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Author Spotlight: Studying the Impact of Maternal Dietary Deficiencies on Long-Term Offspring Health Outcomes
Published on: June 28, 2024
Breastfeeding duration modifies the association between maternal weight status and offspring dietary palmitate
Eva C Diaz1,2,3,4,5, David K Williams1,4,5, Matthew Cotter1,2
1Arkansas Children's Nutrition Center, Little Rock, AR, USA.
Insights
Maternal obesity in early pregnancy may program offspring for higher fat utilization, particularly in boys and those with longer breastfeeding duration. Human milk insulin and leptin levels in mothers with excessive weight may contribute to this effect.
Area of Science:
- Metabolic programming
- Human milk composition
- Childhood metabolic health
Background:
- Offspring of obese rodents exhibit increased fat deposition.
- Limited human data exists on maternal obesity's programming of offspring fuel utilization.
Purpose of the Study:
- To investigate the association between maternal weight status and offspring's dietary palmitate oxidation (DPO) at age 2.
- To explore potential confounders and modifiers in this relationship.
Main Methods:
- Prospective study of 56 women from first trimester of gestation.
- Assessed maternal physical activity, gestational weight gain, and human milk composition.
- Measured offspring's DPO at age 2, alongside dietary quality and feeding practices.
Main Results:
- Offspring of women with excessive weight (EW) had higher DPO compared to normal weight (NW) (P=0.03).
- Breastfeeding duration modified this association, with higher DPO in EW offspring with ≥9 months of breastfeeding.
- Human milk insulin and leptin concentrations were positively associated with DPO.
Conclusions:
- Maternal excessive weight is associated with higher offspring DPO, influenced by breastfeeding duration.
- Higher human milk insulin and leptin in mothers with excessive weight may explain the findings.
- Further research is needed to confirm these associations.
Background:
Offspring of obese rodents develop a metabolic phenotype that favors fat deposition. Data regarding the impact of maternal obesity programing of offspring fuel usage in humans is scarce.
Objective:
The objective of this study was to explore the association between maternal weight status and dietary palmitate oxidation (DPO) in 2-y-old offspring, taking into consideration potential confounders and modifiers.
Methods:
Women (n = 56) were enrolled by the first trimester of gestation. Maternal physical activity (PA; measured with accelerometers) at enrollment and gestational weight gain (GWG) were measured. Offspring sex, race, and breastfeeding (BF) duration were self-reported. Human milk (HM) composition was determined at 6 mo postpartum. At age 2 y, dietary quality [healthy eating index (HEI)] and parental feeding practices [Child Feeding Questionnaire (CFQ)] were assessed. DPO in 2-y-olds (2-yo-DPO) was measured using deuterated palmitic acid. Generalized linear regression analysis was used to model the associations of 2-yo-DPO with maternal weight status [normal weight (NW), BMI <25 (in kg/m2) compared with excessive weight (EW), BMI ≥25].
Results:
DPO was higher in offspring of women with EW compared with NW (2.1 ± 1.2%/h compared with 1.4 ± 0.7%/h, P = 0.03). Maternal weight status interacted with BF duration in association with 2-yo-DPO (log ß: 0.05, P = 0.04). Specifically, 2-yo-DPO was higher in the EW compared with NW group if BF duration was ≥9 mo. HM insulin (log ß: 0.35, P = 0.002) and HM leptin (log ß: 0.81, P = 0.001) concentrations directly associated with 2-yo-DPO. PA (log ß: 0.06, P = 0.013), parental feeding restriction (log ß: 0.05, P < 0.0001), and male sex (log ß: 0.54, P < 0.001) were positively associated with 2-yo-DPO. HEI was negatively associated with 2-yo-DPO (log ß:-0.03, P < 0.0001).
Conclusions:
Higher 2-yo-DPO in offspring of women with EW compared with NW were driven by BF duration. Higher HM insulin and leptin concentrations in women with EW may explain these finding. More studies are needed to confirm these results. This trial was registered at clinicaltrials.gov as NCT03281850.
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