Hyperandrogenism Explained: Excess Androgens in PCOS

Introduction

Hyperandrogenism — the state of elevated androgens or excessive sensitivity to them — is the defining hormonal hallmark of PCOS. It is responsible for the most visible and often most distressing clinical features: hirsutism (excess hair

The Androgens Involved

Androgens are a group of sex hormones that include:

• Testosterone: The primary clinical androgen. In PCOS
• both total and free testosterone may be elevated (due to low SHBG). Free testosterone is the biologically active fraction.
• Androstenedione: An androgen precursor from both ovaries and adrenal glands — often elevated in PCOS.
• DHEA-S (dehydroepiandrosterone sulphate): Almost exclusively adrenal in origin; elevated in about 30–35% of PCOS women
• indicating adrenal hyperandrogenism.
• 11-oxygenated androgens (11-ketotestosterone
• 11β-hydroxyandrostenedione): A recently characterised class of adrenal androgens with high androgenic potency. A 2023 review identified these as particularly relevant to PCOS metabolic risk.
• SHBG (sex hormone-binding globulin): Not an androgen itself
• but low SHBG (caused by hyperinsulinaemia) elevates free testosterone by reducing the protein-bound fraction.

Where Excess Androgens Come From

Ovarian Theca Cells

In PCOS, ovarian theca cells are intrinsically hyperactive in androgen production, even when stimulated with normal LH levels. When the already elevated LH and hyperinsulinaemia stimulate these cells, androgen output is further amplified. This is the primary source of excess testosterone in most PCOS phenotypes.

Adrenal Glands

Approximately 20–30% of PCOS women have elevated adrenal androgens (DHEA-S

Clinical Manifestations of Hyperandrogenism

Hirsutism

Hirsutism is the growth of coarse, dark, terminal hair in androgen-sensitive areas: upper lip, chin, sideburns, neck, chest, periareolar area, lower abdomen, inner thighs, and back. It is graded using the modified Ferriman-Gallwey (mFG) score. Scores ≥8 are considered indicative of hirsutism in most populations. Hirsutism is present in 70–80% of women with PCOS and is often the symptom causing the most distress.

Management: Combined oral contraceptives containing anti-androgenic progestins (drospirenone, cyproterone acetate, dienogest) reduce androgen production and increase SHBG, decreasing free testosterone. Spironolactone (anti-androgen) reduces hirsutism with consistent use over 6–12 months. Physical methods: laser hair removal (most effective long-term) and electrolysis; shaving, waxing, and eflornithine cream are shorter-term options.

Acne

Androgen-driven acne in PCOS is typically persistent, predominantly on the lower face and jawline, and often resistant to standard topical treatments. Androgens stimulate sebaceous gland activity, increasing sebum production and promoting Cutibacterium acnes overgrowth. Management: COCs (particularly drospirenone-containing

Androgenic Alopecia

Frontal or crown hair thinning (female-pattern hair loss) affects approximately 20% of PCOS women. Androgens shorten the anagen (growth) phase of hair follicles. Treatments: topical minoxidil (most effective

Biochemical Hyperandrogenism

Some women with PCOS have elevated androgens on blood tests but no visible clinical signs (possibly because their hair follicles are less androgen-sensitive). This "biochemical-only" hyperandrogenism still contributes to metabolic risk and confirms the PCOS diagnosis.

Testing for Hyperandrogenism

Labs: Free testosterone (calculated using total testosterone and SHBG, or measured by equilibrium dialysis) is the most sensitive marker. DHEA-S for adrenal androgen assessment. Androstenedione in specific cases. Note: Many commercial labs use inadequate assays for female testosterone measurement — liquid chromatography/tandem mass spectrometry (LC-MS/MS) is the gold standard.

References: Azziz R et al., J Clin Endocrinol Metab 2006; 2023 International PCOS Guideline; Handelsman DJ, Clin Endocrinol 2018 (testosterone assays); Pretorius E et al. — 11-oxygenated androgens, J Endocrinol 2023.