Age at adiposity rebound in childhood is associated with PCOS diagnosis and obesity in adulthood-longitudinal analysis of BMI data from birth to age 46 in cases of PCOS.


Journal

International journal of obesity (2005)
ISSN: 1476-5497
Titre abrégé: Int J Obes (Lond)
Pays: England
ID NLM: 101256108

Informations de publication

Date de publication:
07 2019
Historique:
received: 25 05 2018
accepted: 20 12 2018
revised: 21 11 2018
pubmed: 6 2 2019
medline: 23 5 2020
entrez: 6 2 2019
Statut: ppublish

Résumé

Adiposity rebound (AR), the second BMI rise in childhood at around the age of 6 years, is associated with obesity and metabolic alteration in later life. Given that polycystic ovary syndrome (PCOS) has a strong metabolic component, early life growth patterns could reveal a risk of PCOS. Thus, we aimed to investigate the associations between age at AR and PCOS diagnosis and BMI later in life. This study is part of a prospective, population-based longitudinal study, where women with PCOS diagnosis by age 46 (n = 280) were compared with asymptomatic women (CTRLs, n = 1573). Weight and height data from birth to age 13 years, at age at menarche, and at ages 31 and 46 years were analyzed RESULTS: Women with PCOS had lower birth weight (3357 ± 477 vs. 3 445 ± 505 g, p < 0.001), earlier age at AR (5.2 ± 1.0 vs. 5.6 ± 0.90 years, p < 0.001) and higher BMI from AR onwards compared with controls. Early timing of AR was associated with PCOS diagnosis independently of BMI (OR 1.62, 95% Cl 1.37-1.92). Women with PCOS and early AR had higher BMI at 31 and 46 years when compared to controls with early AR. The age at AR did not associate with T levels at ages 31 or 46 years. Early AR was associated with PCOS diagnosis and high BMI in adulthood. Adolescent girls with early AR and persisting obesity should be screened for PCOS symptoms, such as persistent irregular cycles and hirsutism.

Sections du résumé

BACKGROUND
Adiposity rebound (AR), the second BMI rise in childhood at around the age of 6 years, is associated with obesity and metabolic alteration in later life. Given that polycystic ovary syndrome (PCOS) has a strong metabolic component, early life growth patterns could reveal a risk of PCOS. Thus, we aimed to investigate the associations between age at AR and PCOS diagnosis and BMI later in life.
MATERIALS AND METHODS
This study is part of a prospective, population-based longitudinal study, where women with PCOS diagnosis by age 46 (n = 280) were compared with asymptomatic women (CTRLs, n = 1573). Weight and height data from birth to age 13 years, at age at menarche, and at ages 31 and 46 years were analyzed RESULTS: Women with PCOS had lower birth weight (3357 ± 477 vs. 3 445 ± 505 g, p < 0.001), earlier age at AR (5.2 ± 1.0 vs. 5.6 ± 0.90 years, p < 0.001) and higher BMI from AR onwards compared with controls. Early timing of AR was associated with PCOS diagnosis independently of BMI (OR 1.62, 95% Cl 1.37-1.92). Women with PCOS and early AR had higher BMI at 31 and 46 years when compared to controls with early AR. The age at AR did not associate with T levels at ages 31 or 46 years.
CONCLUSIONS
Early AR was associated with PCOS diagnosis and high BMI in adulthood. Adolescent girls with early AR and persisting obesity should be screened for PCOS symptoms, such as persistent irregular cycles and hirsutism.

Identifiants

pubmed: 30718819
doi: 10.1038/s41366-019-0318-z
pii: 10.1038/s41366-019-0318-z
pmc: PMC6760596
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1370-1379

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Auteurs

E Koivuaho (E)

Department of Obstetrics and Gynaecology, PEDEGO Research Unit, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.

J Laru (J)

Department of Obstetrics and Gynaecology, PEDEGO Research Unit, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.

M Ojaniemi (M)

Department of Children and Adolescents, PEDEGO Research Unit, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.

K Puukka (K)

NordLab Oulu, Department of Clinical Chemistry, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.

J Kettunen (J)

Computational Medicine, Faculty of Medicine, University of Oulu, Oulu, Finland.
Biocenter Oulu, University of Oulu, Oulu, Finland.

J S Tapanainen (JS)

Department of Obstetrics and Gynaecology, PEDEGO Research Unit, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.
Department of Obstetrics and Gynaecology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.

S Franks (S)

Institute of Reproductive and Developmental Biology, Department of Surgery & Cancer, Imperial College London, London, UK.

M-R Järvelin (MR)

Biocenter Oulu, University of Oulu, Oulu, Finland.
Center for Life Course Health Research, University of Oulu, Oulu, Finland.
Department of Epidemiology and Biostatistics, MRC-PHE Centre for Environment and Health, School of Public Health, Imperial College London, London, UK.
Unit of Primary Care, Oulu University Hospital, Oulu, Finland.

L Morin-Papunen (L)

Department of Obstetrics and Gynaecology, PEDEGO Research Unit, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland.

S Sebert (S)

Biocenter Oulu, University of Oulu, Oulu, Finland.
Center for Life Course Health Research, University of Oulu, Oulu, Finland.
Department of Genomic of Complex Diseases, School of Public Health, Imperial College London, London, UK.

T T Piltonen (TT)

Department of Obstetrics and Gynaecology, PEDEGO Research Unit, Medical Research Center, University of Oulu and Oulu University Hospital, Oulu, Finland. terhi.piltonen@oulu.fi.

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