Late-night eating increases risks of developing obesity and diet-related diseases, experts flag

05 Oct 2022 --- As the number of people suffering from obesity and obesity-related diseases continues to grow in the US, a new study reveals that late-night eating leads to less burning of calories versus caloric intake and increases appetite and adipogenesis – the creation of fat cells in the body. 

“We wanted to test the mechanisms that may explain why late eating increases obesity risk,” states Dr. Frank A. J. L. Scheer, director of the medical chronobiology program in the Brigham’s division of sleep and circadian disorders at Harvard University, US.

“Previous research by us and others had shown that late eating is associated with increased obesity risk, increased body fat, and impaired weight loss success,” he explains. “We wanted to understand why.”

The three adipose creators
In the US, it is estimated that 42% of adults suffer from obesity and have the potential to develop a host of chronic noncommunicable diseases, including several types of cancer and diabetes. 

Late-eating was found to cause lower lipolysis and increased adipogenesis.According to the authors, though warnings against midnight snacking have been used for generations, very few studies have attempted to comprehensively investigate its effects on the three main factors in obesity: appetite, caloric expenditure and the creation of fatty tissues. 

The results reveal that eating later significantly affected the hunger and appetite-regulating hormones ghrelin and leptin. Most notable was a decrease in leptin, a hormone that signals satiety and fullness to the brain. Leptin levels were not only more suppressed when eating later, but they stayed suppressed for over 24 hours, meaning that those who ate later were hungrier for longer amounts of time.

Furthermore, those who ate later in the day burned fewer calories and burned them at slower rates. They also exhibited increased molecular adipogenesis and decreased lipolysis – the process by which triglycerides are broken down – meaning that not only was new adipose tissue being created, but the metabolic process that breaks down the chemicals that become fat was also less effective. 

“In this study, we asked, ‘Does the time that we eat matter when everything else is kept consistent?’” expounds Dr. Nina Vujović, first author of the study. “And we found that eating four hours later makes a significant difference for our hunger levels, the way we burn calories after we eat, and the way we store fat.”

No feeding after midnight
The randomized-crossover study, published in Cell Metabolism, included 16 participants with body mass indexes in the categorical ranges of overweight or obese. Each participant followed one early meal schedule protocol for six days in which they ate meals at one hour, five hours and ten minutes and then again at nine hours and 20 minutes after waking.The study found that those who ate later had an increased appetite and a lack of satiety.

After a 3 to 12-week washout period, they followed a late meal protocol where they ate meals at five hours and ten minutes, nine hours and 20 minutes and again at 13 hours and 30 minutes after waking.

They also followed strict bedtime and wake-up schedules and fed the exact same meals for both phases of the experiment. Additionally, biopsies were performed on the participants’ adipose tissue, and blood tests were taken to determine individual baselines for caloric expenditure, adipogenesis and ghrelin and leptin levels.

The authors believe the results show that late eating behaviors and habits play a significant role in physiological and molecular mechanisms that lead to obesity. 

“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,” Scheer underscores.

“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.”

Edited by William Bradford Nichols