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Int J Epidemiol. 2016 Oct;45(5):1445-1457. Epub 2016 Aug 18.

Effects of hormonal contraception on systemic metabolism: cross-sectional and longitudinal evidence.

Author information

1
Computational Medicine, Faculty of Medicine, University of Oulu & Biocenter Oulu, Oulu, Finland.
2
NMR Metabolomics Laboratory, School of Pharmacy, University of Eastern Finland, Kuopio, Finland.
3
Department of Obstetrics and Gynecology, Oulu University Hospital, University of Oulu and Medical Research Center Oulu, Oulu, Finland.
4
National Institute for Health and Welfare, Helsinki, Finland.
5
Institute for Molecular Medicine (FIMM), University of Helsinki, Helsinki, Finland.
6
Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland.
7
Clinic for General and Interventional Cardiology, University Heart Center Hamburg, Hamburg, Germany.
8
German Center for Cardiovascular Research (DZHK e.V.), partner site Hamburg, Lübeck, Kiel, Germany.
9
Department of Medicine, University of Turku and Division of Medicine, Turku University Hospital, Finland.
10
Department of Clinical Physiology, University of Tampere and Tampere University Hospital, Tampere, Finland.
11
Department of Clinical Chemistry, Fimlab Laboratories, School of Medicine, University of Tampere, Tampere, Finland.
12
Estonian Genome Center, University of Tartu, Tartu, Estonia.
13
Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland.
14
Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Turku, Finland.
15
Medical Research Council Integrative Epidemiology Unit at the University of Bristol, Bristol, UK and.
16
School of Social and Community Medicine, University of Bristol, Bristol, UK.
17
Computational Medicine, Faculty of Medicine, University of Oulu & Biocenter Oulu, Oulu, Finland, mika.ala-korpela@com.

Abstract

BACKGROUND:

Hormonal contraception is commonly used worldwide, but its systemic effects across lipoprotein subclasses, fatty acids, circulating metabolites and cytokines remain poorly understood.

METHODS:

A comprehensive molecular profile (75 metabolic measures and 37 cytokines) was measured for up to 5841 women (age range 24-49 years) from three population-based cohorts. Women using combined oral contraceptive pills (COCPs) or progestin-only contraceptives (POCs) were compared with those who did not use hormonal contraception. Metabolomics profiles were reassessed for 869 women after 6 years to uncover the metabolic effects of starting, stopping and persistently using hormonal contraception.

RESULTS:

The comprehensive molecular profiling allowed multiple new findings on the metabolic associations with the use of COCPs. They were positively associated with lipoprotein subclasses, including all high-density lipoprotein (HDL) subclasses. The associations with fatty acids and amino acids were strong and variable in direction. COCP use was negatively associated with albumin and positively associated with creatinine and inflammatory markers, including glycoprotein acetyls and several growth factors and interleukins. Our findings also confirmed previous results e.g. for increased circulating triglycerides and HDL cholesterol. Starting COCPs caused similar metabolic changes to those observed cross-sectionally: the changes were maintained in consistent users and normalized in those who stopped using. In contrast, POCs were only weakly associated with metabolic and inflammatory markers. Results were consistent across all cohorts and for different COCP preparations and different types of POC delivery.

CONCLUSIONS:

Use of COCPs causes widespread metabolic and inflammatory effects. However, persistent use does not appear to accumulate the effects over time and the metabolic perturbations are reversed upon discontinuation. POCs have little effect on systemic metabolism and inflammation.

KEYWORDS:

amino acids; combined oral contraceptive pills; cytokines; fatty acids; hormonal contraception; hormones; inflammation; lipoproteins; metabolomics; progestin-only contraceptives; risk factors

PMID:
27538888
PMCID:
PMC5100613
DOI:
10.1093/ije/dyw147
[Indexed for MEDLINE]
Free PMC Article

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