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Sökning: onr:"swepub:oai:DiVA.org:uu-273748" > Obesity and risk of...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003826naa a2200577 4500
001oai:DiVA.org:uu-273748
003SwePub
008160118s2014 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:130242973
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2737482 URI
0247 a https://doi.org/10.1093/jnci/dju2522 DOI
0247 a http://kipublications.ki.se/Default.aspx?queryparsed=id:1302429732 URI
040 a (SwePub)uud (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Thrift, Aaron P4 aut
2451 0a Obesity and risk of esophageal adenocarcinoma and Barrett's esophagus :b a Mendelian randomization study.
264 c 2014-09-30
264 1b Oxford University Press (OUP),c 2014
338 a print2 rdacarrier
520 a BACKGROUND: Data from observational studies suggest that body mass index (BMI) is causally related to esophageal adenocarcinoma (EAC) and its precursor, Barrett's esophagus (BE). However, the relationships may be affected by bias and confounding.METHODS: We used data from the Barrett's and Esophageal Adenocarcinoma Genetic Susceptibility Study: 999 patients with EAC, 2061 patients with BE, and 2169 population controls. We applied the two-stage control function instrumental variable method of the Mendelian randomization approach to estimate the unbiased, unconfounded effect of BMI on risk of EAC and BE. This was performed using a genetic risk score, derived from 29 genetic variants shown to be associated with BMI, as an instrument for lifetime BMI. A higher score indicates propensity to obesity. All tests were two-sided.RESULTS: The genetic risk score was not associated with potential confounders, including gastroesophageal reflux symptoms and smoking. In the instrumental variable analyses (IV), EAC risk increased by 16% (IV-odds ratio [OR] = 1.16, 95% confidence interval [CI] = 1.01 to 1.33) and BE risk increased by 12% (IV-OR = 1.12, 95% CI = 1.00 to 1.25) per 1kg/m(2) increase in BMI. BMI was statistically significantly associated with EAC and BE in conventional epidemiologic analyses.CONCLUSIONS: People with a high genetic propensity to obesity have higher risks of esophageal metaplasia and neoplasia than people with low genetic propensity. These analyses provide the strongest evidence to date that obesity is independently associated with BE and EAC, and is not due to confounding or bias inherent in conventional epidemiologic analyses.
7001 a Shaheen, Nicholas J4 aut
7001 a Gammon, Marilie D4 aut
7001 a Bernstein, Leslie4 aut
7001 a Reid, Brian J4 aut
7001 a Onstad, Lynn4 aut
7001 a Risch, Harvey A4 aut
7001 a Liu, Geoffrey4 aut
7001 a Bird, Nigel C4 aut
7001 a Wu, Anna H4 aut
7001 a Corley, Douglas A4 aut
7001 a Romero, Yvonne4 aut
7001 a Chanock, Stephen J4 aut
7001 a Chow, Wong-Ho4 aut
7001 a Casson, Alan G4 aut
7001 a Levine, David M4 aut
7001 a Zhang, Rui4 aut
7001 a Ek, Weronica E4 aut
7001 a MacGregor, Stuart4 aut
7001 a Ye, Weiminu Karolinska Institutet4 aut
7001 a Hardie, Laura J4 aut
7001 a Vaughan, Thomas L4 aut
7001 a Whiteman, David C4 aut
7102 a Karolinska Institutet4 org
7730 t Journal of the National Cancer Instituted : Oxford University Press (OUP)g 106:11q 106:11x 0027-8874x 1460-2105
8564 u https://academic.oup.com/jnci/article-pdf/106/11/dju252/17313117/dju252.pdf
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-273748
8564 8u https://doi.org/10.1093/jnci/dju252
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:130242973

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