The last two decades have seen an increase in the prevalence of asthma, eczema, and allergic rhinitis in developed countries.
This increase has been paralleled by a fall in the consumption of saturated fat and an increase in the amount of polyunsaturated fat in the diet.
This is due to a reduction in the consumption of animal fat and an increase in the use of margarine and vegetable oils containing oméga-6 polyunsaturated fatty acids (PUFAs), such as linoleic acid.
There is also evidence for a decrease in the consumption of oily fish which contain oméga-3 PUFAs, such as eicosapentaenoic acid.
In a number of countries, there are social class and regional differences in the prevalence of allergic disease, which are associated with differences in the consumption of PUFAs.
Linoleic acid is a precursor of arachidonic acid, which can be converted to prostaglandin E2 (PGE2), whereas eicosapentaenoic acid inhibits the formation of PGE2.
PGE2 acts on T-lymphocytes to reduce the formation of interferon-gamma (IFN-gamma) without affecting the formation of interleukin-4 (IL-4).
This may lead to the development of allergic sensitization, since IL-4 promotes the synthesis of immunoglobulin E (IgE), whereas IFN-gamma has the opposite effect.
Changes in the diet may explain the increase in the prevalence of asthma, eczema and allergic rhinitis. (...)
Mots-clés Pascal : Asthme, Allergie, Régime alimentaire, Graisse, Prostaglandine E2, Eczéma, Grande Bretagne, Royaume Uni, Europe, Epidémiologie, Facteur risque, Homme, Appareil respiratoire pathologie, Bronchopneumopathie obstructive, Immunopathologie, Arachidonique acide dérivé, Peau pathologie
Mots-clés Pascal anglais : Asthma, Allergy, Diet, Grease, Prostaglandin E2, Eczema, Great Britain, United Kingdom, Europe, Epidemiology, Risk factor, Human, Respiratory disease, Obstructive pulmonary disease, Immunopathology, Arachidonic acid derivatives, Skin disease
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 97-0155466
Code Inist : 002B06C02. Création : 21/05/1997.