GLP-1s, fertility + the pressure to stay this

 Hi ladies <3 

I want to talk about GLP-1s and fertility because I feel like we have somehow turned this into another black-and-white conversation when it is SO not black and white.

And this one feels especially personal to me.

After years of IVF, losses, obsessing over embryos, hormones, inflammation, supplements, food, workouts, literally EVERYTHING—and now being pregnant—I understand how badly you can want to feel like you're doing everything “right” for your fertility.

But I also understand the other voice.

The one that still wants to be thin.

I don't think we talk about that enough.

You can desperately want a baby AND still feel uncomfortable gaining weight.

You can be TTC and still want your jeans to fit.

You can know intellectually that your body needs nourishment and still feel really good when a medication makes you less hungry, less puffy and five pounds thinner.

Both things can exist at the same time.

And this is exactly why I think we need a much more nuanced conversation about GLP-1s in women who are thinking about pregnancy.

Because I am pro-GLP-1 when it is the right tool for the right woman.

But fertility is probably the perfect example of why context matters more than the medication itself.

FOR ONE WOMAN, A GLP-1 MAY ACTUALLY HELP GET HER BODY CLOSER TO OVULATING NORMALLY.

Think about a woman with insulin-resistant PCOS.

Maybe her A1c is creeping up.

Fasting insulin is high.

She has elevated androgens.

Her cycles are 45, 60, 90 days—or she isn't ovulating consistently at all.

She has significant visceral fat and metabolic dysfunction.

THAT is a very different patient than the already-lean 32-year-old taking a small dose because she likes feeling “less inflamed.”

And hormonally, there is a reason.

With insulin-resistant PCOS, chronically elevated insulin can stimulate the ovaries to produce more androgens and can decrease SHBG, meaning more testosterone is biologically available.

Higher androgen activity can interfere with normal follicular development.

Which means you can end up with the classic PCOS situation:

 

Lots of follicles. Not a lot of ovulation.

So if we improve insulin sensitivity and the overall metabolic environment, we may also improve the hormonal environment in which the ovary is trying to function.

And there is actually research behind this.

One meta-analysis of 11 randomized trials involving 840 women with PCOS found GLP-1 treatment was associated with improvements in insulin resistance, SHBG, testosterone, menstrual regularity and natural pregnancy rates. 

For the right woman, they may be an incredibly useful metabolic optimization tool before pregnancy.

AND THEN THERE'S THE OTHER WOMAN.

And honestly, this is the woman I'm increasingly concerned about and I have talked to so many of them at Raeya.

She doesn't have insulin resistance.

Her A1c is beautiful.

She's already lean.

She has regular-ish cycles.

But she feels so much better on a small dose of a GLP-1.

Less hungry.

Less bloated.

Less “inflamed.”

She can eat whatever she wants because she barely wants very much of it.

And maybe she's 5–10 pounds thinner than she would naturally be without it.

She tells me:

“But I feel SO much better on it.”

Okay.

But if you're trying to make a baby, I want to ask another question:

Does your hypothalamus think there is enough energy available to reproduce?

Because your reproductive system is paying attention to MUCH more than inflammation.

It is paying attention to whether your body has adequate energy coming in.

And one of the hormones involved in that conversation is leptin.

LEPTIN ISN'T JUST A “FULLNESS HORMONE.”

Leptin is made primarily by fat cells and helps communicate information about energy availability to the brain.

Your hypothalamus is essentially receiving signals all day long asking:

Do we have enough energy?

Are we adequately nourished?

Is this an environment where reproduction makes sense?

When energy availability becomes too low—whether because of significant calorie restriction, excessive exercise, weight loss or a combination of those things—leptin and insulin signaling can fall.

And that matters because those metabolic signals communicate with the reproductive axis.

Low energy availability can suppress kisspeptin and GnRH signaling, which then affects LH and FSH—the hormones your brain uses to communicate with your ovaries.

And eventually?

Ovulation can become irregular.

Progesterone can suffer because you need to ovulate to make meaningful luteal progesterone.

Cycles can lengthen.

Periods can disappear altogether.

This isn't woo-woo “your body doesn't feel safe” language. There is actual neuroendocrinology behind it. Reviews of low energy availability describe reduced GnRH signaling and changes in leptin, insulin and kisspeptin as part of the mechanism by which inadequate nutrition can temporarily suppress reproductive function.

THIS is why thinner is not always more fertile.

And I know that can be hard to hear.

Especially when we have spent our entire lives being told that thinner = healthier.

I HAD TO LEARN THIS TOO.

After everything I went through with IVF, I became SO focused on optimization.

What supplement?

What hormone?

What inflammatory marker?

What food?

What workout?

What can I control?

And I think anyone who has struggled with fertility understands that mentality because when pregnancy isn't happening, you will do basically anything to figure out WHY.

But there is a point where “optimization” can become another form of restriction.

And fertility is one area where more restriction is absolutely not always better.

Sometimes the woman with insulin-resistant PCOS really does need to improve her metabolic health before pregnancy.

Sometimes the woman doing IVF may benefit from getting her A1c, insulin, blood pressure and overall metabolic health into a healthier place before another retrieval or transfer.

But sometimes?

The optimization IS eating more.

It's gaining five pounds.

It's pulling back on exercise.

It's getting enough carbohydrates.

It's allowing body fat to come back up.

It's coming OFF the GLP-1.

It's realizing that “I don't have food noise anymore” isn't automatically a fertility benefit if the reason you don't have food noise is because you're barely hungry enough to adequately nourish yourself.

And THAT distinction matters.

WHAT ABOUT MISCARRIAGE?

This is another place I want us to be careful with language.

We know PCOS is associated with a higher miscarriage risk, and the reasons appear to be multifactorial. Insulin resistance, hyperinsulinemia, obesity, hyperandrogenism, oxidative stress and chronic inflammation are all being investigated as pieces of that puzzle.

So when I have a woman preparing for pregnancy with an A1c of 5.8, significant insulin resistance, elevated inflammatory markers and PCOS, I care about improving those things BEFORE conception.

Not because a GLP-1 is a “miscarriage prevention drug.”

It isn't.

But because I don't only care about getting you pregnant.

I care about the metabolic environment you're bringing that pregnancy into.

That distinction is SO important.

THIS IS WHY WE TEST.

This is probably the biggest thing I want you to take away from this email.

Before deciding whether a GLP-1 belongs anywhere near your fertility plan, I want to understand the woman.

Not her Instagram body.

Not whether she'd like to lose seven pounds 😂

HER physiology.

What's her A1c?

Fasting glucose?

Fasting insulin?

Triglycerides?

Inflammatory markers?

Testosterone and free testosterone?

SHBG?

DHEA-S?

LH and FSH?

Estradiol?

Is she actually ovulating?

What does her luteal progesterone look like?

How long are her cycles?

How much is she eating?

How much is she exercising?

Has she recently lost weight?

Is her BMI already low?

And depending on the picture, I may also care about leptin.

Because two women can walk into RAEYA asking the exact same question—

“Should I stay on my GLP-1 while I'm trying to get pregnant?”

—and get two completely different answers.

GOOD.

That's how medicine should work.

One may need a period of metabolic optimization before conception.

The other may need us to stop trying to make her smaller and start convincing her body that there is plenty of energy available to ovulate, build an endometrium and support a pregnancy.

AND ONE IMPORTANT THING:

GLP-1 medications are not pregnancy medications and generally are not continued during pregnancy. If you're actively TTC, your medication and timing need to be discussed with your prescribing provider and fertility team; washout recommendations vary by drug.

So please don't read this email and independently start, stop or change a GLP-1.

My point is actually the opposite.

There shouldn't be a universal GLP-1 fertility protocol.

There should be a protocol for YOU.

And maybe that's what years of fertility treatment ultimately taught me more than anything:

You cannot bully the female body into reproducing.

Sometimes we need to correct insulin resistance.

Sometimes we need to lower metabolic dysfunction.

Sometimes we need medication.

Sometimes we need MORE food.

Sometimes we need MORE body fat.

Sometimes we need to stop chasing thinness long enough to give the reproductive system what it has been asking us for.

And sometimes we need to accept that the body we feel most aesthetically comfortable in isn't necessarily the exact body composition our hormones function best in.

That is a hard conversation.

But I think women deserve to have it.

At RAEYA, this is exactly why we're so obsessed with looking at the whole picture—your labs, hormones, cycle, symptoms, nutrition, body composition, goals AND where you are in your fertility journey.

Because I don't want to tell every woman to take a GLP-1.

And I don't want to tell every woman to avoid one.

I want to understand why we're using it in the first place.

That's the difference.

xx
Kelley