Interpreting Ovarian Reserve: AMH, AFC, FSH & Clinical Decision-Making

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Ovarian reserve testing is widely used — but interpretation requires nuance.

In this episode, Dr. Erica Bove reviews a practical framework for interpreting AMH, antral follicle count (AFC), FSH, and estradiol in clinical practice, with emphasis on how those values influence treatment strategy.

Discussion includes:

• AMH as a surrogate for cohort size and medication responsiveness

• AFC correlation and discordance with AMH

• Elevated FSH as a compensated ovarian state

• Brain–ovary feedback physiology

• FSH resistance and stimulation response

• IVF medication dosing considerations

• Predicting ovarian response and hyperstimulation risk

• Why ovarian reserve is not synonymous with fertility

Rather than weighting one marker over another, Dr. Bove outlines a physiology-based framework that integrates laboratory values, age, genetics, and reproductive goals into individualized treatment planning.

This discussion is part of Season 1 of the Love & Science Fertility Framework: The Biology Beneath the Surface — a series examining the physiology that drives reproductive outcomes.

Transcript

Hello, my loves. And welcome back to the Love and Science podcast. Today, what I want to talk about is how I interpret ovarian reserve values. This is a really,
really important thought process because it really does affect so many things about, you know, what the values are and then what treatment options are available. So we just had a robust episode on mularian hormone and everything that that represents. But basically, the antimularian hormone comes from the small antipollocals. And basically, that is a surrogate marker for how many eggs somebody has left in their body. And so if somebody has a low antimularian hormone, that means that they have low egg reserve. If somebody has a high antimulary hormone, that means that there's still a lot of eggs to work with. And, you know, this is not a fertility test. I will be clear because we see people with low antimularyin hormones get pregnant all the time. But it really does portend response to medications in a treatment settings such as canatotropins, IVF. And so, you know, when we look at as an REI, when I look at endemulary hormone levels, first of all, I think about, okay, like, is this low compared to where the averages are for somebody's age? So if somebody is is 32 and has AMH of 0 .4, you know, I'm going to get worried about that in
terms of their reproductive timeline. Also, you know, if I'm like thinking about
medication dosing, if I'm doing IVF and somebody has an antemuloran hormone of 10, you better believe I'm going to be a little bit stingier on my medications because I know they're going to go farther just because somebody has a lot of eggs in there. And I also don't want to make them sick with hyperstimulation syndrome. So AMH is an excellent marker for how many eggs somebody has left in their body, you know, specifically relative to their age. Okay. So then another test that we have, which actually correlates with the antimilarian hormone, has an ultrasound -based test, which is called the antropholical count. The best time to get an antifolical count is during the follicular phase, right? When somebody's on their period, actually, you know, as gynecologist, we think that's totally acceptable to sweep through the ovaries and really count how many follicles between two to nine millimeters are there. And in general, if that number is above 10, then we're like, okay, that's a reasonable barren reserve. But if that number is less than 10, just like when the AMH is less than one, that suggests that there's fewer eggs to work with in a given cycle. The premise behind the AFC is that we don't just go through one egg in a given month.
We go through groups of eggs. I like to say that eggs are social. And so as we
get older and as our body is recognized,
and my body's recognizing a low egg number, that number might shrink to like four,
five, six, you know, follicles. Again, this is highly individualized. But because the
body recognizes a lower egg number, it conserves, which means there's fewer of those
follicles available when we go to try to stimulate them, say, in an IVF process.
And so the AMH and the AFC, they tend to correlate with each other. If they are
discordant, you know, that's always interesting because I always ask myself, okay, is
this person smoking? Does this person carry extra weight? You know, what is the FSH?
What's the estrogen aisle, which we'll talk about in a second. But, you know, the
antifolical count suggests how many eggs could I get to you in an IVF cycle, you
know, if I got the whole cohort of this month? And so somebody's AMH is low,
I might really be bold with my medications so that I can get as many eggs as
possible. You can't always get the whole cohort, but there's tips and tricks and
protocols that we like to try to make sure that we're optimizing as much as
possible. I always tell my patients, you pay the same amount, whether I get 15 eggs
or three eggs. And so let's do our best to get as many eggs as possible. Okay. So
then there's the follicle stimulating hormone in the estrogen. So this requires an
explanation of physiology. if you're a female physician, perhaps you remember this
from medical school, but maybe very vaguely. So the ovaries and the brain are always
in a conversation with each other. These tests are blood tests, right? They're
hormones. And the ovaries make estrogen and the anterior pituitary makes follicle
stimulating hormone or FSH. And so when the ovaries are doing a fine job,
right, doing what they're supposed to do, the follicle stimulating hormone is in a
normal range, right? But as we get older, especially, and our ovaries are having a
harder time doing their job, the brain then recognizes that and compensates and sends
a stronger signal so that the ovaries then can better do their job. So, for
instance, say the estrogen ovaries are having a hard time making estrogen, the brain
recognizes that an FSH of eight isn't cutting it for the ovaries to do their job.
It might turn up that signal to like 12, 13, 15. And then the ovaries are like,
oh, yeah, I get it. I'll do my job now. Thanks for knocking a little harder right
on the system. And so then, you know, although that the cycles keep going, I
consider this like a compensated state because the ovaries are, you know, being
stimulated by more and more and more FSAH to be able to do their job. Now, why
does this matter? This matters because any treatments that we do for the most part
in the fertility world are going to work too.
to create a response. And so you might hear the term FSAH resistance. I love
getting FSAH and estrogen because it helps me understand, you know, what resistance
might I have to overcome to be able to kick somebody's ovaries into gear. Sometimes
I use estrogen priming. That's a great way to lower the body's FSAH without, you
know, too much suppression to be able to then get a cohort. You know, it's one of
our newer strategies in the last 10 years. But I think it's really important to
understand, you know, if the FSH is 20, 2530, why might an IVF cycle not work?
It's because the body is already living in a C of FSH. And when we give our
hormones from the outside world, it's just not seeing that much of a difference.
It's also why in primary overemufficiency, a lot of times people are just as
successful at home as in the clinic because we really can't get a change in that
delta for the most part. So what I would say is there's three different ways that
we can look at ovarian reserve. One of them is the antinulinarian hormone blood
test. Another is the antifolical count ultrasound. Another is the combination of the
follicle stimulating hormone in the estrogen. You know, I go through those in a lot
of detail in other podcasts, but I think understanding like antimilarian hormone,
we start at a certain level, it goes down, down. So the asymptote is actually like
zero, right? FSAH is, goes up, up, up with time. And so it's really infinity,
right? I might see an FSAH of like 80, 100, 120. That means that somebody's ovaries
are really not doing well and the brain is working awfully hard. So it's interesting
that the asymptote for AMH is zero. And then, you know, FSAH, the sky's a limit.
So that's kind of an interesting thing to think out in and of itself. And then the
antrololic account ultrasound really suggests how many eggs is this person going
through in a given month and how many eggs might I have access to that might
respond to stimulation if we do a cycle. So, you know, do I put more weight on
one than the other? I really don't because I believe that this has to be
interpreted in the context of each person's fertility story, each person's genetics,
these persons' family building goals and all those things. But I think that there
are certain correlations that we know about, for instance, you know, AMH with
medication dose and FSAH with resistance that really help us shape each treatment
plan in a very thoughtful and scientific way. So I hope this was helpful. Until the
next time, you know, I love you. Bye.