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New Insight brought back home from the Espghan 50th Annual Meeting, Prague 11–12 May 2017.

Breast-milk as the Natural Functional Food:

Nutrition and the gut microbiota to brain development

(A report by Saptawati Bardosono)

Following all the talks regarding to the use pre and probiotics during the two days meeting, the following are the reports:

Milk, is the only food ever “designed” specifically to feed human, in which its composition is used as gold standard for estimating nutrient and energy requirements for infants, and manufacturing infant formulas. We still need to understand thoroughly what is in human milk and what it all does may improve human health than other food, which makes human milk or breast milk as natural functional food.

Human milk has long been considered sterile unless contaminated or collected from infected gland. And, even as human milk banks it is a pasteurize milk, in which no one would have ever suggested adding bacteria back to the milk. Until recently, formula manufactures would not dream of adding bacteria to their products. But, why the paradigm shift? It is because of the evolution of methods and then the fact that nothing is likely sterile. As now we characterizing microbial communities in human milk, i.e. diverse bacterial genera identified in every sample with high level of variability among women and in which there are bacterial fingerprints within a woman (McGuire, Espghan 2017). Again, the paradigm shift as milk, even when produced by healthy women, contains bacteria, and many of these bacteria would/could be considered as potentially pathogenic.

There are several factors that are believed associated with variation in the milk microbiome, such as:

  • Time of postpartum, i.e. milk microbial community structure is relatively stable over time,

  • Delivery mode, i.e. C-section associated with decrease diversity in milk, increase total bacteria, and trend toward higher relative abundance of propionibacterium,

  • Maternal diet, i.e. there is positive correlations between fermiculates to total energy, lipids, carbohydrates and fiber in diet, additionally when women consume probiotic bacteria, they find their way to the milk,

  • Other milk components, i.e. HMO and immune cells. HMO stimulate growth of milk-derived Staphylococcus, and milk also have immune cell distributions in which there is a relationship between immune cells in milk ad microbial community in milk,

  • Childcare, i.e. increase of milk microbiome diversity related to the increase of social networks,

  • Maternal genetics and environmental microbial exposure, i.e. skin, infant mouth, environment and maternal GI tract are the origin of milk microbiota.

Starting to learn the evolution of gut symbiont, then Lactobacillus reuteri can be used as a model of vertebrae gut symbiont evolution. Along the way, there is a diversification of the gut symbiont Lactobacillus reuteri as a result of host-driven evolution. This happened to all vertebrae species, i.e. rodent, poultry, pig and also human. Specifically for Lactobacillus reuteri, the epithelial selection is highly specific in rodent as compare to the non-rodents, i.e. pig and human, because there is a fundamentally different trend of genome evolution in Lactobacillus reuteri. The phenomenon is caused by several factors, including the very homogeneous, smaller genome, reductive evolution, and population bottleneck. It is also evident in human population, in which the gut microbiota in rural Papua New Guineans significantly different as compared to the Americans.

What are the roles of Lactobacillus reuteri? From the animal study, firstly, it plays role as aryl hydrocarbon receptor (AHR) ligands derived from tryptophan catabolism from the diet that works in lamina propria of the gut as protection against colitis. Secondly, it plays role in the astrocyte as protection against central nervous system inflammation. Thus, Lactobacillus reuteri is beneficial both for gastrointestinal tract and the brain of the host. However, there is a harmful issue for the “modern” lifestyle that might have been unfavorable to L. reuteri. For further detailed, please find it in Marsland, Nature Medicine, 2016.

Next is, what is already known about L. reuteri?

  • Wu et al (2013) from Neurogastroenterol Motil 25, explained how L. reuteri DSM 17938 increased colon propulsive peristaltis. Dunn’s multiple comparisons tests shows how loperamide decreases propulsive contractile clusters frequency and velocity ex vivo and decreases defecation frequency in vivo. And, decreased motility ex vivo or in vivo is reversed by L. reuteri DSM 17938;

  • Perez-Burgos et al (2015) from J Physiol 593(17):3943-57 shows how L. reuteri DSM 17938 block the capsaicin stimulation of transient receptor potential cation channel subtype V1 (TRPV1) as receptor within minutes to reduce pain.

In conclusion on the issues, the following are the mode of action of L. reuteri DSM 17938:

  1. Decreased inflammation

  2. Reduced dysbiosis

  3. Improved gut motility

  4. Decreased visceral pain.