Perimenopause & Menopause

This marker sits in Sense -- signals being produced, detected and acted on.

Pituitary gonadotropins. FSH rises as the ovarian follicle pool depletes and estrogen/inhibin-B feedback weakens; LH follows a similar but less clinically-used pattern. In reproductive years these drive follicle development and ovulation (see `Fertility-Women.md`); across the menopause transition, a sustained rise reflects the ovary running out of follicles to recruit.

Typical range: No single perimenopausal cutoff exists. FSH commonly runs >25 IU/L in late perimenopause and >30-40 IU/L postmenopause (assay-dependent), but the defining STRAW+10 staging system explicitly notes FSH and estradiol keep shifting until roughly 2 years after the final menstrual period, after which they stabilize. A single FSH drawn during perimenopause can be in the "premenopausal" range one cycle and "menopausal" range the next. (source: Harlow SD et al., STRAW+10 executive summary, Fertility and Sterility/Climacteric, 2012, PMC3340903)

Food first: None -- this is not a nutrition-modifiable marker. Its clinical value in perimenopause is mainly to support (not solely determine) a staging picture already suggested by age and symptoms.

When to see someone: Don't rely on a single FSH draw to rule in or out perimenopause -- because levels fluctuate wildly cycle to cycle during the transition, a "normal" FSH doesn't exclude perimenopause and an elevated one drawn during a still-cycling phase doesn't confirm menopause. See the dedicated section below on the limits of hormone testing in perimenopause.

The primary circulating estrogen. In perimenopause, ovarian follicle activity becomes erratic -- estradiol doesn't decline smoothly, it can swing from very low to higher-than-premenopausal-peak levels cycle to cycle as the ovary intermittently over- and under-responds to rising FSH, before settling into a consistently low postmenopausal range.

Typical range: Reproductive-age reference ranges (see `Fertility-Women.md`) don't apply during the transition. Postmenopausal (12+ months without a period): typically <20 pg/mL. During perimenopause itself, a single value can legitimately fall anywhere from postmenopausal-low to premenopausal-peak, which is exactly why it isn't used alone to stage the transition.

Food first: Adequate fiber intake supports healthy estrogen metabolism/excretion generally, but won't reverse the ovarian decline driving perimenopause. A Mediterranean-style eating pattern and healthy body-fat range support hormone physiology broadly.

When to see someone: Postmenopausal oestrogen sitting well below the premenopausal reference range is the expected physiology, not a deficiency to correct with supplements.

Produced by the corpus luteum after ovulation; in perimenopause, ovulation becomes increasingly irregular and anovulatory cycles (no corpus luteum, no progesterone rise) become common well before periods stop altogether -- often the earliest hormonal shift of the transition.

Typical range: Same conventional ranges as reproductive years apply *when ovulation occurs* (see `Fertility-Women.md`), but anovulatory cycles -- increasingly frequent through perimenopause -- simply won't show a luteal-phase rise at all, which is a normal feature of the transition, not automatically a problem requiring correction.

Food first: General reproductive/metabolic health support; no specific "progesterone food" exists.

When to see someone: Progesterone (as a prescription) is a real, evidence-based intervention used in menopause hormone therapy specifically to protect the uterine lining in women taking estrogen who still have a uterus -- that is a medical decision, not something achieved through diet or supplements. Don't substitute herbal approaches for that conversation.

This marker sits in Sense -- signals being produced, detected and acted on.

Same hormone used as an ovarian-reserve marker in fertility testing (see `Fertility-Women.md`), repurposed here as a predictor of *when* menopause will occur, since it reflects the size of the remaining follicle pool that must be exhausted before periods stop.

Typical range: No fixed "menopause-timing" cutoff exists; AMH is interpreted as a trend relative to age. In a large individual-patient-data meta-analysis, AMH was a significant predictor of time to menopause, and adding AMH to age alone modestly improved prediction accuracy overall (C-statistic 84% for age alone vs. 86% for age+AMH) and substantially improved prediction specifically of *early* menopause (C-statistic 52% for age alone vs. 80% for age+AMH). A separate study found a single AMH measurement in late-reproductive-age women showed a strong percentage of correct predictions (C-statistic 0.86, improving to 0.90 with age added). (source: Depmann M et al., Journal of Clinical Endocrinology & Metabolism, 2018, individual patient data meta-analysis, doi: 10.1210/jc.2018-00724; Tehrani FR et al., PMC5509971)

Food first: None for the number itself. General health -- not smoking, healthy weight, managing autoimmune conditions -- is associated with *later* average menopause age in observational data, but this is population-level association, not a proven individual intervention.

When to see someone: Be skeptical of any product marketed to "predict your exact menopause date" from AMH alone -- even the best meta-analyses show individual predictions carry real uncertainty (wide confidence intervals), especially for women who are not already close to the transition. AMH is more useful for flagging *early* menopause risk than for pinpointing an exact age for an average-risk woman.

This marker sits in Sense -- signals being produced, detected and acted on.

Testosterone in women is made by the ovaries and adrenal glands; unlike estrogen and progesterone, it does not drop sharply at menopause -- it declines gradually across the 30s and 40s and largely levels off by the time of the menopause transition itself.

Typical range: Same conventional ranges as in `Fertility-Women.md` apply (roughly 15-70 ng/dL total, highly assay-dependent), though there is no separate menopause-specific reference range. A classic cross-sectional study found total testosterone and free androgen index were significantly lower in women in their 40s than in their 20s, but did not fall further across natural menopause itself -- the decline is driven by chronological aging, not the menopause transition per se. A newer cross-sectional midlife cohort similarly found blood testosterone concentrations declining roughly 25% from age 40 through the late 50s, continuing a trajectory that started well before perimenopause, with levels stabilizing or slightly rising after that. (source: Davison SL et al., Journal of Clinical Endocrinology & Metabolism, 2005, PMID 15827095; cross-sectional midlife cohort, eBioMedicine, 2025)

Food first: No specific food or supplement reliably restores testosterone to a younger baseline. General metabolic health -- adequate protein, resistance training, healthy body composition -- supports whatever endogenous production remains.

When to see someone: Over-the-counter DHEA and testosterone precursors are hormonally active and unregulated for dose and purity -- the issue is that you cannot verify what you are actually taking. Testosterone therapy for women is a legitimate medical option in selected cases (better established outside the US, mainly for low libido); it belongs in a clinical conversation rather than a supplement aisle.

An adrenal androgen precursor that can be converted peripherally to testosterone and estrogen; unlike ovarian hormones, DHEA-S is adrenal in origin and follows its own age-related decline curve, largely independent of ovarian menopause.

Typical range: Peaks in the mid-20s and declines roughly 10% per decade thereafter -- by age 75, levels run roughly 80% lower than the mid-20s peak. For midlife women specifically, one reference cites roughly 1.0-3.0 mcg/mL for ages 35-45 versus 0.7-1.6 mcg/mL for ages 45-55 (assay-dependent, no universal "optimal" replacement target). Contrary to the assumption of a smooth decline, longitudinal data through the menopause transition show adrenal androgens don't always fall in a straight line -- some women show a transient *increase* in late perimenopause before declining further. (source: menopausal transition stage-specific changes in circulating adrenal androgens, PMC3366025)

Food first: General metabolic and stress-management support is reasonable, but nothing in the literature reliably restores DHEA-S to a younger baseline.

When to see someone: DHEA is sold over-the-counter in the US and has real androgenic side effects (acne, hair growth/loss, voice changes, mood changes) at supplemental doses. Given the null ovarian-reserve RCT and the hormone's downstream conversion to both testosterone and estrogen, self-prescribing DHEA for "anti-aging" or menopause symptoms should be done under clinical supervision, not casually.

This marker sits in Sense -- signals being produced, detected and acted on.

A liver-made protein that binds testosterone and estradiol, controlling how much circulates "free" and biologically active. During perimenopause, fluctuating estrogen can shift SHBG production (estrogen tends to raise it, so falling/erratic estrogen can lower it), which changes how much of a woman's remaining testosterone is bioavailable even if the total testosterone number looks unchanged.

Typical range: Same conventional range as in `Fertility-Women.md` applies, roughly 20-130 nmol/L in women (lab-dependent); one source cites a narrower 30-90 nmol/L band. No separate menopause-specific target exists.

Food first: A lower-glycemic, higher-fiber dietary pattern and maintaining muscle mass through resistance training support healthy insulin sensitivity, which is the more evidence-grounded lever on SHBG than any single supplement.

When to see someone: Treat boron/DIM marketing claims skeptically, same as in the fertility context.

This marker sits in Sense -- signals being produced, detected and acted on.

Pituitary signal to the thyroid; included here because hypothyroidism and perimenopause produce a strikingly overlapping symptom picture -- fatigue, weight gain, brain fog, mood changes, sleep disruption, and temperature dysregulation appear in both, making it easy for a genuine thyroid problem to be dismissed as "just menopause" (or vice versa). Autoimmune thyroid disease (Hashimoto's) also becomes more common in the same midlife window as perimenopause, so the two frequently coexist rather than being either/or. (source: Thyroid Dysfunction: An Alternate Plausibility in Perimenopausal Women, PMC10266572; EMAS position statement on thyroid disease and menopause, Maturitas, 2024)

Typical range: See `Function-Health-Hyman.md` and `Thyroid.md` for the full conventional range and functional-optimal opinion range discussion -- nothing menopause-specific changes the reference range itself.

Food first: Same as `Thyroid.md`.

When to see someone: Given the symptom overlap, a reasonable clinical step for a perimenopausal woman with prominent fatigue, weight gain, or mood symptoms is to actually check TSH (and antibodies if there's a personal/family autoimmune history) rather than assume it's hormonal transition by default -- an inexpensive test that can meaningfully change the plan.

Standard glycemic-control markers (see `Function-Health-Hyman.md` Metabolic section for full detail on each). Relevant here because insulin resistance measurably worsens across the menopause transition independent of age and body-weight change in longitudinal SWAN data -- women who entered the study with normal insulin sensitivity often showed meaningful deterioration by late perimenopause and early postmenopause, suggesting the hormonal transition itself, not just aging or weight gain, drives part of the shift. (source: El Khoudary SR et al., SWAN progress report, Menopause, 2019)

Typical range: Same conventional ranges as `Function-Health-Hyman.md` (fasting glucose 70-99 mg/dL normal, HbA1c <5.7% normal). No separate menopause-specific cutoff exists, though the observation above means a woman's HOMA-IR trajectory across this window is worth watching even if any single value still looks "normal."

Food first: Same evidence-backed levers as general metabolic health -- lower-glycemic eating pattern, adequate fiber and protein, resistance training (muscle is the body's largest glucose sink and directly counters the menopause-related insulin-resistance shift), consistent sleep.

When to see someone: None specific beyond reading these three together rather than singly -- fasting insulin often moves before glucose or HbA1c do.

See `Function-Health-Hyman.md` Heart & Lipids section for full marker-by-marker detail. Menopause-specific relevance: SWAN found sharp, clinically meaningful increases in LDL-C and ApoB concentrated in the one-year window surrounding the final menstrual period -- larger than the annual changes seen before or after that window -- meaning the lipid shift is tied to the hormonal transition itself, not smooth aging. HDL cholesterol and HDL particle number actually rose across the transition in the same data, but with an adverse shift in HDL subclass composition (more small, less large HDL particles), which complicates the usual "higher HDL is better" read. Higher post-transition LDL particle number and ApoB were associated with greater carotid artery thickening and coronary calcification over follow-up. (source: El Khoudary SR et al., lipid changes around the final menstrual period, Stroke/PMC5183479; SWAN LDL subclass and HDL ancillary studies, PMC10539013)

Typical range: Same conventional ranges as `Function-Health-Hyman.md`.

Food first: Same as `Function-Health-Hyman.md` -- replace saturated fat with unsaturated fat, add soluble fiber, cut refined sugar, include fatty fish.

When to see someone: A single "worse" lipid panel drawn right around the final menstrual period may partly reflect this well-documented transition-related shift rather than a new, unrelated problem -- still worth addressing, but useful context when discussing trends with a clinician.

This marker sits in Maintain -- the cleanup and defence system, and whether it is switched on.

See `Function-Health-Hyman.md` for the general marker description. SWAN longitudinal data found systemic inflammation shifts around the menopause transition are not one-size-fits-all: distinct hs-CRP trajectory patterns exist across women (a "low-rise" group whose hs-CRP increases after the final period, a "medium-stable" group, and a "high-decline" group whose already-elevated hs-CRP falls around the transition), and these patterns track with pre-menopausal body weight and race/ethnicity rather than following one universal curve. (source: Trajectories of C-Reactive Protein Over the Menopause Transition, SWAN, PMC10736740)

Typical range: Same conventional cutoffs as `Function-Health-Hyman.md` (<1.0 mg/L low risk, 1.0-3.0 average, >3.0 high risk).

Food first: Same as `Function-Health-Hyman.md`.

DEXA (dual-energy X-ray absorptiometry) measures bone mineral density and reports it as a T-score (standard deviations from a young healthy adult reference). CTX (C-terminal telopeptide) is a marker of bone *resorption* (breakdown), and P1NP (procollagen type 1 N-terminal propeptide) is a marker of bone *formation* -- together, "bone turnover markers." All three matter here because bone remodeling accelerates sharply at menopause: falling estrogen removes a brake on osteoclast (bone-resorbing) activity, and resorption temporarily outpaces formation, driving the fastest bone loss of a woman's life in the first 5-10 years after the final period.

Typical range: DEXA T-score: -1.0 to +1.0 normal, -1.0 to -2.5 osteopenia, ≤-2.5 osteoporosis (WHO diagnostic criteria). CTX and P1NP have assay-specific reference ranges and are **not used to diagnose osteoporosis** -- their main validated clinical use is monitoring response to osteoporosis treatment (a good antiresorptive response shows CTX dropping substantially within 3-6 months; anabolic treatment shows P1NP rising). The International Osteoporosis Foundation and International Federation of Clinical Chemistry specifically recommend serum P1NP and CTX as the reference markers for this monitoring role. (source: Vasikaran S et al., IOF-IFCC bone turnover marker position paper, Osteoporosis International, 2011, PMID 21184054; Bone Turnover Markers: Basic Biology to Clinical Applications, Endocrine Reviews, 2023)

Food first: See Bone Nutrients section below. Weight-bearing and resistance exercise is also a major, well-established lever for bone density that isn't a nutrient but deserves mention alongside diet.

When to see someone: Bone turnover markers cannot diagnose osteoporosis on their own and do not reliably predict an individual's fracture risk by themselves -- DEXA remains the diagnostic standard. A single "high" CTX in an otherwise healthy midlife woman is expected physiology during the menopause transition, not automatically a disease state requiring treatment; interpret trends with a clinician, ideally alongside DEXA.

This marker sits in Transform -- the cofactors enzymes need to turn fuel into usable energy.

These three regulate calcium homeostasis together (see `Function-Health-Hyman.md` for the full physiology) and matter specifically here because postmenopausal bone loss increases the stakes of getting calcium/vitamin D status right; PTH rises when either vitamin D or calcium is insufficient, pulling calcium from bone to keep blood levels normal at bone's expense.

Typical range: See `Function-Health-Hyman.md` for the full conventional ranges (vitamin D: deficient <20 ng/mL, sufficient ≥30 ng/mL per Endocrine Society; calcium 8.5-10.5 mg/dL). No separate menopause-specific reference range exists for any of the three, though guidance on *intake targets* does shift at menopause (see Bone Nutrients section below).

Food first: See Bone Nutrients section below.

When to see someone: See `Function-Health-Hyman.md` -- vitamin D toxicity is rare but real at sustained high doses; calcium excess has its own debated cardiovascular question, addressed in detail below.