Obesity is a serious epidemic affecting an estimated 650 million adults worldwide, including 42% of the adult US population). Obesity is a major contributor to the global burden of chronic disease and disability, as it elevates the risk for a wide range of health issues including diabetes, cardiovascular disease, certain cancers, and COVID-19 mortality. For this reason, prevention and treatment of obesity has been identified as a global imperative.
Behavioral interventions targeting obesity have been mostly aimed at reducing dietary energy intake and/or increasing energy expenditure via increased physical activity. However, these behavioral interventions are often only transiently effective, as a complex array of factors beyond diet and exercise influence energy balance and contribute to obesity risk.
One such factor is the circadian timing system, which is tightly interwoven with energy metabolism. The influence of the circadian system and its interaction with time of eating on metabolism has been demonstrated at the whole-body physiology level and at the molecular level, for example in adipocytes.
New study show the impact of late eating
Vujovic, Scheer and their team studied 16 patients with a body mass index (BMI) in the overweight or obese range. Each participant completed two laboratory protocols: one with a strictly scheduled early meal schedule, and the other with the exact same meals, each scheduled about four hours later in the day. In the last two to three weeks before starting each of the in-laboratory protocols, participants maintained fixed sleep and wake schedules, and in the final three days before entering the laboratory, they strictly followed identical diets and meal schedules at home. In the lab, 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 how eating time affected molecular pathways involved in adipogenesis, or how the body stores fat, investigators collected biopsies of adipose tissue from a subset of participants during laboratory testing in both the early and late eating protocols, to enable comparison of gene expression patterns/levels between these two eating conditions.
Results revealed that eating later had profound effects on hunger and appetite-regulating hormones leptin and ghrelin, which influence our drive to eat. Specifically, levels of the hormone leptin, which signals satiety, were decreased across the 24 hours in the late eating condition compared to the early eating conditions.
When participants ate later, they also burned calories at a slower rate and exhibited adipose tissue gene expression towards increased adipogenesis and decreased lipolysis, which promote fat growth. Notably, these findings convey converging physiological and molecular mechanisms underlying the correlation between late eating and increased obesity risk.
This study shows the impact of late versus early eating. Here, they isolated these effects by controlling for confounding variables like caloric intake, physical activity, sleep, and light exposure, but in real life, many of these factors may themselves be influenced by meal timing.
Nina Vujović et al, (October 4, 2022). Late isocaloric eating increases hunger, decreases energy expenditure, and modifies metabolic pathways in adults with overweight and obesity. Cell Metabolism. Retrieved from : https://www.cell.com/cell-metabolism/fulltext/S1550-4131(22)00397-7?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1550413122003977%3Fshowall%3Dtrue