Xiumei Hong1, Liming Liang2, Qi Sun3, Corinne A Keet4, Hui-Ju Tsai5, Yuelong Ji6, Guoying Wang6, Hongkai Ji7, Clary Clish8, Colleen Pearson9, You Wang6, Robert A Wood4, Frank B Hu10, Xiaobin Wang11. 1. Department of Population, Family and Reproductive Health, Center on the Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Md. Electronic address: xhong3@jhu.edu. 2. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Mass; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston Mass. 3. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Mass; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass. 4. Division of Pediatric Allergy and Immunology, Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, Md. 5. Department of Population, Family and Reproductive Health, Center on the Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Md; Institute of Population Health Sciences, National Health Research Institute, Zhunan, Taiwan. 6. Department of Population, Family and Reproductive Health, Center on the Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Md. 7. Department of Biostatistics, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Md. 8. Broad Institute of MIT and Harvard University, Cambridge, Mass. 9. Department of Pediatrics, Boston University School of Medicine and Boston Medical Center, Boston, Mass. 10. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Mass; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Mass; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Mass. 11. Department of Population, Family and Reproductive Health, Center on the Early Life Origins of Disease, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Md; Division of General Pediatrics & Adolescent Medicine, Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, Md.
Abstract
BACKGROUND: The prevalence of IgE-mediated food allergy (FA) is increasing worldwide, but the underlying mechanisms are poorly understood. OBJECTIVE: We sought to examine the role of maternal lipidomic profiles in risk of FA development in offspring and to investigate the potential modification effects by timing of first solid-food introduction. METHODS: This report included 1068 mother-child dyads from the Boston Birth Cohort. Maternal lipid metabolites in plasma were assessed by using liquid chromatography tandem mass spectrometry. Food sensitization (FS) was defined as a specific IgE level of 0.35 kU/L or greater to any of the 8 common food allergens determined by using ImmunoCAP. FA was defined based on FS, clinical symptoms, and food avoidance. Logistic regression was applied to analyze associations between maternal metabolites and risk of FS and FA in offspring and to explore potential effect modifications. RESULTS: Of the 1068 children, 411 had FS, and 132 had FA. Among the 209 metabolites, maternal triacylglycerols (TAGs) of shorter carbon chains and fewer double bonds were associated with greater risk of FA, whereas TAGs of longer carbon chains and more double bonds were significantly associated with lower risk of FA in offspring. These associations were stronger in children with delayed solid-food introduction (≥7 months of age) than those with earlier solid-food introduction (P = .010 for interaction between the maternal TAG score and timing of solid-food introduction). No significant association was found for FS. CONCLUSION: This is the first study to demonstrate a link between maternal TAGs and risk of FA in offspring and potential risk modification by timing of solid-food introduction.
BACKGROUND: The prevalence of IgE-mediated food allergy (FA) is increasing worldwide, but the underlying mechanisms are poorly understood. OBJECTIVE: We sought to examine the role of maternal lipidomic profiles in risk of FA development in offspring and to investigate the potential modification effects by timing of first solid-food introduction. METHODS: This report included 1068 mother-child dyads from the Boston Birth Cohort. Maternal lipid metabolites in plasma were assessed by using liquid chromatography tandem mass spectrometry. Food sensitization (FS) was defined as a specific IgE level of 0.35 kU/L or greater to any of the 8 common food allergens determined by using ImmunoCAP. FA was defined based on FS, clinical symptoms, and food avoidance. Logistic regression was applied to analyze associations between maternal metabolites and risk of FS and FA in offspring and to explore potential effect modifications. RESULTS: Of the 1068 children, 411 had FS, and 132 had FA. Among the 209 metabolites, maternal triacylglycerols (TAGs) of shorter carbon chains and fewer double bonds were associated with greater risk of FA, whereas TAGs of longer carbon chains and more double bonds were significantly associated with lower risk of FA in offspring. These associations were stronger in children with delayed solid-food introduction (≥7 months of age) than those with earlier solid-food introduction (P = .010 for interaction between the maternal TAG score and timing of solid-food introduction). No significant association was found for FS. CONCLUSION: This is the first study to demonstrate a link between maternal TAGs and risk of FA in offspring and potential risk modification by timing of solid-food introduction.
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