PCOS Blood Test UK: Which Hormones to Check, What Results Mean & How Diagnosis Actually Works

1. What is PCOS — and why is it so often missed?

Polycystic ovary syndrome is a hormonal disorder characterised by a combination of excess androgens (male hormones), irregular or absent ovulation, and — in many but not all cases — polycystic- appearing ovaries on ultrasound. Despite the name, the “cysts” are actually immature follicles that have stalled mid-development, not true cysts.

The condition is remarkably heterogeneous. Some women present with acne and irregular periods at 16. Others discover it only when trying to conceive in their 30s. Some have elevated testosterone; others have normal androgens but insulin resistance and anovulation. This variability is precisely why a single blood test or a single ultrasound cannot diagnose PCOS in isolation.

According to the Royal College of Obstetricians and Gynaecologists, PCOS is associated with significantly increased long-term risks of type 2 diabetes (up to 5–10 times higher), cardiovascular disease, endometrial cancer, non-alcoholic fatty liver disease, and obstructive sleep apnoea. Early identification — and metabolic monitoring — changes outcomes.

The diagnostic delay is partly systemic (NHS guidelines focus on excluding other causes rather than confirming PCOS), partly educational (many GPs receive minimal training on the condition), and partly biological (symptoms overlap with thyroid dysfunction, adrenal hyperplasia, and normal adolescent hormonal flux). Blood testing is the single most useful step a woman can take to cut through ambiguity.

2. The Rotterdam criteria: how PCOS is actually diagnosed

The international gold standard for PCOS diagnosis is the Rotterdam criteria, endorsed by ESHRE, ASRM, and reaffirmed in the 2023 international evidence-based guideline. You need two out of three:

Crucially, other causes of androgen excess and anovulation must be excluded — thyroid disease, non-classical congenital adrenal hyperplasia (CAH), Cushing's syndrome, and hyperprolactinaemia. This is why a comprehensive blood panel is essential: it simultaneously investigates PCOS and rules out mimics.

The Rotterdam system identifies four phenotypes of PCOS (A through D), ranging from the classic presentation (all three criteria) to the mildest form (irregular cycles + polycystic ovaries, no androgen excess). Your phenotype affects your metabolic risk profile, your treatment options, and which blood markers will be abnormal.

3. Which hormones does a PCOS blood test check?

A thorough PCOS assessment requires more markers than the NHS typically runs. Here is the full panel, why each marker matters, and whether the NHS routinely includes it.

The gap between what a comprehensive PCOS assessment requires and what the NHS typically runs is significant. Many women receive a testosterone and TSH result, are told both are “normal,” and are sent home — without SHBG, fasting insulin, DHEA-S, or LH:FSH ratio ever being checked.

4. Testosterone & free androgen index: the androgen picture

Testosterone is the primary diagnostic androgen in PCOS. But there is an important nuance: only 1–3% of circulating testosterone is biologically active (“free”). The rest is bound to sex hormone-binding globulin (SHBG) and albumin. A woman with normal total testosterone but suppressed SHBG may have excess free androgen activity — and will experience the same symptoms as someone with overtly elevated testosterone.

The free androgen index (FAI) captures this. It is calculated as (total testosterone ÷ SHBG) × 100. An FAI above 5 is considered elevated in women and supports the biochemical hyperandrogenism criterion of the Rotterdam criteria, even if total testosterone is within the reference range.

Why is SHBG so often low in PCOS? Because insulin suppresses SHBG production by the liver. This creates a vicious cycle: insulin resistance → low SHBG → more free testosterone → more androgen-driven symptoms → more visceral fat → more insulin resistance. Breaking this cycle is the rationale for insulin- sensitising interventions (metformin, inositol, dietary modification).

When to test: testosterone, SHBG, and FAI should be measured in the early follicular phase (days 2–5 of your cycle) for reliable interpretation. If your periods are absent or irregular, a random sample is acceptable — but note this on your request. Hormonal contraception must be stopped for at least 3 months before androgen testing, as it artificially raises SHBG and masks androgen excess.

5. LH:FSH ratio: why it matters and when it misleads

In a normal menstrual cycle, LH and FSH are roughly equal in the early follicular phase, with LH surging mid-cycle to trigger ovulation. In classic PCOS, hypothalamic GnRH pulse frequency increases, favouring LH secretion over FSH. The result is an elevated LH:FSH ratio — often quoted as >2:1 or >3:1.

This ratio is found in approximately 60% of women with PCOS, according to a Human Reproduction study. It is more common in lean PCOS than in overweight PCOS, where insulin resistance may blunt the LH elevation.

Important limitation: the LH:FSH ratio is not a Rotterdam criterion. It is a supportive finding, not a diagnostic one. A normal ratio does not exclude PCOS. The 2023 international guideline specifically warns against using LH:FSH ratio as a standalone diagnostic marker. Its value lies in adding context to an already-suspicious picture.

Timing matters: LH and FSH must be measured in the early follicular phase (days 2–5). A mid-cycle sample will catch the LH surge and produce a misleadingly high ratio. If your periods are absent, any random sample is acceptable — but both hormones should be drawn simultaneously.

6. Fasting insulin & HOMA-IR: the metabolic root

Insulin resistance is present in an estimated 50–70% of women with PCOS, including lean women with normal BMI. Yet the NHS typically screens only with HbA1c or fasting glucose — both of which remain normal until insulin resistance has progressed to prediabetes or overt diabetes. By that point, years of compensatory hyperinsulinaemia have already driven androgen excess, weight gain, and metabolic damage.

Fasting insulin is the earliest detectable marker of insulin resistance. Combined with fasting glucose, it allows calculation of the HOMA-IR index (Homeostatic Model Assessment of Insulin Resistance): fasting insulin (µU/mL) × fasting glucose (mmol/L) ÷ 22.5. A HOMA-IR above 2.0 suggests insulin resistance; above 2.5 is strongly indicative.

Research published in The Journal of Clinical Endocrinology & Metabolism demonstrated that fasting insulin identified insulin resistance in PCOS women who had completely normal fasting glucose and HbA1c. The glucose-based tests missed them entirely.

Why this matters for treatment: if insulin resistance is driving your PCOS, then interventions targeting insulin (metformin, inositol, GLP-1 medications, dietary modification, resistance training) are likely to be far more effective than anti-androgens alone. Without testing fasting insulin, you are guessing at the mechanism.

7. DHEA-S: the adrenal androgen the NHS rarely tests

DHEA-S (dehydroepiandrosterone sulphate) is produced almost exclusively by the adrenal glands, unlike testosterone which comes from both the ovaries and adrenals. Measuring DHEA-S serves two purposes in a PCOS workup.

First, it identifies adrenal-source androgen excess. Approximately 20–30% of women with PCOS have elevated DHEA-S alongside ovarian androgens. These women may respond differently to treatment — ovarian suppression (combined pill) alone may not fully resolve symptoms if the adrenals are a significant contributor.

Second, it helps exclude non-classical congenital adrenal hyperplasia (NCAH). NCAH, caused by 21-hydroxylase deficiency, affects roughly 1–5% of women presenting with PCOS symptoms and is often mistaken for PCOS. Isolated DHEA-S elevation with a suspicious 17-OH progesterone level warrants further investigation with an ACTH stimulation test.

The NHS rarely includes DHEA-S in initial PCOS investigations. The NICE fertility guideline CG156 mentions measuring total testosterone and SHBG but does not mandate adrenal androgens. This means adrenal contributors — and NCAH mimics — go undetected in the standard pathway.

8. AMH: ovarian reserve and PCOS severity

Anti-Müllerian hormone (AMH) is produced by the small antral follicles in the ovaries. In PCOS, the excess of stalled follicles means AMH levels are typically 2–3 times higher than in women without the condition. The 2023 international evidence-based guideline for the first time included AMH as a potential alternative to ultrasound for the polycystic ovarian morphology criterion.

An AMH above 35 pmol/L (approximately 5 ng/mL) in reproductive-age women is strongly suggestive of PCOS, according to research published in The Journal of Clinical Endocrinology & Metabolism. Higher AMH levels correlate with greater follicle count, more severe anovulation, and higher androgen levels — making it a useful severity marker as well as a diagnostic one.

Why this matters: ultrasound is the traditional method for assessing polycystic ovarian morphology, but it is operator-dependent, requires a transvaginal probe (which not all women are comfortable with), and is not available via primary care without a referral. AMH is a simple blood test that can be drawn alongside the rest of the hormone panel.

Limitation: AMH declines naturally with age. A “normal” AMH in a 38-year-old may still be elevated relative to her age-matched peers if she has PCOS. Age-specific reference ranges are essential for interpretation. AMH is also not available on the NHS outside fertility clinic referrals.

9. Thyroid & prolactin: ruling out mimics

Both thyroid dysfunction and hyperprolactinaemia can produce symptoms that are virtually indistinguishable from PCOS: irregular periods, anovulation, weight changes, fatigue, hair changes, and mood disturbance.

Hypothyroidism is particularly important to exclude. An underactive thyroid increases TRH, which stimulates prolactin release, which suppresses GnRH, which disrupts the menstrual cycle. It also reduces SHBG (increasing free androgen levels) and can cause weight gain. A woman with subclinical hypothyroidism may meet PCOS diagnostic criteria on blood tests alone — but the root cause is treatable thyroid disease, not PCOS.

Prolactin elevation can be caused by pituitary microadenomas (prolactinomas), medications (SSRIs, antipsychotics, metoclopramide), hypothyroidism, or stress. Mild elevation (<1,000 mIU/L) is common and usually benign. Levels above 1,000 warrant further investigation.

A complete PCOS workup should always include TSH, Free T4, and prolactin. The NHS usually tests TSH, but may omit Free T4 and prolactin — missing secondary hypothyroidism and hyperprolactinaemia respectively.

10. Reference ranges: what's normal vs what's diagnostic

These ranges are indicative and vary between laboratories. Always interpret results against the specific reference ranges provided on your lab report. Blood should ideally be drawn in the early follicular phase (days 2–5) after an overnight fast.

A critical point: laboratory “normal” ranges are statistical constructs based on the general population. A total testosterone of 1.7 nmol/L is technically “within range” but sits at the very top — and in the context of low SHBG, irregular periods, and clinical signs of androgen excess, it is diagnostically significant. Context matters more than cut-offs.

11. The NHS PCOS pathway: what gets tested and what gets missed

The NHS approach to suspected PCOS is outlined in NICE CG156 (fertility) and general primary care guidance. The typical pathway looks like this:

The problem with step 4 is clear: a normal total testosterone does not rule out PCOS. SHBG may be suppressed (increasing free androgen), the LH:FSH ratio may be abnormal, fasting insulin may reveal metabolic drivers, and DHEA-S may show adrenal contribution. None of these are typically checked in the initial NHS investigation.

For women trying to conceive, the pathway eventually reaches a fertility clinic where more comprehensive testing occurs. But for women not seeking fertility treatment — those who want to understand their symptoms, manage acne or hirsutism, monitor metabolic risk, or simply get a diagnosis — the NHS pathway often stops before it has meaningfully started.

12. GP blood test vs Helvy: what's the difference?

If your GP offers to test and investigate comprehensively, take it — it is free and clinically valid. Private testing is most valuable when the initial NHS investigation stops at testosterone and TSH, when you cannot get a timely appointment, or when you want fasting insulin and SHBG — markers the NHS rarely includes in a primary care PCOS investigation.

13. Common result patterns and what they mean

14. Frequently asked questions