RISKS FACTORS FOR FOOD ALLERGY FOR THE LATIN AMERICAN POPULATION. Speaker: Emilia María Hidalgo Castro. Food allergy or Allergic Food Hipersensibility is defined as an adverse immunologic reaction caused by immunologic mechanisms mediated or not by IgE. It is a complex disease influenced by polygenetic heritance and environmental factors. Epidemiologic studies have provided data on a number of emerging thoughts about risk factors of food allergy but information is variable and controversial. Risks factors can be classified on prenatal and postnatal. Prenatal risks factors. 1. Genetic risks. Only a small number of studies have investigated the association between genetic traits and susceptibility to food allergy. a. Specific genes: -the promoter polymorphism 159T/C in the CD14 gene is more common in subjects with food allergy.1 - STAT-6 G allele frequency is increased in nut allergy patients.2 -IL-10 gene polymorphism was associated with food allergy .3 -IL-13 polymorphism was associated with food allergy.4 b. Familial associations: a child has 7 fold increased risk for peanut allergy if he or she has a parent or sibling with peanut allergy. For monozygotic twins, a child has 64% more risk for developing peanut allergy if his or her twin sibling has peanut allergy.5 2. Intrauterine sensitization. In children with at least one allergic parent it has been demonstrated that high IgE levels at birth are associated with food allergy urticaria in the first year of life.6 3. Maternal ingestion: controversy about maternal ingestion of allergen during pregnancy being risk factor.7 Maternal peanut consumption during pregnancy and breast feeding showed a dose-response association with peanut IgE >5 in the infant. Consumption during pregnancy was a significant predictor.8 4. Caesarean birth: among children with allergic mothers a study reported that caesarean section was associated with 7 fold increased risk of parentally perceived reactions to egg, fish and nuts, and 4 fold increased risk of confirmed egg allergy.9 5. Maternal age: children whose mothers are aged 30 and over have increased risk for developing food allergy.10 6. Sex: boys appear to be at higher risk than girls for food allergy. 11 7. Race/ethnicity: racial and ethnic differences have not been explored widely but in the United States of America the National Health and Nutrition Examination Survey study reported that non- Hispanic blacks had increased food allergy (OR 3.1).¹° Postnatal risk factors. 1. Associated atopic disease: family history of atopy and presence of atopic dermatitis are risks factors for the development of both sensitization to food and confirmed food allergy.12 Having atopic dermatitis in infancy is a risk for developing food allergy. Atopic dermatitis in the first 6 months of life has been associated with increased risk for milk, egg and peanut allergies.⁵ 2. Lack of breast feeding: many prospective, observational studies reported that exclusive breast feeding for at least 4-6 months decrease cumulative incidence of cow´s milk allergy until 18 months and atopic dermatitis until 3 years.13 3. Early introduction of solid foods: introduction of complementary foods before 4-6 months of age has been associated with a higher risk of atopic dermatitis14 and food allergy.15 4. Birth weight and gestational age: there appears to be an association between very low birth weight <1000 g and gestational age <28 weeks with food allergy (RR 2.15 and 1.9 respectively). 16 5. Exposure route: lack of ingestion exposure during period of environmental exposure may increase risk.17It is argued that low-doses exposure to environmental food (table tops, hands and dust) penetrates the skin barrier and is taken up by the Langerhan´s cells leading to TH2 response and IgE production. In contrast early high-doses oral consumption leads to TH1 and regulatory cells responses inducing tolerance.⁵ 6. Dietary constituents: a. Reduced consumption of ɯ-3 polyunsaturated fatty acids and increased consumption of ɯ-6 leads to the production of PGE2. PGE2 reduces IFγ production by T lymphocytes, thus resulting in increased production of IgE by B cells. This has been proposed to explain the increase in prevalence of allergic diseases but there few data to support or refute this hypothesis respect to food allergy.⁵ b. Vitamin D: one study report that infants who had vitamin D supplementation had increased risk for food allergy.18 In contrast, other study links the vitamin D deficiency with food allegy. 19 This controversy remains unresolved. 7. Obesity: may be an inflammatory state associated with increased risk for food allergy.20 8. Anti-acid medications: anti-ulcer drugs inhibit peptic digestion and turn harmless food proteins into allergenic molecules, which are able to perform sensitization and to elicit allwergy.21 1 Cochrane S, Beyer K, Clausen M, WjSt M, Hiller R, Nicolleti C, Szepfalusi Z, Savelkoul,H. Breiteneder H, Manios Y,Crittenden, Burney P. Factors influencing the incidence and prevalence of food allergy. Allergy 2009; 64: 1246-55. 2 Amoli MM, Hand S, Hajeer AH, Jones KP, Rolf S, Sting C, et al. Polymorphism inthe STAT6 gene encodes risk for nut allergy. Genes Immun 2002;3:220-4. 3 Campos Alberto EJ, Shimojo N, Suzuki Y, Mashimo Y, Arima T, Matsuura T, et al.IL-10 gene polymorphism, but not TGF-beta1 gene polymorphisms, is associatedwith food allergy in a Japanese population. Pediatr Allergy Immunol 2008; Jan 16 4 Liu X, Beaty TH, Deindl P, Huang SK, Lau S, Sommerfeld C, et al. Associations between specific serum IgE response and 6 variants within the genes IL4, IL13, and IL4RA in German children: the German Multicenter Atopy Study. J Allergy Clin Immunol 2004;113:489-95. 5 Gideon Lack MD.Epidemiologic risks for food allergies. J Allergy Clin Immunol 2008;121:1331-6. 6 Kaan et al. Cord Blood IgE: its determinants and prediction of development of asthma and other allergic disorders at 12 months. Ann Allergy Asthma Immunol 2000;84:37– 42. 7 Muraro et al. Dietary prevention of allergic diseases in infants and small children Part III: Critical review of published prereviewed observational and interventional studies and final recommendations. Pediatr Allergy Immunol 2004: 15: 291–307 8 Sicherer SH, Wood RA, Stablein D, Lindblad R, Burks AW, Liu AH et al. Maternal consumption of peanut during pregnancy is asspciated with peanut sensitization in atopic infants. J Allergy Clin Immunol 2010;126:1191-7. 9 Merete Eggesbo, Grete Botten, Hyein Stigum, Per Nafatad, Per Magnus. Is delivery by cesarean section a risk factor for food allergy? J Allergy Clin Immunol 2003; 112: 420-426 10 Anahita F. Dioun, Sion Kim Harris, Patricia L. Hibberd. Is maternal age at delivery related to childhood food allergy? Pediatric Allergy and Immunology 2003;14: 307–311. 11 Liu AH, Jaramillo R, Sicherer SH, Wood RA, Bock SA, Burks AW, et al. 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J Allergy Clin Immunol Feb 2005;S242. 17 Sicherer SH. Epidemiology of food allergy. J Allergy Clin Immunol 2011;127:594-602. 18 Milner JD, Stein DM, McCarter R, Moon RY. Early infant multivitamin supplementation is associated with increased risk for food allergy and asthma. Pediatrics 2004;114:27-32. 19 Camargo CA, Clark S, Kaplan MS, Lieberman P, Wood RA. Regional differences in EpiPen prescriptions in the United States: the potential role of vitamin D. J Allergy Clin Immunol 2007;120:131-6. 20 Visness CM, London SJ, Daniels JL, Kaufman JS, Yeatts KB, Siega-Riz Al et al. Association of obesity with IgE levels and allergy symptoms in children and adolescents: results from the National Health and Nutrition Examination Survey 2005-2006. J Allergy Clin Immnunol 2009;123: 1163-9. 21 Pali-Schöll I, Jensen-Jarolim E. Anti-acid medication as a risk factor for food allergy. Allergy 2011; 66: 469-477.