World Health Organization (WHO) recommends exclusive breastfeeding for the first six months after which breastfeeding can continue alongside suitable, complementary, solid foods(1).
One of the many reasons for recommending exclusive breastfeeding for the first six months of life is that breastfed infants have lower levels of atopic disease compared to those fed on infant formula(2).
Breastmilk achieves this beneficial effect through a number of factors, many of which are not completely understood.
“One mechanism that has been researched increasingly in recent years is the way that compounds within breastmilk stimulate the growth of «friendly» bacteria in the gut of the growing infant.”
The intestinal tract of the unborn infant is relatively sterile. During vaginal delivery and as the infant starts to breastfeed, the infant comes into contact with ‘friendly’ bacteria such as Bifidobacteria and Lactobacilli which enter the gut and gradually begin to colonize it(3).
Human milk oligosaccharides
The bacterial population creates an intestinal microbiota whose composition plays an important role in the infant’s digestion, protects against the development of pathogenic bacteria such as E. coli, Clostridia and Eubacteria and stimulates the development of the immune system(4).
Studies have shown significant differences between the microbiota of breastfed and bottle-fed infants(5) and also between infants with and without atopic disease(6). A microbiota with high levels of Bifidobacteria and low counts of Clostridia is associated with a reduced risk of allergy(7).
“A crucial constituent of breastmilk that contributes to the growth of beneficial bacteria is a class of compounds known as human milk oligosaccharides.”
Human milk oligosaccharides cannot be digested by the infant. But unlike dietary fiber, which passes through the infant’s gut virtually unchanged, human milk oligosaccharides are selectively fermented by the beneficial bacteria. Products of this fermentation include short-chain fatty acids which are absorbed by the infant and lower the pH of the gut to levels that inhibit the growth of pathogens(3).
The link between the gut microbiota and subsequent development of atopic disease has led a number of researchers to investigate whether non-digestible or fermentable compounds could be used as a nutritional ingredient to modify the infant gut microflora and thus help protect against atopic dermatitis (or atopic eczema) and allergic symptoms (or manifestations).
In several dietary intervention studies researchers used a mixture of short chain galacto-oligosaccharides and long-chain fructo-oligosaccharides (GOS/FOS 9:1) to mimic the effect of oligosaccharides within breastmilk(8). The study enrolled healthy, full-term babies born to parents with a history of atopic eczema, allergic rhinitis or asthma.
The infants’ mothers were all advised to breastfeed their infants, but those who switched to formula feeding within the first two weeks were randomly assigned to a milk formula that was supplemented either with the GOS/FOS 9:1 carbohydrates or an inactive carbohydrate placebo. Of these infants, 134 were followed-up for two years(8).
The results showed that, by the end of the study, the infants fed GOS/FOS 9:1 formula had a significantly lower incidence of atopic dermatitis, recurrent wheezing and allergic urticaria compared to the placebo group(8).
A more recent follow-up to that study of 92 children has shown the anti-allergenic effect of the GOS/FOS 9:1 mixture and showed that, in high-risk infants, the reduced risk of atopic dermatitis and certain allergic symptoms lasts beyond infancy until at least five years of age(9).
Halting the allergic march
The importance of offering protection against atopic dermatitis and certain allergic symptoms is two-fold. Not only is the condition unpleasant and irritating for the child at the time, it is also considered one of the stages in the pediatric ‘allergic march’ in which allergies might follow atopic dermatitis to allergic rhinoconjunctivitis and finally to asthma. Childhood allergy places a significant burden on the NHS, and any intervention that can halt or avoid the onset of this progression and reduce the need for treatment is to be welcomed.
Naturally occurring oligosaccharides in breastmilk are just one of the many remarkable ways in which breastfeeding offers infants the very best start in life. The more we learn about the various constituents within breastmilk (including recently discovered small amounts of Bifidobacteria and lactobacilli), the more we understand how the benefits of breastfeeding extend beyond nutrition and into the realms of immune system development.
1. World Health Organization. Breastfeeding [Online]. WHO. Available at: http://www.who.int/topics/breastfeeding/en/ [Accessed July 2013].
2. Kelly D, Coutts AG. Early nutrition and the development of immune function in the neonate, Proc Nutr Soc 2000; 59(2):177-85.
3. Boehm G, Moro G. Structural and functional aspects of prebiotics used in infant nutrition, J Nutr 2008; 138(9); 1818-28.
4. Gibson GR, Wang X. Regulatory effects of bifidobacteria on the growth of other colonic bacteria, J Appl Bacteriol 1994; 77(4):412-20.
5. Harmsen HJ et al. Analysis of intestinal flora development in breast-fed and formula-fed infants by using molecular identification and detection methods, J Pediatr Gastroenterol Nutr 2000; 30(1):61-7.
6. Watanabe S et al. Differences in fecal microflora between patients with atopic dermatitis and healthy control subjects, J Allergy Clin Immunol 2003; 111(3):587-91.
7. Björkstén B et al. Allergy development and the intestinal microflora during the first year of life, J Allergy Clin Immunol 2001; 108(4):516-20.
8. Arslanoglu S et al. Early dietary intervention with a mixture of prebiotic oligosaccharides reduces the incidence of allergic manifestations and infections during the first two years of life, J Nutr 2008; 138(6):1091-5.
9. Arslanoglu S et al. Intestinal microbiology in early life: specific prebiotics can have similar functionalities as human-milk oligosaccharides, J Biol Regul Homeost Agents 2012; 26 S: 49-59.