Editing Hygiene hypothesis (section)

== Overview ==

The idea of a link between parasite infection and immune disorders was first suggested in 1968<ref name="MaizelsMcSorley2014">{{cite journal |last1=Maizels |first1=R. M. |last2=McSorley |first2=H. J. |last3=Smyth |first3=D. J. |title=Helminths in the hygiene hypothesis: sooner or later? |journal=Clinical & Experimental Immunology |date=July 2014 |volume=177 |issue=1 |pages=38–46 |doi=10.1111/cei.12353 |pmid=24749722 |pmc=4089153 }}</ref> before the advent of [[DNA sequencing#High-throughput sequencing (HTS) methods|large scale DNA sequencing techniques]]. The original formulation of the hygiene hypothesis dates from 1989, when David Strachan proposed that lower incidence of [[infection]] in early childhood could be an explanation for the rise in allergic diseases such as [[asthma]] and [[hay fever]] during the 20th century.<ref name=strachan2000>{{cite journal |last1=Strachan |first1=D. |title=Family size, infection and atopy: the first decade of the 'hygiene hypothesis' |journal=Thorax |date=1 August 2000 |volume=55 |issue=90001 |pages=2S–10 |doi=10.1136/thorax.55.suppl_1.s2 |pmid=10943631 |pmc=1765943 }}</ref>

The hygiene hypothesis has also been expanded beyond allergies, and is also studied in the context of a broader range of conditions affected by the immune system, particularly [[inflammatory disease]]s.<ref name="ShuYuen2018">{{cite journal |last1=Shu |first1=Shang-An |last2=Yuen |first2=Agatha W. T. |last3=Woo |first3=Elena |last4=Chu |first4=Ka-Hou |last5=Kwan |first5=Hoi-Shan |last6=Yang |first6=Guo-Xiang |last7=Yang |first7=Yao |last8=Leung |first8=Patrick S. C. |title=Microbiota and Food Allergy |journal=Clinical Reviews in Allergy & Immunology |date=18 December 2018 |volume=57 |issue=1 |pages=83–97 |doi=10.1007/s12016-018-8723-y |pmid=30564985 |s2cid=56476417 }}</ref> These include [[type 1 diabetes]],<ref name=stene2001>{{cite journal |last1=Stene |first1=Lars C |last2=Nafstad |first2=Per |title=Relation between occurrence of type 1 diabetes and asthma |journal=The Lancet |date=February 2001 |volume=357 |issue=9256 |pages=607–608 |doi=10.1016/S0140-6736(00)04067-8 |pmid=11558491 |s2cid=7457497 }}</ref> multiple sclerosis,<ref name=raison2010>{{cite journal |last1=Raison |first1=Charles L. |last2=Lowry |first2=Christopher A. |last3=Rook |first3=Graham A. W. |title=Inflammation, Sanitation, and Consternation |journal=Archives of General Psychiatry |date=December 2010 |volume=67 |issue=12 |pages=1211–1224 |doi=10.1001/archgenpsychiatry.2010.161 |pmid=21135322 |pmc=3724429 }}</ref><ref name="Haga2017"/> and also some types of depression<ref name=raison2010 /><ref name=rook2013>{{cite journal |last1=Rook |first1=Graham A. W. |last2=Lowry |first2=Christopher A. |last3=Raison |first3=Charles L. |title=Microbial 'Old Friends', immunoregulation and stress resilience |journal=Evolution, Medicine, and Public Health |date=2013 |volume=2013 |issue=1 |pages=46–64 |doi=10.1093/emph/eot004 |pmid=24481186 |pmc=3868387 }}</ref> and cancer.<ref name=rook2011>{{cite journal |last1=Rook |first1=Graham A. W. |last2=Dalgleish |first2=Angus |title=Infection, immunoregulation, and cancer |journal=Immunological Reviews |date=March 2011 |volume=240 |issue=1 |pages=141–159 |doi=10.1111/j.1600-065X.2010.00987.x |pmid=21349092 |s2cid=39495585 }}</ref><!---Deleted "{{specify|date=March 2015}}" because it seems hard to be more specific than the cite info provided by the author in the </ref>. ---> For example, the global distribution of multiple sclerosis is negatively correlated with that of the helminth ''[[Trichuris trichiura]]'' and its incidence is negatively correlated with ''[[Helicobacter pylori]]'' infection.<ref name="Haga2017"/> Strachan's original hypothesis could not explain how various allergic conditions spiked or increased in prevalence at different times, such as why respiratory allergies began to increase much earlier than food allergies, which did not become more common until near the end of the 20th century.<ref name="BloomfieldRook2016"/>

In 2003, Graham Rook proposed the [[Old Friends hypothesis (biology)|"old friends" hypothesis]] which has been described as a more rational explanation for the link between microbial exposure and inflammatory disorders.<ref name=rook2003>{{cite journal |last1=Rook |first1=Graham A.W. |last2=Martinelli |first2=Roberta |last3=Brunet |first3=Laura Rosa |title=Innate immune responses to mycobacteria and the downregulation of atopic responses |journal=Current Opinion in Allergy and Clinical Immunology |date=October 2003 |volume=3 |issue=5 |pages=337–342 |doi=10.1097/00130832-200310000-00003 |pmid=14501431 |s2cid=45020780 }}</ref> The hypothesis states that the vital microbial exposures are not colds, influenza, measles and other common childhood infections which have evolved relatively recently over the last 10,000 years, but rather the microbes already present during mammalian and human evolution, that could persist in small hunter-gatherer groups as microbiota, tolerated latent infections, or carrier states. He proposed that [[coevolution]] with these species has resulted in their gaining a role in immune system development.{{citation needed|date=May 2023}}

Strachan's original formulation of the hygiene hypothesis also centred around the idea that smaller families provided insufficient microbial exposure partly because of less person-to-person spread of infections, but also because of "improved household amenities and higher standards of personal cleanliness".<ref name=strachan2000 /> It seems likely that this was the reason he named it the "hygiene hypothesis". Although the "hygiene revolution" of the nineteenth and twentieth centuries may have been a major factor, it now seems more likely that, while public health measures such as [[sanitation]], [[potable water]] and [[garbage collection]] were instrumental in reducing our exposure to [[cholera]], [[typhoid]] and so on, they also deprived people of their exposure to the "old friends" that occupy the same environmental habitats.<ref name=stanwellsmith>{{cite journal |first1=Rosalind Stanwell |last1=Smith |first2=Sally F. |last2=Bloomfield |first3=Graham A. |last3=Rook |title=The Hygiene Hypothesis and its implications for home hygiene, lifestyle and public health |journal=Home Hygiene & Health |date=September 2012 |url=https://www.ifh-homehygiene.org/review-best-practice/hygiene-hypothesis-and-its-implications-home-hygiene-lifestyle-and-public-0 }}</ref>

The rise of [[autoimmune disease]]s and [[acute lymphoblastic leukemia]] in young people in the developed world was linked to the hygiene hypothesis.<ref>{{cite journal |last1=Smith |first1=Malcolm A. |last2=Simon |first2=Richard |last3=Strickler |first3=Howard D. |last4=McQuillan |first4=Geraldine |last5=Gloeckler Ries |first5=Lynn A. |last6=Linet |first6=Martha S. |title=Evidence that childhood acute lymphoblastic leukemia is associated with an infectious agent linked to hygiene conditions |journal=Cancer Causes & Control |date=1998 |volume=9 |issue=3 |pages=285–298 |doi=10.1023/A:1008873103921 |pmid=9684709 |s2cid=25397922 }}</ref><ref name=Okada2010>{{cite journal |last1=Okada |first1=H. |last2=Kuhn |first2=C. |last3=Feillet |first3=H. |last4=Bach |first4=J.-F. |title=The 'hygiene hypothesis' for autoimmune and allergic diseases: an update |journal=Clinical & Experimental Immunology |date=11 March 2010 |volume=160 |issue=1 |pages=1–9 |doi=10.1111/j.1365-2249.2010.04139.x |pmid=20415844 |pmc=2841828 }}</ref><ref>{{cite journal |last1=Greaves |first1=Mel |title=A causal mechanism for childhood acute lymphoblastic leukaemia |journal=Nature Reviews Cancer |date=August 2018 |volume=18 |issue=8 |pages=471–484 |doi=10.1038/s41568-018-0015-6 |pmid=29784935 |pmc=6986894 }}</ref> [[Autism]] may be associated with changes in the gut microbiome and early infections.<ref>{{cite journal |last1=Vallès |first1=Yvonne |last2=Francino |first2=M. Pilar |title=Air Pollution, Early Life Microbiome, and Development |journal=Current Environmental Health Reports |date=29 September 2018 |volume=5 |issue=4 |pages=512–521 |doi=10.1007/s40572-018-0215-y |pmid=30269309 |pmc=6306492 |bibcode=2018CEHR....5..512V }}</ref> The risk of chronic inflammatory diseases also depends on factors such as diet, pollution, physical activity, obesity, socio-economic factors, and stress. Genetic predisposition is also a factor.<ref name= rockgaw /><ref name=filippi2008>{{cite journal |last1=Filippi |first1=C. M. |last2=von Herrath |first2=M. G. |title=Viral Trigger for Type 1 Diabetes: Pros and Cons |journal=Diabetes |date=29 October 2008 |volume=57 |issue=11 |pages=2863–2871 |doi=10.2337/db07-1023 |pmid=18971433 |pmc=2570378 }}</ref><ref name=rook2012>{{cite journal |last1=Rook |first1=Graham A. W. |title=Hygiene Hypothesis and Autoimmune Diseases |journal=Clinical Reviews in Allergy & Immunology |date=17 November 2011 |volume=42 |issue=1 |pages=5–15 |doi=10.1007/s12016-011-8285-8 |pmid=22090147 |s2cid=15302882 |doi-access=free }}</ref>