October 2011, VOLUME128 /ISSUE Supplement 3

Maternal Antenatal Peanut Consumption and Peanut and Rye Sensitization in the Offspring at Adolescence

AS Kemp, AL Ponsonby, T Dwyer, JA Cochrane, A Pezic, G Jones. Clin Exp Allergy. 2011;41(2):224231
  1. Lara S. Ford, MD, MPH,
  2. Scott H. Sicherer, MD
  1. New York, NY


To examine the influence of antenatal peanut ingestion on peanut and rye sensitization.


The 373 participants were drawn from a cohort of 1437 children born in Tasmania in 1988 and 1989, selected from all births for being at elevated risk of sudden infant death syndrome. Those who were not lost to follow-up and who subsequently agreed to participate at age 8 in studies on bone density, blood pressure, high-density lipoprotein cholesterol, and vitamin D and at age 16 in a study of bone health and allergy were included.


The mothers completed a hospital interview shortly after delivery that included a food-frequency questionnaire of diet in the third trimester and family history of asthma. Those mothers who ingested peanut at least once per month were regarded as eating peanut. Peanut and rye sensitization at age 16 were determined by using the ImmunoCAP test (Phadia, Uppsala, Sweden). An allergen-specific immunoglobulin E (IgE) level of >0.35 kU of antibody (kUA)/L was regarded as a positive result.


The peanut sensitization rate was 14%. In the entire cohort (N = 310), there was no association between antenatal peanut ingestion and peanut sensitization (P = .17). However, there was a strong association between antenatal peanut ingestion and decreased risk of rye sensitization and peanut sensitization in those (n = 201) without a family history of asthma (rye odds ratio [OR]: 0.30 [95% confidence interval (CI): 0.14–0.63], P = .001; peanut OR: 0.18 [95% CI: 0.04–0.78], P = .02). There was an increased risk of rye sensitization in those (n = 108) with a family history of asthma and antenatal peanut ingestion (rye OR: 2.69 [95% CI: 1.11–6.51], P = .03). It was considered that these sensitizations were likely to be related to the presence of IgE antibodies to cross-reacting carbohydrate epitopes common to rye and peanut allergens, which are not the epitopes thought to typically contribute to clinical disease.


Antenatal peanut ingestion might influence the development of IgE antibody to cross-reacting carbohydrate epitopes in later life, and avoidance might inadvertently increase sensitization in some people. Genetic factors might modify this association.


This study is the first to obtain prospective data on antenatal peanut consumption in a population-based cohort rather than one with a family history of allergy. Selection bias is likely to have been limited, because the subjects were initially recruited for a study of nonatopic conditions, but there was a substantial loss to follow-up that might have introduced unrecognized bias. The fact that the results were not significant overall, but were significant and meaningful when considered according to family history of asthma, adds to the evidence that the relationship between sensitization and disease, and antenatal and early life exposure to allergens, is complex and depends on multiple factors.