In a prospective cohort study, poorer maternal diet quality during pregnancy was associated with higher odds of infants developing both colic and eczema, but not either condition alone.
Investigators analyzed data from 1,324 mother-infant pairs participating in Project Viva, a prospective cohort established in Massachusetts between 1999 and 2002. Participants were recruited during early pregnancy without selection for atopic risk. Maternal dietary intake was assessed using food frequency questionnaires administered during early and midpregnancy. The researchers calculated Mediterranean Diet Scores (MDS) and Dietary Inflammatory Index (DII) values and evaluated consumption of commonly allergenic foods. Infants were assessed at a median age of 6.3 months. Higher MDS values indicated greater adherence to a Mediterranean-style diet, whereas higher DII values reflected greater dietary inflammatory potential.
The primary outcome was the co-occurrence of colic and eczema, compared with neither condition. Colic was identified through maternal reports of episodes of inconsolable crying and distress occurring sometimes or often, whereas eczema was based on maternal reports of a clinician diagnosis. Analyses accounted for maternal demographic characteristics, smoking, and atopic history.
Among the 1,324 infants, 61 (5%) had both colic and eczema, 273 (21%) had colic alone, and 152 (11%) had eczema alone. In fully adjusted analyses, each 1-point increase in mean MDS was associated with 15% lower odds of both conditions. Conversely, each 1-point increase in DII was associated with 34% higher odds of the combined outcome.
Both conditions occurred in 7% of infants whose mothers were in the lowest quartile of MDS, compared with 4% in the highest quartile, and in 7% of those in the highest DII quartile versus 3% in the lowest. Neither dietary score was significantly associated with colic alone or eczema alone.
Each additional weekly serving of seafood was associated with 25% lower odds of combined colic and eczema. The combined outcome occurred in 6% of infants in the lowest quartile of maternal seafood intake, compared with 3% in the highest quartile.
Greater maternal nut and peanut consumption showed a marginal association with higher odds of colic without eczema, but not the combined outcome. Dairy and egg consumption showed no statistically significant associations with any outcome. The investigators noted that existing evidence does not support prenatal dietary restrictions to prevent infant allergy.
Subgroup analyses suggested that associations between maternal dietary quality and infant colic differed according to eczema status and maternal history of atopy. Among infants with eczema, each 1-point increase in DII was associated with 47% higher odds of colic, whereas no clear association was observed among infants without eczema. Higher MDS was associated with lower estimated odds of colic among infants with eczema, although the association was not statistically significant. Associations between dietary quality measures and colic also appeared stronger among infants whose mothers had a history of atopy.
The study had several limitations. Colic symptoms and eczema diagnoses were based on maternal reports rather than independent medical record verification, potentially introducing outcome misclassification. Only 61 infants had both conditions, limiting the precision of estimates for the combined outcome. Missing dietary and infant outcome information may have introduced selection bias, and residual confounding remained possible. The cohort was recruited more than 2 decades before publication, which, along with participants' access to prenatal care and insurance, may limit generalizability.
The observational study cannot establish causality or determine whether prenatal dietary changes could prevent infant colic and eczema. Further research is needed to clarify the underlying biological mechanisms.“We hypothesize that this outcome combination may reflect a specific, immune endotype of colic,” wrote lead study author Emily Oken, MD, of Harvard Medical School and the Harvard Pilgrim Health Care Institute, and colleagues.
The study was supported by an anonymous donor and the National Institutes of Health. Dr Oken reported research grants; Dr Nadeau disclosed research funding, equity interests, consulting fees, patents, and advisory roles; and Dr Lightdale reported industry consulting fees. No other disclosures were reported.
Source: JAMA Network Open
