- Top of page
- Growing evidence for the second wave
- Current prevalence of ‘challenge positive’ IgE-mediated food allergy even higher than anticipated
- A new generation, a new disease profile?
- The usual suspects or new causal pathways?
- Mechanisms of environmental influence?
- A role for transgenerational epigenetic effects: an amplifying effect of maternal allergy?
- Different processes governing oral tolerance compared with tolerance to inhaled allergens
- The implications for rapidly urbanizing developing regions: anticipating a tsunami?
- Food allergens – friends or foe?
- A final word
To cite this article: Prescott S, Allen KJ. Food allergy: Riding the second wave of the allergy epidemic. Pediatr Allergy Immunol 2011; 22: 155–160.
Food allergy is a substantial and evolving public health issue, recently emerging over the last 10–15 yr as a ‘second wave’ of the allergy epidemic. It remains unclear why this new phenomenon has lagged decades behind the ‘first wave’ of asthma, allergic rhinitis and inhalant sensitization. In regions like Australia, which lead the respiratory epidemic, challenge-proven IgE-mediated food allergy now affects up to 10% of infants. Although their parents were among the first generation to experience the large-scale rise in allergic diseases, disorders of oral tolerance were previously uncommon. Of further concern, this new generation appears less likely to outgrow food allergy than their predecessors with long-term implications for disease burden. Allergic disease has been linked to the modern lifestyle including changing dietary patterns, changing intestinal commensal bacteria and vehicular pollution. It is not yet known whether the rise in food allergy is a harbinger of earlier and more severe effects of these progressive environmental changes or whether additional or unrelated lifestyle factors are implicated. New studies suggest environmental factors can produce epigenetic changes in gene expression and disease risk that may be potentially heritable across generations. The rising rates of maternal allergy, a strong direct determinant of allergic risk, could also be amplifying the effect of environmental changes. Preliminary evidence that non-Caucasian populations may be even more susceptible to the adverse effects of ‘westernisation’ has substantial global implications with progressive urbanization of the more populous regions in the developing world. Unravelling the environmental drivers is critical to curtail a potential tsunami of allergic disease.