Scientists reveal that shifting meals earlier could counteract genetic risk for obesity, helping at-risk adults keep the weight off years after dieting.
Study: Early meal timing attenuates high polygenic risk of obesity. Image credit: nehophoto/Shutterstock.com
A study published in the journal Obesity reported that early eating can reduce the genetic risk of obesity, and that each hour of delay in the midpoint of meal intake (the average timing between breakfast and dinner, including snacks) can lead to poor body weight maintenance in adults with overweight or obesity.
Background
Meal timing as a lifestyle factor can potentially influence weight management and obesity risk by altering metabolism, energy expenditure, and body weight regulatory processes. Moreover, meal timing as a rhythmically occurring event can act as a cue in regulating the body’s circadian rhythms. In this way, any change in meal timing can induce changes in circadian rhythms in metabolic function, leading to adverse cardiometabolic outcomes, including obesity.
Meal timing-related metabolic outcomes may vary from person to person. While some people may experience weight loss benefits from specific meal timing strategies, others may not experience the same. It is important to decipher the impact of a person’s genetic makeup on meal timing-related metabolic changes.
Genetic factors play a crucial role in determining obesity risk. Studies have identified several genes that substantially increase obesity risk. Genetic research uses a polygenic risk score to determine a person’s genetic predisposition to obesity. However, genetic factors do not exclusively contribute to obesity risk; complex interactions between genetic and lifestyle factors are vital in determining obesity risk.
Most studies investigating the impact of lifestyle factors on obesity risk have chosen meal components (food intake) over meal timing as the primary modulator. In the current study, researchers primarily aimed at exploring the impact of meal timing on weight management in adults with different levels of genetic predisposition to obesity.
The study
The study included 1195 overweight and obese adults from the Obesity, Nutrigenetics, Timing, and Mediterranean (ONTIME) study. All of them were undergoing dietary obesity treatments in six weight-loss clinics in Spain.
Participants were categorized as early and late eaters based on their estimated meal timing. Polygenic risk scores for body mass index (BMI) were estimated to determine their genetic predisposition to obesity.
Appropriate statistical analyses were carried out to determine the impact of meal timing on participants’ BMI, weight-loss effectiveness, and long-term weight-loss maintenance. The interaction of meal timing with 97 already-known BMI-related genetic variants was analyzed for more in-depth interpretations.
However, the researchers found that meal timings and polygenic risk scores did not significantly interact to affect weight-loss percentage or speed during the active dietary treatment phase; the effects were specific to BMI at baseline and long-term weight regain.
Key findings
The study found a significant association between meal timing and BMI. This association remained significant even after adjusting for potential confounding factors, including total energy intake, physical activity, sleep duration, educational level, and carbohydrate, protein, and fat intakes.
At long-term follow-up (averaging 12 years post-treatment), the participants exhibited 2.2% greater body weight with each hour of meal timing delay, indicating poor long-term weight-loss maintenance following dietary obesity treatment.
The study also found significant associations of polygenic risk scores for BMI with participants’ BMI and meal timing interactions. Participants with a high genetic predisposition to obesity exhibited an increase in BMI by more than 2 kg/m2 for each hour of meal timing delay. However, this relationship was not seen in participants with medium or low genetic risk, and there was no overall correlation between genetic risk and meal timing.
The exploratory analyses identified two genetic variants that nominally interacted with meal timing for BMI in different directions depending on whether they may be protective or promoters of obesity.
Study significance
The study findings reveal that early eating can attenuate the high genetic risk of obesity in overweight or obese adults. Late eating, on the other hand, can lead to poorer long-term weight maintenance after a dietary weight loss treatment among adults with a higher genetic predisposition to obesity.
Previous studies have identified various modifiable lifestyle factors crucial for long-term weight maintenance following obesity management treatments. These factors include regular high-intensity physical activity, consumption of a low-calorie or low-fat diet, regular breakfast eating, body weight monitoring, and maintaining a consistent eating pattern across weekdays and weekends. The current study adds early meal timing as a potential modifiable lifestyle factor.
According to the study findings, early eating is particularly beneficial for individuals with a higher genetic risk of obesity, but not for individuals with a medium or low genetic predisposition to obesity. These findings highlight the significance of personalized obesity management strategies based on an individual’s genetic makeup.
The variations in metabolic responses to meal timing observed among participants may be due to genetic variations in clock genes. Clock genes maintain circadian rhythms that regulate various physiological processes, including metabolism.
Meal timing may also influence the balance between energy intake and expenditure by regulating the timing and distribution of nutrient intake throughout the day. In this context, evidence indicates that eating a heavy meal later in the day can lead to lower energy expenditure and subsequent weight gain. However, the current study found no impact of energy intake and dietary composition on the observed associations.
As the study is observational, causality cannot be inferred, and the self-reporting of dietary intake and meal timing introduces possible recall bias. Furthermore, the sample was predominantly female (81%), and only 456 of the 1195 participants were recontacted for long-term weight maintenance outcomes. The study involved a specific population of overweight or obese adults enrolled in the ONTIME study, which may restrict the generalizability of the findings.
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