Women in their late 30s and early 40s who notice that something has shifted. And they’re told over and over again:
This is just what happens.

But what they’re almost never told is that it might be hormonal.

Testosterone is an important hormone for women too, and it begins to decline in your late 20s. By your early 40s, the decline mirrors estrogen and is measurable, meaningful, and almost universally unaddressed. An important concept that we have discussed before is that your ovary, which is the primary site of testosterone production, changes its hormonal output years before perimenopause begins, and those changes may show up in desire before they show up anywhere else.

As a reproductive endocrinologist, I see this constantly. Women who have been to their OB/GYN, who have been told their labs are normal, and who have been handed a referral to couples therapy for a problem that might have a hormonal explanation. This is a clinical gap, and it starts earlier than almost anyone is talking about.

This week I’m joined by Dr. Kelly Casperson, a board-certified urologist, author of “You Are Not Broken” and “The Menopause Moment,” and one of the most important voices in women’s sexual health, for a conversation about desire, hormones, and why the window to address both opens much earlier than medicine currently acknowledges.

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Your sex drive is a window into your health

Your sex drive is not an isolated switch that simply turns on or off. It is connected to your hormones, your medications, your sleep, your stress, your pelvic health, your relationship, and whether sex is physically and emotionally pleasurable for you.

A change in desire is not a diagnosis, and low desire is not automatically a problem that needs to be fixed. If you are not distressed by it, then it may not be a problem at all. But if your desire has changed and that change bothers you, it deserves more than a shrug. It deserves a real conversation about what changed, when it changed, and what else was happening in your body at the time.

Low libido: one phrase can describe many different problems

When you say, “I have a low libido,” what do you actually mean?

Do you never think about sex? Do you want to want it, but the feeling never arrives? Are you interested mentally, but your body does not respond? Does sex hurt? Can you become aroused once intimacy begins, but rarely feel the urge to initiate it? Are you able to orgasm? Has sex stopped feeling pleasurable? Or do you simply want sex less often than your partner does?

These are not the same problem, and they should not be treated as though they are.

“Never assume that what you think low libido means is what they think low libido means because you’re both talking about low libido, but you’re actually having very different conversations.” — Dr. Kelly Casperson

Desire, arousal, orgasm, and pain are separate parts of sexual function. They can overlap, but each one gives us different information. If your primary issue is pain, simply telling you to “work on your libido” misses the point. If your body can become aroused but you rarely experience spontaneous desire, that may reflect a completely normal pattern of responsive desire. If your interest changed shortly after starting a medication, that timeline matters.

The first step is not trying to increase your sex drive. The first step is defining what has actually changed.

Responsive desire: Hollywood taught you the wrong model

Many women believe desire is supposed to appear spontaneously. You are expected to be going about your day, suddenly think about sex, and immediately feel ready for it. That model exists, but it is not the only normal way to experience desire.

For many women, desire is responsive. You may not start with an urgent desire for sex. Instead, you begin with willingness, connection, touch, or curiosity. As your nervous system shifts into a state where you feel safe and present, your body may become aroused, and desire can follow.

That does not mean consenting to sex you do not want. Responsive desire requires genuine willingness and the freedom to stop. It means recognizing that you may not always need to feel desire before intimacy begins. Sometimes desire appears after your brain and body have been given enough time, attention, and stimulation to respond.

This is especially important if your days are filled with work, parenting, caregiving, decision-making, and constant stimulation. Your body may not move immediately from answering emails or putting children to bed into sexual arousal. Context matters. Time matters. Feeling safe enough to become present in your body matters.

Painful sex: treat the pain before blaming desire

If sex hurts, it makes sense that you would stop wanting it. Your brain is designed to protect you. When an experience repeatedly causes pain, burning, tearing, or discomfort, your body learns to anticipate that pain. Desire may decrease because your nervous system no longer associates sex with pleasure.

Pain with sex can have many causes, but especially hormone related ones. Hormonal changes may contribute to dryness, reduced blood flow, changes in genital sensation, and thinner or less elastic vaginal tissue. These changes can occur during perimenopause and menopause, but they may also appear while breastfeeding, postpartum, or when certain medications suppress estrogen (including hormonal birth control).

Local vaginal estrogen and systemic hormone therapy are different treatments with different purposes, but both can be helpful. Local therapy primarily targets vaginal and urinary tissue. Systemic therapy circulates throughout the body and may be considered when you have broader symptoms. Neither is the right answer for every person, and not all sexual pain is hormonal. Pelvic floor dysfunction, vulvar conditions, infections, endometriosis, scar tissue, and other medical issues may also need to be evaluated.

But pain should never be dismissed as something you simply have to tolerate. And you should not be expected to manufacture desire for an experience your body has learned will hurt.

Good sex: are you having something worth wanting?

Hormones matter, but they are not the whole story. Dr. Casperson uses food as an analogy. You can have a normal appetite and still have no interest in eating something that is consistently unappealing. Desire does not exist independently of the experience you are being asked to desire.

If sex is rushed, predictable, painful, disconnected, focused entirely on your partner, or consistently ends before you experience pleasure, your lack of interest may not be evidence that something is wrong with you. This is one of the most important questions in the entire conversation.

Many couples focus on frequency. How often are you having sex? Who initiates? Is that number normal? But frequency alone tells you very little about whether the sex is pleasurable, connected, or satisfying.

There is no universally correct amount of sex. The goal is not to reach a number that makes your relationship look healthy from the outside. The goal is to understand what intimacy means to you, what makes sex pleasurable for you, and whether both people can talk honestly about what they want.

Your period: not a hormonal all-clear

One of the biggest misunderstandings I see is the belief that if you are still having regular periods, your hormones must be fine.

Your menstrual cycle is important information, but it does not tell us everything about your hormonal environment. Ovarian hormone production does not remain completely unchanged until the day your periods stop, but your hormones start changing well before your periods end.

Hormones change over time, and those changes may affect different parts of your health at different moments. Desire may change. Sleep may become less restorative. Mood may shift. Vaginal tissue may feel different. Arousal may take longer. You may feel less like yourself, even while your periods continue to arrive.

And these symptoms interact. If you are not sleeping, if your mood is different, if you are uncomfortable in your body, or if sex has begun to hurt, all of that can affect desire. Desire is an outward reflection of everything else that is going on inside your body. Not every change in your 30s or 40s must be caused by hormones, but your hormones should be a part of the conversation and not dismissed because you are not yet in menopause.

Medications: the side effect nobody mentioned

If your desire changed, look at the timeline. Did it happen after starting or changing an antidepressant? After beginning hormonal birth control? After adding a medication that affects sleep, mood, blood pressure, or blood flow? Did it happen postpartum or while breastfeeding?

Some medications can affect desire, arousal, lubrication, genital sensation, or orgasm. That does not mean the medication is bad, or that you should stop taking it. It means sexual side effects should be included in informed consent and discussed as part of your overall health.

Hormonal birth control can be transformative. It can prevent pregnancy, regulate bleeding, reduce pain, improve acne, and help manage conditions such as endometriosis. But it can also change hormone availability in ways that may affect sexual function for some women. Your experience matters, even if that side effect does not happen to everyone.

Never stop a prescription medication without speaking with the clinician managing it. But do not assume you must silently accept a sexual side effect that affects your quality of life. There may be another dose, another medication, or another way to approach the underlying problem.

Hormones: where estrogen, progesterone, and testosterone fit

There are multiple different hormones that are all import in libido and desire.

Estrogen supports blood flow, vaginal tissue, lubrication, and genital sensation. Progesterone can influence sleep and mood. Testosterone plays a role in sexual desire, motivation, arousal, and other aspects of how you feel in your body.

But hormone treatment must be individualized. Vaginal estradiol treatment can be a powerful option for many women. The strongest evidence for testosterone therapy is in appropriately evaluated women with hypoactive sexual desire disorder, particularly after menopause, although some expert guidance also discusses carefully selected women in the later reproductive years.

There is currently no FDA-approved testosterone product specifically dosed for women in the United States, so treatment is prescribed off-label. That does not automatically make it inappropriate, but it does make clinician experience, careful dosing, informed consent, and monitoring especially important.

But more is not better. Excess testosterone can cause acne, unwanted hair growth, scalp hair changes, and voice changes, some of which may not be reversible. Long-lasting pellets can be difficult to adjust or remove if the dose is too high. I do not recommend pellets. I still remember the patient I saw in fellowship with an enlarged clitoris and voice deepening from pellet treatment with too much testosterone. Any discussion about treatment should include what form is being prescribed, why it is being recommended, how you will be monitored, and what side effects to watch for.

Hormones are one part of the picture. Pain, medications, sleep, stress, relationship dynamics, and the quality of the sexual experience still matter. The right treatment depends on identifying which pieces are affecting you.

So what do you actually DO with this information?

1. Start by getting specific. Instead of saying, “My libido is low,” describe what has changed in your own words. Did you stop thinking about sex? Does your body take longer to become aroused? Is sex uncomfortable? Has orgasm become more difficult? Do you enjoy intimacy once it begins, but rarely initiate it? Did the change begin after pregnancy, breastfeeding, a new medication, hormonal birth control, surgery, or a shift in your cycle?

2. Write down the timeline before your appointment. Include changes in your periods, sleep, mood, vaginal comfort, medications, and overall health. You are looking for patterns, and presenting accurate information to aid in diagnosis.

3. Ask for an evaluation that goes beyond a single laboratory result. Labs are useful in the right context, but “normal” does not always explain your symptoms, and symptoms cannot always be reduced to one number. You can bring questions such as:

   1. Could pain, vaginal dryness, or pelvic floor dysfunction be affecting my desire?

   2. Could one of my medications be contributing?

   3. Could hormonal changes be playing a role even though I still have periods?

   4. Am I experiencing low desire, difficulty with arousal, pain, or a combination?

   5. What treatment options have evidence for my specific symptoms?

   6. If you recommend hormone therapy, what are the benefits, risks, dose, and monitoring plan?

   7. When should I see a menopause specialist, pelvic floor physical therapist, sexual-medicine clinician, or another specialist?

4. If your concerns are repeatedly dismissed, it is reasonable to seek another opinion. Sexual health is health. You deserve a clinician who is willing to define the problem with you and discuss your options honestly.

The bottom line

Your sex drive is not a measure of your worth, and it is not something that you should just have to “deal” with. I know that if you have been dismissed or gaslit before, you learn to mistrust your body. I want you to get to a place where you trust your body again and you feel confident advocating for your health. You deserve it.

“I care desperately that you are educated and you’re empowered to be an advocate for yourself.” — Dr. Kelly Casperson

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This week’s guest: Dr. Kelly Casperson is a board-certified urologist, author of “You Are Not Broken” and “The Menopause Moment,” and one of the most important voices in women’s sexual health.

If this helped you understand your desire differently, share it with someone else who may be struggling with the same questions. Listen to the full episode of the As a Woman podcast wherever you get your podcasts—listen now on Spotify or Apple.

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I review studies in women’s health, hormones, fertility, and ovarian aging almost every single day, but this really stopped me. In a new survey of more than seven thousand American women over thirty-five, one in three could not say what stage of reproductive life they were in. Not that they “didn’t feel like sharing,” but they really could not say. They had options including the words premenopause, perimenopause, and postmenopause, and 1 in 3 women picked “I’m unsure.”

And that uncertainty was highest (42%!) in the women who were most likely to actually be going through it, those in the 40-to-44 age group. These are often women who are done with their families and not sure what is coming next. As someone who is 44, this is me, my friends, and many of my current and former patients (and probably a lot of you who started following me when you were trying to grow your family and stuck around). How do you know when you are going through perimenopause? Are there symptoms you should know about?

I have spent my career saying that women should not have to fail before they learn about their body. This study is that sentence turned into proof that the current approach to women’s health is failing us all.

So this week I break the study down this study and what you need to know to determine what life stage you are actually in, and I’m questioning WHY we diagnose perimenopause and menopause the way that we do. Menopause is defined as no menstrual cycles for one year and ovarian failure—again, we require failure before action. I do not think this serves women who want to be proactive in their health.

Happy reading and thank you so much for being here.

XO, Nat.

Study: Exploring Prevalence and Drivers of Perimenopause Uncertainty Among U.S. Women: A Mixed-Methods Study

Journal: Menopause

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Why this study caught my attention:

A new study published in Menopause, the journal of The Menopause Society, surveyed 7,640 American women aged 35 and up and asked a deceptively simple question: do you know what reproductive stage you’re in? A third of them said no. Among women aged 40 to 44, the group where perimenopause most often begins, it climbed above 40%. The researchers asked why, and we see the real life confusion behind ovarian aging: missed cycles, competing diagnoses, and far too many women being told they were “too young” to be in perimenopause. Dismissed, gaslit, and turned away. Unfortunately things we see commonly in women’s health.

Add in the fact that perimenopausal symptoms overlap almost perfectly with thyroid disease, anemia, depression, anxiety, PMOS (previously PCOS), and chronic inflammation, stress, and insulin resistance. What you get is exactly what this study measured: a whole lot of women with real symptoms and no clear answer.

I’ve spent years telling women that perimenopause is officially a clinical diagnosis, but the truth is, I diagnose it every single day as low ovarian reserve. We know that your egg count drops before your cycle changes. And symptoms begin with the hormone changes that precede abnormal cycles. As a reproductive endocrinologist, I believe that we have more tools to diagnose reproductive life stage than we have been using.

So today I am reviewing:

• What is perimenopause

• A breakdown of this study

• The argument for ovarian reserve testing to aid in perimenopause diagnosis

• What you should do if you think you are in peri

What is perimenopause

If a third of women can’t name their reproductive life stage, then understanding what perimenopause really is must be at least part of the problem.

Perimenopause is the transition into menopause. I like to think about it as the time period when your egg count starts dropping and your hormones start responding as such, but this change actually starts well before menopause itself.

Menopause is only a single day. The one-year anniversary of your final period, diagnosed looking backward. Everything in the years leading up to that day is perimenopause, and postmenopause is everything after. But menopause is something we can only define AFTER it has happened (or after you have been suffering for that fact).

The word perimenopause literally means “around menopause,” and “around” is a pretty large time period since peri can last anywhere from about 4-10 years for most women. It usually begins in the mid-forties, with a median onset around 45, but it can start in the late thirties, depending your own trajectory of ovarian aging. In the U.S., roughly two million women enter perimenopause every year.

For most of your reproductive life, a pool of small follicles in your ovaries keeps a steady conversation going with your brain, producing estrogen and progesterone in a predictable monthly rhythm. As that follicle pool shrinks with age, the conversation gets erratic. You may not know that all the resting follicle still talk back to the brain signaling what is happening. As that pool gets smaller (the number of eggs outside the vault decreases), then the feedback will change, and the hormone response does as well.

Estrogen doesn’t just get lower, but it fact it swings—from high to low. I like to describe it as a stubborn ovary. It just doesn’t respond until it then does, and then it miss shoots and over produces. Even the odds of having twins is higher as you are in perimenopause because more FSH is being sent from the brain (trying hard to stimulate that stubborn ovary) and then the ovary over responds when it does, resulting in more than one egg ovulating. In that cycle if you don’t get pregnant, you will have significantly higher estrogen levels (double) what you “normally” would if you were ovulating just one.

That single fact explains almost every symptom. Hot flashes and night sweats from the brain working overtime, yes. But also think of all the symptoms connected to the hormone fluctuations with peri: waking up from sleep at 3 a.m., anxiety or low mood swings, brain fog, heart palpitations, joint aches, decrease in libido, mid section weight gain, low energy, and then eventually heavier or lighter or closer-together or further apart periods. Your period symptoms are typically some of the later ones to appear, which makes sense. The hormone abnormalities that LED to the abnormal cycles were already brewing. Around 60% of women will have symptoms significant enough to affect daily life.

But read that again because your period can stay regular through much of this. Up to a 25% of women don’t have a significant cycle change during perimenopause. The classic teaching that “your periods get irregular first” simply doesn’t hold for many women. So if you’re waiting for your cycle to fall apart before you get help or trust your body, you may be waiting on a signal that never comes, while everything else is already telling you the truth.

Perimenopause is not a disease. It’s a universal, normal transition. But it is likely you were never told what to expect or when to get help. I’m reviewing below this study in detail, why I believe ovarian reserve testing can be used to aid in perimenopause diagnosis, and what you should do if you think you are in peri.

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AskNat The column where you ask and I answer like the doctor-friend you wish was in the room with you. Real questions from real women, straight from my inbox. General education, never a substitute for your own doctor.

Welcome friends-

Your questions this week are great, and some of you were asking very similar things! As always, these are real questions from your submissions, cleaned up so no one is identifiable, and answered the way I would if you were sitting across from me. I will tell you what I tell my own patients—explaining what we know and what we don’t. This is not personal medical advice, and I am not your doctor. But you deserve to understand your body, and that is what we are here to do.

For a limited time, AskNat is open to all subscribers as a free trial but it will soon be a paid subscriber only offering. Only paid subscribers can ask questions, upgrade now. Once you subscribe you will see the question box at the bottom of the article.

Questions answered this week:

1. “Can you discuss mosaic embryos and their success rate? Which mosaic embryos would you prioritize first?”

2. “My luteal phase is 9 days. Is this normal?”

3. “I just had a chemical pregnancy and I’m so scared to try again, but I feel like I should because I read on your Substack that chances are higher after. Can you tell us more?”I just had a chemical pregnancy and I’m scared to try again (and is it true chances go up after?)

4. “What’s a safe dose of inositol in pregnancy and breastfeeding? I have PMOS and a history of gestational diabetes, and took 1 g/day (myo-inositol) last pregnancy with no side effects.”

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1.“Can you discuss mosaic embryos and their success rate? Which mosaic embryos would you prioritize first?”

A mosaic embryo is an embryo that had genetic testing and came back essentially with a mixed result—some normal cells and some cells that are abnormal. There are different types of mosaic embryos, so this is a really good question.

When we do preimplantation genetic testing for aneuploid (PGT-A), we take a biopsy of around 5-8 cells from the trophectoderm (the cells that become the placenta). Each cell is then evaluated to see if it is genetically normal or not. Note, unless we are looking at PGT-M, which is an extra layer of screening, then we are not looking at single gene disorders (like the gene that carries cystic fibrosis or the gene that carries the BRCA mutation). For PGT-A we are simply evaluating if the cells have the normal number of chromosomes, or is part of a chromosome is missing or duplicated.

The two main type of mosaic embryos include low level mosaic embryos and high level mosaic embryos. The easiest way to think about this is that low level mosaic (LLM) embryos have most the cells normal and a high level mosaic has most the cells abnormal (HLM). Now, in the early days of PGT-A, the labs didn’t report out LLM vs HLM instead everything was grouped as either ‘normal” or “abnormal” and in this time LLM embryos were put into the “normal” group and HLM were put in the “abnormal” group. Since we now detect and report mosaicism, we see the highest birth rates with embryos that are genetic euploid (normal) or about 65% per transfer.

LLM embryos should be considered for transfer but as a second line, with a cumulative live birth rate of around 30%—which is still a good number, but lower than euploid embryos. HLM embryos have a much lower love birth rate (usually around 5% or less) and many clinics will not transfer these embryos. We prioritize small chromosome defects (segmental breaks) over whole chromosome abnormalities, and there are some chromosome defects that may not be worth the risk.

We have patients see a genetic counselor who specializes in embryo testing and a high risk MFM prior to transferring a mosaic embryo. Sometimes patients decide to proceed with fetal testing (like an amniocentesis) if they get pregnant to get a confirmatory karyotype of the baby if the PGT-A was a mosaic embryo. Note, a CVS sampling also tests the placenta so that would not be appropriate in this case because the same tissue line is being testing for both.

All that said, it does depend which chromosome the defect is on and what type of abnormality it is. We now know that embryos which come back as segmentally aneuploid still have a live birth rate of over 20%! So even not all “abnormal” embryos are created equally and we have to think about where the chromosome issue it.

Remember that when we take a biopsy of an embryo we are taking 5-8 cells out of hundreds. It is a blind snapshot and may not reflect the actually fetal cells (since we are taking the biopsy from the cells that become the placenta). Also complicating the picture is the fact that the embryo is still growing and developing and can self correct itself—sometimes pushing out abnormal cells so the embryo inside is healthier. This is the problem with a mosaic embryo, when we have 2 cell lines we don’t really know which one reflects the status of the baby.

The good news is that many perfectly normal children have been born from mosaic embryos, and probably from well before we even knew we were transferring them! If you do PGT-A, I would prioritize transferring 1) euploid embryos first, 2) LLM with partial chromosome abnormalities 3) LLM with whole chromosome abnormalities, 4) segmental aneuploid, 5) HLM. Of course, anytime the PGT-A comes back as anything except euploid, you should ask to talk to genetics, even if not required by your clinic. This will set you up to be in the best position to get the data you need to have to make an informed decision.

2. “My luteal phase is 9 days. Is this normal?”

A 9 day luteal phase is not normal. A short luteal phase is defined as a luteal phase of less than 11 days. If we think back to the menstrual cycle, the lute, phase is a sign of normal ovulation. A follicle grows as the egg matures, the follicle ruptures and the egg ovulates, then the follicle reforms and becomes the corpus luteum making progesterone. This entire process is under direct control of the brain, which is highly sensitive to the world around you.

A short luteal phase is the first stage of ovulatory dysfunction. Meaning this: if you don’t grow the best follicle (which becomes the foundation for the corpus luteum), you won’t have a great corpus luteum. Said another way: if the brain can’t stimulate the follicular and ovulatory phase, I’ve lost confidence we can send out enough LH to support progesterone.

There are some medical reasons for a shorty luteal phase: thyroid disease, elevated prolactin, hypothalamic dysfunction (which encompasses energy deficit, chronic stress, chronic inflammation and even insulin resistance). Sometimes a short luteal phase is a sign of low ovarian reserve (although classically we see a shorter follicular phase in this as the first cycle change).

Tests I recommend to start with include: thyroid panel (including antibodies), prolactin, fasting insulin, and AMH. Sometimes the treatment is straightforward, sometimes luteal progesterone treatment (starting 2-3 days after ovulation) or ovulation induction can be helpful.

3. “I just had a chemical pregnancy and I’m so scared to try again, but I feel like I should because I read on your Substack that chances are higher after. Can you tell us more?”I just had a chemical pregnancy and I’m scared to try again (and is it true chances go up after?)

A chemical pregnancy is one where you get a positive pregnancy test but the pregnancy miscarries prior to seeing it on ultrasound. In the past, some doctors didn’t “count” a chemical pregnancy loss as a “real” pregnancy loss. I call this a lot of BS, and as someone who has had a lot of losses, I never believed this. I am happy to report that guidelines have changed on this one and now all losses count.

In fact, in a study looking at women after a pregnancy loss, women who started trying again at 0-3 months after their loss (as compared to >3 months after their loss) had higher odds of conceiving and conceived faster. There was no higher chance of a second chemical pregnancy after one loss.

After one pregnancy loss, your loss of having another pregnancy loss are not higher. This does change after multiple pregnancy losses, so please consider getting an evaluation if you have had 2 or more losses.

From someone who had 4 losses herself, sending you huge hugs. It sucks, it makes you question everything—your future, your body. But more than anything know that pregnancy loss occurs on average in 1 out of 4 pregnancies, you are not alone.

4. “What’s a safe dose of inositol in pregnancy and breastfeeding? I have PMOS and a history of gestational diabetes, and took 1 g/day (myo-inositol) last pregnancy with no side effects.”

.PMOS (previously PCOS) is characterized by abnormal insulin metabolism, and inositol is a first-line treatment approach that can be very helpful. Inositol, specifically myoinositol works as an insulin sensitizer and a mainstay in PMOS treatment because better insulin signaling results in improves ovulation and symptoms.

For general PMOS management, the doses studied are usually around 2-4g of myo-inositol per day.

In pregnancy trials, myoinositol at roughly 2g twice daily (about 4 g/day) was used, appeared safe, and was associated with a lower rate of developing gestational diabetes in high-risk groups. So the dose you took last time, 1 g/day, is on the lower end of what’s been studied, and the trial-level dose is higher which should make us feel confident that you haven’t done any harm, and I let my patients continue myoinositol in pregnancy for this reason (to lower the GDM risk).

For breastfeeding, we just don’t have the same data. On the pro side, it is a natural substance and normally present in breastmilk, so generally considered low risk. In fact, early data looks like it may even help improve fetal brain development (win!). That said, we always want to think about the full picture and you should discuss with your doctor.

Overall, inositol is one of the safer options we have for PMOS and it is ok to continue in fertility treatments, pregnancy, and breastfeeding—BUT you should absolutely discuss with your OB-GYN in case there is something about your history or medications that modifies your personal risk.

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Before you go

None of us should have to fail before we understand our own bodies, and none of us should have to figure it out alone at midnight with a search bar. Paid subscribers can submit questions below to have them answered in AskNat.

XO, Nat

Once you subscribe you will see the question box at the bottom of the article.

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In this edition of Fertility Q&A, I’m answering your questions about ovulation tracking, recurrent chemical pregnancies, PMOS (formerly PCOS), low sperm motility, failed embryo transfers, Hashimoto’s, unexplained infertility, IUI, and when it may be time to take the evaluation one step further.

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1. “My cycles are regular, and I track ovulation with test strips and my Oura Ring. When they give me different dates, which day am I actually ovulating?”

I usually say that the truth is somewhere in between. An ovulation predictor kit detects the rise in luteinizing hormone, or LH, that happens before ovulation. One of the most common misconceptions I hear is thinking that the OPK test is positive when you are ovulating. But since LH is the hormone that causes ovulation, a positive OPK is a representation of the LH surge and reflects the day BEFORE ovulation.

Basal body temperature rises after ovulation once the ovary begins making progesterone since progesterone raises your core body temp by 0.4 degrees F. This makes temperature helpful for confirming that ovulation likely occurred, but it is not always as useful for predicting your fertile window in real time. The exception here is when BBT is connected to a wearable and an app like natural cycles (disclaimer, I am a natural cycles medical advisory board member but this is because I support the product so much).

If you get a positive LH test one day and see a temperature shift after that, the day following your positive LH surge is often the best estimate of when you ovulated.

The way you use an ovulation predictor kit matters too. LH is released from the brain in the early morning hours, but it takes time to reach the urine. I recommend testing between 10 a.m. and 2 p.m. rather than first morning urine. If you are using a traditional test strip, a faint line is not a positive test (unlike a pregnancy test) since we all have some LH in our bodies at baseline. The test line needs to be as dark as or darker than the control line to indicate a true surge. If you find the lines difficult to interpret, a digital test may be easier because it simply tells you whether a surge has been detected.

No single wearable or test is going to identify the exact moment of ovulation. The most useful information comes from looking at the pattern created by your LH testing, temperature, cervical mucus, and cycle history together.

2. “I have had four chemical pregnancies in the last four years. My blood work and ultrasounds always come back normal. Could this mean my uterus is not strong enough, and what can I do to prepare my body for implantation?”

First, I am so sorry for everything you have been through. Four chemical pregnancies are real losses, and they deserve a real evaluation. Recurrent loss does not mean that your body is weak or incapable of holding a pregnancy.

A regular ultrasound is helpful, but it is not a complete evaluation of the uterine cavity. I always describe the uterus as a potential space. We picture it as an open triangle, but most of the time the two walls are resting against each other. A polyp, scar tissue, a uterine septum, or another structural difference may be sitting inside that space without being visible on a standard ultrasound.

To see the cavity more clearly, we need to separate those walls. A saline sonogram does this by placing fluid inside the uterus while we watch with ultrasound. An HSG is a similar test that uses contrast and an x-ray, which allows us to examine the uterine cavity and see whether the fallopian tubes are open. A hysteroscopy places a small camera directly inside the uterus. Each test gives us different information, and after recurrent losses, I would want to know whether the uterine cavity and fallopian tubes have been fully evaluated rather than relying only on a regular ultrasound.

Anatomy is only one part of the recurrent pregnancy loss evaluation. You also should have testing for thyroid disease, antiphospholipid antibody syndrome, insulin resistance, inflammation, genetic factors, and a DNA sperm fragmentation. The exact testing should be individualized, but after four chemical pregnancies, I would not accept “everything looks fine” without a complete evaluation.

3. “I have PMOS and have been told different things about fasting and working out before eating. Is fasted exercise okay for me?”

Working out fasted is not automatically harmful. If you enjoy exercising first thing in the morning, feel good doing it, and consistently meet your protein, fiber, and overall nutrition needs later in the day, exercising before breakfast may work well for you. The support of fasted exercise is that you can still build muscle without eating immediately beforehand. That is different from saying every woman should work out fasted or that fasting is beneficial in every hormonal situation.

When someone has PMOS and insulin resistance, I prefer the term time-restricted eating rather than fasting. A reasonable approach is an overnight interval of approximately 12 hours without food, ideally finishing dinner at least three hours before bed and not by pushing the first meal later and later into the day. With insulin resistance, going too long without eating can cause the liver to release more glucose and may work against what we are trying to accomplish metabolically.

If you are trying to regulate your cycle, improve insulin sensitivity, or get pregnant, a balanced morning meal may be more advantageous. If your cycles are regular, you feel well, you prefer to work out immediately after waking, and you are meeting your nutritional needs, the answer may be different. For the situation described in this question, with PMOS and active fertility goals, I would favor eating in the morning while maintaining a reasonable overnight eating interval.

4. “I’m 34 and have been trying to conceive for a year and a half. My cycles and saline sonogram are normal, my AMH is 1.4, and my husband has slightly low sperm motility. What should we consider next?”

An AMH of 1.4 is a little lower than I would expect at 34, but it does not mean you are about to run out of eggs or enter menopause. AMH gives us information about ovarian reserve, or the quantity of eggs remaining. It does not tell us whether you can or cannot get pregnant naturally, and it is not a direct measure of egg quality.

The first question I would ask is how many children you hope to have. If you are trying for one child, we may think about your timeline differently than if you are at the beginning of building a larger family. A slightly lower ovarian reserve becomes relevant when we are making a long-term family-building plan, because we are not only thinking about getting pregnant today. We are also thinking about whether you hope to return for another pregnancy several years from now.

Because your AMH is a little lower than I would expect at 34, I would also ask why. Depending on your history, I would consider ferritin, fasting insulin, thyroid disease, autoimmune disease, endometriosis, and other signs of inflammation.

I also do not live in the world where slightly low sperm motility is automatically “no big deal.” Moving is one of sperm’s main jobs. If they are not swimming well, it may be more difficult for them to reach the egg. This is one situation in which IUI may be helpful because we prepare the sperm and place them higher in the reproductive tract. I describe it as moving the players farther down the field, essentially giving them a better starting position.

Low motility should also prompt us to look at male lifestyle and medical factors. Sperm develop over approximately 90 days, so alcohol, cannabis, heat exposure, excess sugar, inflammation, sleep, and overall metabolic health may be relevant. Lifestyle will not explain or correct every case of low motility, but the result deserves more context. I would consider repeating the semen analysis, looking for possible contributors, and having a real conversation about whether IUI makes sense given how long you have already been trying.

5. “I had my saline sonogram on cycle day nine. Does it matter which day of the cycle this test is performed?”

We generally perform a saline sonogram or HSG after menstrual bleeding has ended but before you get close to ovulation, often around cycle days 6 through 10. We want to examine the uterine cavity while the endometrial lining is still thin.

Here is my imperfect analogy. Imagine that I am looking for a tree stump in a yard. If the grass is tall, I may walk right past it. If the yard has just been mowed, the stump becomes much easier to see. The same concept applies inside the uterus—a polyp or other small finding may be harder to identify once the endometrial lining has become thick (when the grass is tall).

Cycle day nine is therefore a very reasonable time for the test in someone with a typical cycle. The exact timing may change if you have very short, long, or irregular cycles, but the principle is the same: after bleeding and before ovulation, when the lining is thin and the chance of an early pregnancy is low.

6. “I have lean PMOS and made 13 blastocysts from one retrieval, but I have now had five unsuccessful euploid embryo transfers. My doctor thinks it may be an embryo or lab issue. How do I know whether we are missing endometriosis or another implantation problem?”

Even if you love your doctor, at this point it is time to go see another fertility specialist for a second opinion. Have them review your complete records, including the stimulation protocol, embryo development, laboratory information, transfer protocols, uterine lining, medications, and every test that has or has not been performed.

One of the hardest problems in IVF is separating an embryo issue from an implantation issue. Not every euploid embryo will become a baby, even in an ideal situation. At the same time, recurrent implantation failure does exist, and after multiple failed euploid transfers, it is reasonable to question whether there is something about the uterine environment or transfer protocol that has not been addressed.

I have seen patients complete another IVF cycle and make new embryos that behave differently because it was a different month with different exposures. I have seen endometriosis surgery change the outcome. I have also seen patients benefit when we changed a protocol or added medications. The data supports that 95% of people will get pregnant after 4-5 euploid embryo transfers. Each case should be individualized.

If the uterine cavity has only been evaluated with ultrasound, I would ask about hysteroscopy. A hysteroscopy allows us to place a camera inside the uterus and directly inspect the cavity. After this many unsuccessful transfers, I would want to know that someone has truly laid eyes on the inside of the uterus.

Other things to think about: undiagnosed endometriosis, protocols for recurrent implantation failure (such as 2 months of letrozole with lupron), recurrent pregnancy loss labs, chronic endometritis testing/treatment. Add on that should be individualized include ERA testing, steroids, and blood thinners.

7. “Can creatine cause endometriosis to progress?”

There is currently no human data that creatine causes endometriosis to progress. Creatine has a well-established role in muscle function, and we are learning more about its potential benefits for brain health and women’s health over time. Human data has shown that inflammatory markers decrease with creatine supplementation. However, concern exists due to lab model showing that creatine accumulates in endometriosis lesions and it increases vascular growth—potentially promoting progression.

I do not routinely tell my patients with endometriosis that they cannot take it, but endo is complicated. If you notice a worsening of symptoms, know that for you, creatine may not be the right answer. Even within women with endometriosis, the expression of estrogen and progesterone receptors can vary between people, and endometriosis lesions do not behave exactly the same way in every body. That individual variation is part of what makes the disease so difficult to study and treat.

My general position is that creatine does not need to be automatically restricted simply because someone has endometriosis. If you are taking creatine and feel like your endometriosis symptoms are worse, then consider not adding it to your stack.

8. “I’m 32, have Hashimoto’s and an AMH of 1.5, and I want to start trying to conceive this year. Where should I begin?”

With Hashimoto’s, the first step is making sure your thyroid is well controlled and that you have a clear medication plan for pregnancy. I would review your thyroid function, including your TSH and thyroid antibodies, with the clinician managing your Hashimoto’s and discuss the type of thyroid replacement medication you are taking.

There are two primary thyroid hormones, T3 and T4. T4 is especially important during pregnancy because it crosses the placenta and supports the developing baby. If you take a combination medication, talk with your endocrinologist about whether the balance is appropriate for pregnancy, often patients need more T4 in pregnancy because this is what can help the baby. Since the fetal thyroid gland does not start working until 11 weeks, all fetal thyroid hormones comes directly from mom in the first trimester. Thyroid hormone requirements also rise quickly once you become pregnant, so this is not a conversation I would wait to have until after a positive test.

I would also recommend tracking ovulation. Thyroid disease can interfere with regular ovulation even when you are having periods, so use LH testing, basal body temperature, cervical mucus, or a combination of these methods to confirm what your body is doing. Your partner should complete a semen analysis as well.

This is exactly the kind of situation where a preconception appointment can be incredibly helpful. Your OB-GYN, reproductive endocrinologist, endocrinologist, or a maternal-fetal medicine specialist can review your medications, draw the appropriate labs, and create a plan before pregnancy. The last thing you want is to get pregnant and suddenly wonder what to do with your medications.

9. “I conceived my first child easily, but after having my IUD removed I had a miscarriage followed by two chemical pregnancies. Every time I get pregnant, it ends in a loss. What should I do?”

This is the point when I would recommend a complete fertility and recurrent pregnancy loss evaluation. We sometimes assume that because we had a baby before, or because we are still able to get pregnant, we do not need testing. Neither assumption is true. Secondary infertility is real, and recurrent loss deserves an evaluation even when a previous pregnancy was uncomplicated.

Certain conditions can develop or worsen over time. Endometriosis can create a significant inflammatory burden and contribute to infertility. Adenomyosis occurs when tissue similar to the uterine lining grows into the muscular wall of the uterus. It may cause heavy periods, but some women have regular cycles and do not recognize that anything has changed. Pregnancy, delivery, uterine procedures, and other events can also change the anatomy of the uterine cavity.

I have cared for patients who developed scar tissue inside the uterus after giving birth or after a pregnancy loss. They had no idea it was there, and it was contributing to infertility or pregnancy loss. In some cases, a relatively straightforward uterine surgery corrected the problem, but someone first had to look inside the cavity and identify it. This is why having a period, even a regular one, cannot be the only information we use to evaluate the uterus.

I would consider blood work, ultrasound, and a complete uterine cavity evaluation. After recurrent losses, genetic testing may also be appropriate. A karyotype is a blood test that looks at the chromosomes of both partners and can identify something called a balanced translocation.

I think about chromosomes like children standing in a kindergarten line. If two children switch places but everyone is still present and accounted for, the line may function normally. The problem can appear when we divide that line in half to create an egg or sperm. The groups may no longer contain the correct amount of genetic information, which can lead to pregnancy loss. A person with a balanced translocation can be completely healthy and may already have a healthy child, so previous success does not rule it out.

This is recurrent pregnancy loss and you deserve a full evaluation.

10. “I’m 32 and have been trying to conceive for eight months. My HSG and my husband’s semen analysis were normal, and my blood work was reassuring. Do you think IUI could be successful?”

When someone has regular ovulation, reassuring ovarian reserve, open fallopian tubes, and a normal semen analysis, we often use the diagnosis unexplained infertility. I prefer to think of it as undiagnosed infertility. Something is interfering with conception, but our current testing has not shown us exactly what it is.

Unexplained infertility is still an important diagnosis because we have studies specifically looking at treatment in this group. If you continue trying through intercourse alone after reaching this diagnosis, the chance of pregnancy may be approximately 4% to 5% per month. For someone your age without infertility, we would expect that monthly chance to be closer to 20%.

One treatment option is ovarian stimulation combined with IUI. Medication helps more than one follicle develop, and the IUI places prepared sperm higher in the reproductive tract. We are playing the odds: more eggs, more sperm, and a better starting position. I describe it as moving the players farther down the field so we have a better chance of lining up the shot.

That does not bring the monthly chance of pregnancy all the way back to baseline. In unexplained infertility, ovarian stimulated plus an IUI cycle improves pregnancy rate to about 8-10% chance. That means most individual cycles will still not result in pregnancy, but we have improved the odds compared with continuing the same thing indefinitely. IUI is also relatively low risk and less expensive than IVF, which makes it a reasonable first treatment for many people.

If you want to consider an IUI, I would try a limited number of properly stimulated IUI cycles, typically up to three, and then reassess. Continuing through six or more cycles can cost significant time, money, and emotional energy without continuing to offer the same benefit.

IVF is the more successful option because it allows us to control and observe many more steps. We can retrieve multiple eggs, fertilize them in the laboratory, watch embryo development during the first five days, consider genetic testing, and synchronize an embryo transfer with the uterine environment. IVF can sometimes overcome a problem we have not been able to diagnose because it removes or controls so many variables.

Whether IUI or IVF makes the most sense depends on how long you have been trying, how many children you hope to have, your ovarian reserve, your treatment goals, and how quickly you want to move. But yes, based on the information in this question, IUI is a reasonable option to discuss at your fertility appointment.

And in all scenarios, it is important to make sure we have done everything we can to really look into why you have infertility and think about what may be going on.

11. “Who is the best candidate for IUI?”

The clearest candidates are people who need donor sperm, including single women and same-sex female couples. If there are no other fertility concerns, placing donor sperm inside the uterus allows them to approach the expected pregnancy rate for their age and reproductive health.

IUI can also be a particularly good option for mild male-factor infertility when the primary issue is low motility. If the sperm are not moving quickly, placing them higher in the reproductive tract gives them a closer starting position. To return to the football analogy, if the players are slow, starting them at the 50-yard line may help.

That same strategy is less effective when the sperm concentration is very low or morphology is significantly abnormal. If there are not enough players on the field, or if the players are not capable of doing the job, moving them closer may not solve the underlying problem. IUI is not equally effective for every form of male-factor infertility, which is why the complete semen analysis matters.

12. “I’m 31 and have Hashimoto’s and a history of thyroid cancer with a total thyroidectomy and radioactive iodine treatment. I have been trying for six months since my IUD was removed. Should I be concerned?”

It is hard to answer this question without a complete evaluation, especially because your thyroid history adds another factor that deserves attention. At six months, you are reaching the point when fertility should be returning to its expected baseline after IUD removal. You could decide to continue trying for another six months, but you are also completely reasonable to gather more information now. I would want to review your thyroid function and medication, confirm that you are ovulating, evaluate your ovarian reserve if it has not been checked, assess the reproductive anatomy, and have your partner complete a semen analysis.

A fertility evaluation does not obligate you to start treatment. If everything is reassuring, you may decide to keep trying for another three to six months. You will have made that choice with real information rather than continuing to wonder whether you should be doing more.

If something is abnormal, you have the opportunity to address it and accelerate care. That is why I am always in favor of getting the data when a question like this is taking up significant space in your mind.

The bottom line

There is so much nuance in fertility medicine. If everything keeps coming back normal but you still do not have an answer, it may be time to look at the anatomy more closely, review what testing has actually been done, or get a second opinion.

Your time matters.

XO, Nat

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We talk about estrogen constantly (to be fair, estrogen is my favorite hormone), and I remember sitting with interviewing her for my podcast talking about hormones and the brain and she told me progesterone was her favorite hormone. I laughed at our different takes, but this stuck with me. A researcher who studies hormones and the brain, and she loves progesterone, maybe I should give it more of a chance.

Perhaps my reasons for not loving progesterone are my own pregnancy losses? Was my body unable to make the progesterone I needed when I was trying to conceive? Maybe we need to think about progesterone not as a second tier reproductive hormone, but as one of the most powerful signals your brain receives.

Today I am reviewing the science of progesterone as a brain hormone and why it matters throughout your reproductive life. Maybe you are trying to conceive, maybe you are avoiding pregnancy, maybe you are in perimenopause wondering what is going on.

There is a big difference in progesterone and progestins, and we can look at what happens in our brains with premenstrual dysphoric disorder (PMDD) as a great starting point.

Study: Neurosteroids and Premenstrual Dysphoric Disorder

Journal: The British Journal of Psychiatry

Read the Study

Why this study caught my attention:

We typically think about hormones as being high or low, forgetting that your hormones are a dynamic communication system in your body. They talk to organs, they respond, and a single level is typically not diagnostic. And one concept that I talk about a lot with my fertility patients is that lab values do NOT tell the entire story. You have your own internal reference range, determined by your brain. Learning to lean into your body, and how it feels, and learn what normal is for you.

This review asks that exact question: does the same hormone at the same level impact each woman differently?

This is especially important to me because I see women get dismissed for progesterone related symptoms all the time. Maybe it is PMS, PMDD, short luteal phase, recurrent pregnancy loss, perimenopause or sleep issues. Across the board, these complaints are often not taken seriously, are attributed to anxiety or over reacting, and yet there is a real mechanism behind what is happening that we deserve to understand so we can advocate for our health the best

So today I am reviewing:

• What progesterone actually does in your brain

• The relationship between PMDD, mood disorders, and hormones

• A breakdown of this study

• Recommendations for PMDD

• Recommendations for perimenopause

First, what progesterone actually does in your brain

Progesterone is not constantly available in your cycle. Most progesterone you make comes from the corpus luteum after ovulation. Remember that a follicle grows and egg, that follicle ruptures after ovulation, and then the same follicle reforms to become a corpus luteum—a progesterone producing cyst.

One big misconception is that progesterone is constantly produced, and it is not. Progesterone is made in pulses from the corpus luteum, stimulated directly from LH pulses from the brain. This means that after ovulation progesterone can range anywhere from 3-40 ng/mL. You can see that one difficulty with progesterone measurement is exactly that. How do you know if “enough” progesterone is released if it is made in pulses?

The second half of the menstrual cycle, the time after ovulation, is known as the luteal phase. Normal progesterone production and luteal phase length are important for implantation and conception. But beyond pregnancy you may not know that the luteal phase is giving you crucial details about your hormone health. In fact, a short luteal phase (<11 days in length) is the first sign of an ovulation disorder. Too often we think about ovulatory issues being a yes or no—you either ovulate or you do not. But in reality, ovulation is a spectrum and it can move from working perfectly through a variety of stages of dysfunction: starting with a short luteal phase, then a long follicular phase, irregular cycles, and eventually amenorrhea (no periods).

Luteal phase deficiency (LPD) is a clinical, and not a lab diagnosis. Having a short luteal phase or bleeding in the luteal phase are hallmarks of a LPD, but no blood level will tell us that the luteal phase is “normal” since blood progesterone levels fluctuate throughout your luteal phase. A luteal progesterone level is only helpful in confirming that you did ovulate, with a value of > 3 ng/mL being confirmatory that ovulation did in fact occur.

Importantly, this story changes with pregnancy. When a pregnancy makes hCG (the pregnancy hormone), hCG and LH bind to the same receptor and now progesterone is being constantly stimulated to be released (and at an increasing signal as hCG rises as the pregnancy progresses). One mistake people often use is looking at “normal” progesterone levels in early pregnancy and assuming mid-luteal progesterone should be the same.

Just because something is difficult to measure doesn’t mean it isn’t important. In addition to normal ovulation, progesterone is important in mood, brain function, and sleep via allopregnanolone.

When progesterone is made after ovation, a portion is converted into a compound called allopregnanolone which is what you really need to understand. Allopregnanolone acts on a receptor in the brain called GABA-A, which is the same receptor targeted by anti anxiety medications and alcohol. I want you to think about GABA being your nervous system’s main calming signal. When allopregnanolone binds to GABA-A it enhances the calming effect. This is why progesterone in the luteal phase can feel steadying and result in a better night’s sleep.

So if you’ve ever heard me say that progesterone is a “calming” hormone—this is what I mean. But what this study asked is if allopregnanolone crosses the brain and “calms” it then shouldn’t more of it be better and less of it be worse? But actually, that’s not what most people experience.

Allopregnanolone follows a biphasic curve: where at high concentrations it is calming and sedative but at lower or fluctuating levels it may actually do the opposite triggering anxiety, irritability and even low mood. This means the same molecule on the same receptor has different effects depending not only on dose but also on your own brain. This means two women can have the identical progesterone levels and different experiences based on how their GABA-A receptors respond, and this is important for you to understand.

In perimenopause, progesterone levels tend to fluctuate immensely due to the abnormal communication between the brain and ovary seen with a lower ovarian reserve. This means ovulation become abnormal—maybe happening earlier (you might see shorter cycles), maybe happening later (long cycles), or maybe you have irregular cycles and no clue when you are ovulating. These progesterone fluctuations become more severe—resulting in noticeable symptoms.

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AskNat The column where you ask and I answer like the doctor-friend you wish was in the room with you. Real questions from real women, straight from my inbox. General education, never a substitute for your own doctor.

Welcome friends-

This week most of the questions are about hormones beyond fertility. As always, these are real questions from your submissions, cleaned up so no one is identifiable, and answered the way I would if you were sitting across from me. I will tell you what the science says, where the science is thin, and what I would want my own sister to know. None of this is personal medical advice, because I am not your doctor and I have not seen your chart. But you deserve to understand your body, and that is what we are here to do.

For a limited time, AskNat is open to all subscribers as a free trial but it will soon be a paid subscriber only offering. Only paid subscribers can ask questions, upgrade now.

Questions answered this week:

1. “I’m 46. My hot flashes are getting worse and my cycles are shorter, and my weight and blood sugar are creeping up even though nothing about how I eat has changed. Is this perimenopause, and are these connected?”

2. “A wellness clinic ran a hormone panel, told me I have ‘estrogen dominance,’ and put me on compounded progesterone and testosterone creams. Is that a real diagnosis?”

3. “I’ve been exhausted for a year, my hair is thinning, I’ve gained weight, and my periods are heavier. Everyone says it’s stress. How do I know if it’s my thyroid, and what should I ask them to test?”

4. “How long should we actually try before getting help? I keep hearing ‘a year,’ but I’m 37 and don’t want to waste time.”

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1. “I’m 46. My hot flashes are getting worse and my cycles are shorter, my weight and blood sugar are creeping up even though nothing about how I eat has changed. Is this perimenopause, and are these connected?”

Yes, this sounds like perimenopause, and yes, those things are connected, more than you have probably been told.

Perimenopause is the stretch of menstrual changes as your egg count winds down, and it has a classic evolution: cycles first get a little shorter with earlier ovulation, then longer with later ovulation, then irregular and skipping, and eventually they stop. It can last anywhere from two to ten years, and here is the part most women are never told: the hormone shifts and symptoms begin while you are still getting periods (and specifically while your periods are still regular). So you do not have to have stopped cycling to be in it. Shorter, less predictable cycles plus worsening hot flashes at 46 yo this squarely.

Estrogen is not only a reproductive hormone, it is a metabolic one. It helps your cells respond to insulin, helps your muscle pull sugar out of your blood, and keeps fat from settling around your organs. As estrogen declines through perimenopause, insulin resistance tends to rise, and the long-term data show it rises independent of aging and independent of your habits. That is why your weight and blood sugar can drift even when nothing about your eating changed. It is not a willpower failure. It is a hormone shift. And there is striking new research suggesting your metabolism and your hot flashes are part of the same story: higher insulin around this age has been linked to earlier and longer hot flashes, even independent of body weight.

So here is what I would do. Track your cycles now, because it flags the subtle changes early and buys you time. Ask for the metabolic labs (a fasting insulin and glucose, lipids, and A1c), plus a thyroid panel (including thyroid antibodies), since thyroid can mimic all of this. Pull the levers that actually move insulin: protein and fiber at meals, strength training, and real sleep. And treat hormone therapy as a genuine, evidence-based conversation, for your symptoms and, as a bonus, your metabolism. You are not falling apart, and it is not in your head.

2. “A wellness clinic ran a hormone panel, told me I have ‘estrogen dominance,’ and put me on compounded progesterone and testosterone creams. Is that a real diagnosis?”

This one frustrates me because “estrogen dominance” is not a real, defined medical diagnosis (and often patients are mistreated because of this!). This is a marketing phrase, not a condition with agreed-upon criteria, and it is very often used to sell you compounded creams from the exact clinic that just diagnosed you.

Here is why the panel misled you: your hormones swing dramatically across a single cycle, by design. A one-time blood draw is a snapshot of a moving target, so an estrogen or progesterone number means almost nothing unless we know precisely where you were in your cycle when it was drawn. “High estrogen, low progesterone” is literally the normal state in your follicular phase and is perfectly normal. Labeling that “dominance” is like taking a photo of a wave and diagnosing the ocean.

And the treatment is not the harmless “balancing” it is sold as. Compounded progesterone and testosterone can suppress ovulation. I have seen a woman put on progesterone and testosterone cream for “estrogen dominance” who was, in effect, handed a form of birth control by the very clinic promising to help her hormones, and whose partner was started on testosterone “for fatigue,” which can shut down his own sperm production. The treatment can quietly cause the problems it claims to fix. That story is in my book for a reason.

None of this means hormones do not matter or that real conditions do not exist.

Thyroid disease, PMOS, perimenopause, hypothalamic dysfunction, and a true luteal phase progesterone issue are real, and we diagnose them with properly timed testing interpreted against your symptoms, not a single scary panel with a cream attached. My rule of thumb for you: be very skeptical of any place that diagnoses you and sells you the treatment in the same visit.

3. “I’ve been exhausted for a year, my hair is thinning, I’ve gained weight, and my periods are heavier. Everyone says it’s stress. How do I know if it’s my thyroid, and what should I ask them to test?”

“It’s just stress” is what a lot of women hear right before a real, treatable diagnosis gets missed. Your cluster of symptoms is a classic thyroid picture.

Your thyroid sets your metabolic thermostat. In hypothyroidism, an underactive thyroid, your whole metabolism slows down, and that produces almost exactly your list: fatigue, weight gain, hair thinning, and heavier or more irregular periods. The most common cause is an autoimmune condition called Hashimoto’s, where the immune system gradually dials down the gland.

For your thyroid, the most sensitive early sign is an elevated TSH, sometimes even when your actual thyroid hormones (T3 and T4) still read in the normal range. TSH is essentially your brain shouting louder to squeeze more hormone out of a struggling gland, so it rises first. That means a “normal T4” by itself does not rule this out, and you want the TSH specifically.

So what to ask for: a TSH], a free and total T4, T3, and thyroid antibodies (TPO and TG) to check for Hashimoto’s.

You should also ask for a ferritin, because iron deficiency causes its own fatigue and hair loss, and a vitamin D, since deficiency is common and adds to fatigue. If it is your thyroid, the good news is that it is very treatable, usually with a single daily thyroid hormone, and treatment often reverses the symptoms you have been told to just live with.

4. “How long should we actually try before getting help? I keep hearing ‘a year,’ but I’m 37 and don’t want to waste time.”

I have been pushing back on the trying to conceive for a year narrative before getting testing for a while. I understand that recommendations have to come from some place, but this delay in testing doesn’t help most people.

Infertility is technically defined as not conceiving after twelve months of regular, unprotected sex. But that number was built around younger couples, and it is a starting point, not a universal law. In fact, this is the longest you should try before getting an evaluation: under 35, twelve months of trying before an evaluation is reasonable. From 35 to 39, get evaluated after six months. At 40 or older, do not wait, seek help right away or after just a cycle or two. At 37, that puts you at about six months, and there is genuinely no harm in a preconception check-in now.

My personal recommendation (and preference), would be for everyone to get testing before they conceive. Why should you have to try and fail before you find out your tubes are blocked? or your partner has no sperm? or that your egg count is low? I have sat across from too many women who wish they could get this time back and make difference decisions.

And do not wait the full window, at any age, if there are red flags: irregular or absent periods, known PMOS or endometriosis, prior pelvic surgery or infection, a history of miscarriage, or any known concern on the sperm side.

Two things to hold onto. Most couples who will conceive do so within the first six months of trying, so seeking care is not panic, it is just refusing to lose months you cannot get back. And an evaluation is not a fast track to IVF. It is confirming that you ovulate, that your tubes are open, and a semen analysis, because it takes two. Simple testing that either reassures you or finds something fixable. You should not have to fail for a year before someone is willing to look.

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Before you go

If one of these gave you language for your next appointment, that is the whole point. So much of what scares us about our bodies is really just information no one ever sat down and explained. None of us should have to fail before we understand our own bodies, and none of us should have to figure it out alone at midnight with a search bar.

XO, Nat

Paid subscribers can submit questions below to have them answered in AskNat.

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Here’s what I think really happened. Women have been asking good, specific questions about their bodies for decades, and too many of us walked out of appointments without a real answer. When the medical system doesn’t give you the information you need, you go looking for it somewhere else. Social media rushed into that gap. Some of what it surfaced was overdue and important. A lot of it was fear dressed up as education.

You don’t need blind reassurance and you don’t need scary headlines. You need the honest version, with the actual numbers and the actual nuance, so you can decide what’s right for your body. That’s why I wanted to have this conversation, and I wanted to have it with someone I trust to hold the same standard.

This week, I sat down with Dr. Fran Haydanek, a board-certified OB/GYN, residency faculty member, and one of the most trusted physician voices in women’s health on social media. Together, we tackle the biggest birth control myths and viral hormone claims, separating what’s supported by evidence from what’s misunderstood, oversimplified, or simply untrue. Our goal wasn’t to talk you into the pill or out of it. It was to give you what we think every woman deserves before she makes that decision for herself.

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Does the pill treat PMOS (formerly PCOS), or does it only mask it?

You’ve probably seen the claim that the pill doesn’t treat PMOS, it only masks it. There’s a grain of truth in there, and it’s almost always stated without the context that makes it useful.

The pill doesn’t cure PMOS. Nothing does, because there’s no single medication that fixes every piece of it. But “doesn’t cure” is not the same as “does nothing.” If you’re not ovulating regularly, your uterine lining can keep building without shedding the way it should, and over time that matters for your long-term health. Birth control protects that lining by creating predictable, scheduled bleeding. It can also lower androgen activity, which is what’s driving the acne and the excess facial or body hair for a lot of women with PMOS. Those are real medical benefits, not a magic trick.

What the pill doesn’t do on its own is address the insulin resistance, the metabolic piece, the inflammation, the sleep, the nutrition, or every underlying reason you’re not ovulating. So the honest answer is the one in the middle. The pill can genuinely treat certain parts of PMOS while other parts still need their own evaluation and care. Symptom management isn’t fake, and it isn’t the whole story either. What’s right for you depends on your symptoms, your health risks, and whether you’re trying to prevent pregnancy, control bleeding, or conceive.

Does birth control ruin your hormones?

Hormonal birth control changes your hormone signaling. That’s not a side effect, that’s the mechanism. The pill quiets the conversation between your brain and your ovaries that normally leads to ovulation, so while you’re on it, you’re not running a typical ovulatory cycle. None of that means your hormones are permanently ruined.

The medication itself clears your system fast. The pill has a half-life of roughly 28 hours. Your body does not need a cleanse, a detox tea, a liver supplement, or a several-hundred-dollar protocol to get rid of it. It’s already gone.

What actually happens for a lot of women after stopping is that their symptoms come back. Maybe you started the pill for irregular periods, acne, painful or heavy cycles, or signs of PMOS. It controlled those things for years. When they return, it feels like the pill caused the problem. In most cases it didn’t. It was managing a condition that was there the whole time and got quiet while you were on it.

This is exactly why I’m careful with the phrase “post birth control syndrome.” The symptoms are real. I believe you. But the explanation matters, and “the pill caused this problem so I need a detox” is usually not it. The better move isn’t a cleanse. It’s to ask why the symptoms are showing up and whether there’s an underlying condition that finally deserves a name. Not in your head, and worth actually diagnosing.

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When should you stop the pill before trying to conceive?

For most people, there’s no medical rule that you have to wait several months after stopping the pill before you try. You can ovulate and conceive soon after you come off it.

But “you don’t have to wait” isn’t the same as “wait until the exact month you want to be pregnant.” Coming off a little earlier gives you something valuable: a look at what your natural cycle is actually doing. Are you ovulating consistently? Are your cycles landing in a normal range and staying reasonably consistent? Is your luteal phase long enough, meaning at least around 11 days? Are signs of PMOS, thyroid disease, or hypothalamic dysfunction becoming visible now that the pill isn’t smoothing everything over?

Stopping earlier also buys you time to fix a problem before a pregnancy timeline is bearing down on you. That’s especially true if the reason you started the pill in the first place was irregular cycles. The pill can hand you predictable bleeding, but scheduled withdrawal bleeds tell us nothing about whether you’ll ovulate on your own once you stop. The right timing here depends on your method, your history, and how soon you want to be pregnant. I usually recommend at least 3-6 months yo be able to detect your cycle, learn to track, and identify any problems early. If you did not have any periods (continuous pill use or the progestin-IUD), then I recommend stopping 6 months before you want to conceive to allow for endometrial recovery and cycle tracking.

Does birth control cause infertility?

For the overwhelming majority of people, no. Once you stop hormonal contraception, the signaling between your brain and ovaries starts coming back. How fast ovulation returns varies by person and by method. Infertility is defined as failure to conceive at 12 months of trying, and no option has been show to increase the risk of infertility in the general population.

Exceptions may include Depo-Provera shot and the progestin IUD. The Depo-Provera shot, which can delay the return of ovulation for up to 18 months after your last injection. That delay isn’t permanent infertility, but it’s absolutely something to factor in when you’re deciding when to stop. Long-term progestin IUD use hasn’t been studied, and recent data shows an association with a higher risk of intrauterine adhesions. Although the overall risk is still low, this is something to consider if you do not conceive after stopping. As a fertility doctor, this is one thing that I take seriously and I like to see patients remove their IUD 6 months before conceiving so we can evaluate cycle regularity, flow, and consider an earlier identification of problems if things seem off. All of that said, as Dr. Fran points out, you can conceive the cycle you stop contraception, so always make sure you are making the decision best for you.

And let’s put another myth to rest: the pill does not “save” your eggs. Your ovarian reserve declines over time no matter what you’re doing, whether you’re ovulating, pregnant, breastfeeding, or on contraception. The pill stops you from ovulating a dominant follicle each month, but it does not stop eggs from leaving the resting pool and being lost along the way. It doesn’t destroy your fertility, and it doesn’t freeze your reproductive age in place either. Both of those are stories, not physiology.

Can birth control affect fertility testing or egg freezing?

Here’s a nuance that trips people up. Birth control doesn’t cause infertility, but it can absolutely change what a fertility doctor sees on a given day. Because hormonal contraception suppresses ovarian activity, it can lower your AMH, reduce the number of small follicles visible on ultrasound, and affect how your ovaries respond during an egg freezing cycle. That’s a snapshot being altered, not your real reserve.

The practical takeaway: if you’re considering egg freezing or fertility testing, tell your doctor exactly what type of birth control you’re using and how long you’ve been on it. That’s what lets them decide whether to test now or whether a stretch off contraception would give you a clearer picture. One AMH on a suppressed cycle does not define your reserve, your future, or your worth.

What do the Depo-Provera brain tumor headlines actually mean?

Seeing “birth control” and “brain tumor” in the same headline is frightening, and I understand why the fear arrives faster than the math. So let’s slow it down.

The concern is about meningioma, a tumor that grows from the tissues surrounding the brain and spinal cord. Most meningiomas aren’t cancerous, but depending on size and location they can still cause real problems, so this is a fair thing to discuss. What you can’t do is understand your risk from a headline.

To actually make sense of a number like this, we have to look at the baseline odds of the outcome in the first place, how much the absolute risk changes, how long the medication was used, and how all of that stacks up against the benefits and the alternatives. A relative increase can sound enormous while the absolute number of women affected stays very small. That doesn’t make the risk meaningless. It means you deserve the real context, so your decision comes from information instead of adrenaline.

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Patients changed the conversation about IUD pain

For years, women were told IUD insertion would feel like a quick pinch. For some women, that’s accurate. For plenty of others, it’s intensely painful. Both of those are true at the same time, and for a long time medicine only acknowledged the first one.

Women talking openly about what insertion actually felt like is the reason the field is finally rethinking how we counsel patients and what pain management we offer. That’s not misinformation. That’s patients spotting a gap before the system was ready to admit it existed. The right response was never to wave away women’s experiences. It’s to listen, take it seriously, investigate it, and then separate what happened from any shaky explanation that got attached to it. You deserve to know what to expect before an insertion, and you deserve to talk through your options for managing the pain and choose what feels right for you.

Permanent contraception should be treated as a real decision

Dr. Fran became (even more) internet famous when she created a list of physicians who would help you achieve permanent contraception even if you did not have children.

A salpingectomy removes the fallopian tubes and should be considered permanent. If both tubes are gone and you later want to be pregnant, you’d generally need IVF, because the egg and sperm no longer have a way to meet. Removing the tubes may also lower the risk of certain ovarian cancers, since many cancers we used to think started in the ovaries are now believed to begin in the fallopian tubes.

This isn’t a decision to make casually. You should understand the permanence, the surgical risks, the alternatives, and the future reproductive implications. But you’re also an adult with the right to make decisions about your own body. Good counseling helps you make an informed choice. It does not put up arbitrary walls based on your age, your marital status, or someone else’s guess that you might change your mind.

Is estrogen dominance real?

“Estrogen dominance” has become the catch-all explanation for heavy periods, weight gain, mood swings, breast tenderness, fatigue, brain fog, and infertility. The trouble is that your hormones don’t work in isolation, and they don’t sit still. Estrogen rises and falls across the cycle. Progesterone rises after ovulation. What any single hormone result means depends entirely on when it was drawn, whether you ovulated that cycle, what symptoms you have, and what else is going on in your body.

A tidy label can feel like relief, especially after years of being told your symptoms were normal and being sent home. I get the appeal. But a label can also end the investigation right when it should be starting. The same problem applies to “adrenal fatigue.” Your exhaustion is real, but adrenal fatigue isn’t a diagnosed disorder of the adrenal glands. Fatigue has a long list of real causes we can actually test for: poor sleep, iron deficiency, thyroid dysfunction, metabolic disease, chronic stress, undereating, depression, autoimmune disease, and more. Before you buy supplements for a condition you were diagnosed with on your phone, ask whether your symptoms have actually been worked up.

What is the Dutch test?

The Dutch test uses dried urine samples to measure hormones and their metabolites at several points, and it’s marketed as a more complete window into cortisol, estrogen, progesterone, and the rest. I understand why it’s appealing. When you’ve had symptoms for a long time and standard testing hasn’t explained them, a thick, detailed report feels like someone is finally looking hard enough.

But more data isn’t the same as better care. A test can measure something accurately without that measurement explaining your symptoms, and it can generate an impressive report without changing your treatment or improving your health. The Dutch test also tends to run hundreds of dollars out of pocket, and the results often lead to more supplements, more repeat testing, and protocols that aren’t backed by strong evidence.

Most OB/GYNs don’t order it routinely because its clinical usefulness hasn’t been established for a lot of the claims made about it. That doesn’t make every number on it meaningless but checking serum levels is cheaper and more valid. For the Dutch test, I would skip.

Book the appointment you actually need

An annual wellness exam is built for preventive care. Depending on your age and history, that might mean a Pap, a breast exam, screening recommendations, contraceptive counseling, and a general check-in. What it usually isn’t built for is a deep evaluation of months of pelvic pain, abnormal bleeding, fatigue, or a complicated medication concern. When you bring a long list of real problems to a short preventive slot, you can walk out feeling dismissed, your doctor feels rushed, and the thing that mattered most to you never got addressed.

So sometimes the most powerful sentence you can say is, “I’d like to book a separate appointment to work up this problem.” I wish our system made this easier, and I hope it will. But in the system we’ve actually got, booking the right type of visit changes how much time, testing, and follow-up your concern gets. That’s not a workaround. That’s you advocating for yourself effectively.

The bottom line

Women didn’t become skeptical of birth control out of nowhere. Too many were handed a prescription with no real explanation. Too many had side effects brushed off. Too many felt dismissed when their experience didn’t match the reassurance they were given. That skepticism is earned, and I take it seriously.

But swapping one oversimplified story for the opposite one doesn’t get you better care. Birth control isn’t harmless for every single person, and it isn’t toxic for every single person. It doesn’t cure every hormonal condition, but it can meaningfully treat certain symptoms. It doesn’t create every problem that shows up after you stop it. It doesn’t destroy your fertility, it doesn’t preserve your eggs, and it doesn’t require a detox. It can be the right tool, the wrong tool, or one piece of a bigger plan, and which one it is depends on you.

The point of this episode isn’t to talk you into birth control or to scare you off it. It’s to give you enough real information to ask sharper questions and make a decision that fits your body, your health, and your plans. You can handle the nuance. You should not have to fail, or be frightened, before you understand your own body, and you deserve care and health education that believe that too.

XO, Nat

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This week’s guest: Dr. Fran Haydanek, is a board-certified OB/GYN, residency faculty member, and physician educator known for making complicated women’s health topics accessible and evidence-based.

If this helped you better understand birth control, share it with someone you think would benefit. Listen to the full episode of the As a Woman podcast wherever you get your podcasts—listen now on Spotify or Apple.

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A new study published in early 2026 went looking for the answer in a specific place: the energy chemistry inside the cells of the ovary. Researchers compared the support cells that feed the egg in younger women versus women over 35, measured their metabolism directly, and found something clean and striking. The aging ovary shifts how it makes energy, losing the efficient energy making factory.

This week I’m breaking that study down in plain language, then using it to make sense of the supplements you’re being sold: the real CoQ10 evidence, and the NAD+ and NMN hype showing up in IV bags and pricey clinics. What’s proven, what’s promising, and what’s just a beautifully marketed drip.

Study: Age-related mitochondrial energy metabolism reprogramming occurs in granulosa cells during ovarian aging

Journal: Frontiers in Endocrinology

Read the Study

Why this study caught my attention:

A mature egg is the largest cell in your body and one of the most energy-hungry cells. When it resumes maturation and lines up its chromosomes to split them evenly, that job is astonishingly energy-intensive. It runs on ATP, the cell’s energy currency, and that ATP is made by mitochondria, the tiny power plants packed inside the egg and inside the cells that surround it.

An egg carries more mitochondria than almost any other cell you have.

So when we say “egg quality,” a huge part of what we’re really talking about is power. Does the egg have clean, abundant energy at the exact moment it needs to do the hardest thing it will ever do?

This new study, published in Frontiers in Endocrinology in early 2026, went after that question in real women. That’s why it caught my attention. Not a mouse or in vitro study, but actual ovarian cells, from actual women, at different ages, with the energy chemistry measured directly.

So today I am reviewing:

• What’s actually happening inside an egg

• Why the granulosa cells matter

• A breakdown of this study

• What prior research showed

• What you should do with this information

First, what’s actually happening inside an egg

Did you know that your eggs are frozen in a state of meiosis (cell division) since before you were born? Every egg you have was frozen partway through cell division while you were still a fetus inside your own mother. It sits there, mid-step, for decades. Then, in the cycle it’s finally called up, it has to wake up and finish a division it started twenty or thirty or forty years ago.

That finishing step is the most important. The egg has to pull its chromosomes apart and sort them into exactly the right number, no extras and no missing pieces. When we get it right, you have a genetically normal egg. But when things go wrong, you get an egg with the wrong chromosome count, which is the single biggest reason older eggs lead to failed cycles and miscarriage.

This is the machinery behind the numbers I’m always quoting: roughly 65 percent of embryos are genetically normal at 35 and under, closer to 40 percent by the late 30s, around 20 percent by the mid-40s. That decline is, at its core, a story of an aging egg struggling to sort its chromosomes cleanly.

Building the meiotic spindles that separate the chromosomes, then pulling them apart evenly, burns an enormous amount of ATP in a very short window. Which brings us to the mitochondria. Your egg is packed with more mitochondria than any other cell in your body, hundreds of thousands of them, because it needs a massive power reserve on hand for that one moment.

But, the egg largely runs on the mitochondria it already has, and those mitochondria have been sitting inside it, aging right along with you, the entire time. The power plants are getting older and more run down over time—impacted by inflammation, fibrosis, and other ovarian changes seen with aging.

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I know that feeling personally. I’ve had four pregnancy losses, including an ectopic pregnancy, so when a patient sits across from me and asks how long she has to wait, I know she isn’t really asking about a calendar. She’s asking whether her body is okay, and whether she’s allowed to hope again.

Most people don’t realize there are several different types of pregnancy loss, and each one comes with a different answer about trying again. So let’s go through them one at a time, and I’ll tell you what has to happen before you can start trying after each.

Watch the full breakdown here:

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A chemical pregnancy

You ovulated, the egg was fertilized, an embryo formed, and it started to implant. We know it implanted because you got a positive pregnancy test, and hCG (the pregnancy hormone we detect on a pregnancy test) is only made by a pregnancy. Then the level dropped and you started bleeding, before you ever reached six weeks or saw anything on ultrasound. This is called a chemical (or biochemical) pregnancy loss.

I am so tired of people being told a chemical pregnancy doesn’t count. It absolutely counts. You were pregnant, you proved it with a pregnancy test. You had a pregnancy loss. It was just very early. This idea was propagated because ASRM previously said that chemical pregnancy losses didn’t “count” in the evaluation of a recurrent pregnancy loss (RPL). After experiencing a chemical loss myself, I’ll tell you that they do count, I’ve always counted them in my patient’s reproductive history and in the evaluation for RPL, and finally ASRM has changed their recommendations (see later in this article for those details).

What does a chemical pregnancy loss do to your cycle? This one surprises people. hCG talks back to your brain and stops it from sending out FSH, which is the hormone you need to grow a follicle. So while hCG is present, you won’t ovulate.

Say you were pregnant for a week and then started bleeding. That week acted like a pause. The moment hCG drops and the bleeding starts, your brain is released from suppression, FSH goes back out, and a new follicle starts growing almost immediately. Your cycle stays in the same four week rhythm, it’s just shifted. If you always got your period the first week of the month, now it lands in the second. Nothing is broken. The clock just moved.

This is also why a chemical pregnancy can be mistaken for a late period if you aren’t testing. Back before urine tests could detect such low levels, this was often written off as a cycle that ran five weeks instead of four. If you notice sore breasts, nausea, sensitivity to smell or taste, food aversions, or extreme fatigue, take a test. You deserve to know what’s happening in your own body.

When you can try again? Immediately.

I don’t make my patients wait at all after one chemical pregnancy loss and no additional testing is required. In fact, the early pregnancy loss study, a landmark New England Journal of Medicine paper, showed a higher rate of pregnancy in the cycles immediately after a loss.

The exception is if you’ve had two or more losses, even if every one of them was a chemical pregnancy, you qualify for a recurrent pregnancy loss evaluation. More testing is needed.

A spontaneous miscarriage

The pregnancy was seen on ultrasound, and then you started bleeding and passed the pregnancy without medical intervention. The bleeding might feel like a heavy period, maybe a little clottier. Your symptoms fade afterward and your hCG drops. The further along you were, the higher your hCG was, and the longer it takes to resolve.

When you can try again? Once your pregnancy test is negative.

Sometimes small remnants of placental tissue are left behind. Those remnants keep making hCG, and they are highly inflammatory inside the uterus, potentially resulting in scar tissue. We don’t want to take a bad situation and compound it by adding a uterine factor on top of it so it is important to make sure hCG drops to zero (your pregnancy test is negative).

That negative test usually comes within four to six weeks, and your period tends to arrive right around the same time. Then you can start trying. I don’t require a normal cycle in between but I want a negative pregnancy test.

If you’re still testing positive at six weeks out, tell your doctor, even if you’ve had bleeding or something that looked like a period. That warrants a blood hCG and possibly an ultrasound and/or saline sonogram to check for retained products of conception, and it means waiting to try until we sort it out.

A missed miscarriage

For a missed miscarriage, you had a positive pregnancy test and were further along in the pregnancy to have it confirmed intrauterine on ultrasound. But then the pregnancy stopped developing, resulting in a loss, but without any bleeding. You go in for an ultrasound and find an empty sac, which may be called a blighted ovum or an anembryonic pregnancy, or a pregnancy that stopped growing, or a pregnancy with no heartbeat.

This is where we have to make a decision. We can wait and hope your body passes the tissue on its own. If it does, great. If it doesn’t, we need to intervene, because a pregnancy that’s no longer growing inside your body can lead to a septic miscarriage, which is an infected pregnancy loss. An infection inside the uterus is a breeding ground for destruction of the functional layer of the endometrium, and that means scarring.

Options for treatment:

Misoprostol (Cytotec) drops your progesterone and causes the uterus to cramp and expel the pregnancy. I’ll be blunt—I don’t love this option. I’ve had it, and I do prescribe it, but the cramping is intense, and it can cause nausea, vomiting, and severe pain. If you choose it, clear your calendar, stay home, and have someone with you. If you have heavy bleeding that won’t stop, that’s an incomplete miscarriage and it’s an emergency. Call your doctor or go to the ER.

Misoprostol also doesn’t always work completely. You still need to follow for a negative pregnancy test, and if you needed more than one round of misoprostol to excel the pregnancy or to remove retained placental tissue, you have a risk for uterine scaring. Needing 2 or 3 rounds is always a red flag for me and I would want you to ask about a saline sonogram afterwards.

A D&C is an aspiration procedure using suction. Very early pregnancies can often be done in the office with a cervical block while you’re awake or in the operating room with light anesthesia. It is a quick procedure, and it typically drops hCG faster and involves less overall bleeding than misoprostol.

No procedure is without risk. A D&C carries a small risk of perforation or scar tissue, though that’s less common now that we use suction instead of sharp instruments, and much less common outside of an emergency. Most D&Cs after a loss will not predispose you to scarring. I’ve had one myself, and I preferred it to misoprostol both mentally and physically. But this is your choice, and both options should be offered to you when both are appropriate.

When you can try again: negative test, plus a look inside your uterus. Here’s my extra layer of caution. If you needed misoprostol or a D&C for any reason, even if this was your first loss, I want a saline sonogram before you try again. I want to confirm the cavity has healed, that there’s no retained tissue or scar tissue, and that there isn’t something structural that contributed to the loss in the first place.

My recommendation is that if one round of misoprostol didn’t work, consider just proceeding with definitive treatment with a D&C. Ultimately, this is an individualized choice and you should discuss with your doctor what makes sense for you.

Once you have a negative test and a normal cavity, everything resumes as it did before. Ovulation comes back. None of this causes long term harm unless scarring developed.

A second trimester loss or beyond

Losses later in pregnancy carry more risk to the uterus. If you went into pre-viable labor and needed a manual extraction of the placenta or a D&C at that stage, scarring is more likely, because the placenta had invaded more deeply.

When you can try again? Negative pregnancy test and ask for a saline sonogram. This is a circumstance where I’m conservative. I would rather look and feel good about it than assume things are fine and deal with infertility later. If your doctor doesn’t suggest a saline sonogram and you fit this picture, ask. It’s worth advocating for.

An ectopic pregnancy

An ectopic pregnancy is one that is outside the uterus, usually in the fallopian tube. These are non-viable, and they can become an emergency of early pregnancy, because a tube that gets big enough can rupture. That causes intense abdominal pain and heavy internal bleeding, and it can mean urgent surgery to remove or repair the tube.

Sometimes we can trend levels and wait, but only with very close medical management. Otherwise it’s methotrexate or surgery, depending on the location, the size, and the surgeon.

Methotrexate is a folic acid antagonist. Folic acid drives cell division in early pregnancy, so blocking it stops the pregnancy from progressing. You have to follow it closely with hCG at four and seven days to make sure it’s working, and this part matters: you can still rupture a tube even after receiving it.

When you can try again after methotrexate? You must wait 3 months. This is the one real waiting period in the whole list. Methotrexate can stay in your system for up to three months, so we pause for three months regardless of how quickly your hCG returns to zero.

I’ve had methotrexate. It’s not fun. It felt like getting hit by a truck, which honestly surprised me, because I hadn’t fully appreciated how much it affects every cell in your body. But this wait time is important and real.

But I’ll tell you what those three months became for me. I used them to get as healthy as I possibly could, not as some strategy to get pregnant, but to take charge of a situation that had taken all my control away. That’s when I started learning about inflammation and insulin resistance. That’s when I changed my lifestyle. And that’s ultimately what led to me getting pregnant. Sometimes a forced pause turns out to be the thing you needed.

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What the new ASRM guidance says about RPL

If you’ve had more than one loss, then you should know that in June 2026, the American Society for Reproductive Medicine updated its guidance on recurrent pregnancy loss for the first time since 2012, and it moves in a direction I’ve been advocating for in this exact conversation.

A few things stand out. ASRM confirms the threshold is two or more losses, and it says those losses do not have to be consecutive to warrant an evaluation. It explicitly recognizes very early losses confirmed by a blood or urine test, which is the chemical pregnancy loss I refuse to let anyone dismiss. It recommends chromosome testing of the pregnancy tissue when possible as a first step, because knowing whether a loss was genetic changes everything about what comes next. It recommends evaluating the uterine cavity, which is the saline sonogram I keep asking you to advocate for. And it recommends screening for treatable conditions like thyroid disease and diabetes, while steering away from tests and treatments that sound appealing but don’t have evidence behind them.

The guidance isn’t perfect, and there are till some testes that I think are important—testing for insulin resistance (fasting insulin) and not just diabetes or autoimmune testing, especially for autoimmune thyroid disease (thyroid antibodies and a full thyroid panel), and testing for endometriosis and andenomyosis, for example. I still believe RPL needs a full evaluation offered and discussed, with individualized testing and treatment. But this is certainly a step in the right direction.

Even with recurrent loss, and often without any intervention at all, ASRM notes that 50 to 80 percent of patients go on to have a successful pregnancy. Two losses does not mean your body has failed you. It means you’ve earned a real workup and real answers.

Bring these questions to your appointment

• What type of pregnancy loss was this?

• Is my hCG confirmed back to zero or negative?

• Did I need any management, and if so, should I have a saline sonogram before we try again?

• I’ve had two or more losses. Can we start a recurrent pregnancy loss evaluation, including chromosome testing of the tissue?

• If I’m choosing between misoprostol and a D&C, are both appropriate for me?

The bottom line

Unless you had an ectopic pregnancy treated with methotrexate, you don’t have to wait a set amount of time. You need a negative pregnancy test, and if your miscarriage needed management, you need to know your uterus has healed. That’s it. Not a magic number of cycles.

I know that a pregnancy loss makes you doubt your own body, your future, and everything you had pictured for yourself. Please don’t carry it alone. Find one person you can be fully honest with, and find a provider you trust to answer your questions and explain why any of this may or may not apply to you.

I see you. I am you. Huge hugs.

XO, Nat

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AskNat The column where you ask and I answer like the doctor-friend you wish was in the room with you. Real questions from real women, straight from my inbox. General education, never a substitute for your own doctor.

Hi friends!

Welcome to round 2 of AskNat. As always, these are real questions from your submissions, cleaned up so no one is identifiable, and answered the way I would if you were sitting across from me. I will tell you what the science says, where the science is thin, and what I would want my own sister to know. None of this is personal medical advice, because I am not your doctor and I have not seen your chart. But you deserve to understand your body, and that is what we are here to do.

For a limited time, AskNat is open to all subscribers as a free trial but it will soon be a paid subscriber only offering. Only paid subscribers can ask questions, upgrade now.

Questions answered this week:

1. “Is it ok to if my multivitamin has biotin in it?”

2. “Could you do an ideal ‘what to eat in a day’ for someone TTC, and maybe foods to really avoid during this stage?”

3. “Can you speak on the data behind acupuncture and fertility outcomes?”

4. “Should I take myo-inositol for PCOS (PMOS)?”

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1. “Is it ok to if my multivitamin has biotin in it?”

Biotin is vitamin B7, an essential nutrient, and 30 mcg is right around the normal daily intake. At that dose it will not harm you and having it in a prenatal is standard. So the amount in your bottle is a non-issue.

The concern with biotin is not safety but that doses over 300 mcg interfere with common lab tests. Biotin can bind the lab assay and cause false high or low results (each hormone responds differently). This can mean if we are checking your hormones, monitoring your thyroid, The “hair, skin, and nails” and beauty supplements often contain 5,000 to 10,000 mcg, which is a few hundred times what is in your prenatal, and at those levels biotin can skew results on assays that use it in their chemistry. That includes many hormone tests that we rely on. You can end up misdiagnosed, retested, or worried for no reason, and the culprit is a supplement no one thought to mention.

I recommend staying under 300 mcg of biotin a day (the amount in a prenatal is typically lower than this). Sneaky places are hair, skin, and nails (or any beauty supplement) and greens powders and collagen products. If you are taking high-dose biotin supplement, tell whoever is ordering your bloodwork, and it is generally recommended to stop it a week before getting bleed drawn so your results can be accurate.

2. “What should a ‘day of eating’ look like for TTC, and what should I avoid?”

No single food that makes or breaks conception. What actually moves the needle is the overall pattern, and the one with the most support is anti-inflammatory and looks a lot like a Mediterranean way of eating. The goal with your nutrition is to decrease inflammation and improve insulin sensitivity. The truth is that this is the healthiest dietary pattern throughout our entire life.

Insulin resistance is one of the most common and most fixable drivers of ovulation problems (it is central to PMOS, previously PCOS), so the goal of most meals is steady blood sugar rather than spikes and crashes. In practice that means building meals around fiber and protein instead of processed foods. A day might look like a real breakfast with protein and fat rather than a sugary coffee and a pastry, meals centered on vegetables, whole grains, legumes, and healthy fats like olive oil, nuts, and avocado. And if you eat meat, fish has the highest nutrient value and should be prioritized. Two nutrients worth being intentional about are folate (leafy greens, legumes, plus your prenatal) and omega-3 fatty acids (fish, chia seeds flax seeds, walnuts).

In a study looking at the "Time to Conceive" prospective cohort at UNC (this is the same cohort I worked with in fellowship), ~900 women aged 30–44 trying to conceive naturally. Women who took an omega-3 supplement had a fecundability ratio of 1.51 (95% CI 1.12–2.04)versus non-users, meaning roughly 1.5x the odds of conceiving in a given cycle.

On things to limit: toxins and foods with limited nutritional value. I recommend avoiding alcohol, cannabis, and smoking. Ultra-processed foods should be limited. Caffeine does not have to go to zero, just keep it moderate.

The foods you eat do matter, and they can be a powerful took to decrease inflammation and improve your insulin sensitivity. But you don’t have to be perfect, each day is a new opportunity to make the best choices you can in that moment.

3. “What does the data actually say about acupuncture and fertility?”

Here is the mechanism and where it may help. Acupuncture places tiny needles at specific points to lower inflammation, improve circulation, and promote relaxation. For many women it genuinely decreases stress and anxiety, which matters most in high-stress stretches like an IVF cycle. There is also evidence it can improve blood flow to the uterus in women dealing with implantation failure, and that women with low ovarian reserve may see a small increase in the number of eggs retrieved during IVF. So if you are running into unexpected or disappointing outcomes on your journey, I think acupuncture is a reasonable option to consider.

A study published in JAMA in 2018 compared real acupuncture against “sham” acupuncture (pressure, no needle insertion) during IVF, and it found no benefit of real over sham. That does not mean acupuncture cannot help you. It more likely means the response is individual, and that sham has its own benefits too, which makes a true difference hard to detect. Look at what both groups shared: time in a calm space, off your phone, alone with your thoughts, with nothing to do but be present. A lot of what helps here is the stress reduction itself.

A 2024 review pooling 25 trials and nearly 4,800 women found higher rates with acupuncture than with controls, both for clinical pregnancy (43.6% versus 33.2%) and for live birth (38.0% versus 28.7%).

Acupuncture is certainly something you can try and for many women it has a benefit. Just use a simple test: if you finish a session and feel that real drop in stress, that “aaah,” then it is doing something valuable for you and it is worth keeping. If you do not get that reduction, you do not need to force it or spend money you do not have on it. Do it because it calms you, not because you are afraid of what happens if you skip it. To learn more about acupuncture and fertility, listen to my episode with Sadie Minkoff.

4. “Should I take myo-inositol for PCOS (PMOS)?”

Insulin resistance sits at the center of PMOS (previously PCOS). When your cells stop responding well to insulin, your body pushes out more of it to compensate, and that excess insulin tells the ovary to make more androgens, which is a big part of what disrupts ovulation. So a major target for treatment is addressing the underlying insulin signaling.

Myo-inositol is a molecule your cells use as a messenger inside the insulin and gonadotropin (FSH and LH) signaling pathways. It helps your cells hear the insulin signal better, which improves insulin sensitivity, and it helps move glucose into the ovary. This results in better insulin sensitivity, more regular menstrual cycles, and an improved ovarian response to FSH. That is why it can help restore ovulation for many women with PMOS, and it tends to be well tolerated, which is a real advantage over some other options. You can even find it in food, in things like nuts, beans, quinoa, oats, and citrus, though supplementing is what gets you to the studied doses.

Some small studies have shown that myoinositol may directly improve fertility parameters. A 2016 systematic review of randomized controlled trials in women with PCOS found that inositol improved insulin sensitivity and helped restore ovulation, which is exactly why it has become a first-line option many of us recommend. Myo-inositol may help beyond regulating your cycle— in IVF it has been linked to better outcomes, particularly in women who respond poorly to stimulation, likely because the same improvements in insulin signaling and ovarian response to FSH carry into a stimulated cycle. A 2021 randomized trial found that 4 g of myo-inositol improved fertility outcomes in poor ovarian responders going through assisted reproduction.

Bottom line: if you have PMOS with irregular cycles, myo-inositol is a reasonable, well-tolerated first step, and the dose used in most studies is 2 grams twice a day (4 grams total), often in the 40-to-1 ratio of myo-inositol to D-chiro-inositol. Give it about three months before you judge it, since cycle changes take time, and pair it with the foundational work that also targets insulin resistance: strength training, protein and fiber at your meals, and real sleep.

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Before you go

If you this and thought “I never knew that,” then you are exactly who this column is for. None of us should have to fail before we get to understand our own bodies, and none of us should have to figure it out completely alone at midnight with a search bar.

XO, Nat

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Wait a year before you ask for help. Wait until 35 to start worrying. Wait until you have “failed” before anyone actually looks. And while you wait, those same myths hand you the bill and the blame. I have sat across from too many women who did everything they were told to do, trusted the advice, followed the rules, and still ended up wondering what was happening. And too often, there are fertility myths that have propagated our actions and beliefs.

Fertility misinformation is not harmless. It delays testing, delays diagnosis, and delays treatment, and worst of all, it teaches women to blame their own bodies for things that were never their fault. My goal is the same as it was on the mic: take the blame off your body, and put the information back in your hands.

This week I went solo to bust the fertility myths that quietly cost women the most, the ones that make you wait, second-guess yourself, and blame your body.

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Myth 1: You have to wait 12 months to get a fertility evaluation.

This is the one I would change first if I could change only one thing. Yes, infertility is defined as trying for 12 months without success, but that is the outer limit, not a waiting requirement. You can get evaluated at any point before then, and I want you to. Here is the math that makes waiting illogical: if you are under 35, about 72% of people conceive in the first six months of trying. So if you are not pregnant at six months, why wait another six for a much smaller remaining chance (only 13% will get pregnant in those next 6 months) instead of simply checking that ovulation, tubes, and sperm are all working? Getting the data in hand is not jumping the gun. It is being proactive about a life goal. You will not be pushed into fertility treatments and you can always keep trying longer.

Myth 2: Your fertility falls off a cliff at age 35.

The “cliff at 35” is a labeling artifact, not biology. Egg quality does decline with age, both because the chromosomes inside your eggs accumulate wear over time and because our metabolic and cellular health declines too. But at 35, most women still have a genuinely good chance of conceiving. The steeper, year-over-year drop really begins after 37. Where age matters most is if you want more than one child, because you have to account for the time it takes to conceive, be pregnant, and recover before trying again. So if you are older, the move is not despair, it is earlier testing and proactive planning.

Myth 3: Birth control causes infertility.

The pill works by telling your brain to stop sending FSH and LH, so you do not ovulate. But eggs are still leaving the “vault” of your ovary the whole time, at the same rate they always would, and dying off unstimulated. Birth control does not speed up, slow down, or change your long-term ovarian reserve. It can lower your AMH reading while you are on it, because the cells that make AMH get suppressed when you are not ovulating, but that is a drop in cellular activity, not a true loss of eggs. Across contraceptive types, there is no higher rate of infertility a year after stopping, with one exception: the Depo Provera shot can suppress ovulation for up to 18 months, so stop it more than two years before trying. Two real caveats: continuous pill or IUD use can thin the uterine lining (a tip-off is no periods or very light ones), so consider stopping three to six months early to let estrogen rebuild your lining, and while you are on hormonal contraception you cannot read your ovulation signs, so coming off and tracking early can surface fixable problems before you are behind and gives your uterine lining time to recover—I recommend stopping these 6 months before you want to conceive.

Myth 4: IVF guarantees a baby.

IVF is remarkable, but it is limited by the eggs and sperm we actually get, and that gets harder with age. Even in the best lab, there is a ceiling: a genetically normal (euploid) embryo carries about a 65% chance of live birth per transfer. Cumulatively, after three euploid transfers, roughly 90 to 95% of people will have a pregnancy, so most people do succeed, with an asterisk: if you have enough genetically normal embryos. A 40-year-old with an average egg count might get zero to one euploid embryo per cycle, meaning three cycles just to bank three embryos, and that is if everything goes well. Time, resources, and biology are all real constraints. One cycle is not a guarantee, which is exactly why the lifestyle and timing work still matters.

Myth 5: Most infertility is a female problem.

It is a clean 50/50 split between male and female factors, because eggs and sperm are equally essential. And here is the hopeful part: sperm are far easier to influence. About 1,500 sperm are made every second, and each one takes roughly 72 days to develop plus about 18 days to travel out, so a man can change his habits today and have meaningfully different sperm in about three months. We can improve egg quality too, just not as dramatically, since eggs are in the body for life. This is why I push for an early semen analysis. It is inexpensive and easy, and I have seen couples try for years only to discover the partner had no sperm in the ejaculate the whole time. Fertility is a team sport.

Myth 6: If you had one baby, the next will be easy.

There is some truth here, people who have conceived before tend to have a higher monthly odds of. conceiving again, but secondary infertility (conceiving before, then struggling for the next) is a real problem. The culprits are often the diseases that show up with time: insulin resistance and metabolic dysfunction, autoimmune disease and chronic inflammation, endometriosis or adenomyosis, and frequently male factor, because it is a completely different sperm sample than years ago. Take a struggle to conceive number two just as seriously as you would the first.

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Myth 7: Men should “save up” sperm for ovulation day.

Abstaining to stockpile sperm backfires. Sperm are made continuously, and the body is designed to clear them out and keep a fresh supply ready. The longer they sit, the more die off and the more debris accumulates. The only reason we ask for two to three days of abstinence is to standardize a semen analysis. For actually trying, daily or every-other-day sex is great, and daily ejaculation can even help men with motility issues. Keep the longest gap to one to three days, because at four days and beyond sperm damage climbs, and it gets worse at seven-plus. These sperm are ready to go.

Myth 8: If your cycles are regular, you do not need to track ovulation.

Regular does not mean normal. Ovulatory dysfunction happens in stages, and the earliest one, a short luteal phase, can occur while your cycles still look perfectly regular. Next comes delayed ovulation and a longer follicular phase, then irregular cycles, then missed periods. The early stages are exactly where I would rather catch and treat a problem, and the causes are worth knowing: thyroid disease, prolactin issues, hypothalamic dysfunction, autoimmune disease, chronic inflammation, insulin resistance, and early PMOS (previously PCOS). A luteal phase defect means a luteal phase of 11 days or less, or spotting during it, and you cannot know your luteal length without knowing your true ovulation day. Apps that use only a calendar are giving you an estimate, not a real ovulation date. Learn to track with cervical mucus, basal body temperature, or an ovulation predictor kit or urinary hormone monitor. Too many doctors ask “are your cycles regular?”, hear yes, and move on. It is on you to know what is actually happening.

Myth 9: There is nothing you can do to improve egg quality.

This narrative makes me genuinely angry, because it sends women to “just do IVF” when even in IVF we can only work with the eggs you grow inside your body. Yes, the chromosomal side of egg quality is partly a function of time. But the metabolic health of the egg is very much in your influence, and it matters enormously. The mitochondria that power your eggs get passed to the embryo, mitochondrial health reflects your metabolic health, and insulin resistance and chronic inflammation are proven in studies to produce fewer mature eggs, fewer normal embryos, lower pregnancy rates, and longer time to pregnancy. Your eggs become most sensitive to your environment in roughly the 300 days before ovulation, and especially the final 60 to 90, and even more so the last 30. So it is never too soon to start. If smoking harms egg quality, and every fertility doctor agrees it does, then it makes no sense to pretend other sources of toxins and inflammation are irrelevant. It all runs through the same inflammatory pathway.

Myth 10: Your AMH tells you whether you are fertile.

I love AMH testing, and it is widely misread in both directions. AMH comes from the cells around each follicle that has left the vault, so it naturally fluctuates 25 to 30% month to month, because your body does not release a perfectly even number of eggs each cycle. A normal AMH tells you that right now you have a normal number of eggs in play. It does not tell you where you started, where you will end, your rate of decline, or your egg quality. A low AMH does not mean you are infertile, and as long as you are ovulating you can absolutely still conceive. But I also push back on the flat claim that AMH says nothing about natural fertility, because the very things that lower AMH, autoimmune disease, chronic inflammation, endometriosis, smoking, also contribute to infertility. The real value of AMH is knowledge and timing: a low number is a reason to look at your inflammation and genetics, think about whether and when you want children, and consider whether to act sooner, so you are the one making the decisions instead of having them made for you.

Myth 11: You need to lie with your legs up or avoid peeing after sex.

Good, moving sperm leave the acidic vagina and head into the cervix and uterus within minutes, chasing the egg. What leaks back out if you stand up is mostly the ejaculate, the alkaline fluid whose job was to protect the sperm from vaginal acidity on the way in. There is no reason to trap it, and holding your urine to “keep sperm in” mostly just sets you up for a urinary tract infection. Get up, go to the bathroom. No position or post-sex ritual changes your odds.

Myth 12: You cannot get pregnant on your period. Usually true, but not always.

For most people, most of the time, no. But as you get older your cycles shorten, because a more stubborn ovary prompts your brain to release more FSH, which recruits an egg faster, so you ovulate earlier. Since sperm can survive up to five days and periods can last four to seven, an early ovulation can overlap with the tail of your period. This is also why cycles shorter than 25 days make calendar-based natural family planning unreliable. Less likely is not the same as impossible, which is one more reason to actually know your own cycle.

The take home message

Most of these myths either make you wait when you should act, or make you blame yourself when you should investigate. The antidote is the same every time. Understand your own body, track what is actually happening, test early instead of waiting to “fail,” and treat your metabolic and inflammatory health as the lever it truly is. You should not have to fail before you learn how your body works.

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A new analysis of the long-running SWAN study followed women from their mid-forties across the next decade and asked a simple question: does your metabolic health before menopause predict how your menopause actually goes? The answer was striking. Women with higher fasting insulin at age 47, years before their final period, went on to start hot flashes earlier and have them longer. And insulin predicted this even after accounting for body weight, which means this is not just a story about BMI or weight. It is a story about the hormone insulin, quietly shaping one of the most disruptive experiences of midlife.

Below, I break down exactly what they found, what insulin resistance actually is, why estrogen was a metabolic hormone all along, and the specific, doable things that move insulin, because this is one finding where the takeaway is genuinely in your hands.

Study: Insulin Levels Early in Perimenopause Inform Vasomotor Symptom Incidence Across the Menopausal Transition

Journal: The Journal of Clinical Endocrinology & Metabolism

Read the Study: https://pubmed.ncbi.nlm.nih.gov/41482729/

Why this study caught my attention:

If you have followed me for any length of time, you know that your ovary is not just a reproductive organ, it is an endocrine organ wired into your whole body. I often talk about the ovary and insulin as it impacts fertility, but this study shows another important example—the influence of metabolic health, insulin. and perimenopause. When we talk about hot flashes and night sweats, we talk about estrogen. We almost never talk about insulin. This paper says we should.

What really interested me is that the metabolic signal showed up years early, and it held up independent of body weight. This is extremely important because it bridges the gap—menopause may be a transition we all go through, but your experience is something you can influence by the choices you make right now. This is taking charge of your future health now.

So today I am reviewing:

• What is insulin resistance

• How estrogen is a metabolic hormone

• A breakdown of this study

• What prior research showed

• How to improve your insulin sensitivity

First, what insulin resistance actually is

Insulin is the hormone that lets your cells take use glucose for energy. Insulin resistance is when your cells stop responding well to insulin’s signal, so your body compensates by making more and more of it to get the same job done. The result is chronically high insulin, or hyperinsulinemia.

I like to use this analogy—imagine that insulin is a salesman coming to the door of your cell. Glucose can’t open the door to the cell, it needs insulin knocking for it. You answer the door, glucose goes into the cell, and both insulin and glucose lower in the bloodstream. Now insulin resistances happens when your cell gets sick of seeing the salesman. Let’s just imagine a salesman coming to your door all the time. What would you do? You would stop answering. Eventually the salesman starts banging on the door, you go and finally answer—and now glucose can go into the cell.

This is insulin resistance. Your cell will respond to insulin, but it needs a much higher insulin signal than normal. This is hyperinsulinemia. But high insulin levels in your blood is not benign. It causes high inflammation, impacts brain and ovarian signaling, and actually changes how the ovary functions.

One important thing to know is that high insulin appears before full-blown insulin resistance. So elevated fasting insulin is often the earliest visible sign that this system is starting to strain, long before your blood sugar ever looks abnormal on a standard test.

That early-warning quality is exactly why measuring insulin, and not just glucose or a HgbA1c, matters. A normal fasting glucose can sit on top of years of rising insulin because your body is quietly working harder to keep that glucose looking fine.

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Here is what I want you to know before you get there: how we prepare your body for that transfer is not an afterthought, and it is not the same for everyone. The protocol matters. And most patients are never told there is a choice at all.

So today I am breaking down the frozen embryo transfer, or FET, and the five different protocols we use to get your body ready. My goal is not to tell you which one is right for you, because I cannot do that without knowing your history. My goal is to help you understand what exists so you can walk into your clinic and ask a much better question: which protocol are we doing, and why?

Watch the full breakdown here:

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Why the protocol matters

Once we have an embryo, we are in a powerful position. In a natural month, there can be a mismatch between when the embryo is ready and when the uterine lining is ready. In IVF we get to remove that guesswork. The embryo is frozen and waiting, so we can take our time getting the lining exactly where we want it, then pair them up.

There are multiple different protocols, but I want to review the way I sort them in my brain as five different protocol strategies, running from least to most aggressive. I want to be clear that least aggressive does not mean least successful, and most aggressive does not mean best. These are simply different tools, and the right one depends on you.

First, a word about success rates

When we transfer a genetically normal (euploid) embryo, our success rate is about 65% per embryo. That means even when everything is perfect, one transfer may not work. That is heartbreaking, but it does not always mean we need to change the protocol.

Here is the number that gives me hope: the cumulative success rate after two transfers is around 85%. So if I liked how things looked the first time, I am often doing something very similar the second time on purpose.

We only start rethinking the protocol when the pattern tells us to. Officially, recurrent implantation failure is defined as three genetically normal embryos that have not worked. Once we are there, we absolutely need more testing and a fresh look at the plan. But embryos are not a limitless resource, so sometimes we pull in your history sooner: past miscarriages, known or suspected PCOS, known or suspected endometriosis, your reason for infertility, and what your lining looked like during your IVF cycle. All of it shapes the choice.

The 5 protocols, from least to most aggressive

1. Pure natural cycle

No medications at all. You track your own ovulation, grow your lining with your own estrogen, and make your own progesterone from the corpus luteum after you ovulate. We place the embryo in your natural implantation window, which is roughly five to seven days after ovulation.

The upside is that you are not taking or paying for extra medication. The downside is timing, because you have to catch ovulation precisely, and honestly we like more control than this gives us. There is also a fair question to ask: if your natural cycles never got you pregnant, why would this one be different? For that reason I do not love this option for recurrent implantation failure, unexplained infertility, or long-standing primary infertility.

2. Modified natural cycle

Same idea, a little more control. You still use your own estrogen to build the lining and your own progesterone to open the window, but we help ovulation along, usually with letrozole or with FSH shots, and then a trigger shot so we can pin down timing. We also add a little vaginal progesterone as a bonus, since you are already making some yourself.

This one is well tolerated, faster, and may be associated with better birth outcomes and a possibly lower risk of preeclampsia for some patients. Many women also grow a better lining on their own estrogen than on synthetic estrogen, so this can be a good fit if you have a history of thin lining or Asherman’s. In addition if you have gotten pregnant without IVF in the past, this may more closely mimic the cycle in which you had success. The tradeoff is that it is less predictable. You do not get a tidy calendar, because we are following your body.

3. Controlled (medicated) cycle

Here we grow the lining with estrogen you take (estradiol as pills, patches, or injections), monitor with ultrasound, and there is no ovulation because the ovaries are not driving the cycle. Because you are not making any progesterone of your own, you have to use intramuscular progesterone, known as PIO or progesterone in oil. Bigger needle, not fun, but it does the job.

This is probably the most common protocol in the US, and it shines when we cannot rely on your body to ovulate, or in cases of ovarian failure or menopause. It is not my personal favorite, because we miss out on some of the benefits of the natural and more advanced protocols, but it gives us clean calendar control and it works.

4. Medicated cycle with Lupron

This is one of my preferred medicated approaches. It looks like the controlled cycle, but we add Lupron, a GnRH agonist. Lupron first dumps out the FSH and LH the pituitary is holding, then shuts down further production, which creates a suppressive, quieting effect. Started in the luteal phase or overlapped with birth control pills, it avoids the initial flare.

Why do this? Lupron suppresses adenomyosis and endometriosis, calming chronic inflammation that can quietly work against implantation. If you have known endo or adeno, or symptoms that strongly suggest it even without a formal diagnosis, this is often where I want to be.

5. Recurrent implantation failure protocol

The most involved option. This is typically two months of Lupron suppression paired with daily letrozole, so we really down-regulate everything. You will be low on estrogen and it is not a comfortable stretch, but then we typically grow the lining with estradiol and support with progesterone. Think of it as an even deeper level of immune and inflammatory control for the situations that need it.

Sometimes you can try a down-regulation with lupron for months and then a modified natural approach, but the ovaries may be slower to respond after being suppressed for a while. It’s all about choosing the best option for the patient.

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Progesterone: the piece people get wrong

Progesterone opens and closes the implantation window, and it is essential to holding the pregnancy until the placenta takes over around 9-10 weeks. Lose it before then and you lose the pregnancy. So how you replace it matters, and it depends entirely on your protocol.

If you are on a cycle where you make no progesterone of your own (a fully medicated cycle), the data is no longer up for debate: you need progesterone in oil. You can take it daily or every other day, and you can layer vaginal progesterone on top. If you are ovulating in any natural or modified cycle and making your own progesterone, you can usually get away with vaginal progesterone only, because you are just supplementing. That distinction is profound, and it is worth confirming with your clinic.

Before you transfer, two things I insist on

Look inside the uterus. I require a saline sonogram, an HSG, or a hysteroscopy within six months of transfer. There is nothing worse than repeated failed transfers when no one ever checked the cavity and there was scar tissue or a polyp getting in the way the whole time.

Ask about the add-ons. Some extras have not been shown to harm and may help, with mixed evidence. Baby aspirin is common, and sometimes a short course of steroids or antibiotics. None of these is magic, but they are reasonable to discuss.

What to do with all of this

You do not need to memorize five protocols. You need to walk into your clinic informed enough to have a real conversation.

Bring these questions to your next appointment:

• Which protocol are we doing, and why is it the right one for my history?

• What did my lining look like during my IVF cycle? (This is one of the highest natural estrogen states you will ever be in, so a thin lining then tells us something now.)

• Given my history of endometriosis, PCOS, thin lining, or prior losses, should we be considering a different approach?

• Am I making my own progesterone in this cycle, and does that mean I need PIO or just vaginal progesterone?

• Have we looked inside my uterus in the last six months?

There is no single protocol that is right for everyone. If your clinic has a default, that is fine, and there may a good reason for it. But you deserve an honest conversation about the risks and benefits for your specific situation, and the willingness to get creative when something is not working.

You are not being difficult by asking why. You are being an informed partner in your own care. And the more you understand about what exists, the better the decisions we can make together.

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AskNat The column where you ask and I answer like the doctor-friend you wish was in the room with you. Real questions from real women, straight from my inbox. General education, never a substitute for your own doctor.

A quick hello before we start

Every week, hundreds of you send questions. Some make me laugh, some make me tear up, and almost all of them make me think, “so many women are wondering this exact thing and have no one to ask.” So I am starting a column for it. This is AskNat.

Here is how it works. You send the questions. I pull the ones that will help the most people, and I answer them the way I would if you were sitting across from me. I will always tell you what the science says, where the science is thin, and what I would want my own sister to know. None of this is personal medical advice, because I am not your doctor and I have not seen your chart. But you deserve to understand your body, and that is what we are here to do. Let’s get into it.

For a limited time, AskNat is open to all subscribers as a free trial but it will soon be a paid subscriber only offering. Only paid subscribers can ask questions, upgrade now.

Questions answered in this week:

1. “You mentioned that CoQ10 should be around 600 mg a day, and my expensive prenatal doesn’t come close. Can you clarify the dose, and is there research behind it?”

2. “What does it mean if I have about a 28-day follicular phase every cycle? My cycles have always been long.”

3. “I’m 33, after a tough first IVF cycle where very few eggs made it, what does that say about my ovarian reserve and my chances?

4. “Five months after I stopped breastfeeding I feel awful. I have heavy, irregular periods, mood swings, anxiety, a racing heart. My doctor prescribed a progesterone-only pill without any testing first. Could that make things worse?”

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1. “You mentioned that CoQ10 should be around 600 mg a day, and my expensive prenatal doesn’t come close. Can you clarify the dose, and is there research behind it?”

I love CoQ10, but often the dose in prenatals (if any) is less than the dose studied for fertility. But how does CoQ10 even help?

Your egg is one of the most energy-hungry cells in your entire body, and it runs on its mitochondria, the little power plants inside the cell. CoQ10 is a nutrient those power plants use to make energy. We know that the mitochondria are important for egg health and function, and mitochondrial health can support egg quality, especially as we get older and that energy production gets less efficient. The dose studied for fertility benefits is 600 mg per day, and it is usually split through the day (200 mg three times) because it is fat-soluble, so it absorbs better in divided doses taken with food. The ubiquinol form tends to absorb better than plain ubiquinone but both are sufficient.

A randomized controlled trial of 186 women under 35 with diminished ovarian reserve, given 600 mg of CoQ10 per day (200 mg three times daily) for 60 days before an IVF cycle, versus a control group. The CoQ10 group had more eggs retrieved, more mature eggs, a higher fertilization rate, and more high-quality embryos, and fewer cycles were canceled for poor response or poor embryo development (cancellation for poor embryo development dropped from about 22.9% to 8.3%). This is why we recommend 600 mg, split as 200 mg x3. , works over the ~60-day egg-development window" point in the column.

Even though your eggs are in your body your entire life, the 60-90 days before ovulation appear to be when they are most susceptible to the environment of your body. This was reflected in the study starting CoQ10 60 days before the cycle started. Also - I take this as good news because it means that changes you start now can have a positive impact on your egg quality. Also important to note that research is mostly small studies, often in IVF patients looking at egg response, so I would call CoQ10 reasonable and low-risk rather than magic. I recommend buying a separate supplement for CoQ10 as most prenatal will only have about 200 mg at most.

2. “What does it mean if I have about a 28-day follicular phase every cycle? My cycles have always been long.”

Somewhere along the way we were all handed the idea that a “normal” cycle is 28 days with ovulation on day 14. That number is a textbook average, not a rule, and it barely describes anyone. Only about 13% of women actually have a 28-day cycle, and even among those who do, only around 10% truly ovulate on day 14. So a longer follicular phase is not automatically a problem. It is a variation, and variation is the norm.

Your cycle has two halves. The follicular phase is the run-up, from your period until ovulation, where a follicle is growing and estrogen is being made, and this is the part that varies from person to person and even cycle to cycle. The luteal phase is the second half, after ovulation, when a corpus luteam makes progesterone, and it should be fairly fixed (and we want the luteal phase to be at least 11 days in length to be normal).

Longer follicular phases and longer overall cycles are very common with PMOS (previously PCOS). The issue is usually less about the length itself and more about two things: making sure ovulation is really happening, and catching a fertile window that arrives on a later and sometimes irregularly. This is an example of a time where you need an evaluation.

That said, a 28-day follicular phase is too long. Your ovaries are taking a long time to respond to FSH signals from the brain (and likely using this time to make significant androgens and feeding back into insulin resistance, which is a huge problem for PMOS). A normal cycle length can be anywhere between 25-35 days, and needs to be consistent for you (within 1-2 days of expected each month). In all circumstances, ovulating this late in your cycle is telling us there is some miscommunication between the brain and ovary.

The good news for PMOS is that it responds well to ovulation support and improving insulin resistance. But we always want to rule out other potential causes, such as thyroid, prolactin, congenital adrenal hyperplasia, before we assume a diagnosis of PMOS. Treating insulin resistance should be a mainstay for all PMOS patients, and medications like inositol, metformin, and GLP-1 agonists are some options that can work exceptionally well.

3. “I’m 33, after a tough first IVF cycle where very few eggs made it, what does that say about my ovarian reserve and my chances?”

We often say that IVF can be both diagnostic and therapeutic. Meaning, we are trying to help you get pregnant, but we are learning about your body along the way. One hard cycle can feel like a verdict on your fertility, but it is not. It is a single data point, and one data point does not define your reserve, your future, or your worth.

Here is the distinction that changes how this feels. Ovarian reserve is a quantity question: how many eggs are in the pool. Quality is a different question entirely: how many of those eggs are chromosomally normal and able to grow into a healthy embryo. They are not the same thing, and it is quality, not the raw number, that most determines whether an embryo keeps developing. That is also why a single retrieval is only a one time snapshot. The numbers genuinely bounce around from cycle to cycle. Even the AMH blood test, the one we use to estimate reserve, can vary by up to 28% from one month to the next in the same woman. So one cycle that disappointed you is not a promise that the next one looks the same.

I recommend a protocol review with your doctor. We use the best information we can to choose the best protocol, but sometimes what looks good on paper isn’t what is really best for you. Remember that for IVF, we are trying to override the normal brain-ovary communication system. Your body wants to ovulate just one egg. We want to get all eggs available to us this month. Sometimes the combination of suppression + stimulation doesn’t get the job done. And it is worth it to review the data and try again with a different protocol using the data we now have about your body.

I review failed IVF cycles in this video which can breakdown some more details and questions to consider asking your doctor, big hugs.

4. “Five months after I stopped breastfeeding I feel awful. I have heavy, irregular periods, mood swings, anxiety, a racing heart. My doctor prescribed a progesterone-only pill without any testing first. Could that make things worse?”

First of all, asking questions about your body should always be encouraged. That is you advocating for yourself.

The months after you stop breastfeeding are one of the largest hormonal shifts a woman goes through, second only to the immediate postpartum period. Prolactin falls, your cycles wake back up, and estrogen and progesterone start swinging again after a long quiet stretch. That transition on its own can produce exactly what you are describing: heavy or unpredictable bleeding, mood swings, and that wired, racing-heart anxiety. So some of this may simply be your system recalibrating. But “may be” is not “definitely,” and that gap is the whole reason your instinct was right.

Here is what I want ruled out before anyone assumes this is only hormones settling. First, your thyroid. Postpartum thyroiditis is common, it tends to show up in exactly this window, and its symptoms read almost like a copy of your list: racing heart, anxiety, mood changes, and cycle changes. It is very treatable once it is found, but someone has to actually test for it. Second, your iron. Heavy periods are a leading cause of iron deficiency (and about 1 in 10 women have genuinely heavy menstrual bleeding), and low iron will make you feel exhausted, anxious, and unwell in a way that has nothing to do with your mood being “off.” You can have iron deficiency without having anemia. A simple ferritin level tells that story. These are basic labs, and asking for them is completely reasonable.

Postpartum we can see irregular ovulation, heavy bleeding, and hormone fluctuations. Sometimes women have irregular or absent ovulation postpartum, which is coming at a time of significant low estrogen and can lead you to feel terrible. Sometimes with irregular ovulation the progesterone only pill is helpful, but other times it adds an extra layer of hormone disruption.

The progestin-only pill is a good contraceptive choice if you are still breastfeeding as the combination birth control pill can sometimes decrease milk supply. But progestin-only pill users sometimes report irregular bleeding and you do have to take the pill at the same time every day or ovulation can occur. It isn’t the wrong choice to try postpartum, but it may not be the right choice, and it certainly seems like there are other medical conditions that need to be ruled out first.

I wouldn’t say “do not take it” but “ask for testing first.” You are allowed to go back and say, “before we try a medication, can we check my thyroid and my ferritin?” A good clinician will say yes. Feeling this unwell is not something you are supposed to white-knuckle through, and it is not in your head.

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Before you go

If you this and thought “I never knew that,” then you are exactly who this column is for. None of us should have to fail before we get to understand our own bodies, and none of us should have to figure it out completely alone at midnight with a search bar.

XO, Nat

Paid subscribers can submit questions below to have them answered in AskNat.

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Pregnancy is the most sophisticated stress test the female body will ever undergo. Blood volume climbs by nearly 50%. Cardiac output rises dramatically. The vascular system is pushed to pressures it has never seen. The hormonal environment shifts in ways that are profound and complex. And the immune system somehow learns to tolerate a genetically foreign life growing inside it. As Amanda put it, pregnancy is a stress test on your entire body, head to toe—your brain, your eyes, your gums, your airway, your intestines, your blood, all of it.

For nine months, the body is pushed to its absolute physiologic limit. And then the baby is born, and we send mom home. What almost nobody does is stop and read what the stress test actually revealed.

This week I sat down with one of my dearest friends and most trusted colleagues, Dr. Amanda Horton, a double board-certified maternal-fetal medicine specialist, to talk about what your pregnancy reveals about your future health, and why so much of that priceless information gets quietly thrown away.

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Your pregnancy is a window into your future health

I say all the time that your fertility is a health marker: the ability to get pregnant reflects a certain state of metabolic and cellular health. Amanda takes that one step further. What happens during pregnancy, under that extraordinary pressure, is some of the most revealing health data a woman will ever generate.

Preeclampsia. Gestational diabetes. Preterm birth. A small baby. Postpartum hemorrhage. We file these away as “pregnancy complications,” but they are biological signals — the body under maximum load, showing us something about its vascular health, its metabolic function, its immune regulation, and its hormonal resilience. Sometimes those are green flags. Sometimes they are red flags. Either way, they are information.

“Even though you deliver, they stay with you. Your obstetric history is your future history.” — Dr. Amanda Horton

The tragedy is that we rarely connect the dots. Cardiology, primary care, and rheumatology too often treat your pregnancy history as a single throwaway line on an intake form when it may be one of the strongest predictors of what’s coming.

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Preeclampsia: a plumbing problem with a long memory

Preeclampsia affects roughly 5–8% of pregnancies worldwide, and it is far more than “high blood pressure of pregnancy.” It’s a vascular problem that starts in the placenta. The placenta is supposed to remodel your blood vessels into wide, low-resistance channels that flood the baby with nutrition. In preeclampsia, that remodeling goes wrong and the vessels stay narrow and high-pressure. The placenta then starts sending out distress signals that hit your kidneys (spilling protein), your liver, your brain, and your heart.

Those vascular changes have memory. Having a hypertensive disorder of pregnancy raises your future cardiovascular risk by roughly three to four times, and up to eight times if you also delivered preterm, because that severity signals just how significant the vascular insult was. Heart disease is the number one killer of women, and these are exactly the “risk enhancers” our standard cardiac models still don’t know how to account for.

And delivery isn’t the finish line. Postpartum preeclampsia can appear days to weeks after birth. Exhausted new parents explain away the warning signs—a headache that won’t quit, shortness of breath, dramatic swelling, sudden weight gain, not being able to lie flat. Please hear this: that is not normal, and it can be an emergency. Call your doctor.

What to do with a preeclampsia diagnosis:

• Get a blood pressure cuff for home. Most of us don’t own one and you need it in those first weeks.

• If your blood pressure hasn’t normalized by six weeks postpartum, that’s essential hypertension. Don’t walk around with it untreated but see a primary care doctor.

• Tell every future doctor. Ask what your cardiovascular risk is and whether you need added screening like an Lp(a).

• In a future pregnancy, low-dose aspirin (81 mg), started at 12–16 weeks, can cut the risk of a hypertensive disorder by about 25% in the highest-risk women. We have almost nothing else that works that well.

Gestational diabetes: please don’t “game” the test

Gestational diabetes is diabetes diagnosed during pregnancy, and its own category, not type 1 or type 2. Your friend and mine, the placenta, makes a hormone called human placental lactogen that drives insulin resistance, which peaks between 24 and 28 weeks. That’s exactly why we screen then: we’re catching you at your most insulin-resistant.

Here’s why it matters for your future: a gestational diabetes diagnosis is associated with roughly a tenfold higher risk of developing type 2 diabetes later and probably higher. It also travels with high blood pressure in pregnancy, so good blood sugar control supports good blood pressure control.

Which brings me to the internet trend of trying to “game” the one-hour or three-hour glucose test. Amanda and I both feel strongly: don’t. Gestational diabetes isn’t caused by the cupcake at your baby shower but it’s the placenta. Manipulating the test doesn’t protect you; it just hides your own data. And poorly controlled blood sugar has real consequences—bigger babies, harder deliveries, and newborns born with dangerously low blood sugar who can end up in the NICU. You deserve the real information, and so does your baby.

A few practical notes: Rescreen 4–12 weeks postpartum so you’ll learn whether it resolved, whether you have lingering insulin resistance, or whether you now have diabetes. If you come in with known insulin resistance, PCOS, or prior gestational diabetes, we screen earlier (often late first trimester). And remember that hemoglobin A1c is unreliable in pregnancy that’s why challenging your body with a glucose load is the better test.

Preterm birth and small babies: cardiovascular red flags

A small-for-gestational-age baby often reflects placental dysfunction, and it’s a recognized cardiovascular risk enhancer for the mother. Did you know that having a baby born small raises your own risk of heart disease later in life?

Spontaneous preterm birth affects about 10–12% of pregnancies, and many women have no risk factors at all. But once you’ve had one, your risk in a future pregnancy jumps to 30–50%. That’s a staggering number, and it comes wrapped in trauma and misplaced guilt for so many parents.

One myth worth killing: bed rest. It feels intuitive to “take it easy” when you’re high-risk but the data now show that activity restriction is associated with higher rates of preterm birth, not lower. Your body, and especially your vascular system, is meant to move. (It’s the same story in fertility—more sedentary, worse outcomes. We get patients up and out after an embryo transfer; there’s no bed rest, and yes, they can go get their French fries.)

If you’ve had a preterm birth: start with a consult to understand why it happened. Was it infection, cervical insufficiency, a uterine shape difference (like a septum or bicornuate uterus), or placental pathology? From about 16 to 24 weeks we can monitor cervical length on ultrasound, and when the cervix shortens we have to consider options like nightly vaginal progesterone or, in select cases, a cerclage (a “belt” stitch to support the cervix).

When birth itself leaves a mark: hemorrhage and retained placenta

Placental abruption, retained placenta, and postpartum hemorrhage all tend to recur so your OB always needs to know your history. And I want to spend a moment on retained placenta, because it’s my world.

Normally the placenta detaches within about eight minutes of delivery (sometimes up to 30). When it’s stuck, often because of prior uterine surgery, a D&C, or infection, it can lead to hemorrhage and, in the worst cases, placenta accreta. In the moment, the entire focus is on stopping the bleeding and saving your life, as it should be. But retained placenta is one of the top causes of uterine scarring (Asherman’s syndrome) that I see afterward. It often gets missed because postpartum estrogen is low, you’re breastfeeding, you’re not having a period, and everyone chalks the absent cycle up to breastfeeding. If your bleeding continues, or something feels off, advocate for an evaluation of the uterus. The sooner we intervene to remove the adhesions and provide hormonal support, the better the healing.

Platelets: the labs nobody revisits

Your platelet count naturally drops in pregnancy, sometimes markedly in the third trimester (we call it gestational thrombocytopenia), and honestly, we can’t always tell it apart from an autoimmune condition like ITP. Your white blood cell count rises. Your hemoglobin shifts with dilution. These changes are usually normal but they should return to baseline by around six weeks postpartum.

This is one more reason not to skip the postpartum visit. A simple CBC gives you a real baseline. If your platelets are still low, that’s a reason to see a hematologist because pregnancy may have unmasked something worth diagnosing.

So what do you actually DO with this information?

This is the part that matters, because knowledge without action is just anxiety. Here’s where Amanda and I landed:

• Get a preconception visit — even with a high-risk or MFM doctor. It’s a conversation, not a test you can fail, and it lets us establish your true baseline before pregnancy masks it. (Your blood pressure naturally drops in early pregnancy, which can hide pre-existing hypertension entirely.)

• Find a primary care doctor — and tell them your OB history. Their intake form gives it one line; you may have to advocate for it to be taken seriously.

• Know your numbers, especially your blood pressure. Ask what screening you need and how often.

• Don’t skip the postpartum visit, and get a real baseline before you assume everything reset.

• Optimize chronic conditions before pregnancy — IBD well-controlled for 4–6 months, lupus and MS stable, thyroid dosing sorted (your needs rise the moment you’re pregnant; many people double up two days a week).

• Come back to the foundations: about 150 minutes of moderate cardio a week, good sleep, minimizing processed foods and environmental toxins, staying hydrated, and eating plant-forward. The unglamorous basics genuinely move the needle.

Bring these questions to your next appointment

• “I had preeclampsia / gestational diabetes / a preterm birth / a small baby / a postpartum hemorrhage. What does that mean for my long-term risk?”

• “Do I need earlier or extra screening like blood pressure, lipids or Lp(a), glucose?”

• “Should I have a blood pressure cuff at home?”

• “If I want another pregnancy, what should I do differently and when should I come in?”

The bottom line

Just because you’ve delivered does not mean the risk is gone — but it also doesn’t mean you’re powerless. Your pregnancy generated some of the most valuable health data you will ever have access to. Don’t let it get filed away in a chart nobody reopens.

Read the results. And bring someone with you into the conversation who’s willing to read them, too.

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This week’s guest: Dr. Amanda Horton is a double board-certified maternal-fetal medicine specialist and perinatologist who cares for the most complex, high-risk pregnancies and a voice I trust completely.

If this helped you see your own history differently, share it with someone who’s pregnant, postpartum, or planning. Listen to the full episode of the As a Woman podcast wherever you get your podcasts—listen now on Spotify or Apple.

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Hi friends and welcome — I’m really glad you’re here.

You just joined a space where I answer the women’s health questions I get asked over and over — about fertility, hormones, ovarian aging, and what’s actually happening in your body. No fear-mongering, no fluff. Just honest, evidence-based answers. We will dive into latest research so that you can make…

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I think every woman should have her AMH tested. Not because she’s trying to get pregnant, but as a baseline biomarker of her own body.

This is a controversial thing for a fertility doctor to say. But I think the current standard of “wait until you’re struggling” is one of the clearest examples of how women’s medicine gets it backwards.

I strongly believe that you should not have to fail to learn about your own body.

We don’t apply “wait and see” to anything else in medicine. We check your cholesterol before you have a heart attack. We check your blood pressure before you have a stroke. We check your blood sugar before you’re diabetic, your bone density before you break a hip, your blood counts before you’re symptomatic. The entire logic of preventive medicine is that data early, when you can still act on it, is a gift.

And then we get to a woman’s reproductive lifespan, one of the most time-sensitive systems in her entire body, and suddenly the advice flips. Suddenly the official position is: don’t look. Don’t test. You might worry. Come back when you’ve been trying and failing for a year. I find that indefensible.

The establishment position (and why they hold it)

In 2019, the American College of Obstetricians and Gynecologists released Committee Opinion 773, “The Use of Antimüllerian Hormone in Women Not Seeking Fertility Care.” Its position is that AMH should not be used as a screening test for fertility potential in the general population. The reasoning is that a single AMH value doesn’t predict your ability to get pregnant naturally, and that testing might cause anxiety or push women toward aggressive, unnecessary interventions.

This is not false. A woman with a low AMH can conceive naturally, especially if she’s still ovulating. Anyone who tells you your number means you can or can’t have a baby is misunderstanding the test.

But why is your AMH low? What does that mean for your health now? What does that mean for your fertility? There are absolutely circumstances when a low AMH is directly correlated with a circumstance that causes infertility (endometriosis is one great example).

But the solution to “this test is often explained badly” is not “hide the test.” It’s “explain it well.” We don’t ban cholesterol screening because some people panic at their LDL. We teach people what it means.

What AMH actually is

I like to use an analogy of a vault inside your ovary.

AMH, anti-Müllerian hormone, is made by the cells surrounding your small developing follicles. More follicles, higher AMH; fewer follicles, lower AMH. Unlike older tests, it’s relatively stable across your cycle, which makes it an easy screening test for roughly how many eggs you have in reserve at a given moment.

Now the limitations:

• It does not directly measure egg quality. There is no test for egg quality.

• It does not predict natural conception. As long as you’re ovulating, your AMH doesn’t tell you your odds this month.

• A single value is a snapshot. AMH varies up to 28% month to month, and one measurement can’t tell you your rate of decline — only where you are right now.

• Hormonal birth control lowers it temporarily (the pill by up to ~24%, the ring ~22%, the implant ~23%, hormonal IUDs only ~7%), returning to baseline about two months after stopping.

If AMH can’t tell you any of that, why do I think you should have it tested?

Because of what it can tell you.

In my professional opinion, AMH is essential if you want kids one day (but not yet), are about to start trying to conceive, or in the midst of trying. But the other part of AMH that nobody tells you is that it can be helpful even AFTER you have completed your family.

AMH is the single best biomarker we have for ovarian reserve and, increasingly, for your reproductive lifespan. This means AMH is more than just a fertility test.

A 2023 systematic review in Human Reproduction Update confirmed AMH as a meaningful predictor of the timing of menopause. Lower AMH for your age correlates with earlier menopause and earlier onset of perimenopausal symptoms. I see this clinically as well, as AMH gets lower and lower, at some point the ovary will eventually stop responding to stimulation meds—this is ovarian failure.

The argument that a low AMH will cause too much “fertility anxiety” is paternalistic because this is information about the arc of your own hormonal life—which affects your bones, your heart, and your brain, not just your ability to have children.

And in fertility, it matters more than we previously realized. A 2024 cohort study of over 3,150 women found that lower AMH was associated with a longer time to pregnancy. It’s the number that tells a fertility doctor how you’ll respond to egg freezing or IVF, and how to plan for it. And critically—when I see a low AMH in a young woman, my first question isn’t “you’re doomed.” It’s “why?” Because some causes of low ovarian reserve (endometriosis, autoimmune disease, smoking) are things we want to catch and address, sometimes for reasons that have nothing to do with fertility. To wave off a low AMH as meaningless without ever asking why it’s low is, frankly, a huge miss.

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The reframe: test it as a biomarker, and trend it

Here’s the shift I’m actually arguing for. The critics treat AMH as a one-time crystal ball, prove that it’s a bad crystal ball, and conclude you shouldn’t look. But that was never the right way to use it.

You use it the way you use every other biomarker: as a baseline you establish early and track over time. One AMH value tells you a moment. Two or three values, spaced out over years, tell you a trajectory—and trajectory is where the real information lives.

Imagine knowing at 28 that your ovarian reserve was tracking lower than expected for your age, not as a verdict, but as a nudge to think about your timeline, get evaluated for a cause, or consider freezing eggs while you have the most options. Imagine the opposite: reassurance that you have one less thing to quietly worry about. Either way, you got to make an informed decision before the window narrowed, instead of finding out in a fertility clinic at 39 that you wish you’d known sooner. That is the entire point.

I will tell you EVERY patient I have ever had who has a low AMH for her age wishes she had that information sooner. Not that there is a one size fits all approach, but you can’t make decisions on data you don’t know. You should be making your fertility decisions, not time.

About that “anxiety” argument

The objection I have the biggest problem with is that testing will scare women. Personally, this is not a reason to withhold data. In fact, I think this is a paternalistic view—women are smart, resilient, and can handle most anything that is thrown at them. The scariest thing, in fact, is not having any data at all. The unknown is always the scariest.

The anxiety doesn’t come from the data. It comes from a number handed over without context, by someone who doesn’t have the time (or the training) to explain it. Of course that’s frightening. But the answer to “we explain this badly” is to explain it well and not to decide, on a woman’s behalf, that she can’t handle knowing something true about her own body. I trust women with their cholesterol. I trust them with their mammograms. I trust them with this.

Even the guidance is starting to move

ACOG’s more recent guidance has already softened, acknowledging AMH as a “useful, albeit imperfect, predictor of ovarian reserve” for women planning to delay childbearing, and issuing newer statements on counseling women proactively about ovarian-factor fertility decline. The ground is shifting from “don’t tell them” toward “tell them, carefully.” That’s the right direction. I’d just like us to move faster.

What I actually recommend

So that I’m not misunderstood, here’s the balanced version:

Test your AMH as a baseline, ideally in your late 20s or early 30s, or whenever you first think about it, and understand what it is: a measure of ovarian reserve and reproductive lifespan, not a pregnancy prediction and not a life sentence. Don’t make a single drastic decision off a single value. Interpret it in context, talk to a fertility doctor if it is low—get an antral follicle count and look for reasons why your AMH may be low (endometriosis, autoimmune disease, etc). If it’s low, treat that as the beginning of a conversation and evaluation, not the end of one.

Most of the time, your result will be reassuring and you’ll have lost nothing but the cost of a blood test. Occasionally, it will catch something early enough to change your life. That means AMH has a small downside, potentially enormous upside, and is exactly why I test for so many other things in medicine. Your ovaries deserve the same respect.

Because I’ll say it one more time, since it’s the whole reason I do this work: you should not have to fail before you’re allowed to understand your own body.

Is the Future of Women’s Health Ovarian Age?

We have been asking the wrong question.

For decades, women have asked me one question more than any other. “When will I run out of eggs?”

It’s understandable. We all know fertility declines with age, so we naturally want to know when our ovaries will stop working. Unfortunately, medicine has never had a satisfying answer. we have simplified fertility to simply being a byproduct of your age for years. And yes, age is important, but it is not the full story.

And labs are often misinterpreted or vary based on your cycle day.

As I was promoting and talking about The Fertility Formula I noticed a common question. I was setting the stage that chronic inflammation influences ovarian function and fertility, and many interviewers and listeners asked, “Does this mean inflammation also impacts menopause?” Well, if chronic inflammation is associated with diminished ovarian reserve, premature menopause, and poor ovarian function, could the opposite be true as well? Even if we can’t prevent ovarian failure, can we slow it down? Can we delay ovarian failure to the latest we each personally could have? Can we extend our own ovarian function?

But we would need a way to track and measure the trajectory of your ovaries for this to be true.

This month, I found myself reading several papers that all pointed toward the same idea.

Women’s health is beginning to move away from measuring isolated hormone values and toward measuring trajectories.

Not just: What is your AMH?

But: Where are your ovaries headed?

A new concept: ovarian age

One of the most interesting papers published this past year came from researchers at Peking University.

Instead of simply reporting an AMH level, they asked a different question—Could we estimate an individual’s endocrine ovarian age?

The idea fascinated me enough that I decided to run my own results.

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This week, I’m breaking down the science about ovarian aging based on a recent article in Nature.

Ovarian Aging Begins Before Menopause: New Research Suggests the Ovary Ages Long Before It Stops Working

Journal: Nature Aging (June 2026)

Read the study:
https://www.nature.com/articles/s43587-026-01140-z

Why this study caught my attention

If you’ve followed me for any length of time, you’ve probably heard me say that the ovary is much more than an organ that stores eggs. It is an endocrine organ that loves to make hormones (and estrogen is its favorite). For too long, we have simplified the function of the ovary to be a storage center for eggs to ovulate, and once we are out of eggs the ovary stops working.

I often use the analogy of an ovarian vault. Imagine you are born with all the eggs you are ever going to have in a vault inside your ovary. Ovarian formation begins surprisingly early when you are still a fetus. At 20 week gestation (as a baby still in your mom’s womb), you will have the most eggs you will ever have—6 to 7 million. From there, a rapid loss of 80% of your eggs occurs before you are ever born, resulting in having only 1-2 million eggs present at birth. Oocyte loss continues until you have only 300,000-500,000 by the time you start your first menstrual cycle.

Throughout your reproductive life:

• follicles are recruited (one egg grows inside each follicle)

• most undergo atresia (most eggs die)

• only a small percentage ovulate (400 total in your lifetime)

• eventually the follicle pool becomes critically low

• menopause occurs

This “egg depletion” model has explained ovarian aging for decades, but interestingly, women still have around 1,000 follicles remaining at menopause. So menopause isn’t triggered because the ovary reaches zero eggs. Something else is happening within the ovarian tissue itself that makes the ovary no longer able to respond when our vault gets near-empty.

Ovarian aging is much more than just losing eggs. But even when we talk about ovarian aging, we almost always reduce the conversation to one question: How many eggs do you have left?

This paper argues that we’ve been asking the wrong question. Instead, we should be asking: How healthy is the ovarian environment that supports those eggs?

This is the question that is actually important for our health now, in the future, and for aging as a woman.

What did the researchers actually do?

This wasn’t a clinical trial, but it was a laboratory study using mice, which are commonly used to model reproductive aging because many of the cellular pathways involved in ovarian aging are conserved across mammals.

The investigators used spatial transcriptomics, a cutting-edge technology that allows scientists to map not only which genes are active but where those genes are active within intact tissue. Think of it like Google Maps for gene expression. Traditional RNA sequencing tells us which genes are turned on. This allows us to know which cells are talking to each other, where inflammation is occurring, and how tissue organization changes over time. That level of detail simply wasn’t possible a few years ago.

What did they discover?

1. Aging starts before reproductive function stops

One of the most interesting observations was that the ovaries already showed evidence of aging while the animals were still cycling normally. In other words, ovarian aging begins well before menopause. The researchers observed:

• loss of normal tissue organization

• impaired coordination between different ovarian cell populations

• altered communication between follicles and surrounding support cells

• early inflammatory changes (chronic inflammation plays a role)

This is remarkably similar to what we see clinically. Women experience perimenopause symptoms and declining fertility years before they experience irregular menstrual cycles. Meaning, the function of the ovaries is impaired before we are out of eggs.

2. The immune system becomes much more active

One of the biggest findings was the dramatic increase in immune cells within aging ovaries. Specifically, the researchers identified increases in numerous types of immune cells, including: macrophages, T lymphocytes, and inflammatory signaling pathways.

These immune cells appeared to be actively communicating with granulosa cells (the cells responsible for nurturing developing eggs) and producing pro-inflammatory signals that could interfere with normal follicle development.

3. Cell-to-cell communication begins breaking down

The ovary is an incredibly coordinated organ. Every month follicles grow, hormones are made, ovulation occurs, and the ovary remodels itself. The study found that this coordination becomes increasingly disorganized with age. The authors describe a loss of “spatiotemporal coordination,” meaning the normal timing and location of cell signaling begins to deteriorate making it harder for the ovary to do it’s job well. Think of it like an orchestra where the musicians are still playing but nobody is playing in synchrony.

4. Tissue cleanup appears less efficient

You may not know that part of normal cell function includes clearing out damage. In this study, the investigators also found evidence that aging ovaries become less efficient at clearing damaged cells and cellular debris. This impaired “housekeeping” is something we see in many aging organs.

If damaged cells aren’t removed efficiently, inflammation can increase, fibrosis can develop, and tissue function gradually declines. This plays a role in how the ovarian cells age faster than other cells in the body.

Strengths and Limitations of this study

One reason I think this paper is important is because of its methodology. Rather than simply measuring hormone levels or follicle counts, they created a detailed map of ovarian aging.

As exciting as this work is, it is important to remember that this is an animal study. Mouse ovaries are not identical to human ovaries.

Also, the study identifies associations between immune-cell infiltration and ovarian aging but cannot prove that inflammation causes ovarian aging. It’s possible that inflammation is a consequence of aging rather than its primary driver.

Further, we don’t yet know whether modifying these inflammatory pathways would meaningfully delay menopause, although this is an exciting potential area of investigation.

How does this fit with previous research?

Over the past five years we’ve seen several major themes emerge in ovarian aging research:

• chronic low-grade inflammation (”inflammaging”)

• mitochondrial dysfunction

• immune-cell activation

• fibrosis

• altered extracellular matrix remodeling

• disrupted ovarian blood supply

This new study integrates many of these observations into a single framework by showing how these processes interact spatially within the ovary. This is supporting data that cell communication and inflammation contribute to the change in ovarian function seen with age, beyond just running out of eggs.

Does this change what I recommend to patients?

Not yet. But it does reinforce why I continue to emphasize the foundations that influence inflammatory and metabolic health:

• anti-inflammatory eating

• regular exercise and building muscle

• adequate sleep

• avoiding smoking and other toxins

• treating insulin resistance when present

• reducing chronic inflammatory burden where possible

Essentially, we want to reduce chronic inflammation where possible and treat insulin resistance where we can. Although we don’t have evidence that these interventions prevent menopause, they certainly support the biological environment that the ovary depends on and likely play a role in extending ovarian function as long as possible.

For decades we’ve viewed ovarian aging as an issue of egg quantity. Increasingly, the science suggests we should also think about ovarian quality—the health of the tissue, immune system, blood vessels, and support cells that allow those eggs to function.

I suspect this shift, from counting eggs to understanding the ovarian ecosystem, will define the next decade of reproductive medicine.

This is the kind of breakdown I’ll be doing every single week — reading the actual research so you don’t have to, and translating it into what it means for your body and your decisions.

Everything like this post stays free. If you want to go deeper, paid subscribers get a weekly deep-dive essay, a monthly live Q&A where I answer your questions directly, and access to the chat.

I’m also opening founding-member spots for the readers who want to build this with me from the beginning.

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And if you’re here for the free work — I’m genuinely glad you are. Forward this to one woman who’d want to understand her ovaries better than anyone ever explained to her.

XO, Nat.

Infertility Warning Signs

One of the most common questions I get asked is: How will I know if I’m going to have trouble getting pregnant? Can I test my fertility? I want to be pregnant one day, but not now.

One of the hardest things is that while I can test your fertility right now and identify if something is wrong at this moment, none of that guarantees you’ll be able to get pregnant in the future. However, one of the biggest sources of regret I see is when someone has warning signs that something is wrong but didn’t know about them. This can lead to months or even years of trying to conceive when, in reality, they should have sought fertility treatment sooner.

That’s why this is so important. Here are six of the top signs or symptoms that may indicate a higher chance of infertility.

Disclaimer: Some people will have these signs and symptoms and still not have infertility. Nothing is 100%, but this information can help guide you on whether you should seek an evaluation sooner, consider fertility preservation (like egg freezing), or get fertility testing done at an earlier stage.

1. Painful Periods or Painful Intercourse

Painful periods, specifically severe pain during menstruation, or pain with intercourse (especially deep penetration or certain positions), can be a sign of endometriosis. Endometriosis is a chronic inflammatory disorder with an autoimmune component. It causes inflammation and can lead to scarring, which may reduce egg count and make it harder to conceive.

Some people with endometriosis have no symptoms, while others experience debilitating period pain. A good rule of thumb is:

• If your periods interfere with daily life causing you to cancel plans, miss work, or avoid activities then you should be evaluated.

• If you experience vomiting or fainting due to period pain, that is NOT normal and may indicate endometriosis.

2. Irregular or Absent Periods

Your period is a vital sign of your reproductive health. If you’re not on hormonal contraception and your periods are not regular and predictable, something may be off. This can include:

• Irregular cycles

• Skipped months

• Abnormal spotting or bleeding

Potential causes include hormone dysfunction, thyroid disease, polycystic ovary syndrome (PCOS), or hypothalamic dysfunction. I’ve seen many cases where someone has been trying to conceive for a year but has only had a few periods—meaning they’ve only had a few chances to get pregnant. If your cycles are not regular, seek an evaluation before trying to conceive.

3. Low Libido or Erectile Dysfunction in Your Partner

For male partners, issues such as low libido or erectile dysfunction can indicate low testosterone levels. Testosterone is produced at the same time as sperm, so low testosterone can also mean low sperm count. If your partner is experiencing these symptoms, a semen analysis should be done earlier rather than later.

Important: If your male partner is taking testosterone supplements, this can act as male birth control and suppress sperm production entirely. This should be addressed before trying to conceive.

4. History of Chlamydia or Gonorrhea

A history of chlamydia or gonorrhea can increase the risk of tubal infertility. These infections can spread from the cervix to the uterus and fallopian tubes, causing scarring and blockages. This can lead to ectopic pregnancies or make natural conception impossible without IVF.

If you have a history of these STIs and are struggling to conceive, a tubal evaluation should be done. This can be performed via:

• Hysterosalpingogram (HSG): An X-ray dye test to check if the tubes are open.

• Saline Infusion Sonohysterogram (SIS): A water-based ultrasound test for tubal patency.

5. Underweight or Overweight BMI

Your weight plays a crucial role in fertility. Both underweight and overweight individuals may have difficulties conceiving.

• Underweight individuals may experience hormonal disruptions that impair ovulation and implantation.

• Overweight individuals may experience inflammation and hormonal imbalances that affect egg quality and uterine lining.

Studies on donor egg recipients show that those with a normal BMI have the highest success rates, while those with very low or high BMIs have lower pregnancy rates—even when using high-quality eggs.

If you plan to conceive in the future, working towards a healthy BMI can optimize your fertility.

6. Personal or Family History of Autoimmune Disease

Autoimmune diseases are increasingly common and often take 7–10 years to diagnose. Many women are diagnosed in their mid-30s to mid-40s, meaning they may experience unexplained infertility or recurrent pregnancy loss before receiving a diagnosis.

Autoimmune diseases often run in families. Even if your family members have different conditions, a family history of autoimmune disorders should prompt an earlier evaluation if you’re having trouble conceiving.

You can also learn this and so much more in my new book The Fertility Formula.

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When Should You See a Fertility Doctor?

The standard guidelines for seeing a fertility specialist are:

• Under 35 years old: If not pregnant after one year of regular, unprotected intercourse.

• 35 and older: If not pregnant after six months.

• 40 and older: Ideally, get an evaluation before trying to conceive.

However, these guidelines assume everything is functioning normally. If you have any of the above warning signs, it’s wise to seek an evaluation sooner before you want to conceive.

WHAT DOES FERTILITY TESTING INCLUDE?

Basic fertility testing evaluates:

• Uterus and fallopian tubes (HSG or SIS)

• Egg count (ovarian reserve) through blood tests like AMH

• Semen analysis for male partners

While these tests provide insight into your fertility at the moment, they cannot predict the future. However, if an issue is detected now, you may choose to adjust your plans, freeze eggs, or seek treatment sooner—giving you more control over your fertility journey.

By staying informed and proactive, you can make empowered decisions about your reproductive health. If you resonate with any of these warning signs, don’t wait—seek an evaluation and take control of your fertility today.

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Imagine your ovary as a vault where all your eggs are kept. Every month, a group of eggs comes out of that vault, and this process starts even before you're born. Here’s a timeline of what happens:

• At five months in utero: You have the highest number of eggs you will ever have—about 6 to 7 million.

• At birth: The number decreases to about 1 to 2 million.

• At puberty: You have around 100,000 to 200,000 eggs.

• Over your lifetime: You will ovulate about 400 eggs at most.

• Menopause: You reach a point where there are no longer enough eggs to respond to hormonal signals from the brain.

This natural decline in egg count happens to everyone and is an inevitable part of aging.

How Your Ovaries Release Eggs

Each month, your ovary releases a group of eggs, and this happens even before you ever get your first period. Every egg grows inside a follicle, a fluid-filled structure visible on ultrasound, but the egg itself is microscopic.

• When your ovaries are full of eggs, more are released each month.

• As your egg count declines, fewer eggs are released monthly.

• The "vault keeper" inside the ovary determines how many eggs to send out based on how full the ovary is.

The Role of Hormones in Puberty and Ovulation

Puberty isn't just about getting your period—it’s the maturation of your brain, ovaries, and adrenal glands.

• The brain starts sending out follicle-stimulating hormone (FSH) to encourage egg growth.

• Before ovulation, estrogen levels rise until they trigger a luteinizing hormone (LH) surge.

• This LH surge causes a follicle to rupture, releasing the egg—this is ovulation.

• After ovulation, the follicle transforms into the corpus luteum, which produces progesterone to support a potential pregnancy.

If pregnancy does not occur, progesterone levels drop, signaling the uterus to shed its lining—this is your period.

Understanding Egg Loss and Ovarian Reserve

Egg loss is continuous, regardless of external factors like birth control or pregnancy. Important facts:

• You lose the most eggs before birth. The most dramatic loss happens between 5 months in utero and birth.

• Birth control doesn’t preserve eggs. Your body continues releasing eggs from the vault each month, but they do not ovulate—they simply die off.

• Pregnancy and breastfeeding do not stop egg loss. Even if you're not ovulating, eggs continue to be lost every month.

• Menopause occurs when the ovary no longer has enough eggs to respond. The brain keeps sending high levels of FSH, but the ovary cannot produce a response.

Signs of Declining Ovarian Reserve

As you approach menopause, you may notice changes in your cycle:

• Shortening cycles: Your cycle interval becomes shorter because eggs are responding faster to FSH.

• High estrogen and low AMH: Early signs of ovarian aging include a drop in Anti-Müllerian Hormone (AMH) and increased estrogen levels.

• Longer cycles and skipped periods: As your ovarian reserve gets very low, it takes longer for the brain’s signals to stimulate an egg to grow.

Once you have gone 12 months without a period, you are officially in menopause.

How We Measure Ovarian Reserve

We can assess your ovarian reserve using these tests:

• Anti-Müllerian Hormone (AMH): The most reliable test, made by the cells surrounding follicles. A higher AMH indicates a greater number of eggs.

• Follicle-Stimulating Hormone (FSH): Measured on cycle days 2-3. Higher FSH indicates lower ovarian reserve.

• Antral Follicle Count (AFC): An ultrasound measurement of how many small follicles are visible in the ovaries.

Typical AMH levels by age:

• 30 years old: AMH ~2-4, AFC ~20

• 35 years old: AMH ~1.5-3, AFC ~15

• 40 years old: AMH ~1-1.5, AFC ~10

Does Egg Freezing or IVF Make You Run Out of Eggs Faster?

It does not. When we do egg freezing or IVF, we can only retrieve the eggs that were already recruited from the vault that month. These eggs would have been lost if we didn’t retrieve them. You’re not using up more eggs—you’re just giving those eggs a chance instead of letting them die.

Final Thoughts

Your ovarian reserve is unique to you, and a single test only tells us where you are right now—not where you started or how fast you're losing eggs. Understanding this process helps you make informed decisions about your reproductive health.

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