Studies are revealing more and more interesting facts about cortisol – “Death Hormone”.  In a separate article, we briefly cited various studies that link the death hormone to aging, immune deficiencies, telomere shortening, stress, and a number of debilitating chronic conditions.  This article reviews studies that have established links between cortisol and cancer. Cancer biology has long been linked to psychological factors, which are crucial determinants of progression through various biological pathways. Researchers have carried out studies to try and unravel the actual mechanisms through which psychological stress plays a role in cancer.  Indeed the association between cortisol and malignant diseases has been suspected for more than four decades.  A study conducted by Azzopardi et al. in 1970 showed that a number of patients with bronchial carcinoma presented with endocrine disturbances that could be linked to the tumor. This included a case of Cushing’s syndrome (Azzopardi, Freeman, & Pool, 1970) . Cushing’s syndrome is a condition that describes the effects of a prolonged exposure to high levels of cortisol.

A review conducted by Brody (1970) showed that patients dying from carcinoma of the bronchus, as well as other sites within the body, were found to have increased levels of cortisol and that rose significantly as death approached.  The findings were made in a study carried out to establish causes of diminished or absent reactions to tuberculin in treatment of tuberculosis.  The review suggested that the loss of sensitivity to tuberculin could be due to increased levels of circulating steroids (Brody, 1970) .

A study was carried out by Cohen et al. (2012) on the association between survival in patients with renal cell carcinoma and depressive symptoms and cortisol rhythmicity . Two hundred and seventeen patients with metastatic renal carcinoma were included in the study (n = 217). The findings strongly indicated that depressive symptoms are key predictors of survival in renal cell carcinoma (RCC) patients with possible links to dysregulation of cortisol and the inflammatory biology (Cohen, et al., 2012) .

Another study investigated fluctuations in diurnal variations of cortisol levels and their relationship with metastatic breast cancer. In the majority of healthy health individuals, cortisol shows a diurnal variation which it peaks in the morning and continues to decline as the day progresses (Stone, et al., 2001) . The findings of this study indicated that women with metastatic breast cancer had a visibly flatter diurnal cortisol rhythms compared to healthy controls. Those with elevated severity showed a raised mean cortisol levels, a reduced waist circumference, and a flattening diurnal cortisol rhythms (Abercrombie, et al., 2003) . Therefore, the study confirmed that metastatic disease is associated with a poorly modulated cortisol functioning, and the most sick have the worst cortisol dysregulation and most progressive cachexia (Abercrombie, et al., 2003) . The study did not however show any links between biological indicators and psychological measures.
Cortisol was also linked to progression of ovarian cancer in one study. A study researching on “diurnal cortisol dysregulation, functional disability, and depression in women with ovarian cancer” showed a greater association of cortisol dysregulation with functional disability, fatigue and vegetative depression (Weinrib, et al., 2010) .

Several other studies have shown that cortisol levels may relate to cancer in one way or another. A review conducted by Friedenreich & Thune on physical activity and cancer concluded that physical activity may decrease the risk of prostate cancer. This study did not however show what magnitude of physical activity is necessary to control prostate cancer (Friedenreich & Thune, 2001). Other studies have shown that increased physical activity results in an increase in circulating cortisol level (Wellhoener, Born, Horst, & Chistoph, 2004 ;Hill, et al., 2008 ). Therefore, it is interesting to understand how an increase in the level of circulating cortisol reduces the risk of prostate cancer. This is in addition to the finding that psychological stress increases the risk of cancer (Kirchheimer, 2003) .

Another interesting link between cortisol and cancer comes from telomere studies. Cortisol has long been established as one the physiological pathways that play a role in many diseases observed in the aging process. A study conducted by Epel et al. showed that telomere shortening was linked to elevations in urinary catecholamines and cortisol in a section of caregiver subjects (2006) .

A study contacted by Willeit et al. (2010) investigated on the relationship between Telomere length and risk of incident cancer and cancer mortality. The study was carried to get more understanding on the theoretical assumption that critically short telomeres lead to replicative cell senescence and chromosomal instability and may thereby increase cancer risk. The findings of the study showed that short telomere length at baseline was linked with incident cancer independent of other cancer risk factors (Willeit, et al., 2010) .

Summary: Cortisol seems to play a very in important role in the development and progression of cancer. A number of cancerous conditions have been linked to cortisol dysregulation. These includes renal carcinoma and flattened cortisol rhythmicity; fluctuations in diurnal variations in cortisol and metastatic breast cancer; progression of ovarian cancer and diurnal cortisol dysregulation . Cancer has also been linked to a number of biological pathways that cortisol in which cortisol plays an active role. These include telomere shortening and psychological and physiological stress. Interventions which reduce over-all circulating levels of cortisol while maintaining the rhythmicity of diurnal cortisol fluctuations may be beneficial in preventing or treating certain cancers, but this finding needs further research.

Azzopardi, J. G., Freeman, E., & Pool, G. (1970). Enfocrine and Metabolic Disorders in Bronchial Carcinoma. British Medical journal , 4,528 - 530 .

Brody, A. J. (1970). Tuberculin anergy . Br Med J, 4: 573.

Brody, A. J. (1970)

Cohen, L., Cole, S. W., Sood, A. K., Prinsloo, S., Kirschbaum, C., Arevalo, J. G., . . . Pisters, L. (2012). Depressive Symptoms and Cortisol Rhythmicity Predict Survival in Patients with Renal Cell Carcinoma: Role of inflammatory Signaling. PLos ONE, 7(8):e4224.

Cohen, L., Cole, S. W., Sood, A. K., Prinsloo, S., Kirschbaum, C., Arevalo, J. G., . . . Pisters, L. (2012)

Stone, A. A., Scwartz, J. E., Smyth, J., Kirschbaum, C., Cohen, S., Hellhammer, D., & Grossman, S. (2001). Individual differences in the diurnal cycle of salivary free cortisol: a replication of flattened cycles for some individuals. Psychoneuroendocrinology, 26, 295–306.

Abercrombie, H. C., Giese-Davis, J., Sephton, S., Epel, E. S., Turner-Cobb, J. M., & Spiegel, D. (2003). Flattened Cortisol rhythms in metastatic breast cancer patients . Psychoneuroendocrinology.

Abercrombie, H. C., Giese-Davis, J., Sephton, S., Epel, E. S., Turner-Cobb, J. M., & Spiegel, D. (2003).

Weinrib, A., Sephton, S. E., Degeest, K., Penedo, F., Bender, D., Zimmerman, B., & Lubaroff, D. (2010). Diurnal cortisol dysregulation, functional disability, and depression in women with ovarian cancer. Cancer, 116(18): 4410-4419.

Wellhoener, P., Born, J., Horst, L., & Chistoph, D. (2004). Elevated Resting and Exercise-Induced Cortisol Levels after Mineralocorticoid Receptor Blockade with Canrenoate in Healthy Humans . The Journal of Clinical Endocrinology & Metabolism, 89 (10): 5048-5052.

Hill, E. E., Zack, E., Battaqlini, C., Viru, M., Viru, A., & Hackney, A. C. (2008). Exercise and circulating cortisol levels: the intensity threshold effect. J Endocrinol Invest, 31(7): 587 -91.

Kirchheimer, S. (2003, October 1). How Sleep Affects Cancer. Retrieved from WebMD:

Epel, J. L. (2006). Cell aging in relation to stress arousal and cardiovascular disease risk factors. Psychoneuroendocrinology, 31:277-287.

Willeit, P., Willeit, J., Mayr, A., Weger, S., Oberhollenzer, F., Brandstatter, A., . . . Kiechl, S. (2010). Telomere length and risk of incident cancer and cancer mortality. JAMA, 7;304(1): 69-75.

Friedenreich, C. M., & Thune, I. (2001). A reveiw of physical Activity and prostate Cancer Risk. Cancer Causes & Control , 12(5):461-475.

Author's Bio: 

Dr. Steven Petrosino received his Baccalaureate (BA) degree in both Science and English from Penn State University in 1975, pursued his Masters degree (American Studies) with honors at Penn State in 1977-1978, and graduated Summa Cum Laude with a Doctorate in Nutrition from Lasalle University in 1995. He currently is enrolled in a Ph.D. program at Walden University (Public Health). In 1996-1998 he was involved in external post-doctoral research at the Ohio State University in the Department of Cancer Prevention and Natural Products Research. In 2002, he was enrolled in a post-doctoral external course (Immunobiology) at the University of Pennsylvania.

Dr. Petrosino is currently employed as a Senior Medical Science Liaison with Human Genome Sciences, Inc. He is married to the former Lynn Tutoli, and he and his wife reside in Dublin, OH. They have two children, Angela Petrosino Johnson, (32) and Aaron (28). Visit his website here: