Genetic variation alone cannot account for a dramatic increase in disease prevalence over such a short time frame. Emerging evidence suggests that twenty-first century environmental interventions, including widespread antibiotic use, consumption of a high-fat/low fiber diet, elimination of previously common enteropathogenesis (including Helicobacter pylori and helminthic parasites), reduced exposures to infectious disease, Caesarean birth, and formulafeeding, may have perturbed the mutually beneficial interactions established over millions of years of coevolution with the bacteria that comprise our commensal microbiota (Cho and Blaser, 2012). This dysbiosis can predispose genetically susceptible individuals to allergic disease