We're About to Define "Normal Menopause." We Should Be Nervous About What We're Using as the Baseline.
After decades of being medicine's most underfunded, least-discussed transition, menopause is finally having its moment. In the US, the FDA is revisiting the black-box warnings on hormone therapy. Here at home, the Australian Government has just launched its first-ever national menopause and perimenopause campaign, "Could This Be Perimenopause?", backed by a $792.9 million women's health package, new Medicare-funded menopause health assessments, and cheaper access to hormone therapy on the PBS. Over 100,000 Australian women have already had a menopause health assessment since it became Medicare-eligible last July. This is overdue, and I'm genuinely glad it's happening.
But I have a concern sitting underneath the momentum, and I want to name it before the data hardens into doctrine: the women whose bodies we're studying right now, to define what menopause is, are not a neutral baseline. They are the most chemically exposed¹, dietarily disrupted², and sedentary³ cohort of women in human history, carrying a chronic stress load our bodies were never built for. When we describe "what menopause does" using this population, we may not be describing menopause. We may be describing menopause happening on top of forty years of accumulated environmental damage, and mistaking the sum for the transition itself.
Why we live decades beyond our reproductive years
There's something worth understanding before we get to any of that: why does menopause happen at all? Across the animal kingdom, it's extraordinarily rare for a female to live long past the point she can reproduce, evolutionarily, that's expensive, and nature is not usually generous with expenses it can't recoup. Yet humans do it. So do orcas and short-finned pilot whales, and almost nothing else.
The leading explanation, built from decades of fieldwork by anthropologist Kristen Hawkes among Hadza hunter-gatherers in Tanzania, is known as the grandmother hypothesis: post-reproductive women who kept provisioning food and care for their grandchildren measurably improved those children's survival and freed their daughters to have more children sooner. A 2008 review spanning dozens of historical and ethnographic populations worldwide found the same pattern holding up again and again, a grandmother's presence was consistently linked to better odds for her grandchildren. Killer whales tell a strikingly parallel story: post-reproductive female orcas lead their pods to food during lean years, drawing on decades of accumulated ecological memory, and researchers tracking Pacific Northwest pods have found adult sons had meaningfully better survival odds while their mothers were still alive. Some evolutionary biologists now think the fuller picture involves a second mechanism too, reduced reproductive competition between mothers and daughters, rather than the grandmother effect alone explaining it entirely. But the throughline across every credible account is the same: this stage of life was not designed as decline. It was selected for, because older females, freed from continued reproduction, became more valuable to the survival of their family and community alive and active than they would have been having another child.
That's not folklore. It's a robust finding in evolutionary biology, replicated across human populations and, independently, in a handful of long-lived whale species that arrived at the same pattern on a completely separate branch of the tree of life. I find it hard to read that evidence and still see the modern experience of menopause, invisibility, dismissal, a slow shrinking rather than a stepping forward, as anything other than what it likely is: not a biological failure, but a mismatch between what this stage of a woman's life evolved to be and the conditions she's actually living it in.
Less estrogen doesn't cause this. It just stops hiding it.
Estrogen isn't just a reproductive hormone. It plays a measurable role in how the body metabolises and clears foreign chemical compounds, and it exerts protective effects on bone, vasculature, and inflammatory regulation. Here's my reading of the mechanism: perimenopause doesn't cause a woman's vulnerability to whatever she's been exposed to over her lifetime, it reveals it, as declining follicle numbers mean less estrogen production, and less of the hormonal buffering that's been quietly absorbing decades of exposure to plastics, pesticide residues, and industrial compounds.
This isn't speculative. Researchers analysing U.S. National Health and Nutrition Examination Survey data found that women with the highest exposure to certain long-lived endocrine-disrupting chemicals, PCBs, certain pesticide residues, phthalates, reached menopause two to four years earlier than their lower-exposure peers, and were up to six times more likely to already be menopausal at a given age. Multiple mechanistic reviews since have converged on oxidative stress and follicular depletion as plausible pathways. The chemical burden isn't a footnote to the hormonal story. I think it may be co-authoring it.
The "universal" symptom checklist isn't universal
If declining estrogen alone explained the modern Western menopause experience, the hot flashes, the sleep disruption, the mood volatility, the brain fog, the irritability, we'd expect to see it show up more or less consistently wherever women stop menstruating. We don't. Vasomotor symptoms are reported by roughly six in ten women in Europe and the US, compared to under three in ten in Japan, a gap medical anthropologist Margaret Lock first documented decades ago and later cross-cultural reviews have continued to confirm. Rural Mayan women in Guatemala and the Yucatán, studied across several small cohorts, showed similar reproductive hormone profiles to North American women but reported markedly fewer classic symptoms, and in several accounts, anticipated menopause with something closer to relief than dread.
The honest reading of this isn't "ancestral women had it easy", some populations report different symptoms, not none, and the data is thin and contested. But the pattern is too consistent to wave away: diet, movement, chemical load, and cultural framing are doing real biological work here, not just coloring how symptoms are perceived. Lower lifelong exposure to endocrine disruptors, higher phytoestrogen intake, and different inflammatory baselines are live explanations sitting alongside the cultural ones, and most of the research to date hasn't been designed to tell them apart.
Why the timing of this research boom matters
Here's the part I'm particularly uncomfortable about. Reference ranges in medicine are usually built by sampling a population and cutting off the extremes, typically the bottom and top 2.5%. That method quietly assumes the sampled population is healthy to begin with. It often isn't. Take ferritin: a 2023 paper in the American Society of Hematology's own education program made the case plainly, because 30-50% of women have no measurable iron stores in their bone marrow, using this standard method produces a "normal" lower limit built from a sample where nearly half were already iron-depleted. The range wasn't wrong by accident. It was wrong because the population it was drawn from wasn't well to start with. Vitamin B12 tells a similar story: several large studies have argued the standard lower limit misses widespread, symptomatic deficiency, because the "normal" population it was calculated from already included a lot of quietly deficient people. In both cases, "statistically normal" and "biologically adequate" have pulled apart, not through a labelling error, but because the reference group itself wasn't the healthy baseline it was assumed to be.
I fear menopause research is about to do the same thing, except this time, we have biomonitoring, cross-population data, and decades of exposure science that earlier reference-range mistakes were made without. I think we're capable of asking whether "normal" post-menopausal bone loss, symptom severity, and risk are biology, or a generation's environmental load quietly mistaken for it. We already know the vasomotor symptom gap between Japan and the West is real and unresolved. So will we be courageous enough to ask the harder version of that same question: is this a woman's biological experience because of the transition itself, or is it her experience depending on where and how she lives?
If the current cohort's chemical exposure, food environment, and activity levels are unlike anything experienced by any prior generation of women, then the "normal" we're about to enshrine in guidelines, hormone therapy protocols, and public understanding for the next thirty years risks being a description of adaptation to harm, dressed up as biology. Even the architects of Australia's own campaign have acknowledged this gap directly: when asked what the government is doing to address how much remains unknown, Assistant Minister Rebecca White pointed to updated clinical guidelines currently in progress, noting plainly that women have long been dismissed or under-supported by the very professionals meant to help them. That's an honest admission, and I think it's precisely the moment to ask what baseline those new guidelines will be built on.
That doesn't mean distrust the new research. It means fund the comparison work alongside it: exposure histories, dietary reconstruction, cross-cultural cohorts, and honest acknowledgment of what we don't yet know how to separate. We finally have the attention. I think we owe women a "normal" that means healthy, not merely common.
But we are where we are. So what do we actually do?
The obvious objection to all of this is fair: fascinating history of science problem, but I'm 47 and not sleeping. What's the plan? The answer isn't to wait for perfect research. It's to recognise that perimenopause is not just a diagnostic blind spot, it's a rare, forced pause where most women start paying attention to their bodies with real intent, often for the first time since their twenties. That attention is the lever. Used well, this transition can become the moment a woman resets her baseline toward optimal rather than merely adapted, not by chasing a symptom checklist, but by reducing the load her body has been quietly buffering for decades.
This isn't a detox cleanse. The credible version of "clean up your exposure" looks unglamorous: cutting back on plastic food packaging and canned goods, choosing fresh and organic over ultra-processed and conventional, being more deliberate about personal care products, and treating movement and sweat as physiological maintenance. Trials testing these exact changes reducing plastics and processed food exposure, personalised report-back on measured chemical burden, show they reliably lower measurable exposure. What's genuinely still unproven is whether lowering exposure alone measurably improves menopausal symptoms; the studies designed to test that outcome are only just being funded. That gap is worth naming honestly, because overpromising here is exactly the kind of inflated claim that got women's health research distrusted in the first place.
What the research does support is that this transition is a legitimate biological inflection point, bone density, cardiovascular risk, and metabolic regulation all shift meaningfully here, which makes it a uniquely high-leverage window for intervention regardless of the exposure question. Collectively, that argues for treating perimenopause less as a problem to survive and more as an initiation: the one moment in midlife when biology, attention, and motivation align. If we're going to spend the next decade studying what "normal" menopause looks like, the most useful thing any woman can do in the meantime is refuse to let normal and optimal quietly become the same word.
There's a load in this equation that doesn't show up in a blood panel. Most women arrive at perimenopause having spent two, sometimes three decades running the emotional infrastructure of a household, managing everyone else's health, schedules, moods, and needs before their own. That's not incidental to the biology; it compounds it. And this isn't only true for mothers. Plenty of women moved through this same decades-long stretch of life differently, building careers, carrying households or aging parents, holding communities together in ways that don't get called caregiving but function exactly like it. The grandmother hypothesis explains why this stage evolved around care for kin, but it was never only about biological motherhood; it's about the accumulated cost of being the one who holds things together, in whatever form that took. Chronic stress has its own well-established hormonal and inflammatory signature regardless of the shape a woman's life has taken, and honestly, just being human at full stretch for that long leaves a mark. A body that has spent years in "manage everyone else first" mode often has little practical capacity left for tuning into its own signals. Part of resetting the baseline is not just what you stop putting in your body, but what you stop deprioritising about yourself. That takes more than a supplement or a spreadsheet, it takes actively unlearning the habit of coming last, and giving yourself permission to treat this transition as worth the same attention you've spent years giving everyone else.
Notes
¹ Most chemically exposed: Over 80,000 synthetic chemicals are registered for commercial use in the US alone, with roughly 1,000 new ones added each year, fewer than 10% have been tested for human health effects. Persistent synthetic chemical pollutants have accumulated in the environment and food webs globally since World War II, and are now documented in wildlife, human blood, and breast milk worldwide. This is a specifically post-WWII phenomenon; no prior generation lived inside this density and diversity of synthetic compounds.
² Most dietarily disrupted: Ultra-processed food (UPF) intake among US adults rose from 53.5% to 57% of total daily calories between 2001 and 2018 alone. The exponential rise of ultra-processed foods in the food system dates specifically to the 1980s, paralleling the timeline of rising global obesity rates. Other countries show even starker shifts, Sweden saw a 142% increase in UPF consumption between 1960 and 2010; Canada's UPF share doubled between 1938 and 2001.
³ Most sedentary: The decline in physical activity across all domains of daily life occurred earlier than the major dietary shifts, driven by the same modernisation forces, chiefly the reduction of physically demanding manual labour, with more recent shifts toward television, smartphones, and other sedentary leisure activities adding further sedentary time on top of that.
References
Note: full citations for the numbered claims in the Notes section above:
Health and Environment Alliance / Health & Environment (n.d.). Biomonitoring: synthetic chemical registration and testing rates.
Thornton, J. et al. (2002), cited in Linking Empirical Estimates of Body Burden of Environmental Chemicals and Wellness using NHANES Data. Documentation of post-WWII global accumulation of persistent synthetic chemical pollutants in environment, wildlife, and human tissue.
Juul, F. et al. (2022). Ultra-processed food consumption among US adults from 2001 to 2018. American Journal of Clinical Nutrition.
Nutrition transition and ultra-processed food prevalence (2021). PMC, cross-national UPF consumption trend data (Sweden, Canada).
Hawkes, K., O'Connell, J.F., Blurton Jones, N.G., Alvarez, H. & Charnov, E.L. (1998). Grandmothering, menopause, and the evolution of human life histories. PNAS, 95(3), 1336–1339.
Sear, R. & Mace, R. (2008). Who keeps children alive? A review of the effects of kin on child survival. Evolution and Human Behavior, 29(1), 1–18.
Brent, L.J.N., Franks, D.W., Foster, E.A., Balcomb, K.C., Cant, M.A. & Croft, D.P. (2015). Ecological knowledge, leadership, and the evolution of menopause in killer whales. Current Biology, 25(6), 746–750.
Croft, D.P., Johnstone, R.A., Ellis, S., Nattrass, S., Franks, D.W., Brent, L.J.N., Mazzi, S., Balcomb, K.C., Ford, J.K.B. & Cant, M.A. (2017). Reproductive conflict and the evolution of menopause in killer whales. Current Biology, 27(2), 298–304.
Foote, A.D. (2008). Mortality rate acceleration and post-reproductive lifespan in matrilineal whale species. Biology Letters, 4(2), 189–191.
Cooper, A. et al. Analysis of NHANES data (1999–2008) on endocrine-disrupting chemical exposure and menopause timing, reported via Chemistry World (2024).
Aydemir, D. & Ulusu, N.N. (2023). Impact of endocrine-disrupting chemicals on premature and early menopause. Frontiers in Endocrinology.
Wu, M., Harlow, S., Randolph, J., Gold, E. & Park, S. (2024/2025). Environmental effects on menopause timing and reproductive aging. Seminars in Reproductive Medicine.
Lock, M. (1998). Menopause: lessons from anthropology. Psychosomatic Medicine; Melby, M.K., Lock, M. & Kaufert, P. (2005). Culture and symptom reporting at menopause. Human Reproduction Update.
Nappi, R.E. et al. (2021), cited in Whelan, Dempsey & Chi (2026) scoping review of cross-cultural vasomotor symptom prevalence.
Flint, M. (1975). The menopause: reward or punishment? Psychosomatics; supplementary Mayan cohort data summarized via Women in Balance and Women's Health Network.
Frontiers in Reproductive Health (2025). Scoping review of menopause symptom prevalence across ethnic groups.
Sant'Anna, T.M. et al. (2023). Sex, lies, and iron deficiency: a call to change ferritin reference ranges. Hematology, American Society of Hematology Education Program.
MTHFR Support Australia (2015, ongoing community data). Vitamin B12 reference range and subclinical deficiency.
Australian Government Department of Health, Disability and Ageing (2026). "Could This Be Perimenopause?" national menopause and perimenopause campaign; Assistant Minister Rebecca White, public remarks on menopause guideline development.
FIGO (2022). Nutritional interventions and endocrine-disrupting chemical exposure: a semi-structured review.
REED Study protocol (2024). Personalized endocrine-disrupting chemical exposure reduction via biomonitoring report-back.