Issue: August 2012
July 02, 2012
2 min read

Children with higher genetic risk more likely to develop adult chronic obesity

Issue: August 2012
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Genetic risk for obesity in children upped the odds of developing chronic obesity in adulthood, according to data from a 38-year prospective study.

The New Zealand-based study, designed by Daniel W. Belsky, PhD, and colleagues, was composed of 1,037 patients (91% eligible births, 52% male) in a 38-year prospective longitudinal study of a representative birth cohort. Participants were born between April 1972 and March 1973 in Dunedin, New Zealand, and assessed at birth, ages 3, 5, 7, 9, 11, 13, 15, 18, 21, 26, 32 and 38 years (95% retention).

Researchers developed a 32-single nucleotide polymorphism (SNP) genetic risk score (GRS) from published genome-wide association studies. Of the 32 GRS SNPs genotyped using a commercially available array, 29 were called successfully in 95% of the cohort. Final score was constructed from these SNPs.

Participants carried 15 to 36 risk alleles and GRS values ranged from 13.71 to 35.04 after weighting.

Parental BMI was also available for 97.82% of the cohort and was used to measure familial disposition to obesity.

Role of genetic risk

At each assessment, participants’ height and weight were recorded. According to data, participants who met obesity criteria for at least 50% of six measurements from ages 15 to 38 years were labeled chronically obese.

Participants aged 15 to 18 years of the Dunedin Study (5.5%) had BMIs in the obese range, and by ages 21 to 26 years, 11.2% met criteria for obesity. By ages 32 to 38, researchers found that 22.3% met criteria for obesity.

Moreover, participants with an increased risk for obesity were 1.61 to 2.41 times more likely to become obese in their second, third and fourth decades of life, and 1.9 times more likely to be chronically obese, compared with children at low risk, based on Poisson regression models used in the study

Researchers reported, “In the life-course growth model, higher GRSs predicted higher mean levels of BMI (P<.001), faster growth in childhood (P<.001) and faster growth in adulthood (P=.02).”

In addition to gaining weight more rapidly, children at higher genetic risk reached adiposity rebound earlier and at a higher BMI than those at lower genetic risk for obesity.

Furthermore, genetic associations with risk for growth and obesity remained independent of family history.


Jose R. Fernandez, PhD, of the department of nutrition sciences at the University of Alabama at Birmingham, commented on the study’s potential clinical implications.

“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,” Fernandez wrote in an accompanying editorial.

“We should keep in perspective that for obesity-related outcomes the environment plays a pivotal role. Developing effective public health interventions to prevent obesity will require population-specific genetic studies that incorporate socially and culturally sensitive behavioral and environmental factors,” Fernandez wrote.

For more information:

Belsky DW. Arch Pediatr Adolesc Med. 2012;166:515-521.

Fernandez JR. Arch Pediatr Adolesc Med. 2012;166:576-577.

Disclosure: Drs. Belsky and Fernandez report no relevant financial disclosures.