Chronic ACTH autoantibodies Disrupt HPA Axis in CFS.

Ema

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And yet none of the current conventional adrenal testing will uncover this possibly dysregulation...

Med Hypotheses. 2005;65(2):287-95.
Chronic ACTH autoantibodies are a significant pathological factor in the disruption of the hypothalamic-pituitary-adrenal axis in chronic fatigue syndrome, anorexia nervosa and major depression.
Wheatland R.
Author information

Abstract
Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis is a commonly recognized feature of many pathological conditions. Abnormal adrenal responses to experimental manipulation have been well documented in patients suffering from chronic fatigue syndrome, anorexia nervosa and major depression.

Yet no defect of any single organ, gland or brain region has been identified as a cause of these abnormalities.

The disruption of the HPA axis that occurs in these conditions can be understood if an interfering factor is present in these patients. Evidence indicates that this interfering factor is adrenocorticotropin hormone (ACTH) autoantibodies.

Chronic high levels of ACTH autoantibodies will significantly disrupt the HPA axis and force the body to compensate for an impaired cortisol response. The resulting effect of chronic ACTH autoantibody interference is the manifestation of adrenocortical insufficient symptoms and psychological disturbances. Some symptoms of chronic fatigue syndrome, anorexia nervosa and major depression, such as anxiety, are the adverse effects of mechanisms compensating for less effective ACTH due to autoantibodies.

Furthermore, these patients engage in extraordinary behaviors, such as self-injury, to increase their cortisol levels. When this compensation is inadequate, symptoms of adrenocortical insufficiency appear.

Corticosteroid supplements have been demonstrated to be an effective treatment for chronic fatigue syndrome, anorexia nervosa and major depression. It allows the patients to have the corticosteroids they require for daily functioning and daily stressors. This therapy will relieve the patients of their symptoms of adrenocortical insufficiency and permit their cortisol-stimulating mechanisms to operate at levels that will not cause pathological problems.

PMID:

15885924

[PubMed - indexed for MEDLINE]
 

peggy-sue

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Interesting, particularly in the light of the NICE "do not recommend corticosteroids for "CFS" instructions", they are specifically prohibited.:eek:
 

Ema

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A LOT of damage has been done, in my opinion, to very sick people by not differentiating between replacing physiological levels of cortisol and applying pharmacological super-doses of steroids to reduce inflammation and suppress immune response.

The first has largely been shown to not only be beneficial, but absolutely necessary for proper immune response to fighting off an infection whereas the latter is not helpful at all. The dose has always made the poison, right?

All we hear about are the dangers and not the benefits which have left generations of people running scared of proper steroid replacement...and have gotten approx zero research into the variety of ways our endocrine and immune systems interact.
 

peggy-sue

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But the powers that be were only to happy to start stuffing women full of hormones for contraception.

Without doing any studies whatsoever on the long term effects - particularly those of the effects on personality and mood.:mad:
I found one, once.
It had made the finding that women on the pill tend to choose much more violent/aggressive partners.

(Might explain how the vile-ex got his claws into me!)

I understand exactly what you're saying Ema, but I still reckon hormones and corticosteroids need a heck of a lot more study before messing about with putting them in people.

But I've always been of the opinion that depression is hormonal.:p
 

anciendaze

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My own opinion is that the problem is less about levels of hormone than about defective regulation. The hormone finally gets around a blockage in the cascade of signals, but arrives much later than needed. I often find that I start the day with symptoms suggesting I have low levels of cortisol, including signs of inflammation. At the end of a long day I often have a serious problem slowing down, but those symptoms of inflammation are much less.

One feature I've noted, which has never been of interest to doctors, is that I am very sensitive to prednisone. After one shot, needed to open my sinuses so I could get on an airplane, I did not sleep for 48 hours. Doctor response, "Well, that is a little unusual."

Tests for cortisol levels in urine, which many here have had, collect over 24 hours, which loses any information about when in the cycle it was excreted. You can have a phase lag which completely wrecks your ability to sleep at night, but no one will notice. I suspect this also happens with ADH, causing nocturia. ACTH is involved in regulation of both cortisol and ADH.
 
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