Fries, Eva, Hesse, Judith, Hellhammer, Juliane et al. · Psychoneuroendocrinology · 2005 · DOI
Some people with ME/CFS, fibromyalgia, and PTSD have abnormally low levels of cortisol, a stress hormone their body normally produces. This review suggests that this low cortisol may develop after the body's stress system works overtime for a long time. Interestingly, while low cortisol contributes to symptoms like fatigue, pain, and stress sensitivity, it may also provide some protective benefits to the body.
Understanding how and why cortisol levels become abnormally low in ME/CFS is crucial for developing targeted treatments and explaining the paradoxical symptom profile of high stress sensitivity alongside fatigue and pain. This review connects ME/CFS to a broader mechanistic framework shared with other stress-related conditions, potentially opening new therapeutic avenues and validating the biological basis of the illness.
This review does not establish causation—it cannot prove that hypocortisolism causes ME/CFS symptoms or that treating low cortisol will resolve the condition. The proposed HPA axis hyperactivity-to-hypocortisolism model is based partly on animal data and requires validation in human ME/CFS populations. The claimed 'protective effects' of hypocortisolism remain speculative and are not clearly defined or quantified in the abstract.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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