Maternal Dairy Consumption and Hematochezia in Exclusively Breastfed Infants.

Background: When an exclusively breastfed infant develops hematochezia, the pediatrician may recommend elimination of dairy and soy products from a mother's diet, but there is limited scientific evidence to indicate that altering the maternal diet will lead to resolution of the problem.

Research Aim: To estimate the likelihood that maternal dairy and soy avoidance will resolve rectal bleeding in an exclusively breastfed infant.

Methods: This was a prospective, longitudinal, one-group pre/post study involving mothers of exclusively breastfed infants at least 2 weeks but less than 6 months of age with a positive stool guaiac test in the absence of an intestinal lesion or other explanation for the blood.

Rapid resolution of milk protein intolerance in infancy.

Objectives: Infants with milk protein intolerance are usually switched to a casein hydrolysate or amino acid-based formula, which they continue to receive until 1 year of age, when they are rechallenged with a cow's-milk or soy protein formula. To investigate whether some of these infants actually become tolerant sooner, this study gathered preliminary data for establishing an empirical timetable for the resolution of milk protein intolerance.

Methods: This prospective, longitudinal cohort study enrolled infants <4 months of age receiving either breast milk or a cow's-milk or casein hydrolysate formula who presented to a pediatric subspecialty practice during an 18-month period and had a positive stool guaiac test.

Ω-3 fatty acids prevent hepatic steatosis, independent of PPAR-α activity, in a murine model of parenteral nutrition-associated liver disease.

Objectives: ω-3 Fatty acids (FAs), natural ligands for the peroxisome proliferator-activated receptor-α (PPAR-α), attenuate parenteral nutrition-associated liver disease (PNALD). However, the mechanisms underlying the protective role of ω-3 FAs are still unknown. The aim of this study was to determine the effects of ω-3 FAs on hepatic triglyceride (TG) accumulation in a murine model of PNALD and to investigate the role of PPAR-α and microsomal triglyceride transfer protein (MTP) in this experimental setting.