The Hygiene Hypothesis -- Redefine, Rename, or Just Clean It Up?

Linda Brookes, MSc; Laurence E. Cheng, MD, PhD


April 06, 2015

In This Article

Origin of the Hygiene Hypothesis

The "hygiene hypothesis" has been a topic of contention ever since the term was first coined in 1989 by Professor David Strachan (St George's, University of London, London, United Kingdom). Derived from his study showing that a child's risk of developing allergic rhinitis ("hay fever") was inversely related to the number of older siblings in the family,[1] Professor Strachan suggested that allergic diseases were prevented in the younger siblings by "infection in early childhood, transmitted by unhygienic contact with older siblings." At that time, this was interpreted as an explanation for the increased prevalence of allergic diseases in Western countries, with the assumption that opportunities for infection had been reduced through the higher standards of hygiene achieved in those countries.

Initially, the "hygiene hypothesis," which Professor Strachan later admitted "owed more to an alliterative tendency than to [an] aspiration to claim a new scientific paradigm,"[2] was greeted with skepticism. Additional studies, however, provided further support for the idea that microbial exposure in early life protects against allergic rhinitis, eczema, and asthma.[3,4,5,6,7] As the prevalence of allergic diseases in children continues to rise in the West, especially in the United States,[8,9] the hygiene hypothesis is now frequently cited as evidence that Western households are "too clean" and that progress in public hygiene has been achieved at the expense of protection against allergy in early childhood. The hypothesis has been extended to explain food allergy[10] and a wide range of other conditions such as autoimmune diseases (type 1 diabetes and multiple sclerosis), inflammatory bowel disease, some cancers,[11] and Alzheimer disease.[12]

The term "hygiene hypothesis" has been criticized as being too vague, including by Professor Strachan himself.[2] Other concepts have been proposed as more accurate descriptions of the model, including: the "microbial hypothesis" (avoiding an overemphasis on cleanliness)[13] and the "old friends hypothesis" (implying that microbes that were beneficial for immune system development have been eliminated or replaced).[14] The "biodiversity hypothesis" expands the hygiene hypothesis to the living environment in general,[15] and the "biome depletion" model views the hygiene hypothesis as an evolutionary mismatch that works in tandem with other mismatches, such as inflammatory diets or vitamin D deficiency, which undermine immune function in westernized societies.[16]

Others have contended that reduced microbial exposure early in life cannot be the sole explanation for changes in allergic disease prevalence, given that some regions have a high prevalence of allergic diseases along with high infection rates.[9] It is generally agreed that more epidemiologic and clinical studies are needed as well as basic research into the mechanisms underlying the protective effects of microbial exposure. As Professor Strachan wrote, "Over 25 years of epidemiological and immunological investigation...little progress has been made in identifying the biologically relevant exposures which 'explain' the frequently replicated epidemiological observations linking allergic sensitization and atopic disease (inversely) to family size and to 'unhygienic' environments."[2]

For further clarification of the current understanding of the hygiene hypothesis and its implications for the advice physicians should give parents and caregivers of young children about "hygiene in the home," Medscape approached Dr Laurence E. Cheng, MD, PhD, Assistant Professor in the Department of Pediatrics at the University of California, San Francisco School of Medicine and the Mary E. and Oscar L. Frick, MD Endowed Chair in Allergy. Dr Cheng is using basic and translational approaches to research patients with allergic diseases, including food allergy, atopic dermatitis, and asthma. He was coauthor of a recent review on the role of allergic inflammatory responses in maintaining tissue homeostasis[17] as well as an editorial accompanying an observational study of children's allergies.[18]


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