Lauren B Shomaker1,2,3, Nichole R Kelly4,5,6, Courtney K Pickworth4, Omni L Cassidy4,5, Rachel M Radin4,5, Lisa M Shank4,5, Anna Vannucci4,5, Katherine A Thompson4, Sara A Armaiz-Flores4, Sheila M Brady4, Andrew P Demidowich4, Ovidiu A Galescu4, Amber B Courville7, Cara Olsen8, Kong Y Chen9, Eric Stice10, Marian Tanofsky-Kraff11,12, Jack A Yanovski13. 1. Section on Growth and Obesity, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Hatfield Clinical Research Center, 10 Center Drive, Building 10, Room 1-3330, MSC 1103, Bethesda, MD, 20892-1103, USA. lauren.shomaker@colostate.edu. 2. Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences (USUHS), 4301 Jones Bridge Road, Bethesda, MD, 20814-4712, USA. lauren.shomaker@colostate.edu. 3. Department of Human Development and Family Studies and Colorado School of Public Health, Colorado State University, 303A Behavioral Sciences Building, 410 Pitkin Street, Campus Delivery 1570, Fort Collins, CO, 80523-1570, USA. lauren.shomaker@colostate.edu. 4. Section on Growth and Obesity, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Hatfield Clinical Research Center, 10 Center Drive, Building 10, Room 1-3330, MSC 1103, Bethesda, MD, 20892-1103, USA. 5. Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences (USUHS), 4301 Jones Bridge Road, Bethesda, MD, 20814-4712, USA. 6. Department of Human Development and Family Studies and Colorado School of Public Health, Colorado State University, 303A Behavioral Sciences Building, 410 Pitkin Street, Campus Delivery 1570, Fort Collins, CO, 80523-1570, USA. 7. Nutrition Department, Mark O. Hatfield Clinical Center, NIH, Bethesda, MD, USA. 8. Biostatistics, Department of Preventive Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA. 9. Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, MD, USA. 10. Oregon Research Institute, Eugene, OR, USA. 11. Section on Growth and Obesity, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Hatfield Clinical Research Center, 10 Center Drive, Building 10, Room 1-3330, MSC 1103, Bethesda, MD, 20892-1103, USA. marian.tanofsky-kraff@usuhs.edu. 12. Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences (USUHS), 4301 Jones Bridge Road, Bethesda, MD, 20814-4712, USA. marian.tanofsky-kraff@usuhs.edu. 13. Section on Growth and Obesity, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), Hatfield Clinical Research Center, 10 Center Drive, Building 10, Room 1-3330, MSC 1103, Bethesda, MD, 20892-1103, USA. jy15i@nih.gov.
Abstract
BACKGROUND: Prospective data suggest depressive symptoms worsen insulin resistance and accelerate type 2 diabetes (T2D) onset. PURPOSE: We sought to determine whether reducing depressive symptoms in overweight/obese adolescents at risk for T2D would increase insulin sensitivity and mitigate T2D risk. METHOD: We conducted a parallel-group, randomized controlled trial comparing a 6-week cognitive-behavioral (CB) depression prevention group with a 6-week health education (HE) control group in 119 overweight/obese adolescent girls with mild-to-moderate depressive symptoms (Center for Epidemiological Studies-Depression Scale [CES-D] ≥16) and T2D family history. Primary outcomes were baseline to post-intervention changes in CES-D and whole body insulin sensitivity index (WBISI), derived from 2-h oral glucose tolerance tests. Outcome changes were compared between groups using ANCOVA, adjusting for respective baseline outcome, puberty, race, facilitator, T2D family history degree, baseline age, adiposity, and adiposity change. Multiple imputation was used for missing data. RESULTS:Depressive symptoms decreased (p < 0.001) in CB and HE from baseline to posttreatment, but did not differ between groups (ΔCESD = -12 vs. -11, 95 % CI difference = -4 to +1, p = 0.31). Insulin sensitivity was stable (p > 0.29) in CB and HE (ΔWBISI = 0.1 vs. 0.2, 95 % CI difference = -0.6 to +0.4, p = 0.63). Among all participants, reductions in depressive symptoms were associated with improvements in insulin sensitivity (p = 0.02). CONCLUSIONS: Girls at risk for T2D displayed reduced depressive symptoms following 6 weeks of CB or HE. Decreases in depressive symptoms related to improvements in insulin sensitivity. Longer-term follow-up is needed to determine whether either program causes sustained decreases in depressive symptoms and improvements in insulin sensitivity. TRIAL REGISTRATION NUMBER: The trial was registered with clinicaltrials.gov (NCT01425905).
RCT Entities:
BACKGROUND: Prospective data suggest depressive symptoms worsen insulin resistance and accelerate type 2 diabetes (T2D) onset. PURPOSE: We sought to determine whether reducing depressive symptoms in overweight/obese adolescents at risk for T2D would increase insulin sensitivity and mitigate T2D risk. METHOD: We conducted a parallel-group, randomized controlled trial comparing a 6-week cognitive-behavioral (CB) depression prevention group with a 6-week health education (HE) control group in 119 overweight/obese adolescent girls with mild-to-moderate depressive symptoms (Center for Epidemiological Studies-Depression Scale [CES-D] ≥16) and T2D family history. Primary outcomes were baseline to post-intervention changes in CES-D and whole body insulin sensitivity index (WBISI), derived from 2-h oral glucose tolerance tests. Outcome changes were compared between groups using ANCOVA, adjusting for respective baseline outcome, puberty, race, facilitator, T2D family history degree, baseline age, adiposity, and adiposity change. Multiple imputation was used for missing data. RESULTS:Depressive symptoms decreased (p < 0.001) in CB and HE from baseline to posttreatment, but did not differ between groups (ΔCESD = -12 vs. -11, 95 % CI difference = -4 to +1, p = 0.31). Insulin sensitivity was stable (p > 0.29) in CB and HE (ΔWBISI = 0.1 vs. 0.2, 95 % CI difference = -0.6 to +0.4, p = 0.63). Among all participants, reductions in depressive symptoms were associated with improvements in insulin sensitivity (p = 0.02). CONCLUSIONS:Girls at risk for T2D displayed reduced depressive symptoms following 6 weeks of CB or HE. Decreases in depressive symptoms related to improvements in insulin sensitivity. Longer-term follow-up is needed to determine whether either program causes sustained decreases in depressive symptoms and improvements in insulin sensitivity. TRIAL REGISTRATION NUMBER: The trial was registered with clinicaltrials.gov (NCT01425905).
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