Background:
Some infants experience excessive weight gain during exclusive breastfeeding. The cause is unknown, but variation in human milk composition might play a role. Several human milk koligosaccharides (HMOs) have been associated with growth velocity in breastfed infants, and it has been suggested that the mechanism could be through an effect on infant gut microbiota composition.
Objective:
The purpose of this exploratory study was to evaluate if HMO composition was different in milk fed to infants with excessive weight gain compared to infants with normal weight gain. Furthermore, we aimed to examine if HMO composition was associated with growth velocity and change in body composition and if there were maternal determinants of HMO composition.
Materials and Methods:
We recruited 13 high weight-gain (HW) and 17 normal weight-gain (NW) breastfed infants, collected human milk and anthropometry data at 5 and 9 months, and analyzed HMO composition by high performance liquid chromatography.
Results:
In the HW group eight out of 11 infants received milk from secretor mothers and in the NW group 15 out of 17. Comparing milk from Secretor mothers only, four HMO's were significantly different between the HW and NW group at 5 months and two remained significant at 9 months. Total HMO concentrations as well as total HMO-bound fucose at 5 months were positively associated with both fat mass index (FMI) and weight velocity from 0 to 5 months (all
p
< 0.025). 2′-fucosyllactose (2′-FL) was positively associated with weight velocity from 0 to 5 months and FMI at 5 months. In contrast, lacto-N-neotetraose was lower in the HW group (
p
= 0.012) and negatively associated with height-for-age Z-scores (
p
= 0.008), weight velocity from 0 to 5 months (
p
= 0.009) and FMI (
p
= 0.033). Maternal BMI at 5 months was negatively associated with 6′-sialyllactose and sialyl-lacto-N-tetraose (LSTb) and positively with 2′-FL, total HMO and total HMO-bound fucose (all
p
≤ 0.03).
Conclusion:
In a small cohort, we found significantly different HMO concentrations in milk to exclusively breastfed infants with excessive weight gain, suggesting that some HMOs, including 2′-FL, which is the most abundant HMO and currently added to some infant formula, could be part of the cause for the excessive weight gain.
A daily administration of a combination of subsp and for 6 months did not reduce the number of days absent from child care in healthy infants at the time of enrollment in child care.
In adults, dietary protein seems to induce weight loss and dairy proteins may be insulinotropic. However, the effect of milk proteins in adolescents is unclear. The objective was to test whether milk and milk proteins reduce body weight, waist circumference, homeostatic model assessment, plasma insulin, and insulin secretion estimated as the plasma C-peptide concentration in overweight adolescents. Overweight adolescents (n = 203) aged 12-15 y with a BMI of 25.4 ± 2.3 kg/m(2) (mean ± SD) were randomized to 1 L/d of skim milk, whey, casein, or water for 12 wk. All milk drinks contained 35 g protein/L. Before randomization, a subgroup of adolescents (n = 32) was studied for 12 wk before the intervention began as a pretest control group. The effects of the milk-based test drinks were compared with baseline (wk 0), the water group, and the pretest control group. Diet and physical activity were registered. Outcomes were BMI-for-age Z-scores (BAZs), waist circumference, plasma insulin, homeostatic model assessment, and plasma C-peptide. We found no change in BAZ in the pretest control and water groups, whereas it was greater at 12 wk in the skim milk, whey, and casein groups compared with baseline and with the water and pretest control groups. The plasma C-peptide concentration increased from baseline to wk 12 in the whey and casein groups and increments were greater than in the pretest control (P < 0.02). There were no significant changes in plasma C-peptide in the skim milk or water group. These data suggest that high intakes of skim milk, whey, and casein increase BAZs in overweight adolescents and that whey and casein increase insulin secretion. Whether the effect on body weight is primary or secondary to the increased insulin secretion remains to be elucidated.
Background/Objectives: High protein intake has been associated with increased growth. This may be linked to increased concentrations of insulin-like growth factor I (IGF-I), which seems to be influenced by the diet, especially its protein component. The short-term effects of high protein intake in late infancy are not known. The objective was to investigate the effects of high protein intake in the form of whole milk (WM) on growth and IGF-I from 9 to 12 months of age. Subjects/Methods: Healthy infants (n ¼ 83) were randomized to receive either WM or infant formula and fish oil or no fish oil (2 Â 2 design). Anthropometric variables, IGF-I concentrations, serum urea nitrogen (SUN) and diet were recorded before and after the intervention. Results: Intake of WM significantly increased the protein energy percentage (PE%; Pp0.001) and SUN (P ¼ 0.01), whereas there was no effect on size. The milk intervention increased IGF-I in boys (P ¼ 0.034) but not in girls. Intake of fish oil had no effect on the outcomes. Including all infants in the analysis there was a significant correlation between weight and IGF-I at 12 months (r ¼ 0.316, P ¼ 0.017), and PE% was positively associated with IGF-I after adjusting for sex and breastfeeding at both 9 (r ¼ 0.329, P ¼ 0.015) and 12 months (r ¼ 0.272, P ¼ 0.044). Conclusions: Randomization to WM had no overall effect on growth. However, the positive effect of WM on IGF-I in boys and the positive association between PE% intake and IGF-I at 9 and 12 months is consistent with the hypothesis that a high milk intake stimulates growth.
At 9 months, breastfeeding still had a strong negative effect on insulin concentrations, which were positively associated with weight gain and current waist circumference, while glucose concentrations were associated with subcutaneous fat. These results are of interest in disentangling the association between early growth and later risk of disease.
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