Breast feeding and insulin levels in low birth weight neonates: A randomized study.

ABSTRACT

Objective. To evaluate the influence of early infancy feeding practices on fasting insulin levels, as marker of insulin resistance, in low birthweight neonates. Methods. Eighty successive low birth weight (<2.5 kg) neonates <10 days of age born at >38 wk of gestation at this tertiary care centre, were successively invited for participation in the study; parents of 52 (65%) consented to participate. Group 1 children (n=26) were randomized to receive only breast feeding and Group 2 (n=26) received fortified breast feeding with a commercially available human milk fortifier. Routine anthropometry and evaluation of health status was performed. The babies were followed-up every 15 day up to three months. 4-hour fasting glucose and insulin levels were measured at baseline and at 3 month. Statistical analyses were performed using t-test and Mann-Whitney test. Results. In excusively breast-fed Group 1 neonates vs Group 2 the mean birthweight was similar (1.99+0.23 vs 1.87+0.30 kg). There was no difference in body length, head circumference and chest circumference. Mean hemoglobin levels, fasting glucose (63.9+9.8 vs 64.3+8.0 mg/dl) and fasting insulin levels (1.44+1.19 vs 1.73+1.38 μU/ml), were also similar. At three month follow-up in Group 1 children receiving exclusive breast feeding, there was significantly lower weight as compared to Group 2 (3.40+0.3 vs 4.75+0.5 kg, p<0.01). This was associated with significantly lower fasting glucose (79.0+9.4 vs 85.6+8.4 mg/dl) and fasting insulin levels (6.95+4.27 vs 15.73+3.29 μU/ml) (p<0.001).The difference persisted even after adjustment for weight gain in Group 2 (weight adjusted insulin 11.26+3.3 μU/ml; p<0.001). Conclusions. Low birthweight neonates fed fortified breast milk had greater fasting insulin levels compared to those with exclusive breast feeding, at three month of age. The difference persisted after adjustment for excessive gain in fortified milk fed neonates and, suggests adverse glucometabolic programming.