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Hormonal alterations in adolescent chronic fatigue syndrome

Discussion in 'Latest ME/CFS Research' started by shrewsbury, Mar 7, 2010.

  1. shrewsbury

    shrewsbury member

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    Fred Springfield posted this to co-cure yesterday

    Hormonal alterations in adolescent chronic fatigue syndrome.

    Journal: Acta Paediatr. 2010 Mar 1. [Epub ahead of print]

    Authors: Wyller VB, Evang JA, Godang K, Solhjell KK, Bollerslev J.

    Affiliation: Division of Paediatrics, Oslo University Hospital, Oslo, Norway.

    NLM Citation: PMID: 20199497


    Abstract
    Aim: The chronic fatigue syndrome is associated with alterations in the hypothalamus-pituitary-adrenal axis and cardiovascular autonomic nervous activity, suggesting a central dysregulation. This study explored differences among adolescent chronic fatigue syndrome patients and healthy controls regarding antidiuretic hormone, the renin-angiotensin-aldosterone-system, sex hormones and cardiac peptides.

    Methods: We included a consecutive sample of 67 adolescents aged 12-18 years with chronic fatigue syndrome diagnosed according to a thorough and standardized set of investigations, and a volunteer sample of 55 healthy control subjects of equal gender and age distribution. Hormones were assayed with standard laboratory methods.

    Results: Among patients, plasma antidiuretic hormone was significantly decreased and serum osmolality and plasma renin activity were significantly increased (p </= 0.001). Serum concentration of aldosterone, cortisol, NT-proBNP and sex hormones were not significantly different in the two groups.

    Conclusion: Chronic fatigue syndrome in adolescents is associated with alterations in hormonal systems controlling osmolality and blood volume, possibly supporting a theory of central dysregulation.
    Enid, taniaaust1 and Merry like this.
  2. beesknees

    beesknees Senior Member

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    Interesting. Thank you for posting.
  3. ukme

    ukme Senior Member

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    Very good. So now I wonder what they are going to do with that information?
  4. Dolphin

    Dolphin Senior Member

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    Definition

    Definition used:
    taniaaust1 likes this.
  5. Dolphin

    Dolphin Senior Member

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    There were 2 other statistically significant differences not mentioned in abstract

    There were 2 other statistically significant differences not mentioned in abstract:

    1st number: median, they call the other two confidence intervals (but I wonder do they mean interquartile ranges or the ranges covering 95% - a confidence interval would be more if one didn't know the value I would have thought):

    Variables* CFS patients Controls
    Serum albumin (g ⁄ L) 45‡ (44–46) 43 (43–44)

    Male CFS; Female CFS; Male Control; Female control
    Serum sex hormon binding globuline (nmol ⁄ L) 24 (17–28) 52 (38–59) 31 (24–38) 45 (42–56)

    ‡p < 0.001 for differences between CFS-patients and controls, Wilcoxon–Mann–Whitney’s test.
    p <0.05 for differences between male CFS-patients and male controls, Wilcoxon–Mann–Whitney’s test.
    ---------------
    The lower values for serum cortisol in CFS were nearly significant:
  6. Dolphin

    Dolphin Senior Member

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    The differences in ADH were quite dramatic:

    One obvious factor that might explain the ADH results isn't relevant here:
    I recall this crowd are a bit into deconditioning.
    However, they say the following:
    The authors mention sustained arousal which is Wyller's pet theory
    a couple of times in the discussion but my guess is there are plenty of other ways to view the data.
  7. August59

    August59 Daughters High School Graduation

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    Isn't low serum ADH and high serum PRA the recommended lab test results to confirm adrenal insuffiency?
  8. Dolphin

    Dolphin Senior Member

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    I don't know what the cut off points are - maybe somebody could look. The authors do say:
    One can sometimes find that on average a group's levels are lower than normal but still most or all of the values are within the "normal" range.
  9. CBS

    CBS Senior Member

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    There is no way to for an individual patient or a patient group to have values below the reference range for ADH.

    In this study, the ADH levels in the patient group (which do not meet the criteria for CFS), unlike the control group, are not "normally distributed." The analysis there for uses non-parametric (the results are not on a standard normal curve and therefore measures of variance are inappropriate). The WilcoxonMannWhitneys measure employed by the authors uses expected rank order of a continuous variable versus the observed rank order. The bottom line was that the ADH values clustered very tightly towards the bottom of the scale (see the confidence interval) in a dramatic fashion but because their ADH test was only sensitive to 0.6 pmol ⁄ L. The bottom of the reference range for ADH is always reported as something along the lines of LE 0.4 pmol/L.

    Here's my summary of the ADH portion of this article:


    • The strong association of CFS with lower levels of ADH appears even more striking given the relaxed diagnostic criteria for the CFS group (three consecutive months of disabling fatigue was sufficient for inclusion and no accompanying symptoms were required.).
    • The relaxed diagnostic criteria and the statement that some variables were appraised not to follow an approximate normal distribution together raise the question of whether or not stricter inclusion criteria and a possibly more homogeneous CFS cohort would have produced an even stronger association between CFS and low levels of ADH (the WilcoxonMannWhitneys test, used for non-parametric analysis, relies upon ranking and ignores variance). In this study, the CFS cohort had an ADH level confidence interval of 0.3 pmol/L while the control group had a CI of 1.7 pmol/L.
    • If it were available, a look at the authors raw data with an eye towards the association between ADH levels and the number of consecutive months of fatigue and/or accompanying symptoms may be revealing. The authors noted that in some cases No detectable concentration [of ADH] is put equal to the lowest detection limit, i.e. 0.6 pmol ⁄ L. I wonder if there were a number of these cases in the CFS group along with a subset of more typical readings, resulting in a skewed or bimodal distribution.
    • Lastly, I have a minor quibble with the authors' statement All median values for both groups were within normal reference ranges. There is no attainable ADH value that is below the reference range of the test as the lower detection limit of the test is actually higher than the bottom of the reference range.
  10. MeSci

    MeSci ME/CFS since 1995; activity level 6

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    I just came across the abstract for this paper today. I have suffered from significant polyuria since at least 1996 and from ME/CFS since 1995. I have had to fight for a prescription of desmopressin, which has made life a great deal easier, although in the past few years I seem to have developed another type of polyuria as well which does not respond to desmopressin, so I presume it to be a solute diuresis, perhaps driven by Na/lactate loss due to lactic acidosis. (I have twice suffered from severe hyponatraemia, but seem to be preventing a recurrence of this through diet and supplementation.)

    As the formal spot-checks for urine osmolality were botched/variable, I did tests myself at home for a while, using a wine hydrometer and conversion methods. Perceived polyuria was consistent with low, sometimes very low, osmolality. This was before the solute diuresis arrived to complicate matters.

    Doctors in the UK are alarmingly ignorant about polyuria, and the ones I have seen will not even recognise that normal urine production depends on body mass! When I initially suggested to the first doctor that he test for antidiuretic hormone he replied that it was a strange thing to test for, so it was never done.
  11. August59

    August59 Daughters High School Graduation

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    It is not just the UK that don't want to do the test. US doctors do not want to do because I don't think they would know what to do if the results come back abnormal. They are under such a drive to see so many patients a day that they would not have time to do 15 minutes worth of research.

    I told my new primary care physician that I wanted him to help me if he would in doing some follow-up blood work in reference to my CFS and he cut his eyes at me and said he would entertain the thought of helping with the test, but he wasn't sure on what to do with the blood work when it comes back. I said I would be glad to help him with that to.

    I see him in 2 more weeks and I quess we will see
  12. richvank

    richvank Senior Member

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    Hi, all.

    For what it's worth, the GC-MCB hypothesis explains the low ADH as being due to glutathione depletion in the hypothalamus and pituitary. The same explanation applies to other hormones secreted by the hypothalamus and pituitary that contain cysteine residues, either themselves or their prohormones. These include ACTH and oxytocin.
    The problem with ACTH explains the HPA axis dysfunction in ME/CFS.

    It's interesting that they found normal levels of aldosterone in the kids. Two studies have found low aldosterone in adults with ME/CFS.

    Best regards,

    Rich
    Battery Muncher likes this.
  13. taniaaust1

    taniaaust1 Senior Member

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    I hate it when they can use whatever defination they like and still call it a CFS study. This study seeing no other symptoms other then fatigue were required.. is a "chronic fatigue" study rather then even a CFS study which fits any CFS defination. They should be force to issue a correction.

    Still very interesting results.. I wonder how many of these adolesents will end up developing CFS in the future.
  14. Snow Leopard

    Snow Leopard Senior Member

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    Interestingly Vasopressin/ADH is also the only consistent precursor that is consistent with neuroendocrine pattern (hypocortisol, but CRH is normal!), and POTS symptoms.

    Vasopressin/ADH is not a specitic biomarker, but it is important to consider its role in CFS IMO.
  15. Battery Muncher

    Battery Muncher Senior Member

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    I might be talking out of my backside here, but...

    I vaguely remember, from the days where I was trying out nootropics, that desmopressin OR vasopressin OR both (I can't remember) was used to boost memory.

    Could low ADH help explain the short term memory problems in ME? (Of course, low ADH may just be the underlying symptom of a deeper problem - as Rich Vank has suggested)

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