Hair and salivary cortisol in a cohort of women with chronic fatigue syndrome.

[Murph]

Hair and salivary cortisol in a cohort of women with chronic fatigue syndrome.
Roerink ME1, Roerink SHPP2, Skoluda N3, van der Schaaf ME4, Hermus ARMM2, van der Meer JWM2, Knoop H5, Nater UM3.
Author information
Abstract
Hypocortisolism has been found in CFS patients in blood, urine, and saliva. It is unclear if hypocortisolism can also be demonstrated using long-term cortisol measurements, such as cortisol in hair. In addition, the interaction between the HPA axis and the immune system, both expected to play an important role in CFS, is unclear. The objective of the current study was to compare hair and salivary cortisol concentrations in a cohort of female CFS patients to those in healthy controls, and to test the effect of an interleukin-1 receptor antagonist (anakinra) on the HPA axis. Salivary cortisol concentrations of 107 CFS patients were compared to 59 healthy controls, with CFS patients showing a decreased cortisol awakening response (4.2 nmol/L ± 5.4 vs 6.1 nmol/L ± 6.3, p = 0.036). Total cortisol output during the day did not differ significantly in saliva, but there was a trend to lower hair cortisol in a subset of 46 patients compared to 46 controls (3.8 pg/mg ± 2.1 vs 4.3 pg/mg ± 1.8, p = 0.062). After four weeks of treatment with either daily anakinra (100 mg/day) or placebo, there was a slight decrease of hair cortisol concentrations in the anakinra group compared to an increase in the placebo group (p = 0.022). This study confirms the altered dynamics of the HPA axis in a group of CFS patients, and for the first time shows that this might also be present for long-term cortisol measures.

 

[ljimbo423]

The objective of the current study was to compare hair and salivary cortisol concentrations in a cohort of female CFS patients to those in healthy controls, and to test the effect of an interleukin-1 receptor antagonist (anakinra) on the HPA axis.

Interesting study. I wonder how much better a response they could have had with multiple cytokine receptor antagonists?

I think there is a really good chance HPA axis dysfunction plays a significant role in ME/CFS. I also think there are probably multiple cytokines effecting the HPA.

There's a good chance HPA axis dysfunction also plays a big role in thyroid, adrenal dysfunction and maybe many other dysfunctions in ME/CFS.

One piece of a much larger picture though.

Jim

 

[datadragon]

Low cortisol is the end result of depleted nutrients (adrenal burnout phase) usually the depletion is mainly caused from various ongoing stressors to the body, although one can be deficient by poor intake of a particular nutrient. I have only shared a general overview of how I believe it works getting to that point of HPA axis dysfunction (burnout) which is a factor in allowing many of the symptoms of ME/CFS and Adrenal Fatigue to be able to occur here:

https://forums.phoenixrising.me/index.php?posts/980149

-- the interaction between the HPA axis and the immune system, both expected to play an important role in CFS, is unclear.

TH1 is later supressed and allows viruses to reactivate, which would be an additional issue that some face with CFS.

Here is some information on some of the details of the process and effects on the body. Magnesium is a cofactor in more than 300 enzyme systems that regulate diverse biochemical reactions in the body including ATP energy.
https://coppertoxic.com/adrenals
https://coppertoxic.com/flowchart - click to enlarge, zoom controls on lower right then.
https://www.drlam.com/articles/adrenalexhaustion.asp