Hygiene Hypothesis

edit

Hygiene hypothesis, a concept initially theorized by immunologists and epidemiologists, has been proved to have a strong connection with evolutionary mismatch through recent year studies. Hygiene hypothesis states that the profound increase in allergies, autoimmune diseases, and some other chronic inflammatory diseases is related to the reduced exposure of the immune system to antigens. Such reduced exposure is more common in industrialized countries and especially urban areas, where the inflammatory chronic diseases are also more frequently seen.[1][2] Recent analysis and studies have tied the hygiene hypothesis and evolutionary mismatch together. Some researchers suggest that the overly sterilized urban environment changes or depletes the microbiota composition and diversity. Such environmental conditions favor the development of the inflammatory chronic diseases because human bodies have been selected to adapt to a pathogen-rich environment in the history of evolution.[3] For example, studies have shown that change in our symbiont community can lead to the disorder of immune homeostasis, which can be used to explain why antibiotic use in early childhood can result in higher asthma risk.[3] Because the change or depletion of the microbiome is often associated with hygiene hypothesis, the hypothesis is sometimes also called “biome depletion theory”.


  1. ^ Garn, Holger; Renz, Harald. "Epidemiological and immunological evidence for the hygiene hypothesis". Immunobiology. 212 (6): 441–452. doi:10.1016/j.imbio.2007.03.006.
  2. ^ Prokopakis, Emmanuel; Vardouniotis, Alexios; Kawauchi, Hideyuki; Scadding, Glenis; Georgalas, Christos; Hellings, Peter; Velegrakis, George; Kalogjera, Livije. "The pathophysiology of the hygiene hypothesis". International Journal of Pediatric Otorhinolaryngology. 77 (7): 1065–1071. doi:10.1016/j.ijporl.2013.04.036.
  3. ^ a b Sironi, Manuela; Clerici, Mario (2010-06-01). "The hygiene hypothesis: an evolutionary perspective". Microbes and Infection. 12 (6): 421–427. doi:10.1016/j.micinf.2010.02.002.