Baseline PCOS — Insulin Resistance Drives the Syndrome
Hyperinsulinemia pushes ovarian theca cells to overproduce androgens.
- ~10%: Women affected (of reproductive age)
- ~70%: Insulin resistance (of PCOS patients)
- ~4/yr: Baseline ovulation (cycles, often anovulatory)
- 1.5–2×: Androgen elevation (above normal range)
Insulin resistance as the root driver
Insulin resistance forces the pancreas to secrete more insulin.
Excess insulin binds ovarian theca cell receptors directly.
This amplifies LH-driven androgen synthesis abnormally.
Downstream reproductive consequences
High androgens block normal follicle selection each cycle.
Follicles stall, and ovulation becomes rare or absent.
Irregular cycles and infertility commonly follow.
Hyperinsulinemia, not androgens alone, is the primary treatable driver.
Why insulin sensitizers make sense
Two therapies target insulin signaling from different angles.
Metformin acts mainly in the liver and muscle.
Inositol acts mainly inside the ovarian cell itself.
This 3D companion
The mechanism and dose-response model are identical to the 2D original: the same computeMetrics() formulas for insulin sensitivity, androgen level, ovulation frequency and side-effect burden. Here the liver and ovary are real orbitable 3D meshes with molecule particles, follicle spheres and signaling pulses placed in actual depth rather than flat canvas sprites.