Estradiol makes clotting self-sustaining

This proposed hypothesis asks whether estradiol, an estrogen hormone, can make blood clotting sustain itself even when liver-driven activation is reduced. In reconstituted blood, linked clotting enzymes could cross a tipping point and amplify one another until thrombin, the enzyme that drives clot formation, surges. Blood depleted of immunoglobulins, immune proteins, and containing unmodified fibrinogen, the clot-forming protein, would test whether reaction rates predict a fading or expanding burst. A selective block could remove the excess while matched thrombin still starts downstream clotting. That pattern would favor propagation over direct activation of factor XIII, a clot-stabilizing enzyme. Testing needs selective inhibitors and time-resolved enzyme assays.