The hygiene theory: fact or fiction?
OBJECTIVE
The "hygiene hypothesis" offers a potentially credible and parsimonious explanation for the increasing prevalence of allergy noted in many westernized populations. The authors review recent evidence both for and against this hypothesis.


RESULTS
A strong body of epidemiologic evidence indicates that the original observations, namely of a birth order effect and increased risk of atopic disorders in those born into small, affluent households, are robust findings. Improved hygiene is believed to mediate its effect through decreased exposure to infectious agents in early life, and recent evidence has focused attention on the importance of the gastrointestinal microbial environment. In particular, infection with hepatitis A, Helicobacter pylori, and toxoplasma in those living in temperate climates, and geoheminths in those living in endemic areas, have been shown to be associated with reduced risk of atopic manifestations. It is postulated that these infections exert their effect through critically altering T-helper (Th)1/Th2 regulation, which is supported by the examination of the cytokine profiles of cord mononuclear cells when exposed to gastrointestinal flora and, furthermore, emerging evidence on the benefits of probiotics on symptoms of atopic dermatitis. Attempts to identify an inverse relation between Th1- and Th2-mediated disorders (as might be predicted by the Th1/Th2 paradigm) have, however, yielded conflicting results, raising the possibility that this model may be something of an oversimplification.


CONCLUSIONS
The hygiene hypothesis remains a credible but nonspecific explanation for observed variations over time, place and persons at risk for developing atopic allergic disorders. More prospective studies are needed to unravel which infectious agents exert a protective effect and the time period of importance for sensitization. The clinical implications of these advances in our understanding of the etiology of atopic allergic disorders are currently limited.
Sheikh
Aziz
A
Division of Community Health Sciences: GP Section, University of Edinburgh, UK. aziz.sheikh@ed.ac.uk
Strachan
David P
DP
D000328:Adult; D001722:Birth Order; D015984:Causality; D002648:Child; D002675:Child, Preschool; D003140:Communicable Disease Control; D004781:Environmental Exposure / Q000592:standards*; D041981:Gastrointestinal Tract / Q000276:immunology / Q000382:microbiology; D006801:Humans; D006920:Hygiene / Q000592:standards*; D006967:Hypersensitivity / Q000453:epidemiology* / Q000209:etiology / Q000276:immunology / Q000517:prevention & control; D007223:Infant; D007231:Infant, Newborn; D019936:Probiotics / Q000627:therapeutic use; D012307:Risk Factors; D012959:Socioeconomic Factors