Cancer Is Depressing

Science Signaling  09 Jun 2009:
Vol. 2, Issue 74, pp. ec189
DOI: 10.1126/scisignal.274ec189

A relationship exists between health and mood. Individuals suffering from disease are more likely to suffer from depression and mood disorders, and depression is associated with increased severity of symptoms, and even death, in certain diseases, including cancer. Proinflammatory cytokines, such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor–α (TNF-α), can trigger behaviors associated with depression. Pyter et al. found that rats with induced mammary tumors exhibited more depressive behaviors and behaviors associated with anxiety than did control rats or rats treated with the cancer-inducing agent, but before tumor formation. The mammary tumors produced increased IL-1β compared with normal mammary tissue. In addition, the abundances of the proinflammatory mediators IL-1β, IL-6, and TNF-α and the antiinflammatory mediator IL-10 were all elevated in the hippocampus of rats with mammary tumors compared with the control rats. Corticosterone, produced by the adrenal gland under the control of the hypothalamus and pituitary gland, reduces proinflammatory responses, and its production is stimulated by stress. Although the rats with tumors exhibited no change in circulating basal corticosterone concentrations, the tumor-carrying rats showed a significantly smaller increase in corticosterone than did control rats in response to a swim stressor. Furthermore, rats with tumors had increased mRNA for both the mineralocorticoid and glucocorticoid receptors in the hypothalamus, suggesting that peripheral tumors influence the hypothalamic-pituitary-adrenal axis. The relationship between cancer and the immune system is complex, not only affecting tumor progression but also potentially affecting prognosis by influencing patient mood and ability to cope with stress.

L. M. Pyter, V. Pineros, J. A. Galang, M. K. McClintock, B. J. Prendergast, Peripheral tumors induce depressive-like behaviors and cytokine production and alter hypothalamic-pituitary-adrenal axis regulation. Proc. Natl. Acad. Sci. U.S.A. 106, 9069–9074 (2009). [Abstract] [Full Text]