The incidence of allergic diseases is increasing concomitantly with improvements in living standards and the adoption of a western lifestyle. Although the reduced exposure to microbial products is one possible cause, recent evidence indicates diet as a key factor influencing the development of allergic diseases.
Epidemiological studies indicate a crucial role of both maternal and early childhood food exposure in the development of allergic diseases, with the inclusion of food allergens in maternal and early childhood diet possibly being beneficial for the prevention of allergy and asthma.
Animal models show that the transfer of allergens, immune complexes and immunosuppressive cytokines to the suckling baby through breast milk enables the generation of regulatory T cells in neonates, which can protect them from later developing allergies.
Obesity exacerbates early-onset (allergic) asthma, but can also induce asthma in adults. Immune responses that are associated with the development of allergy are influenced by factors produced by adipose tissue and hence could be differentially affected in lean and obese individuals.
Several classes of dietary components affect the development and homeostasis of the immune system by preventing or potentiating the development of allergy. The complex mechanisms of action of these dietary components involve specific receptors.
Although the anti-inflammatory effects of omega-3 polyunsaturated fatty acids are well established, their precise role in the development of allergy requires further investigation to understand their potential role in a 'prophylactic diet'.
Clinical studies indicate that diet supplementation with fibre, vitamin A and/or vitamin D during the perinatal period has beneficial effects in terms of preventing allergic diseases.
The incidence of allergic diseases is increasing, both in developed and developing countries, concomitantly with the rise in living standards and the adoption of a 'western lifestyle'. For two decades, the hygiene hypothesis — which proposes that the lack of early childhood exposure to infectious agents increases susceptibility to allergic diseases in later life — provided the conceptual framework for unravelling the mechanisms that could account for the increased incidence of allergic diseases. In this Review, we discuss recent evidence that highlights the role of diet as a key factor influencing immune homeostasis and the development of allergic diseases through a complex interplay between nutrients, their metabolites and immune cell populations. Although further investigations are still required to understand these complex relationships, recent data have established a possible connection between metabolic homeostasis and allergic diseases.
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The authors thank B. Staels (Lille, France) for critical reading of the manuscript and F. Aguila (Nice, France) for help with the figures. They sincerely apologize to all of their colleagues whose important work could not be cited owing to space constraints. Work related to this review is funded in part by Fondation pour la Recherche Médicale (to V.J. and D.D.); European Genomic Institute for Diabetes (EGID) grant ANR-10-LABX-46 (to D.D.); Region Nord-Pas-de-Calais (to D.D.), and National Health and Medical Research Council grant APP1068890 (to L.M.).
The authors declare no competing financial interests.
- Allergic diseases
Diseases caused by an inappropriate initiation of type 2 immune responses to innocuous environmental antigens that result in several conditions, including asthma, allergic rhinitis, food allergy and atopic dermatitis.
A respiratory disorder that is characterized by reversible expiratory airflow limitation or bronchial hyperresponsiveness, and has various clinical, biological and therapeutic characteristics.
Recognized as the main source of active and passive immunity in early life. Breast milk contains antibodies that react with infectious agents present in the mother's environment, and confers passive immunity to the breastfed child against infectious agents that the child is likely to encounter shortly after birth.
- Oral tolerance
An immune state induced by the oral administration of innocuous antigens (such as food proteins) that leads to local and systemic unresponsiveness.
- G protein-coupled receptors
(GPCRs). A large family of receptors that have seven transmembrane domains and are implicated in various signal transduction pathways and cellular responses.
Defined by a body mass index of the 95th percentile or above for age and sex standards.
- Polyunsaturated fatty acid
(PUFA). An unsaturated fatty acid with a carbon chain that has more than one double bond per molecule.
- Mediterranean diet
A diet based on a high consumption of olive oil, fish and vegetables.
- Vitamin A
A vitamin that is oxidized into retinal, which in turn is converted into retinoic acid (RA). Oxidation to retinal is mediated by alcohol dehydrogenases (ADHs) or retinol dehydrogenases (RDHs) and then by retinal dehydrogenases (RALDHs; also known as aldehyde dehydrogenases (ALDHs)), producing all-trans-RA and 9-cis-RA.
- Immune complexes
Complexes of antigen bound to antibody and, sometimes, to components of the complement system. The levels of immune complexes are increased in many autoimmune disorders, in which they become deposited in tissues and cause tissue damage.
Contained in oils and fats, triglycerides give rise to free fatty acids after their breakdown by pancreatic lipases. Dietary fats are dissolved in micelles by bile salts in the upper part of the gastrointestinal tract and are subsequently taken up by enterocytes.
- White adipose tissue
A type of adipose tissue that specializes in energy storage and is most commonly found in subcutaneous and visceral adipose tissues.
Cytokines that are secreted by adipocytes.
- Peroxisome proliferator-activated receptors
(PPARs). Nuclear receptors that are activated by many ligands, including food-derived saturated fatty acids, and that function as transcription factors to regulate the expression of genes that are involved in both metabolism and immune functions.
Modification of the commensal (gut) bacterial flora.
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Julia, V., Macia, L. & Dombrowicz, D. The impact of diet on asthma and allergic diseases. Nat Rev Immunol 15, 308–322 (2015). https://doi.org/10.1038/nri3830
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