Eating less meat may help prevent obesity for adults with high genetic risk
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Key takeaways:
- Plant-based diet indices did not mediate associations between polygenic risk scores for obesity and body composition measures.
- Meat intake mediated the link between polygenic risk score and BMI.
Adhering to a diet containing less meat may be beneficial for people with a high genetic risk for obesity, according to data published in Obesity.
"We found it interesting that while overall adherence to a plant-based dietary pattern did not appear to be relevant in the relationship between genetic risk of obesity and obesity-related outcomes, certain food groups could be relevant,” Daiva E. Nielsen, PhD, associate professor in the School of Human Nutrition at McGill University, told Healio. “These were meat and whole grains, which were identified as mediators of obesity genetic risk, meaning that they partly contribute to the relationship between obesity genetic risk scores and obesity-related outcomes. Lower intake of meat and higher intake of whole grains showed beneficial patterns of relationships with obesity-related outcomes.”
Nielsen and colleagues obtained data from the CARTaGENE study that investigated genetic, environmental and lifestyle factors that contribute to health. The study included 2,258 adults aged 40 to 69 years who had genotype and dietary data available and had BMI and waist circumference collected during follow-up. Dietary intake was assessed using the Canadian adaptation of the U.S. NIH Diet History Questionnaire. Three plant-based dietary indices assessed whether participants adhere to an overall plant-based diet, a healthy plant-based diet or an unhealthy plant-based diet. Two polygenic risk scores (PRSs) were calculated, PRS-Khera and PRS-Locke. BMI, waist circumference and body fat percentage were measured at assessment centers during baseline. Weight and waist circumference were self-reported during follow-up.
Adults had a lower BMI (beta = –0.09), lower waist circumference (beta = –0.09) and lower body fat percentage (beta = –0.07) with each 1 U increase in overall plant-based diet index score. Each 1 U increase in healthy plant-based diet index score was also associated with a lower BMI (beta = –0.09), body fat percentage (beta = –0.08) and waist circumference (beta = –0.11).
Higher PRSs for both models were associated with higher BMI, body fat percentage and waist circumference at baseline and follow-up. None of the plant-based diet index scores mediated the association between PRS and obesity.
“Results from our study suggest that greater adherence to a healthful (but not unhealthful) plant-based dietary pattern is linked to lower BMI, waist circumference and percentage of body fat,” Nielsen said. “This relationship appears to be largely independent of genetic risk scores for obesity, suggesting that a healthful plant-based dietary pattern may be beneficial for obesity prevention and management in all adults.”
Within food groups, eating more meat had a 2.26% mediation effect on the association between PRS-Khera and body fat percentage (P = .01). When stratified by sex, eating more meat mediated the association between PRS-Khera and BMI (mediation effect, 2.54%; P = .02) and waist circumference (mediation effect, 3.31%; P = .02) for women. Among men, eating more whole grains mediated the association between PRS-Khera and BMI (mediation effect, 2.06%; P = .007), body fat percentage (mediation effect, 3.19%; P = .006) and waist circumference (mediation effect, 2.74%; P = .006).
“Obesity is a complicated condition,” Nielsen said. “The genetic factors that contribute to obesity may interact with various lifestyle factors, particularly diet. Further research is needed to better understand dietary strategies that may be more effective for promoting healthy weight management among individuals with higher genetic risk of obesity. Intervention studies that evaluate the effects of targeted dietary strategies according to severities of obesity genetic risk will be highly valuable for advancing knowledge on this topic.”
For more information:
Daiva E. Nielsen, PhD, can be reached at daiva.nielsen@mcgill.ca.
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