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why is me/cfs incidence higher after puberty (in women only?)

Discussion in 'General ME/CFS Discussion' started by xena, Nov 10, 2015.

  1. xena

    xena Senior Member

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    hi everyone, i'm curious about why we think this is....

    i believe KDM had some kind of explanation for it. i personally had biotoxin expsure from 11-13 but only seem to have gone into full scale me/cfs at puberty
     
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  2. Kati

    Kati Patient in training

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    I do not have references to provide you but there are 2 known peaks of increased incidence at least in women, the first one is during puberty, as teen and the second peak is in the middle age, 35-50.

    This would suggest the influence of hormones in disease process but at the moment, more research is needed.
     
    Last edited: Nov 10, 2015
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  3. Hip

    Hip Senior Member

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    There is a study on this:

    Two age peaks in the incidence of chronic fatigue syndrome/myalgic encephalomyelitis: a population-based registry study from Norway 2008–2012

    For ME/CFS onset, the study found there were two peaks in the figures: a first peak in the age group 10 to 19 years, and a second peak in the age group 30 to 39 years.

    The first peak of people coming down with ME/CFS from 10 to 19 years might involve Epstein-Barr virus as a trigger, because EBV is picked up in the teenage years.
     
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  4. xena

    xena Senior Member

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  5. WillowJ

    WillowJ คภภเє ɠรค๓թєl

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    WA, USA
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  6. pattismith

    pattismith Senior Member

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    [/QUOTE]
    Thank you for this article Xena
    Interesting as the article makes a possible connection between ME in women and genetic polymorphism in the Cytochrome P450,

    with impaired CYP3A and CYP1A2 activity (slow metabolizers), and/or increase CYP1B1 activity (fast metabolizers).

    it would be interesting to know the genetic status of members for these CYP and see if it matches!

    I do myself suspect to carry slow CYP, as I had several side effects with drugs,

    salicylic acid
    coffee
    ephedrine
    Amitriptyline

    Coffee is metabolized by CYP1A2 so I may be concerned by an inactivated variant on this gene.
    Salicylic acid is metabolized by CYP2C9
    Amitriptyline by CYP3A4, so again I may have impaired CYP3A4,

    It would be consistent with the hypothesis in the article...

    Maybe someone here knows about ones genetic polymorphism for CYP3A4 and CYP1A2, to see if the hypothesis correlates with us?



    interesting as my first symptoms started around 13 years old and progressed slowly, and I had a big "crash at 35 years old"...
     

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