In light of the OMF scientists proposing that CFS serotonin receptors could be negatively affected in order to cope with high serotonin levels (due to the tryptophan/kyneurenine issue), this interested me as years ago ME doctor/researcher from Belgium, Kenny De Meirleir, mentioned that he believes ME patients have altered hormone receptors, e.g. effectively giving patient signs of hypothyroidism, yet their blood thyroid markers (sans RT3) are essentially normal.
So I wonder if it's 'just' the serotonin receptors 'adapt' (potentially causing a functional depression without actual depression), but other receptors could have adapted like this also in ME CFS, such as KDM mentioned?
Also I was thinking if that happened, all of these effects, including low GH due to pituitary problems may be explained by a process of wide spread neuroinflammation affecting the way our brains control hormones? If so, this might explain why so many of our hormone levels although altered, aren't altered enough to meet clinical definitions of deficiency or excess states, yet in long term ME CFS patients we can still have the classic symptoms of these conditions - such as hair loss, premature greying of hair, weight gain/weight loss, female health problems etc.
It always interested me why the tragic fatal ME CFS subsets with dorsal root ganglionitis found on autopsy, not only are usually female, but I've read at least one of these young women reported entering the menopause in their 20's, which now might make sense if the brain is getting zapped on it's receptors, or in some way, trying to adapt?
Just a thought.