Why PMOS raises androgens

If you have a PCOS diagnosis, what you have is now formally called PMOS (polyendocrine metabolic ovarian syndrome), the new name confirmed by global consensus in May 2026. The diagnostic criteria did not change. The clinical condition did not change. Hyperandrogenism, the elevated androgen activity that drives much of what is visible in PMOS, remains one of the three diagnostic criteria.

If you have been treated for acne, prescribed hair removal, and told to "just manage" facial hair growth separately, by different specialists, with different products, no one has explained the pathway. All three are downstream of one mechanism.

What androgens are

Androgens are a family of hormones including testosterone, dehydroepiandrosterone (DHEA and its sulfated form DHEA-S), and dihydrotestosterone (DHT, the most potent in this group). Every woman produces them. They are essential for libido, bone density, muscle, and mood. The framing of androgens as "male hormones that women should not have" is wrong; the relevant variables are level, source, and biological activity.

In PMOS, the issue is not that androgens are present. It is that levels and activity are elevated, and that this elevation drives visible features. Approximately 60 to 80 percent of women with PMOS show biochemical hyperandrogenism, meaning elevated testosterone or related markers on blood work. Many more have clinical hyperandrogenism, meaning visible androgenic features (acne, hirsutism, androgenetic hair thinning) whether or not the blood panel flags it. The 2023 International Guideline treats either form as meeting the hyperandrogenism criterion for PMOS diagnosis.

The androgens in PMOS come from two sources. Most attention goes to the ovary. The adrenal glands are also a meaningful contributor. Approximately 20 to 30 percent of women with PMOS have elevated DHEA-S, an adrenal-source androgen, alongside or independent of elevated ovarian androgens. This is part of why a complete PMOS workup tests DHEA-S as well as testosterone and SHBG; the source of the androgen excess shapes the right intervention.

The pathway, start to finish

This is the core mechanism. It is the single most useful thing to understand about why androgenic features cluster in PMOS.

Step 1: insulin resistance. Cells respond less efficiently to insulin’s signal. The pancreas compensates by releasing more insulin. Glucose levels in the blood often stay in the normal range while insulin climbs. The 2026 Lancet rename consensus reports approximately 85 percent of people with PMOS overall have insulin resistance, and approximately 75 percent of women with PMOS at a lean body weight do. The mechanism page on insulin resistance in PMOS covers this in depth.

Step 2: elevated insulin reaches the ovary. The ovarian theca cells carry insulin receptors. When stimulated, they increase testosterone production. This is the central insulin-to-androgen link in the ovarian source.

Step 3: insulin suppresses SHBG. Sex hormone-binding globulin is a protein made by the liver that binds testosterone in the blood and keeps it inactive. Insulin suppresses SHBG production. When SHBG drops, more of the testosterone already in circulation becomes biologically active, meaning more free testosterone reaches skin, hair follicles, and ovarian tissue. Total testosterone on a lab report can look unremarkable while free testosterone is elevated.

Step 4: more testosterone gets converted to DHT. DHT is the more potent androgen and the one that most directly acts on hair follicles, sebaceous glands, and other androgen-sensitive tissues.

Step 5: visible features emerge. Acne (oil gland stimulation), hirsutism (terminal hair growth in androgen-sensitive areas), androgenetic hair thinning (scalp), and contributions to cycle irregularity (the LH-FSH balance is disrupted in parallel). These are not four problems. They are four expressions of the same upstream activity.

The adrenal source operates in parallel. Adrenal androgens contribute to the overall androgen burden, particularly in the 20 to 30 percent of women with PMOS who show elevated DHEA-S. Adrenal-source androgens do not run through the insulin-to-theca-cell pathway the same way ovarian-source ones do, which is one reason a single intervention rarely addresses everything in everyone.

Why "just cut sugar" misses the mechanism

A frequent piece of well-meaning advice in the PMOS community is to cut sugar. The mechanism above explains why this is mostly a miss.

Insulin resistance is a chronic state, not a meal-by-meal response. A woman with PMOS and insulin resistance can eat a low-sugar meal and still have elevated fasting insulin, because the underlying resistance has not gone away. Reducing sugar in a given meal is fine, sometimes useful, but it is not the lever that moves the upstream variable. The interventions that move the upstream variable are the ones that change how the body handles insulin over weeks to months: sleep, resistance training, an overall dietary pattern oriented around protein, fibre, and meal composition, and where indicated, medications that act directly on insulin signalling.

This is why lifestyle changes are slow to show results on androgenic features. The upstream mechanism has to genuinely shift, not just be quiet on a given day.

What actually moves androgens

The broad principle: anything that improves insulin sensitivity tends, over time, to lower free androgens. Direct anti-androgen interventions can produce faster surface improvements without addressing the upstream picture. Both have their place; knowing which is which is the useful part.

Foundation interventions (2023 Guideline first-line). Resistance training, an overall dietary pattern oriented around protein, fibre, and meal composition (not restriction), adequate sleep, and mental health support. Sustained changes over weeks to months show measurable improvement in free testosterone and SHBG. Effect sizes are modest individually; they compound. The PMOS treatment hierarchy covers the foundation framing in more detail.

Metformin. The most-studied insulin-sensitising medication for PMOS. Improves fasting insulin, modestly lowers androgens, and has decades of safety data. First-line pharmacological option per the 2023 Guideline. Engages the upstream mechanism.

Inositol. Meta-analyses suggest modest improvement in insulin sensitivity and ovulation. The 2023 Guideline rates the evidence as limited and inconclusive. Reasonable as an adjunct, particularly for people who cannot tolerate metformin. The evidence summary on inositol covers the fuller picture.

Combined oral contraceptives (COCs). Suppress ovarian androgen production and increase SHBG. They engage two of the downstream steps directly but do not address insulin resistance and do not improve underlying ovulatory function once stopped. Useful for symptom control while other changes take effect, or as longer-term management depending on goals. Not a foundation intervention; not an insulin-sensitising one.

Anti-androgens (spironolactone). Block androgen receptors. Do not engage insulin resistance, but directly reduce hair and skin features. Used adjunctively in PMOS when symptom relief is urgent and foundation interventions plus metformin are not producing the visible effects on a timeline that works for the person. Reliable contraception is required during anti-androgen therapy. The PMOS treatment hierarchy covers where anti-androgens sit in the broader order.

GLP-1 receptor agonists. Newer medications with growing evidence for metabolic, weight, and cycle outcomes in PMOS, with adjacent effects on androgenic features. Off-label for PMOS-specific use outside of obesity or type 2 diabetes indications. The evidence summary on GLP-1s in PMOS covers this in depth.

What to ask a clinician

If you have been offered hormonal contraception or topical acne treatments without a conversation about insulin resistance, three questions have high leverage:

Has my fasting insulin been tested, or only fasting glucose? Glucose alone misses early to moderate insulin resistance because the pancreas compensates by releasing more insulin while glucose stays in range.

What are my SHBG and free testosterone, not just total testosterone? SHBG is one of the most informative single markers in a PMOS workup; total testosterone alone can look normal while free testosterone is elevated.

Has DHEA-S been checked, to see if there is an adrenal contribution? This shapes whether the intervention picture is purely insulin-and-ovarian or includes an adrenal component.

These questions clarify whether the proposed treatment plan engages the mechanism or only the surface. Both can be appropriate, depending on goals; the distinction is worth knowing.

A note on the experience

Acne, facial and body hair growth, and scalp hair thinning are among the most distressing features of PMOS, not because they are medically dangerous, but because of what they do to how someone feels in the mirror. The medical system often treats them as cosmetic. They are not. They are endocrine features with endocrine causes, downstream of a defined mechanism in a recognised condition.

Taking them seriously, including asking the insulin and SHBG and DHEA-S questions that explain them, is part of taking the condition seriously.