- Last Updated: 07 November 2015 07 November 2015
Mediators (immune, endocrine, neuroendocrine, psychosocial)
An Immune Cascade chart was used to illustrate how various immune response processes are activated in response to an infection. Basically, the helper T-cell function in individuals with CFS no longer remains balanced; instead, it shifts to a TH-2 pattern, which in turn, triggers pro-inflammatory cytokines.
More recent endocrinology studies show evidence of reduced cortisol output (by the adrenals) via several mechanisms, such as heightened negative feedback, heightened receptor function and impaired ACTH and cortisol responses to challenge. Research data also supports DHEA functional abnormality, abnormal serotonin function, and IL-6 increase associated with low cortisol. (The low cortisol is mediated by a hypothalamic dysregulation of Cortisol Releasing Hormone.) In spite of these findings, Dr. Klimas stated that cortisol treatment, especially long-term, is not being recommended. The following two studies address this issue:
Cleare AJ, “The Neuroendocrinology of Chronic Fatigue Syndrome,” Endocrine Reviews 24 (2) (2003): 236-252.
Papanicolaou DA et al (representing a large US panel), “Neuroendocrine Aspects of Chronic Fatigue Syndrome," Neuroimmunomodulation 11(2) (2004): 65-74.
Some of the latest research on Autonomic Nervous System abnormalities in CFS (as shown on the chart for ANS) and other sources, are as follows:
- Haemodynamic Instability Score taken during tilt table testing predicts CFS with 90% sensitivity. 1
- Heart rate variability as a predictor of CFS. 2
- Gastric emptying delayed in 23 out of 32 CFS subjects. 3
1. Naschitz J, “The Head-up Tilt Test with Haemodynamic Instability Score in Diagnosing Chronic Fatigue Syndrome,” QJM 96(2) (2003): 133-42.
2. Yamamoto et al, “A Measure of Heart Rate Variability Is Sensitive to Orthostatic Challenge in Women with Chronic Fatigue Syndrome,” Experimental Biology and Medicine 228 (2003):167-174.
3. Burnet R, “Gastric Emptying is Slow in Chronic Fatigue Syndrome,” BMC Gastroenterology 4 (2004): 32.