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Article: Lifecourse infectious origins of sexual inequalities in central adiposity

TitleLifecourse infectious origins of sexual inequalities in central adiposity
Authors
KeywordsCentral obesity
Infection
Sex
Socio-economic position
Issue Date2011
PublisherOxford University Press. The Journal's web site is located at http://ije.oxfordjournals.org/
Citation
International Journal Of Epidemiology, 2011, v. 40 n. 6, p. 1556-1564 How to Cite?
AbstractBackground: Social disparities in obesity are often more marked among women than men, possibly due to social factors. Taking a life-history perspective, we hypothesized that childhood infections could be relevant via sex-specific effects of immune system activation on sexual development and, hence, body shape. Methods: We used multivariable linear regression to assess the sex-specific, adjusted associations of 'childhood' pathogens [0 (n = 1002), 1 (n = 2199), 2 (n = 3442) or 3 (n = 4833) of HSV1, CMV and hepatitis A antibodies] and 'adult' pathogens [0 (n = 5836), 1 (n = 3018) or ≥2 (n = 720) of HSV2, HHV8 and hepatitis B or C) with waist-hip ratio (WHR) and body mass index (BMI) standard deviations (SDs) using NHANES III (1988-94). As validation, we assessed associations with height. Results: 'Childhood' pathogens were positively associated with WHR among women [0.18 SD, 95% confidence interval (95% CI) 0.04-0.32 for 3, compared with 0], but not men (-0.04 SD, 95% CI -0.15 to 0.08), adjusted for age, education, race/ethnicity, smoking and alcohol. Further adjustments for leg length barely changed the estimates. There were no such sex-specific associations for BMI or for adult pathogens. 'Childhood', but not 'adult', pathogens were negatively associated with height, adjusted for age, sex, education and race/ethnicity. Conclusions: These observations are consistent with the lifecourse hypothesis that early exposure to infections makes women vulnerable to central obesity. This hypothesis potentially sheds new light on the developmental origins of obesity, and is consistent with the generally higher levels of central obesity among women than men in developing populations. Published by Oxford University Press on behalf of the International Epidemiological Association. © The Author 2011; all rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/144607
ISSN
2015 Impact Factor: 7.522
2015 SCImago Journal Rankings: 4.381
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSchooling, CMen_HK
dc.contributor.authorJones, HEen_HK
dc.contributor.authorLeung, GMen_HK
dc.date.accessioned2012-02-03T06:15:42Z-
dc.date.available2012-02-03T06:15:42Z-
dc.date.issued2011en_HK
dc.identifier.citationInternational Journal Of Epidemiology, 2011, v. 40 n. 6, p. 1556-1564en_HK
dc.identifier.issn0300-5771en_HK
dc.identifier.urihttp://hdl.handle.net/10722/144607-
dc.description.abstractBackground: Social disparities in obesity are often more marked among women than men, possibly due to social factors. Taking a life-history perspective, we hypothesized that childhood infections could be relevant via sex-specific effects of immune system activation on sexual development and, hence, body shape. Methods: We used multivariable linear regression to assess the sex-specific, adjusted associations of 'childhood' pathogens [0 (n = 1002), 1 (n = 2199), 2 (n = 3442) or 3 (n = 4833) of HSV1, CMV and hepatitis A antibodies] and 'adult' pathogens [0 (n = 5836), 1 (n = 3018) or ≥2 (n = 720) of HSV2, HHV8 and hepatitis B or C) with waist-hip ratio (WHR) and body mass index (BMI) standard deviations (SDs) using NHANES III (1988-94). As validation, we assessed associations with height. Results: 'Childhood' pathogens were positively associated with WHR among women [0.18 SD, 95% confidence interval (95% CI) 0.04-0.32 for 3, compared with 0], but not men (-0.04 SD, 95% CI -0.15 to 0.08), adjusted for age, education, race/ethnicity, smoking and alcohol. Further adjustments for leg length barely changed the estimates. There were no such sex-specific associations for BMI or for adult pathogens. 'Childhood', but not 'adult', pathogens were negatively associated with height, adjusted for age, sex, education and race/ethnicity. Conclusions: These observations are consistent with the lifecourse hypothesis that early exposure to infections makes women vulnerable to central obesity. This hypothesis potentially sheds new light on the developmental origins of obesity, and is consistent with the generally higher levels of central obesity among women than men in developing populations. Published by Oxford University Press on behalf of the International Epidemiological Association. © The Author 2011; all rights reserved.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://ije.oxfordjournals.org/en_HK
dc.relation.ispartofInternational Journal of Epidemiologyen_HK
dc.subjectCentral obesityen_HK
dc.subjectInfectionen_HK
dc.subjectSexen_HK
dc.subjectSocio-economic positionen_HK
dc.subject.meshCommunicable Diseases - complications - epidemiology - virology-
dc.subject.meshHealth Behavior-
dc.subject.meshHealth Status Disparities-
dc.subject.meshObesity, Abdominal - epidemiology - etiology - immunology-
dc.subject.meshSexual Development - immunology-
dc.titleLifecourse infectious origins of sexual inequalities in central adiposityen_HK
dc.typeArticleen_HK
dc.identifier.emailSchooling, CM:cms1@hkucc.hku.hken_HK
dc.identifier.emailLeung, GM:gmleung@hku.hken_HK
dc.identifier.authoritySchooling, CM=rp00504en_HK
dc.identifier.authorityLeung, GM=rp00460en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/ije/dyr128en_HK
dc.identifier.pmid22158667-
dc.identifier.scopuseid_2-s2.0-83455213401en_HK
dc.identifier.hkuros198158en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-83455213401&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume40en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1556en_HK
dc.identifier.epage1564en_HK
dc.identifier.isiWOS:000297868500018-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridSchooling, CM=12808565000en_HK
dc.identifier.scopusauthoridJones, HE=8238349700en_HK
dc.identifier.scopusauthoridLeung, GM=7007159841en_HK
dc.identifier.citeulike10428065-

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