Early human development · 2026
Beyond maternal weight: Independent contributions of paternal and maternal obesity to fetal macrosomia in a Peruvian nationwide survey.
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Briceño-Chavez Jhofree Einstein, Delgado-Toro Holly Estrella, Ballena-Caicedo Jhosmer, Mestanza Rossmery Leonor Poemape, Castillo Marcos Francisco Garavito, Zuzunaga-Montoya Fiorella E, Vera-Ponce Víctor Juan
Аннотация
INTRODUCTION: Fetal macrosomia is associated with short- and long-term perinatal complications. Although the role of maternal obesity is well established, the father's independent contribution has been less studied, particularly in middle-income countries such as Peru, where the prevalence of parental obesity has increased steadily over the past decade.
OBJECTIVE: To evaluate the association between obesity in both parents and fetal macrosomia in father-mother-newborn triads nationwide in Peru.
METHODS: Analytical cross-sectional study using data from the Peruvian Demographic and Family Health Survey (ENDES) 2015-2024 (excluding 2020). We assembled 30,593 triads with complete information. Exposures were paternal and maternal obesity (body mass index [BMI] ≥30 kg/m2); the outcome was fetal macrosomia (>4000 g). We estimated weighted prevalences, prevalence ratios (PRs) using Poisson regression with robust variance, dose-response curves using restricted cubic splines, and multiplicative interactions.
RESULTS: The prevalence of macrosomia was 6.7% (95% confidence interval [CI]: 6.2-7.2). Obesity affected 22.7% of fathers and 26.2% of mothers. After multivariable adjustment, paternal obesity (PR 1.30; 95% CI: 1.11-1.53) and maternal obesity (PR 1.71; 95% CI: 1.48-1.97) were independently associated with macrosomia. The dose-response gradient was steeper in mothers (overweight PR 1.55; obesity PR 2.26) than in fathers (significant from obesity onward, PR 1.26). A suggestive multiplicative interaction was observed when both parents had obesity (PR 1.38; 95% CI: 1.01-1.90).
CONCLUSIONS: Obesity in both parents was independently associated with fetal macrosomia, with a biologically coherent dose-response gradient and a tendency toward synergy when both exposures coexisted. This pattern supports incorporating paternal nutritional status into obstetric risk stratification and into strategies to prevent adverse perinatal outcomes.
OBJECTIVE: To evaluate the association between obesity in both parents and fetal macrosomia in father-mother-newborn triads nationwide in Peru.
METHODS: Analytical cross-sectional study using data from the Peruvian Demographic and Family Health Survey (ENDES) 2015-2024 (excluding 2020). We assembled 30,593 triads with complete information. Exposures were paternal and maternal obesity (body mass index [BMI] ≥30 kg/m2); the outcome was fetal macrosomia (>4000 g). We estimated weighted prevalences, prevalence ratios (PRs) using Poisson regression with robust variance, dose-response curves using restricted cubic splines, and multiplicative interactions.
RESULTS: The prevalence of macrosomia was 6.7% (95% confidence interval [CI]: 6.2-7.2). Obesity affected 22.7% of fathers and 26.2% of mothers. After multivariable adjustment, paternal obesity (PR 1.30; 95% CI: 1.11-1.53) and maternal obesity (PR 1.71; 95% CI: 1.48-1.97) were independently associated with macrosomia. The dose-response gradient was steeper in mothers (overweight PR 1.55; obesity PR 2.26) than in fathers (significant from obesity onward, PR 1.26). A suggestive multiplicative interaction was observed when both parents had obesity (PR 1.38; 95% CI: 1.01-1.90).
CONCLUSIONS: Obesity in both parents was independently associated with fetal macrosomia, with a biologically coherent dose-response gradient and a tendency toward synergy when both exposures coexisted. This pattern supports incorporating paternal nutritional status into obstetric risk stratification and into strategies to prevent adverse perinatal outcomes.