People with higher genetic risk scores usually have a greater chance of becoming chronically obese when they are adults, researchers from Duke University, Durham, N.C. report in Archive of Pediatrics and Adolescent Medicine. Certain genetic characteristics lead to rapid growth during childhood, and a higher risk of obesity during adulthood, the authors added.

The researchers explain that obesity can be inherited and GWASs (genome-wide association studies) have started to reveal the molecular roots of heritability by identifying SNPs (single-nucleotide polymorphisms) which are associated with higher BMIs (body mass indexes).

Daniel W. Belsky, Ph.D., and team wrote:

“In this study, we asked how SNPs with replicated GWAS evidence for association with adult BMI relate to growth across the first four decades of life and to adult obesity in a birth cohort followed up prospectively from birth through 38 years of age.”

The researchers gathered data on 1,037 New Zealanders who were members of the Dunedin Multidisciplinary Health and Development Study. 52% of them were males. They were all born between April 1972 and March 1973. They were assessed every few years up to the age of 38 years.

Participants with higher GRSs (genetic risk scores) had greater BMIs between ages 3 to 38 for every age assessed. Children identified with a high genetic risk were found to have a 1.61 to 2.41 times higher chance of becoming obese during their teens to late thirties , and 1.90 times more likely to become chronically obese across over three assessments compared to the other kids.

Children at higher genetic risk experienced more severe adiposity rebound than other kids. Adiposity rebound means gaining fat after losing weight – piling the pounds back on. Adiposity rebound also appeared to occur earlier on among kids at higher genetic risk.

Children of normal weight at higher genetic risk, whose parents were overweight, were found to have faster growth and a greater chance of becoming obese.

The authors explained that genetic score risk contributed “independent and additive information” to predicting how much children might grow and/or become obese later on in life – this data went beyond family history data.

In the same journal, the authors concluded:

“Thus, the results present compelling evidence that SNPs identified in GWASs of adult BMI and other obesity-related phenotypes predispose to more rapid growth in childhood, leading to increased risk for obesity in adulthood, and provide information not forthcoming from a simple analysis of family history.”

Jose R. Fernandez, Ph.D., of the University of Alabama at Birmingham, wrote:

“This study provides clear evidence regarding the role of biological risk attributed to the development of obesity and suggests that genetic risk for obesity affects fat accumulation through accelerated growth in early childhood.

Further insights and implications of the study, however, cause concern as much as they fascinate. Given that the associations identified were independent of parental body mass index, the findings from Belsky et al may imply a degree of genetic determinism that challenges overall public health recommendations worldwide in a simple question: What about the role of the environment across the life span?

Attempting to translate the findings from Belsky and colleagues to clinical practice would be naïve at this point when more research is clearly needed to fully understand the genetic basis of many complex traits. … Until we know more, and perhaps after we know more, preventive behaviors should be each individual’s priority so that we all achieve the best health possible regardless of genetic profiles. Without taking this approach, we might risk the mistake of allowing genetic predisposition to become genetic determinism.”

Written by Christian Nordqvist