The most abundant solid component in breast milk, after lactose and fats
Fats and Lactose in Human Milk Infographic
Within the 3 categories of HMOs, summarized below are 5 of the most abundant HMOs found in human milk. HMOs may support development in ways other prebiotics cannot.1-4
Preclinical research suggests that HMOs play complementary roles in the gut because of their unique structures.5,7
In several cellular culture studies, each HMO acts as a receptor decoy to block specific pathogen adhesion.
Preclinical research also suggests that HMOs may act as immune cell modulators to help balance immune response.5,25,26
Preclinical research suggests that HMOs may play a beneficial role in the brain through communication via 1) circulation and 2) the vagus nerve.27-39
Fucose, sialic acid, and microbiota-derived metabolites may be absorbed through circulation, where they can travel to the brain to support cognitive development.27-39
Microbiota-derived metabolites may activate the vagus nerve and thus stimulate the developing brain.32,39
Human milk concentrations of 2'-FL and 6'-SL HMO have been associated with measures of improved cognitive outcomes through 24 months of age.40,41
Each HMO feeds good bacteria in the gut.
Different HMOs may play different functions via two pathways to the brain.
Each HMO may play a role in blocking pathogen adhesion.5,8-24,‡
* Nonfucosylated; containing N-acetylglucosamine. Plaza-Díaz J, et al. Nutrients. 2018;10(8):1038.
† Most abundant in most mothers’ milk.
‡ In cellular culture.
References: 1. Goehring KC, et al. PLoS One. 2014;9(7):e101692. 2. Ruhaak LR, et al. Anal Bioanal Chem. 2014;406(24):5775-5784. 3. Bode L. Nutr Rev. 2009;67(suppl 2):S183-S191. 4. Bode L, et al. Adv Nutr. 2012;3(3):383S-391S. 5. Walsh C, et al. J Funct Foods. 2020;72:104074. 6. Bode L. Glycobiology. 2012;22(9):1147-1162. 7. Bode L. Nestle Nutr Inst Workshop Ser. 2020;94:115–123. 8. Ruiz-Palacios GM, et al. J Biol Chem. 2003;278(16):14112–14120. 9. Weichert S, et al. Nutr Res. 2013;33(10):831–838. 10. Yu Z-T, et al. J Nutr. 2016;146(10):1980–1990. 11. El-Hawiet A, et al. Glycobiology. 2015;25(8):845–854. 12. Facinelli B, et al. J Matern Fetal Neonatal Med. 2019;32(17):2950–2952. 13. Weichert S, et al. J Virol. 2016;90(9):4843–4848. 14. Koromyslova A, et al. Virology. 2017;508:81–89. 15. Duska-McEwen G, et al. Food Nutr Sci. 2014;5:1387–1398. 16. Laucirica DR, et al. J Nutr. 2017;147(9):1709–1714. 17. Jantscher-Krenn E, et al. Br J Nutr. 2012;108(10): 1839–1846. 18. Lin AE, et al. J Biol Chem. 2017;292(27):11243–11249. 19. Angeloni S, et al. Glycobiology. 2005;15(1):31–41. 20. Simon PM, et al. Infect Immun. 1997;65(2):750–757. 21. Mysore JV, et al. Gastroenterology. 1999;117(6):1316–1325. 22. Kim J, et al. Infect Immun. 2019;87. doi:10.1128/IAI.00694-18. 23. Hester SN, et al. Br J Nutr. 2013;110(7):1233–1242. 24. Idota T, et al. Biosci Biotechnol Biochem. 1995;59(3):417–419. 25. Oberholzer A, et al. Crit Care Med. 2000;28(suppl 4):N3-N12. 26. Donovan SM, et al. Ann Nutr Metab. 2016;69(suppl 2):41-51. 27. Oliveros E, et al. Nutrients. 2018;10(10):1519. 28. Jacobi SK, et al. J Nutr. 2016;146(2):200–208. 29. Lis-Kuberka J, et al. Nutrients. 2019;11(2):306. 30. Mudd AT, et al. Nutrients. 2017;9(12):1297. 31. Tarr AJ, et al. Brain Behav Immun. 2015;50:166–177. 32. Vázquez E, et al. PLoS One. 2016;11(11):e0166070. 33. Vázquez E, et al. J Nutr Biochem. 2015;26(5):455–465. 34. Wang B, et al. Am J Clin Nutr. 2007;85(2):561–569. 35. Wang B. Annu Rev Nutr. 2009;29:177–222. 36. Wang B. Adv Nutr. 2012;3(3):465S–472S. doi: 10.3945/an.112.001875. 37. Krug M, et al. Brain Res. 1994;643(1-2):130–135. 38. Matthies H, et al. Brain Res. 1994;725(2):276–280. 39. Al-Khafaji AH, et al. J Funct Foods. 2020;74. doi:10.1016/j.jff.2020.104176. 40. Oliveros E, et al. J Nutr Food Sci. 2021;4(1):024. 41. Berger PK, et al. PLoS One. 2020;15(2):e0228323.
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