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Chinese Journal of Obesity and Metabolic Diseases(Electronic Edition) ›› 2026, Vol. 12 ›› Issue (02): 140-148. doi: 10.3877/cma.j.issn.2095-9605.2026.02.009

• Evidence based Medicine • Previous Articles    

Interplay between genetic polymorphisms and environmental factors in childhood obesity: a meta-analysis

Pin Zhang1, Weiting Yuan2, Hongye Yang3,†()   

  1. 1Department of Clinical Laboratory, Jiangyin Maternal and Child Health Hospital, Jiangyin 214400, China
    2Department of Medical Education, Jiangyin Maternal and Child Health Hospital, Jiangyin 214400, China
    3Department of Pediatrics, Jiangyin Third People’s Hospital, Jiangyin 214400, China
  • Received:2026-06-18 Online:2026-05-31 Published:2026-09-17
  • Contact: Hongye Yang

Abstract:

Objective

To investigate the relationship between genetic polymorphisms and environmental factors, we conducted a meta-analysis.

Methods

According to the PRISMA guidelines, we conducted a systematic search across all relevant databases from the inception of the search until April 1, 2026. We also retained studies that addressed the interaction between obesity-related gene polymorphisms and modifiable environmental factors in overweight or obese children and adolescents. Continuous outcomes were summarized as standardized mean differences (SMD) and dichotomous outcomes as odds ratios (OR), with effect sizes combined under a random-effects model; heterogeneity was assessed by I2 statistic, and publication bias was judged qualitatively from funnel plots.

Results

23 studies meet the criteria. For FTO effect-allele carriers versus non-carriers, the pooled SMD was -0.13 (95%CI: -0.34 to 0.08, I2= 39%), a difference that did not reach statistical significance. Nine studies addressed the MC4R-diet interaction: carriers of the rs17782313 C allele showed a pooled OR of 1.35 (95%CI: 1.19 to 1.53, I2=0%, P<0.0001), roughly a 35% higher risk than non-carriers, with effect directions consistent and the result robust across studies. Eight studies informed the sleep analysis, where insufficient sleep carried a pooled OR for overweight/obesity of 1.54 (95%CI: 1.26 to 1.87, I2= 53%, P<0.0001); given the moderate-to-high heterogeneity, this estimate should be read with caution.

Conclusion

Childhood obesity is a result of both genetic predisposition and modifiable environmental factors, with genetic factors contributing to the risk.

Key words: Childhood obesity, Gene–environment interaction, Genetic polymorphism, Diet, Sleep duration

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