Article

Fruit and vegetable consumption in relation to allergy: disease-related modification of consumption? J Allergy Clin Immunol

Unit of Environmental Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
The Journal of allergy and clinical immunology (Impact Factor: 11.48). 05/2011; 127(5):1219-25. DOI: 10.1016/j.jaci.2010.11.019
Source: PubMed

ABSTRACT

Previous largely cross-sectional studies suggest that fruit and vegetable consumption reduces the risk of allergic disease in children, but results are conflicting.
To investigate the association between current fruit or vegetable intake and allergic disease in 8-year-old Swedish children, and to evaluate the potential effect of disease-related modification of consumption.
Cross-sectional data were obtained from a Swedish birth cohort study. Information on fruit and vegetable consumption as well as symptoms and diagnoses of allergic diseases was obtained by parental questionnaires at the 8-year follow-up. Allergen-specific IgE levels against food and inhalant allergens were obtained from blood samples collected at age 8 years. In total, 2447 children were included. Data were analyzed with logistic regression.
An inverse relation was observed between total fruit consumption and rhinitis (odds ratio, highest vs lowest quartile, 0.62; 95% CI, 0.45-0.86; P for trend, .002), whereas no association was observed for total vegetable intake. In analyses of individual foods, intake of apples/pears and carrots was inversely associated with rhinitis, asthma, and atopic sensitization. Fifty percent of the children with rhinitis were sensitized against birch pollen, which may cross-react with apples and carrots. After exclusion of children who reported food-related allergic symptoms, most of the observed inverse associations moved toward the null and became nonsignificant.
We confirm the inverse associations between fruit intake and allergic disease in children observed in earlier studies. However, our data also indicate that disease-related modification of consumption contributed to this association.

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    • "A healthy eating pattern was identified as being protective against the development of food allergy with the possible mechanism being the immunomodulatory effect of nutrients found in fruit and vegetables which were a feature of the observed healthy eating pattern along with a predominantly home-cooked diet[13]. Fruit and vegetables are good sources of vitamin C, betacarotenes , folate and oligo-saccharides all of which have been shown to have immunomodulatory actions323334. Also, home processed foods may have a higher microbial load than commercially prepared foods[35]and this may offer protection from the development of allergic disease as suggested by the " Hygiene Hypothesis "[36]. "
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    ABSTRACT: Background: The prevalence of food hypersensitivity in the UK is still largely open to debate. Additionally its pathogenesis is also unclear although it is known that there are differing phenotypes. Determining its prevalence, along with identifying those factors associated with its development will help to assess its clinical importance within the national setting and also add to the debate on appropriate prevention strategies. Methods: A population based birth cohort study conducted in Hampshire, UK as part of the EuroPrevall birth cohort study. 1140 infants were recruited with 823 being followed up until 2 years of age. Infants with suspected food reactions were assessed including specific IgE measurement and skin prick testing. Diagnosis of food hypersensitivity was by positive double-blind, placebo-controlled food challenge (DBPCFC) where symptoms up to 48 h after the end of the food challenge were considered indicative of a food hypersensitivity. Factors associated with food hypersensitivity and its two phenotypes of IgE-mediated and non-IgE-mediated disease were modelled in a multivariable logistic regression analysis. Results: Cumulative incidence of food hypersensitivity by 2 years of age was 5.0 %. The cumulative incidence for individual food allergens were hens' egg 2.7 % (1.6-3.8); cows' milk 2.4 % (1.4-3.5); peanut 0.7 % (0.1-1.3); soy 0.4 % (0.0-0.8); wheat 0.2 % (0.0-0.5) and 0.1 % (0.0-0.32) for fish. The cumulative incidence of IgE-mediated food allergy was 2.6 % with 2.1 % reacting to hens' egg. For non-IgE-mediated food allergy the cumulative incidence was 2.4 % (cows' milk 1.7 %). Predictors for any food hypersensitivity were wheeze, maternal atopy, increasing gestational age, age at first solid food introduction and mean healthy dietary pattern score. Predictors for IgE mediated allergy were eczema, rhinitis and healthy dietary pattern score whereas for non-IgE-mediated food allergy the predictors were dog in the home, healthy dietary pattern score, maternal consumption of probiotics during breastfeeding and age at first solid food introduction. Conclusions: Just under half the infants with confirmed food hypersensitivity had no demonstrable IgE. In an exploratory analysis, risk factors for this phenotype of food hypersensitivity differed from those for IgE-mediated food allergy except for a healthy infant diet which was associated with less risk for both phenotypes.
    Full-text · Article · Dec 2015
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    • "Also, total energy intake was not assessed, and this could contribute to potential confounding in analyses. Reverse causality is also a possibility [50], such that those diagnosed with AS/HF might purposefully eat more fruits and vegetables in efforts to bolster health and control symptoms or attacks. Lastly, there are a number of fruits and vegetables that are high in histamine or other biogenic amines, and histamine intolerance may play a role in the observed relationship with fruits and vegetables. "
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    ABSTRACT: Background There is abundant research relevant to genetic and environmental influences on asthma and hayfever, but little is known about dietary risk factors in Australian adults. This study’s purpose was to identify dietary factors associated with lifetime asthma (AS) and asthma or hayfever (AS/HF) diagnosis in Australian middle-aged and older adults. Methods From The 45 and Up Study baseline self-report data, this study included 156,035 adult men and women. Participants were sampled from the general population of New South Wales, Australia in 2006–2009. About 12% of participants reported ever receiving an AS diagnosis (men 10%; women 14%) and 23% reported AS/HF diagnosis (men 19%; women 26%). Following principle components factor analysis, dietary items loaded onto one of four factors for men (meats/cheese; fruits/vegetables; poultry/seafood; grains/alcohol) or five factors for women (meats; fruits/vegetables; poultry/seafood; cereal/alcohol; brown bread/cheese). Logistic regression was used to analyze the associations between dietary factors and AS or AS/HF diagnosis. Results For men, the meats/cheese factor was positively associated with AS (AOR = adjusted odds ratio for highest versus lowest quintile = 1.18, 95%CI = 1.08, 1.28; Ptrend = 0.001) and AS/HF (AOR for highest versus lowest quintile = 1.22, 95%CI = 1.14, 1.29; Ptrend < 0.001). Poultry/seafood was also associated with AS/HF in men (AOR for highest versus lowest quintile = 1.11, 95%CI = 1.04, 1.17; Ptrend = 0.002). For women, significant risk factors for AS/HF included meats (AOR for highest versus lowest quintile = 1.25, 95%CI = 1.19, 1.31; Ptrend = 0.001), poultry/seafood (AOR for highest versus lowest quintile = 1.06, 95%CI = 1.01, 1.12; Ptrend = 0.016), and fruits/vegetables (AOR for highest versus lowest quintile = 1.07, 95%CI = 1.02, 1.12; Ptrend = 0.011). In contrast, the cheese/brown bread dietary factor was protective against AS in women (AOR for highest versus lowest quintile = 0.88, 95%CI = 0.82, 0.94; Ptrend < 0.001). Conclusions Generally, diets marked by greater intakes of meats, poultry, and seafood were associated with diagnosed AS and AS/HF. Taken together, these findings suggest that adherence to a more meat-based diet may pose risk for AS and AS/HF in Australian adults.
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    No preview · Article · Dec 2012 · The Journal of allergy and clinical immunology
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