Human milk oligosaccharides

Human milk oligosaccharides (HMO) are with concentrations between 1 ‑ 15 g/l the third largest fraction of components in human milk (Donovan and Comstock. 2016). They comprise approx. 200 individual oligosaccharide isoforms. The high concentration coupled with structural diversity are characteristic for human milk. Lactose, the most abundant and dietary carbohydrate in human milk is also an integral component of HMO. In contrast to lactose, HMO are indigestible and do not contribute to energy intake. They reach the colon intact, exert their effects often via gut microbiota and are absorbed in low concentrations, only (Bode. 2012).

  1. Evidence indicates that HMO play a remarkable role in the observed short- and long-term benefits of breastfeeding, especially its immune protection and support of cognitive development. HMO are promoting growth of specific bacteria (Bode. 2012); and individual HMO isoforms are prebiotic candidates that possibly affect health (Gibson et al. 2017⁠; Sakanaka et al. 2019).
  2. HMO bind intestinal pathogens reducing susceptibility for infections (Triantis et al. 2018);
  3. By shaping gut microbiota, HMO modulate the systemic and mucosal immune system indirectly, for example by reducing use of medication (Puccio et al. 2017), reducing mortality (Kuhn et al. 2015) or reducing risk of respiratory and enteric diseases (Stepans et al. 2006⁠; Triantis et al. 2018).
  4. Certain HMO isoforms may be potential substrates for neurological cells (Wang. 2009) and suspected to influence cognitive development in infancy favourably (Berger et al. 2020).

Although laboratory research on the isolated HMO fraction from mother's milk has been ongoing for many decades, technological advances from the last decade are now allowing production of individual HMO isoforms on industrial scale. To date, the European Union allows four HMO to be added to infant food: 2'‑fucosyllactose (2'FL), lacto-N-neo-tetraose (LNnT), difucosyllactose (DiFL), and lacto‑N‑tetraose (LNT) (EU/2016/375⁠; EU/2016/376⁠; EU/2019/1979⁠; EU/2020/484). Whether these isolated components are capable of mimicking the diverse HMO fraction present in breast milk remains to be determined. Nevertheless, HMO either as natural fraction or industrially generated isolated isoforms hold the potential to play a key role for healthy infant development (Bode. 2012).

  • Human milk oligosaccharide terminology

    The literature on human milk oligosaccharides is diverse and stretches over many decades. Certain terms are used synonymously. We summarised these terms here:

    • The oligosaccharide fraction of human milk
    • consists of 200+ HMO species or isoforms or molecules or types.
    • Together, these form a HMO profile (e.g. HPLC analysis) or cluster or conglomerate.
    • The cluster/profile/conglomerate can be split into three HMO categories
    • in which HMO with a specific structure are sorted or grouped by their residues.
    • These structures are all built from the same three to five residues or molecules or monomers or building blocks that are monosaccharides and
    • differ in the combination of building blocks and glycosidic bond i.e. connection type.
  • Structural diversity – Human milk oligosaccharide building blocks

    All human milk oligosaccharides (HMO) can be described with an equation such as this:

    To break down this complicated seeming equation, we start with the three to five monosaccharides or monomers that are the building blocks of HMO (Figure 412-3). Depending on the way these five building blocks are combined together with a number of different structural ways to connect, they form more than 200 HMO isoforms (Thurl et al. 2010).


    The disaccharide lactose is a combination of D‑glucose (Glu, blue circle Figures 412-3 and 412-4) with D-galactose (Gal, yellow circle, Figures 412-3 and 412-4) connected via a β1-4 bond (Figure 412-5). As free disaccharide or dimer, lactose is the major carbohydrate in mother's milk and thus called milk sugar. Lactose is a core component of all HMO isoforms: It is located at the terminal end of all HMO and further modified by the addition of galactose, N‑acetyllactosamine, fucose, or sialic acid, elongated and branched in various ways to form the multitude of known HMO isoforms (Figure 412-4) (Bode. 2012⁠, 2006).

    The type of connection – that is the glycosidic bond – plays a crucial role in HMO formation. It can define the 3D structure, thus determine interaction of the HMO to microorganisms (decoy receptor) or access of enzymes and other metabolites, and therefore affect functionality of the HMO isoform that was synthesised.

    As example Figure 412-6 shows the two HMO building blocks lacto‑N-biose and N-acetyllactosamine. Both are dimers from two of the five monomers: D-galactose and N‑acetylglucosamine (yellow circle, blue square; Figures 412-3 and 412-4). The only difference lies in the β1‑3 bond to form lacto‑N‑biose (Gal β1‑3 N‑acetlyglucosamine, Figure 412-6) compared with the β1‑4 bond that forms N‑acetyllactosamine (Gal β1‑4 N‑acetlyglucosamine, Figure 412-6). Fucose (red triangle, Figure 412-4) and sialic acid (purple diamond, Figure 412-4) can be added in α1‑2, α1‑3, α1‑4 and α2‑3, and α2‑6 bonds, to the lactose molecules, lactose-N‑biose or N‑acetyllactosamine, respectively (Bode. 2006).

  • Structural diversity – Human milk oligosaccharides can be categorised by their residues

    Human milk oligosaccharides structures are described by a basic blueprint (Figure 412-3): Lactose is a core component linked with at least one further residue or unit. Based on the presence of these residues, HMO can be sorted into three different categories:

    1. Fucosylated HMO (Figure 412-7) are linked with at least one L-fucose residue.
    2. Sialylated or acidic HMO (Figure 412-8) are oligosaccharides linked with at least one sialic acid residue.
    3. Non-fucosylated or neutral HMO (Figure 412-9) are linked with at least one galactose, N‑acetyllactosamine, or lacto‑N‑biose unit. They are neither linked with fucose nor sialic acid (Ayechu-Muruzabal et al. 2018⁠; Kunz et al. 2000).

    Non-fucosylated neutral human milk oligosaccharides are the most diverse and extensive category representing between 42 ‑ 55% of the entire human milk oligosaccharide fraction, followed by fucosylated human milk oligosaccharides with 35 ‑ 50%. Sialylated, acidic human milk oligosaccharides are the least extensive category, representing approx. 13% of total human milk oligosaccharides (Donovan and Comstock. 2016).

  • Human milk oligosaccharides may be prebiotics

    Since 2017, prebiotics are defined by the The International Scientific Association for Probiotics and Prebiotics (ISAPP) as “a substrate that is selectively utilized by host microorganisms conferring a health benefit.” This statement keeps a microbiota-mediated health benefit, but does not restrict a prebiotic component to be a food or carbohydrate nor are the effects limited to the gastro-intestinal tract (Gibson et al. 2017). This definition still requires that a prebiotic substance (1) reaches the microorganisms intact, (2) that selected, not all, microorganisms use the prebiotic candidate as substrate, and (3) that the beneficial effect to the host is mediated via actions of these microorganisms (La Fata et al. 2017).

    HMO meet the first and second set of requirements, whereas the third set is actively under investigation. HMO are resistant to digestive enzymes which makes them predominantly indigestible fibres and are unaffected by intestinal pH (Engfer et al. 2000⁠; Gnoth et al. 2000); only 1-2% of HMO are absorbed. Consequently, many HMO are reaching the colon intact (Obermeier et al. 1999) where individual isoforms are candidate prebiotics by serving as nutrient source for specific colonic microbiota species (Gibson et al. 2017).

    The HMO fraction as total has been associated with the establishment of a favourable intestinal microbiome (Kunz. 2012). When comparing the gut microbiome of breastfed and non-breastfed infants, different bacterial composition was identified (Harmsen et al. 2000). The predominance of Bifidobacteria species in breastfed infants was attributed to HMO presence (Kunz. 2012). When adding the two industrially generated HMO isoforms 2'‑fucosyllactose and lacto-N-neo-tetraose as mixture to infant formula, a shift of the stool microbiota composition was detected towards a similar composition to that of breastfed infants (Steenhout et al. 2016). Similarly, in vitro studies on cell lines are supporting a HMO-mediated growth advantage for beneficial over pathogenic bacteria (Sela and Mills. 2010). Individual HMO types, including 2'‑fucosyllactose, 3‑fucosyllactose, lacto‑difucotetraose, 3'‑sialyllactose, and 6'‑sialyllactose, promote the growth of Bifidobacteria strains (B. infantis, B. bifidus, B. breve, B. longum), Bacteroides genera, and specific Lactobacillus species (Lactobacillus delbrueckii) (Lewis et al. 2015⁠; Yu et al. 2012). This may be due to the specialised ability of B. breve, B. infantis, and most B. longum species of using fucosylated HMO as growth substrate that these pathogens lack (Sakanaka et al. 2019). In contrast, the same HMO isoforms cannot be used as growth substrate by many pathogens, including Escherichia coli, Clostridium perfringens, Streptococcus agaltictiae, Enterobacter, Acinetobacter baumannii (Ackerman et al. 2018⁠; Underwood et al. 2015⁠; Yu et al. 2013) or Streptococcus aureus, the latter being one of the most frequent causes for bacterial infections in infants (Lin et al. 2017).

    Besides directly affecting microbiota growth by serving as substrate of particular species, HMO are indirectly promoting bacterial growth via cross-feeding (Smith et al. 2019). When bacterial strains ferment HMO and other prebiotic substrates in the intestinal lumen the left-overs and bacterial metabolites serve other bacterial strains as growth substrate (Sela and Mills. 2010). This supports the development of a healthy and diverse microbiota ecosystem.

    Demonstrating the third set of requirements for a prebiotic classification of HMO – that is the demonstration of health benefits mediated via colonic microorganisms – has been difficult. This is because – until about 2000 – HMO could only be extracted from mother's milk and tested small-scale in laboratory settings. Since then, technological advancements have been making individual HMO isoforms available for large scale clinical studies or commercial productions (Bode et al. 2016) and data from clinical safety and/or efficacy studies have been slowly accumulating (Reverri et al. 2018).

    Health benefits associated with HMO include

    • anti-inflammatory properties: Pro-inflammatory cytokine concentrations in circulation were lower for infants fed formula with 2'-fucosyllactose in comparison to infants fed formula without (Goehring et al. 2016),
    • bifidogenicity,
    • decreased intestinal pH: Many beneficial bacteria strains are associated with short-chain fatty acid (SCFA) production (Yu et al. 2013). SCFA reduce intestinal pH, which is a mechanism of prebiotics that inhibits pathogen infection by creating unfavourable growth conditions (Ríos-Covián et al. 2016),
    • pathogen deflection and decoy effect.

    More information around prebiotics is available here.

  • Human milk oligosaccharides deflect pathogens

    Breastfed infants may receive a clinically relevant infection protection that is mediated by human milk oligosaccharides. High HMO concentrations are associated with a reduced risk of diarrhoea (Morrow et al. 2004⁠; Stepans et al. 2006), an effect that seems to be particularly related to fucosylated HMO (Newburg et al. 2004). In addition, the risk for respiratory and bronchial infections seems to be reduced and may be related to 2'‑fucosyllactose and lacto‑N‑neo‑tetraose (Puccio et al. 2017⁠; Stepans et al. 2006).

    HMO are capable of binding to pathogens as decoy receptors and thereby blocking the attachment of pathogens to glycans in the intestine (Bode. 2012⁠; Triantis et al. 2018). Interactions between glycan structures and carbohydrate-binding proteins are a common metabolic process. They mediate selective substance uptake and cellular signal recognition (Taylor and Drickamer. 2014). Pathogens make use of this process because various cells in the intestine and respiratory tract have glycan structures on their surface. These represent binding targets to microbial pathogens. HMO show structural similarities to these surface glycans and some isoforms use the same mechanism of inhibiting pathogen infection: HMO either bind to the pathogen itself or they bind competitively to the cell surface, thereby blocking the interaction sites of pathogens or the receptor docking sites, respectively (Plaza-Diaz et al. 2013⁠; Triantis et al. 2018). This way, human milk oligosaccharides protect mechanically from infection.

    Representatives of each HMO category bind specifically to bacteria or viruses and bacterial toxins. Sialylated HMO (Figure 412-8) prevent adhesion of E. coli (Angeloni et al. 2005⁠; Facinelli et al. 2019) and fucosylated HMO (Figure 412-7) bind to various pathogens, including Campylobacter jejuni (Ruiz-Palacios et al. 2003⁠; Weichert et al. 2013), Helicobacter pylori (Xu et al. 2004), Salmonella enterica, Pseudomonas aeruginosa and enteropathogenic E. coli (EPEC) (Weichert et al. 2013). In addition, fucosylated HMO prevent adhesion of (intestinal) viruses such as Norwalk or Noroviruses by blocking their docking sites (decoy receptor) (Koromyslova et al. 2017⁠; Laucirica et al. 2017⁠; Shang et al. 2013). The efficacy of pathogen inhibition is structurally dependent; e.g. 2'-fucosyllactose has greater inhibition capacity on Campylobacter jejuni than 3'‑fucosyllactose (Weichert et al. 2013).

    HMO not only bind pathogens but also their toxins: Fucosylated HMO bind heat-stable enterotoxin of E. coli in vitro (Newburg et al., 1990) and may mitigate the activity of different bacterial exotoxins such as toxin A and B of Clostridium difficile, Shiga toxin type 1, and type 2 holotoxin (El-Hawiet et al. 2015⁠; Nguyen et al. 2016).

    Many of the protective effects of breast milk may be related to HMO presence, concentrations, and composition of the HMO fraction. However, a direct effect of specific HMO isoforms or the HMO cluster with reduced disease incidence has not been demonstrated yet. Since breast milk is rich in bioactive compounds – many of which are involved in immune protection – not all preventive effects can be dedicated to the HMO cluster or individual isoforms (Ballard and Morrow. 2013). Clinical data are needed to clearly identify the extent and mechanisms behind preventative effects hypothesised for HMO. Nevertheless, HMO deflect various pathogens and are thereby promising prebiotic candidates contributing significantly to microbiota-mediated health benefits (Triantis et al. 2018).

  • Human milk oligosaccharide composition is genetically regulated

    Human milk can be sorted into four groups dependent on gene activation – that is on the Lewis positive/negative (Le gene) and secretor/non‑secretor (Se gene) status. These milk groups differ mostly in fucosylated HMO (Kumazaki and Yoshida. 1984⁠; Thurl et al. 1997). Sialylated and neutral non-fucosylated HMO (Figures 412-7 and 412-8) are abundant with relatively stable concentrations in all groups (Kunz et al. 2017⁠; Thurl et al. 2017).

    Enzymes define the HMO isoforms. Theoretically a great number of structures are possible. About 200 isoforms are present in human milk because the enzymes for their construction limit the possibilities of what building blocks are added where within the molecule (Figures 412-3, 412-4, and 412-5) (Kobata. 2010⁠; Zivkovic et al. 2010). Generally, 13 core structures are found in human milk (Urashima et al. 2012).

    Fucosylated HMO are generated by two different enzymes (Figure 412‑7): Fucosyltransferase‑2 encoded by the secretor (Se) gene (Kumazaki and Yoshida. 1984) and fucosyltransferase‑3 encoded by the Lewis blood group (Le) gene (Xu et al. 1996). Both genes are known to control blood group antigens (Dotz and Wuhrer. 2016⁠; Shen et al. 1968).

    Dependent on the genetic phenotype, the Le and Se genes can either be active or inactive (Kumazaki and Yoshida. 1984⁠; Shen et al. 1968). Individuals with active Se gene are “secretors” or "Se+" (Kumazaki and Yoshida. 1984) and individuals with active Le gene are “Le‑positive” or "Le+" (Xu et al. 1996).

    Le-positive secretors (Le+/Se+) express high oligosaccharide concentrations and all fucosylated human milk oligosaccharide isoforms from both fucosyltransferase‑2 and ‑3. Le-negative secretors (Le-/Se+) express similar oligosaccharide concentrations but are lacking the human milk oligosaccharides from fucosyltransferase‑3 such as lacto-N-fucopentaose‑II and ‑III. Presence of the HMO isoform 3'-fucosyllactose in this milk group is under debate because recent reports state its absence (Kunz et al. 2017) but older reports stated presence of 3'‑fucosyllactose (Ayechu-Muruzabal et al. 2018⁠; Thurl et al. 2010⁠; Thurl et al. 1997). If fucosyltransferase‑3 is responsible to generate 3'‑fucosyllactose it would be logical to expect its absence from this group.

    Le-positive non-secretors (Le+/Se-) express lower total oligosaccharide concentrations compared to the other groups. Because fucosyltransferase‑2 is absent, this group lacks the 2'-fucosyllactose, the most abundant human milk oligosaccharide isoform in the majority of milk samples (Kunz et al. 2017). Less than 1% of women are Le-negative non‑secretors (Le-/Se-) and compositional data of their milks are scarce. Total HMO concentrations have not been reported to date but are estimated to be comparable to Le-positive non-secretors (Thurl et al. 1997). Fucosylated human milk oligosaccharides are barely traceable and sialylated HMO take higher precedence in the total oligosaccharide fraction compared to the other milk groups.

    Although both enzymes are absent in Le-negative non‑secretors, traces of fucosylated HMO are detectable in these milk samples. This observation indicates that Le and Se-independent fucosyltransferases with very low efficacy exist (Erney et al. 2000⁠; Thurl et al. 1997). Their biological relevance remains to be determined.

  • Why are human milk oligosaccharides a hot topic in infant nutrition?

    Publications on HMO have almost quadrupled since 2010 (National Library of Medicine This is because novel processing techniques allow production of certain HMO isoforms on industrial scale (Faijes et al. 2019⁠; Sprenger et al. 2017). Until the turn of this millennium, human milk oligosaccharides could only be extracted from mother's milk, their function tested small scale and limited to laboratory settings (Bode et al. 2016⁠; Furuike et al. 2003). Cow's or goat's milk are poor sources for milk oligosaccharides because concentrations are low and lack the diversity of those in human milk (Zeuner et al. 2019).

    These generated molecules are structurally identical to those isolated from mother's milk. Four of these – 2'‑fucosyllactose (2'‑FL) – lacto‑N‑neotetraose (LNnT) – the mixture of 2'‑fucosyllactose with difucosyllactose (DiFL) – and as of April 2020, lacto‑N‑tetraose (LNT) arepermitted on the European market and in food for infants (EU/2016/375⁠; EU/2016/376⁠; EU/2019/1979⁠; EU/2020/484).

    As part of the novel food application process in Europe, a safety evaluation is made by the European Food Safety Agency (EFSA) on behalf of the European Commission. Novel food applications are currently ongoing for 3'‑ and 6'-sialyllactose (3'‑SL and 6'‑SL, respectively) []. As a consequence, communication on these components in foods is increasing in parallel to the novel scientific insights on their function and potential health benefits generated at high pace.

    More information around prebiotics is available here.

  • The most abundant human milk oligosaccharides that have been identified from milk samples around the world

    Table 412- 1 The table represents the most abundant human milk oligosaccharides that have been identified from milk samples around the world. Presence and concentrations of these respective HMO isoforms in an individual sample are affected by ethnicity yet additionally by individual genetic traits and lactation stage but little by maternal intake (Urashima et al. 2012). Structures, symbols and coloration of the respective HMO isoform are shown according to guidelines for glycans (Neelamegham et al. 2019); the images were drawn with the DrawGlycan tool at (Cheng et al. 2017) defining Gal, galactose as yellow circle, Glc, glucose as blue circle, Fuc, L-fucose as red triangle, Neu5Ac, sialic acid as purple diamond, GlcNAc, N-acetyllactosamine as blue square. The chemical terminology as per International Union of Pure and Applied Chemistry (IUPAC, explains the structures and bonds between monomers. Glycosidic bonds are represented by α and β terminology. The lactose dimer in each HMO is emphasised in bold. Monomers in brackets are bound to the monomer following after the bracket.

  • Maximum concentrations of isolated human milk oligosaccharides allowed as per European Commission

    Table 412- 2 Maximum concentrations of isolated human milk oligosaccharides allowed as per European Commission.


    Products for infants younger than 12 months

    Baby food for infants and young children




    Follow-on formula

    Processed cereal-based food

    Milk-based drinks or similar

    Safety evaluation by EFSA

    Age range1

    0-6 months

    6-12 months

    6 - ≤ 36 months


    HMO isoform and EU legislation implementing the respective HMO as novel food in Europe






    (EU/2016/375⁠; EU/2017/2470⁠; EU/2019/1979)

    1.2 g/l alone

    or in combination with lacto-N-neotetraose;

    1.6 g/l as specific mix with difucosyllactose

    1.2 g/l alone or in combination with lacto-N-neotetraose;

    1.2 g/l as specific mix with difucosyllactose

    12 g/kg for products other than beverages alone or 10 g/kg as specific mix with difucosyllactose;

    1.2 g/l for liquid food ready to use alone or as specific mix with difucosyllactose

    1.2 g/l alone, in a specific mix with difucosyllactose or at a 2:1 ratio with lacto-N-neotetraose

    (EFSA NDA. 2015a)


    (EU/2016/375⁠; EU/2017/2470)



    6 g/kg for products other than beverages; 0.6 g/l for liquid food ready to use;

    0.6 g/l

    (EFSA NDA. 2015b⁠, 2015c)

    Mix lacto‑N‑neotetraose + 2'‑fucosyllactose

    (EU/2016/375⁠; EU/2017/2470)

    0.6 g/l in combination with 1.2 g/l of 2'‑fucosyllactose at a ratio of 1:2

    0.6 g/l in combination with 1.2 g/l of 2'‑fucosyllactose at a ratio of 1:2

    6 g/kg for products other than beverages;

    0.6 g/l for liquid foods

    0.6 g/l in combination with 2'FL at a ratio of 1:2 in the final product

    (EFSA NDA. 2015b)








    Mix difucosyllactose + 2'‑fucosyllactose2


    1.6 g/l of the mixture

    1.2 g/l of the mixture

    1.2 g/l (beverages)

    10 g/kg for products other than beverages

    1.2 g/l (beverages)

    10 g/kg for products other than beverages

    (EFSA NDA. 2019a)



    0.8 g/l

    0.6 g/l

    0.6 g/l (beverages)

    5 g/kg for products other than beverages

    0.6 g/l (beverages)

    5 g/kg for products other than beverages

    (EFSA NDA et al. 2019b)



    0.2 g/l

    0.15 g/l

    0.15 g/l in a ready to feed product ;

    1.25 g/kg for products other than beverages

    0.15 g/l in a ready to feed product;

    1.25 g/kg for products other than beverages

    (EFSA NDA. 2020a)



    0.4 g/l

    0.3 g/l

    0.3 g/l in a ready to feed product;

    2.5 g/kg for products other than beverages

    0.3 g/l in a ready to feed product;

    2.5 g/kg for products other than beverages

    (EFSA NDA. 2020b)








    1Age range and product descriptions as per Regulation EU/2013/609 .

    2Mix contains ≥ 75% 2'‑FL and ≥ 5% DiFL (w/w in % of dry matter) EU/2019/1979

    3Novel food applications for 3'‑SL and 6'‑SL have been submitted to the European Commission beginning 2019 []

    4Values proposed by EFSA

    The maxima are given for products ready to feed or according to preparation instructions of the manufacturer (EC/2006/125⁠; EU/2016/375). Products should bear a statement that "these products should not be used if breast milk or other foods containing [the added HMO isoform or mixture] are consumed at the same day" (EU/2019/1979⁠; EU/2020/484). Concentrations for Foods for Special Medical Purposes (FSMP) are dependent on the nutrient requirements of the patient population that needs the particular product.

  • References

    Ackerman, D L, Craft, K M, Doster, R S, Weitkamp, J-H, Aronoff, D M, Gaddy, J A, Townsend, S D. Antimicrobial and Antibiofilm Activity of Human Milk Oligosaccharides against Streptococcus agalactiae, Staphylococcus aureus, and Acinetobacter baumannii 2018. ACS infectious diseases 4 (3), 315–324. doi 10.1021/acsinfecdis.7b00183. 

    Angeloni, S, Ridet, J L, Kusy, N, Gao, H, Crevoisier, F, Guinchard, S, Kochhar, S, Sigrist, H, Sprenger, N. Glycoprofiling with micro-arrays of glycoconjugates and lectins 2005. Glycobiology 15 (1), 31–41. doi 10.1093/glycob/cwh143. 

    Ayechu-Muruzabal, V, van Stigt, A H, Mank, M, Willemsen, L E M, Stahl, B, Garssen, J, Van't Land, B. Diversity of Human Milk Oligosaccharides and Effects on Early Life Immune Development 2018. Frontiers in pediatrics 6, 239. doi 10.3389/fped.2018.00239. 

    Ballard, O and Morrow, A L. Human milk composition: nutrients and bioactive factors 2013. Pediatric clinics of North America 60 (1), 49–74. doi 10.1016/j.pcl.2012.10.002. 

    Berger, P K, Plows, J F, Jones, R B, Alderete, T L, Yonemitsu, C, Poulsen, M, Ryoo, J H, Peterson, B S, Bode, L, Goran, M I. Human milk oligosaccharide 2'-fucosyllactose links feedings at 1 month to cognitive development at 24 months in infants of normal and overweight mothers 2020. PloS one 15 (2), e0228323. doi 10.1371/journal.pone.0228323. 

    Bode, L. Recent advances on structure, metabolism, and function of human milk oligosaccharides 2006. The Journal of nutrition 136 (8), 2127–2130. doi 10.1093/jn/136.8.2127. 

    Bode, L. Human milk oligosaccharides: every baby needs a sugar mama 2012. Glycobiology 22 (9), 1147–1162. doi 10.1093/glycob/cws074. 

    Bode, L, Contractor, N, Barile, D, Pohl, N, Prudden, A R, Boons, G-J, Jin, Y-S, Jennewein, S. Overcoming the limited availability of human milk oligosaccharides: challenges and opportunities for research and application 2016. Nutrition reviews 74 (10), 635–644. doi 10.1093/nutrit/nuw025. 

    Cheng, K, Zhou, Y, Neelamegham, S. DrawGlycan-SNFG: a robust tool to render glycans and glycopeptides with fragmentation information 2017. Glycobiology 27 (3), 200–205. doi 10.1093/glycob/cww115. 

    Donovan, S M and Comstock, S S. Human Milk Oligosaccharides Influence Neonatal Mucosal and Systemic Immunity 2016. Annals of nutrition & metabolism 69 Suppl 2, 42–51. doi 10.1159/000452818. 

    Dotz, V and Wuhrer, M. Histo-blood group glycans in the context of personalized medicine 2016. Biochimica et biophysica acta 1860 (8), 1596–1607. doi 10.1016/j.bbagen.2015.12.026. 

    EC/2006/125. Commission Directive 2006/125/EC of 5 December 2006 on processed cereal-based foods and baby foods for infants and young children (Codified version) (Text with EEA relevance): EUR-Lex - 32006L0125 - EN - EUR-Lex 2006. 

    EFSA NDA. Safety of 2′‐O‐fucosyllactose as a novel food ingredient pursuant to Regulation (EC) No 258/97 2015a. EFSA Journal 13 (7), 1313. doi 10.2903/j.efsa.2015.4184. 

    EFSA NDA. Safety of lacto‐N‐neotetraose and 2′‐O‐fucosyllactose as novel food ingredients in food supplements for children 2015b. EFSA Journal 13 (11), 4299, 32. doi 10.2903/j.efsa.2015.4299.

    EFSA NDA. Safety of lacto‐N‐neotetraose as a novel food ingredient pursuant to Regulation (EC) No 258/97 2015c. EFSA Journal 13 (7), 4183. doi 10.2903/j.efsa.2015.4183. 

    EFSA NDA. Safety of 2’‐fucosyllactose/difucosyllactose mixture as a novel food pursuant to Regulation (EU) 2015/2283: EFSA-Q-2018-00374 2019a. EFSA Journal 17 (6), 5717. doi 10.2903/j.efsa.2019.5717. 

    EFSA NDA. Safety of 3’‐Sialyllactose (3’‐SL) sodium salt as a novel food pursuant to Regulation (EU) 2015/2283 2020a. EFSA Journal 18 (5), 6098, 1–22. doi 10.2903/j.efsa.2020.6098. 

    EFSA NDA. Safety of 6′‐Sialyllactose (6′‐SL) sodium salt as a novel food pursuant to Regulation (EU) 2015/2283 2020b. EFSA Journal 18 (5), 6097. doi 10.2903/j.efsa.2020.6097. 

    EFSA NDA, Turck, D, Castenmiller, J, Henauw, S de, Hirsch‐Ernst, K I, Kearney, J, Maciuk, A, Mangelsdorf, I, McArdle, H J, Naska, A, Pelaez, C, Pentieva, K, Siani, A, Thies, F, Tsabouri, S, Vinceti, M, Cubadda, F, Engel, K‐H, Frenzel, T, Heinonen, M, Marchelli, R, Neuhäuser‐Berthold, M, Poulsen, M, Sanz, Y, Schlatter, J R, van Loveren, H, Colombo, P, Knutsen, H K. Safety of lacto‐N‐tetraose (LNT) as a novel food pursuant to Regulation (EU) 2015/2283 2019b. EFSA Journal 17 (12), 5907. doi 10.2903/j.efsa.2019.5907. 

    El-Hawiet, A, Kitova, E N, Klassen, J S. Recognition of human milk oligosaccharides by bacterial exotoxins 2015. Glycobiology 25 (8), 845–854. doi 10.1093/glycob/cwv025. 

    Engfer, M B, Stahl, B, Finke, B, Sawatzki, G, Daniel, H. Human milk oligosaccharides are resistant to enzymatic hydrolysis in the upper gastrointestinal tract 2000. The American journal of clinical nutrition 71 (6), 1589–1596. doi 10.1093/ajcn/71.6.1589. 

    Erney, R M, Malone, W T, Skelding, M B, Marcon, A A, Kleman-Leyer, K M, O'Ryan, M L, Ruiz-Palacios, G, Hilty, M D, Pickering, L K, Prieto, P A. Variability of human milk neutral oligosaccharides in a diverse population 2000. Journal of pediatric gastroenterology and nutrition 30 (2), 181–192. doi 10.1097/00005176-200002000-00016. 

    EU/2013/609. Regulation (EU) No 609/2013 of the European Parliament and of the Council of 12 June 2013 on food intended for infants and young children, food for special medical purposes, and total diet replacement for weight control and repealing Council Directive 92/52/EEC, Commission Directives 96/8/EC, 1999/21/EC, 2006/125/EC and 2006/141/EC, Directive 2009/39/EC of the European Parliament and of the Council and Commission Regulations (EC) No 41/2009 and (EC) No 953/2009: EUR-Lex - 32013R0609 - EN - EUR-Lex. 

    EU/2016/375. Commission Implementing Decision (EU) 2016/375 of 11 March 2016 authorising the placing on the market of lacto-N-neotetraose as a novel food ingredient under Regulation (EC) No 258/97 of the European Parliament and of the Council (notified under document C(2016) 1419): EU CELEX_32016D0375. 

    EU/2016/376. Commission Implementing Decision (EU) 2016/376 of 11 March 2016 authorising the placing on the market of 2′-O-fucosyllactose as a novel food ingredient under Regulation (EC) No 258/97 of the European Parliament and of the Council (notified under document C(2016) 1423): CELEX_32016D0376. 

    EU/2017/2470. Commission Implementing Regulation (EU) 2017/2470 of 20 December 2017 establishing the Union list of novel foods in accordance with Regulation (EU) 2015/2283 of the European Parliament and of the Council on novel foods: EUR-Lex - 32017R2470 - EN - EUR-Lex. 

    EU/2019/1979. Commission implementing Regulation (EU) 2019/1979 of 26 November 2019 authorising the placing on the market of 2'-Fucosyllactose/Difucosyllactose mixture as a novel food under Regulation (EU) 2015/2283 of the European Parliament and of the Council and amending Commission Implementing Regulation (EU) 2017/2470 (Text with EEA relevance): CELEX_32019R1979.  

    EU/2020/484. Commission Implementing Regulation (EU) 2020/484 of 2 April 2020 authorising the placing on the market of lacto-N-tetraose as a novel food under Regulation (EU) 2015/2283 of the European Parliament and of the Council and amending Commission Implementing Regulation (EU) 2017/2470 (Text with EEA relevance): EUR-Lex - 32020R0484 - EN - EUR-Lex. 

    Facinelli, B, Marini, E, Magi, G, Zampini, L, Santoro, L, Catassi, C, Monachesi, C, Gabrielli, O, Coppa, G V. Breast milk oligosaccharides: effects of 2'-fucosyllactose and 6'-sialyllactose on the adhesion of Escherichia coli and Salmonella fyris to Caco-2 cells 2019. The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians 32 (17), 2950–2952. doi 10.1080/14767058.2018.1450864. 

    Faijes, M, Castejón-Vilatersana, M, Val-Cid, C, Planas, A. Enzymatic and cell factory approaches to the production of human milk oligosaccharides 2019. Biotechnology advances 37 (5), 667–697. doi 10.1016/j.biotechadv.2019.03.014. 

    Furuike, T, Yamada, K, Ohta, T, Monde, K, Nishimura, S-I. An efficient synthesis of a biantennary sialooligosaccharide analog using a 1,6-anhydro-β-lactose derivative as a key synthetic block 2003. Tetrahedron 59 (27), 5105–5113. doi 10.1016/S0040-4020(03)00711-7. 

    Gibson, G R, Hutkins, R, Sanders, M E, Prescott, S L, Reimer, R A, Salminen, S J, Scott, K, Stanton, C, Swanson, K S, Cani, P D, Verbeke, K, Reid, G. Expert consensus document: The International Scientific Association for Probiotics and Prebiotics (ISAPP) consensus statement on the definition and scope of prebiotics 2017. Nature reviews. Gastroenterology & hepatology 14 (8), 491–502. doi 10.1038/nrgastro.2017.75. 

    Gnoth, M J, Kunz, C, Kinne-Saffran, E, Rudloff, S. Human milk oligosaccharides are minimally digested in vitro 2000. The Journal of nutrition 130 (12), 3014–3020. doi 10.1093/jn/130.12.3014. 

    Goehring, K C, Marriage, B J, Oliver, J S, Wilder, J A, Barrett, E G, Buck, R H. Similar to Those Who Are Breastfed, Infants Fed a Formula Containing 2'-Fucosyllactose Have Lower Inflammatory Cytokines in a Randomized Controlled Trial 2016. The Journal of nutrition 146 (12), 2559–2566. doi 10.3945/jn.116.236919. 

    Harmsen, H J, Wildeboer-Veloo, A C, Raangs, G C, Wagendorp, A A, Klijn, N, Bindels, J G, Welling, G W. Analysis of intestinal flora development in breast-fed and formula-fed infants by using molecular identification and detection methods 2000. Journal of pediatric gastroenterology and nutrition 30 (1), 61–67. doi 10.1097/00005176-200001000-00019. 

    Kobata, A. Structures and application of oligosaccharides in human milk 2010. Proceedings of the Japan Academy. Series B, Physical and biological sciences 86 (7), 731–747. doi 10.2183/pjab.86.731. 

    Koromyslova, A, Tripathi, S, Morozov, V, Schroten, H, Hansman, G S. Human norovirus inhibition by a human milk oligosaccharide 2017. Virology 508, 81–89. doi 10.1016/j.virol.2017.04.032. 

    Kuhn, L, Kim, H-Y, Hsiao, L, Nissan, C, Kankasa, C, Mwiya, M, Thea, D M, Aldrovandi, G M, Bode, L. Oligosaccharide composition of breast milk influences survival of uninfected children born to HIV-infected mothers in Lusaka, Zambia 2015. J Nutr 145 (1), 66–72. doi 10.3945/jn.114.199794. 

    Kumazaki, T and Yoshida, A. Biochemical evidence that secretor gene, Se, is a structural gene encoding a specific fucosyltransferase 1984. Proceedings of the National Academy of Sciences of the United States of America 81 (13), 4193–4197. doi 10.1073/pnas.81.13.4193. 

    Kunz, C. Historical aspects of human milk oligosaccharides 2012. Advances in nutrition (Bethesda, Md.) 3 (3), 430S-9S. doi 10.3945/an.111.001776. 

    Kunz, C, Meyer, C, Collado, M C, Geiger, L, García-Mantrana, I, Bertua-Ríos, B, Martínez-Costa, C, Borsch, C, Rudloff, S. Influence of Gestational Age, Secretor, and Lewis Blood Group Status on the Oligosaccharide Content of Human Milk 2017. Journal of pediatric gastroenterology and nutrition 64 (5), 789–798. doi 10.1097/MPG.0000000000001402. 

    Kunz, C, Rudloff, S, Baier, W, Klein, N, Strobel, S. Oligosaccharides in human milk: structural, functional, and metabolic aspects 2000. Annual review of nutrition 20, 699–722. doi 10.1146/annurev.nutr.20.1.699. 

    La Fata, G, Rastall, R A, Lacroix, C, Harmsen, H J M, Mohajeri, M H, Weber, P, Steinert, R E. Recent Development of Prebiotic Research-Statement from an Expert Workshop 2017. Nutrients 9 (12). doi 10.3390/nu9121376. 

    Laucirica, D R, Triantis, V, Schoemaker, R, Estes, M K, Ramani, S. Milk Oligosaccharides Inhibit Human Rotavirus Infectivity in MA104 Cells 2017. The Journal of nutrition 147 (9), 1709–1714. doi 10.3945/jn.116.246090. 

    Lewis, Z T, Totten, S M, Smilowitz, J T, Popovic, M, Parker, E, Lemay, D G, van Tassell, M L, Miller, M J, Jin, Y-S, German, J B, Lebrilla, C B, Mills, D A. Maternal fucosyltransferase 2 status affects the gut bifidobacterial communities of breastfed infants 2015. Microbiome 3. doi 10.1186/s40168-015-0071-z. 

    Lin, A E, Autran, C A, Szyszka, A, Escajadillo, T, Huang, M, Godula, K, Prudden, A R, Boons, G-J, Lewis, A L, Doran, K S, Nizet, V, Bode, L. Human milk oligosaccharides inhibit growth of group B Streptococcus 2017. The Journal of biological chemistry 292 (27), 11243–11249. doi 10.1074/jbc.M117.789974. 

    Morrow, A L, Ruiz-Palacios, G M, Altaye, M, Jiang, X, Guerrero, M L, Meinzen-Derr, J K, Farkas, T, Chaturvedi, P, Pickering, L K, Newburg, D S. Human milk oligosaccharides are associated with protection against diarrhea in breast-fed infants 2004. The Journal of pediatrics 145 (3), 297–303. doi 10.1016/j.jpeds.2004.04.054. 

    Neelamegham, S, Aoki-Kinoshita, K, Bolton, E, Frank, M, Lisacek, F, Lütteke, T, O'Boyle, N, Packer, N H, Stanley, P, Toukach, P, Varki, A, Woods, R J. Updates to the Symbol Nomenclature for Glycans guidelines 2019. Glycobiology 29 (9), 620–624. doi 10.1093/glycob/cwz045. 

    Newburg, D S, Ko, J S, Leone, S, Nanthakumar, N N. Human Milk Oligosaccharides and Synthetic Galactosyloligosaccharides Contain 3'-, 4-, and 6'-Galactosyllactose and Attenuate Inflammation in Human T84, NCM-460, and H4 Cells and Intestinal Tissue Ex Vivo 2016. The Journal of nutrition 146 (2), 358–367. doi 10.3945/jn.115.220749. 

    Newburg, D S, Pickering, L K, McCluer, R H, Cleary, T G. Fucosylated oligosaccharides of human milk protect suckling mice from heat-stabile enterotoxin of Escherichia coli 1990. The Journal of infectious diseases 162 (5), 1075–1080. doi 10.1093/infdis/162.5.1075. 

    Newburg, D S, Ruiz-Palacios, G M, Altaye, M, Chaturvedi, P, Meinzen-Derr, J, Guerrero, M L, Morrow, A L. Innate protection conferred by fucosylated oligosaccharides of human milk against diarrhea in breastfed infants 2004. Glycobiology 14 (3), 253–263. doi 10.1093/glycob/cwh020. 

    Nguyen, T T H, Kim, J W, Park, J-S, Hwang, K H, Jang, T-S, Kim, C-H, Kim, D. Identification of Oligosaccharides in Human Milk Bound onto the Toxin A Carbohydrate Binding Site of Clostridium difficile 2016. Journal of microbiology and biotechnology 26 (4), 659–665. doi 10.4014/jmb.1509.09034. 

    Obermeier, S, Rudloff, S, Pohlentz, G, Lentze, M J, Kunz, C. Secretion of 13C-labelled oligosaccharides into human milk and infant's urine after an oral 13Cgalactose load 1999. Isotopes in environmental and health studies 35 (1-2), 119–125. doi 10.1080/10256019908234084. 

    Plaza-Diaz, J, Gomez-Llorente, C, Campaña-Martin, L, Matencio, E, Ortuño, I, Martínez-Silla, R, Gomez-Gallego, C, Periago, M J, Ros, G, Chenoll, E, Genovés, S, Casinos, B, Silva, A, Corella, D, Portolés, O, Romero, F, Ramón, D, La Perez de Cruz, A, Gil, A, Fontana, L. Safety and immunomodulatory effects of three probiotic strains isolated from the feces of breast-fed infants in healthy adults: SETOPROB study 2013. PloS one 8 (10), e78111. doi 10.1371/journal.pone.0078111. 

    Puccio, G, Alliet, P, Cajozzo, C, Janssens, E, Corsello, G, Sprenger, N, Wernimont, S, Egli, D, Gosoniu, L, Steenhout, P. Effects of Infant Formula With Human Milk Oligosaccharides on Growth and Morbidity: A Randomized Multicenter Trial 2017. Journal of pediatric gastroenterology and nutrition 64 (4), 624–631. doi 10.1097/MPG.0000000000001520. 

    Reverri, E J, Devitt, A A, Kajzer, J A, Baggs, G E, Borschel, M W. Review of the Clinical Experiences of Feeding Infants Formula Containing the Human Milk Oligosaccharide 2'-Fucosyllactose 2018. Nutrients 10 (10). doi 10.3390/nu10101346. 

    Ríos-Covián, D, Ruas-Madiedo, P, Margolles, A, Gueimonde, M, Los Reyes-Gavilán, C G de, Salazar, N. Intestinal Short Chain Fatty Acids and their Link with Diet and Human Health 2016. Frontiers in microbiology 7, 185. doi 10.3389/fmicb.2016.00185. 

    Ruiz-Palacios, G M, Cervantes, L E, Ramos, P, Chavez-Munguia, B, Newburg, D S. Campylobacter jejuni binds intestinal H(O) antigen (Fuc alpha 1, 2Gal beta 1, 4GlcNAc), and fucosyloligosaccharides of human milk inhibit its binding and infection 2003. The Journal of biological chemistry 278 (16), 14112–14120. doi 10.1074/jbc.M207744200. 

    Sakanaka, M, Hansen, M E, Gotoh, A, Katoh, T, Yoshida, K, Odamaki, T, Yachi, H, Sugiyama, Y, Kurihara, S, Hirose, J, Urashima, T, Xiao, J-z, Kitaoka, M, Fukiya, S, Yokota, A, Lo Leggio, L, Abou Hachem, M, Katayama, T. Evolutionary adaptation in fucosyllactose uptake systems supports bifidobacteria-infant symbiosis 2019. Science Advances 5 (8). doi 10.1126/sciadv.aaw7696. 

    Sela, D A and Mills, D A. Nursing our microbiota: molecular linkages between bifidobacteria and milk oligosaccharides 2010. Trends in microbiology 18 (7), 298–307. doi 10.1016/j.tim.2010.03.008. 

    Shang, J, Piskarev, V E, Xia, M, Huang, P, Jiang, X, Likhosherstov, L M, Novikova, O S, Newburg, D S, Ratner, D M. Identifying human milk glycans that inhibit norovirus binding using surface plasmon resonance 2013. Glycobiology 23 (12), 1491–1498. doi 10.1093/glycob/cwt077. 

    Shen, L, Grollman, E F, Ginsburg, V. An enzymatic basis for secretor status and blood group substance specificity in humans 1968. Proceedings of the National Academy of Sciences of the United States of America 59 (1), 224–230. doi 10.1073/pnas.59.1.224. 

    Smith, N W, Shorten, P R, Altermann, E, Roy, N C, McNabb, W C. The Classification and Evolution of Bacterial Cross-Feeding 2019. Front. Ecol. Evol. 7, 153, 153. doi 10.3389/fevo.2019.00153. 

    Sprenger, G A, Baumgärtner, F, Albermann, C. Production of human milk oligosaccharides by enzymatic and whole-cell microbial biotransformations 2017. Journal of biotechnology 258, 79–91. doi 10.1016/j.jbiotec.2017.07.030. 

    Steenhout, P, Sperisen, P, Martin, F-P, Sprenger, N, Wernimont, S, Pecquet, S, Berger, B. Term infant formula supplemented with human milk oligosaccharides (2'-fucosyllactose and Lacto-N-neotetraose) shifts stool microbiota and metabolic signatures closer to that of breastfed infants. 2016. FASEB J. 2016 (30), 275–277. 

    Stepans, M B F, Wilhelm, S L, Hertzog, M, Rodehorst, T K C, Blaney, S, Clemens, B, Polak, J J, Newburg, D S. Early consumption of human milk oligosaccharides is inversely related to subsequent risk of respiratory and enteric disease in infants 2006. Breastfeeding Medicine 1 (4), 207–215. doi 10.1089/bfm.2006.1.207. 

    Taylor, M E and Drickamer, K. Convergent and divergent mechanisms of sugar recognition across kingdoms 2014. Current opinion in structural biology 28, 14–22. doi 10.1016/ 

    Thurl, S, Henker, J, Siegel, M, Tovar, K, Sawatzki, G. Detection of four human milk groups with respect to Lewis blood group dependent oligosaccharides 1997. Glycoconjugate journal 14 (7), 795–799. doi 10.1023/a:1018529703106. 

    Thurl, S, Munzert, M, Boehm, G, Matthews, C, Stahl, B. Systematic review of the concentrations of oligosaccharides in human milk 2017. Nutrition reviews 75 (11), 920–933. doi 10.1093/nutrit/nux044. 

    Thurl, S, Munzert, M, Henker, J, Boehm, G, Müller-Werner, B, Jelinek, J, Stahl, B. Variation of human milk oligosaccharides in relation to milk groups and lactational periods 2010. The British journal of nutrition 104 (9), 1261–1271. doi 10.1017/S0007114510002072. 

    Triantis, V, Bode, L, van Neerven, R J J. Immunological Effects of Human Milk Oligosaccharides 2018. Frontiers in pediatrics 6, 190. doi 10.3389/fped.2018.00190. 

    Underwood, M A, German, J B, Lebrilla, C B, Mills, D A. Bifidobacterium longum subspecies infantis: champion colonizer of the infant gut 2015. Pediatric research 77 (1-2), 229–235. doi 10.1038/pr.2014.156. 

    Urashima, T, Asakuma, S, Leo, F, Fukuda, K, Messer, M, Oftedal, O T. The predominance of type I oligosaccharides is a feature specific to human breast milk 2012. Advances in nutrition (Bethesda, Md.) 3 (3), 473S-82S. doi 10.3945/an.111.001412. 

    Wang, B. Sialic acid is an essential nutrient for brain development and cognition 2009. Annual review of nutrition 29, 177–222. doi 10.1146/annurev.nutr.28.061807.155515. 

    Weichert, S, Jennewein, S, Hüfner, E, Weiss, C, Borkowski, J, Putze, J, Schroten, H. Bioengineered 2'-fucosyllactose and 3-fucosyllactose inhibit the adhesion of Pseudomonas aeruginosa and enteric pathogens to human intestinal and respiratory cell lines 2013. Nutrition research (New York, N.Y.) 33 (10), 831–838. doi 10.1016/j.nutres.2013.07.009. 

    Xu, H-T, Zhao, Y-F, Lian, Z-X, Fan, B-L, Zhao, Z-H, Yu, S-Y, Dai, Y-P, Wang, L-L, Niu, H-L, Li, N, Hammarström, L, Borén, T, Sjöström, R. Effects of fucosylated milk of goat and mouse on Helicobacter pylori binding to Lewis b antigen 2004. World Journal of Gastroenterology : WJG 10 (14), 2063–2066. doi 10.3748/wjg.v10.i14.2063. 

    Xu, Z, Vo, L, Macher, B A. Structure-function analysis of human alpha1,3-fucosyltransferase. Amino acids involved in acceptor substrate specificity 1996. The Journal of biological chemistry 271 (15), 8818–8823. doi 10.1074/jbc.271.15.8818. 

    Yu, Z-T, Chen, C, Kling, D E, Liu, B, McCoy, J M, Merighi, M, Heidtman, M, Newburg, D S. The principal fucosylated oligosaccharides of human milk exhibit prebiotic properties on cultured infant microbiota 2012. Glycobiology 23 (2), 169–177. doi 10.1093/glycob/cws138. 

    Yu, Z-T, Chen, C, Newburg, D S. Utilization of major fucosylated and sialylated human milk oligosaccharides by isolated human gut microbes 2013. Glycobiology 23 (11), 1281–1292. doi 10.1093/glycob/cwt065. 

    Zeuner, B, Teze, D, Muschiol, J, Meyer, A S. Synthesis of Human Milk Oligosaccharides: Protein Engineering Strategies for Improved Enzymatic Transglycosylation 2019. Molecules (Basel, Switzerland) 24 (11). doi 10.3390/molecules24112033. 

    Zivkovic, A M, German, J B, Lebrilla, C B, Mills, D A. Human milk glycobiome and its impact on the infant gastrointestinal microbiota 2010. Proceedings of the National Academy of Sciences of the United States of America 108 (Suppl 1), 4653–4658. doi 10.1073/pnas.1000083107. 


More about breastfeeding