Evidence map›Paper›PMID 36074951›Full record

ArticleEuropean journal of endocrinology2022

Polycystic ovary syndrome and leukocyte telomere length: cross-sectional and longitudinal changes.

Johanna Pölönen, Pekka Pinola, Justiina Ronkainen, Alex I Blakemore, Jessica L Buxton, Juha S Tapanainen, Stephen Franks, Terhi T Piltonen, Sylvain Sebert, Laure Morin-Papunen

Abstract read
In one paragraph

Article in European journal of endocrinology, 2022. 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. Review
  3. Review
  4. Article
  5. Article
  6. Obesity contributes to telomere shortening in polycystic ovary syndrome.Reproductive sciences (Thousand Oaks, Calif.) · 2024
    Article
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

10 authors.

Johanna PölönenDepartment of Obstetrics and Gynecology, University of Oulu and Oulu University Hospital, Medical Research Center, PEDEGO Research Unit, Oulu, Finland.ORCID 0000-0003-2795-5619
Pekka PinolaDepartment of Obstetrics and Gynecology, University of Oulu and Oulu University Hospital, Medical Research Center, PEDEGO Research Unit, Oulu, Finland.ORCID 0000-0001-6356-723X
Justiina RonkainenCenter for Life Course Health Research, University of Oulu, Oulu, Finland.
Alex I BlakemoreDepartment of Life Sciences, College of Health, Medicine and Life Sciences, Brunel University London, London, UK.
Jessica L BuxtonDepartment of Biomolecular Sciences, School of Life Sciences, Pharmacy and Chemistry, Kingston University London, London, UK.
Juha S TapanainenDepartment of Obstetrics and Gynecology, University of Oulu and Oulu University Hospital, Medical Research Center, PEDEGO Research Unit, Oulu, Finland.
Stephen FranksDepartment of Metabolism, Digestion and Reproduction, Institute of Reproductive and Developmental Biology, Imperial College London, London, UK.ORCID 0000-0002-3712-0335
Terhi T PiltonenDepartment of Obstetrics and Gynecology, University of Oulu and Oulu University Hospital, Medical Research Center, PEDEGO Research Unit, Oulu, Finland.ORCID 0000-0002-9921-7300
Sylvain SebertCenter for Life Course Health Research, University of Oulu, Oulu, Finland.
Laure Morin-PapunenDepartment of Obstetrics and Gynecology, University of Oulu and Oulu University Hospital, Medical Research Center, PEDEGO Research Unit, Oulu, Finland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Telomeres are DNA-protein complexes that protect chromosome ends from DNA damage and are surrogate biomarkers of cellular aging. Current evidence, almost entirely from cross-sectional observations, supports negative associations between leukocyte telomere length (LTL) and adverse lifestyle factors and cardiometabolic risk factors. Polycystic ovary syndrome (PCOS), the most common gynecological endocrine disorder, is associated with inflammation and oxidative stress, both factors associated with accelerated telomere attrition. We therefore hypothesized that LTL would be shorter and decrease more rapidly in women with PCOS in comparison to a control population. Design: This is a population-based cohort study comprising women of Northern Finland Birth Cohort 1966, with clinical examinations at ages 31 and 46. The sample included self-reported PCOS (age 31, n = 190; age 46, n = 207) and referent women (age 31, n = 1054; age 46, n = 1324) with data on LTL. Methods: The association between LTL and PCOS at ages 31 and 46 was analyzed by linear regression models adjusted for BMI, smoking, alcohol consumption and socioeconomic status at the corresponding age. Results: Women with PCOS had similar mean LTL at ages 31 and 46 (P > 0.4 for both). The mean LTL change between ages 31 and 46 did not differ between groups (P = 0.19). However, we observed a significant LTL attrition between ages 31 and 46 in the reference population (P < 0.001), but not in women with PCOS (P = 0.96). Conclusions: This finding may suggest a difference in the LTL attrition rate in women with PCOS, an unexpected finding that might affect their risk of age-related disease. Further research is needed to clarify the underlying mechanisms.

Indexed as

Polycystic Ovary SyndromeAdultBiomarkersCohort StudiesCross-Sectional StudiesDNAFemaleHumansLeukocytesLongitudinal StudiesMiddle AgedTelomereBiomarkersDNA

Identifiers

PMID36074951
PMCPMC9578080

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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 OpenQuestion graph.