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A Little Poisoning Along the Road to ME/CFS
Looking at my symptoms, many of which are far less these days and some are gone, it would be easy to figure that I'd just been dealing with some heavy-duty menopausal issues.
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ACTH autoantibodies disrupt HPA axis in ME/CFS.

Discussion in 'Latest ME/CFS Research' started by Ema, Feb 11, 2013.

  1. Ema

    Ema Senior Member

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    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.

    Source

    The Endocrine Research Project, 574 Sims Road, Santa Cruz, CA 95060, USA. rwheatla@query.com

    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.
     
  2. Valentijn

    Valentijn Activity Level: 3

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    Sounds like it's purely speculative at present, but it does present an interesting avenue for further research.
     
  3. lansbergen

    lansbergen Senior Member

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    Realy??????? Do CFS patient do this?
     
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  4. Valentijn

    Valentijn Activity Level: 3

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    Maybe our muscles are doing it for us, so we don't have to :p
     
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  5. lansbergen

    lansbergen Senior Member

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    :lol::lol::lol:
     
  6. Enid

    Enid Senior Member

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    Interesting Ema - endocrine function/dysfunction as part of the whole picture - just wish they would keep away from the emotive term depression - don't recall it.
     
  7. alex3619

    alex3619 Senior Member

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    Cortisol is not hugely helpful for us, though many do benefit at lower doses, and our biggest problem is an abnormal pattern of cortisol release: too little in the day, too much at night. Its not a deficiency state as such. I cannot comment on this paper properly as I have not read it, but with respect to CFS (and ME) it may not be a valid hypothesis. That doesn't mean we don't have such autoantibodies though: we know we make a lot of autoantibodies and its an underinvestigated area.
     
  8. Ema

    Ema Senior Member

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    When your cortisol is low, you will find the most creative ways to stimulate the release. For me, this certainly involved self-injury behavior from time to time. Plus self injurious behavior from drugs and alcohol that also functioned to stimulate cortisol. Troubles with alcohol and/or nicotine seem to be very common in the Addison's population. Those substances must work VERY well to stimulate cortisol.

    Certainly this won't apply to all ME/CFS people (maybe to very few!) but I agree that it needs further investigations. I think there must be autoantibodies to just about everything!

    Ema
     
  9. lansbergen

    lansbergen Senior Member

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    In my opion understimulated A7 nAchR would have the shame effect.
     
  10. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    I self-harmed due to high stress levels from childhood until my twenties. The simple self-harm merged into other harmful-but-relieving behaviours such as heavy drug use (including alcohol). Self-harm and drug use relieve emotional distress, at least partly by stimulating the release of endorphins, but of course I didn't know that at the time. One just finds out by chance that it helps, so one keeps doing it.
     
  11. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    Incidentally, the Wheatland paper, albeit a rather strange one, is cited by de Meirleir et al in a paper discussed here.

    Although Wheatland doesn't cite conclusive evidence for autoantibodies against ACTH, it fits with so much else, e.g. that we seem to have high levels of autoantibodies, that our cortisol levels are (often/inappropriately) low, and that the Synacthen test makes us produce cortisol normally (so doctors assume that there is nothing wrong with our cortisol production).

    What I can't figure out is how autoantibodies against ACTH could explain our apparently-reversed diurnal cortisol secretion. I did a lot of clicking around today to try to find answers and think I came across a paper that suggested an alternative way for the body to make cortisol but goodness knows what it was! Something to do with DHEA? That was involved somewhere anyway! Too tired to look again today.
     
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