The numbers are alarming: atopic disorders — which include atopic dermatitis (eczema), food allergy, asthma, and allergic rhinitis (“hay fever”) — are currently estimated to affect up to 30% of the population, with many children experiencing lifelong symptoms.
Scientists have determined that the microbiomes of those with atopy differ from those from healthy individuals, but that leads to a number of questions including whether the difference is a cause or effect of atopy, and how early in a child’s development the microbiomes begin to differ.
To get an early snapshot of an infant’s metabolome at birth, researchers can study the infant’s meconium. Meconium is the first stool sample passed after birth. The meconium metabolome reflects a wide range of fetal exposure as it begins forming in the fetal gut by gestational week 16 and is not passed until the first few days of life. Not only is meconium a rich source of metabolites reflecting perinatal influences, but it also contains the starting material for the initial microbiota.
In a study published in the journal Cell Reports: Medicine, researchers looked for metabolic signatures within the meconium that might influence both microbiota maturation and immune development.
Data from meconium samples of 950 infants enrolled in the Canadian Healthy Infant Longitudinal Development (CHILD) cohort along with sequential stool samples collected within the first 2 years of life were analyzed.
The researchers found that reduced meconium metabolic richness was associated with IgE-mediated allergic sensitization — atopy, as diagnosed via standardized skin prick testing — to common allergens at 1 year of age.
They also found that select metabolites present within the meconium were associated with changes detected months later in key bacteria important for driving microbiota maturation in the first year of life as well as the atopy phenotype. They concluded that deficiency in microbiota maturation and immune development likely begins in utero, and these findings may be valuable to identifying at-risk infants and revealing directly modifiable metabolic targets to prevent allergic sensitization.
The authors noted that the study was limited by the relatively small number (100) of infants whose meconium metabolites were profiled requiring further confirmation of the results in larger and more diverse populations.
