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Volume 122, Issue 1, Pages 49-54.e3 (July 2008)


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Prospective study of breast-feeding in relation to wheeze, atopy, and bronchial hyperresponsiveness in the Avon Longitudinal Study of Parents and Children (ALSPAC)

Leslie Elliott, MPH, PhDa, John Henderson, MDcd, Kate Northstone, MScc, Grace Y. Chiu, PhDe, David Dunson, PhDb, Stephanie J. London, MD, DrPHaCorresponding Author Informationemail address

Received 10 January 2008; received in revised form 31 March 2008; accepted 2 April 2008. published online 12 May 2008.

Background

Breast-feeding clearly protects against early wheezing, but recent data suggest that it might increase later risk of atopic disease and asthma.

Objective

We sought to examine the relationship between breast-feeding and later asthma and allergy outcomes by using data from the Avon Longitudinal Study of Parents and Children, a large birth cohort in the United Kingdom.

Methods

We used adjusted logistic regression models to evaluate the association between breast-feeding and atopy at age 7 years, bronchial responsiveness to methacholine at age 8 years, and wheeze at ages 3 and 7½ years. Bayesian methods were used to assess the possibility of bias caused by an influence of early wheezing on the duration of breast-feeding, as well as selection bias.

Results

Breast-feeding was protective for wheeze in the first 3 years of life (odds ratio [OR] of 0.80 [95% CI, 0.70-0.90] for ≥6 months relative to never) but not wheeze (OR, 0.98; 95% CI, 0.79-1.22), atopy (OR, 1.12; 95% CI, 0.92-1.35), or bronchial hyperresponsiveness (OR, 1.07; 95% CI, 0.82-1.40) at ages 7 to 8 years. Bayesian models adjusting for the longer duration of breast-feeding among children with wheezing in early infancy produced virtually identical results.

Conclusions

We did not find consistent evidence for either a deleterious effect or a protective effect of breast-feeding on later risk of allergic disease in a large prospective birth cohort of children with objective outcome measures and extensive data on potential confounders and effect modifiers. Neither reverse causation nor loss to follow-up appears to have materially biased our results.

a Epidemiology Branch, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC

b Biostatistics Branch, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC

c Department of Social Medicine, University of Bristol, Bristol, United Kingdom

d Department of Respiratory Medicine, Bristol Royal Hospital for Children, Bristol, United Kingdom

e Westat, Inc, Research Triangle Park, NC

Corresponding Author InformationReprint requests: Stephanie J. London, MD, DrPH, NIEHS, PO Box 12233, MD A3-05, Research Triangle Park, NC 27709.

 The UK Medical Research Council, the Wellcome Trust, and the University of Bristol provide core support for ALSPAC. The analysis was supported by the Division of Intramural Research, National Institute of Environmental Health Sciences, USA.

 Disclosure of potential conflict of interest: The authors have declared that they have no conflict of interest.

PII: S0091-6749(08)00618-0

doi:10.1016/j.jaci.2008.04.001


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