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Folate intake and atopic eczema in Japanese school children

Published online by Cambridge University Press:  06 September 2018

A. Nishide
Affiliation:
International Research Institute of Disaster Science, Tohoku University, Sendai, Japan
H. Matsubara
Affiliation:
Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan
M. Nagai
Affiliation:
Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan
S. Kure
Affiliation:
Tohoku Medical Megabank Organization, Tohoku University, Sendai, Japan Department of Pediatrics, Graduate School of Medicine, Tohoku University, Sendai, Japan
S. Kuriyama
Affiliation:
International Research Institute of Disaster Science, Tohoku University, Sendai, Japan
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Abstract

Type
Abstract
Copyright
Copyright © The Authors 2018 

A previous cross-sectional study has shown a tendency towards a lower risk of atopic eczema with a higher folate intake, and the significant interaction effect between folate intake and MTHFR (C677 T) genotype, which reflects impaired folate metabolism in Danish adults(Reference Husemoen, Toft and Fenger1). However, the other study has reported both dietary folate intake and C677 T genotype were not associated with self-reported atopic eczema in children and their mother in the UK(Reference Granell, Heron and Lewis2). To gain insight into folate intake in the risk of atopic eczema, the aim of this study was to examine association between folate intake and atopic eczema.

We conducted a cross-sectional study involving seven elementary schools in Miyagi prefecture, Japan. Brief self-administered diet history questionnaire (BDHQ)(Reference Sasaki, Yanagibori and Amano3) and International Study of Asthma and Allergies in Childhood (ISAAC)(Reference Haileamlak, Lewis and Britton4) were distributed to the parents of all school Japanese children in first grade to fifth grade aged 6 yr to 11 yr on 29th August, 2017 (n = 1397). Study participants were 403 children whose parents returned the questionnaires (response rate: 28·8%). Of these, we analysed 401 children who were completely answered BDHQ and ISSAC. The exposure variable was the energy-adjusted folate intake assessed using BDHQ which was categorized at quartile points. The presence of atopic eczema was defined as “yes” for the following both question in ISAAC; “Has your child ever had an itchy rash which was coming and going for at least 6 months” and “Has your child had this itchy rash at any time in the last 12 months?”. We used logistic regression analysis to estimate odds ratio (OR) and 95% confidence interval (CI) for prevalence of atopic eczema in quartile of folate intake adjusting for confounders. The lowest quartile category of folate intake was used as a reference category.

Values are odds ratio (OR) and for prevalence of atopic eczema in quartile of folate intake. *Adjustment for age, sex, school (seven categories), Obesity Index: {(real weight – standard weight)/standard weight × 100}(Reference Ikiuo, Hashimoto and Murata5)

Compared with folate intake in the first quartile, its intake in 2nd-4th quartiles had no significant association with a lower prevalence of atopic eczema. No significant linear trend existed (P for trend = 0·202), indicating that the quartiles with higher folate intake did not have less prevalence of atopic eczema. This study has several limitation that we did not actually observe the diet contents and the symptoms, because these data were obtained from self-administered questionnaires. However, these self-administered questionnaires have been used in previous several studies. Secondary, information on C677 T genotype was not available in this study. In conclusion, even though point estimates in 2nd-4th quartiles showed lower than 1st quartile, the results did not show any significant association between amount of folate intake and prevalence of atopic eczema. To determine the association between folate intake and allergic diseases, further studies with consideration of impaired folate metabolism by polymorphism of methylene-tetra-hydro folate reductase C677 T are needed.

References

1.Husemoen, LLN, Toft, U, Fenger, M et al. (2006) Int J Epidemiol 35, 954961.Google Scholar
2.Granell, R, Heron, J, Lewis, S et al. (2008) Clin Expe Allergy 38, 320328.Google Scholar
3.Sasaki, S, Yanagibori, R, Amano, K (1998) JEpidemiol 8, 203215.Google Scholar
4.Haileamlak, A, Lewis, SA, Britton, J et al. (2005) Brit J Dermatol 152, 735741.Google Scholar
5.Ikiuo, K, Hashimoto, R, Murata, Ml (2010) Child Health 69, 613.Google Scholar