Obesity is a serious epidemic that affects some 650 million adults worldwide. Obesity is a significant contributor to the global burden of chronic disease and disability, raising the risk of a wide range of health problems, including diabetes, cardiovascular disease, certain cancers, and mortality by COVID-19. For this reason, the prevention and treatment of obesity have been identified as a global imperative.
Behavioural interventions targeting obesity have primarily been aimed at reducing dietary energy intake or increasing energy expenditure through increased physical activity. However, they are often only transiently effective, as a complex set of factors beyond diet and exercise influence energy balance and contribute to obesity risk.
The influence of the circadian system and its interaction with mealtime on metabolism has been demonstrated at the physiology level of the whole body and the molecular level, for example, in adipocytes. Therefore, the circadian timing of food intake has been proposed as a factor that can alter energy balance and act as a modifiable risk factor for obesity.
Researchers at Brigham and Women’s Hospital (USA) studied 16 patients with a body mass index (BMI) in the range of overweight or obese to find out the influence of sleep and weight. Each participant completed two laboratory protocols: one with a strictly scheduled early meal time and the other with the same meals about four hours later in the day. In the last two to three weeks, before starting each of the protocols in the laboratory, the participants maintained fixed sleep-wake schedules. They strictly followed identical diets and meal times in the previous three days before entering the laboratory. At home.
In the lab, the participants regularly documented their hunger and appetite, provided frequent small blood samples throughout the day, and had their body temperature and energy expenditure measured. To measure the effect of mealtime on molecular pathways involved in adipogenesis and how the body stores fat, the researchers took biopsies of fatty tissue from a subgroup of participants during laboratory tests. , both in the early and late feeding protocol, to be able to compare the patterns and levels of gene expression between these two feeding conditions.
The results revealed that eating later had profound effects on hunger and the appetite-regulating hormones leptin and ghrelin, which influence our desire to eat. Specifically, levels of the hormone leptin, which signals satiety, decreased over 24 hours in the late-eating condition compared to the early-eating needs. They also burned calories slower and showed adipose tissue gene expression toward increased adipogenesis and decreased lipolysis, which promotes fat growth. Notably, these findings convey converging physiological and molecular mechanisms underlying the correlation between eating late and the increased risk of obesity.
These findings not only jibe with a large body of research suggesting that eating later may increase the likelihood of developing obesity, but they also shed new light on how this might occur. Using a randomized crossover study and strictly controlling for behavioural and environmental factors such as physical activity, posture, sleep, and light exposure, the researchers could detect changes in the different control systems involved in energy balance, an indicator of how our body uses the food we eat.
In future studies, the team intends to recruit more women to increase the generalizability of their findings to a broader population. Although this study’s cohort only included five female participants, the study was set up to control the menstrual phase, reducing confounding.
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