🧬 PCOS Endometrial Hyperplasia Risk Simulator

Chronic Anovulation in PCOS

No ovulation means no corpus luteum ever forms.

• ~10%: PCOS prevalence (reproductive-age women)
• up to 100%: Anovulatory cycles (in PCOS patients)
• 0: Corpus luteum formed (without ovulation)
• primary: Progesterone source lost (luteal production absent)

Why ovulation stalls

High LH and insulin block follicle maturation.

No corpus luteum forms

Without a ruptured follicle, no progesterone source exists.

Cycle irregularity results

Periods become infrequent, unpredictable, or absent.

Unopposed Estrogen Exposure

Estrogen keeps building tissue with nothing to oppose it.

• ~0: Progesterone level (ng/mL without ovulation)
• ongoing: Estrogen source (follicular and peripheral)
• absent: Opposition mechanism (no luteal phase)
• growth-only: Endometrial signal (unbalanced stimulation)

Estrogen keeps signaling

Follicular and peripheral estrogen production continues unchecked.

Progesterone normally opposes it

Progesterone usually limits and matures the lining.

Peripheral aromatization adds fuel

Adipose tissue converts androgens into extra estrogen.

Endometrial Proliferation Without Shedding

The lining thickens progressively over unopposed months.

• ~28 days: Normal shedding cycle (typical menstrual cycle)
• months: Anovulation duration (lining keeps growing)
• rising: Endometrial thickness (no shedding trigger)
• increasing: Glandular crowding (proliferative overgrowth)

Growth without a stop signal

No progesterone withdrawal means no shedding trigger.

Glands crowd together

Proliferative glands multiply and pack more densely.

Thickness accumulates monthly

Each unopposed month adds more tissue depth.

Hyperplasia and Cancer Risk

Prolonged unopposed estrogen raises hyperplasia risk sharply.

• low: Simple hyperplasia risk (early unopposed exposure)
• rises: Atypical hyperplasia risk (with duration untreated)
• up to 29%: Cancer progression risk (untreated atypical hyperplasia)
• duration: Key driver (months of unopposed estrogen)

Simple to complex hyperplasia

Glandular crowding progresses toward structural complexity.

Atypia raises stakes

Cellular atypia signals a precancerous change.

Time is the driver

Longer unopposed exposure means higher cumulative risk.

Progestin Therapy Protects the Endometrium

Progestin restores balance and triggers protective shedding.

• 10–14 days: Cyclic progestin (monthly withdrawal bleed)
• daily: Continuous progestin (IUD or pill option)
• high: Hyperplasia regression (with adequate therapy)
• substantial: Risk reduction (restored opposition)

Progestin opposes estrogen

It counters growth signaling and matures the lining.

Shedding is restored

Withdrawal bleeding clears accumulated tissue safely.

Long-term protection

Regular progestin use lowers hyperplasia risk durably.