Are the dangers of childhood food allergy exaggerated?
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ABSTRACT:
SUBMITTER: Colver A
PROVIDER: S-EPMC1557974 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Background:The role of infant feeding for food allergy in children is unclear and studies have not addressed simultaneous exposures to different foods. The goal of this study was to analyze existing data on feeding practices that represent realistic exposure and assess the risk of food allergy symptoms and food allergy in children. Methods:The Infant Feeding Practices Study II conducted by the CDC and US-FDA enrolled pregnant women and collected infant feeding information using nine repeated surveys. Participants were re-contacted after 6 years. Food allergy data were collected at 4, 9, 12, and 72?months. In total, 1387 participants had complete infant feeding pattern data for 6 months and information on food allergy symptoms and doctors' diagnosed food allergy. Feeding patterns constituted six groups: 3-months of feeding at breast followed by mixed feeding, 3-months of breast milk and bottled milk followed by mixed feeding, 1-month of feeding at breast followed by mixed feeding, 6-months of mixed feeding i.e., concurrent feeding of breast milk, bottled milk and formula, 2-3?months of formula followed by formula and solid food, and formula and solid food since the first month. To estimate risks of food allergy, we used linear mixed models, controlling for potential confounders. Results:Of the 328 children with food allergy symptoms in infancy and at 6 years, 52 had persistent symptoms from infancy. Children exposed to mixed feeding had a higher risk of food allergy symptoms (Risk Ratio [RR] 1.54; 95% Confidence Interval [CI] 1.04, 2.29) compared to 3-months of feeding at breast adjusted for confounding. No statistically significant risk of infant feeding patterns was found for doctors' diagnosed food allergy. Paternal allergy posed a higher risk for food allergy symptoms (RR 1.36; 95% CI 1.01, 1.83). Prenatal maternal smoking increased the risk for doctors' diagnosed food allergy (RR 2.97; 95% CI 1.53, 5.79). Conclusions:Analysis of this prospective birth cohort suggest that introduction of multiple feeding source may lead to food allergy symptoms. Future efforts are needed to determine acceptable approaches to improve the ascertainment of food allergy in children and the role of infant feeding.
| S-EPMC6813109 | biostudies-literature
Project description:BackgroundChildhood food allergy and asthma rates are increasing. The hygiene hypothesis has been proposed as an explanation for the increased incidence of allergic disease.ObjectiveTo describe the association of childhood food allergy and asthma with hygiene factors, such as the number of siblings, antibiotic use, infection history, pet exposure, child care exposure, and maternalchild factors.MethodsChildren ages 021 years old (N = 1359) were recruited for a cross-sectional family-based study, including children with food allergy and children without food allergy, and their siblings. We assessed the associations between childhood food allergy and asthma with hygiene factors.ResultsOf the 1359 children, 832 (61.2%) had food allergy, and 406 (30%) had asthma. In the adjusted analysis, the prevalence of food allergy was increased if there was a history of skin infection (prevalence ratio [RRR] 1.12 [95% confidence interval {CI}, 1.011.24]) or eczema (RRR 1.89 [95% CI, 1.702.10]). The prevalence of asthma was increased with a history of respiratory syncytial virus infection (RRR 1.60 [95% CI, 1.341.90]) or eczema (RRR 1.54 [95% CI, 1.271.86]). A greater number of siblings were associated with a decreased prevalence of food allergy (RRR 0.79 [95% CI, 0.750.84]) and asthma (RRR 0.82 [95% CI, 0.740.91]).ConclusionOur findings supported the accumulating evidence of an association between skin infections and eczema with food allergy. Because these results could be subject to recall bias, additional prospective studies are needed to substantiate these findings.
| S-EPMC5080537 | biostudies-literature
Project description:The development of food allergy has been reported to be related with the changes in the gut microbiome, however the specific microbe associated with the pathogenesis of food allergy remains elusive. This study aimed to comprehensively characterize the gut microbiome and identify individual or group gut microbes relating to food-allergy using 16S rRNA gene sequencing with network analysis. Faecal samples were collected from children with IgE-mediated food allergies (n = 33) and without food allergy (n = 27). Gut microbiome was profiled by 16S rRNA gene sequencing. OTUs obtained from 16S rRNA gene sequencing were then used to construct a co-abundance network using Weighted Gene Co-expression Network Analysis (WGCNA) and mapped onto Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. We identified a co-abundance network module to be positively correlated with IgE-mediated food allergy and this module was characterized by a hub taxon, namely Ruminococcaceae UCG-002 (phylum Firmicutes). Functional pathway analysis of all the gut microbiome showed enrichment of methane metabolism and glycerolipid metabolism in the gut microbiome of food-allergic children and enrichment of ubiquinone and other terpenoid-quinone biosynthesis in the gut microbiome of non-food allergic children. We concluded that Ruminococcaceae UCG-002 may play determinant roles in gut microbial community structure and function leading to the development of IgE-mediated food allergy.
| S-EPMC7923212 | biostudies-literature
Project description:Food allergies affect up to 6% of young children and 3%-4% of adults. They encompass a range of disorders that may be IgE and/or non-IgE mediated, including anaphylaxis, pollen food syndrome, food-protein-induced enterocolitis syndrome, food-induced proctocolitis, eosinophilic gastroenteropathies, and atopic dermatitis. Many complex host factors and properties of foods are involved in the development of food allergy. With recent advances in the understanding of how these factors interact, the development of several novel diagnostic and therapeutic strategies is underway and showing promise.
| S-EPMC3049383 | biostudies-other
Project description:BackgroundImmunoglobulin E-mediated food allergy (FA) affects children and adults with variable age of onset. Phenotype and quality of life (QoL) differences between childhood-onset FA (COFA) and adult-onset FA (AOFA) are not known.ObjectiveTo identify phenotypic and QoL differences between AOFA and COFA.MethodsA cross-sectional study of adults (≥18 years old) seen at Northwestern Memorial HealthCare clinics between 2002 and 2017 with an International Classification of Diseases ninth and tenth revision diagnosis of FA. Subjects completed a FA history survey and a FA QoL questionnaire. FA characteristics and QoL scores were compared between groups.ResultsAmong 294 consented subjects, 202 had a clinical history consistent with labeled immunoglobulin E-mediated FA. The onset of FA symptoms occurred before age 18 years (COFA) in 80 subjects and after age 18 years in 122 (AOFA) subjects. Shellfish reactions were most common in AOFA-labeled subjects (28%), whereas tree nut reactions were the most common in COFA-labeled subjects (55%) compared with other triggers. Hives (68% vs 52%, P = .03), facial swelling (69% vs 50%, P = .009), wheezing (56% vs 29%, P < .001), and vomiting (41% vs 22%, P = .005) were more often observed in COFA compared with AOFA. Total QoL was significantly reduced in COFA compared with AOFA (3.6 vs 3.0, P = .003) along with specific domains related to the following: allergen avoidance and dietary restriction (3.7 vs 3.1, P = .006), emotional impact (3.9 vs 3.2, P = .003), and risk of accidental exposure (3.6 vs 2.8, P = .001).ConclusionThere are differences in specific food triggers and symptoms in adult-onset and childhood-onset labeled FA. Adults labeled with childhood-onset FA have reduced QoL.
| S-EPMC8483056 | biostudies-literature
Project description: Not available
| S-EPMC6433125 | biostudies-literature
Project description:BackgroundAlterations in the intestinal microbiome are prospectively associated with the development of asthma; less is known regarding the role of microbiome alterations in food allergy development.MethodsIntestinal microbiome samples were collected at age 3-6 months in children participating in the follow-up phase of an interventional trial of high-dose vitamin D given during pregnancy. At age 3, sensitization to foods (milk, egg, peanut, soy, wheat, walnut) was assessed. Food allergy was defined as caretaker report of healthcare provider-diagnosed allergy to the above foods prior to age 3 with evidence of IgE sensitization. Analysis was performed using Phyloseq and DESeq2; P-values were adjusted for multiple comparisons.ResultsComplete data were available for 225 children; there were 87 cases of food sensitization and 14 cases of food allergy. Microbial diversity measures did not differ between food sensitization and food allergy cases and controls. The genera Haemophilus (log2 fold change -2.15, P=.003), Dialister (log2 fold change -2.22, P=.009), Dorea (log2 fold change -1.65, P=.02), and Clostridium (log2 fold change -1.47, P=.002) were underrepresented among subjects with food sensitization. The genera Citrobacter (log2 fold change -3.41, P=.03), Oscillospira (log2 fold change -2.80, P=.03), Lactococcus (log2 fold change -3.19, P=.05), and Dorea (log2 fold change -3.00, P=.05) were underrepresented among subjects with food allergy.ConclusionsThe temporal association between bacterial colonization and food sensitization and allergy suggests that the microbiome may have a causal role in the development of food allergy. Our findings have therapeutic implications for the prevention and treatment of food allergy.
| S-EPMC5921051 | biostudies-literature
Project description:Food allergy poses a significant clinical and public health burden affecting 2-10% of infants. Using integrated DNA methylation and transcriptomic profiling, we found that polyclonal activation of naive CD4+ T cells through the T cell receptor results in poorer lymphoproliferative responses in children with immunoglobulin E (IgE)-mediated food allergy. Reduced expression of cell cycle-related targets of the E2F and MYC transcription factor networks, and remodeling of DNA methylation at metabolic (RPTOR, PIK3D, MAPK1, FOXO1) and inflammatory genes (IL1R, IL18RAP, CD82) underpins this suboptimal response. Infants who fail to resolve food allergy in later childhood exhibit cumulative increases in epigenetic disruption at T cell activation genes and poorer lymphoproliferative responses compared to children who resolved food allergy. Our data indicate epigenetic dysregulation in the early stages of signal transduction through the T cell receptor complex, and likely reflects pathways modified by gene-environment interactions in food allergy.
| S-EPMC6098117 | biostudies-literature
Project description:Food allergy in children is increasing and the perception of food allergy among parents is even more common. In a questionnaire-based study of 702 children aged 6 to 48 months in four primary care settings, the aim was to determine the prevalence of perception vs. proven food allergy, parental anxiety and general pediatrician knowledge of food allergy. In 95/702 children (13.5%) parentally-reported food was associated reactions. IgE and/or skin prick test (SPT) and/or an open provocation test were performed in 48 (6.8%) and allergy was proven in 38 (5.4%) children. Discrepancy between parental perception and proven allergy is significant (p < 0.001), especially for food other than milk, egg and peanut (p < 0.001). Allergy to milk was the most common. Allergy to peanut was significantly more common in children ?2 years (p < 0.05). Severe reactions occurred in 5/95 (5.2%) of all children and in 5/38 (13.1%) of allergic children, in 3/5 caused by peanut. Parents of children with proven allergy do not experience high degree of anxiety. The perception of food allergy among general pediatricians is limited, and in children with severe reactions precautionary measures and information to parents were insufficient. Parents and general pediatricians need additional education in food allergy.
| S-EPMC4928769 | biostudies-literature
Project description:BackgroundFilaggrin is an epidermal protein that has a role in skin barrier function. Filaggrin loss-of-function (FLG-LOF) mutations are a significant risk factor for eczema and atopy, but their association with food allergy (FA) is less clear.ObjectiveWe explored the longitudinal relationship between 3 common FLG-LOF mutations and FA using the Isle of Wight birth cohort.MethodsFA diagnosis was based on recognized allergic reactions within 4 hours after exposure to known food allergens. Food allergen sensitization (FAS) was identified by using skin prick tests conducted between 1 and 18 years of age to a range of food allergens. Three FLG mutations were genotyped in 1150 (79%) of 1456 children. The temporal relationships between FA, FAS, and eczema in children with FLG mutations were explored by using path analysis with total, direct, and indirect effect models.ResultsThere was a significant total effect of FLG-LOF mutations on the risk of FA in later childhood at the ages of 10 (odds ratio, 31.46; 95% CI, 2.86 to >100) and 18 (odds ratio, 4.25; 95% CI, 1.55-11.61) years. Path analysis showed that there was no direct effect of FLG-LOF mutations on FA at any age; however, an indirect effect was found on FA at all ages through eczema and FAS in the earlier years.ConclusionFLG-LOF mutations are associated with FA in older children through eczema and FAS during early childhood. Our results highlight a biologically plausible pathway, which suggests that skin barrier function is important in the development and persistence of FA.
| S-EPMC4186905 | biostudies-literature