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      Chronotype: Implications for Epidemiologic Studies on Chrono-Nutrition and Cardiometabolic Health

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          ABSTRACT

          Chrono-nutrition is an emerging research field in nutritional epidemiology that encompasses 3 dimensions of eating behavior: timing, frequency, and regularity. To date, few studies have investigated how an individual's circadian typology, i.e., one's chronotype, affects the association between chrono-nutrition and cardiometabolic health. This review sets the directions for future research by providing a narrative overview of recent epidemiologic research on chronotype, its determinants, and its association with dietary intake and cardiometabolic health. Limited research was found on the association between chronotype and dietary intake in infants, children, and older adults. Moreover, most of the evidence in adolescents and adults was restricted to cross-sectional surveys with few longitudinal cohorts simultaneously collecting data on chronotype and dietary intake. There was a gap in the research concerning the association between chronotype and the 3 dimensions of chrono-nutrition. Whether chronotype modifies the association between diet and cardiometabolic health outcomes remains to be elucidated. In conclusion, further research is required to understand the interplay between chronotype, chrono-nutrition, and cardiometabolic health outcomes.

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          Circadian Misalignment Augments Markers of Insulin Resistance and Inflammation, Independently of Sleep Loss

          Shift workers, who are exposed to irregular sleep schedules resulting in sleep deprivation and misalignment of circadian rhythms, have an increased risk of diabetes relative to day workers. In healthy adults, sleep restriction without circadian misalignment promotes insulin resistance. To determine whether the misalignment of circadian rhythms that typically occurs in shift work involves intrinsic adverse metabolic effects independently of sleep loss, a parallel group design was used to study 26 healthy adults. Both interventions involved 3 inpatient days with 10-h bedtimes, followed by 8 inpatient days of sleep restriction to 5 h with fixed nocturnal bedtimes (circadian alignment) or with bedtimes delayed by 8.5 h on 4 of the 8 days (circadian misalignment). Daily total sleep time (SD) during the intervention was nearly identical in the aligned and misaligned conditions (4 h 48 min [5 min] vs. 4 h 45 min [6 min]). In both groups, insulin sensitivity (SI) significantly decreased after sleep restriction, without a compensatory increase in insulin secretion, and inflammation increased. In male participants exposed to circadian misalignment, the reduction in SI and the increase in inflammation both doubled compared with those who maintained regular nocturnal bedtimes. Circadian misalignment that occurs in shift work may increase diabetes risk and inflammation, independently of sleep loss.
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            Short sleep duration and dietary intake: epidemiologic evidence, mechanisms, and health implications.

            Links between short sleep duration and obesity, type 2 diabetes, hypertension, and cardiovascular disease may be mediated through changes in dietary intake. This review provides an overview of recent epidemiologic studies on the relations between habitual short sleep duration and dietary intake in adults from 16 cross-sectional studies. The studies have observed consistent associations between short sleep duration and higher total energy intake and higher total fat intake, and limited evidence for lower fruit intake, and lower quality diets. Evidence also suggests that short sleepers may have irregular eating behavior deviating from the traditional 3 meals/d to fewer main meals and more frequent, smaller, energy-dense, and highly palatable snacks at night. Although the impact of short sleep duration on dietary intake tends to be small, if chronic, it may contribute to an increased risk of obesity and related chronic disease. Mechanisms mediating the associations between sleep duration and dietary intake are likely to be multifactorial and include differences in the appetite-related hormones leptin and ghrelin, hedonic pathways, extended hours for intake, and altered time of intake. Taking into account these epidemiologic relations and the evidence for causal relations between sleep loss and metabolism and cardiovascular function, health promotion strategies should emphasize improved sleep as an additional factor in health and weight management. Moreover, future sleep interventions in controlled studies and sleep extension trials in chronic short sleepers are imperative for establishing whether there is a causal relation between short sleep duration and changes in dietary intake.
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              Endogenous circadian system and circadian misalignment impact glucose tolerance via separate mechanisms in humans.

              Glucose tolerance is lower in the evening and at night than in the morning. However, the relative contribution of the circadian system vs. the behavioral cycle (including the sleep/wake and fasting/feeding cycles) is unclear. Furthermore, although shift work is a diabetes risk factor, the separate impact on glucose tolerance of the behavioral cycle, circadian phase, and circadian disruption (i.e., misalignment between the central circadian pacemaker and the behavioral cycle) has not been systematically studied. Here we show--by using two 8-d laboratory protocols--in healthy adults that the circadian system and circadian misalignment have distinct influences on glucose tolerance, both separate from the behavioral cycle. First, postprandial glucose was 17% higher (i.e., lower glucose tolerance) in the biological evening (8:00 PM) than morning (8:00 AM; i.e., a circadian phase effect), independent of the behavioral cycle effect. Second, circadian misalignment itself (12-h behavioral cycle inversion) increased postprandial glucose by 6%. Third, these variations in glucose tolerance appeared to be explained, at least in part, by different mechanisms: during the biological evening by decreased pancreatic β-cell function (27% lower early-phase insulin) and during circadian misalignment presumably by decreased insulin sensitivity (elevated postprandial glucose despite 14% higher late-phase insulin) without change in early-phase insulin. We explored possible contributing factors, including changes in polysomnographic sleep and 24-h hormonal profiles. We demonstrate that the circadian system importantly contributes to the reduced glucose tolerance observed in the evening compared with the morning. Separately, circadian misalignment reduces glucose tolerance, providing a mechanism to help explain the increased diabetes risk in shift workers.
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                Author and article information

                Journal
                Adv Nutr
                Adv Nutr
                advances
                Advances in Nutrition
                Oxford University Press
                2161-8313
                2156-5376
                January 2019
                26 November 2018
                26 November 2018
                : 10
                : 1
                : 30-42
                Affiliations
                [1 ]Brain, Performance, and Nutrition Research Center, Northumbria University, Newcastle-upon-Tyne, United Kingdom
                [2 ]Nestlé Research Center, Institute of Nutritional Sciences, Lausanne, Switzerland
                [3 ]Clinical Epidemiology and Biostatistics, School of Medical Sciences, Örebro University, Örebro, Sweden
                [4 ]School of Life Sciences, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland
                [5 ]Department of Diabetes and Circadian Rhythms, Nestlé Institute of Health Sciences, Lausanne, Switzerland
                [6 ]Department of Epidemiology, Erasmus MC, University Medical Center, Rotterdam, Netherlands
                [7 ]Faculty of Epidemiology and Population Health, London School of Hygiene and Tropical Medicine, London, United Kingdom
                [8 ]Faculty of Health and Medical Sciences, University of Surrey, Guildford, United Kingdom
                [9 ]Saw Swee Hock School of Public Health, National University of Singapore and National University Health System, Singapore
                [10 ]Nestlé Health Science, Vevey, Switzerland
                [11 ]Experimental Myology and Integrative Physiology Cluster, Plymouth Marjon University, Plymouth, United Kingdom
                Author notes
                Address correspondence to LGK (e-mail: leonidas.karagounis@ 123456nestle.com )
                Author information
                http://orcid.org/0000-0003-1030-3470
                http://orcid.org/0000-0002-9279-9707
                http://orcid.org/0000-0003-2830-6813
                http://orcid.org/0000-0001-6944-1750
                http://orcid.org/0000-0002-7354-8734
                http://orcid.org/0000-0003-2403-3387
                Article
                nmy070
                10.1093/advances/nmy070
                6370261
                30500869
                251f86d5-1e29-4b0a-9de1-51865899490c
                © 2018 American Society for Nutrition.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@ 123456oup.com

                History
                : 18 April 2018
                : 02 July 2018
                : 20 August 2018
                Page count
                Pages: 13
                Categories
                Review

                chrono-nutrition,chronotype,nutrition,circadian rhythm,cardiometabolic health,epidemiology

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