PCOS
Polycystic Ovary Syndrome

PCOS
Protocol

PCOS is not one condition — it has four distinct phenotypes with different hormonal profiles and metabolic risks. Understanding your phenotype determines the most targeted intervention.

1 in 10
women of reproductive age have PCOS
70–80%
of PCOS cases involve insulin resistance
4
distinct phenotypes — each needs different management
55–100%
ovulation restoration with 5–10% weight reduction
Rotterdam Criteria

The Four PCOS Phenotypes

Diagnosis requires 2 of 3 criteria: hyperandrogenism, anovulation, polycystic ovarian morphology on ultrasound.

Phenotype A
Hyperandrogenism + Anovulation + Polycystic ovaries
Classic PCOS — most common and most severe metabolic phenotype. High androgen levels, insulin resistance, and anovulation. Responds well to insulin-sensitising interventions.
Phenotype B
Hyperandrogenism + Anovulation (no PCO morphology)
Androgenic and anovulatory but ovaries appear normal on ultrasound. Metabolic risk similar to Phenotype A. Often missed if diagnosis relies on ultrasound alone.
Phenotype C
Hyperandrogenism + Polycystic ovaries (ovulatory)
Androgenic with polycystic morphology but regular ovulation. Lower metabolic risk than A/B. Fertility may be preserved but androgen excess still requires management.
Phenotype D
Anovulation + Polycystic ovaries (no hyperandrogenism)
Non-androgenic PCOS — mildest metabolic phenotype. Often associated with insulin resistance without elevated androgens. Best prognosis for fertility with lifestyle intervention.
The Biology

Key Mechanisms in PCOS

  • →Insulin resistance is present in 70–80% of women with PCOS, regardless of body weight. Hyperinsulinaemia directly stimulates ovarian theca cell androgen synthesis via insulin receptor activation, independent of LH stimulation.
  • →Insulin suppresses hepatic SHBG synthesis, increasing free testosterone and free oestradiol. Elevated free androgens impair follicular maturation, causing follicular arrest at the small antral stage — producing the characteristic 'string of pearls' appearance on ultrasound.
  • →The resulting anovulation prevents progesterone production in the luteal phase, creating unopposed oestrogen exposure of the endometrium — increasing the long-term risk of endometrial hyperplasia.
  • →Normalising insulin sensitivity is the most effective single intervention for restoring ovulation in PCOS. A 5–10% reduction in body weight in overweight women with PCOS restores ovulation in 55–100% of cases.
Evidence-Based Supplementation

PCOS Supplement Protocol

Myo-inositol
2–4 g/day
With meals
Improves FSH receptor signalling in granulosa cells; reduces insulin resistance; restores ovulation in 60–70% of anovulatory PCOS women over 3–6 months
D-chiro-inositol
50–100 mg/day
With meals (40:1 ratio with myo-inositol)
Mediates insulin action in ovarian theca cells; reduces androgen synthesis; improves oocyte quality
Berberine
500 mg 2–3×/day
With meals
AMPK activator — comparable to metformin for insulin sensitisation; reduces androgen levels; improves menstrual regularity
N-acetylcysteine (NAC)
600 mg 2–3×/day
Between meals
Antioxidant; improves insulin sensitivity; reduces androgen levels; comparable to metformin in some RCTs for ovulation induction
Vitamin D3
Target 100–150 nmol/L
With largest meal
Reduces insulin resistance, androgen levels, and inflammatory markers in PCOS; improves AMH-to-AFC ratio
Omega-3 DHA/EPA
2–3 g/day
With meals
Reduces triglycerides, inflammatory cytokines, and free testosterone; improves insulin sensitivity
Spearmint tea
2 cups/day
Any time
Reduces free testosterone via anti-androgenic activity; improves LH:FSH ratio; evidence from RCTs for hirsutism reduction
Magnesium glycinate
300–400 mg/day
Evening
Improves insulin receptor sensitivity; reduces cortisol; improves sleep quality — all relevant to PCOS management
PCOS Protocol — Quick Reference
One-page PDF cheat sheet · Supplement doses, food priorities & action steps
Download PDF
Your Protocol

Action Plan

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Dietary Foundation

Supplement Protocol

Movement & Monitoring