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Anorexia nervosa, autoimmunity and the hygiene hypothesis
Summary The hypothesis proposed is that anorexia nervosa (AN) is an autoimmune disease caused by delayed exposure to common micro-organisms in which auto-antibodies to regulatory peptides and hypothalamic neurons, which cross react with microbial antigens, disturb appetite and lead to decreased inta...
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Published in: | Medical hypotheses 2012-06, Vol.78 (6), p.772-775 |
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description | Summary The hypothesis proposed is that anorexia nervosa (AN) is an autoimmune disease caused by delayed exposure to common micro-organisms in which auto-antibodies to regulatory peptides and hypothalamic neurons, which cross react with microbial antigens, disturb appetite and lead to decreased intake of food. IgG, IgA and IgM auto-antibodies to a range of regulatory peptides concerned with appetite and mood are found in patients with AN. The regulatory peptides show sequence homology with common micro-organisms of the microbial flora. Auto-antibodies to α melanocyte stimulating hormone (αMSH) are positively correlated with AN psychopathology. But patients with bulimia nervosa (BN) and normal healthy controls also have a similar range of auto-antibodies at comparable levels. The incidence of AN is rising in developed countries, the disease is more common in females than in males, the peak incidence is in the teenage years, there is seasonal variation in the month of birth and the disease is more common in higher socio-economic groups. These are all features which are consistent with the hygiene hypothesis. But there is no evidence that the disease is more common in first born than in later born children. There is a paucity of data on early life events such as attendance at nursery and exposure to pets. Genetic factors are important but the data on major histocompatibility complex (MHC) gene polymorphisms are contradictory. The epidemiological and serological data are consistent with the hypothesis under investigation but key questions in relation to the hygiene hypothesis have not been posed. A large case control study of AN epidemiology is indicated. MHC gene polymorphisms should be assessed. There is, however, sufficient evidence to justify a trial of pooled immunoglobulin therapy in patients with life threatening AN. |
doi_str_mv | 10.1016/j.mehy.2012.03.002 |
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IgG, IgA and IgM auto-antibodies to a range of regulatory peptides concerned with appetite and mood are found in patients with AN. The regulatory peptides show sequence homology with common micro-organisms of the microbial flora. Auto-antibodies to α melanocyte stimulating hormone (αMSH) are positively correlated with AN psychopathology. But patients with bulimia nervosa (BN) and normal healthy controls also have a similar range of auto-antibodies at comparable levels. The incidence of AN is rising in developed countries, the disease is more common in females than in males, the peak incidence is in the teenage years, there is seasonal variation in the month of birth and the disease is more common in higher socio-economic groups. These are all features which are consistent with the hygiene hypothesis. But there is no evidence that the disease is more common in first born than in later born children. There is a paucity of data on early life events such as attendance at nursery and exposure to pets. Genetic factors are important but the data on major histocompatibility complex (MHC) gene polymorphisms are contradictory. The epidemiological and serological data are consistent with the hypothesis under investigation but key questions in relation to the hygiene hypothesis have not been posed. A large case control study of AN epidemiology is indicated. MHC gene polymorphisms should be assessed. There is, however, sufficient evidence to justify a trial of pooled immunoglobulin therapy in patients with life threatening AN.</description><identifier>ISSN: 0306-9877</identifier><identifier>EISSN: 1532-2777</identifier><identifier>DOI: 10.1016/j.mehy.2012.03.002</identifier><identifier>PMID: 22465467</identifier><language>eng</language><publisher>United States: Elsevier Ltd</publisher><subject>Adolescent ; Anorexia Nervosa - epidemiology ; Anorexia Nervosa - etiology ; Anorexia Nervosa - immunology ; Autoantibodies - blood ; Autoantibodies - immunology ; Autoimmunity - immunology ; Female ; Humans ; Hygiene Hypothesis ; Immunoglobulin A - immunology ; Immunoglobulin G - immunology ; Immunoglobulin M - immunology ; Internal Medicine ; Male ; Models, Biological</subject><ispartof>Medical hypotheses, 2012-06, Vol.78 (6), p.772-775</ispartof><rights>Elsevier Ltd</rights><rights>2012 Elsevier Ltd</rights><rights>Copyright © 2012 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c411t-98fc36a9a5da4adc337a636b3188d1b37cad5215a75cba9e8ed4447c3d24c8323</citedby><cites>FETCH-LOGICAL-c411t-98fc36a9a5da4adc337a636b3188d1b37cad5215a75cba9e8ed4447c3d24c8323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22465467$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Acres, Meghan J</creatorcontrib><creatorcontrib>Heath, Joseph J</creatorcontrib><creatorcontrib>Morris, James A</creatorcontrib><title>Anorexia nervosa, autoimmunity and the hygiene hypothesis</title><title>Medical hypotheses</title><addtitle>Med Hypotheses</addtitle><description>Summary The hypothesis proposed is that anorexia nervosa (AN) is an autoimmune disease caused by delayed exposure to common micro-organisms in which auto-antibodies to regulatory peptides and hypothalamic neurons, which cross react with microbial antigens, disturb appetite and lead to decreased intake of food. IgG, IgA and IgM auto-antibodies to a range of regulatory peptides concerned with appetite and mood are found in patients with AN. The regulatory peptides show sequence homology with common micro-organisms of the microbial flora. Auto-antibodies to α melanocyte stimulating hormone (αMSH) are positively correlated with AN psychopathology. But patients with bulimia nervosa (BN) and normal healthy controls also have a similar range of auto-antibodies at comparable levels. The incidence of AN is rising in developed countries, the disease is more common in females than in males, the peak incidence is in the teenage years, there is seasonal variation in the month of birth and the disease is more common in higher socio-economic groups. These are all features which are consistent with the hygiene hypothesis. But there is no evidence that the disease is more common in first born than in later born children. There is a paucity of data on early life events such as attendance at nursery and exposure to pets. Genetic factors are important but the data on major histocompatibility complex (MHC) gene polymorphisms are contradictory. The epidemiological and serological data are consistent with the hypothesis under investigation but key questions in relation to the hygiene hypothesis have not been posed. A large case control study of AN epidemiology is indicated. MHC gene polymorphisms should be assessed. There is, however, sufficient evidence to justify a trial of pooled immunoglobulin therapy in patients with life threatening AN.</description><subject>Adolescent</subject><subject>Anorexia Nervosa - epidemiology</subject><subject>Anorexia Nervosa - etiology</subject><subject>Anorexia Nervosa - immunology</subject><subject>Autoantibodies - blood</subject><subject>Autoantibodies - immunology</subject><subject>Autoimmunity - immunology</subject><subject>Female</subject><subject>Humans</subject><subject>Hygiene Hypothesis</subject><subject>Immunoglobulin A - immunology</subject><subject>Immunoglobulin G - immunology</subject><subject>Immunoglobulin M - immunology</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Models, Biological</subject><issn>0306-9877</issn><issn>1532-2777</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNp9kU1r3DAQhkVJaLab_oEeio851M7ow5YNJbAsSRsI5JDkLLTSbFdb29pKdqj_fWQ27SGHnAbB875iniHkC4WCAq0u90WHu6lgQFkBvABgH8iClpzlTEp5QhbAocqbWsoz8inGPQA0gtcfyRljoipFJRekWfU-4F-nsx7Ds4_6W6bHwbuuG3s3TJnubTbsMNtNvxz28zz49I4unpPTrW4jfn6dS_J0c_24_pnf3f-4Xa_uciMoHdL3W8Mr3ejSaqGt4VzqilcbTuva0g2XRtuS0VLL0mx0gzVaIYQ03DJhas74klwcew_B_xkxDqpz0WDb6h79GFVSQakUkBZfEnZETfAxBtyqQ3CdDlOCZq5SezUrU7MyBVwlZSn09bV_3HRo_0f-OUrA9yOAactnh0FFk1wYtC6gGZT17v3-qzdx07reGd3-xgnj3o-hT_4UVTFl1MN8tPlmlAFQaIC_AI62kZ0</recordid><startdate>20120601</startdate><enddate>20120601</enddate><creator>Acres, Meghan J</creator><creator>Heath, Joseph J</creator><creator>Morris, James A</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20120601</creationdate><title>Anorexia nervosa, autoimmunity and the hygiene hypothesis</title><author>Acres, Meghan J ; Heath, Joseph J ; Morris, James A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c411t-98fc36a9a5da4adc337a636b3188d1b37cad5215a75cba9e8ed4447c3d24c8323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adolescent</topic><topic>Anorexia Nervosa - epidemiology</topic><topic>Anorexia Nervosa - etiology</topic><topic>Anorexia Nervosa - immunology</topic><topic>Autoantibodies - blood</topic><topic>Autoantibodies - immunology</topic><topic>Autoimmunity - immunology</topic><topic>Female</topic><topic>Humans</topic><topic>Hygiene Hypothesis</topic><topic>Immunoglobulin A - immunology</topic><topic>Immunoglobulin G - immunology</topic><topic>Immunoglobulin M - immunology</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Models, Biological</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Acres, Meghan J</creatorcontrib><creatorcontrib>Heath, Joseph J</creatorcontrib><creatorcontrib>Morris, James A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Medical hypotheses</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Acres, Meghan J</au><au>Heath, Joseph J</au><au>Morris, James A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anorexia nervosa, autoimmunity and the hygiene hypothesis</atitle><jtitle>Medical hypotheses</jtitle><addtitle>Med Hypotheses</addtitle><date>2012-06-01</date><risdate>2012</risdate><volume>78</volume><issue>6</issue><spage>772</spage><epage>775</epage><pages>772-775</pages><issn>0306-9877</issn><eissn>1532-2777</eissn><abstract>Summary The hypothesis proposed is that anorexia nervosa (AN) is an autoimmune disease caused by delayed exposure to common micro-organisms in which auto-antibodies to regulatory peptides and hypothalamic neurons, which cross react with microbial antigens, disturb appetite and lead to decreased intake of food. IgG, IgA and IgM auto-antibodies to a range of regulatory peptides concerned with appetite and mood are found in patients with AN. The regulatory peptides show sequence homology with common micro-organisms of the microbial flora. Auto-antibodies to α melanocyte stimulating hormone (αMSH) are positively correlated with AN psychopathology. But patients with bulimia nervosa (BN) and normal healthy controls also have a similar range of auto-antibodies at comparable levels. The incidence of AN is rising in developed countries, the disease is more common in females than in males, the peak incidence is in the teenage years, there is seasonal variation in the month of birth and the disease is more common in higher socio-economic groups. These are all features which are consistent with the hygiene hypothesis. But there is no evidence that the disease is more common in first born than in later born children. There is a paucity of data on early life events such as attendance at nursery and exposure to pets. Genetic factors are important but the data on major histocompatibility complex (MHC) gene polymorphisms are contradictory. The epidemiological and serological data are consistent with the hypothesis under investigation but key questions in relation to the hygiene hypothesis have not been posed. A large case control study of AN epidemiology is indicated. MHC gene polymorphisms should be assessed. There is, however, sufficient evidence to justify a trial of pooled immunoglobulin therapy in patients with life threatening AN.</abstract><cop>United States</cop><pub>Elsevier Ltd</pub><pmid>22465467</pmid><doi>10.1016/j.mehy.2012.03.002</doi><tpages>4</tpages></addata></record> |
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subjects | Adolescent Anorexia Nervosa - epidemiology Anorexia Nervosa - etiology Anorexia Nervosa - immunology Autoantibodies - blood Autoantibodies - immunology Autoimmunity - immunology Female Humans Hygiene Hypothesis Immunoglobulin A - immunology Immunoglobulin G - immunology Immunoglobulin M - immunology Internal Medicine Male Models, Biological |
title | Anorexia nervosa, autoimmunity and the hygiene hypothesis |
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