Poor sleep quality is associated with impaired glucose tolerance in women after gestational diabetes
Introduction
In epidemiologic studies, sleep disturbances are associated with several metabolic and vascular diseases, e.g. a modestly increased risk of coronary heart disease in women Ayas et al. (2003) and a higher prevalence of obesity and type 2 diabetes mellitus (Type 2 DM) in the general population (Knutson and Van Cauter, 2008). Experimental disruption of sleep in humans rapidly leads to an impairment of glucose tolerance via increased insulin resistance (Meisinger et al., 2005, Knutson and Van Cauter, 2008, Spiegel, 2008, Tasali et al., 2008, Buxton et al., 2010, Knutson, 2012, Morselli et al., 2012).
Pregnancy and the postpartum period are times during which most women experience an impaired sleep quality, both with respect to sleep duration and sleep interruptions (Mindell and Jacobson, 2000).
Women with GDM represent a high-risk group for the development of Type 2 DM. The overall risk of Type 2 DM after a pregnancy complicated by GDM is increased 7.4-fold compared to women after a normoglycemic pregnancy (Reutrakul et al., 2011). A BMI of 30 kg/m2 or more, gestational age at diagnosis of GDM of less than 24 weeks, an antenatal 1 h plasma glucose level of over 200 mg/dl and a requirement for insulin therapy have been identified as risk factors for early progression to after GDM (Kim et al., 2002).
Given the association of sleep and glucose metabolism and the very common state of ‘sleep deprivation’ in new mothers, we wanted to test whether impaired sleep is associated with poor post-partum glucose metabolism in women after GDM. Findings in this high-risk group were compared to a control group of women after a normoglycemic pregnancy. In addition, we tried to identify risk factors for a poor sleep quality in the post-GDM cohort.
Section snippets
Study population
Data were derived from the PPS-Diab (“Prediction, Prevention and Sub-classification of Type 2 Diabetes”) study. This is a prospective, mono-center observational study, which started recruitment in November 2011. The study population consisted of women who had gestational diabetes (pGDM) during their last pregnancy and women after normoglycemic pregnancy as controls in a 2:1 ratio. The cohorts were recruited consecutively from the Diabetes Center and the obstetrics department of the Klinikum der
Baseline characteristics
109 women were included in the study between November 1, 2011 and May 31, 2013. No information from the PSQI questionnaire was documented for 18 participants; hence, those were excluded from further analysis. The final sample consisted of 91 women, thereof 61 after GDM and 30 after normoglycemic pregnancy.
Significant differences between post-GDM patients and controls were found for fasting plasma glucose, 2 h plasma glucose in the OGTT, the Matsuda insulin sensitivity index and the systolic
Conclusion
The main findings of this study are patients with a history of GDM still show significantly impaired glucose sensitivity compared to controls, which significantly correlates with sleep quality respectively sleep duration. Within the GDM group sleep duration was significantly decreased in patients with impaired insulin sensitivity. Sleep quality measured by PSQI is again strongly associated to subjective stress perception and not to factors like time since delivery and the older siblings in the
Funding sources
This work was funded by the Helmholtz Zentrum München, Deutsches Zentrum für Diabetesforschung and Klinikum der Universität München [German Center for Diabetes Research and the University Clinic, Munich].
Author contributions
AL, JS, KGP, UF, SK, MI and HK contributed to the study conception and design. KT, MF, FB, MW, UF, UH and SH recruited study participants and collected data. Data extraction and statistical analyses were carried out by MR and DK. HK and UF wrote the first draft of the manuscript and all authors contributed with critical comments to the final version. All authors have seen and approved the final version. AL is the guarantor of this work and, as such, had full access to all the data in the study
Conflicts of interests
None.
Acknowledgments
We are grateful to all study participants without whom our work would not be possible. We also thank Sarah Michel for language editing of this manuscript. This work was funded by the Helmholtz Zentrum München, Deutsches Zentrum für Diabetesforschung and Klinikum der Universität München [German Center for Diabetes Research and the University Clinic, Munich].
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These authors contributed equally to this work.