Nutrition
Late food intake relative to chronotype is associated with poorer metabolic health
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Ainhoa Pérez
Alumni
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MPH, MSc.
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A study has evaluated the relationship between food intake and individual chronotype, showing that greater desynchronization between the two is associated with alterations in glucose metabolism and higher levels of adiposity.
CONCLUSION AND CLINICAL RELEVANCE This study reinforces the role of the circadian rhythm in glycemic metabolism, beyond the quality and quantity of food in the diet. The desynchronization between eating and chronotype could constitute a metabolic mechanism common to different pathologies. The findings support personalized dietary strategies based on chronotype, especially in people with a late chronotype. Thus, advancing energy intake may be a preventive measure against insulin resistance, which is associated with the development of diabetes, hypertension, adiposity, cardiovascular risk, etc. The reduced effectiveness of insulin in the afternoon and the interference of nighttime melatonin with its signaling could explain the glycemic deterioration observed in those with a later mid-caloric point.
Taken together, these data point to the synchronization of eating schedules with the biological clock as a tool for improving insulin sensitivity and reducing cardiometabolic risk. Some limitations of the study include its observational design, the use of self-reported records, and the exclusion of people with pathologies, which restricts the generalization of the findings. Therefore, although the associations are consistent and the characterization of chronobiological mechanisms in metabolic health is strong, experimental studies are still needed to prospectively evaluate chrononutritional interventions tailored to individual genetic and metabolic profiles.
PATHOPHYSIOLOGY AND MECHANISMS
The activity of the cells in our body is not constant, following hourly cycles of greater and lesser activation. This circadian system is coordinated by a central clock in the hypothalamus that is sensitive to light and dark cycles, and peripheral clocks in almost all organs and tissues, following their own endogenous rhythms and modulated by the central clock and other physiological aspects. Peripheral clocks respond strongly to eating schedules, so eating late or at irregular times disrupts the circadian synchronization of cells, hormones, and organs, a phenomenon known as chronodisruption. Alterations in eating schedules and late food intake have been linked to endocrine disturbances, glucose metabolism, increased adiposity, and an increased risk of cardiometabolic diseases. However, alterations adjusted for individual chronotype have been less explored.STUDY
A recent study (Vahlhaus et al., 2025) analyzed the metabolic impact of eating schedules and individual chronotype. Forty-six pairs of twins, aged 18 to 70, participated in the study, in which their meal times were analyzed for five consecutive days. Chronotype was determined using the Munich Chronotype Questionnaire, and circadian synchronization was estimated using the difference between the midpoint of daily energy intake and the midpoint of sleep. Glycemic, anthropometric, and body composition parameters were assessed using dual-energy X-ray absorptiometry, and an oral glucose tolerance test was performed to measure metabolic response. In addition, the heritability of sleep and eating patterns was calculated.MAIN RESULTS
The results showed poorer metabolic health as the discrepancy between meal times and individual chronotype increased. Specifically, the greater the discrepancy between the time at which the midpoint of caloric intake was reached and the midpoint of sleep, the lower the insulin sensitivity, with higher fasting insulin levels, greater insulin resistance, and higher levels of abdominal adiposity. Metabolic alterations were significant even after adjusting for age, sex, daily energy intake, and sleep duration. In contrast, reaching the midpoint of daily caloric intake early in the individual circadian cycle was associated with a better glycemic profile, lower body mass index, and greater pancreatic beta cell capacity. Participants with a late chronotype tended to concentrate their intake at later times, reinforcing the link between chronobiology and diet, showing significant heritability in various aspects, which demonstrates the genetic predisposition of dietary patterns.CONCLUSION AND CLINICAL RELEVANCE This study reinforces the role of the circadian rhythm in glycemic metabolism, beyond the quality and quantity of food in the diet. The desynchronization between eating and chronotype could constitute a metabolic mechanism common to different pathologies. The findings support personalized dietary strategies based on chronotype, especially in people with a late chronotype. Thus, advancing energy intake may be a preventive measure against insulin resistance, which is associated with the development of diabetes, hypertension, adiposity, cardiovascular risk, etc. The reduced effectiveness of insulin in the afternoon and the interference of nighttime melatonin with its signaling could explain the glycemic deterioration observed in those with a later mid-caloric point.
Taken together, these data point to the synchronization of eating schedules with the biological clock as a tool for improving insulin sensitivity and reducing cardiometabolic risk. Some limitations of the study include its observational design, the use of self-reported records, and the exclusion of people with pathologies, which restricts the generalization of the findings. Therefore, although the associations are consistent and the characterization of chronobiological mechanisms in metabolic health is strong, experimental studies are still needed to prospectively evaluate chrononutritional interventions tailored to individual genetic and metabolic profiles.
#chronobiology #chrononutrition #chronotype #chronodisruption
References:
Vahlhaus, J et al, 2025. Later eating timing in relation to an individual internal clock is associated with lower insulin sensitivity and affected by genetic factors. eBioMedicine, 116, 105737. https://doi.org/10.1016/j.ebiom.2025.105737
* The news published on studies do not represent an official position of ICNS, nor a clinical recommendation.
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