Supplementation with Bifidobacterium animalis subsp. Lactis BB-12 is effective in managing infant colic. - GreenMedInfo Summary
The therapeutic efficacy of Bifidobacterium animalis subsp. lactis BB-12in infant colic: A randomised, double blind, placebo-controlled trial.
Aliment Pharmacol Ther. 2020 Jan ;51(1):110-120. Epub 2019 Dec 3. PMID: 31797399
Rita Nocerino
BACKGROUND: The pathogenesis of infant colic is poorly defined. Gut microbiota seems to be involved, supporting the potential therapeutic role of probiotics.
AIMS: To assess the rate of infants with a reduction of≥50% of mean daily crying duration after 28 days of intervention with the probiotic Bifidobacterium animalis subsp. lactis BB-12(BB-12). Secondary outcomes were daily number of crying episodes, sleeping time, number of bowel movements and stool consistency.
METHODS: Randomized controlled trial (RCT) on otherwise healthy exclusively breastfed infants with infant colic randomly allocated to receive BB-12 (1 × 10 CFU/day) or placebo for 28 days. Gut microbiota structure and butyrate, beta-defensin-2 (HBD-2), cathelicidin (LL-37), secretory IgA (sIgA) and faecal calprotectin levels were assessed.
RESULTS: Eighty infants were randomised, 40/group. The rate of infants with reduction of≥50% of mean daily crying duration was higher in infants treated with BB-12, starting from the end of 2nd week. No infant relapsed when treatment was stopped. The mean number of crying episodes decreased in both groups, but with a higher effect in BB-12 group (-4.7 ± 3.4 vs -2.3 ± 2.2, P < 0.05). Mean daily stool frequency decreased in both groups but the effect was significantly higher in the BB-12 group; stool consistency was similar between the two groups. An increase in Bifidobacterium abundance (with significant correlation with crying time reduction), butyrate and HBD-2, LL-37, sIgA levels associated with a decrease in faecal calprotectin level were observed in the BB-12 group.
CONCLUSIONS: Supplementation with BB-12 is effective in managing infant colic. The effect could derive from immune and non-immune mechanisms associated with a modulation of gut microbiota structure and function.