. This will accelerate the growth of the tumor.

The findings imply that the faster a cancer patient emotionally copes with the thought of cancer, the better their chances of inhibiting tumor growth and reversing the cancer. This further solidifies the importance of cancer programs designed to keep cancer patients from breaking down while undergoing chemotherapy.

Conclusion

This experiment not only links stress to cancer development, but it also painted a clearer picture of the mechanisms surrounding cancer cell formation and apoptosis. I believe it will help doctors and nurses form more effective ways to improve success rate of cancer patients. It implies the importance of mind-body relaxation and stress management in over-all health maintenance and cancer-prevention.


WORKS CITED:
1. Kulik, George, Sazzad Hassan, Daniele Baiz, Dana Yancey, Ashok Pullikuth, and Anabel Flores. “Behavioral Stress Accelerates Prostate Cancer Development in Mice.” Thesis. Department of Cancer Biology, Wake Forest School of Medicine, 2013. The Journal for Clinical Investigation Vol.123.2 (2013): 874-86. Print

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