Abstract

The prevalences of allergic diseases, asthma, atopic dermatitis, allergic rhinitis and lately food allergy have been increasing over the last decades. It has been suggested that the prevalence of allergic diseases has reached a plateau in high income countries, while it is still on the rise in low and middle income countries. Generally, allergic diseases more often set on in childhood than in adulthood and affected children contribute more to the rise in allergic disease prevalence than affected adults. Epidemiological evidence suggests that not all atopic dermatitis and asthma cases are attributable to atopic sensitization. Indeed, mainly genetic association studies have prompted the unravelling of barrier dysfunction as a mainstay in the patho-mechanisms leading to atopic dermatitis and to asthma with atopic sensitization secondary to this dysfunction. Epidemiological research on risk and protective factors for allergic disease, acting against the background of genetic susceptibility, has produced an enormous body of evidence. Prominent observations are the 'sibling effect' and the 'farm effect' which gave rise to the 'hygiene hypothesis' and later the 'biodiversity hypothesis'. Future epidemiological research is required to evaluate and refine these hypotheses in light of the paradigm shift from atopic sensitization to barrier dysfunction with ever increasing options for environmental characterization, currently, e.g., 'omics'-techniques in microbiology and metabolism, and with ever increasing options for phenotyping of allergic techniques, including, e.g., high-resolution time series of symptoms using, e.g., sensing technologies.

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