Edad intermedia escolar

Páginas: 13 (3175 palabras) Publicado: 22 de noviembre de 2010
Published in Volume 118, Issue 10 (October 1, 2008)
J Clin Invest. 2008;118(10):3265–3268. doi:10.1172/JCI37171.
Copyright © 2008, American Society for Clinical Investigation
Citations reported by Scopus (9)
Prenatal maternal diet affects asthma risk in offspring
Rachel L. Miller
Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College ofPhysicians and Surgeons, New York, New York, USA.
Address correspondence to: Rachel. L. Miller, Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, PH8E, 630 W. 168th Street, New York, New York 10032, USA. Phone: (212) 305-7759; Fax: (212) 305-2277; E-mail: rlm14@columbia.edu.
First published September 18, 2008
Recently,epigenetic-mediated mechanisms — which involve heritable changes in gene expression in the absence of alterations in DNA sequences — have been proposed as contributing to asthma. In this issue of the JCI, Hollingsworth and colleagues report on the effect of prenatal maternal dietary intake of methyl donors on the risk of allergic airway disease in offspring in mice and show that these effects involveepigenetic regulation (see the related article beginning on page 3462). Supplementation of the maternal diet with methyl donors was associated with greater airway allergic inflammation and IgE production in F1 and, to some extent, F2 progeny. Site-specific differences in DNA methylation and reduced transcriptional activity were detected. If these findings are confirmed, a new paradigm for asthmapathogenesis may be emerging.
See the related article beginning on page 3462.
More and more, it seems that our traditional view of asthma as a complex disease that is mediated by a genetic predisposition and childhood or later environmental exposures needs updating. At this point, a mounting body of literature has established that prenatal exposures can influence the risk for developing asthma (1).This link has been most firmly documented in epidemiological studies of prenatal exposure to cigarette smoke and subsequent wheeze. For example, in a large prospective Danish cohort study of over 11,000 children, maternal smoking at the 36th week of gestation was associated with transient wheezing in children before age 3 years (2). In a Stockholm cohort of over 4,000 newborns, maternal smokingduring but not following pregnancy was associated with an increased risk of recurrent wheezing in offspring up to age two years (3). In mouse models, exposure during pregnancy to an air pollutant aerosol (residual oil fly ash) led to a greater susceptibility to an asthma-like phenotype in the offspring mice (4).
Prenatal diet and atopy risk
The relationship between a mother’s diet duringpregnancy and the child’s subsequent risk of developing asthma or atopy has become a topic of growing investigation. Reduced maternal intake of vitamin E, vitamin D, and zinc during pregnancy all have been associated with a greater risk of development of asthma and wheezing symptoms in 5-year-old children (5, 6). Most recently, Chatzi and colleagues found that adherence to a Mediterranean diet duringpregnancy was associated with protection from persistent wheeze and atopy in children (7). Frequent maternal intake of fish during pregnancy also reduced the risk of food and possibly inhalant allergic sensitizations (8). Daily consumption of nut products during pregnancy has been associated with asthma in the child by age 8 years (9). However, in a recent meta-analysis of four clinical studies,avoidance of specific food antigens during pregnancy did not appear to influence the risk of development of atopic disease in the child (10). Combined, these studies suggest that the prenatal diet can alter the intrauterine environment in complex and possibly inconsistent ways.
So how does this happen? Epigenetic regulation
Current hypotheses tend to consider either immune-mediated or...
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