I don't know if this is relevant to any of your cases, but I figured it wouldn't hurt to point out that estradiol (And possibly other estrogens - that was just the only form they tested.) increases the
sensitivity and
quantity of the TRPV1 receptor. It used to be called VR-1 or the capsaicin receptor. This receptor senses capsaicin,
dust, and other irritants and causes
bronchoconstriction in asthma and
chemical sensitivity. Testosterone, DHEA, and
somatostatin desensitize the receptor, while progesterone is neutral.
My own sensitivities are to mold VOCs and dust, and my symptoms are muscle tension/tension headache/anxiety (depends on exposure level), 10 pounds water retention (weight is stable, but socks squish dents into my legs only during the summer), and asthma (when in southeastern states). I can confirm that DHEA desensitizes something in me: almost certainly TRPA1, since that receptor can be triggered by mold VOCs (presumed to be disulfides and/or dialdehydes) and I don't think TRPV1 can. TRPA1 can also be activated by
dust so my dust sensitivity cannot prove a partial role for TRPV1. I haven't tried deliberately elevating estrogen to see if that would make things worse. My estradiol has ranged from 23 pg/ml (taking Arimidex) to 38 (baseline) up to 55 (taking a bodybuilding supplement "aromatase inhibitor") with no noticeable effects.
Before I got sensitized by mold, the only time I got asthma was when I overdosed on calcium. I was playing with 2(?) gram doses of calcium pyruvate and didn't think the calcium would be a big deal. I was also probably getting almost 1000 mg from food and 1000 mg more from a calcium supplement, so we're talking about a disgusting excess of calcium. With a family history of prostate cancer, I should have been treating 1000 mg as my upper limit...