Continued research into the human microbiome (gut flora) has now discovered human milk oligosaccharides health benefits (HMO). In a nutshell, human milk oligosaccharides support the lining of the gastrointestinal system, increase beneficial gastrointestinal bacteria, especially bifidobacterium and decrease the adherence of pathogens to the inside of the lining of the gastrointestinal system. But how and why?
An oligosaccharide, simply stated is a type of undigestible carbohydrate. It is technically a prebiotic, a term recognized by many with GI tract problems as “food for the good bacteria”. Many probiotics contain prebiotics and most of them have the potential to cause unexpected GI tract problems like gas, bloating, stomach aches or loose bowels. Not so with human milk oligosaccharides.
Human Milk Oligosaccharides
There have been more than 200 human milk oligosaccharides identified and 2′ FL is the most abundant. In comparison with bovine milk withless than 40 oligosaccharides identified, human milk has 100-300 times more total oligosaccharides. They resist the acidic pH of the stomach, are not affected by digestive enzymes and reach the colon intact – an area where bifidobacterium thrives. Once arriving in the colon, they work to change the chemistry of the bowel in a remarkably positive way.
Not only do levels of beneficial bacteria increase, but human milk oligosaccharides act as decoys for many bacterial, viral and protozoan pathogens. They confuse these organisms causing them to bind to the HMO and not human cells. These pathogens are then excreted and do no harm.
No wonder breast milk has always been the “gold standard” for infant nutrition. These same benefits can also be seen in children and adults.
For Metagenics supplement containing HMO’s:
1. Bode L. Human milk oligosaccharides: every baby needs a sugar mama. Glycobiology.
2. Jaff MS. Higher frequency of secretor phenotype in O blood groups benefits in
prevention and/or treatment of some diseases. Int J Nanomedicine. 2010;5:901-905.
3. Kobata A. Structures and application of oligosaccharides in human milk. Proc Jpn Acad
Ser B Phys Biol Sci. 2010;86:731-747.
4. Engfer MB, Stahl B, Finke B, Sawatzki G, Daniel H. Human milk oligosaccharides are
resistant to enzymatic hydrolysis in the upper gastrointestinal tract. Am J Clin Nutr.
5. Gibson GR, Scott KP, Rastall RA, et al. Dietary prebiotics: Current status and new
definition. Food Science and Technology Bulletin: Functional Foods. 2010;7:1-19.
6. Yu ZT, Chen C, Kling DE, et al. The principal fucosylated oligosaccharides of human milk
exhibit prebiotic properties on cultured infant microbiota. Glycobiology. 2013;23:169-177.
7. Lievin V, Peiffer I, Hudault S, et al. Bifidobacterium strains from resident infant human
gastrointestinal microflora exert antimicrobial activity. Gut. 2000;47:646-652.
8. Sharon N. Carbohydrate-lectin interactions in infectious disease. Adv Exp Med Biol.
9. Kunz C, Rudloff S, Baier W, Klein N, Strobel S. Oligosaccharides in human milk:
structural, functional, and metabolic aspects. Annu Rev Nutr. 2000;20:699-722.
10. Newburg DS, Ruiz-Palacios GM, Morrow AL. Human milk glycans protect infants against
enteric pathogens. Annu Rev Nutr. 2005;25:37-58.
11. Ruiz-Palacios GM, Cervantes LE, Ramos P, Chavez-Munguia B, Newburg DS.
Campylobacter jejuni binds intestinal H(O) antigen (Fuc alpha 1, 2Gal beta 1, 4GlcNAc),
and fucosyloligosaccharides of human milk inhibit its binding and infection. J Biol Chem.
12. Morrow AL, Ruiz-Palacios GM, Altaye M, et al. Human milk oligosaccharides are
associated with protection against diarrhea in breast-fed infants. J Pediatr. 2004;145:297-
13. Coppa GV, Zampini L, Galeazzi T, et al. Human milk oligosaccharides inhibit the
adhesion to Caco-2 cells of diarrheal pathogens: Escherichia coli, Vibrio cholerae, and
Salmonella fyris. Pediatr Res. 2006;59:377-382.
14. Shang J, Piskarev VE, Xia M, et al. Identifying human milk glycans that inhibit norovirus
binding using surface plasmon resonance. Glycobiology. 2013;23:1491-1498.
15. Weichert S, Jennewein S, Hufner E, et al. Bioengineered 2′-fucosyllactose and 3-
fucosyllactose inhibit the adhesion of Pseudomonas aeruginosa and enteric pathogens to
human intestinal and respiratory cell lines. Nutr Res. 2013;33:831-838.
16. Angeloni S, Ridet JL, Kusy N, et al. Glycoprofiling with micro-arrays of glycoconjugates
and lectins. Glycobiology. 2005;15:31-41.
17. Kuntz S, Kunz C, Rudloff S. Oligosaccharides from human milk induce growth arrest via
G2/M by influencing growth-related cell cycle genes in intestinal epithelial cells. Br J Nutr.
18. Kuntz S, Rudloff S, Kunz C. Oligosaccharides from human milk influence growth-related
characteristics of intestinally transformed and non-transformed intestinal cells. Br J Nutr.
19. Rudloff S, Pohlentz G, Borsch C, Lentze MJ, Kunz C. Urinary excretion of in vivo (1)(3)Clabelled
milk oligosaccharides in breastfed infants. Br J Nutr. 2012;107:957-963.
20. Obermeier S, Rudloff S, Pohlentz G, Lentze MJ, Kunz C. Secretion of 13C-labelled
oligosaccharides into human milk and infant’s urine after an oral [13C]galactose load.
Isotopes Environ Health Stud. 1999;35:119-125.
21. Eiwegger T, Stahl B, Schmitt J, et al. Human milk-derived oligosaccharides and plant derived
oligosaccharides stimulate cytokine production of cord blood T-cells in vitro.
Pediatr Res. 2004;56:536-540.
22. Bode L, Kunz C, Muhly-Reinholz M, et al. Inhibition of monocyte, lymphocyte, and
neutrophil adhesion to endothelial cells by human milk oligosaccharides. Thromb
23. Bode L, Rudloff S, Kunz C, Strobel S, Klein N. Human milk oligosaccharides reduce
platelet-neutrophil complex formation leading to a decrease in neutrophil beta 2 integrin
expression. J Leukoc Biol. 2004;76:820-826.
24. Schilling JD, Mulvey MA, Vincent CD, Lorenz RG, Hultgren SJ. Bacterial invasion
augments epithelial cytokine responses to Escherichia coli through a lipopolysaccharidedependent
mechanism. J Immunol. 2001;166:1148-1155.
25. He Y, Liu S, Kling DE, et al. The human milk oligosaccharide 2′-fucosyllactose modulates
CD14 expression in human enterocytes, thereby attenuating LPS-induced inflammation.