Understanding the Connection Between PCOS and Hirsutism
Polycystic ovary syndrome (PCOS) is the most common hormonal disorder in women of reproductive age, affecting 6–12% of the population. Among its many manifestations, hirsutism—the growth of coarse, dark, terminal hair in a male-pattern distribution on the face, chest, abdomen, and back—is one of the most distressing. Understanding why hirsutism develops in PCOS, and how to effectively treat it, requires a clear understanding of the underlying hormonal dysregulation.
What Is Hirsutism?
Hirsutism refers specifically to androgen-dependent hair growth in women that follows a male pattern. It is distinct from hypertrichosis, which refers to generalized fine hair growth unrelated to androgens. The Ferriman-Gallwey scoring system is the standard clinical tool for assessing hirsutism severity, rating hair growth across nine androgen-sensitive body areas.
Hirsutism affects approximately 70–80% of women with PCOS and is directly caused by androgen excess. However, the severity of hirsutism does not always correlate perfectly with androgen levels measured in serum, because the sensitivity of hair follicles to androgens varies substantially between individuals—a phenomenon driven by differences in local 5-alpha reductase activity, the enzyme that converts testosterone to its more potent form, dihydrotestosterone (DHT), within the hair follicle itself.
Androgen Excess in PCOS
In PCOS, elevated androgens—primarily testosterone, DHEA-S (dehydroepiandrosterone sulfate), and androstenedione—drive hirsutism through several overlapping mechanisms. The ovaries in PCOS produce excess androgens due to abnormal LH (luteinizing hormone) signaling, which overstimulates the theca cells that synthesize testosterone. The adrenal glands also contribute excess DHEA-S in approximately 20–30% of PCOS cases.
Elevated androgens stimulate androgen-sensitive hair follicles to transition from producing fine, light vellus hairs to producing coarse, pigmented terminal hairs. This transformation is largely irreversible once established—which is why early treatment of androgen excess is more effective than treating long-established hirsutism.
The Role of SHBG
Sex hormone binding globulin (SHBG) is a protein produced by the liver that binds testosterone and estradiol in the bloodstream, rendering them biologically inactive. Only "free" (unbound) testosterone can enter cells and exert androgenic effects. In PCOS, SHBG levels are frequently low—sometimes profoundly so—due to elevated insulin levels, which suppress hepatic SHBG production.
This means that even when total testosterone is only modestly elevated, the free testosterone fraction can be dramatically high if SHBG is suppressed. A woman with a total testosterone of 60 ng/dL and SHBG of 15 nmol/L may have more androgenic effect at the follicle level than a woman with testosterone of 80 ng/dL and SHBG of 60 nmol/L. This is why measuring free testosterone and SHBG—not just total testosterone—is essential for a complete androgenic assessment.
Insulin Resistance: The Central Driver
Insulin resistance is present in 50–70% of women with PCOS, regardless of weight. Excess insulin has two direct androgenic effects: it stimulates ovarian testosterone production by binding to insulin-like growth factor receptors on theca cells, and it suppresses hepatic SHBG production, increasing free androgen availability.
This creates a self-reinforcing cycle: insulin resistance raises androgens, androgens worsen fat distribution and insulin sensitivity, and worsening insulin resistance further elevates androgens. Breaking this cycle—through lifestyle modification, insulin-sensitizing agents like metformin or inositol, and hormonal therapy—is central to managing both PCOS and its androgenic manifestations.
Comprehensive Treatment Approach
Treating hirsutism in PCOS requires targeting the underlying hormonal and metabolic dysfunction, not just the cosmetic manifestation. A comprehensive approach includes:
Insulin sensitization: Weight loss (even 5–10% of body weight) in overweight women significantly reduces androgen levels and SHBG suppression. Metformin and inositol (particularly myo-inositol) improve insulin sensitivity, reduce androgen production, and can restore ovulatory function.
Hormonal therapy: Oral contraceptives containing anti-androgenic progestins suppress ovarian androgen production and increase SHBG. Spironolactone, a mineralocorticoid antagonist with anti-androgenic properties, blocks androgen receptors and reduces 5-alpha reductase activity at the follicle level.
Bioidentical progesterone: Natural progesterone has mild anti-androgenic properties and can help restore hormonal balance in PCOS without the side effects associated with synthetic progestins. It also supports cycle regularity and addresses the progesterone deficiency that accompanies chronic anovulation.
Cosmetic approaches: Laser hair removal and eflornithine cream are effective adjuncts for established hirsutism. However, without addressing the androgenic driver, cosmetic treatments must be repeated indefinitely.
A Personalized Hormonal Evaluation Is Essential
Every woman with PCOS has a unique hormonal profile. Effective treatment requires understanding not just androgen levels but also insulin dynamics, SHBG, LH/FSH ratios, DHEA-S, prolactin, thyroid function, and metabolic markers. A one-size-fits-all approach leaves many women undertreated.
Dr. Kenton Bruice, MD, offers comprehensive hormonal evaluations for women with PCOS and hirsutism at his clinics in Denver, Aspen, and St. Louis. If you are struggling with unwanted hair growth and other PCOS symptoms, schedule a consultation with Dr. Bruice to explore a personalized treatment approach.