About 20% of people have an inactive FUT2 gene and cannot secrete particular antigens in their body fluids or intestinal tract. These “non-secretors” are more resistant to pathogens that use FUT2 antigens to infect cells, but they are more susceptible to some other pathogens. Non-secretors also have a lower diversity of “healthy” gut bacteria, and may be at increased risk for autoimmune diseases including type 1 diabetes, psoriasis and inflammatory bowel disease. However, these associations are unclear because most studies rely on self-reported information rather than firm diagnoses or biological test results.

FUT2 antigens are also secreted in breast milk. They are attached to breast milk sugars that are not digested by babies, but provide a specialized food source for the babies’ gut bacteria. These bacteria influence the baby’s growth, immunity and metabolism throughout life. A mother’s secretor status therefore affects her baby’s gut bacteria, which in turn affects the baby’s development and health, including its susceptibility to infections and autoimmune disease later in childhood.

Thus, both maternal and infant FUT2 secretor status can affect the health of breastfed children. However, few studies examining FUT2 have accounted for breastfeeding or maternal secretor status, so it is unclear how a ‘match’ or ‘mismatch’ in mother/baby secretor status might impact the baby’s gut bacteria and risk of infections or autoimmune disease. We will address this intriguing issue using available information, genetic data, medical diagnoses and biological test results from the ALSPAC cohort.