The prevalence of peanut allergy among children in Western countries has doubled in the past 10 years, reaching rates of 1.4-3.0%. This allergy is the leading cause of anaphylaxis and death due to food allergy.

Peanut allergy develops early in life and is rarely outgrown. Clinical practice guidelines from the UK in 1998 and from the US in 2000 recommended the exclusion of allergenic foods from the diets of infants at high risk for allergy, and from the diets of their mothers during pregnancy and lactation. However, studies in which food allergens have been eliminated from the diet have consistently failed to show that elimination from the diet prevented the development of IgE-mediated food allergy. In 2008, recommendations for the avoidance of allergens were withdrawn. The question of whether early exposure or avoidance is the better strategy to prevent food allergies remains open. 

These authors had previously observed that the risk of the development of peanut allergy was 10 times as high among Jewish children in the UK as it was in Israeli children of similar ancestry. In the UK infants typically do not consume peanut-based foods in the first year of life, whereas in Israel, peanut-based foods are usually introduced in the diet when infants are approximately seven months of age, and their median monthly consumption of peanut protein is 7.1g. This finding prompted the hypothesis that the early introduction of peanuts to the diet may actually offer protection from the development of peanut allergy.

The primary prevention of allergy targets non-sensitised persons, whereas secondary prevention targets those who are known to be sensitised on the basis of test results for allergen-specific IgE or reactions on skin-prick testing. The Learning Early about Peanut Allergy (LEAP) trial was conceived to determine whether the early introduction of dietary peanut could serve as an effective primary and secondary strategy for the prevention of peanut allergy. 

A total of 640 infants with severe eczema, egg allergy, or both were randomly assigned to consume or avoid peanuts until 60 months of age. Participants, who were at least four months but younger than 11 months of age at randomisation were assigned to separate study cohorts on the basis of pre-existing sensitivity to peanut extract, which was determined with the use of a skin-prick test – one consisting of participants with no measurable wheal after testing and the other consisting of those with a wheal measuring 1-4mm in diameter. The primary outcome, which was assessed independently in each cohort, was the proportion of participants with peanut allergy at 60 months of age.

Among the 530 infants in the intention-to-treat population who initially had negative results on the skin-prick test, the prevalence of peanut allergy at 60 months of age was 13.7% in the avoidance group and 1.9% in the consumption group (p < 0.001). Among the 98 participants in the intention-to-treat population who initially had positive test results, the prevalence of peanut allergy was 35.3% in the avoidance group and 10.6% in the consumption group (p = 0.004). There was no significant between-group difference in the incidence of serious adverse events. Increases in levels of peanut-specific IgG4 antibody occurred predominantly in the consumption group; a greater percentage of participants in the avoidance group had elevated titres of peanut-specific IgE antibody. A larger wheal on the skin-prick test and a lower ratio of peanut-specific IgG4:IgE were associated with peanut allergy.

The early introduction of peanuts significantly decreased the frequency of the development of peanut allergy among children at high risk for this allergy and modulated immune responses to peanuts.