1. Scope

What is covered:

• Systemic menopausal hormone therapy (MHT/HRT): oestrogen (transdermal or oral estradiol; conjugated equine oestrogen [CEE]) with or without a progestogen (micronised progesterone preferred, or synthetic progestins), plus tibolone and combined oestrogen–bazedoxifene where relevant.
• Low-dose vaginal (local) oestrogen for genitourinary syndrome of menopause (GSM).
• Off-label systemic testosterone in women.
• HRT in premature ovarian insufficiency (POI) and early menopause.
• Framing for a UK private longevity clinic: symptom control, bone protection, and the evidence (and its limits) for HRT influencing ageing biomarkers, morbidity and mortality.

What is NOT covered: contraception, management of hormone-sensitive cancers, fertility treatment, gender-affirming hormone therapy, and detailed osteoporosis pharmacotherapy (bisphosphonates, denosumab). Compounded “bioidentical” hormone regimens are addressed only to advise against them.

Positioning: This summary is adjunctive to conventional primary and secondary care, not a substitute. Longevity-specific and off-label uses are flagged throughout. It assumes prescribing by a clinician competent in menopause care, with shared decision-making and documented informed consent.

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2. Background and pathophysiology

Biological rationale relevant to ageing:

• The menopause transition produces a relatively abrupt loss of ovarian 17β-estradiol, accelerating changes across multiple organ systems: bone resorption, unfavourable shifts in lipids and body composition, endothelial and vascular changes, vasomotor instability, urogenital atrophy, and sleep/mood disruption.
• Oestrogen acts via ER-α/ER-β and membrane receptors, influencing endothelial nitric oxide, lipid metabolism, osteoclast activity, and CNS thermoregulation. This provides mechanistic plausibility for effects on cardiometabolic and skeletal ageing — but mechanistic plausibility is not proof of hard-outcome benefit.

Human evidence on ageing biomarkers (surrogate — interpret cautiously):

• In the UK Biobank cohort (n≈117,000), ever-use of HT was associated with a modestly lower phenotypic-age discrepancy (β −0.17 years) and this mediated ~13% of the HT–mortality association (Liu & Li, 2024; observational, residual confounding likely). The absolute effect is small (≈0.25 years of “delayed” phenotypic ageing).
• Cross-sectional/longitudinal analyses of sex hormones against six epigenetic clocks (Berlin Aging Study II) found no consistent association, suggesting sex hormones play at most a minor role in epigenetic-clock ageing in older adults (Schmid et al., 2025).
• A 2026 narrative synthesis concluded HT “may favourably influence certain senescence markers and biological-age discrepancy,” but that biomarkers lack validated thresholds and clinical translation remains premature (Castaneda et al., 2026).

Interpretive caveat: No robust data link HRT-induced changes in epigenetic clocks, phenotypic age, or SASP/senescence markers to hard clinical outcomes. These should be regarded as surrogate/mechanistic only and must not be presented to patients as proven anti-ageing benefits.

Preclinical data (clearly separated): Rodent/in-vitro work supports oestrogen effects on mitochondrial bioenergetics, endothelial function and cellular senescence. This is hypothesis-generating only and carries no weight in the recommendations below.

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3. Evidence base and grading

Types of evidence available: Multiple large RCTs (WHI CEE+MPA n=16,608; WHI CEE-alone n=10,739; HERS; WISDOM), Cochrane systematic reviews, USPSTF evidence reports/meta-analyses, and large nationwide/observational cohorts (UK QResearch/CPRD; Danish registry; UK Biobank). Key limitation for longevity practice: most RCT participants were >60 years and often >10 years post-menopause — a population indirect to the typical newly-menopausal or early-menopausal longevity patient.

GRADE-style certainty and strength of recommendation by outcome (higher-certainty outcomes first):

Outcome	Direction & magnitude	Certainty (GRADE)	Main downgrading domains	Strength of recommendation
Vasomotor symptom relief	Large benefit; HRT most effective treatment	High	None major	Strong: offer for bothersome VMS
Fracture reduction	RR ~0.73–0.79 (combined & oestrogen-only)	High/Moderate	Indirectness (older cohorts)	Conditional: offer where bone protection is a goal, but not sole indication for prevention per USPSTF
Invasive breast cancer (E+P)	Increased, RR ~1.24–1.28; rises with duration	Moderate–High (harm)	—	Recommend against using combined HRT for prevention; counsel risk
Breast cancer (oestrogen-only)	Little/no increase; WHI signalled possible reduction	Moderate	Inconsistency	Informs route/regimen choice
VTE (oral)	Increased; oral RR ~1.6, higher first year	Moderate (harm)	Mostly observational for route	Strong: prefer transdermal to mitigate
VTE (transdermal)	No significant increase	Low–Moderate	Observational only	Preferred route
Stroke	Increased, esp. oral & older age (RR ~1.3–1.4)	Low–Moderate (harm)	Imprecision	Caution; avoid oral in high-risk
Coronary heart disease	E+P little/no difference overall; possible harm year 1; timing-dependent signal	Moderate	Inconsistency, indirectness	Recommend against HRT for CHD prevention
All-cause mortality	Neutral in RCTs (pooled HR ~0.99); observational cohorts suggest lower mortality, esp. early initiation & POI	Moderate (neutral in RCT)	Confounding in cohorts	Only in research / do not use HRT with the primary aim of extending lifespan
Type 2 diabetes	Reduced incidence (E+P HR ~0.81)	Moderate	Self-report	Ancillary benefit; not a standalone indication
Gallbladder disease	Increased (RR ~1.6–1.8)	Moderate (harm)	—	Counsel
Probable dementia (age ≥65, E+P)	Increased (HR ~2.05)	Low (harm)	Single trial, imprecision	Recommend against starting in older women for cognition
Biological-age/epigenetic biomarkers	Small, inconsistent	Very low	Observational, surrogate, no hard-outcome link	Only in research
Testosterone – female sexual function (HSDD, postmenopausal)	Benefit: ~+1 satisfying event/month	High	—	Conditional: offer transdermal, physiological dose, off-label
Testosterone – cognition/bone/mood/wellbeing	No demonstrated benefit	Moderate–High (no effect)	Small samples	Recommend against for these indications
</mdtable>

Overall evidence statement: Moderate-to-high-certainty RCT evidence supports HRT for symptom relief and fracture reduction and defines its principal harms (breast cancer with combined therapy, VTE/stroke especially oral). RCTs show neutral all-cause mortality; observational cohorts suggesting a survival advantage are confounded and cannot support prescribing HRT as a longevity/chronic-disease-prevention intervention. Any anti-ageing claim rests on surrogate biomarkers of very low certainty.

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4. Patient selection and indications

Who may benefit within a longevity clinic:

• Symptomatic peri-/postmenopausal women within ~10 years of menopause and aged <60 (“window of opportunity”) with bothersome vasomotor or genitourinary symptoms — the group with the most favourable benefit–risk profile (Shifren, Crandall & Manson, 2019; Manson et al., 2024). Guideline-based.
• Women with POI or early menopause (<45 years) — HRT recommended until at least the average age of natural menopause (~51) for symptom control and primary prevention of osteoporosis and (probable) cardiovascular/cognitive risk; WHI risk data should not be extrapolated to this group (ESHRE/ASRM/IMS, 2025; ACOG, 2017; Stuenkel & Gompel, 2023). Guideline-based, STRONG.
• Women prioritising bone health where HRT is otherwise indicated for symptoms (fracture reduction is a genuine ancillary benefit). Guideline-based; not a sole prevention indication per USPSTF.
• Postmenopausal women with distressing hypoactive sexual desire disorder despite adequate oestrogenisation — off-label physiological transdermal testosterone. Guideline/consensus-based (off-label).

Clinical scenarios where longevity framing must be tempered:

• “Middle-aged adults with high cardiometabolic risk”: HRT is not a cardiovascular prevention tool; existing risk factors must be controlled first, and transdermal route preferred.
• “Older adults / frailty”: initiating systemic HRT de novo in women >60 or >10 years post-menopause carries a less favourable profile (stroke, VTE, dementia signal).
• “Athletic/performance-seeking individuals”: no evidence supports systemic HRT or testosterone for performance/longevity in eugonadal women; testosterone benefit is confined to HSDD.

Exclusion criteria / high-risk groups (avoid or specialist input): current/prior breast cancer or other oestrogen-dependent malignancy; undiagnosed abnormal vaginal bleeding; active or prior VTE/PE, arterial thromboembolic disease (MI, stroke), or known thrombophilia (factor V Leiden, protein C/S or antithrombin deficiency, antiphospholipid syndrome); active liver disease; pregnancy. High cardiovascular risk, migraine with aura, uncontrolled hypertension, high VTE risk, and prior gallbladder disease warrant caution and route modification.

Regulatory and ethical status:

• On-label: systemic HRT for moderate–severe menopausal VMS and GSM; some products for osteoporosis prevention; HRT in POI. Bijuva (estradiol/progesterone) is FDA-approved for VMS in women with a uterus.
• Off-label: testosterone in women (no female-specific licensed product in most of the UK/US — use a fractionated regulator-approved male transdermal formulation); use of HRT specifically to modify ageing biomarkers or extend lifespan.
• Only in research / registry: HRT prescribed with the primary aim of slowing biological ageing or preventing chronic disease in asymptomatic women. Compounded “bioidentical” hormones should be avoided (unregulated absorption, overdose risk).

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5. Assessment and baseline work-up

History: menopausal status and time since final menstrual period; symptom inventory (VMS severity/impact, GSM, sleep, mood, libido/HSDD with associated distress); personal and family history of breast/ovarian/endometrial cancer, VTE, cardiovascular and cerebrovascular disease, migraine with aura, liver/gallbladder disease, osteoporosis/fracture; smoking, alcohol, BMI; medications and interactions; reproductive history and (for POI) fertility wishes.

Examination: blood pressure, BMI/waist, breast awareness check, and pelvic/vaginal assessment where GSM or bleeding is present.

Baseline investigations:

• Not routinely required to diagnose menopause in women ≥45 with typical symptoms.
• FSH to support diagnosis of POI/early menopause (raised on two occasions), plus consideration of the underlying-cause workup for POI (karyotype, FMR1 premutation, autoimmune/adrenal screen) — refer per POI guidance.
• Lipids, HbA1c/fasting glucose, LFTs, U&E as part of cardiometabolic risk stratification.
• Cardiovascular risk assessment (e.g. QRISK) before initiation.
• Mammography per national screening; cervical screening up to date.
• DXA where osteoporosis risk or bone-protection is a consideration.
• Baseline total/free testosterone (and SHBG) before considering testosterone therapy.

Risk stratification (benefit vs harm):

• Favourable: age <60, <10 years post-menopause, bothersome symptoms, low CVD/VTE/breast-cancer risk → benefit likely outweighs harm.
• Intermediate: moderate cardiometabolic or VTE risk → use transdermal estradiol + micronised progesterone; optimise modifiable risk first.
• Unfavourable: >60 or >10 years post-menopause, high VTE/stroke/breast-cancer risk → generally avoid systemic HRT for prevention; local vaginal oestrogen remains appropriate for GSM.

Baseline documentation (to enable follow-up): symptom scores; blood pressure, BMI, lipids, HbA1c; QRISK; DXA if done; indication, regimen, route, dose, and start date; explicit record of shared decision-making, off-label status where relevant, and consent. If ageing biomarkers (phenotypic age, epigenetic clocks) are measured, document that they are surrogate, research-grade endpoints without validated thresholds.

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6. Dosing regimens and practical implementation

General principles (guideline-based): lowest effective dose for symptom control; transdermal estradiol preferred (lower VTE and probably stroke risk than oral); women with a uterus require adequate progestogen for endometrial protection; micronised progesterone preferred over synthetic progestins (more favourable VTE and probably breast profile).

Typical systemic regimens (robust human data):

• Transdermal estradiol: patch 25–100 µg/24 h twice weekly, or gel/spray equivalent; titrate to symptom control.
• Oral estradiol: 1–2 mg daily (use only if transdermal not preferred and VTE risk is low).
• Endometrial protection (uterus present):
  • Micronised progesterone 100 mg daily (continuous, no bleed) or 200 mg for 12–14 days/month (sequential/cyclical).
  • LNG-IUS provides endometrial protection and contraception.
  • Synthetic progestins or combined patches are alternatives.
• Regimen choice: sequential/cyclical for perimenopausal women still bleeding; continuous combined once postmenopausal (≥1 year amenorrhoea or age-appropriate).

POI / early menopause (higher physiological replacement):

• Transdermal estradiol 100–150 µg/day (or oral estradiol 2 mg) — higher than standard postmenopausal doses — with cyclical micronised progesterone 100–200 mg for 12–14 days/month; continue until ~age 51 then reassess. Combined oral contraceptive is an acceptable alternative, especially if contraception is needed, though MHT is generally preferred. Guideline-based (ESHRE/ASRM/IMS 2025; ACOG; NICE).

Genitourinary syndrome of menopause:

• Low-dose vaginal oestrogen (estradiol tablet/ring/cream) — effective, minimal systemic absorption, no progestogen required, and considered safe long-term including (with oncology input) in many breast-cancer survivors.

Testosterone (off-label, physiological dosing only):

• Transdermal, targeting premenopausal physiological range; where no female-specific product exists, use a fractionated dose of a regulator-approved male transdermal formulation (e.g. a small daily fraction of a 1% gel). Avoid oral testosterone (adverse lipids), injectables, pellets and compounded preparations (supraphysiological/unpredictable levels). Consensus-based (Davis et al., 2019).

Titration: start low, review symptoms at ~3 months, adjust dose/route; there is a dose–response for symptom relief and for bone density. No “loading” regimen is used.

Regimens requiring caution / not supported by robust data:

• Supraphysiological or “optimisation-to-youthful-levels” hormone targeting — no robust human outcome data; mechanistic plausibility only.
• Systemic DHEA for sexual dysfunction — RCTs show no benefit (Davis, 2024).
• HRT dosing driven by epigenetic-clock or phenotypic-age targets — research only.

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7. Monitoring, safety and follow-up

Monitoring plan:

• Clinical: symptom response, unscheduled/breakthrough bleeding (investigate persistent or new bleeding after 3–6 months), blood pressure, BMI, breast awareness, and adherence.
• Laboratory/imaging: serum estradiol monitoring is not routinely required (except sometimes to check absorption/adherence with transdermal, and not recommended to titrate in POI). Maintain routine mammographic and cervical screening. DXA as clinically indicated.
• Testosterone: baseline and periodic total testosterone to avoid supraphysiological levels, plus clinical review for androgenic effects; lipids if any oral exposure.
• Ageing biomarkers (optional, research-grade): if tracked, record as exploratory; do not alter dosing solely to change a biomarker.

Suggested timepoints: review at ~3 months after initiation or dose change; then annually with a formal benefit–risk reassessment. There is no arbitrary age- or duration-based stopping rule — continue while benefits outweigh risks (NAMS; NICE 2024).

Adverse effects and safety profile (per 10,000 women, from USPSTF/WHI where available):

• Common/early: breast tenderness, bleeding, bloating, nausea, headache, skin reaction to patches; androgenic effects (acne, hair growth) with testosterone.
• Increased risks (combined E+P over ~5.6 y): invasive breast cancer (~51 more), stroke (~52 more), VTE (~120 more), gallbladder disease (~260 more), urinary incontinence, and probable dementia when started at ≥65 (~88 more).
• Oestrogen-only: stroke, VTE and gallbladder disease increased; breast-cancer risk little/no increase; VTE and stroke risk substantially lower with transdermal route.
• Serious but rare: pulmonary embolism, stroke, and (combined therapy) breast cancer.

Required actions for abnormal findings:

• New/persistent unscheduled bleeding → investigate (TVUS ± endometrial biopsy); refer per suspected-cancer pathways as appropriate.
• Symptoms/signs of VTE or stroke → stop HRT immediately and manage acutely.
• New breast lump/abnormal mammogram → urgent breast referral; withhold pending assessment.
• New migraine with aura, uncontrolled hypertension, or significant LFT derangement → reassess route/continuation.
• Androgenic side effects on testosterone → reduce dose/stop; reversible except possibly voice/clitoral change.

Interactions: oral oestrogen is affected by hepatic enzyme inducers (some anticonvulsants, rifampicin) and interacts with thyroid-hormone binding (monitor TFTs in treated hypothyroidism); transdermal route avoids much first-pass interaction. Consider additive VTE risk with other prothrombotic drugs.

Special populations: HRT is contraindicated in pregnancy (and testosterone is teratogenic/contraindicated); it is not a treatment during breastfeeding. In hepatic impairment, systemic HRT is contraindicated/avoided. In renal impairment, no specific dose adjustment but assess comorbid CVD/VTE risk. In frailty/advanced age, avoid initiating systemic HRT for prevention; favour local vaginal oestrogen for GSM.

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8. Contraindications and cautions

Absolute contraindications: current or past breast cancer or other oestrogen-dependent malignancy; undiagnosed abnormal genital bleeding; active or recent VTE/PE or known high-risk thrombophilia; active arterial thromboembolic disease (MI, stroke); active liver disease with abnormal LFTs; pregnancy; hypersensitivity to the preparation.

Relative contraindications / specialist advice: high cardiovascular risk or established CHD; migraine with aura (favour transdermal, avoid oral); uncontrolled hypertension; high VTE risk (obesity, thrombophilia trait, immobility) — use transdermal only; prior gallbladder disease; strong family history of breast cancer or hormone-sensitive cancer; otosclerosis; history of endometrial hyperplasia.

Harm likely to outweigh benefit with current evidence:

• Initiating systemic HRT in women >60 years or >10 years post-menopause for chronic-disease/mortality prevention.
• Using HRT solely to prevent CHD, dementia, or to slow biological ageing — USPSTF recommends against HRT for chronic-disease prevention; mortality is neutral in RCTs.
• Compounded/”bioidentical” hormones and supraphysiological testosterone.

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9. Practical management scenarios

Scenario A — Symptomatic, newly menopausal woman with cardiometabolic risk factors

Recommendation: Offer HRT for bothersome symptoms (conditional/strong for symptoms), NOT as CVD prevention.

• Assessment: confirm bothersome VMS/GSM; QRISK; lipids, HbA1c, BP, BMI; breast/cervical screening current; exclude contraindications.
• Shared decision-making/consent: explain symptom benefit and fracture benefit; small absolute increases in breast cancer (if combined) and stroke/VTE; that HRT does not treat cardiovascular risk and is not given for prevention. Optimise modifiable risk (statin, antihypertensive, glycaemia, smoking) first.
• Initiation: transdermal estradiol (lowest effective dose) + micronised progesterone if uterus present. Avoid oral oestrogen given VTE/stroke concern.
• Monitoring/follow-up: 3-month review, then annual benefit–risk reassessment; ongoing cardiometabolic management.
• Escalate/stop: any VTE/stroke symptoms, new breast finding, or persistent unscheduled bleeding.

Scenario B — Older, frail woman with multimorbidity considering HRT de novo

Recommendation: Avoid initiating systemic HRT for prevention/longevity; restrict systemic use to compelling refractory symptoms only.

• Assessment: clarify indication; if the goal is chronic-disease prevention or “anti-ageing,” this is not supported and the stroke/VTE/dementia profile is unfavourable in this group.
• Shared decision-making: for GSM, offer low-dose vaginal oestrogen (favourable safety, no progestogen needed). For isolated bone concern, prefer bone-specific agents.
• Initiation: systemic HRT only if severe, refractory VMS after weighing risks; if used, transdermal and lowest dose.
• Monitoring/follow-up: close review; low threshold to stop.
• Escalate/stop: any thrombotic/cerebrovascular event, cognitive concern, or new bleeding.

Scenario C — Woman already under specialist care (e.g. breast-cancer survivor with distressing GSM)

Recommendation: Restrict/co-manage; systemic HRT generally contraindicated.

• Assessment: confirm oncology status and current endocrine therapy.
• Shared decision-making/consent: systemic HRT is contraindicated after breast cancer; distressing GSM unresponsive to non-hormonal measures may warrant low-dose vaginal oestrogen after explicit oncology input (evidence supports safety of low-dose vaginal oestrogen including in many survivors, but decision must be individualised with the oncologist).
• Initiation: non-hormonal first (moisturisers/lubricants); vaginal oestrogen only with oncology agreement.
• Monitoring/follow-up: joint oncology review.
• Escalate/refer: defer to specialist team for any change.

Scenario D — POI / early menopause (<45 years)

Recommendation: Offer HRT until ~age 51 (strong, guideline-based).

• Assessment: confirm diagnosis (FSH ×2, cause workup); DXA; cardiovascular baseline; fertility wishes.
• Consent: explain that WHI risks do not apply; HRT here is replacement to physiological levels, reducing osteoporosis and probably cardiovascular/cognitive risk; HRT is not contraceptive.
• Initiation: transdermal estradiol 100–150 µg/day + cyclical micronised progesterone (or COC if contraception preferred).
• Monitoring/follow-up: annual review; reassess continuation at ~51.
• Escalate/stop: standard HRT red flags; involve fertility services as needed.

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10. Research gaps and future directions

• Longevity/mortality: RCTs show neutral all-cause mortality; observational survival signals are confounded. There is no RCT evidence that HRT extends lifespan or healthspan in asymptomatic women — this should remain research/registry only.
• Ageing biomarkers: epigenetic clocks, phenotypic age, SASP/senescence and telomere measures lack validated thresholds and proven links to hard outcomes in women; prospective interventional studies with clinical endpoints are needed before clinical use.
• Modern formulations: most RCT harm data derive from oral CEE±MPA; transdermal estradiol + micronised progesterone likely have a better VTE/stroke (and possibly breast) profile, but this is largely observational and unproven in RCTs.
• Timing hypothesis: the critical-window concept for cardiovascular and cognitive benefit remains inconclusive and needs dedicated early-initiation RCTs.
• Testosterone in women: robust only for postmenopausal HSDD; long-term safety (breast, cardiovascular), premenopausal use, and non-sexual indications remain unproven and need adequately powered long-duration trials, plus a licensed female-specific product.
• POI: optimal estrogen dose/route and long-term endometrial protection at higher doses are under-studied.

Bottom line for longevity practice: HRT is a well-evidenced treatment for menopausal symptoms, GSM, POI and (as an ancillary benefit) fracture reduction, with harms that are manageable through patient selection, transdermal route and micronised progesterone. It should not be prescribed as a lifespan-extension or generic anti-ageing intervention; any such use is off-label, surrogate-driven, and belongs in research settings with explicit informed consent.

Footnote

The pivotal points that a longevity clinician should note:

– Symptom relief and fracture reduction are high/moderate-certainty benefits from RCTs, but all-cause mortality is neutral in the WHI randomised trials (pooled HR ~0.99), and the 2026 Danish nationwide cohort found no mortality increase but only a small survival signal confined to sustained use and to oophorectomised women. Observational “younger biological age” and lower-mortality findings (UK Biobank) are confounded surrogate data, and epigenetic-clock studies show no consistent hormone effect — hence the explicit “only in research” grading for any anti-ageing indication.[1][2][3][4][5][6][7][8][9]

– USPSTF recommends against HRT for chronic-disease prevention because combined therapy raises breast cancer, stroke, VTE, gallbladder disease and (age ≥65) dementia, which is why the document separates symptom/replacement indications from prevention framing.[2]

– Route matters: transdermal estradiol carries little to no VTE excess versus oral, across a meta-analysis and large UK case-control data, and micronised progesterone/estradiol regimens have the lowest thrombotic risk — the basis for the transdermal-first recommendation.[10][11][12][13][14]

– POI is a distinct, guideline-strong indication with higher physiological dosing until ~51, where WHI risk data should not be applied.[15][16][17]

– Testosterone is evidence-based only for postmenopausal HSDD at physiological transdermal doses (off-label), with no proven cognitive, bone or wellbeing benefit and inadequate long-term safety data.[18][19][20]

Important caveat: NICE NG23 was updated in 2024; the specific recommendation numbers cited here derive from the 2016 JAMA summary of the guideline, so verify current NG23 wording before local protocol adoption.[1][21]

 

Figure 2 Mortality Outcomes in the Women’s Health Initiative Hormone Therapy Trials During the 18-Year Cumulative Follow-up Manson JE, Aragaki AK, Rossouw JE, et al. Menopausal Hormone Therapy and Long-Term All-Cause and Cause-Specific Mortality: The Women’s Health Initiative Randomized Trials. Jama. 2017;318(10):927-938. doi:10.1001/jama.2017.11217.

 

Figure 4 Mortality Outcomes During the 18-Year Cumulative Follow-Up According to 10-Year Age Groups at Randomization Manson JE, Aragaki AK, Rossouw JE, et al. Menopausal Hormone Therapy and Long-Term All-Cause and Cause-Specific Mortality: The Women’s Health Initiative Randomized Trials. Jama. 2017;318(10):927-938. doi:10.1001/jama.2017.11217.

 

Table 3 Summary of Evidence by Outcome: Estrogen Plus Progestin Trials Enrolling Generally Healthy Postmenopausal Persons 50 Years or Older Gartlehner G, Patel SV, Reddy S, et al. Hormone Therapy for the Primary Prevention of Chronic Conditions in Postmenopausal Persons: Updated Evidence Report and Systematic Review for the US Preventive Services Task Force. Jama. 2022;328(17):1747-1765. doi:10.1001/jama.2022.18324.

 

Table 2 Summary of Evidence by Outcome: Estrogen-Only Trials Enrolling Generally Healthy Postmenopausal Persons 50 Years or Older Gartlehner G, Patel SV, Reddy S, et al. Hormone Therapy for the Primary Prevention of Chronic Conditions in Postmenopausal Persons: Updated Evidence Report and Systematic Review for the US Preventive Services Task Force. Jama. 2022;328(17):1747-1765. doi:10.1001/jama.2022.18324.

 

Figure 2.1 Comparison 2 HT plus testosterone versus HT on sexual function, Outcome 1 Change scores of sexual function. Somboonporn W, Davis S, Seif MW, Bell R. Testosterone for Peri- And Postmenopausal Women. The Cochrane Database of Systematic Reviews. 2005;(4):CD004509. doi:10.1002/14651858.CD004509.pub2.

 

Table 1 Representative Guideline Recommendations for HRT in Women with Primary Ovarian Insufficiency.* Stuenkel CA, Gompel A. Primary Ovarian Insufficiency. The New England Journal of Medicine. 2023;388(2):154-163. doi:10.1056/NEJMcp2116488.

 

Figure Approach to Initiating Menopausal Hormone Therapy Shifren JL, Crandall CJ, Manson JE. Menopausal Hormone Therapy. Jama. 2019;321(24):2458-2459. doi:10.1001/jama.2019.5346.

 

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