Re: Theory as to why some people so sensitive to Calcium-D-Glucarate

Powers reduced calcium D-glucarate's (CDG) action to a single mechanism — inhibition of bacterial beta-glucuronidase — arguing it only matters for patients who actually have substantial beta-glucuronidase activity, using a house-fire/shed-fire analogy. He said he suspects androsterone will turn out to be absurdly elevated in many patients, particularly in PSSD, based on ongoing lab testing, while acknowledging others likely have the opposite pattern with the switch thrown the other way. He criticized two decades of research fixated on allopregnanolone, noting that absurd 3α metabolite elevations (a 28x multiplier versus controls) in the original PFS studies were never followed up. He framed the disease state as a derangement of the normal neurosteroid order — one steroid absurdly high, another low, in either direction — with normalization as the goal, and explained the indomethacin panic reactions as occurring only in patients whose THDOC is actually the out-of-band molecule. He closed with the model that the disease is roughly fifteen different switch-flips, up or down, differing per person — which is why "X crashed me" anecdotes dominate discussion and why CDG may simply not address a given individual's specific dysfunction.