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. Participants agreed to follow a dairy and soy elimination/rechallenge protocol, maintain a food diary, and have their infant re-tested at 3-week intervals to determine the outcome of the dietary changes. One participant was lost to follow-up, leaving a final sample size of N = 19. RESULTS: All infants continued to test positive for blood in the stool after their mothers eliminated foods containing dairy or soy. Therefore, 0% (0/19) of infants responded to their mother's restricted diet, 95% confidence interval (one-sided [0%, 15%]). CONCLUSION: Given these results, we must call into question the rationale for advising breastfeeding mothers to eliminate dairy and soy from their diet in response to their infant's unexplained rectal bleeding.

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. After having been successfully switched to a casein hydrolysate or amino acid formula, infants who had guaiac-negative stools for at least 2 consecutive months were rechallenged with the formula that had necessitated the most recent switch. RESULTS: Of the 25 patients enrolled in the study, 16 completed the food challenge and data collection protocol. Negative stool guaiac tests following rechallenge indicated resolution of milk protein intolerance by the time subjects reached an average age of 6.7 ±â€Š1.0 months (mean ±â€Šstandard deviation). By the age of 7 months, milk protein intolerance was resolved in 12 of the 16 infants, the remainder having resolved by 10 months. CONCLUSIONS: It may be reasonable to treat infants with milk protein intolerance for 2 to 3 months with a hypoallergenic formula, then rechallenge them at 6 months of age, usually without causing recurrence of the hematochezia. Rechallenging before 12 months old could result in cost savings to families and insurers.

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. METHODS: 129S1/SvImJ wild-type or 129S4/SvJaePparatm/Gonz/J PPAR-α knockout mice were fed chow and water (controls); oral, fat-free PN solution only (PN-O); PN-O plus intraperitoneal (IP) ω-6 FA-predominant supplements (PN-ω-6); or PN-O plus IP ω-3 FA (PN-ω-3). Control and PN-O groups received sham IP injections of 0.9% NaCl. Hepatic histology, TG and cholesterol, MTP activity, and PPAR-α messenger RNA were assessed after 19 days. RESULTS: In all experimental groups, PN feeding increased hepatic TG and MTP activity compared with controls. Both PN-O and PN-ω-6 groups accumulated significantly greater amounts of TG when compared with PN-ω-3 mice. Studies in PPAR-α null animals showed that PN feeding increases hepatic TG as in wild-type mice. PPAR-α null mice in the PN-O and PN-ω-6 groups demonstrated variable degrees of hepatic steatosis, whereas no evidence of hepatic fat accumulation was found after 19 days of oral PN plus IP ω-3 FAs. CONCLUSIONS: PN induces TG accumulation (steatosis) in wild-type and PPAR-α null mice. In PN-fed wild-type and PPAR-α null mice given IP ω-3 FAs, reduced hepatic TG accumulation and absent steatosis are found. Prevention of steatosis by ω-3 FAs results from PPAR-α-independent pathways.