A new study published in the journal Cell Metabolism shows that late eating may cause decreased energy expenditure, increased appetite, and molecular changes in adipose tissue, increasing the risk of obesity.
At a Glance
Compared to early eating, late eating:
- Doubled the odds of waketime hunger,
- Decreased 24-h leptin levels by 6% and increased the 24-h ghrelin: leptin ratio by 12%,
- Lowered 24h energy expenditure by 5%,
- Significantly decreased 24-h core body temperature (CBT),
- Significantly altered adipose tissue gene expression favoring increased lipid storage.
Obesity is a global health issue contributing to the incidence of chronic diseases, including diabetes, high blood pressure, heart disease, stroke, musculoskeletal disorder, cancer, and COVID-19 mortality.
In the USA, obesity affects 42% of the adult population. An increasing trend in obesity is also prevalent in Canada, exceeding 30% among adults aged 40–69 years (Lytvyak et al., 2022). Globally, 39% of adults aged 18 years and over were overweight in 2016 (WHO).
Dietary Intervention, Mealtime, and Weight Loss
Lifestyle interventions like reducing total calorie intake or increasing energy expenditure have been the primary choice for many people to combat weight gain.
The strategy is effective to some extent, but growing evidence from animal and observational studies supports the idea that the timing of calorie intake itself plays a significant role in energy balance (Arble et al., 2009, Salgado-Delgado et al., 2010).
Despite evidence showing consumption of food, independent of amount or content, during the night plays a significant role in weight gain (McHill et al., 2017), and avoiding food at night may be a useful, practical strategy for weight loss (Kahleova et al., 2017), little is known about the molecular mechanisms by which the timing of meal would modulate energy balance.
Late Eating Increases Obesity Risks
In a new study published in Cell Metabolism (Vujovic et al., 2022), scientists from Brigham and Women’s Hospital investigated why late eating increases obesity risk.
In the randomized, controlled, crossover trial (ClinicalTrials.gov NCT02298790), the Vujović, Scheer research team investigated 16 patients with the following inclusion criteria:
1. BMI between 25 and 37.9 kg-2,
2. Adults with regular sleep-wake timing,
3. Non-smokers,
4. Completion of medical and psychological screening tests,
5. Able to spend 14 consecutive days in the sleep laboratory.
Before beginning the laboratory phase trial, all participants maintained a fixed sleep/wake cycle for 2-3 weeks, including consumption of a calculated, timed, identical, pre-prepared diet during the final three days at home.
In the laboratory, each participant completed two phases of strictly scheduled study protocol: early eating and late eating. Late eating usually started four hours after early eating timing.
They consumed identical meals, recorded their hunger and appetite, and provided blood samples. They had their body temperature and energy expenditure measured. In addition, the investigator collected biopsies of adipose tissue.
Outcome
Results showed that eating later decreased the level of satiety control hormone leptin by 6% (p = 0.171) and increased the 24-h ghrelin : leptin ratio by 12% (p = 0.0063), revealing late eating increases hunger.
Measured by indirect calorimetry 12 times over an 18 h period, energy expenditure was significantly lowered in the late eating condition than in the early eating condition, with participants expending 59.4 ± 13.9 fewer kcal per waking day (5.03% less) than in early eating condition.
Measuring core body temperature (CBT) continuously across the entire 24-h sleep/wake cycle, the investigator found that late eating significantly lowers the 24-h CBT (p = 0.019).
In larger scale studies, where tight control of all these factors is not feasible, we must at least consider how other behavioral and environmental variables alter these biological pathways underlying obesity risk.
F. Scheer
The investigators also analyzed the differential expression and pathway enrichment using mRNA from biopsies samples.
They observed differential expression in early and late eating conditions revealing the involvement of several pathways related to lipid metabolism, p38 MAPK signaling, modulation of receptor tyrosine kinases, TGF-β signaling, and autophagy.
More Read
The outcome of the study is simply stunning. The participants consumed identical meals both in early and late eating conditions. However, eating later affects the level of hunger and appetite regulation hormones, increasing urges to eat.
Eating later also burned calories at a slower rate and exhibited adipose tissue gene expression towards increased adipogenesis and decreased lipolysis, which promotes fat growth.
Significance
“This study shows the impact of late versus early eating. Here, we 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,” said lead author Scheer.
“In larger scale studies, where tight control of all these factors is not feasible, we must at least consider how other behavioral and environmental variables alter these biological pathways underlying obesity risk. “
