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      A longitudinal study of depression and gestational diabetes in pregnancy and the postpartum period

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          Abstract

          Aims/hypothesis

          Depression and glucose intolerance commonly co-occur among non-pregnant individuals; however, the temporal relationship between gestational diabetes (GDM) and depression during pregnancy and the postpartum period is less understood. Our objective was to assess longitudinal associations between depression early in pregnancy and GDM risk, as well as GDM and subsequent risk of postpartum depression.

          Methods

          Data came from the prospective National Institute of Child Health and Human Development Fetal Growth Studies-Singleton cohort (2009–2013), and had been collected at 12 US clinical centres. Pregnant women without psychiatric disorders, diabetes or other chronic conditions before pregnancy were followed throughout pregnancy (n=2477). Only women with GDM and matched controls were followed up at 6 weeks postpartum (n=162). GDM was ascertained by a review of the medical records. Depression was assessed in the first (8–13 gestational weeks) and second (16–22 weeks) trimesters and at 6 weeks postpartum using the Edinburgh Postnatal Depression Scale. Postpartum depression was defined as a depressive symptom score ≥10 or antidepressant medicine use after delivery. RR and 95% CI we adjusted for pre-pregnancy BMI and other risk factors. GDM was considered to be the outcome for the first set of analyses, with depression in the first and second trimesters as the exposures. Postpartum depression was considered as the outcome for the second set of analyses, with GDM as the exposure.

          Results

          Overall, comparing the highest and lowest quartiles of first-trimester depression scores, the scores from the highest quartile were associated with a significant twofold (95% CI 1.06, 3.78) increased risk of GDM, but this was attenuated to 1.72-fold (95% CI 0.92, 3.23) after adjustment; the second-trimester results were similar. The risk was stronger and significant in both trimesters among non-obese women ( p for trend 0.02 and 0.01, respectively), but null for obese women. Women with persistently high depression scores in both trimesters had the greatest risk of GDM (highest vs lowest quartile in both trimesters: adjusted RR 3.21, 95% CI 1.00–10.28). GDM was associated with an adjusted 4.62-fold (95% CI 1.26, 16.98) increased risk of subsequent postpartum depression.

          Conclusions/interpretation

          This prospective study demonstrates a modest association between depressive symptoms early in pregnancy and an increased risk of incident GDM, as well as between GDM and subsequent postpartum depression risk, highlighting pregnancy and the postpartum period as an important susceptible time window during the life course for the interplay between depression and glucose intolerance phenotypes. GDM risk associated with elevated depressive symptoms was particularly high among non-obese women and women with symptoms persisting across the first two trimesters of pregnancy.

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          Most cited references27

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          The Hyperglycemia and Adverse Pregnancy Outcome Study

          OBJECTIVE To determine associations of gestational diabetes mellitus (GDM) and obesity with adverse pregnancy outcomes in the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) Study. RESEARCH DESIGN AND METHODS Participants underwent a 75-g oral glucose tolerance test (OGTT) between 24 and 32 weeks. GDM was diagnosed post hoc using International Association of Diabetes and Pregnancy Study Groups criteria. Neonatal anthropometrics and cord serum C-peptide were measured. Adverse pregnancy outcomes included birth weight, newborn percent body fat, and cord C-peptide >90th percentiles, primary cesarean delivery, preeclampsia, and shoulder dystocia/birth injury. BMI was determined at the OGTT. Multiple logistic regression was used to examine associations of GDM and obesity with outcomes. RESULTS Mean maternal BMI was 27.7, 13.7% were obese (BMI ≥33.0 kg/m2), and GDM was diagnosed in 16.1%. Relative to non-GDM and nonobese women, odds ratio for birth weight >90th percentile for GDM alone was 2.19 (1.93–2.47), for obesity alone 1.73 (1.50–2.00), and for both GDM and obesity 3.62 (3.04–4.32). Results for primary cesarean delivery and preeclampsia and for cord C-peptide and newborn percent body fat >90th percentiles were similar. Odds for birth weight >90th percentile were progressively greater with both higher OGTT glucose and higher maternal BMI. There was a 339-g difference in birth weight for babies of obese GDM women, compared with babies of normal/underweight women (64.2% of all women) with normal glucose based on a composite OGTT measure of fasting plasma glucose and 1- and 2-h plasma glucose values (61.8% of all women). CONCLUSIONS Both maternal GDM and obesity are independently associated with adverse pregnancy outcomes. Their combination has a greater impact than either one alone.
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            Evidence for a differential role of HPA-axis function, inflammation and metabolic syndrome in melancholic versus atypical depression.

            The hypothalamic-pituitary-adrenal (HPA) axis and the inflammatory response system have been suggested as pathophysiological mechanisms implicated in the etiology of major depressive disorder (MDD). Although meta-analyses do confirm associations between depression and these biological systems, effect sizes vary greatly among individual studies. A potentially important factor explaining variability is heterogeneity of MDD. Aim of this study was to evaluate the association between depressive subtypes (based on latent class analysis) and biological measures. Data from 776 persons from the Netherlands Study of Depression and Anxiety, including 111 chronic depressed persons with melancholic depression, 122 with atypical depression and 543 controls were analyzed. Inflammatory markers (C-reactive protein, interleukin-6, tumor necrosis factor-α), metabolic syndrome components, body mass index (BMI), saliva cortisol awakening curves (area under the curve with respect to the ground (AUCg) and with respect to the increase (AUCi)), and diurnal cortisol slope were compared among groups. Persons with melancholic depression had a higher AUCg and higher diurnal slope compared with persons with atypical depression and with controls. Persons with atypical depression had significantly higher levels of inflammatory markers, BMI, waist circumference and triglycerides, and lower high-density lipid cholesterol than persons with melancholic depression and controls. This study confirms that chronic forms of the two major subtypes of depression are associated with different biological correlates with inflammatory and metabolic dysregulation in atypical depression and HPA-axis hyperactivity in melancholic depression. The data provide further evidence that chronic forms of depressive subtypes differ not only in their symptom presentation, but also in their biological correlates. These findings have important implications for future research on pathophysiological pathways of depression and treatment.
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              Constructs of depression and distress in diabetes: time for an appraisal.

              Depression presents in roughly 20% of people with diabetes worldwide, and adversely affects quality of life and treatment outcomes. The causes of depression in diabetes are poorly understood, but research suggests a bi-directional association, at least for type 2 diabetes. Inconsistent findings regarding prevalence and depression treatment outcomes in patients with diabetes seem partly attributable to inconsistencies in the definition and measurement of depression and in distinguishing it from diabetes-distress, a psychological concept related to depression. We review evidence suggesting that diabetes-distress and depression are correlated and overlapping constructs, but are not interchangeable. Importantly, diabetes-distress seems to mediate the association between depression and glycaemic control. We propose a model to explain the direct and indirect effects of depression and diabetes-distress on glycaemic control. Additionally, using emerging insights from data-driven approaches, we suggest three distinct symptom profiles to define depression in patients with diabetes that could help explain differential associations between depression and metabolic abnormalities, and to tailor interventions for depression. Future research should focus on further refining depression profiles in patients with diabetes, taking into account the natural history of diabetes and depression, clinical characteristics, and diabetes-distress. The assessment of diabetes-distress and depression in research and clinical practice will be essential to identify high-risk patients with different mental health needs.
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                Author and article information

                Journal
                0006777
                3399
                Diabetologia
                Diabetologia
                Diabetologia
                0012-186X
                1432-0428
                21 September 2016
                19 September 2016
                December 2016
                01 December 2017
                : 59
                : 12
                : 2594-2602
                Affiliations
                [1 ]Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Drive, MSC 7004, Bethesda, MD 20817, USA
                [2 ]Office of the Director, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA
                [3 ]Biostatistics and Bioinformatics Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA
                Author notes
                Corresponding author: C. Zhang, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6710B Rockledge Drive, MSC 7004, Bethesda, MD 20817, USA, zhangcu@ 123456mail.nih.gov
                Article
                PMC5101167 PMC5101167 5101167 nihpa817108
                10.1007/s00125-016-4086-1
                5101167
                27640810
                66362148-dbe1-4422-991f-6670332b89a9
                History
                Categories
                Article

                Depression,Pregnancy,Gestational diabetes,Postpartum
                Depression, Pregnancy, Gestational diabetes, Postpartum

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