Dr Michelle Leary

THE 3 PHASES OF MENOPAUSE — and what nobody tells you about the timeline.

✨ PREMENOPAUSE
Regular cycles. Predictable ovulation. A hormonal choreography that supports sleep, mood, metabolism, and brain function.

But the transition out of this phase begins long before cycles become irregular. Years before perimenopause, many women start having anovulatory cycles — where ovulation simply doesn’t occur. And if you don’t ovulate, you don’t make meaningful progesterone.

That matters more than most women are ever told.

Progesterone is not just a fertility hormone. It is neuroactive — interacting with GABA receptors, influencing sleep depth, and modulating anxiety circuits.

So when women in their late 30s or early 40s notice subtle sleep disruption, increased anxiety, or a sense that their stress tolerance has changed — hormones may already be shifting, even if labs still look “normal.”

✨ PERIMENOPAUSE
Estrogen does not decline smoothly. It can be highly variable — sometimes even elevated — while progesterone drops due to inconsistent ovulation. Estrogen volatility + progesterone deficiency. That combination drives most of what women feel during this phase. It can last a decade.

✨ MENOPAUSE
Defined as 12 consecutive months without a period. No ceremony. Just a calendar milestone — and the beginning of a different hormonal landscape.

Menopause is not a failure of the body. It is a phase shift. A biologic transition that every woman who lives long enough will experience — and one that deserves far more literacy, nuance, and compassion than it has historically received. And perhaps most importantly: menopause is not the end of vitality.
It is the beginning of a different hormonal landscape — one that, when understood and supported well, can still be vibrant, cognitively sharp, metabolically strong, and deeply alive.

Michelle Leary, ND, IFMCP

For the first time in modern history, menopause is stepping out of the shadows and into real conversation. Podcasts, books, research funding, group chats, late-night voice notes between friends — women are finally talking about it openly. And as someone in my 40s, I have to say, I love being a woman in this era.

And I’ll be honest — there’s something deeply empowering about understanding what your body is doing in this phase of life. Not fearing it. Not catastrophizing it. But actually getting curious about it.

Because once you understand the physiology, the mystery fades. And in its place, you get context.

Learn more on the blog! https://drmichelleleary.com/menopause-what-is-it-really/

Menopause: What Is It, Really? Menopause isn’t a sudden hormonal cliff. Explore the science of ovarian aging, perimenopause, progesterone loss, estrogen fluctuations, and how to understand this biologic transition with clarity and confidence.

If your patient been doing everything “right” and still not getting the results they hoped for, I want you to hear this: the problem may not be what they’re doing — it may be what’s going undetected.

Any pathological process in the body can potentially impact the health of the egg or s***m, but for women, the stakes are simply higher. Untreated health conditions such as PCOS/PMOS, endometriosis, Hashimoto’s thyroiditis and hypothyroidism, undiagnosed celiac disease, and vitamin D deficiency can all contribute to subfertility or infertility depending on the extent of the disease process. In the case of PCOS/PMOS, women may not ovulate at all, making natural conception impossible. Endometriosis may lead to inflammation and scarring and can contribute to tubal dysfunction or occlusion, making fertilization difficult.

These patients aren’t failing their fertility journey — they’re being failed by a workup that hasn’t gone far enough. When a patient presents with subfertility and no clear explanation, that’s not the end of the diagnostic conversation. That’s where it should begin. As clinicians, we have the tools to look deeper. The question is whether we’re asking the right questions.

Michelle Leary, ND, IMFCP

One of the most important factors in fertility is, without question, the health of the egg. Don’t get me wrong—s***m health is mission critical, and male factor infertility is real. But by definition, the faster, more motile s***m are more likely to reach the egg. (Nature is rude.) Still, s***m DNA fragmentation and chromosomal abnormalities can contribute to infertility and early pregnancy loss.

In most cycles, one egg is released. If that egg is chromosomally abnormal, that cycle will not result in a healthy full-term birth. There is significant controversy in reproductive endocrinology about whether you can “increase egg quality.” The reason is we know, with a very high level of certainty, that egg quality declines with age—especially via increased aneuploidy risk. This, combined with insulin resistance, PCOS, metabolic syndrome, inflammation, nutrient deficiencies, and environmental exposures can contribute to challenges becoming and staying pregnant.

There are animal studies and human trials (particularly in IVF settings) suggesting that certain supports—like Coenzyme Q10—may improve some markers of oocyte/embryo quality, though results vary and data are not uniformly conclusive. Vitamin D status has also been associated with certain fertility outcomes, particularly in assisted reproduction and in the context of immune/endometrial receptivity. Glutathione-related pathways (oxidative stress defense) are biologically relevant to oocyte health, though direct clinical outcomes data are still evolving.

Quick clarification: egg quantity (ovarian reserve) cannot be meaningfully increased by fertility drugs or supplements. What fertility medications can do is recruit and mature more follicles in a given cycle—helpful for assisted reproduction—but they do not create new eggs or reverse ovarian aging. DHEA is sometimes used in diminished ovarian reserve protocols and has mixed evidence; it may influence response in some IVF populations, but it is not accurately described as “increasing egg quantity” in the sense most people mean.

Michelle Leary, ND, IFMCP

PMS and PMDD are often misunderstood as simply “hormone problems.” The reality is more nuanced—and more clinically important.

The strongest and most prevailing theory suggests a combination of predisposition to anxiety or depressive symptoms, coupled with the effect estrogen and progesterone have on the serotonin, γ-aminobutyric acid (GABA), and dopamine systems.

Serotonin, GABA, and dopamine are critical neurotransmitters that can either hinder or enhance mood. During the luteal phase, changes in these sensitive systems can disrupt, antagonize, or augment mood stabilization.

This is why symptoms are not “just in your head”—they are rooted in neuroendocrine physiology.

When symptoms become more severe, it’s important to look deeper at underlying patterns. These patterns are signals—not diagnoses to ignore.

From a functional medicine perspective, the goal is not to suppress symptoms, but to understand why these neurohormonal and inflammatory shifts are occurring in the first place.

Because when you address the root cause, you change the experience of the cycle—not just manage it.

Fertility looks simple from a distance—but when you zoom in, it is one of the most complex biological processes in the human body. Conception requires precise brain-to-o***y signaling, healthy egg and s***m development, chromosomal integrity, ovulation, fertilization, implantation, and a stable hormonal environment. Conditions like PCOS, endometriosis, Hashimoto’s thyroiditis, undiagnosed celiac disease, insulin resistance, and vitamin D deficiency can subtly shift this terrain—often in ways that routine hormone testing alone doesn’t reveal.

Read more on the blog! ➡️ https://drmichelleleary.com/why-fertility-is-more-than-hormones/

Michelle Leary, ND, IFMCP

Excited to share that I’ll be presenting a webinar this Wednesday!

As functional medicine clinicians, we talk a lot about the brain — but how often do we zoom in to the organelle level?
Mitochondria aren’t just the powerhouse of the cell. In neurons, they are central regulators of cellular stress response, repair signaling, and long-term cognitive resilience. When mitochondrial bioenergetics falter, the downstream effects on brain cell function are profound — and increasingly, the research is giving us clinically actionable targets.

In this webinar, I’ll be walking through:
→ Mitochondrial dysfunction’s role in brain and cognitive decline
→ Clinical implications of targeting mitochondrial renewal pathways
→ Emerging preclinical data on how Urolithin A may support brain againg

Would love to see colleagues there
🔗 register here! f09f7f7d-6986-4149-bb11-40516b9e4fd3@4f2a9ea4-e014-4389-9ac5-7a060d837a29" rel="ugc" target="_blank">https://events.teams.microsoft.com/event/f09f7f7d-6986-4149-bb11-40516b9e4fd3@4f2a9ea4-e014-4389-9ac5-7a060d837a29

🧠 The Central Role of Mitochondria in Brain Longevity
📅 Wednesday, April 22 | 11:00 AM PST

What is happening at the level of the mitochondria?

These organelles are far more than energy producers. They regulate inflammation, immune cell differentiation, insulin signaling, lipid metabolism, and neuronal survival. When mitochondrial function is compromised, the downstream effects are systemic — and they look like the chronic disease patterns we see every day in practice.

Cognitive decline, cardiovascular disease, metabolic syndrome, chronic inflammation — the research increasingly points to a shared bioenergetic foundation.

This is why I believe mitochondrial medicine deserves a seat at the table in every functional and integrative practice.

Michelle Leary, ND, IFMCP