Mid-pregnancy weight gain is associated with offspring adiposity outcomes in early childhood.

BACKGROUND: Gestational weight gain (GWG) has been linked to childhood obesity. However, it is unclear if the timing of weight gain influences offspring body composition. A secondary analysis of a clinical trial examined the influence of total, early, and mid-pregnancy GWG on adiposity outcomes in 186 children at birth, 1, 3, and 5 years. METHODS: Early (<15 weeks) and mid-pregnancy GWG (15-32 weeks) were assessed. Anthropometrics and abdominal ultrasound were measured annually in children from birth to 5 years. MRI was performed in a sub-group of 44 children at 5 years to estimate abdominal fat. RESULTS: Almost half of the women (n = 86/186) gained excess weight in pregnancy, and women with a BMI ≥ 25 kg/m2 (n = 33) were more likely to gain in excess. Mid-pregnancy GWG predicted higher weight (g) and subcutaneous fat by ultrasound (mm2) and MRI (cm3) at 5 years [ß: 139.34 g (95% CI: -0.22; 278.90), p = 0.050; ß: 1.42 mm2 (95% CI: 0.06; 2.78), p = 0.041; and ß: 18.56 cm3 (95% CI: 1.30; 35.82) p = 0.036, respectively]. CONCLUSIONS: Mid-pregnancy weight gain was associated with greater fat depots at 5 years, which suggests that the timing of GWG has differential effects on offspring adiposity outcomes. IMPACT: Gestational weight gained in mid-pregnancy is associated with growth and adipose tissue development at 5 years. We observed that maternal weight gain in early and mid-gestation has differential effects on offspring body composition. Mid-pregnancy weight gain (15-32 weeks gestation) appears to influence child growth and abdominal fat accretion which may have implications for long-term metabolic health. Interventions that prevent excessive gestational weight gain in mid-pregnancy may affect obesity risk in early childhood. Prenatal care should stress the importance of optimal weight gain throughout pregnancy.

Evaluation of Maternal Dietary n-3 LCPUFA Supplementation as a Primary Strategy to Reduce Offspring Obesity: Lessons From the INFAT Trial and Implications for Future Research.

Preclinical research suggests that early exposure to LCPUFAs is associated with offspring health outcomes, although evidence in humans is rather unclear. In 2006, we established the Impact of Nutritional Fatty acids during pregnancy and lactation on early human Adipose Tissue development (INFAT) study, a prospective randomized controlled intervention trial that examined whether decreasing the n-6/n-3 LCPUFA ratio during pregnancy and lactation influences offspring adipose tissue development in children up to 5 years. Our results indicate that maternal supplementation with n-3 LCPUFAs does not reduce offspring obesity risk, which is in line with recent publications. This perspective describes the challenges and lessons learned from our clinical trial. We discuss key findings and critically evaluate differences in study design, methodology, and analyses across similar intervention trials that may partly explain heterogeneous results. Summarizing evidence from human trials, we conclude that n-3 LCPUFA supplementation should not be recommended as a primordial strategy to prevent childhood obesity. Instead, it remains unknown whether n-3 LCPUFA supplementation could benefit high-risk subgroups and some vulnerable maternal/child populations. The perspectives offered herein are derived largely from insights gained from ours and similar n-3 LCPUFA intervention trials and help to provide direction for future research that examines the impact of maternal nutritional exposure on offspring health and disease outcomes.

Associations between long-chain PUFAs in maternal blood, cord blood, and breast milk and offspring body composition up to 5 years: follow-up from the INFAT study.

BACKGROUND/OBJECTIVES: Limited research suggests that exposure to long-chain PUFAs (LCPUFAs) during perinatal development can influence adipose tissue expansion later in life. In previous analyses, we observed that maternal LCPUFAs in late gestation promote offspring gestational growth, whereas breast milk n-3 LCPUFAS promote adipogenesis in infants up to 1 year. This follow-up analysis examines these relationships in offspring up to 5 years. SUBJECTS/METHODS: In this observational study of 169 children, relationships between n-3, n-6 LCPUFAs, and the n-6/n-3 LCPUFA ratio in maternal blood at 32 weeks' gestation, cord blood, and breast milk, and anthropometry in offspring from 2 to 5 years were investigated. Body composition was assessed with indirect (i.e., body weight, BMI percentiles, sum of four skinfold thicknesses) and direct (i.e., ultrasonography, magnetic resonance imaging in a subgroup) measurement tools. RESULTS: Maternal and cord blood LCPUFAs were largely not shown to be related to offspring body composition. Breast milk n-3 LCPUFAs were significantly positively related to several measurements of child anthropometry at 2 and 4 y, but only a positive relationship between n-3 LCPUFAs and lean body mass remained statistically significant at 5 y. Breast milk n-6/n-3 LCPUFA ratio was inversely related to weight and BMI percentiles at 2 y, and lean body mass at 4 and 5 y. CONCLUSIONS: Results from this follow-up do not provide sufficient evidence that LCPUFAs in maternal blood, cord blood, and breast milk predict offspring adiposity in children up to 5 years.

Leptin in Maternal Plasma and Cord Blood as a Predictor of Offspring Adiposity at 5 Years: A Follow-up Study.

OBJECTIVE: Perinatal leptin exposure may modulate the risk of adiposity in early childhood. In previous analyses, negative associations between maternal (32 weeks' gestation) and cord blood leptin and offspring body composition at 2 years were observed. METHODS: Associations between maternal/cord blood leptin were assessed with indirect (i.e., body weight, BMI percentiles, sum of 4 skinfold thicknesses), and direct (i.e., ultrasonography, magnetic resonance imaging in a subgroup) growth and adipose tissue (AT) measurements in 120 children aged 3 to 5 years. RESULTS: Maternal leptin was not shown to be associated with offspring body composition in univariate analyses. In adjusted analyses, some weak negative associations were observed with weight and BMI percentiles but not with sum of 4 skinfold thicknesses or calculated body fat at 3 to 5 years. Cord blood leptin was inversely related to offspring body composition, but effect sizes were small and not consistently statistically significant. No evidence of associations with direct AT measurements was observed. CONCLUSIONS: Although some negative relationships with indirect measurements of AT mass were observed, the results of this study do not provide sufficient evidence that maternal plasma or cord blood leptin is clinically relevant predictors of obesity or body fat distribution in early childhood.

Impact of Dietary Macronutrient Intake during Early and Late Gestation on Offspring Body Composition at Birth, 1, 3, and 5 Years of Age.

Dietary intake during pregnancy as a possible modifiable risk factor for childhood obesity is poorly explored. In a prospective observational study, two multivariable regression models were therefore used to associate maternal diet at 15 and 32 weeks’ gestation with offsprings’ body composition and fat distribution at birth, 1, 3, and 5 years. Mean energy intake was 2157 ± 375 kcal (n = 186) in early and 2208 ± 460 kcal (n = 167) in late gestation. The partition model showed mostly no significant associations between maternal diet in early pregnancy and offspring body composition. In late pregnancy, higher fat intake was negatively associated with clinical outcomes at birth, 1, and 5 years. Protein intake was negatively associated with BMI z score (zBMI) at 3 and 5 years. A 10 g increase in fiber was associated with an increase of 3.50 mm² abdominal subcutaneous fat at 1, 172.49 g fat mass at 3, and 0.23 zBMI at 5 years. Results were largely comparable in the substitution model. An incremental increase in fat and protein at the expense of carbohydrates in late but not early pregnancy may be associated with lower fat mass up to 5 years. Findings require confirmation by additional prospective studies.