Prenatal alcohol exposure and childhood atopic disease: A Mendelian randomization approach - 25/12/13
, Clare Rutterford, MSc a, Luisa Zuccolo, PhD b, c, Susan M. Ring, PhD b, George Davey Smith, MD b, c, John W. Holloway, PhD d, A. John Henderson, MD bAbstract |
Background |
Alcohol consumption in western pregnant women is not uncommon and could be a risk factor for childhood atopic disease. However, reported alcohol intake may be unreliable, and associations are likely to be confounded.
Objective |
We aimed to study the relation between prenatal alcohol exposure and atopic phenotypes in a large population-based birth cohort with the use of a Mendelian randomization approach to minimize bias and confounding.
Methods |
In white mothers and children in the Avon Longitudinal Study of Parents and Children (ALSPAC) we first analyzed associations between reported maternal alcohol consumption during pregnancy and atopic outcomes in the offspring measured at 7 years of age (asthma, wheezing, hay fever, eczema, atopy, and total IgE). We then analyzed the relation of maternal alcohol dehydrogenase (ADH)1B genotype (rs1229984) with these outcomes (the A allele is associated with faster metabolism and reduced alcohol consumption and, among drinkers, would be expected to reduce fetal exposure to ethanol).
Results |
After controlling for confounders, reported maternal drinking in late pregnancy was negatively associated with childhood asthma and hay fever (adjusted odds ratio [OR] per category increase in intake: 0.91 [95% CI, 0.82-1.01] and 0.87 [95% CI, 0.78-0.98], respectively). However, maternal ADH1B genotype was not associated with asthma comparing carriers of A allele with persons homozygous for G allele (OR, 0.98 [95% CI, 0.66-1.47]) or hay fever (OR, 1.11 [95% CI, 0.71-1.72]), nor with any other atopic outcome.
Conclusion |
We have found no evidence to suggest that prenatal alcohol exposure increases the risk of asthma or atopy in childhood.
Le texte complet de cet article est disponible en PDF.Key words : Alcohol, ADH1B, Mendelian randomization, prenatal exposure, ALSPAC, pregnancy, birth cohort, asthma, atopy
Abbreviations used : ADH, ALSPAC, GWAS, PCA
Plan
| ☆ | This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
| Supported by the UK Medical Research Council, Wellcome Trust grant 092731, and the University of Bristol who provided core support for ALSPAC. L.Z. was funded by a Medical Research Council Population Health Scientist fellowship (grant G0902144). L.Z. and G.D.S. work in a center that receives funding from the MRC (grant G0600705). |
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| Disclosure of potential conflict of interest: A. J. Henderson has been supported by one or more grants from the UK Medical Research Council and the Wellcome Trust. S. M. Ring has been supported by one or more grants from the UK Medical Research Council (grant 74882) and the Wellcome Trust (grant 076467). L. Zuccolo has been supported by one or more grants from the UK Medical Research Council. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 133 - N° 1
P. 225 - janvier 2014 Retour au numéro
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