Stress, genes, and cytokines
Chapter 10 endnote 8, from How Emotions are Made: The Secret Life of the Brain by Lisa Feldman Barrett.
Some context is:
A chronically imbalanced body budget acts like fertilizer for disease.
During stress (body-budget imbalance), certain genes are turned on that lead the interoceptive network to increase activation of β-adrenergic sympathetic nervous system (SNS) activity. This encourages pro-inflammatory gene expression and discourages anti-viral immune gene expression as cells in the body replicate, and bathes the body in proinflammatory cytokines.[1] (We discussed this in chapter 2 in relation to emotion.) These genetic effects, which researchers have observed in non-human animals such as rats, have been found in breast tissue,[2] in lymph nodes,[3] and in the brain.[4] Even a brief period of these changes can stay with an animal for weeks, months, or even years, carried in its cells, increasing its risk of developing a tumor as well as other diseases.[5] Once a tumor develops, stress-related SNS activity acts like a fertilizer; it changes the micro-environment of tumor cells, making metastasis easier, causing animals to die sooner.[6][7]
If stress is prolonged, the SNS's connections to lymph nodes in the immune system expand (called arborization), increasing inflammatory reactivity and enhancing this entire process.[8][3][9]
Rats have a far simpler stress response than we do, but at least some instances of stress produces similar changes in humans. Stress increases risk for practically every known chronic illness and causes people to die sooner of cancer.[10]
Notes on the Notes
- ↑ Irwin, Michael R., and Steven W. Cole. 2011. "Reciprocal regulation of the neural and innate immune systems." Nature Reviews Immunology 11 (9): 625-632.
- ↑ Williams, J. Bradley, Diana Pang, Bertha Delgado, Masha Kocherginsky, Maria Tretiakova, Thomas Krausz, Deng Pan, Jane He, Martha K. McClintock, and Suzanne D. Conzen. 2009. "A model of gene-environment interaction reveals altered mammary gland gene expression and increased tumor growth following social isolation." Cancer Prevention Research 2 (10): 850-861.
- ↑ 3.0 3.1 Sloan, Erica K., John P. Capitanio, Ross P. Tarara, Sally P. Mendoza, William A. Mason, and Steve W. Cole. 2007. "Social stress enhances sympathetic innervation of primate lymph nodes: mechanisms and implications for viral pathogenesis." Journal of Neuroscience 27 (33): 8857-8865.
- ↑ Drnevich, Jenny, Kirstin L. Replogle, Peter Lovell, Thomas P. Hahn, Frank Johnson, Thomas G. Mast, Ernest Nordeen et al. 2012. "Impact of experience-dependent and-independent factors on gene expression in songbird brain." Proceedings of the National Academy of Sciences 109 (supplement 2): 17245-17252.
- ↑ Slavich, George M., and Steven W. Cole. 2013"The emerging field of human social genomics." Clinical Psychological Science 1 (3): 331-348.
- ↑ Antoni, Michael H., Susan K. Lutgendorf, Steven W. Cole, Firdaus S. Dhabhar, Sandra E. Sephton, Paige Green McDonald, Michael Stefanek, and Anil K. Sood. 2006. "The influence of bio-behavioural factors on tumour biology: pathways and mechanisms." Nature Reviews Cancer 6 (3): 240-248.
- ↑ Cole, Steven W., and Anil K. Sood. 2012. "Molecular pathways: beta-adrenergic signaling in cancer." Clinical Cancer Research 18 (5): 1201-1206.
- ↑ Capitanio, John P., and Steven W. Cole. 2015. "Social instability and immunity in rhesus monkeys: the role of the sympathetic nervous system." Phil. Trans. R. Soc. B 370 (1669): 20140104, doi:10.1098/rstb.2014.0104.
- ↑ Sloan, Erica K., John P. Capitanio, and Steve W. Cole. 2008. "Stress-induced remodeling of lymphoid innervation." Brain, Behavior, and Immunity 22 (1): 15-21.
- ↑ Rappaport, Stephen M. 2012. "Discovering environmental causes of disease." Journal of Epidemiology and Community Health 66 (2): 99-102.