Common Conditions

Three conditions account for a significant proportion of delayed fertility investigations in the UK: PMOS (previously called PCOS), endometriosis, and thyroid dysfunction. They're common, they're often slow to diagnose, and they each have a specific investigation pattern that should be done before anything else is tried. Knowing what those investigations are, and whether you've had them, is the starting point.

PMOS (previously called PCOS) is diagnosed using the Rotterdam criteria: two of three findings are required, irregular or absent periods, clinical or biochemical evidence of elevated androgens (acne, excess hair, elevated testosterone or DHEAS on bloods), and polycystic-appearing ovaries on ultrasound (twelve or more follicles per ovary, or an ovarian volume over 10ml).

You do not need all three. A diagnosis of PMOS based on ultrasound appearance alone, without the other two features, is an incomplete assessment, and many people are told they have PMOS on the basis of an ultrasound finding that doesn't meet the criteria by itself.

Endometriosis has an average diagnostic delay of nearly nine years from symptom onset in the UK, 8 years and 10 months as of Endometriosis UK's 2024 survey data, having increased over the past decade. The reason is partly that pelvic pain gets normalised, and partly that a negative ultrasound does not rule it out, endometriosis is a laparoscopic diagnosis in most cases, which sits outside primary care's remit to arrange. There are also consistent disparities in who gets diagnosed: research has found Black women are around 50% less likely to receive an endometriosis diagnosis than White women, compounding existing delays, UK-specific data by ethnicity is an active area of research.

Symptoms that are generally considered worth raising with a GP include: pain severe enough to limit activity during your period, pain during sex (deep dyspareunia), pain when your bowel or bladder is active during a period, and pain between periods.

Any of these is worth a conversation, particularly if symptoms have been present for some time or have previously been attributed to normal variation.

Thyroid dysfunction is frequently under-investigated in the fertility context. Standard lab reference ranges mark TSH as normal up to roughly 4–5 mIU/L, but ESHRE guidance (2018) and many fertility specialists use a threshold of 2.5 mIU/L for people trying to conceive, though this is not universal and remains an area of debate among reproductive endocrinologists. Subclinical hypothyroidism in this context, TSH elevated above 2.5 but within the standard 'normal' range, is associated with reduced implantation rates and increased miscarriage risk in cohort data, though whether treating it improves outcomes is still being studied.

If your GP has tested your thyroid and said it's normal but hasn't given you the number, asking for the actual value is reasonable. A full thyroid panel includes TSH and free T4 at minimum; if there's any suggestion of thyroid antibodies (Hashimoto's), TPO antibodies should also be checked.

Prolactin and AMH are two further investigations that get inadequately explained when they come back. Elevated prolactin suppresses ovulation, even mildly elevated levels can cause subtle luteal phase problems. Causes include a pituitary microadenoma (benign, treatable), certain medications, and stress at the time of the blood draw (a single high reading often gets repeated because sampling conditions matter).

AMH, anti-Müllerian hormone, reflects ovarian reserve but it is not a fertility sentence. Low AMH means fewer eggs are likely available, not that conception is impossible; it changes the clinical conversation, not the outcome.