Allergic asthma and rhinitis, atopic dermatitis (AD), urticaria and gastrointestinal allergy, are common diseases of infants and children. It was recently estimated that 14% of children suffer from AD, 8% from food allergy, and 12% from asthma (1, 2). The cumulated incidence of these diseases in adolescents has been estimated between 25-35%, while the prevalence is about 20% (3). The phenotypic expression of these illnesses varies extensively, being very mild in some cases, severe in many, and even life threatening in others. Specific IgE antibodies to foods and positive challenge tests to a number of food allergens are frequently present in children with these disorders. Cow's milk (CM) appears to be the most common offending food both in
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Therefore interest has been focused on methods for the prediction and prevention of atopy (5-9). Prevention of IgE-mediated diseases relies on the skill necessary to overcome the natural forces unceasingly working to sensitize humans to produce IgE antibodies. The phenotypic expression of allergic disease ensues from an elaborate interrelationship between the atopy-prone genetic constitution of a child and the experienced environment that surrounds it. Prevention of atopy could potentially be met by selectively interfering with the genetic and environmental factors that appear to be responsible in concert for the final phenotypic expression of atopy.
Human milk has been for centuries the only way of feeding human neonates. Since the beginning of this century CM formulas have become a common breast milk substitute when mother's milk was not available. During this century and especially in the last decade other formulas have been developed in order to reduce the antigen load and therefore the risk of sensitization.
In this paper we will briefly summarize recent data on the environmental factors triggering atopy. In addition, we will report recent knowledge on atopy prevention, also reviewing the so-called hypoallergenic
Therefore interest has been focused on methods for the prediction and prevention of atopy (5-9). Prevention of IgE-mediated diseases relies on the skill necessary to overcome the natural forces unceasingly working to sensitize humans to produce IgE antibodies. The phenotypic expression of allergic disease ensues from an elaborate interrelationship between the atopy-prone genetic constitution of a child and the experienced environment that surrounds it. Prevention of atopy could potentially be met by selectively interfering with the genetic and environmental factors that appear to be responsible in concert for the final phenotypic expression of atopy.
Human milk has been for centuries the only way of feeding human neonates. Since the beginning of this century CM formulas have become a common breast milk substitute when mother's milk was not available. During this century and especially in the last decade other formulas have been developed in order to reduce the antigen load and therefore the risk of sensitization.
In this paper we will briefly summarize recent data on the environmental factors triggering atopy. In addition, we will report recent knowledge on atopy prevention, also reviewing the so-called hypoallergenic