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Nitric oxide and its possible implication in ME/CFS (Part 2 of 2)
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Glucocorticoid Dysregulations and Their Clinical Correlates.

Discussion in 'Other Health News and Research' started by Ema, Mar 9, 2014.

  1. Ema

    Ema Senior Member

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    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2933142/pdf/nihms227231.pdf

    As an introduction to this volume, this chapter will review the basic biology of glucocorticoid release and molecular mechanisms of glucocorticoid receptor function, and will discuss how dysregulation of glucocorticoid action at all levels could contribute to such side effects.

    At the molecular level, glucocorticoid receptor polymorphisms may be associated either with receptor hypofunction or hyperfunction and could thus contribute to differential individual sensitivity to the effects of glucocorticoid treatment.

    Numerous factors regulate hypothalamic-pituitary-adrenal (HPA) axis responsiveness, which could also contribute to individual differences in glucocorticoid side effects.

    One of these is sex hormone status and the influence of estrogen and progesterone on HPA axis function and mood.

    Another is immune system activity, in which immune molecules, such as interleukins and cytokines, activate the HPA axis and alter brain function, including memory, cognition, and mood. The effects of cytokines in inducing sickness behaviors, which overlap with depressive symptomatology, could also contribute to individual differences in such symptomatology.
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