Associate Professor Dr. Masako Fujita and Ph.D. Candidate Nerli Paredes Ruvalcaba co-publish in the American Journal of Human Biology

Department of Anthropology Associate Professor Dr. Masako Fujita, Ph.D. Candidate Nerli Paredes Ruvalcaba and co-authors recently published in the American Journal of Human Biology. The article, titled, “Human milk lactoferrin variation in relation to maternal inflammation and iron deficiency in northern Kenya” explored how nutritional and disease stress among breastfeeding mothers might influence the immune content in mothers’ own milk, focusing on an iron-binding protein called lactoferrin. Lactoferrin is abundant in fluids such as saliva, tears, and milk. In milk, it serves to protect infants against infection. Lactoferrin has come under the spotlight recently because of its preventive and therapeutic potential against COVID-19 when taken as a supplement (made from cow’s milk). The study found that human milk lactoferrin content did not differ between mothers with and without iron deficiency, suggesting that mothers under nutritional stress are able to maintain their delivery of lactoferrin to infants. Moreover, the study found that mothers undergoing inflammation (likely due to infections) delivered more lactoferrin when raising younger infants than mothers without inflammation raising similarly young infants, suggesting that mothers under infectious disease stress might upregulate milk lactoferrin delivery and therefore bolster immune protection for young infants who are at heightened vulnerability to infection.

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Background: Milk lactoferrin is a multi-functional, iron-binding glycoprotein with immunomodulatory effects, protecting infants against infectious diseases.

Aims: This study explored how maternal inflammation/infection and iron-deficiency anemia (IDA) might influence human milk lactoferrin. Lactoferrin might be elevated with maternal inflammation resulting from infectious disease processes. Conversely, lactoferrin might decrease with IDA, corresponding to scarce maternal iron for transfer in milk. In these two hypothesized scenarios, the degree of lactoferrin elevation or decrease might vary with infant vulnerability to infectious diseases or malnutrition. Alternatively, lactoferrin might be unassociated with inflammation/infection or IDA if mothers could buffer it against these conditions.

Materials & Methods: We used cross-sectional data from Ariaal mothers of northern Kenya (n = 200) to evaluate associations between milk lactoferrin and maternal inflammation/infection, IDA, infant age/sex, and the mother-infant variable interactions in multivariate regression models.

Results: Maternal inflammation was associated with higher lactoferrin for younger infants (<~5 months of age) but with lower lactoferrin for older infants. Maternal IDA was unassociated with lactoferrin alone or in interaction with infant variables.

Discussion & Conclusion: Results suggest that mothers of vulnerable young infants deliver more lactoferrin when they have inflammation/infection but mothers with older infants do not, and that maternal delivery of lactoferrin is unaffected by their IDA. Longitudinal research should verify these findings.