obesity in children

A new study has found that dietary protein and fat intake can influence, and indeed enhance the FTO gene-linked risk for obesity in children.


Obesity is a complex trait that is influenced by the interplay of genetic, socioeconomic, cultural, psychological, and lifestyle-related factors. Studies have identified more than 430 genes that are associated with the risk for obesity.In particular, variants of the fat mass and obesity-associated (FTO) gene are associated with obesity in humans.2 The FTO gene has been shown to regulate eating behavior and energy expenditure. There is also evidence suggesting that high saturated fatty acid (SFA) intake and a comparatively low polyunsaturated fatty acid (PUFA) intake in individuals carrying particular variants of the FTO gene can compound the effects of this gene on obesity.3,4

While variants of the FTO gene have been associated with obesity in individuals from diverse populations, this association has not been examined in Latin American populations with a high degree of admixture. A study carried out in the city of Salvador in Brazil examined this relationship in a highly mixed randomly selected group of 1191 children between 4–11 years of age.It also examined the effects of diet on the relationship between FTO variants and obesity in children. The results of the study were recently published in the British Journal of Nutrition.

The participants were classified into underweight, normal weight, overweight, and obese categories after gathering their anthropometric data (height, weight, and age) and determining their basal metabolic indices (BMIs). DNA was extracted from blood samples and sequenced to determine variants of the FTO gene. Dietary information was gathered by using a questionnaire to record foods consumed in the preceding 24-hour period, which was then converted into an energy and macronutrient format.

Data analysis showed that of the 1191 children who participated, 11.2% were overweight or obese. DNA sequencing, analysis of the FTO gene variants, and subsequent statistical evaluation showed a significant association of certain gene variants with obesity. Ten variants located in 3 different non-coding segments(introns) of the gene were found significantly associated.

The study also found that having a particular variant of the FTO gene (rs62048379) not only increased the risk for obesity, but when the protein content in the diet of these individuals was high (above the median value with all participants considered), their risk for obesity was twice as high when compared to individuals who did not possess this variant. Similarly, individuals with the rs62048379 variant on a diet with a PUFA:SFA ratio below the median value for the study group were at a 1.63 times higher risk for obesity than individuals who did not carry the variant. These findings support available data about the benefits of a diet with a high PUFA:SFA ratio.

A limitation of the study was the small size of the sample comprised of children of predominantly African descent; therefore, these results may not be generalizable to other ethnic groups. Other limitations include; using the BMI to determine obesity status, which does not adequately represent body fat composition or distribution, determining dietary intake using a food questionnaire, which may not always be entirely accurate, and the cross-sectional nature of the study with no follow-up, which limits an analysis of the biological mechanisms involved in the variant-diet-obesity link.

Overall, the study’s findings are consistent with previously published results about the role of FTO in the coordinated regulation of energy intake and energy expenditure as well as in emotional eating and binge eating.2,6 There is also some evidence indicating that the FTO protein may have a role in sensing amino acid levels, which in turn may influence body composition.7 However, the mechanism by which dietary SFAs influence FTO-linked obesity is not clear, and delineating these relationships will require further studies.

Written by Usha B. Nair, Ph.D.


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