M J Parsons1, T E Moffitt2, A M Gregory3, S Goldman-Mellor4, P M Nolan1, R Poulton5, A Caspi2. 1. Mammalian Genetics Unit, MRC Harwell, Harwell Science and Innovation Campus, Oxfordshire, UK. 2. 1] Department of Psychology and Neuroscience, Duke University, Durham, NC, USA [2] Institute for Genome Sciences & Policy, Duke University, Durham, NC, USA [3] Department of Psychiatry & Behavioral Sciences, Duke University Medical Center, Durham, NC, USA [4] Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, King's College London, London, UK. 3. Department of Psychology, Goldsmiths, University of London, London, UK. 4. 1] Department of Psychology and Neuroscience, Duke University, Durham, NC, USA [2] Institute for Genome Sciences & Policy, Duke University, Durham, NC, USA [3] Department of Psychiatry & Behavioral Sciences, Duke University Medical Center, Durham, NC, USA [4] Center for Developmental Science, University of North Carolina at Chapel Hill, Durham, NC, USA. 5. Dunedin Multidisciplinary Health and Development Research Unit, Department of Preventive and Social Medicine, School of Medicine, University of Otago, Otago, New Zealand.
Abstract
BACKGROUND: Obesity is one of the leading causes of preventable death worldwide. Circadian rhythms are known to control both sleep timing and energy homeostasis, and disruptions in circadian rhythms have been linked with metabolic dysfunction and obesity-associated disease. In previous research, social jetlag, a measure of chronic circadian disruption caused by the discrepancy between our internal versus social clocks, was associated with elevated self-reported body mass index, possibly indicative of a more generalized association with obesity and metabolic dysfunction. METHODS: We studied participants from the population-representative Dunedin Longitudinal Study (N=1037) to determine whether social jetlag was associated with clinically assessed measurements of metabolic phenotypes and disease indicators for obesity-related disease, specifically, indicators of inflammation and diabetes. RESULTS: Our analysis was restricted to N=815 non-shift workers in our cohort. Among these participants, we found that social jetlag was associated with numerous clinically assessed measures of metabolic dysfunction and obesity. We distinguished between obese individuals who were metabolically healthy versus unhealthy, and found higher social jetlag levels in metabolically unhealthy obese individuals. Among metabolically unhealthy obese individuals, social jetlag was additionally associated with elevated glycated hemoglobin and an indicator of inflammation. CONCLUSIONS: The findings are consistent with the possibility that 'living against our internal clock' may contribute to metabolic dysfunction and its consequences. Further research aimed at understanding that the physiology and social features of social jetlag may inform obesity prevention and have ramifications for policies and practices that contribute to increased social jetlag, such as work schedules and daylight savings time.
BACKGROUND: Obesity is one of the leading causes of preventable death worldwide. Circadian rhythms are known to control both sleep timing and energy homeostasis, and disruptions in circadian rhythms have been linked with metabolic dysfunction and obesity-associated disease. In previous research, social jetlag, a measure of chronic circadian disruption caused by the discrepancy between our internal versus social clocks, was associated with elevated self-reported body mass index, possibly indicative of a more generalized association with obesity and metabolic dysfunction. METHODS: We studied participants from the population-representative Dunedin Longitudinal Study (N=1037) to determine whether social jetlag was associated with clinically assessed measurements of metabolic phenotypes and disease indicators for obesity-related disease, specifically, indicators of inflammation and diabetes. RESULTS: Our analysis was restricted to N=815 non-shift workers in our cohort. Among these participants, we found that social jetlag was associated with numerous clinically assessed measures of metabolic dysfunction and obesity. We distinguished between obese individuals who were metabolically healthy versus unhealthy, and found higher social jetlag levels in metabolically unhealthy obese individuals. Among metabolically unhealthy obese individuals, social jetlag was additionally associated with elevated glycated hemoglobin and an indicator of inflammation. CONCLUSIONS: The findings are consistent with the possibility that 'living against our internal clock' may contribute to metabolic dysfunction and its consequences. Further research aimed at understanding that the physiology and social features of social jetlag may inform obesity prevention and have ramifications for policies and practices that contribute to increased social jetlag, such as work schedules and daylight savings time.
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