Atopy is not a single phenotype, the idea of an “atopic march” from infantile eczema through food allergy to asthma and rhinitis is way too simplistic.
There are different risk groups. Environmental exposure to allergens and microbes in early life is one factor. Farm environment protects. Indoor allergen exposure at 1yr of age is protective against recurrent wheeze at 3 yrs. Reduced bacterial diversity is a risk factor for asthma and atopic wheeze – certain bacteria esp bacteroides and firmacutes seem to be protective.
Viruses also play a role. RSV is associated with later asthma regardless of existing atopy or not, although perhaps not with asthma persisting into adulthood; rhinovirus wheezing in first 3yrs is similarly associated with persistent wheeze, especially in atopic persons.
Heritability of asthma accounts for less than 50% of patients so gene-environment interactions are at least as important. A gene has been found that is associated with early childhood asthma with severe exacerbations (CDHR3).
Animal experiments have already shown that oral administration of bacterial extracts prevents bronchial hyperreactivity. We should therefore encourage less Caesarean sections, more breast feeding, less antibiotic use, more green spaces, more “natural” food preparation and distribution (ie less plastic!).