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  Vol. 283 No. 3, January 19, 2000 TABLE OF CONTENTS
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Protection Against Atopic Diseases by Measles—A Rash Conclusion?

James E. Gern, MD; Scott T. Weiss, MD, MS

JAMA. 2000;283:394-395.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

A major question facing modern medicine is why atopic diseases such as asthma, allergic rhinitis, and atopic dermatitis, which have in common the overproduction of allergen-specific or total IgE, are increasing in prevalence. Atopic diseases are influenced by genetic predisposition and environmental exposures. However, since the spontaneous genetic mutation rate is quite slow, it is clear that changes in the environment are responsible for the increased prevalence of atopic diseases. But which environmental factor(s) is the culprit?

Many theories, based on epidemiologic or experimental data, have been advanced, including improved hygiene1-2; changes in diet3-4; changes in intestinal flora due to increased use of antibiotics5 and altered patterns of infant feeding6; greater exposure to allergens7; obesity and reduced physical activity8; and changes in the prenatal environment.9 One interesting theory is that the reduction of early childhood infectious . . . [Full Text of this Article]

Author Affiliations: University of Wisconsin Medical School, Madison (Dr Gern), and Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass (Dr Weiss).



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RELATED ARTICLE

Measles History and Atopic Diseases: A Population-Based Cross-sectional Study
Mikko Paunio, Olli P. Heinonen, Martti Virtanen, Pauli Leinikki, Annamari Patja, and Heikki Peltola
JAMA. 2000;283(3):343-346.
ABSTRACT | FULL TEXT  


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Atopic Dermatitis and Asthma: Parallels in the Evolution of Treatment
Eichenfield et al.
Pediatrics 2003;111:608-616.
ABSTRACT | FULL TEXT  

Infection: friend or foe in the development of atopy and asthma? The epidemiological evidence
von Mutius
Eur Respir J 2001;18:872-881.
ABSTRACT | FULL TEXT  





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