Research indicates that human breast milk plays a vital role in managing an infant’s microbial composition, known as the microbiome, during their first year, which subsequently reduces the likelihood of developing asthma.
A study led by NYU Langone Health and the University of Manitoba revealed that nursing for more than three months aids in the gradual development of the gut and nasal microbiomes in infants. On the other hand, weaning before three months can hinder this natural progression and has been associated with a greater chance of asthma in preschool children.
Breast milk contains specific elements, including complex sugars known as human milk oligosaccharides, that require particular microbes for digestion. This creates an advantage for microbes that can break down these sugars. Babies weaned from breastfeeding too soon and switched to formula feeding develop different microbial communities, which are tailored to digest formula components. Although these formula-adapted microbes eventually populate all infants, their premature emergence is linked to a heightened risk of asthma, according to the researchers.
“Breastfeeding and human milk regulate the pace and sequence of microbial colonization in an infant’s gut and nasal passages, similar to how a pacemaker impacts heart rhythms,” said Dr. Liat Shenhav, a computational biologist and co-senior investigator of the study. “Proper microbiome growth relies on not just the presence of the right microbes, but also their timely arrival and order,” explained Shenhav, who is an assistant professor at NYU Grossman School of Medicine, as well as at its Institute for Systems Genetics and Department of Microbiology.
The research, which was published in the journal Cell online on September 19, analyzed the microbial variations in the guts and nasal cavities of infants throughout their first year, alongside breastfeeding patterns and milk components from their mothers. This work involved children and mothers from the CHILD Cohort Study, a comprehensive project that has tracked 3,500 Canadian children from fetal development through adolescence.
Thanks to the data from the CHILD Cohort Study, researchers were able to isolate the effects of breastfeeding on an infant’s microbiome from various other environmental influences, such as exposure to smoke during pregnancy, antibiotic use, and the mother’s asthma history.
Even after considering these factors, the duration of breastfeeding stood out as a significant influence on the evolution of a child’s microbial community. The researchers also used insights from these microbial shifts to develop a machine-learning model that accurately forecasts the risk of asthma years ahead. Furthermore, they created a statistical model to determine causal relationships, demonstrating that the main way breastfeeding decreases asthma risk is through influencing the infant’s microbiome.
“The algorithms we created provide crucial insights into how microbial dynamics function during an infant’s first year and how these microbes interact with the baby,” stated Shenhav. “This information goes beyond merely finding associations, as it enhances our capacity to make predictions and delve into causal relationships.
“Our findings emphasize the significant influence of breastfeeding on the infant microbiome and its critical role in promoting respiratory health. By uncovering the protective mechanisms of breast milk, as highlighted in this research, we aim to inform national guidelines on breastfeeding and weaning using data-driven methods.
“With future research, our conclusions may also aid in developing preventive measures against asthma in kids who cannot be breastfed for at least three months,” she added.
The study received funding from the National Institutes of Health grant DP2AI185753, among other sources including Genome British Columbia, the University of British Columbia, the Canadian Institutes of Health Research, and the Canada Research Chair Program. All participants were volunteers from families involved in the CHILD Cohort Study, which was initially supported by the Canadian Institute of Health Research and AllerGen NCE.
In addition to Shenhav and Azad, other co-senior investigators were Padmaja Subbarao from the University of Toronto and Michael Surrette from McMaster University in Hamilton.
Co-investigators included co-first authors Kelsey Fehr and Elinor Simons from the University of Manitoba and co-authors from several institutions such as the University of Toronto, the University of British Columbia, McMaster University, the University of Pennsylvania, the University of California, San Diego, and the University of Alberta, as well as Dalhousie University in Halifax.
