Do advanced glycation end-products cause food allergy?

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Purpose of review

The aim of this study was to appraise the evidence relating to dietary advanced glycation end-products (AGEs), their influence on innate and adaptive immune responses and their possible role in the increasing rate of food allergy that is being observed globally.

Recent findings

The western pattern of diet is high in both AGEs and their substrates and this has been increasing in the last 30 years. AGEs mimic alarmins such as S100 proteins and the high molecular group box 1 (HMBG1), binding to the Receptor for Advanced Glycation End Products (RAGE), which in turn influences innate and adaptive immune responses. AGEs can directly cause mast cell activation and degranulation. Population data from USA and Australia have correlates with the rise in food allergy and sources of AGEs in the diet and this is also reinforced by urban and regional data within countries. The function of the RAGE receptor is inter-twined with Toll-like receptor (TLR) signalling and vitamin D levels. Activation of the RAGE receptor results in loss of epithelial integrity. Animal models studies have shown that dietary compounds that reduce the formation of AGEs can protect from the development of food allergies; however, this has not been shown in humans.


Dietary sources of AGEs and their substrates are a plausible contributor to the increasing prevalence of food allergy, which requires prospective evaluation in human populations.

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