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Updated: May 15, 2026

Assessment of Child Anthropometry in a Large Epidemiologic Study
Published on: February 2, 2017
Reduced genetic influence on childhood obesity in small for gestational age children
Dug Yeo Han1, Rinki Murphy, Angharad R Morgan
1Discipline of Nutrition, FM&HS, The University of Auckland, Auckland, New Zealand. dy.han@auckland.ac.nz
Insights
Genetic factors influencing childhood obesity are less significant in children born small-for-gestational-age (SGA) compared to appropriate-for-gestational-age (AGA) peers. Environmental factors likely play a larger role in SGA children's BMI development.
Area of Science:
- Pediatric Endocrinology
- Genetics
- Metabolic Health
Background:
- Children born small-for-gestational-age (SGA) face higher risks of obesity and metabolic diseases, especially with rapid postnatal growth.
- Investigating the role of common gene variants linked to adult obesity in SGA and appropriate-for-gestational-age (AGA) children's BMI trajectories.
Purpose of the Study:
- To determine if adult obesity-associated gene variants influence postnatal growth (BMI z-score) in SGA and AGA children.
- To compare the impact of genetic risk variants on early childhood BMI between SGA and AGA groups.
Main Methods:
- Genotyped 37 single nucleotide polymorphisms (SNPs) in 547 European children (228 SGA, 319 AGA).
- Assessed obesity using repeated BMI z-score measurements.
- Corrected for multiple testing using the false discovery rate.
Main Results:
- SGA children exhibited lower BMI z-scores at ages 3.5, 7, and 11 years compared to non-SGA children.
- Identified 27 variants in 14 obesity risk genes associated with increased early childhood BMI, primarily in AGA children.
Conclusions:
- Genetic variants have a lesser impact on early childhood BMI in SGA children than in AGA children.
- Non-genetic or environmental factors may be more critical in shaping childhood BMI for SGA individuals.
Background:
Children born small-for-gestational-age (SGA) are at increased risk of developing obesity and metabolic diseases later in life, a risk which is magnified if followed by accelerated postnatal growth. We investigated whether common gene variants associated with adult obesity were associated with increased postnatal growth, as measured by BMI z-score, in children born SGA and appropriate for gestational age (AGA) in the Auckland Birthweight Collaborative.
Methods:
A total of 37 candidate SNPs were genotyped on 547 European children (228 SGA and 319 AGA). Repeated measures of BMI (z-score) were used for assessing obesity status, and results were corrected for multiple testing using the false discovery rate.
Results:
SGA children had a lower BMI z-score than non-SGA children at assessment age 3.5, 7 and 11 years. We confirmed 27 variants within 14 obesity risk genes to be individually associated with increasing early childhood BMI, predominantly in those born AGA.
Conclusions:
Genetic risk variants are less important in influencing early childhood BMI in those born SGA than in those born AGA, suggesting that non-genetic or environmental factors may be more important in influencing childhood BMI in those born SGA.
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