Two types of women in perimenopause: what morning cortisol reveals

Lab finding — week of May 24, 2026 This is week 9 of Lua Labs. Line L2, sub-topic 2.4 — adrenal allostasis in perimenopause.

Carmen is 47 and has felt different for two years

Her cycles used to be 28 days, like clockwork. Now they swing between 24 and 38. One month she ovulates, the next she does not. Some weeks she sleeps well; others she wakes up at 3am with her mind racing. She had labs done: normal estradiol, "borderline" FSH. Her doctor said: "it is not menopause yet".

She is right. It is not. It is something harder to name — and that is why almost no one explains it well.

It is the moment when the ovary starts to fail just as another hormonal system — the adrenal system — has already spent years accumulating wear from caregiving, work and the shifts of life. Two simultaneous hormonal systems entering transition at the same time. And no isolated lab test captures it.

Adrenopause: the parallel decline no one diagnoses

While all clinical attention focuses on ovarian decline (FSH, AMH, estradiol, progesterone), a second hormonal decline happens in parallel and in silence.

The adrenal glands produce DHEA and DHEA-S from a specific zone of their cortex. This process peaks around ages 25-30 and then falls progressively — approximately 1-2% per year — without any menstrual event to signal it. At 47, a woman has approximately 50-60% of the DHEA-S she had at her peak (Sowers et al. 2012, SWAN study).

DHEA-S does not act directly: it is a pre-hormone that is converted inside target cells into active androgens (testosterone) or estrogens (estradiol, estrone) depending on the local enzymes available. Its potency comes from its metabolites.

Cortisol, in contrast, does not decline with age in the same way. Daily production remains relatively stable or even increases during perimenopause (Grub et al. 2021, Swiss Perimenopause Study). What changes is the shape of the curve — and that is what matters.

The result for Carmen at 47: the DHEA-S:cortisol ratio — her most precise indicator of anabolic vs catabolic balance — collapses. Not because cortisol rises dramatically, but because DHEA-S falls steadily while cortisol stays the same or rises. And this ratio is one of the best predictors of accelerated aging, metabolic risk and immunosuppression in the precision medicine literature (Park 2025, n=1,341).

Cortisol is not "one thing" — the heterogeneity of the daytime curve

This point is critical and almost always ignored in the conversation about stress and menopause. "High cortisol" or "low cortisol" does not capture reality. What matters is the full daytime pattern — the shape of the curve, not an isolated point.

In perimenopausal women under chronic stress, there are at least two clearly distinguishable phenotypes:

Phenotype A — "HPA Hyperreactive"

• Pronounced morning peak (very elevated cortisol 20-30 minutes after waking)
• Preserved or increased daytime amplitude
• Evening cortisol still relatively high

How it feels: recent or active chronic stress, fast-response personality, anxiety as the dominant symptom, sleep-onset insomnia (active mind at bedtime), intense hot flashes on waking, morning irritability.

What is happening underneath: the adrenal gland actively responds to a perceived alarm state. The body is in acute overload.

Phenotype B — "Collapsed Allostatic Load"

• Flattened or absent morning peak
• Flat curve all day (low morning cortisol, no reactive peak)
• Evening cortisol relatively high (does not drop at night)

How it feels: prolonged chronic stress or history of burnout, fatigue as the predominant symptom, brain fog, hypersomnia or non-restorative sleep, subclinical depression, diffuse hot flashes with no clear pattern, reduced immune response.

What is happening underneath: the "flat curve" does NOT mean exhausted adrenals. It means the system's set point has recalibrated downward (Cardillo 2026, Frontiers in Endocrinology).

Why this distinction changes everything

It is not cosmetic. It implies:

• Completely different interventions
• Completely different risks
• Completely different developmental trajectories

A woman with Phenotype A who receives "adaptogens for stress" may worsen if they raise her adrenocortical tone. A woman with Phenotype B who receives passive "stress reduction" may not improve — because her problem is lack of rhythmic amplitude, not excess cortisol.

Visceral fat as a source of estrogen: what changes without anyone explaining it to you

When the ovary starts to fail, the body does not run out of estrogens all at once. There is a backup system: peripheral aromatization. An enzyme called CYP19A1 (aromatase) converts androgens into estrogens in adipose tissue, liver, muscle, skin and brain.

The problem is in the substrate and the site (Lee & Den Hartigh 2025):

• The main source of androgens in late perimenopause is no longer the ovary but the adrenal gland via DHEA
• The main site of conversion shifts from the ovary (controlled, pulsatile) to visceral fat (continuous, unregulated)
• Visceral fat predominantly produces estrone (E1), not estradiol (E2). E1 has approximately 10 times less potency and a different metabolism

And here the loop closes: chronically high cortisol increases CYP19A1 activity in visceral fat. Insulin resistance does the same. It is a self-feeding circuit:

cortisol → insulin resistance → visceral fat → more aromatization → more estrone (E1) → lower estrogenic quality

The literature treats these pieces in separate silos. In Carmen, they operate as one system.

"Adrenal fatigue" does not exist — but allostasis does

The term "adrenal fatigue" was popularized in 2001 and has no basis in clinical endocrinology. The adrenal glands of a woman under chronic stress do NOT get "exhausted" — they keep producing cortisol. The real problem is upstream and systemic:

The true mechanism:

• Tissue-level glucocorticoid resistance (tissues stop responding well to cortisol, not that the adrenal stops producing it)
• Dysregulation of hippocampal feedback (Cardillo 2026)
• Loss of circadian amplitude
• Dysbiosis of the estrobolome and progesterobolome (inherited from previous Lua Labs lines)

The body is not "empty of adrenals". It is in allostasis: it has changed its set point to survive in an environment of sustained stress, paying an accumulated cost in other systems (Alebna & Maleki 2021 showed that perimenopausal women with migraine have 63% more allostatic load than those without it).

What Lua can map without touching your blood

In the Lua lab, we propose a digital classifier — the Cortisol Phenotype Classifier (CPC) — that estimates which phenotype each user is in based on patterns the app already captures:

• Morning vs evening energy (daily check-in)
• Type of insomnia (sleep onset vs early waking)
• Hot flash pattern (morning vs diffuse)
• Subjective feeling of stress ("racing mind" vs "overwhelmed-shut down")
• Estimated vagal tone (VTPS, inherited from our L1 line)

The hypothesis we are publicly committing to, ahead of the full data:

Hypothesis 16 — Lua Labs: The daytime cortisol pattern defines two biotypes of perimenopausal adrenal allostasis with qualitatively distinct developmental trajectories, symptom profiles and therapeutic responses — digitally distinguishable without serum biomarkers, with ≥70% accuracy using only Lua check-ins over 14 days.

This is research in progress, not prescription. Lua Labs publishes falsifiable hypotheses before having all the data, to stay honest with its own method.

What we can say today

If you are in perimenopause and feel that your symptoms are "weird" or that generic recommendations do not help you, there is a reason:

There is probably not ONE treatment for perimenopause. There are at least two — and they depend on the shape of your daytime cortisol.

For Phenotype A (racing mind, anxiety, sleep-onset insomnia):

• Caffeine restriction after 12pm
• Magnesium, L-theanine, glycine
• Slow breathing (4-6 cycles/min) before sleep
• Moderate morning aerobic exercise

For Phenotype B (fatigue, brain fog, hypersomnia):

• Morning sunlight 7-8am (10-15 min)
• Protein at breakfast (do not fast)
• AM exercise without fasting
• Adaptogens with evidence (ashwagandha, rhodiola) — the same ones that can worsen Phenotype A

The "when of stress" matters more than the "how much stress". And the when is dictated by your phenotype, not your willpower.

What is next in the lab

This week we close the halfway point of line L2 (HPA-HPO) with four of six sub-topics completed. In the next session, we integrate everything learned about cortisol and the cycle into one unified digital biomarker: the Lua Hormonal Health Index v1.

Every Wednesday we publish a new lab finding. If you want to follow the process, turn on notifications.

References

1. Sowers MF et al. (2012). Menopausal Transition Stage-Specific Changes in Circulating Adrenal Androgens. Menopause 19(6): 658-663. PMID 22415570.
2. Grub J et al. (2021). Steroid Hormone Secretion Over the Course of the Perimenopause. Frontiers in Global Women's Health 2: 774308.
3. Lee AA, Den Hartigh LJ. (2025). Metabolic impact of endogenously produced estrogens by adipose tissue. Frontiers in Endocrinology 16: 1682231.
4. Cardillo G. (2026). Beyond adrenal fatigue: reframing the adrenal stress index. Frontiers in Endocrinology 17: 1785454.
5. Alebna PL, Maleki N. (2021). Allostatic Load in Perimenopausal Women With Migraine. Frontiers in Neurology 12: 649423.
6. Park SB. (2025). Cortisol, DHEA-S, and cortisol/DHEA-S ratio in association with oxidative stress. Frontiers in Endocrinology 16: 1708007.

This article is part of Lua Labs, the digital lab of Lua Care. Lua Labs identifies falsifiable scientific hypotheses about female hormonal health using longitudinal app data and review of recent biomedical literature. It does not constitute medical advice. Before changing your stress management or supplementation, consult your health professional.