Volume 121, Issue 6 , Pages 1455-1459, June 2008
Soy consumption is not a risk factor for peanut sensitization
Background
A recent cohort study suggested that intake of soy milk or soy formula was associated with peanut allergy. If this finding is confirmed, it suggests an avenue for modification of diet as a peanut allergy prevention strategy.
Objective
To investigate the relationship between soy consumption and peanut sensitization in a prospective cohort study of children.
Methods
A total of 620 babies with a family history of allergic disease were recruited. Dietary information was obtained from telephone interviews every 4 weeks from birth until 15 months and then again at 18 months and 2 years. Skin prick tests to peanut, milk, and egg were performed at 6, 12, and 24 months. A wheal size ≥3 mm was considered positive for sensitization.
Results
Children whose parents elected to introduce soy formula or soy milk into their children's diet were more likely to be sensitized to peanuts at 2 years (odds ratio, 2.02; 95% CI, 1.04-3.92; P = .039). However, this relationship was explained by feeding of soy to children who had siblings with milk allergy or were themselves sensitized to milk. After adjusting for these factors, there was no evidence of an association between soy consumption and peanut sensitization (odds ratio, 1.34; 95% CI, 0.64-2.79; P = .434).
Conclusion
The association between soy consumption and peanut sensitization is not causal but merely a result of preferential use of soy milk in infants with a personal or family history of cow's milk allergy. Future studies should take the confounding effects related to dietary modifications by parents into account when investigating the association between diet and childhood allergic diseases.
Key words: Skin prick test, peanut allergy, soy formula, soy milk, risk factors, sensitization
Abbreviations used: MACS, Melbourne Atopy Cohort Study, OR, Odds ratio, SPT, Skin prick test
Funding for the initial development of the Melbourne Atopy Cohort Study was provided by Nestlé Australia. J.K. is a recipient of an Australian Postgraduate Award scholarship. K.J.A., S.D., and L.G. are recipients of National Health Medical Research Council Career Development Awards. A.L. is supported by Dairy Australia, Cooperative Research Center for Asthma, and VicHealth. Funding for analysis was also provided by the Ilhan Food Allergy Research Foundation.
Disclosure of potential conflict of interest: S. Dharmage has received research support from the National Health Medical Research Council, Australia Research Council, and Ilhan Food Allergy Foundation. J. Koplin has received research support from the Ilhan Food Allergy Foundation. L. Gurrin has received research support from National Health Medical Research Council. N. Osborne has received research support from the Ilhan Food Allergy Foundation. M. L. K. Tang was on the advisory board for Nestlé Nutrition Institute, made a presentation at a seminar for Wyeth, and has received research support from Numico, Diroform, and Commonwealth Serum Laboratories. C. Hosking is employed by Melbourne University. D. Hill is on the speakers' bureau for Nutricia International. K. J. Allen has received research support from Ilhan Food Allergy Foundation and the National Health Medical Research Council. The rest of the authors have declared that they have no conflict of interest.
PII: S0091-6749(08)00601-5
doi:10.1016/j.jaci.2008.03.017
© 2008 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Volume 121, Issue 6 , Pages 1455-1459, June 2008

