Evidence mapPaperPMID 40080428Full record

ReviewReproduction (Cambridge, England)2025

POLYCYSTIC OVARY SYNDROME: ORIGINS AND IMPLICATIONS: Polycystic ovary syndrome: an evolutionary metabolic adaptation.

Daniel A Dumesic, Vasantha Padmanabhan, David H Abbott

Abstract readReview
In one paragraph

Review in Reproduction (Cambridge, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Vasantha Padmanabhan
David H Abbott

Funding

Support for National Primate Research CenterP51OD011092 · OREGON HEALTH & SCIENCE UNIVERSITY · 2025 to 2025
$13.7M
UCLA Clinical and Translational Science InstituteUL1TR001881 · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2025 to 2025
$9.9M
Wisconsin National Primate Research Center SupportP51OD011106 · UNIVERSITY OF WISCONSIN-MADISON · 2025 to 2025
$9.9M
Neuroendocrine Actions of Androgens in FemalesP50HD044405 · NORTHWESTERN UNIVERSITY · 2002 to 2005
$4.3M
Sex Steroids Program Premature Ovarian FailureP01HD044232 · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2004 to 2005
$2.3M
Pilot Project ProgramP30ES017885 · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2025 to 2025
$1.4M
NCATS NIH HHS UL1 TR001881NICHD NIH HHS P01 HD044232NICHD NIH HHS P50 HD044405NICHD NIH HHS P50 HD071836NICHD NIH HHS R01 HD098233NICHD NIH HHS R21 HD102172NIEHS NIH HHS P30 ES017885NIH HHS P51 OD011092NIH HHS P51 OD011106
6 · The paper itself

Abstract

In brief: Polycystic ovary syndrome has ancient genetic origins that favored preferential abdominal fat accumulation, ovarian hyperandrogenism and insulin resistance. This review examines how endocrine-metabolic changes in normal-weight hyperandrogenic PCOS women originated as an evolutionary metabolic adaptation to balance enhanced fat storage with increased glucose and fatty acid availability for optimal energy use for survival and reproduction. Abstract: Polycystic ovary syndrome (PCOS) is a common endocrinopathy of reproductive-aged women, characterized by hyperandrogenism, oligo-anovulation and insulin resistance in combination with preferential abdominal fat accumulation. As an ancestral primate trait, PCOS in humans likely underwent relatively recent preferential selection when scarcity of food in hunter-gatherers of the Pleistocene selected for enhanced fat storage and insulin resistance as a survival advantage to maintain glucose homeostasis for brain and reproductive function. As an evolutional model for PCOS, healthy normal-weight women with hyperandrogenic PCOS have subcutaneous (SC) abdominal adipose stem cells that favor exaggerated lipid accumulation during adipocyte development in vitro accompanied by reduced systemic insulin sensitivity and preferential accumulation of highly lipolytic intra-abdominal fat. Programmed by genetic inheritance and epigenetic events during early life, such a metabolic adaptation in PCOS, provides a balance between enhanced SC adipose fat storage and increased circulating glucose and free fatty acid availability as energy substrate for crucial target tissues. The accompanying increased muscle strength and oligo-anovulation in PCOS women of antiquity also enabled sustained energy use during endurance activities in combination with greater time as a rearing advantage for children and a lower risk of maternal mortality. Heritable PCOS characteristics that originally evolved in primates as a genetically and epigenetically enhanced metabolic adaptation to favor fat storage now predispose to lipotoxicity and pregnancy complications, calling for improved preventive healthcare, with early lifestyle and therapeutic choices to optimize the long-term health of PCOS women and their children in today's obesogenic environment.

Indexed as

Adaptation, PhysiologicalBiological EvolutionPolycystic Ovary SyndromeAnimalsFemaleHumansHyperandrogenismInsulin Resistanceandrogen heritabilityfat metabolismhyperandrogenismpolycystic ovary syndrome

Identifiers

PMID40080428
PMCPMC12004336

What Socratic holds

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Registered trials

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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 Socratic graph.