Sugar/Carbohydrate intake and the Barrett’s esophagus-adenocarcinoma continuum Public Deposited

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  • March 19, 2019
  • Li, Nan
    • Affiliation: Gillings School of Global Public Health, Department of Epidemiology
  • 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.
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Rights statement
  • In Copyright
  • Steck, Susan
  • Engel, Lawrence
  • Gammon, Marilie D.
  • Bradshaw, Patrick
  • Shaheen, Nicholas
  • Doctor of Philosophy
Degree granting institution
  • University of North Carolina at Chapel Hill Graduate School
Graduation year
  • 2017

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