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THE EFFECT OF INFLAMMATORY FOODS ON MORBID OBESITY: DOES RACE MATTER?
Cynthia Weber*1, Seyed Mohammad Kalantar Motamedi1, Rami R. Mustafa1, Zhengyi Chen2, Li Li2, Mujjahid Abbas1, Leena Khaitan1
1Surgery, University Hospitals of Cleveland, Cleveland, OH; 2Case Western Reserve University, Cleveland, OH

Introduction: While diet modification remains a mainstay of weight management therapy, there is no perfect diet. The Dietary Inflammatory Index (DII) is a tool that assigns a score based on the inflammatory potential of food constituents, categorizing an individual's diet on a continuum from maximally anti-inflammatory (more negative score) to maximally pro-inflammatory (more positive score). We hypothesized that since obesity is a chronic inflammatory state, obese patients consume foods with higher inflammatory properties. In our study, we sought to determine the relationship between DII and body mass index (BMI) in Caucasians and African Americans (AA).
Methods: Anthropometric and demographic information was obtained from otherwise healthy individuals enrolled in a screening colonoscopy-based study at our institution. Self-reported diet history was used to calculate DII. Subjects were divided into 3 groups defined by tertiles of DII, with increasingly positive scores representing a progressively more inflammatory diet; 1st tertile (DII≥-6.12 and ≤-0.59), 2nd tertile (DII≥ 0.60 and ≤2.31) and 3rd tertile (DII≥ 2.32 and ≤5.88). We investigated the association between DII and BMI using linear regression and DII and morbid obesity (non-obese as BMI<25, morbidly obese as BMI≥40) using logistic regression, controlling for a number lifestyle, economic and educational factors; p<0.05 statistically significant.
Results: 2,407 patients were included in our analysis, (188 morbidly obese and 625 with BMI below 25kg/m2); 1494 Caucasians and 913 AAs. In the pooled population, continuous DII values was not significantly associated with BMI. However, considering tertiles of DII, and when stratified by race, we detected a difference. In Caucasians, an inflammatory diet was associated with a significant increase in BMI (increase of 1.61 kg/m2 and 1.63 kg/m2 in the 2nd and 3rd tertiles compared to the 1st tertile (p<0.01)). Conversely, in AAs, there was no significant between DII tertiles and BMI. Furthermore, within the Caucasian population, morbid obesity was significantly associated with a pro-inflammatory diet, with 5.1 fold higher risk of morbid obesity in the 2nd tertile and a 3.49 fold increased risk in the 3rd tertile compared to the non-obese patients. In AAs we failed to find any statistically significant effect betweent DII and morbid obesity.
Conclusion: We found that a pro-inflammatory diet is a strong predictor of morbid obesity in Caucasians; further proof that diet modification can prove effective in controlling weight within this group. Surprisingly, that relationship does not exist in AAs. This discrepancy between races warrants additional exploration. Perhaps there is a protective genetic effect against inflammatory foods among AAs? By investigating the differences in metabolomic profiles between races we hope to find an answer to this question.




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