Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (742 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The last menstrual period. Permanent cessation of menses (menstruation) is usually defined after 6 to 12 months of amenorrhea in a woman over 45 years of age. In the United States, menopause generally occurs in women between 48 and 55 years of age.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Change of Life, Female.
Where it fits in the MeSH classification
- Broader topics
- Climacteric
- Narrower topics
- Menopause, Premature; Perimenopause; Postmenopause; Premenopause
- See also
- Osteoporosis, Postmenopausal; Estrogen Replacement Therapy; Premenopause; Postmenopause; Hot Flashes
Related concepts
- Menstruation
- Amenorrhea
Research landscape
PubMed indexes 68,666 records tagged with the MeSH heading “Menopause” (counts retrieved 2026-10-31). 11,608 of them (16.9%) were published from 2020 onward, and the busiest period so far is through 1999 with 20,377 records.
Reviews account for 9,989 records (14.5%) and meta-analyses for 1,080. Randomized controlled trials number 7,285 (10.6%) as a share of all records on the topic. Randomized trials make up a comparatively large share of this literature, which means many treatment questions have been tested directly.
Show the data
| Period | Records |
|---|---|
| through 1999 | 20,377 |
| 2000-2009 | 18,354 |
| 2010-2019 | 18,327 |
| 2020 onward | 11,608 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 9,989 | 14.5% |
| Meta-analyses | 1,080 | 1.6% |
| Randomized controlled trials | 7,285 | 10.6% |
Method: PubMed query "Menopause"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Lipoprotein(a) and incident venous thromboembolism in pre- and postmenopausal women, and in men | 2026 | Research article Design not recorded in structured metadata | 6 | cc by PMID 41903523 · DOI · PMC13266305 |
| Menopause, Female Sex Hormones, Skeletal Muscle Mass and Muscle Protein Turnover in Humans | 2026 | Review article Design not recorded in structured metadata | 6 | cc by PMID 41707658 · DOI · PMC12916153 |
| Women's midlife: the front line of Alzheimer prevention | 2026 | Review article Design not recorded in structured metadata | 4 | cc by PMID 41837280 · DOI · PMC12987622 |
Lipoprotein(a) and incident venous thromboembolism in pre- and postmenopausal women, and in men [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Background and aimsElevated lipoprotein(a) [Lp(a)] levels are an established risk factor for atherosclerotic cardiovascular disease, but the association between Lp(a) and venous thromboembolism (VTE) remains unclear.
- Closing excerpt
- ConclusionsElevated Lp(a) was associated with VTE in premenopausal women and in postmenopausal MHT users, suggesting that hormonal context may influence Lp(a)-associated thrombotic risk.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (265 words)
Background and aimsElevated lipoprotein(a) [Lp(a)] levels are an established risk factor for atherosclerotic cardiovascular disease, but the association between Lp(a) and venous thromboembolism (VTE) remains unclear. Sex and hormonal status may modify the relationship between Lp(a) and VTE.MethodsThe present study included participants from the UK Biobank with available baseline Lp(a) data. Individuals with a history of VTE or cancer, as well as those using anticoagulants, were excluded. Multivariable-adjusted Cox models were used to assess the association between Lp(a) levels ≥125 nmol/L and incident VTE in premenopausal women, postmenopausal women, and men. Subgroup analyses stratified premenopausal women by oral contraceptive (OCP) use and postmenopausal women by menopausal hormone therapy (MHT) use.ResultsAmong 55 302 premenopausal women, 129 045 postmenopausal women, and 189 013 men, the proportions with Lp(a) ≥ 125 nmol/L were 14.0%, 19.0%, and 15.0%, respectively. Over a median (interquartile range) follow-up of 13.6 (12.9-14.4) years, 8186 VTE events occurred (cumulative incidence 2.2%). Lp(a) ≥ 125 nmol/L was associated with incident VTE in premenopausal women [adjusted hazard ratio (aHR) 1.32; 95% confidence interval (CI) 1.04-1.66; P = .02] but not in postmenopausal women (aHR 1.03; 95% CI 0.94-1.13; P = .47; Pinteraction = .03) or men (aHR 1.00; 95% CI 0.92-1.08; P = .94). OCP use did not modify the Lp(a)-VTE association among premenopausal women (Pinteraction = .61). However, among postmenopausal MHT users, Lp(a) ≥ 125 nmol/L was associated with higher VTE risk (aHR 1.48; 95% CI 1.03-2.12; P = .03; Pinteraction = .04).ConclusionsElevated Lp(a) was associated with VTE in premenopausal women and in postmenopausal MHT users, suggesting that hormonal context may influence Lp(a)-associated thrombotic risk.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41903523 · DOI · PMC13266305
Menopause, Female Sex Hormones, Skeletal Muscle Mass and Muscle Protein Turnover in Humans [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Sarcopenia describes the loss of muscle mass and function with age.
- Closing excerpt
- Advancements in understanding the role of the menopausal transition in the regulation of muscle mass, and subsequent effectiveness of interventions such as exercise or exogenous hormone provision will enable healthy ageing and sarcopenia prevention in older women.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (280 words)
Sarcopenia describes the loss of muscle mass and function with age. The increase in prevalence of sarcopenia in women appears to coincide with the onset of menopause, which is characterized by large changes to the hormonal milieu such as decreased oestrogen and progesterone concentrations. Although the timing of menopause and sarcopenia may coincide, there is a lack of high-quality evidence demonstrating a link between the two. This narrative review aims to assess evidence for the effects of menopause on muscle mass and muscle protein turnover. Longitudinal (n = 4/5) and cross-sectional (n = 7/11) studies demonstrate a reduction in lean or muscle mass across the menopausal transition with -2.5% and -5.7% reductions in perimenopausal and postmenopausal women, respectively, compared to premenopausal women. Most of this evidence (n = 10/11) is taken through assessment of lean body mass via dual-energy x-ray absorptiometry (DXA), which may underestimate changes in muscle mass. Assessment on changes to muscle protein turnover is largely limited to short-term measures of muscle protein synthesis (MPS), which may be elevated in older women versus younger women (n = 3/7) or age-matched males (n = 4/5). MPS responses to anabolic stimuli, such as resistance exercise (n = 3/4) or protein ingestion (n = 3/6), may be blunted in older women. Evidence assessing muscle protein breakdown (MPB) is lacking; however, evidence from animal and cell models demonstrates the role of estradiol in suppressing MPB, which may contribute to an increase in MPB following menopause. Advancements in understanding the role of the menopausal transition in the regulation of muscle mass, and subsequent effectiveness of interventions such as exercise or exogenous hormone provision will enable healthy ageing and sarcopenia prevention in older women.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41707658 · DOI · PMC12916153
Women's midlife: the front line of Alzheimer prevention [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Nearly two-thirds of patients with Alzheimer disease (AD) are women, most of them postmenopausal.
- Closing excerpt
- The stakes are global, and the opportunity is urgent: to redefine AD prevention through sex-specific, time-sensitive, and biologically informed strategies that translate science into scalable, actionable care.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (197 words)
Nearly two-thirds of patients with Alzheimer disease (AD) are women, most of them postmenopausal. While sex differences in AD have historically been attributed to women's relative longevity, accumulating evidence challenges that view, pointing to female sex-specific biological underpinnings. In particular, neuroendocrine aging and the hormonal shifts that accompany the menopause transition have emerged as potentially modifiable AD risk factors in women. Yet, key neuroendocrine aging-related factors linked to increased AD and dementia risk, such as early menopause, premenopausal bilateral oophorectomy, frequent vasomotor symptoms, and midlife cognitive and mood disturbances, remain underinvestigated. Additionally, although a growing evidence base highlights the potential of menopause hormone therapy for AD prevention, particularly in women undergoing oophorectomy, progress remains hindered by a lack of clinical trials and biomarker-driven studies. This Review calls for a paradigm shift: from viewing AD risk as a byproduct of generalized aging to validating midlife neuroendocrine aging as a distinct window of vulnerability, and an opportunity for prevention. By 2050, over 1.2 billion women worldwide will be in or approaching menopause. The stakes are global, and the opportunity is urgent: to redefine AD prevention through sex-specific, time-sensitive, and biologically informed strategies that translate science into scalable, actionable care.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41837280 · DOI · PMC12987622
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Association of Age at Onset of Menopause and Time Since Onset of Menopause With Cardiovascular Outcomes, Intermediate Vascular Traits, and All-Cause Mortality: A Systematic Review and Meta-analysis [4]
- Research article Association of Endometrial Cancer Risk With Postmenopausal Bleeding in Women: A Systematic Review and Meta-analysis [5]
- Research article Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways [6]
- Research article Body mass index and breast cancer risk according to postmenopausal estrogen-progestin use and hormone receptor status [7]
- Research article Long-term hormone therapy for perimenopausal and postmenopausal women [8]
- Research article Hormonal therapy for menopause and breast-cancer risk by histological type: a cohort study and meta-analysis [9]
References
- Ezzat D, Lopez DM, Claggett BL, Li L, Mohammadnia N, Schuermans A, et al.. Lipoprotein(a) and incident venous thromboembolism in pre- and postmenopausal women, and in men. . 2026. PMID 41903523 · DOI · PMC13266305
- Menzies C, Bowtell R, Shur N, Brook MS. Menopause, Female Sex Hormones, Skeletal Muscle Mass and Muscle Protein Turnover in Humans. . 2026. PMID 41707658 · DOI · PMC12916153
- Mosconi L. Women's midlife: the front line of Alzheimer prevention. . 2026. PMID 41837280 · DOI · PMC12987622
- Muka T, Oliver-Williams C, Kunutsor S, Laven JS, Fauser BC, Chowdhury R, et al.. Association of Age at Onset of Menopause and Time Since Onset of Menopause With Cardiovascular Outcomes, Intermediate Vascular Traits, and All-Cause Mortality: A Systematic Review and Meta-analysis. JAMA Cardiol. 2016. PMID 27627190 · DOI
- Clarke MA, Long BJ, Del Mar Morillo A, Arbyn M, Bakkum-Gamez JN, Wentzensen N. Association of Endometrial Cancer Risk With Postmenopausal Bleeding in Women: A Systematic Review and Meta-analysis. JAMA Intern Med. 2018. PMID 30083701 · DOI · PMC6142981
- Stolk L, Perry JR, Chasman DI, He C, Mangino M, Sulem P, et al.. Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways. Nat Genet. 2012. PMID 22267201 · DOI · PMC3288642
- Munsell MF, Sprague BL, Berry DA, Chisholm G, Trentham-Dietz A. Body mass index and breast cancer risk according to postmenopausal estrogen-progestin use and hormone receptor status. Epidemiol Rev. 2014. PMID 24375928 · DOI · PMC3873844
- Marjoribanks J, Farquhar C, Roberts H, Lethaby A, Lee J. Long-term hormone therapy for perimenopausal and postmenopausal women. Cochrane Database Syst Rev. 2017. PMID 28093732 · DOI · PMC6465148
- Reeves GK, Beral V, Green J, Gathani T, Bull D, Million Women Study Collaborators. Hormonal therapy for menopause and breast-cancer risk by histological type: a cohort study and meta-analysis. Lancet Oncol. 2006. PMID 17081916 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.