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Scientific Overview
Stress and Stress Tolerance
HPA Axis
Circadian Rhythms
Immune System
Placebo Effect
Burnout
Chronic Fatigue Syndrome
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Immune System

The common view among both the general public and the medical profession is that the immune system runs on "autopilot", constantly looking out for infections and mounting an immune response when an infection occurs. Research shows, however, that the health of the immune system can vary widely, and that the immune system is highly influenced by stress.

Although it is known that stress can suppress the immune system, through the action of adrenaline and cortisol, research shows the HPA axis can actually have a positive effect on the immune system, reversing the effects of cortisol and increasing the killing ability of natural killer (NK) cells. ACTH, part of the HPA axis response, has an opposite effect to that of cortisol.

The immune system can be divided into two main branches: Th1 and Th2. The Th1 branch fights viruses, cancer and intracellular bacteria, whereas the Th1 branch fights extracellular bacteria and parasites. The Th2 branch is also responsible for allergic reactions.

Cortisol—the main stress hormone—modulates the immune system rather than suppressing it completely. The overall effect is a shift from Th1 (cell-based immunity) towards the Th2 humoral response (antibodies). A similar shift from Th1 to Th2 is caused by adrenaline.

All types of stress—whether psychological, physical or due to infection—result in similar activation of the HPA axis, and result in an increase in the levels of cortisol in the blood. The activation of the stress system during an infection and resulting shift to the Th2 response is believed to be a protective mechanism which prevents an overactivation of the inflammatory response. During psychological or physical stress, however, this shift to the Th2 response results in a poorer ability to fight viral infections, and increased susceptibility to allergies. A short-term suppression of the Th1 branch of the immune system during a stressful situation is beneficial, as the immune system uses a large amount of energy which would be better channeled to the "flight or fight" response.

Research shows that many CFS patients have a shift towards the Th2 immune response, as well as having a lower than normal immune response in general. This may seem counter-intuitive, as CFS patients tend to have low cortisol (which would favour a Th1 shift). However, the Th2 shift seen in CFS has been shown to be due to increased sensivitity to cortisol in CFS patients' immune cells. This increased sensitivity is common after long-term hypocortisolism, and appears to be a compensation mechanism that allows body tissue to deal with abnormal hormone levels.

Research shows that stress is likely a trigger for autoimmune disease, due to immune dysregulation as a result of hormone changes. Both depression and CFS are associated with increased autoimmune responses, which may be due to stress hormones.

Overall, the immune abnormalities in CFS are likely to be due to the underlying abnormalities in the HPA axis seen in CFS patients, rather than being due to any ongoing infection, as research shows that many CFS patients have no ongoing infections, and the infections that are common in CFS— such as herpesviruses—are known to reactivate during periods of stress. The Th2 shift seen in CFS has a similar effect on the immune system as is seen during stress, and will likely result in similar reactivation of herpesviruses.

References and external links

Wikipedia entry on Th1 and Th2 immune response

Rohleder, N., Wolf, J. M., & Kirschbaum, C. (2003). Glucocorticoid sensitivity in humans-interindividual differences and acute stress effects. Stress: The International Journal on the Biology of Stress, 6(3), 207-222.

Elenkov IJ (2004). "Glucocorticoids and the Th1/Th2 Balance". Annals of the New York Academy of Sciences 1024 (1): 138.146. Bibcode:2004NYASA1024..138E. doi:10.1196/annals.1321.010. PMID 15265778.

Rime B, Ucros CG, Bestgen Y, Jeanjean M, "Type A behaviour pattern: specific coronary risk factor or general disease-prone condition?", Br J Psychol 1989 Sep;62 (Pt 3):229-40

Gatti G, Masera RG, Pallavicini L, Sartori ML, Staurenghi A, Orlandi F, Angeli A, "Interplay in vitro between ACTH, beta-endorphin, and glucocorticoids in the modulation of spontaneous and lymphokine-inducible human natural killer (NK) cell activity.", Brain Behav Immun 1993 Mar;7(1):16-28

Soto NE, Straus SE, "Chronic Fatigue Syndrome and Herpesvirus: the Fading Evidence", Herpes 2000 May;7(2)46-50

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