ingest cdrApp 2017-06-30T21:02:14.954Z aac86417-22f1-4cf6-b34c-2c21f31ce694 modifyDatastreamByValue RELS-EXT fedoraAdmin 2017-06-30T23:55:42.940Z Setting exclusive relation modifyDatastreamByValue RELS-EXT fedoraAdmin 2017-06-30T23:55:55.391Z Setting exclusive relation addDatastream MD_TECHNICAL fedoraAdmin 2017-06-30T23:56:09.200Z Adding technical metadata derived by FITS modifyDatastreamByValue RELS-EXT fedoraAdmin 2017-06-30T23:56:31.009Z Setting exclusive relation addDatastream MD_FULL_TEXT fedoraAdmin 2017-06-30T23:56:42.932Z Adding full text metadata extracted by Apache Tika modifyDatastreamByValue RELS-EXT fedoraAdmin 2017-06-30T23:57:01.043Z Setting exclusive relation modifyDatastreamByValue RELS-EXT cdrApp 2017-07-05T17:44:46.059Z Setting exclusive relation modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2017-12-11T14:28:41.036Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-01-25T01:34:55.986Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-01-27T02:18:16.184Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-03-13T21:55:52.497Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-05-16T19:38:07.732Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-07-10T20:31:23.372Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-07-17T16:46:21.593Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-08-02T16:52:38.502Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-08-08T16:12:40.350Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-08-14T20:36:30.101Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-08-16T16:22:00.132Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-09-21T13:57:00.259Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-09-26T16:50:30.054Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-10-10T17:11:17.041Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-10-11T17:43:34.887Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2019-02-28T00:54:20.197Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2019-03-19T20:11:22.430Z Nan Li Author Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. Spring 2017 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology MARILIE GAMMON Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text Nan Li Author Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. Spring 2017 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. Spring 2017 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. Spring 2017 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017-05 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie D. Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie D. Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation Epidemiology Marilie D. Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 University of North Carolina at Chapel Hill Degree granting institution Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus; carbohydrate; esophageal adenocarcinoma; gastric cardia adenocarcinoma; sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation Epidemiology Marilie D. Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 University of North Carolina at Chapel Hill Degree granting institution Nan Li Creator Department of Epidemiology Gillings School of Global Public Health Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus, carbohydrate, esophageal adenocarcinoma, gastric cardia adenocarcinoma, sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie D. Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus; carbohydrate; esophageal adenocarcinoma; gastric cardia adenocarcinoma; sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Epidemiology Marilie D. Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Nan Li Creator Department of Epidemiology Gillings School of Global Public Health The incidence of esophageal and gastric cardia adenocarcinoma (EA/GCA) has increased rapidly in Westernized countries during the past few decades, whereas survival remains low. Barrett’s esophagus (BE), the only known precursor lesion of EA/GCA, has been increasing. Long-term high sugar/carbohydrate intake may promote carcinogenesis by inducing hyperinsulinemia. In this dissertation, four United States-based case-control studies were pooled to examine the associations between sugar/carbohydrate intake and risk of developing BE, risk of developing EA/GCA, and mortality after a diagnosis of EA/GCA. In total, there were 513 BE cases/528 controls, and 513 EA cases/538 GCA cases/2051 controls. EA/GCA cases were followed for vital status. Dietary intake was assessed by study-specific food frequency questionnaires, and then linked with the University of Minnesota Nutrient Database to harmonize and estimate intake of twelve sugar/carbohydrate measures. Sugar/carbohydrate intake was then pooled using study-specific quantiles and absolute cut-points. Odds ratios and 95% confidence intervals were calculated using: logistic regression for BE incidence; and multinomial logistic regression for EA incidence and GCA incidence as distinct outcomes. Hazard ratios and their 95%CIs were calculated using Cox proportional hazards regression for EA/GCA survival analysis. Sucrose was found to be associated with 79% and 51% increase in risk of developing BE and EA, respectively. Intake of sweetened desserts/beverages was associated with 71% and 55% increase in risk of developing BE and EA, respectively. Added sugar was associated with 71% increase in risk of developing BE, but not with EA. Glycemic index was associated with 58% increase in risk of developing EA, but not with BE. Waist circumference modified the sweetened desserts/beverages-BE association, and body mass index (BMI) modified all of the above positive associations with EA incidence. The sucrose-EA association was modified by frequency of gastroesophageal reflux disease (GERD). If the results from this dissertation are confirmed, there could be potential to reduce risk of BE/EA by reducing intake of sucrose (especially among those with BMI<25 or GERD<weekly) and sweetened desserts/beverages (especially among those with lower waist circumference or BMI<25). Reducing added sugar intake and dietary glycemic index (especially among those with BMI≥25), may also be plausible risk reduction strategies. 2017 Epidemiology Barrett's esophagus; carbohydrate; esophageal adenocarcinoma; gastric cardia adenocarcinoma; sugar eng Doctor of Philosophy Dissertation University of North Carolina at Chapel Hill Graduate School Degree granting institution Marilie D. Gammon Thesis advisor Lawrence Engel Thesis advisor Nicholas Shaheen Thesis advisor Susan Steck Thesis advisor Patrick Bradshaw Thesis advisor text 2017-05 Li_unc_0153D_16742.pdf uuid:72c2c71e-e892-4076-9e84-eae5641b4af1 2019-06-30T00:00:00 proquest 2017-03-14T18:39:52Z application/pdf 3201669 yes