Ovalbumin-sensitized mice avoid drinking egg white solution, an IgE-bound mast cell dependent phenomenon called food aversion, which is seen as a defense mechanism. However, it is not clear whether food aversion happens in other types of food allergy. Thus, we tested if peanut allergy associates with food aversion. Balb/c and C57BL/6 mice were subcutaneously sensitized to peanut protein extract (PPE) and performed a preference test, in which they could choose to drink water or whole peanut extract (WPE). Despite specific IgE and mast cell degranulation, sensitized mice from both strains did not display aversion. They rather preferred drinking WPE as much as control groups. However, after two weeks of WPE exposure as the only source of drinking solution, sensitized Balb/c but not C57BL/6 mice displayed aversion towards WPE during the preference test. At this point, the aversive behavior associated with higher serum levels of MCPT-1 and GDF-15, activation of the amygdala in the brain, as well as inflammation in the intestinal mucosa. Different from egg allergy, in our peanut allergy model food aversion does not happen at the first oral exposure to the allergen, even though mast cells are already equipped with peanut-specific IgE. This points to at least two possibilities: first, WPE ingestion boosts the IgE response, which then becomes strong enough to elicit food aversion; second, other inflammatory stimuli work synergistically with IgE-bound mast cells to drive the late onset of food aversion. Considering the latter, we intend to investigate how other innate immune cells, particularly dendritic cells, orchestrate this food-driven inflammatory response that might favor a late onset of food aversion in this model of peanut allergy.