Abstract
Food allergy originates from physiological fetal Th2 polarization. The normal shift towards Th1 dominance during the first months of life is defective in the atopic infant. Several factors are critical for the development of food allergy. The influence of genetic factors has been shown by familial aggregation studies, and numerous candidate genes have been identified Gene polymorphisms interact with the environment, contributing to fetal programming Heritable epigenetic modifications occur rapidly in response to environmental factors and may explain the recent increase in food allergies and other atopic diseases. Atmospheric agents and the maternal diet during pregnancy may either increase or decrease the risk. Birth conditions, the intestinal microbiota, age at which food diversification begins, and exposure to food allergens and pollutants by inhalation, ingestion and skin contact may all contribute to the onset of food allergy in infancy. Partial prophylaxis is now within reach. Preventive information must be provided to families at high risk of atopy in their offspring.
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