Int. J. Environ. Res. Public Health 2013, 10(11), 5364-5377; doi:10.3390/ijerph10115364
Article
1 Centre for Molecular, Environmental, Genetic and Analytic Epidemiology, University of Melbourne, Parkville, Victoria 3052, Australia2 Murdoch Childrens Research Institute, Parkville, Victoria 3052, Australia3 Department of Allergy and Immunology, Royal Children's Hospital, Parkville, Victoria 3052, Australia4 Department of Paediatrics, University of Melbourne, Parkville, Victoria, Australia† The HealthNuts Study Team is Anne-Louise Ponsonby, David Hill, Melanie Matheson, Melissa Wake, Leone Thiele, Helen Czech, Jana Eckert, Deborah Anderson, Olivia Hamilton, Nadine Bertalli, Jeeva Sanjeevan, Thanh Dang, Tina Tan, Pamela Martin, Nick Osborne, Marnie Robinson, Dean Tey and Giovanni Zurzolo.
* Author to whom correspondence should be addressed.
Received: 1 August 2013; in revised form: 11 October 2013 / Accepted: 14 October 2013 / Published: 25 October 2013
(This article belongs to the Special Issue Food Allergy, Genes and Environment)
Abstract: The apparent rapid increase in IgE-mediated food allergy and its implications are now widely recognized, but little is known about the relationship between family history (an indirect measure of genetic risk) and the risk of food allergy. In a population-based study of 5,276 one year old infants (HealthNuts), the prevalence of oral food challenge-confirmed food allergy was measured. Associations between family history of allergic disease and food allergy in infants were examined using multiple logistic regression. Food allergy was diagnosed in 534 infants. Compared to those with no family history of allergic disease, children meeting the current definition of “high risk” for allergic disease (one immediate family member with a history of any allergic disease) showed only a modest increase (OR 1.4, 95% CI 1.1–1.7) in food allergy, while having two or more allergic family members was more strongly predictive of food allergy in the child (OR 1.8, 95% CI 1.5–2.3). There were also differences in the associations between family history and egg and peanut allergy in the child. Re-defining “high risk” as two or more allergic family members may be more useful for identification of groups with a significantly increased risk of food allergy both clinically and within research studies.
Keywords: food allergy; family history; genetics; heritability; siblings; maternal; paternal; egg allergy; peanut allergy
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