A0186 - Associations of Dietary Fiber and Fat Intake with Barrett’s Esophagus and Stages of Progression to Esophageal Adenocarcinoma

Pranav V. Gwalani, MBBS, MPH¹, Aarti Kumar, BA², Charles Lightdale, MD³, Gary Falk, MD⁴, Gregory Ginsberg, MD⁴, Prasad G. Iyer, MD, FACG⁵, Kenneth K. Wang, MD, FACG⁶, Julian Abrams, MD, MS^7
1Columbia University, Mailman School of Public Health, New York, NY; ²Columbia University Vagelos College of Physicians and Surgeons, New York, NY; ³Columbia University, New York, NY; ⁴University of Pennsylvania, Philadelphia, PA; ⁵Mayo Clinic, Rochester, MN; ⁶Mayo Clinic Rochester, Rochester, MN; ⁷Columbia University Irving Medical Center, New York, NY

Introduction: The incidence of esophageal adenocarcinoma (EAC) has increased dramatically over the past half century. Changes in dietary patterns over this time may partially account for this trend. Prior studies have found inverse associations between fiber intake and both Barrett’s esophagus (BE) and EAC, and studies of fat intake have reported increased risk or no association. However, it is unknown whether fiber or fat intake contribute to neoplastic progression in BE patients.

Methods: We performed a multi-center case-control study of patients with and without BE. We collected demographic, anthropometric, and clinical data and categorized BE by worst degree of histology ever. Subjects completed the NCI DHQII, a validated food frequency questionnaire assessing dietary intake over the preceding 12 months. We used multivariable logistic regression analyses to assess associations of energy adjusted fat and fiber intake with BE and with advanced neoplasia (high grade dysplasia or EAC vs. no dysplasia/indefinite/low grade dysplasia). Four models were developed: 1) fat and fiber intake; 2) Model 1 and EAC risk factors (age, sex, BMI, smoking history, family history); 3) Model 2 and aspirin and statin use; 4) reduced parsimonious model (final model: age, sex, family history).

Results: We enrolled 162 subjects; 108 subjects (37 non-BE, 71 BE; 21 with advanced neoplasia) completed the questionnaire and were analyzed. Compared to controls, BE patients were older and more likely (p< 0.01) to be male, aspirin users, statin users, and ever smokers. BE patients had significantly higher energy-adjusted fiber intake but no difference in fat intake compared to controls. (Figure 1A-B) Adjusted for fat intake, increased fiber intake was associated with reduced odds of BE (per g/1000 kcal, OR 0.81, 95%CI 0.70-0.93), with similar associations in all the models (Table). There was no association between fat intake and BE. There was no significant association between fat or fiber intake and stages of progression to EAC (Figure 1C-D), and neither fat nor fiber intake was associated with advanced neoplasia in multivariable analyses. (Table)

Discussion: Fiber intake was inversely associated with BE but not with stages of progression to EAC. There was no association between fat intake and BE or dysplasia or EAC, but this may reflect our small sample size. Future larger studies are warranted to elucidate the mechanisms by which fiber may protect against the development of BE.




Disclosures:


Pranav V. Gwalani, MBBS, MPH¹, Aarti Kumar, BA², Charles Lightdale, MD³, Gary Falk, MD⁴, Gregory Ginsberg, MD⁴, Prasad G. Iyer, MD, FACG⁵, Kenneth K. Wang, MD, FACG⁶, Julian Abrams, MD, MS⁷. A0186 - Associations of Dietary Fiber and Fat Intake with Barrett’s Esophagus and Stages of Progression to Esophageal Adenocarcinoma, ACG 2022 Annual Scientific Meeting Abstracts. Charlotte, NC: American College of Gastroenterology.