Health
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 min read

Fertility hormone testing and what to check before you start trying to conceive

Here are the 7 biomarkers that actually matter for fertility: AMH, thyroid, prolactin, LH/FSH, testosterone, SHBG, and vitamin D. Learn what each one tells you about your fertility baseline.
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Written by
Robert Jakobson
Published on
August 5, 2026

Here is the scenario. You are 32, you feel well, and you have started thinking seriously about trying to conceive in the next year or two. You book an appointment with your Hausarzt. You mention it. They run a basic blood panel, perhaps a haemogram, thyroid screen. But standard German or European blood workup is designed to detect disease. It is not designed to map the hormonal and nutritional landscape that conception depends on. In Germany, the statutory Gesundheits-Check-up laid down by the Gemeinsamer Bundesausschuss covers exactly five blood values, a lipid profile of total cholesterol, LDL, HDL and triglycerides, plus fasting plasma glucose. Insured people are entitled to it once between 18 and 35, and from 35 onwards every three years. None of those five values are AMH. None are LH or FSH. None are prolactin, SHBG, or a thyroid panel with antibodies. None are vitamin D, in a country where the national health survey found 61.6 percent of adults below 50 nmol per litre of 25-hydroxyvitamin D.

This is not a criticism of German GPs. The consultation model does not allow for it, and the Kassensystem does not fund it. The structural gap is real and well documented. For most conditions, that gap does not matter much. For fertility, it matters more. Because the biomarkers that help explain difficulty conceiving are precisely the ones that never appear in a standard workup.

The window between 28 and 38 is when this gap costs the most. These are the years when most women who are going to think carefully about pregnancy are doing so. They are also the years when ovarian reserve is declining, when polycystic ovary syndrome may still be undiagnosed, when a thyroid abnormality can sit quietly in the background, and when vitamin D levels in Northern Europe are at their lowest through the winter. Testing before anything has gone wrong gives you a baseline to compare against later.

This article covers the seven markers that constitute a meaningful fertility-adjacent hormone panel: what each one measures, why it matters, what the evidence actually says about it, and what an abnormal result means in practice. Not a verdict. Not a reason for alarm. A baseline, which is all good preventive health is.

Aniva's panel includes AMH, TSH, free T4, TPO antibodies, prolactin, LH, FSH, total testosterone, SHBG, and vitamin D as standard, alongside 90+ additional markers, for €199/year, tested at an ISO 15189-certified German laboratory. See the full biomarker list →

AMH: Your Ovarian Reserve Marker

Anti-Müllerian hormone is produced by the granulosa cells surrounding the small developing follicles in your ovaries. Because those follicles represent your remaining egg supply, AMH is the closest thing medicine currently has to a direct measure of ovarian reserve: how many eggs you have left relative to your age. It declines over time as follicles are depleted, and it does so earlier and more sensitively than FSH, the older reserve marker. Unlike most hormone tests, it can be measured at any point in the menstrual cycle, which makes it practical.

All of that makes AMH sound like the decisive fertility number. It is not. And this is where the frequent misreading occurs.

A prospective cohort study of 981 women aged 30 to 44 with no history of infertility, published in JAMA in 2017, found that biomarkers indicating diminished ovarian reserve were not associated with reduced fertility. The 2020 ASRM committee opinion on ovarian reserve testing reaches the same conclusion. Ovarian reserve correlates inversely with age, but there is considerable variation among women of the same chronological age, and in prospective cohort studies markers of ovarian reserve were poor predictors of reproductive potential as measured by fecundability, cumulative probability of pregnancy, or incidence of infertility. AMH is the more sensitive of the two markers only in the sense that it tends to decline before FSH rises.

What AMH does predict well is ovarian response to stimulation, meaning how many eggs you are likely to produce if you undergo IVF or egg freezing. The same ASRM document is blunt about the limits. AMH and antral follicle count have only a weak association with qualitative outcomes such as oocyte quality, clinical pregnancy rates and live birth rates, and an extremely low value should not be used to refuse treatment. For women in their late 30s considering fertility preservation or timed IVF, it is useful data. For a 32-year-old trying to conceive naturally, a low AMH is not a verdict.

One practical caveat. AMH levels may be decreased in women currently using hormonal contraceptives, and ASRM advises that results should be interpreted with caution in those patients. If you have recently stopped hormonal contraception, say so to whoever interprets the result.

AMH reference ranges are assay dependent and vary between laboratories, so a value only means something read against the range your own lab reports. The Time to Conceive cohort described in the ASRM document used a level below 0.7 ng/mL to define low AMH. At the other end of the scale, the 2023 international PCOS guideline accepts a raised AMH as one way to define polycystic ovarian morphology in adults, while stating explicitly that AMH must not be used as a single test to diagnose PCOS and should not yet be used in adolescents.

Thyroid Function

Thyroid hormones act at several points in the reproductive cycle. They affect the maturation of eggs, the receptivity of the uterine lining and the hormonal environment of early pregnancy, and thyroid hormone requirements rise during gestation. Overt thyroid disease is a recognised and treatable cause of irregular cycles, which is why thyroid function belongs in a preconception conversation.

Subclinical hypothyroidism means the TSH sits above the laboratory upper limit while free T4 is still normal. ASRM recommends that laboratory-specific TSH cutoffs be used to diagnose it, since the upper limit of normal differs between labs and between trimesters in pregnancy. It often produces no obvious symptoms, or symptoms easily attributed to stress, poor sleep, or the general demands of a busy life in your 30s.

The TSH threshold question has moved, and this is worth reading carefully because the older advice is still everywhere. Fertility guidance used to suggest targeting a TSH below 2.5 mIU/L before conception. The 2024 ASRM guideline no longer supports that. It recommends counselling women that subclinical hypothyroidism is not associated with an increased risk of miscarriage, and specifically that a TSH between 2.5 and 4.0 mIU/L is not associated with an increased risk of miscarriage. It found moderate evidence that treating subclinical hypothyroidism with levothyroxine does not improve pregnancy loss, clinical pregnancy or live birth, and strong evidence that subclinical hypothyroidism in pregnancy is not associated with adverse neurodevelopmental outcomes in offspring.

TSH alone is still not the whole thyroid picture. Free T4 shows whether the thyroid is producing adequate hormone, and TPO antibodies are the marker for autoimmune thyroid disease. Here too the evidence is weaker than the internet suggests. ASRM found intermediate-quality and conflicting evidence that is insufficient to suggest an association between thyroid antibodies and miscarriage, and insufficient evidence to recommend screening for thyroid autoimmunity in infertile or pregnant women. A positive TPO result is worth knowing and worth mentioning to your doctor, but on its own it does not predict a pregnancy outcome.

Measuring TSH, free T4 and TPO antibodies together describes thyroid function more fully than a single TSH does. That is a reasonable thing to want before pregnancy. It is not the same as a screening recommendation, and ASRM does not make one for antibodies. What it gives you is a documented starting point, which is useful if your thyroid is ever questioned later.

If you want to understand how thyroid function interacts with broader hormonal health, our cortisol article covers the HPA-HPT axis connection in detail.

Prolactin: The Hormone That Silently Blocks Ovulation

Prolactin is best known as the hormone that drives breast milk production after childbirth. Outside of pregnancy and lactation, it operates quietly in the background, until levels rise. Elevated prolactin, called hyperprolactinemia, disrupts the pulsatile release of GnRH from the hypothalamus, which in turn suppresses LH and FSH, which in turn prevents normal ovulation.

The Endocrine Society guideline on hyperprolactinemia recommends excluding medication use, renal failure, hypothyroidism and parasellar tumours before anything else. Where no cause is found, the finding is called idiopathic, and prolactin normalises on its own in approximately 30 percent of those cases. Other causes include a prolactinoma, which is a benign pituitary tumour, and a long list of medications.

There is a practical wrinkle with prolactin testing that many women are never told about. Physiological states including pregnancy, breastfeeding, stress, exercise and sleep can all raise prolactin, as can medication. The Endocrine Society recommends a single measurement of serum prolactin, drawn without excessive venipuncture stress and at any time of day, and recommends against dynamic testing. So a borderline result taken after a rushed journey and a difficult blood draw is worth repeating in calmer conditions before anyone concludes anything from it.

When elevated prolactin is genuinely confirmed, the news is largely good, because it is a treatable cause of ovulatory dysfunction. For symptomatic prolactin-secreting microadenomas or macroadenomas the Endocrine Society recommends dopamine agonist therapy to lower prolactin, decrease tumour size and restore gonadal function, and recommends cabergoline in preference to other dopamine agonists because it normalises prolactin more often and shrinks tumours more often.

The upper limit of normal for prolactin is set by the laboratory that runs the assay, so read your result against the range printed on your own report rather than a number from the internet. A level above that limit, in a sample taken without undue stress, confirms hyperprolactinemia and is worth following up with your doctor.

LH, FSH, and the Ratio That Signals PCOS

Luteinising hormone and follicle-stimulating hormone are the two pituitary signals that orchestrate the menstrual cycle. FSH drives the early development of follicles; LH surges mid-cycle to trigger ovulation. In a normally cycling woman, LH and FSH measured in the early follicular phase are broadly similar to each other, and both are read against the reference range of the laboratory that measured them.

In polycystic ovary syndrome the pituitary often releases disproportionately more LH relative to FSH, reflecting the disrupted hypothalamic signalling that characterises the condition. A raised LH to FSH ratio is a long-standing observation in PCOS. It is worth knowing that the 2023 international PCOS guideline does not include the ratio in its diagnostic criteria at all, so a raised ratio is a hint rather than a finding.

PCOS is the most common endocrine disorder of reproductive-age women. The 2023 international evidence-based guideline puts the global prevalence at 10 to 13 percent using the Rotterdam criteria, broadly similar across world regions, and asks clinicians to be aware of it in all ethnicities. Many of those women are undiagnosed, because the condition presents heterogeneously and is often dismissed as "irregular periods."

That guideline is the current comprehensive framework. In adults, diagnosis requires two of three features, namely clinical or biochemical hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology on ultrasound or a raised AMH, once other causes have been excluded. Where irregular cycles and hyperandrogenism are both present, neither ultrasound nor AMH is needed. AMH as an alternative to ultrasound is new in the 2023 edition and applies to adults only.

An important nuance: LH, FSH, and their ratio are not diagnostic markers for PCOS on their own. The ratio can be normal in confirmed PCOS. These markers should be read in the context of the full hormonal picture of AMH, testosterone, SHBG and clinical features, rather than as standalone verdicts.

If you're planning to conceive and haven't had your full hormone panel checked, Aniva runs LH, FSH, AMH, testosterone, SHBG, prolactin, and full thyroid function as part of its 100+ biomarker annual panel. See what's included →

Testosterone and SHBG: The Androgen Picture in PCOS and Beyond

Elevated androgens, testosterone and its precursors, are central to PCOS. But reading them accurately requires understanding the binding protein that controls how much testosterone your cells can actually use.

SHBG, sex hormone-binding globulin, is a protein produced by the liver that binds to both testosterone and oestrogen, rendering them biologically inactive. Only the free, unbound fraction can enter cells and exert an effect. This is why total testosterone alone can be misleading: a woman can have a normal total testosterone level while experiencing significant hyperandrogenism, because her SHBG is low enough that the free fraction is disproportionately elevated.

The 2023 international PCOS guideline recommends using total and free testosterone to assess biochemical hyperandrogenism, with free testosterone estimated by the calculated free androgen index, which divides total testosterone by SHBG. It also asks laboratories to use tandem mass spectrometry rather than direct immunoassays, which it describes as having limited accuracy and poor sensitivity and precision for diagnosing hyperandrogenism in PCOS. That is worth checking on your own report.

Low SHBG is a common finding in PCOS and is associated with insulin resistance and higher body weight. That is one reason a metabolic view of PCOS matters as much as a hormonal one. The 2023 guideline recommends considering metformin in adults with PCOS and a BMI of 25 or above for metabolic outcomes including insulin resistance, glucose and lipid profiles.

One more thing about SHBG, and it catches a lot of people out. Combined oral contraceptives raise SHBG and reduce gonadotrophin-dependent androgen production, which makes biochemical hyperandrogenism very difficult to assess reliably while you are on the pill. The 2023 guideline says that if androgen testing is imperative, the pill should be withdrawn for a minimum of three months first, with contraception managed another way during that time.

For a deeper look at how SHBG operates across different hormonal contexts, our hormone article explores the interconnections between reproductive and stress hormones.

Vitamin D: The Reproductive Hormone Most Women Haven't Tested

Vitamin D is technically a steroid prohormone, not a vitamin. It regulates gene expression across hundreds of cell types, and ovarian tissue, the uterine endometrium and the placenta all express vitamin D receptors. That is not a coincidence. It reflects a functional role in reproductive biology, even if the clinical implications are still being quantified.

Low vitamin D is frequently reported in women with PCOS, and has been linked in observational work to insulin resistance and to the metabolic features of the condition. The evidence that correcting it changes those features is weaker than the volume of writing on the subject suggests. Treat this as a reason to know your level, not as a treatment claim.

For IVF outcomes the data are suggestive rather than definitive. A 2014 study of 335 women undergoing IVF found clinical pregnancy rates of 20 percent among those with 25-hydroxyvitamin D below 20 ng/mL and 31 percent among those at or above it, with an adjusted odds ratio of 2.15 and a 95 percent confidence interval of 1.23 to 3.77. A 2023 systematic review and meta-analysis of nine randomised trials and three cohort studies, 2,352 patients in total, found that infertile women treated with vitamin D had a significantly higher clinical pregnancy rate than controls, with an odds ratio of 1.70 and a 95 percent confidence interval of 1.24 to 2.34.

Miscarriage is a different question, and the honest answer is that supplementation has not been shown to change it. The same 2023 meta-analysis found no significant difference in miscarriage rate between the supplemented and control groups, with an odds ratio of 0.98 and a 95 percent confidence interval of 0.63 to 1.53.

In Germany, this is not an abstract concern. The Robert Koch Institut's DEGS1 survey of nearly 7,000 adults found a mean 25-hydroxyvitamin D level of 45.6 nmol per litre, with 61.6 percent of participants below 50 nmol per litre and 30.2 percent below 30 nmol per litre. In winter, a quarter of participants sat below 30 nmol per litre. Women planning pregnancy in this country are, statistically, more likely than not to be below the 50 nmol per litre mark heading into their conception window.

There is no agreed optimal vitamin D target for women trying to conceive, and the higher targets quoted around the internet are not backed by guideline evidence. What is true is more mundane. You cannot know where you are without testing, supplementing blind is guessing, and the dose needed to move someone from deficient to sufficient varies substantially between individuals based on body weight, baseline level and absorption. Our article on vitamin D in Northern Europe covers the full context, including cofactors K2 and magnesium.

Aniva includes vitamin D as a standard marker, tested alongside the full reproductive hormone panel and 90+ additional biomarkers, for €199/year. Getting your baseline before you start trying is the difference between supplementing strategically and supplementing hopefully. See the full panel →

What a Complete Fertility-Adjacent Panel Looks Like

Taken together, the markers above constitute a genuinely informative preconception baseline. Not a replacement for your gynaecologist or reproductive endocrinologist, but the data that makes those conversations far more productive.

Here is what that panel covers in plain terms: your ovarian reserve (AMH), the pituitary signals that drive your cycle (LH and FSH), the gland that can disrupt cycles without symptoms (thyroid with antibodies), the pituitary hormone that blocks ovulation when elevated (prolactin), the androgen picture relevant to PCOS and metabolic health (testosterone and SHBG), and the nutrient most often studied in this context (vitamin D).

There is a significant difference between receiving these results as a raw Laborzusendung, a printout of numbers against reference ranges, and receiving them with context. A ferritin of 18 µg/L is "within normal range" on most lab reports. Read alongside your fatigue, your cycle length and your other iron markers, the same number reads very differently, and it is exactly the kind of finding worth raising with your own doctor. The same principle applies across every marker above: the number needs context to be meaningful. Our großes Blutbild guide explains in detail why reference ranges and optimal ranges are not the same thing, and why that gap matters for preventive health.

When to Test and What to Do Next

Timing matters for some of these markers. LH, FSH, and estradiol are conventionally drawn in the early follicular phase, on day 2 to 4 of your menstrual cycle, with day 1 being the first day of your period. AMH, by contrast, is cycle-independent and can be drawn at any time, one of its practical advantages over older reserve markers. Thyroid markers, prolactin, testosterone, SHBG, and vitamin D can also be drawn at any point, though prolactin should be taken in a rested state with the caveats above.

A note on what abnormal results mean in practice. None of the markers above, individually or together, represent an infertility sentence. What they represent is information.

Low AMH narrows the window for fertility preservation decisions and may inform the timing of IVF if that route becomes relevant. A TSH above your laboratory's upper limit is worth discussing with your doctor, though current ASRM guidance is that subclinical hypothyroidism does not by itself raise miscarriage risk and that levothyroxine for it does not improve pregnancy outcomes. Positive TPO antibodies indicate autoimmune thyroid activity worth having on record, even though ASRM found the evidence linking antibodies to miscarriage conflicting and insufficient. Elevated prolactin, once confirmed, responds well to medication in the majority of cases. Raised androgens with low SHBG and irregular cycles put PCOS on the diagnostic table, a condition that, once named, can be managed metabolically, medically, or both. Low vitamin D is correctable with appropriate supplementation once you have a baseline.

The consistent theme: every one of these is an addressable finding, or at minimum a knowable one. The cost of not knowing is having a problem that goes unmanaged for years, quietly complicating something you care about. The cost of knowing is a blood draw, a set of results you can actually read, and a plan.

The best time to get this panel done is before you start trying, ideally 6 to 12 months ahead, while there is time to act on what you find. The second best time could be now.

Aniva's annual panel includes the complete fertility-adjacent hormone profile: AMH, TSH, free T4, TPO antibodies, prolactin, LH, FSH, testosterone, SHBG, vitamin D.  Alongside 100+ additional metabolic, cardiovascular, and nutritional markers. One blood draw, one certified German laboratory, one personalised report. €199 per year. Start your membership →

Sources

This content is for informational purposes only and is not medical advice. Always discuss results with a qualified healthcare professional. Fertility concerns and hormone abnormalities should be assessed by your GP, gynaecologist, or reproductive endocrinologist in the context of your full clinical history.

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