Meal Timing: Its Relation to Metabolism and Heritability in German Adult Twins - European Medical Journal

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Meal Timing: Its Relation to Metabolism and Heritability in German Adult Twins

1 Mins
Diabetes
Authors:
*Olga Pivovarova-Ramich,1-4 Janna Vahlhaus,1,5 Beeke Peters,1,3,6 Silke Hornemann,4 Anne-Cathrin Ost,4,7 Michael Kruse,4 Andreas Busjahn,8 Andreas F.H. Pfeiffer2-4

1. Department of Molecular Metabolism and Precision Nutrition, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
2. Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Endocrinology and Metabolism, Germany
3. German Center for Diabetes Research (DZD), München-Neuherberg, Germany
4. Department of Clinical Nutrition, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
5. University of Lübeck, Germany
6. Department of Human Nutrition, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany
7. University of Leipzig, Germany
8. HealthTwiSt GmbH, Berlin, Germany

*Correspondence to [email protected]
Disclosure:

Busjahn received honoraria for the statistical analysis from HealthTwiSt GmbH. Pivovarova-Ramich has received grants from the German Research Foundation and the European Association of the Study of Diabetes (EASD); and has received payment or honoraria from Novo Nordisk. The other authors declare no conflicts of interest.

Acknowledgements:

The authors thank all study participants for their cooperation. They gratefully acknowledge the technical assistance of Andreas Wagner, Melanie Hannemann, and Anja Henkel. They also thank Elwira Gliwska for her contribution to the algorithm development for the analysis of meal timing.

Citation:
EMJ Diabet. ;12[1]:28-29. https://doi.org/10.33590/emjdiabet/YRCW6549.
Keywords:
Circadian clocks, diabetes, glucose metabolism, heritability, insulin sensitivity, meal timing, twins.

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

INTRODUCTION

Meal timing is a crucial factor influencing metabolic health, which can be explained by the tight interaction between circadian clocks and metabolic homeostasis.1 Recent evidence suggests that meal timing pattern might contribute to obesity and diabetes risk,2 but this topic is still insufficiently studied. This work aimed to investigate the link between individual meal timing pattern and glucose metabolism as well as explore the contribution of genetic and environmental factors to the meal timing architecture.

METHODS

The research was conducted in a German NUtriGenomic Analysis in Twins (NUGAT) cohort (NCT01631123; n=89) comprising 32 monozygotic and 12 dizygotic twin pairs with a BMI of 22.8±2.8 kg/m² and median age of 25.0 years (interquartile range: 22.0).3 Glucose metabolism was assessed using the oral glucose tolerance test. Parameters of meal timing pattern (meal timing itself, daily calorie distribution, and meal number) were extracted from 5-day food records. Circadian timing of the caloric midpoint of the first and last eating events was determined as the time differences relative to the individual chronotype (MSFsc) assessed by the Munich chronotype questionnaire. Heritability of meal timing components was estimated by the ACE model, and bivariate correlation analyses were performed to assess their relation to metabolic traits.

RESULTS

Correlation analysis revealed a number of associations between meal timing components and glucose metabolism parameters. Most associations were found for the calorie midpoint, defined as the time point at which 50% of daily calories were consumed. Indices of insulin sensitivity, Stumvoll Insulin Sensitivity Index (β=0.334; p=2.9×10-4) and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR; β=-0.276; p=0.007), as well as fasting insulin levels (β=-0.278; p=0.008), were significantly associated with the circadian caloric midpoint even after the model adjustment for gender, age, energy intake, and sleep duration (Table 1).

Table 1: Associations of circadian caloric midpoint with insulin sensitivity and fasting insulin.
Linear regression analyses were performed to estimate the strength of association between variables. β are the standardised coefficients; p are the p-values.
HOMA-IR: Homeostatic Model Assessment for Insulin Resistance; ISI: Insulin Sensitivity Index.

The association with the Matsuda Insulin Sensitivity Index was lost after the adjustment for energy intake and sleep duration. BMI and waist circumference also demonstrated robust associations with the circadian caloric midpoint in adjusted models (β=-0.263; p=0.005; and β=-0.194; p=0.014, respectively). All meal timing components showed high or moderate heritability. Meal timing components demonstrated the strong relation to the individual sleep-wake timing and chronotype, both of which also showed a marked genetic impact.

CONCLUSION

Circadian meal timing is associated with insulin sensitivity and shows significant genetic influences, sharing a common genetic architecture with sleep behaviour. These findings help to differentiate (none-)modifiable factors driving individual meal timing, which is important for the development of effective nutritional strategies to combat obesity and diabetes.

References
Kessler K, Pivovarova-Ramich O. Meal timing, aging, and metabolic health. Int J Mol Sci. 2019;20(8):1911. Peters B et al. Meal timing and its role in obesity and associated diseases. Front Endocrinol (Lausanne). 2024;15:1359772. German Institute of Human Nutrition. NUtriGenomic Analysis in Twins (NUGAT). NCT01631123. https://clinicaltrials.gov/study/NCT01631123?tab=results.

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