Testosterone Levels in PCOS: Causes and Treatment

Testosterone levels in PCOS are a central concern for many women living with polycystic ovary syndrome, affecting everything from skin and hair to fertility and menstrual regularity. In PCOS, disrupted hormonal signalling and, in many cases, insulin resistance cause the ovaries to produce excess androgens, including testosterone. Understanding why this happens, what symptoms it causes, how it is tested, and what treatments are available can help women and clinicians make informed decisions about management. This article covers the key clinical facts, aligned with NHS, NICE, and international PCOS guidance.

Why do women with PCOS have high testosterone levels?

Women with PCOS have high testosterone because excess LH stimulates ovarian androgen production, and insulin resistance further raises free testosterone by suppressing SHBG and directly stimulating the ovaries.

Women with polycystic ovary syndrome (PCOS) have raised testosterone levels because of disrupted signalling between the pituitary gland and the ovaries, often compounded by insulin resistance. The mechanisms are heterogeneous: not all people with PCOS have insulin resistance, and lean PCOS phenotypes exist in which ovarian dysfunction is the dominant driver.

In a healthy hormonal cycle, the pituitary releases luteinising hormone (LH) and follicle-stimulating hormone (FSH) in a balanced ratio. In PCOS, LH secretion is disproportionately elevated, which stimulates the ovarian theca cells to produce excess androgens, including testosterone.^[6][1] Where insulin resistance is also present, raised circulating insulin directly stimulates the ovaries to produce more androgens and simultaneously suppresses sex hormone-binding globulin (SHBG) in the liver.^[7][8] SHBG is the protein that binds testosterone in the bloodstream, keeping it biologically inactive. When SHBG levels fall, more free (unbound) testosterone is available to act on tissues throughout the body, amplifying androgenic effects even when total testosterone is only modestly elevated.

The adrenal glands also contribute in some individuals, producing androgens such as dehydroepiandrosterone sulphate (DHEAS) independently of ovarian activity. This means that raised androgens in PCOS can have more than one source, which is why a thorough hormonal assessment is important.

Metformin, an insulin-sensitising agent, can modestly reduce androgen levels in some patients with PCOS, though its effects on testosterone are variable. Its use in PCOS is off-label in the UK.^[3][4] NICE CKS guidance on PCOS and the 2023 International Evidence-Based Guideline for the Assessment and Management of PCOS (Monash University, ESHRE, ASRM) provide further detail on these mechanisms.

What symptoms does raised testosterone cause in PCOS?

Raised testosterone in PCOS most commonly causes hirsutism, persistent acne, and scalp hair thinning; rapid virilisation is a red flag requiring urgent specialist referral.

Raised testosterone in PCOS causes a recognisable cluster of androgenic symptoms, the most common of which are hirsutism (excess facial or body hair), acne, and scalp hair thinning (androgenic alopecia). These features arise because testosterone and its more potent derivative, dihydrotestosterone (DHT), bind to androgen receptors in hair follicles and sebaceous glands, altering their activity.

Hirsutism typically affects the upper lip, chin, chest, abdomen, and inner thighs, following a male-pattern distribution. It is assessed clinically using the modified Ferriman-Gallwey (mFG) score, which helps quantify severity and monitor treatment response.^[9][10] It is worth noting that mFG cut-off thresholds vary by ethnicity and by local clinical practice, so results should be interpreted in context. Acne in PCOS tends to be persistent and often affects the lower face and jawline, though this is a typical pattern rather than a universal one. Scalp hair loss generally follows a diffuse or frontal pattern rather than the vertex-predominant pattern more commonly seen in male androgenic alopecia.

Symptom severity does not always correlate directly with measured testosterone levels. Some individuals experience significant hirsutism with only mildly elevated or even normal total testosterone, because their tissues are more sensitive to androgens or because free testosterone is disproportionately raised due to low SHBG. Conversely, others with biochemically elevated testosterone may have fewer visible symptoms.

Rapid-onset or severe hirsutism, voice deepening, clitoromegaly, or other signs of virilisation are red flags that warrant prompt referral to endocrinology to exclude an androgen-secreting tumour or other serious cause.^[1] These features are distinct from the gradual androgenic changes typical of PCOS.

Beyond cosmetic concerns, raised androgens can contribute to irregular or absent menstrual cycles and reduced fertility by disrupting ovulation. Psychological effects, including reduced self-esteem and anxiety related to visible symptoms, are also well recognised and should be addressed as part of holistic PCOS care, in line with NICE guidance on the condition.

How do doctors in the UK test testosterone levels for PCOS?

UK doctors measure total testosterone, SHBG, and free androgen index as part of the PCOS hormonal screen, ideally in the early follicular phase; COCP use should be stopped beforehand to avoid masking hyperandrogenism.

UK doctors diagnose PCOS using the Rotterdam criteria, which require at least two of three features: irregular ovulation, polycystic ovarian morphology on ultrasound, and clinical or biochemical evidence of hyperandrogenism.^[1][2] Testosterone measurement is central to the biochemical assessment. NICE CKS guidance recommends measuring total testosterone as part of the initial hormonal profile, alongside SHBG, prolactin, and thyroid function (TSH). A pregnancy test should also be performed where relevant. DHEAS and androstenedione may be measured where clinically indicated. LH and FSH are not used diagnostically for PCOS in most current UK guidance, though they may be measured to exclude other conditions such as premature ovarian insufficiency.

Blood tests for testosterone are ideally taken in the early follicular phase of the menstrual cycle (days 2 to 5), or at any time in those with very irregular cycles. The sample should be taken in the morning, when androgen levels are at their daily peak. Free androgen index (FAI), calculated from total testosterone and SHBG, is often more informative than total testosterone alone, as it reflects the biologically active fraction. Factors that alter SHBG (such as obesity, thyroid disease, or use of hormonal contraception) will affect FAI interpretation.

Importantly, the combined oral contraceptive pill (COCP) and anti-androgen medications suppress androgen levels and raise SHBG, which can mask hyperandrogenism on testing. Where possible, these should be stopped for an adequate period (often around three months, though local laboratory protocols should be followed) before androgen testing, to avoid misleading results.

Standard laboratory immunoassays for testosterone are less accurate at the lower concentrations typical in women, and results can vary between laboratories. Results should always be interpreted against local laboratory reference ranges. Some specialist centres use liquid chromatography-tandem mass spectrometry (LC-MS/MS) assays for greater precision, and NICE acknowledges this limitation of standard immunoassays.

If testosterone is markedly elevated (the threshold varies by assay and local laboratory, so clinical judgement and local reference ranges should guide interpretation), or if virilisation or rapid progression of symptoms is present, prompt referral to endocrinology is warranted to exclude other causes such as congenital adrenal hyperplasia (where 17-hydroxyprogesterone measurement is relevant) or an androgen-secreting tumour.

A GP can initiate the initial hormonal screen, and many women are subsequently managed in primary care or referred to a gynaecologist or endocrinologist depending on the complexity of their presentation.

What treatments can lower testosterone in PCOS?

The combined oral contraceptive pill is the most common first-line treatment, suppressing LH and raising SHBG; co-cyprindiol, metformin, and spironolactone are used in selected cases with appropriate safety monitoring.

Several treatments can effectively lower testosterone or reduce its effects in PCOS, and the choice depends on the individual's symptoms, reproductive plans, and any coexisting conditions. Improvements in androgenic symptoms such as hirsutism and acne typically take six to twelve months to become apparent, and realistic expectations should be set at the outset.

The combined oral contraceptive pill (COCP) is commonly used as a first-line hormonal treatment. It suppresses LH secretion, thereby reducing ovarian androgen production, and increases hepatic SHBG synthesis, lowering free testosterone. Preparations containing anti-androgenic progestogens, such as drospirenone, may offer additional benefit for hirsutism and acne.

Co-cyprindiol (cyproterone acetate with ethinylestradiol) is licensed in the UK for severe acne and moderate to severe hirsutism in women when other treatments have not been effective. It is not licensed solely as a contraceptive. Co-cyprindiol carries a higher risk of venous thromboembolism (VTE) than standard COCPs, and the MHRA has issued Drug Safety Updates highlighting this risk, as well as a risk of meningioma with longer-term use of cyproterone acetate.^[12][14] It should only be used after careful individual risk assessment and with appropriate counselling.

Metformin, an insulin-sensitising agent, is considered by NICE CKS for women with PCOS who have evidence of insulin resistance or impaired glucose tolerance. By improving insulin sensitivity, metformin can modestly reduce the insulin-driven stimulus to ovarian androgen production. It is not licensed specifically for PCOS in the UK and is used off-label in this context; its effects on androgen levels are modest and variable.

Spironolactone is sometimes used off-label for hirsutism or acne that has not responded to first-line treatments. It blocks androgen receptors and inhibits androgen synthesis. Because it can raise serum potassium and affect renal function, baseline and periodic monitoring of electrolytes and renal function (U&Es) is required.^[17][18] It interacts with other potassium-sparing agents and ACE inhibitors, among others. Spironolactone must not be used in pregnancy due to the risk of feminisation of a male foetus, so reliable contraception is essential during treatment, and it should be stopped before attempting to conceive. The same applies to co-cyprindiol and other anti-androgens.

Topical eflornithine cream can reduce facial hair growth. Its availability on NHS prescription has fluctuated; patients should check current prescribing status with their GP or dermatologist.

For women seeking to manage weight alongside hormonal symptoms, a clinician may consider whether a weight-management medicine is appropriate. Mounjaro is one option a prescriber may consider after an online consultation with Bolt Pharmacy, a GPhC-registered UK online pharmacy offering prescriber review and pharmacist support, and is only prescribed where clinically appropriate.

If you experience suspected side effects from any medicine used in PCOS management, you can report these to the MHRA via the Yellow Card scheme at yellowcard.mhra.gov.uk.

How do lifestyle changes affect hormone levels in PCOS?

A modest 5 to 10 per cent reduction in body weight can lower circulating androgens, raise SHBG, and improve insulin sensitivity in overweight women with PCOS, supporting more regular ovulation.

Lifestyle modification, particularly weight management and regular physical activity, can meaningfully reduce testosterone levels and improve the broader hormonal profile in PCOS. Clinical studies and the 2023 International Evidence-Based Guideline for the Assessment and Management of PCOS suggest that even a modest reduction in body weight of around 5 to 10 per cent can lower circulating androgens, improve insulin sensitivity, raise SHBG, and restore more regular ovulatory cycles in people with PCOS who are overweight or living with obesity.^[2][21] NICE CKS guidance on PCOS also supports lifestyle advice as a core component of management.

The mechanism is closely linked to insulin resistance. Excess adipose tissue, particularly visceral fat, worsens insulin resistance and promotes androgen production. Reducing caloric intake and increasing physical activity lowers fasting insulin, which in turn reduces the ovarian stimulus to produce testosterone. Both aerobic exercise and resistance training have demonstrated benefit; current evidence suggests that combining the two may be more effective than either alone for improving metabolic and hormonal parameters, though individual responses vary.^[25][23]

Dietary composition also matters. Diets with a lower glycaemic index (GI) may improve insulin sensitivity in some people with PCOS, though the evidence base is still developing and comparative benefits over standard calorie-restricted diets are not consistent across all studies. Reducing ultra-processed foods and refined carbohydrates, while increasing fibre, lean protein, and unsaturated fats, aligns with general healthy eating guidance and supports hormonal balance.

Sleep quality and stress management are increasingly recognised as relevant factors. Chronic sleep deprivation and elevated cortisol from psychological stress can worsen insulin resistance and disrupt the hypothalamic-pituitary-ovarian axis. NICE guidance on PCOS emphasises that lifestyle advice should be offered to all women with the condition, regardless of weight, and should be delivered in a non-stigmatising, supportive manner.

Referral to a dietitian or structured weight management programme may be appropriate for those who need additional support. Access to NHS weight management services depends on local Integrated Care Board (ICB) commissioning criteria, so availability may vary by area.

Scientific References

1. Polycystic ovary syndrome – NICE guideline supporting documentation.
2. Polycystic ovary syndrome – NICE guideline (GID-NG10436).
3. Polycystic ovary syndrome: metformin in women not planning pregnancy (ESUOM6) – resources PDF.
4. Polycystic ovary syndrome: metformin in women not planning pregnancy (ESUOM6) – key points from the evidence.
5. Polycystic ovary syndrome: metformin in women not planning pregnancy (ESUOM6) – overview for healthcare professionals.
6. Gonadotrophin and gonadal steroid response to a single dose of a long-acting agonist of gonadotrophin-releasing hormone in ovulatory and anovulatory women with polycystic ovary syndrome.
7. Insulin signaling in PCOS/PMOS: molecular insights and clinical implications.
8. Relations of Insulin Resistance, Body Weight, Vitamin D Deficiency, SHBG and Androgen Levels in PCOS Patients.
9. Association of ethnicity, Fitzpatrick skin type, and hirsutism: A retrospective cross-sectional study of women with polycystic ovarian syndrome.
10. Clinician vs Self-ratings of Hirsutism in Patients With Polycystic Ovarian Syndrome: Associations With Quality of Life and Depression.
11. Assessing new terminal body and facial hair growth during pregnancy: toward developing a simplified visual scoring system for hirsutism.
12. Cyproterone acetate with ethinylestradiol (co-cyprindiol): balance of benefits and risks remains positive.
13. Co-cyprindiol | Drugs – BNF – NICE.
14. Cyproterone acetate: new advice to minimise risk of meningioma.
15. High-dose cyproterone acetate: potential risk of (multiple) meningiomas.
16. A pregnant woman accidentally treated with spironolactone.
17. Spironolactone | Drugs – BNF – NICE.
18. Spironolactone and renin-angiotensin system drugs in heart failure: risk of potentially fatal hyperkalaemia.
19. Using mass spectrometry to overcome the longstanding inaccuracy of a commercially-available clinical testosterone immunoassay.
20. How low can you go? Analytical performance of five automated testosterone immunoassays.
21. Lifestyle changes in women with polycystic ovary syndrome.
22. Lifestyle changes in women with polycystic ovary syndrome.
23. The Effect of Exercise on Reproductive and Metabolic Outcomes in Women With Polycystic Ovary Syndrome: A Systematic Review and Meta-Analysis.
24. Effects of exercise on reproductive endocrine hormones in adult patients with polycystic ovary syndrome: a systematic review and three-level meta-analysis.
25. Effects of physical activity in women with polycystic ovary syndrome.

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