Re: I collect more and more labs/genome/dutch tests that support my theory on PFS. I really think I have it nailed down. I d...

Powers argued that finasteride is an irreversible "suicide inhibitor" that permanently disables any 5AR enzyme it touches, requiring 2–3 weeks for the enzyme to be degraded and remade — so even a single pill can suffice if the patient's system is already at its limit. He interpreted windows and crashes as substances that increase or worsen metabolite clearance, and suggested cAMP/cGMP gradients may play a role for some patients (particularly PSSD or genital-numbness/ED presentations), where excessive buildup destroys the signal-to-noise ratio. He illustrated transporter overload with ABCC2 (or ABCC5 for cAMP): a struggling exporter given a second job falls further behind, and cited his transgender-medicine experience with COMT, which metabolizes dopamine/adrenaline as well as catechol estrogens, where speeding it up can crash dopamine signaling in slow dopamine producers. He claimed accumulating labs, genomes, and DUTCH tests were finally showing consistent, reliably abnormal findings across nearly all PFS patients — something never previously achieved — and that exceptions still trace to some other near-catastrophic metabolic defect that finasteride converts into a true catastrophe. He framed the whole model through redundancy/entropy metaphors: PFS patients have a hidden specific vulnerability (a video-game character with full hit points but a fatal weakness to fire spells), and he personally lacks that vulnerability because his glucuronidation is intact — closing with dismay at online services selling "DIY fire spells" for hair loss to people unaware of their own vulnerability.