A new study published in the Obesity Journal explores the potential link between plant-based dietary patterns (plant-based dietary indices, PDI) and genetic risk of obesity.
Study: Plant-based dietary patterns and genetic susceptibility to obesity in the CARTaGENE cohort. Image Credit: marilyn barbone/Shutterstock.com
Introduction
Plant-based diets have been associated with health benefits and have contributed to better ecological outcomes. Notably, many of the world’s longest-lived populations have plant components forming a major part of their food, with little to no meat intake, except for fish.
While dietary risk has been earlier reported to affect the genetic risk of obesity, little data has been collated on the impact of plant-based diets and the genetic factors that predispose to obesity.
Genes associated with obesity have been identified with both central and peripheral expression, but their mechanism of action is little understood.
Prior research showed that the genes mediating obesity risk affect eating behaviors, along with other genes activated by factors like stress exposure in early life, leptin levels, physical activity, and depressive symptoms.
Again, these genes are linked to eating behavior via the body mass index (BMI), the most commonly used marker of obesity.
Lifestyle, demographic, and psychological factors act on the genetic factors mediating the association with obesity, but the impact of diet on this pathway is unclear.
Some earlier research indicates that people with a genetic predisposition to obesity eat lower-quality diets and skip meals, explaining the link in part.
About the study
The current study was motivated by the need to identify evidence supporting a causative and interactive effect of plant-based diets on the genetic risk of obesity.
The study was based on data from over 7,000 CARTaGENE cohort participants, all of whom were adults from Quebec, Canada. The mean age was 56 years, and over half was comprised of women.
The mean BMI was 26.7 kg/m2, with the mean waist circumference (WC) being ~93 cm and the body fat percentage being 31%.
The researchers generated two polygenic risk scores (PRSs) for a high body mass index (BMI), among the most commonly used markers for obesity.
These were based on two million single nucleotide polymorphisms (SNPs) for unhealthy individuals and 92 for healthy people.
At follow-up six years later, there were about 2,260 adults with associated obesity data. These were examined for links with the earlier PRSs and PDI scores to identify possible obesity-related relationships.
Further analysis was carried out to ensure that the observed associations were causal, directly or via their moderating effects. This is important because mediation/interaction analyses can help tell us whether these genes are targets for obesity intervention or modify the impact of such intervention.
What did the study show?
The findings show a significant relationship between obesity and the overall PRSs and PDI scores and between those in the “healthy” group.
There was little evidence to suggest that following PDIs had a moderating or mediatorial role in the genetic predisposition to obesity. However, the results suggest a benefit for obese individuals following a more strictly plant-based dietary pattern.
Females were more likely to have healthy PDIs than men, who had a higher risk for unhealthy PDIs. As listed above, the highest PRS quintile was associated with higher BMI and related outcomes and increased odds of a healthy PDI. The latter association was not observed among men.
The PRSs linked to obesity and related outcomes were partly due to the level of meat intake at any given point overall and in females. Obesity outcomes were linked positively to increased meat intake, such that meat-eating was associated with higher BMI, WC, and body fat.
An increase in the overall PDI score was linked to lower BMI, WC, and body fat, as was the healthy PDI. Unhealthy plant-based diets were not related to reduced obesity odds, including higher consumption of fruits and vegetables, with more sugary drinks.
In addition, the whole grain intake partially mediated the association with the BMI in males at any given moment and when followed over time. People with a higher consumption of whole grains were less likely to become obese or suffer related complications. Meat intake did not seem to show any mediation effects.
This may be because “genetic susceptibility to complex disease varies over the life course,” such that genes favoring obesity may be more active in early life. Observed differences between the sexes in the association of different types of food with obesity are worthy of further study.
The two PRSs showed somewhat different results, perhaps because they examined different metabolic pathways activated by food intake.
“This highlights the importance of using a PRS that captures the relevant underlying biological pathways between the exposure and outcome.”
This study was based on French Canadians, and much more work is needed to develop a population-specific PRS that can capture the associations between obesity, cardiometabolic outcomes, and genetic factors interacting with dietary patterns.
What are the implications?
The findings suggest that people with an increased genetic risk of obesity might be well-advised to watch their dietary intake, particularly reducing meat intake and other animal products while including more plant-based products.
“Adherence to healthful plant-based dietary patterns is inversely associated with obesity outcomes irrespective of genetic risk of obesity.”
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