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The immune system of milk (ISOM) creates a mother–infant immune axis that plays an important role in protecting infants against infectious disease (ID). Tradeoffs in the immune system suggest the potential for both protection and harm, so we conceive of two dimensions via which the ISOM impacts infants: promotion of protective activity and control of activity directed at benign targets. High variability in ISOM activity across mother–infant dyads suggests investment the ISOM may have evolved to be sensitive to maternal and/or infant characteristics. We assessed predictors of appropriate and misdirected proinflammatory ISOM activity in an environment of high ID risk, testing predictions drawn from life history theory and other evolutionary perspectives.

We characterized milk in vitro interleukin‐6 (IL‐6) responses toSalmonella enterica(a target of protective immune activity;N = 96) andEscherichia coli(a benign target;N = 85) among mother–infant dyads in rural Kilimanjaro, Tanzania. We used ordered logistic regression and mixture models to evaluate maternal and infant characteristics as predictors of IL‐6 responses.

In all models, IL‐6 responses toS.entericaincreased with maternal age and decreased with gravidity. In mixture models, IL‐6 responses toE.colideclined with maternal age and increased with gravidity. No other considered variables were consistently associated with IL‐6 responses.

The ISOM's capacities for appropriate proinflammatory activity and control of misdirected proinflammatory activity increases with maternal age and decreases with gravidity. These findings are consistent with the hypothesis that the mother–infant immune axis has evolved to respond to maternal life history characteristics.

Folate is an essential nutrient fundamental to human growth and development. Human milk maintains high folate content across the maternal folate status range, suggesting buffering of milk folate with prioritized delivery to milk at the expense of maternal depletion. We investigated whether and how the extent of this buffering may diminish under prolonged nutritional and/or disease stress, while taking into consideration infants' varying vulnerability to malnutrition‐related morbidity/mortality.

A cross‐sectional study analyzed milk specimens from northern Kenyan mothers (n = 203), surveyed during a historic drought and ensuing food shortage. Multiple regression models for folate receptor‐α (FOLR1) in milk were constructed. Predictors included maternal underweight (BMI < 18.5), iron‐deficiency anemia (hemoglobin <12 g/dl and dried‐blood‐spot transferrin receptor >5 mg/L), folate deficiency (hyperhomocysteinemia, homocysteine >12 or 14 μmol/L), inflammation (serum C‐reactive protein >5 mg/L), infant age and sex, and mother‐infant interactions.

In adjusted models, milk FOLR1 was unassociated with maternal underweight, iron‐deficiency anemia and inflammation. FOLR1 was positively associated with maternal folate deficiency, and inversely associated with infant age. There was interaction between infant age and maternal underweight, and between infant sex and maternal folate deficiency, predicting complex changes in FOLR1.

Our results suggest that mothers buffer milk folate against their own nutritional stress even during a prolonged drought; however, the extent of this buffering may vary with infant age, and, among folate‐deficient mothers, with infant sex. Future research is needed to better understand this variability in maternal buffering of milk folate and how it relates to folate status in nursing infants.

This study explored differing levels of macronutrients in breast milk in relation to maternal anemia and hemoglobin.

Archived milk specimens and data from a cross‐sectional sample of 208 breastfeeding mothers in northern Kenya, originally collected in 2006, were analyzed; data included milk fat, maternal hemoglobin concentration, and anemia status (anemia defined as hemoglobin <12 g/dL). Total protein and lactose were measured and energy was calculated. To explore the association between milk outcomes (fat, protein, lactose, and energy) and anemia, regression models were constructed with and without adjustment for maternal age, parity, and time (days) postpartum. The same models were constructed using hemoglobin as a continuous predictor in lieu of dichotomous anemia to explore the role of hemoglobin levels and anemia severity in predicting milk outcomes.

The group comparison indicated significantly higher milk protein and lower milk fat for anemic mothers relative to nonanemic counterparts. After adjustment for maternal age, parity, and time postpartum, maternal anemia was associated with significantly higher milk protein (P = 0.001) and significantly lower milk fat (P = 0.025). Hemoglobin had a significant inverse relationship with milk protein (P = 0.017) and a marginally significant positive relationship with milk fat (P = 0.060) after adjusting for the maternal variables. Neither anemia nor hemoglobin was significant in predicting lactose or milk energy.

Maternal anemia and hemoglobin concentration may be associated with complex changes in milk macronutrients. Future research should clarify the impact of maternal anemia on a range of breast milk components while accounting for other maternal characteristics.

Vitamin A (VA) is an essential micronutrient required for a range of biological functions throughout life. VA deficiency (VAD) claims an estimated 1 million preschool children's lives annually. Human milk is enriched with VA (retinol) from the maternal blood, which originates from the hepatic reserve and dietary intake. Secreting retinol into milk will benefit the nursing infant through breast milk, but retaining retinol is also important for the maternal health. Previous studies found that the public health intervention of high‐dose VA supplementation to lactating mothers did not significantly lower child mortality. The World Health Organization (WHO) recently acknowledged that our understanding about the principle of VA allocation within the maternal system and the secretion into milk is too incomplete to devise an effective intervention.

We present a secondary analysis of data collected among lactating mothers in VAD endemic northern Kenya (n = 171), examining nutritional, inflammatory, and ecological factors that might associate with maternal retinol allocation. Regression models were applied using the outcome milk‐retinol allocation index: milk retinol/(milk retinol + serum retinol).

Ten percent of the sample was identified as VAD. The average milk retinol concentration was 0.1 μmo/L, grossly below what is considered minimally necessary for an infant (1 μmol/L). VAD mothers and mothers with inflammation did not seem to compromise their milk retinol even though their serum retinol was lower than non‐VAD and noninflammation mothers. Breast milk fat concentration positively correlated with milk retinol but not with serum retinol.

This exploratory study contributes toward an understanding of maternal retinol allocation.

Maternal anemia has adverse consequences for the mother‐infant dyad. To evaluate whether and how milk nutrient content may change in ways that could “buffer” infants against the conditions underlying maternal anemia, this study assessed associations between milk macronutrients and maternal iron‐deficiency anemia (IDA), non‐iron‐deficiency anemia (NIDA), and inflammation.

A secondary analysis of cross‐sectional data and milk from northern Kenya was conducted (n = 204). The combination of hemoglobin and transferrin receptor defined IDA/NIDA. Elevated serum C‐reactive protein defined acute inflammation. The effects of IDA, NIDA, and inflammation on milk macronutrients were evaluated in regression models.

IDA (β = 0.077,p =.022) and NIDA (β = 0.083,p =.100) predicted higher total protein (ln). IDA (β = −0.293,p =.002), NIDA (β = −0.313,p =.047), and inflammation (β = −0.269,p =.007) each predicted lower fat (ln); however, anemia accompanying inflammation predictedhigherfat (β = 0.655,p =.007 for IDA and β = 0.468,p =.092 for NIDA). NIDA predicted higher lactose (β = 1.020,p =.003).

Milk macronutrient content both increases and decreases in the presence of maternal anemia and inflammation, suggesting a more complicated and dynamic change than simple impairment of nutrient delivery during maternal stress. Maternal fat delivery to milk may be impaired under anemia. Mothers may buffer infant nutrition against adverse conditions or poor maternal health by elevating milk protein (mothers with IDA/NIDA), lactose (mothers with NIDA), or fat (mothers with anemiaandinflammation). This study demonstrates the foundational importance of maternal micronutrient health and inflammation or infection for advancing the ecological understanding of human milk nutrient variation.