There is a way of telling the story of women's bodies that goes like this. You have your reproductive years. You have babies. Things settle. Years pass. You arrive at perimenopause. The end.

That is not the story. That is a summary of the story, written for a chart in a textbook, and it leaves out the part that matters — which is what is happening underneath, in the system that has to actually do the work of carrying a woman through all of it. The system is the same one. It does not get reset between births. It does not get a fresh start at forty. It is the same nervous system, the same stress response, the same HPA axis, and whatever it has been doing in the years before perimenopause is exactly what it brings with it when perimenopause arrives.

I did not see this when I was inside it. I want to write about it now, because I think there are a lot of women in their thirties and forties who are still being told that postpartum and perimenopause are two separate biological events, and who would be served — really served — by knowing they are not.

I had two babies close together. I was postpartum, and then I was postpartum again. I did not return to baseline between them, but I assumed that was just what happens — that you do not get all the way back to who you were before the first one, before the second one comes. I assumed the depleted, slightly-not-myself version of me was the new mother me, and that with enough time and sleep and intentional living, I would land somewhere recognisable.

Time passed. Sleep was hard to come by. Intentional living was a thing I read about in books and did not have bandwidth to implement. The not-myself feeling did not lift. My periods came back erratic and then heavy. My anxiety did not go anywhere. The version of my body that I had been waiting to return to was not returning.

By thirty-six, I was reading the symptoms as perimenopause. Hot flushes. Cycles that no longer made sense. The waking at 2am. The mood swings. I assumed — like a lot of women do — that I had been postpartum for a while, that was done, and now I was in early perimenopause, that was a separate thing. Two events, side by side. The textbook chart.

What was actually happening was not two events. It was one continuous biological story in which my HPA axis — the stress system that regulates cortisol, that gets reorganised by pregnancy, that takes time to settle after birth — had never settled. The relational stress I wrote about in Vol. 011 was reorganising the same system that was supposed to be recovering from pregnancy. The mould I wrote about in Vol. 015 was adding inflammatory load to the same system that was being asked to stabilise ovarian hormones again. The cortisol mechanism I described in Vol. 012 — chronic HPA activation suppressing the menstrual cycle — was running in postpartum me the same way it would run in perimenopausal me. Same axis. Same biology. Different reproductive window.

The thing my body was reading at thirty-six was not the beginning of perimenopause. It was the cumulative load of a postpartum recovery that had never been allowed to happen, walking into the natural shifts of midlife. Two events in the calendar; one continuous event in the body.

I want to bring the research here because I think it matters that this is not just my experience. There is a body of literature that names exactly what I am describing, and almost no woman in midlife is being given access to it.

In 2023, a group of researchers from Johns Hopkins, Harvard, Penn State, the University of Colorado, the University of Texas, and the Mayo Clinic published a review in Frontiers in Endocrinology with a title that names the whole story: The role of the hypothalamic-pituitary-adrenal axis in depression across the female reproductive lifecycle (Hantsoo et al., 2023). The thesis of the paper is simple and important. The HPA axis — the stress system — is not separate from the reproductive system. They talk to each other. Estrogen and progesterone modulate cortisol. Cortisol modulates ovarian hormones. And at each major reproductive window — puberty, premenstrual phase, pregnancy, postpartum, perimenopause — the HPA axis goes through a reorganisation that changes how the system regulates itself going forward.

What the review establishes, drawing on decades of published research, is that women who experience HPA dysregulation at one reproductive window are at significantly elevated risk at the next one. A woman with postpartum depression has elevated risk for perimenopausal depression. A woman whose HPA axis was sensitised in adolescence has elevated risk in postpartum. A woman whose cortisol response was altered by chronic stress during her reproductive years walks into perimenopause carrying that alteration.

This is not a small finding. It is the difference between treating perimenopausal symptoms as the start of a new hormonal phase and treating them as the visible expression of a stress system that has been adapting and re-adapting for years. The framework most women are handed in their forties is the first one. The truth, as the research describes it, is the second one.

A separate analysis from the Penn Ovarian Aging Study — the same cohort I cited in Vol. 014 — explicitly draws this continuum. Women with a history of major depression during the postpartum period had substantially elevated risk for major depression during the menopausal transition. Same women. Same HPA axis. Different decade of their lives (Bromberger & Epperson, 2018).

This was not happening in spite of the postpartum experience. It was happening because of it. The postpartum window had reorganised the stress system, and the perimenopausal window was meeting that reorganised system, not a fresh one.

If you are reading this and you had a baby in the last ten or fifteen years, and you are now in your late thirties or your forties, and you are wondering whether the symptoms you are experiencing are still postpartum, or finally perimenopause, or maybe both — I want you to know that there is another question worth holding alongside it.

What is more likely happening is that the HPA axis that was reorganised by your postpartum experience never fully settled — because the conditions of postpartum recovery, in most women's actual lives, do not allow it to. Most women do not get the year of low-stress, well-supported, well-resourced recovery that the biology actually requires. They get whatever life had ready for them when the baby arrived. And the system carries forward whatever state it was last left in.

So the symptom cluster you are looking at in your forties — the broken sleep, the cycle changes, the anxiety, the cognitive fog, the inability to feel like yourself — is not necessarily two separate problems with two separate explanations. It is, more often than I think the framework allows for, one continuous reading of a stress system that has been carrying more than it could comfortably carry for a long time, now walking into a window where its compensations are running out.

I have written this with my own arc in mind — postpartum, then perimenopause — because that is the story I lived. But the continuum I am describing is not about having had babies. It is about the HPA axis carrying decades of reproductive-window work, whether or not pregnancy was one of those windows. If you did not have children, your stress system has been doing the same job through other chapters — premenstrual cycles month after month, chronic stress across your twenties and thirties, the cumulative load of relational and work and caregiving and life. The biology is the same. The reproductive windows your body has lived through are just different ones. Your perimenopause is meeting your HPA axis exactly where it has been, regardless of whether children were part of the arc.

The good news in this, if there is good news, is the same news I wrote in Vol. 011 — the system is responsive. When the conditions change, the system changes. The HPA axis carries memory, but it does not carry permanence. When the inputs reduce, when the inflammation comes down, when the relational and environmental loads ease, the system has somewhere to go.

I had my first baby at thirty-three. I had my second at thirty-five. If a clinician — any clinician, at any point in those years — had said to me, "the way you recover from this postpartum window is going to shape how your body meets perimenopause," I would have made different decisions. Not all of them. Some of them I could not have made. But some of them I could.

I would have taken postpartum recovery more seriously, as the years-long undertaking it actually is. I would have taken the chronic stress of my early thirties more seriously, not as something I was supposed to be able to handle because I was young, but as something my biology was reading and recording. I would have asked about my cortisol patterns earlier. I would have asked about my inflammatory markers earlier. I would have understood that the woman walking into perimenopause was going to be a sum of everything the woman in her late twenties and early thirties had been carrying.

I am writing this dispatch in part for the women in their late twenties and thirties who are still in that window. The work you do now — what you choose to take seriously, what conditions you allow your body to recover in, what loads you decide are non-negotiable to reduce — is the work that determines what your body brings to forty-three or forty-seven. It is not too early. It is, in fact, exactly the time.

And I am writing it for the women in their forties who are reading symptoms as perimenopause and wondering if something else is also there. There usually is. The thing that is also there is often the postpartum window your body never finished. Naming it does not make it bigger. It makes it more readable. And once it is readable, you can do something with it.

I stand by you in this, un abrazo.
— Belinda Singkepe Holloway

LE PROTOCOLE: Turning the Research into Intelligence

Three concrete moves for the woman who recognises herself in this.

The AION Atelier Baseline is the panel built to read exactly this continuum — cortisol patterns across the day, sex hormones across the cycle, inflammatory load, metabolic markers — against women's reference ranges, not male-default ones. It is what makes the postpartum-to-perimenopause arc a thing you can actually see in your own data, instead of a thing you are trying to read between the lines of two separate appointments. Begin here.

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THE SOURCES:

Hantsoo, L., Jagodnik, K. M., Novick, A. M., Baweja, R., Lanza di Scalea, T., Ozerdem, A., McGlade, E. C., et al. (2023). The role of the hypothalamic-pituitary-adrenal axis in depression across the female reproductive lifecycle: current knowledge and future directions. Frontiers in Endocrinology, 14, 1295261. DOI: 10.3389/fendo.2023.1295261. PMC10750128. (Multi-institution narrative review — Johns Hopkins, Harvard, Penn State, Colorado, Texas, Mayo Clinic — establishing that the HPA axis goes through reorganisation at each major reproductive window, and that dysregulation at one window predicts vulnerability at the next.)

Bromberger, J. T., & Epperson, C. N. (2018). Depression during and after the perimenopause: impact of hormones, genetics, and environmental determinants of disease. Obstetrics and Gynecology Clinics of North America. PubMed: 25585035. (The Penn Ovarian Aging Study finding that postpartum depression history independently predicts depression during the menopausal transition.)

Metcalf, C. A., et al. (2021). Brain, Behavior, & Immunity – Health, 15, 100280. (Penn cohort inflammatory baseline data, referenced from Vol. 014.)