Prenatal alcohol exposure and childhood atopic disease: a Mendelian randomization approach
Prenatal alcohol exposure and childhood atopic disease: a Mendelian randomization approach
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.
alcohol, ADH1B, mendelian randomization, prenatal exposure, ALSPAC, pregnancy, birth cohort, asthma, atopy
225-232
Shaheen, Seif O.
42e3b3fc-c70c-49e7-8c88-64f2606129ec
Rutterford, Clare
68cae3d5-c98b-4c9f-88a1-1d28866913ea
Zuccolo, Luisa
3d2280df-ab79-4f2e-9b47-4f801e56298d
Ring, Susan M.
55bebe97-d035-43f3-84a6-b57c5ea4c6be
Davey Smith, George
0de6af8f-976a-477d-a944-a98d0c8c1ebb
Holloway, John W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Henderson, A. John
2053b8a0-1b2d-41f6-8b3f-1cf360c88c21
January 2014
Shaheen, Seif O.
42e3b3fc-c70c-49e7-8c88-64f2606129ec
Rutterford, Clare
68cae3d5-c98b-4c9f-88a1-1d28866913ea
Zuccolo, Luisa
3d2280df-ab79-4f2e-9b47-4f801e56298d
Ring, Susan M.
55bebe97-d035-43f3-84a6-b57c5ea4c6be
Davey Smith, George
0de6af8f-976a-477d-a944-a98d0c8c1ebb
Holloway, John W.
4bbd77e6-c095-445d-a36b-a50a72f6fe1a
Henderson, A. John
2053b8a0-1b2d-41f6-8b3f-1cf360c88c21
Shaheen, Seif O., Rutterford, Clare, Zuccolo, Luisa, Ring, Susan M., Davey Smith, George, Holloway, John W. and Henderson, A. John
(2014)
Prenatal alcohol exposure and childhood atopic disease: a Mendelian randomization approach.
Journal of Allergy and Clinical Immunology, 133 (1), .
(doi:10.1016/j.jaci.2013.04.051).
(PMID:23806636)
Abstract
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.
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j.jaci.2013.04.051.pdf
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More information
Accepted/In Press date: 24 April 2013
e-pub ahead of print date: 24 June 2013
Published date: January 2014
Keywords:
alcohol, ADH1B, mendelian randomization, prenatal exposure, ALSPAC, pregnancy, birth cohort, asthma, atopy
Organisations:
Human Development & Health
Identifiers
Local EPrints ID: 354128
URI: http://eprints.soton.ac.uk/id/eprint/354128
ISSN: 0091-6749
PURE UUID: 97d74c6e-7813-43f3-bf4e-3bd57a28a90a
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Date deposited: 02 Jul 2013 08:43
Last modified: 15 Mar 2024 02:56
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Contributors
Author:
Seif O. Shaheen
Author:
Clare Rutterford
Author:
Luisa Zuccolo
Author:
Susan M. Ring
Author:
George Davey Smith
Author:
A. John Henderson
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