ReviewEvolution, medicine, and public health2021
The evolutionary biology of endometriosis.
Review in Evolution, medicine, and public health, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 53 citations in OpenAlex.
- Endometriosis increases the risk of gestational diabetes: a meta-analysis stratified by mode of conception, disease localization and severity.Scientific reports · 2023Pooled it
- Pooled it
- A Systematic Review of Anogenital Distance and Gynecological Disorders: Endometriosis and Polycystic Ovary Syndrome.Frontiers in endocrinology · 2021Pooled it
- Polymorphism of theLife (Basel, Switzerland) · 2026Article
- Selection for Function in Early Life: Implications for Early-Onset Pathologies.Evolutionary applications · 2026Article
- Review
- Epidemiological study and clinical consequences of endometriosis and PCOS co-occurrence in a clinical population of women: a cross-sectional study.BMC women's health · 2026Article
- Gene Polymorphisms Determining Sex Hormone-Binding Globulin Levels and Endometriosis Risk.International journal of molecular sciences · 2025Article
- Hormonal imbalance in umbilical vein cord blood of pregnant women with endometriosis: a propensity score-matched analysis.Reproductive biology and endocrinology : RB&E · 2025Article
- Ameliorative effects ofJournal of traditional and complementary medicine · 2025Article
- Testosterone mediates life-history trade-offs in female mammals.Biological reviews of the Cambridge Philosophical Society · 2025Review
- Smoking and endometriosis: A narrative review.Tobacco induced diseases · 2025Review
- Dysfunction of natural killer cells promotes immune escape and disease progression in endometriosis.Frontiers in immunology · 2025Review
- Similar but Distinct Comorbidity Patterns Between Polycystic Ovary Syndrome and Endometriosis in Korean Women: A Nationwide Cohort Study.Journal of Korean medical science · 2024Article
- Development and Application of a Physiologically Based Pharmacokinetic Model for Elagolix in the Adult and Adolescent Population.Clinical pharmacokinetics · 2024Article
- The kisspeptin system in and beyond reproduction: exploring intricate pathways and potential links between endometriosis and polycystic ovary syndrome.Reviews in endocrine & metabolic disorders · 2024Review
- The evolutionary basis of elevated testosterone in women with polycystic ovary syndrome: an overview of systematic reviews of the evidence.Frontiers in reproductive health · 2024Review
- Polygenic risk score phenome-wide association study reveals an association between endometriosis and testosterone.BMC medicine · 2023Article
- Shorter Anogenital Distance in Women with Ovarian Endometriomas and Adenomyosis, but Not Uterine Leiomyomas.Biomedicines · 2023Article
- Genomic characterisation of the overlap of endometriosis with 76 comorbidities identifies pleiotropic and causal mechanisms underlying disease risk.Human genetics · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We provide the first analysis and synthesis of the evolutionary and mechanistic bases for risk of endometriosis in humans, structured around Niko Tinbergen's four questions about phenotypes: phylogenetic history, development, mechanism and adaptive significance. Endometriosis, which is characterized by the proliferation of endometrial tissue outside of the uterus, has its phylogenetic roots in the evolution of three causally linked traits: (1) highly invasive placentation, (2) spontaneous rather than implantation-driven endometrial decidualization and (3) frequent extensive estrogen-driven endometrial proliferation and inflammation, followed by heavy menstrual bleeding. Endometriosis is potentiated by these traits and appears to be driven, proximately, by relatively low levels of prenatal and postnatal testosterone. Testosterone affects the developing hypothalamic-pituitary-ovarian (HPO) axis, and at low levels, it can result in an altered trajectory of reproductive and physiological phenotypes that in extreme cases can mediate the symptoms of endometriosis. Polycystic ovary syndrome, by contrast, is known from previous work to be caused primarily by high prenatal and postnatal testosterone, and it demonstrates a set of phenotypes opposite to those found in endometriosis. The hypothesis that endometriosis risk is driven by low prenatal testosterone, and involves extreme expression of some reproductive phenotypes, is supported by a suite of evidence from genetics, development, endocrinology, morphology and life history. The hypothesis also provides insights into why these two diametric, fitness-reducing disorders are maintained at such high frequencies in human populations. Finally, the hypotheses described and evaluated here lead to numerous testable predictions and have direct implications for the treatment and study of endometriosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.