Rachel M Radin1, Marian Tanofsky-Kraff2, Lauren B Shomaker3, Nichole R Kelly1, Courtney K Pickworth4, Lisa M Shank2, Anne M Altschul4, Sheila M Brady4, Andrew P Demidowich4, Susan Z Yanovski5, Van S Hubbard6, Jack A Yanovski7. 1. Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, MD 20892-1103, USA; Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA; The Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., Bethesda, MD, USA. 2. Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, MD 20892-1103, USA; Department of Medical and Clinical Psychology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA. 3. Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, MD 20892-1103, USA; Colorado State University, Fort Collins, CO 80523, USA. 4. Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, MD 20892-1103, USA. 5. Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, MD 20892-1103, USA; Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, USA. 6. Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, USA; Division of Nutrition Research Coordination, NIH, USA. 7. Section on Growth and Obesity, Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, MD 20892-1103, USA. Electronic address: jy15i@nih.gov.
Abstract
PURPOSE: Preliminary data in adults suggest that binge eating is associated with greater prevalence of metabolic syndrome (MetS) components. However, there are limited data in youth, and little is known of the role of binge episode size in these relationships. METHODS: We examined the relationship between loss of control eating and metabolic characteristics in a convenience sample of 329 treatment-seeking and non-treatment-seeking adolescent boys and girls. The sample was enriched by design with adolescents who were overweight or obese and with individuals who reported episodes of loss of control over their eating (either objectively large binge episodes, OBEs or subjectively large binge episodes, SBEs, in the past month), as assessed by clinical interview. MetS components (blood pressure, lipids, glucose, and waist circumference) were the primary variables of interest. RESULTS: 46% of the cohort reported loss of control eating; among those, 53% reported SBEs only and 47% reported OBEs. Youth with loss of control eating had higher systolic blood pressure (p=.001) and higher low-density lipoprotein cholesterol (LDL-c) (p=.002) compared to those without loss of control eating, in analyses adjusted for intervention-seeking status, fat mass and sociodemographic characteristics. Youth reporting OBEs had higher LDL-c (p=.013) compared to those reporting only SBEs. CONCLUSIONS: Adolescents reporting loss of control episodes had greater dysfunction in some components of the MetS compared to youth without loss of control; episode size may contribute to metabolic dysfunction. Published by Elsevier Ltd.
PURPOSE: Preliminary data in adults suggest that binge eating is associated with greater prevalence of metabolic syndrome (MetS) components. However, there are limited data in youth, and little is known of the role of binge episode size in these relationships. METHODS: We examined the relationship between loss of control eating and metabolic characteristics in a convenience sample of 329 treatment-seeking and non-treatment-seeking adolescent boys and girls. The sample was enriched by design with adolescents who were overweight or obese and with individuals who reported episodes of loss of control over their eating (either objectively large binge episodes, OBEs or subjectively large binge episodes, SBEs, in the past month), as assessed by clinical interview. MetS components (blood pressure, lipids, glucose, and waist circumference) were the primary variables of interest. RESULTS: 46% of the cohort reported loss of control eating; among those, 53% reported SBEs only and 47% reported OBEs. Youth with loss of control eating had higher systolic blood pressure (p=.001) and higher low-density lipoprotein cholesterol (LDL-c) (p=.002) compared to those without loss of control eating, in analyses adjusted for intervention-seeking status, fat mass and sociodemographic characteristics. Youth reporting OBEs had higher LDL-c (p=.013) compared to those reporting only SBEs. CONCLUSIONS: Adolescents reporting loss of control episodes had greater dysfunction in some components of the MetS compared to youth without loss of control; episode size may contribute to metabolic dysfunction. Published by Elsevier Ltd.
Entities:
Keywords:
Adolescence; Binge eating; Loss of control eating; Metabolic dysfunction
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