Love and Science Fertility

Anti-Müllerian Hormone (AMH) Explained for Physicians: Ovarian Reserve, IVF Dosing & Clinical Applications

Season 1 Episode 2

Use Left/Right to seek, Home/End to jump to start or end. Hold shift to jump forward or backward.

0:00 | 16:40

Download The Physician Fertility Roadmap- a 6-step, evidence-based plan to optimize your fertility over the next 6-12 months. 

https://support.loveandsciencefertility.com/The-Physician-Fertility-Roadmap

What does Anti-Müllerian Hormone (AMH) really tell you about your fertility?

In this episode of the Love and Science Podcast, Dr. Erica Bove, reproductive endocrinologist and fertility specialist, breaks down everything you need to know about AMH — what it is, what it is not, and how it’s actually used in clinical practice.

AMH is often misunderstood as a “fertility test,” but it is more accurately a marker of ovarian reserve — meaning it reflects egg quantity, not egg quality. Dr. Bove explains how AMH levels change over time, what causes fluctuations, and how it influences IVF medication dosing, PCOS diagnosis, egg freezing decisions, and ovarian hyperstimulation risk.

In this episode, we cover:

• What Anti-Müllerian Hormone (AMH) measures

• AMH and ovarian reserve vs. egg quality

• How AMH changes with age

• Why AMH is not a fertility test

• High AMH and PCOS

• Low AMH and what it actually means

• AMH and IVF medication dosing

• Risk of ovarian hyperstimulation syndrome (OHSS)

• AMH and egg freezing decisions

• Birth control, smoking, weight loss, and seasonal variation effects on AMH

• Why age is still the strongest predictor of egg quality

If you’ve ever wondered whether your AMH level predicts your ability to conceive — naturally or through IVF — this episode will give you clear, science-based answers.

Whether your AMH is high, low, or somewhere in the middle, understanding the nuance can help you make informed decisions about your reproductive health and fertility timeline.

This is part of Season 1 of the Love & Science Fertility Framework: The Biology Beneath the Surface — where we unpack the physiology shaping fertility outcomes.

Support the show

As always, please keep in mind that this is my perspective and nothing in this podcast is medical advice.

If you found this conversation valuable, book a consult call with me using this link:

https://www.loveandsciencefertility.com/private-fertility-consult

Follow us on social media:

IG: www.instagram.com/loveandsciencefertility

FB: www.facebook.com/profile.php?id=61553692167183

Please don’t let infertility have the final word. We are here to take the burden from you so that you can achieve your goal of building your family with confidence and compassion. I’m rooting for you always.

In Gratitude,

Dr. Erica Bove

Hello, my loves, and welcome back to the Love and Science Podcast. Today we’re going to talk about anti-Müllerian hormone (AMH) — what it is, what it is not, and how we actually use it in clinical practice.

I’m dating myself here, but when I was a second-year OB/GYN resident in New York City, one of my mentors suggested I give my Grand Rounds that year on anti-Müllerian hormone. At the time, it was still often referred to as Müllerian inhibiting substance (MIS), and virtually nobody had heard of it. It was something fertility clinics were starting to think about checking, but it definitely wasn’t as “bread and butter” as it is today.

Now, so many years later, I’m excited to explain just how relevant AMH is — and also some of the nuances — so that whether your AMH is high, low, or somewhere in the middle, you can understand what it means for your health and (with an asterisk) your fertility.


What is Anti-Müllerian Hormone?

So, what actually is anti-Müllerian hormone? I’m a reproductive endocrinologist, and AMH is truly a hormone. It plays a role in embryologic development — specifically, it inhibits Müllerian (uterine) structures from developing in a male fetus when everything is working correctly.

AMH is also made by the granulosa cells of the ovaries.

Very interestingly, we see that AMH is present during childhood. It tends to peak around the mid-twenties, and then it slowly declines over time until menopause, when it becomes undetectable.

There was a study done by one of my mentors showing that when AMH becomes undetectable, menopause may be “heralded” about six years later. That’s a very specific number, but I do think it points to a real correlation between menopause and cessation of ovarian function — because AMH is a marker of ovarian reserve, meaning it reflects how many eggs are left in the pool.


AMH and FSH: Why High AMH Matters Too

AMH also inhibits follicle-stimulating hormone (FSH). We often talk about low AMH, but I also think about the extremes: if AMH is super high and it’s inhibiting FSH, then maybe someone doesn’t ovulate — like in the context of PCOS.

We do often see a kind of FSH resistance in that context, and sometimes even despite letrozole, it can be hard to get someone to ovulate.


Why AMH Can Change Over Time

I get this question all the time:

“My AMH was 2.0 a year ago and now it’s 0.9. Does that mean I’m falling off a cliff?”

We can talk about it, but yes — we generally see a decline over time. That said, sometimes it seems more rapid, and other times AMH can actually go up. People will say:

“My AMH was 0.6 and I was really worried, but now it’s 1.8 — should I feel reassured?”

So what causes variation over time?


1) Birth Control Pills

One of the biggest factors is birth control pills. We know that the pill can “quiet” the ovaries over time and can reduce AMH.

Is that clinically significant? I would say yes, because we do see that women who have been on long-term birth control pills can sometimes have a diminished response to ovarian stimulation.

So if someone has a lower-than-expected AMH, I often have them come off birth control (with reliable contraception if they still need it) and then recheck AMH in about three months. Very often we’ll see it rise — usually a hormonal effect — and sometimes stimulation response improves as well.

This increase can be meaningful — often around 30% or sometimes even higher.


2) Smoking

Smoking is another big factor. When someone smokes, AMH goes down. And over time, when someone stops smoking, AMH can creep back up — sometimes close to where it would have been without smoking. It’s a dose-dependent response.

We also know smoking affects egg quality.


3) Weight / Weight Loss

Weight can affect AMH too. In the higher ranges of BMI (especially obesity), AMH may be lower than expected. And I’ve seen many times that with meaningful weight reduction, AMH can rise — which is really interesting. We also see improved response to medications in those situations.

So weight optimization can matter when it’s indicated.


4) Seasonal Variation / Vitamin D

There also appears to be seasonal variation. AMH and vitamin D seem correlated. In summer months, AMH can be higher, and in winter months, it can be slightly lower.

I’ve never seen strong data on whether IVF success differs by season, but it is interesting that AMH can fluctuate with sun exposure and vitamin D levels.


How Do We Actually Use AMH in Clinical Practice?

Here’s the number one way I use AMH in my practice: predicting response to medications.

Across the data, AMH correlates best with how someone responds to ovarian stimulation — whether that’s gonadotropin cycles outside of IVF or IVF itself.


AMH and IVF Medication Dosing

I use AMH to help guide IVF dosing.

For example, if someone is 34 and has an AMH of 8, I’m concerned they might over-respond to medications and be at risk for ovarian hyperstimulation syndrome (OHSS). So I would likely start them on a lower gonadotropin dose than I would for someone with a lower AMH, all else equal.

On the other hand, if someone has a low AMH, I may use higher doses of gonadotropins because I’m concerned I won’t reach their full ovarian potential if I under-dose from the beginning. I don’t like to “play catch-up” with IVF meds — I want to recruit the cohort from the start as best as possible.


AMH and Risk of OHSS

High AMH is also a risk factor for OHSS. Studies vary, but some suggest AMH above around 3.5 can increase risk.

Thankfully, we have tools now — like a Lupron trigger and other adjuncts — that can greatly reduce OHSS risk compared to what we used to see years ago.


AMH and PCOS / Ovulation Induction

I also use AMH in PCOS counseling. People with PCOS often have higher AMH than age-matched peers.

If I see a high AMH — like 7, 8, or above — I may not start letrozole at the lowest dose (2.5 mg), because I don’t think it will be enough. That also helps reduce time lost, while still being careful to avoid multiple gestations.


AMH and Egg Freezing Counseling

I also use AMH when counseling patients about egg freezing — and yes, this can be controversial.

For example, if someone is 28 and has an AMH of 0.8, wants a family someday, and has years of training ahead, maybe no partner yet — I might say:

“Your AMH is lower than I would expect for your age. I don’t know your reproductive timeline, but it may be shorter than average — and it may be worth thinking about fertility preservation.”

Sometimes two data points are better than one. If it’s borderline, I might recheck in six months.

I have watched ovarian reserve decline over time, and even drop off — including in cases of primary ovarian insufficiency — so I don’t take this lightly.

And I’m very clear: AMH is not a screening test for fertility. It is not a fertility test. It’s a quantitative marker of ovarian reserve.

However, I do think trends over time can be useful for counseling when fertility is a priority.

There’s a well-known study by Dr. Steiner (around 2013) showing that people with low AMH did not necessarily go on to have worse fertility outcomes later — and that’s important.

But if someone has declining AMH and fertility is a high priority, I think it’s reasonable to use AMH as a counseling tool, because it can be painful to watch a physiologic process that we can’t reverse. Knowledge can be power.


AMH and PCOS Diagnosis

It’s also interesting that newer ASRM guidance suggests a high AMH can be used as part of PCOS diagnosis — potentially in lieu of ultrasound-based follicle count — though they did not define a specific cutoff, likely because AMH assays vary globally.

AMH and antral follicle count often correlate: if someone has many follicles on ultrasound, they often have a high AMH as well.


What AMH Does 


Not


 Tell Us

Here’s the key: AMH is not egg quality. It’s not a qualitative marker. The best predictor we have for egg quality is still age.

Not everyone has the same egg quality at the same age, but in general, egg quality declines over time, especially in the mid-to-late 30s and beyond.

Age is still the most important predictor when someone walks into my office of how likely I am to be able to help them reach their goal.

For example, if someone is 42 and has an AMH of 5, I’m more likely to be able to help than someone who is 42 with an AMH of 0.5 — because it’s easier to find a genetically normal egg when you have more eggs to work with, especially when a high percentage of eggs are abnormal after 40.

But I do want to be clear: there is good data showing that even people with undetectable AMH — including after chemotherapy — can still conceive pregnancies. So I don’t want anyone to think AMH is an “infertility test.”

It reflects physiology — how many eggs are left in the pool. Unlike men, we’re born with all the eggs we’ll ever have, and we lose them over time.

Maybe in the future we’ll be able to take a fibroblast and turn it into an oocyte — many people are researching in vitro gametogenesis — but we’re not there yet. Until then, we work with what we have.


Quick Review

So to review: we talked about what AMH is, how we use it, why it fluctuates, and why it does not necessarily equal fertility.

I hope this has been helpful. I know what people often crave is scientific knowledge about the nuances of their values and their treatment options.

I love you. If you have more science topics for our science series, please let me know. I’m always happy to talk about the frontiers of care.

Until the next time. Bye.