Diagnosis
AMH testing: the most misunderstood number in fertility – what it can and can’t tell you
Article produced in association with Spital Clinic
AMH has become one of the most-requested blood tests in private women’s health. The number it gives back is useful, but only when it is read in context.
AMH testing in the UK has gone mainstream over the past few years. Home-testing kits sell it as a snapshot of “your fertility”.
Private clinics include it in screening packages. On social media, individual AMH results are now routinely treated as a verdict on whether a woman will be able to have children.
That reading isn’t accurate. Anti-Müllerian Hormone (AMH) does carry useful information, but only inside a wider clinical picture.
Looked at on its own, it produces a lot of unnecessary anxiety, and often hides the questions that matter more.
What AMH measures
AMH is a hormone produced by the small follicles in the ovaries, the ones that haven’t yet been recruited for ovulation. Because these follicles are relatively stable across the menstrual cycle, the test can be done on any day, without needing to be timed to a period.
A higher AMH level tends to indicate a larger pool of these follicles. A lower level suggests the pool is smaller. That, broadly, is what the result shows.
The HFEA, the UK’s independent regulator of fertility treatment, describes AMH as an indicator of ovarian reserve, while making clear that fertility test results of this kind “are not guaranteed” as a predictor of fertility outcomes.
Put simply: AMH is a count of what is there. It says nothing about how well the body will use it, and it cannot predict if or when conception will happen.
Where AMH fits in a modern fertility assessment
In current UK private practice, AMH is rarely tested in isolation. A meaningful fertility assessment will pair it with a fuller hormone profile (FSH, LH, oestradiol, prolactin and thyroid function), along with markers such as Day 21 progesterone, vitamin D and rubella immunity where relevant.
This is the structure used in a trying-to-conceive screening, and there is a reason for it: each of these tests answers a different question that AMH on its own cannot.
It is this combination, not the AMH number on its own, that gives a clinician enough information to say anything meaningful about an individual’s reproductive picture.
Misconception 1: “A low AMH means natural pregnancy isn’t possible”
This is the misconception that causes the most distress, and it is consistently wrong.
Several large prospective studies of women in their 30s and 40s trying to conceive naturally have found that women whose biomarkers, including AMH, pointed to a diminished ovarian reserve were no less likely to conceive within twelve cycles than women with reassuring results.
That is why neither UK regulators nor national guidance treat AMH as a test that can predict natural fertility in women who have no known infertility issue.
The reason is simple. Natural conception only requires one good egg, released in a normal cycle, in the right window.
AMH doesn’t measure egg quality, and it doesn’t reveal whether ovulation is happening. A woman with low AMH may still ovulate every month with high-quality eggs.
A woman with high AMH (often the pattern seen in polycystic ovary syndrome) may not be ovulating regularly at all.
The NHS emphasises that age is the strongest single predictor of natural fertility. A 35-year-old with a low AMH and regular cycles is, on average, more likely to conceive naturally than a 40-year-old with a normal AMH and irregular ones.
If AMH comes back low for someone who is trying to conceive, the more useful question isn’t whether pregnancy is still possible (the answer is almost always yes), but whether there is reason to investigate the wider picture now rather than waiting twelve months.
Misconception 2: “A normal AMH means everything is fine”
The opposite assumption is just as risky.
AMH tells you about egg quantity. It does not tell you about:
- Egg quality, which is closely tied to age
- Whether ovulation is happening regularly
- Whether the fallopian tubes are open
- Whether there are structural issues such as fibroids, polyps, ovarian cysts or endometriosis
- Sperm parameters in a male partner
- Whether implantation will succeed
A reassuringly normal AMH at 38 still sits alongside age-related changes in egg quality. A slightly lower-than-average AMH at 28 may carry no real-world implications at all.
That is why no UK clinical body recommends AMH as a routine screening test for healthy women who have no fertility concerns. NICE’s fertility guideline, NG73, treats AMH as one component of a broader investigation, not as a verdict in itself.
Imaging is the natural counterpart to the blood test. A transvaginal pelvic ultrasound directly visualises the small follicles that produce AMH, the antral follicle count. It also picks up structural findings a blood test will never reveal, including ovarian cysts, fibroids, polycystic ovarian morphology, and abnormalities in the uterine cavity. A full ovarian reserve assessment normally includes both.
Where the AMH number actually matters
There are three settings in which AMH carries real, decision-relevant information.
Before IVF or egg freezing. AMH is one of the better predictors of how the ovaries are likely to respond to stimulation medication.
A higher AMH usually predicts more eggs collected per cycle, and a very low AMH may shape decisions about protocol or whether to bank cycles before treatment.
During a fertility investigation. If a couple has been trying for twelve months, or six months if the woman is over 35, AMH becomes part of a wider assessment that should also include ovarian ultrasound, a fuller hormone profile, semen analysis and an assessment of tubal patency.
As context for women planning ahead. Women who want to understand their reproductive options before they are ready to conceive (for example, ahead of a decision about egg freezing) can find AMH informative, provided it is interpreted alongside age, antral follicle count, and other markers, by a clinician who can place the number in context.
Reading the number properly
For anyone who has had an AMH test, three things make the result more useful:
- Pair it with age. A “normal” AMH at 25 means something very different from the same number at 38. Age is doing more work in the equation than the AMH value itself.
- Pair it with imaging. Ultrasound shows what is actually in the ovaries today, rather than relying on a single biochemical marker.
- Read it with a clinician. A number on a screen, with no context, no follow-up and no plan, is the worst way to use a test that, properly interpreted, can be very informative.
AMH is a useful tool. It just isn’t the headline it has often been turned into.
Disclaimer
This article is produced for informational purposes only and does not constitute medical advice, diagnosis or treatment. Clinical guidance referenced reflects published HFEA, NHS and NICE information available as at May 2026. Individual circumstances vary; readers are advised to consult a qualified healthcare professional before acting on any information in this article. This piece was produced in association with Spital Clinic, which provided background clinical information for editorial purposes. Hyperlinks to external sources are included for reference only and do not represent an endorsement of any product, service or organisation.
Menopause is often absent from women’s electronic health records, a study of nearly 396,000 women has found.
Researchers found menopause appeared almost seven times more often in participant surveys than in electronic health records (EHRs).
The findings suggest important reproductive health information, including age at menopause, may often be missing from health records used for research.
Audrey Hendricks, associate professor of bioinformatics at CU Anschutz and the study’s principal investigator, said: “Ultimately, we cannot study what we do not measure. We cannot treat what we do not know.
“Menopause has enormous implications for women’s health, but if we don’t consistently capture when menopause occurs and other important reproductive health information, we limit our ability to understand how this transition affects disease risk and health outcomes.”
Researchers at the University of Colorado Anschutz analysed data from women taking part in the National Institutes of Health’s All of Us Research Program.
They compared menopause information reported by participants in surveys with menopause diagnoses recorded in their electronic health records.
Around 193,000 menopause observations were identified in survey data, compared with approximately 28,000 diagnoses in EHR data.
Menopause was documented in electronic health records for only about 7 per cent of women in the dataset.
Nearly all participants with a menopause diagnosis recorded in their EHR also reported menopause in survey data. However, substantially fewer women had menopause documented in their health records.
Other important information was also frequently unavailable, including age at menopause, which researchers may use when examining links between menopause and chronic disease risk.
Menopause is a physiological transition that can affect cardiometabolic health and many other aspects of women’s health.
Researchers said relatively little is known about how factors including the timing and type of menopause influence health outcomes across diverse populations.
Large-scale programmes such as All of Us combine participant surveys, electronic health records and genomic data, but menopause-related research depends on relevant reproductive health information being available.
Missing menopause information can make it harder to investigate how the transition relates to health and disease.
The findings may also help researchers using All of Us data define menopause-related study populations, design studies and estimate how many participants are needed.
Hendricks said: “We have an enormous opportunity to use large-scale datasets to understand women’s health across the menopause transition and to identify who may be at greater risk for disease.
“But we need to make sure that the information researchers need is actually being collected.
“We must do a better job of capturing women’s health information, including reproductive health and measures related to menopause.”
Researchers said more complete and consistent collection of menopause and reproductive health information could help future studies examine factors such as age at menopause and their relationship with disease risk and health outcomes.
The FDA has granted accelerated approval to AstraZeneca drug Etcamah for certain adults with advanced breast cancer carrying an ESR1 mutation.
Etcamah, also known as camizestrant, was approved in combination with a CDK4/6 inhibitor, either abemaciclib, palbociclib or ribociclib.
The treatment is for adults with hormone receptor-positive, HER2-negative, locally advanced or metastatic breast cancer when an estrogen receptor-1 (ESR1) mutation is detected during aromatase inhibitor and CDK4/6 inhibitor therapy using an FDA-authorised test.
ESR1 mutations are acquired resistance mutations that tumours may develop during treatment with aromatase inhibitors, a type of endocrine therapy commonly used as a front-line treatment for locally advanced or metastatic breast cancer.
Fewer than 5 per cent of patients have the mutation when HR-positive metastatic breast cancer is diagnosed, according to the FDA. After disease progression on an aromatase inhibitor, nearly 40 per cent have the mutation.
Acting FDA commissioner Kyle Diamantas said: “Women living with metastatic breast cancer face an uphill battle as their tumors continuously evolve to escape treatment.
“We owe them every weapon in our arsenal.
“Today’s approval delivers a win to these patients by granting them a targeted therapy designed specifically to overcome resistance, giving them more time before their disease progresses.”
The accelerated approval programme allows earlier approval of drugs that treat serious conditions and fill an unmet medical need based on surrogate or intermediate endpoints.
For Etcamah, approval was based on how long patients lived without their disease worsening, measured from when the resistance mutation was first detected in their blood.
The FDA said it has not yet been confirmed whether intervening when the mutation is detected, rather than waiting until disease progression is confirmed, results in a clinically meaningful benefit. Confirmatory studies are therefore required to verify and describe clinical benefit.
Angelo de Claro, director of the FDA’s Oncology Center of Excellence, said: “I commend both the FDA and the sponsor for their commitment to advancing cancer care and securing this accelerated approval.
“This marks the first FDA approval of a cancer therapy guided by the detection of a resistance mutation in circulating tumor DNA (ctDNA) before imaging tests show that the disease is progressing.
“But additional evidence is needed to confirm clinical benefit.”
Circulating tumour DNA, or ctDNA, consists of small pieces of tumour DNA released into the blood and can allow earlier molecular detection of resistance mutations.
The FDA also authorised the Guardant360 CDx assay as a companion diagnostic to identify patients with breast cancer who have ESR1 mutations for treatment with camizestrant.
Efficacy was assessed in a clinical trial comparing a switch to Etcamah plus a CDK4/6 inhibitor with continued treatment using an aromatase inhibitor plus a CDK4/6 inhibitor.
Estimated median progression-free survival was 16 months in the Etcamah group, compared with 9.2 months in the aromatase inhibitor group.
Etcamah’s prescribing information includes a boxed warning about the risk of irregular heart rhythm when taken with certain other medicines. It also includes warnings about an abnormally slow heart rate and potential harm to an unborn baby.
The FDA convened its Oncologic Drugs Advisory Committee for the application on 30 April 2026.
Four leading cardiovascular health groups have agreed new guidance for healthcare professionals assessing patients with suspected heart attacks.
Historically, some less common forms of heart attack, which evidence shows affect women far more than men, have been classified as less important, with treatment and care often worse as a result.
Experts said women had been receiving less effective treatments that did not always target the specific cause of their heart attack and could even make them more unwell.
The changes were announced in Munich on the opening day of the annual congress of the European Society of Cardiology (ESC).
Professor Bryan Williams, chief scientific and medical officer of the British Heart Foundation, said: “This is a landmark moment, a radical shift in how we define and diagnose heart attacks worldwide which will transform people’s care.
“For decades, women have missed out on accurate diagnoses and treatment.
“This focus on finding less common causes of heart attacks, which predominantly affect women, should help to change that. It could be life-changing for huge numbers of women in the UK and worldwide.”
The new guidance upgrades three types of heart attack that can be up to 10 times more common in women and are often caused by childbirth, exercise and emotional stress.
The most serious cases, previously known as “type 1” and now classed as “primary” heart attacks, had previously prioritised those caused by a clot blocking blood flow to the heart.
Other forms can involve reduced blood flow for different reasons, including the tightening or tearing of coronary arteries. These can be more likely to be missed or treated less urgently.
The guidance also introduces a lower diagnostic threshold for women based on levels of troponin, a protein released into the blood when the heart is injured and damaged.
Previously, women were expected to meet the same troponin threshold as men to receive a diagnosis.
Williams said the streamlined heart attack categories would also help patients understand the cause of their heart attack and what comes next.
The three upgraded types are coronary artery spasm, coronary embolism and spontaneous coronary artery dissection (SCAD).
Coronary artery spasm involves the tightening of an artery, which can deprive the heart muscle of blood and oxygen. It can be caused by emotional stress, exercise or extreme cold.
Coronary embolism occurs when a blood clot or fatty deposit travels to a coronary artery and causes a blockage.
SCAD is caused by a tear in a coronary artery. Around 80 per cent of cases occur in women, and it often happens during or soon after pregnancy.
Professor Nicholas Mills, a cardiologist at the University of Edinburgh who led the international taskforce behind the guidance, said it was “the first time that we’ve had a truly global approach to aligning how we diagnose what is probably the most important diagnosis there is”.
He said: “It kills so many people, and we’ve never got everyone together around the world to agree how we’re going to describe it, classify it, explain it to our patients.
“Our job now is to implement this as widely as possible. It’s just as relevant for the UK as it is for any other country around the world. It is a revolution. It’s going to make care better for patients.”
Mills said there had been “unintended systematic bias against women”, including through the use of the key blood test for diagnosing heart attacks at an average level, which picks up all men but misses some women.
He said: “This is used for all types of heart attack in every emergency department in the world, and we want to make sure that it’s used correctly.”
The guidance was drawn up by the ESC, the American College of Cardiology, the American Heart Association and the World Heart Federation.
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