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Epigenetic regulation: the interface between prenatal and early-life exposure and asthma susceptibility.

ABSTRACT: Asthma is a complex disease with genetic and environmental influences and emerging evidence suggests that epigenetic regulation is also a major contributor. Here, we focus on the developing paradigm that epigenetic dysregulation in asthma and allergy may start as early as in utero following several environmental exposures. We summarize the pathways important to the allergic immune response that are epigenetically regulated, the key environmental exposures associated with epigenetic changes in asthma genes, and newly identified epigenetic biomarkers that have been linked to clinical asthma. We conclude with a brief discussion about the potential to apply newly developing technologies in epigenetics to the diagnosis and treatment of asthma and allergy. The inherent plasticity of epigenetic regulation following environmental exposures offers opportunities for prevention using environmental remediation, measuring novel biomarkers for early identification of those at risk, and applying advances in pharmaco-epigenetics to tailor medical therapies that maximize efficacy of treatment. 'Precision Medicine' in asthma and allergy is arriving. As the field advances this may involve an individually tailored approach to the prevention, early detection, and treatment of disease based on the knowledge of an individual's epigenetic profile.

SUBMITTER: de Planell-Saguer M

PROVIDER: S-EPMC4148423 | biostudies-literature | 2014 Apr

REPOSITORIES: biostudies-literature

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Epigenetic regulation: the interface between prenatal and early-life exposure and asthma susceptibility.

de Planell-Saguer Mariàngels M Lovinsky-Desir Stephanie S Miller Rachel L RL

Environmental and molecular mutagenesis 20131209 3

Asthma is a complex disease with genetic and environmental influences and emerging evidence suggests that epigenetic regulation is also a major contributor. Here, we focus on the developing paradigm that epigenetic dysregulation in asthma and allergy may start as early as in utero following several environmental exposures. We summarize the pathways important to the allergic immune response that are epigenetically regulated, the key environmental exposures associated with epigenetic changes in as ...[more]

PMID: 24323745

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Project description:RATIONALE:Cross-sectional studies have linked intake of high-fructose corn syrup-sweetened beverages with asthma in schoolchildren. OBJECTIVES:To examine associations of maternal prenatal and early childhood intake of sugar-sweetened beverages and fructose with current asthma in midchildhood (median age, 7.7 yr). METHODS:We assessed maternal pregnancy (first- and second-trimester average) and child (median age, 3.3 yr) intake of sugar-sweetened beverages and total fructose using food frequency questionnaires in 1,068 mother-child pairs from Project Viva, a prospective prebirth cohort. In a multivariable analysis, we examined associations of quartiles of maternal and child sugar-sweetened beverage, juice, and total fructose intake with child current asthma in midchildhood, assessed by questionnaire as ever having doctor-diagnosed asthma plus taking asthma medications or reporting wheezing in the past 12 months. RESULTS:Higher maternal pregnancy sugar-sweetened beverage consumption (mean, 0.6 servings/d; range, 0-5) was associated with younger maternal age, nonwhite race/ethnicity, lower education and income, and higher prepregnancy body mass index. Adjusting for prepregnancy body mass index and other covariates, comparing quartile 4 with quartile 1, higher maternal pregnancy intake of sugar-sweetened beverages (odds ratio, 1.70; 95% confidence interval, 1.08-2.67) and total fructose (odds ratio, 1.58; 95% confidence interval, 0.98-2.53) were associated with greater odds of midchildhood current asthma (prevalence, 19%). Higher early childhood fructose intake (quartile 4 vs. quartile 1) was also associated with midchildhood current asthma in models adjusted for maternal sugar-sweetened beverages (odds ratio, 1.79; 95% confidence interval, 1.07-2.97) and after additional adjustment for midchildhood body mass index z-score (odds ratio, 1.77; 95% confidence interval, 1.06-2.95). CONCLUSIONS:Higher sugar-sweetened beverage and fructose intake during pregnancy and in early childhood was associated with childhood asthma development independent of adiposity.

Dataset Information

Epigenetic regulation: the interface between prenatal and early-life exposure and asthma susceptibility.

Publications

Epigenetic regulation: the interface between prenatal and early-life exposure and asthma susceptibility.

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