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Abstract Details
The empirical dietary inflammatory pattern score and the risk of nonalcoholic fatty liver disease and cirrhosis
Hepatol Commun. 2023 Sep 15;7(10):e0263. doi: 10.1097/HC9.0000000000000263.eCollection 2023 Oct 1.
1Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
2Division of Gastroenterology, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts, USA.
3Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
4Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
5Clinical and Translational Epidemiology Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
6Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, Massachusetts, USA.
7Department of Immunology and Infectious Diseases, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA.
Abstract
Background: Diet plays an important role in the pathogenesis of NAFLD. Inflammation is a potential mechanism linking diet to NAFLD development and its progression to cirrhosis.1 We analyzed data from a large, prospective cohort of US women to examine the influence of dietary inflammatory potential on the long-term risk of developing NAFLD and cirrhosis.
Methods: We prospectively followed 96,016 women in the Nurses' Health Study II cohort (1995-2017) who were free of chronic liver disease, including NAFLD, at baseline. The inflammatory potential of the diet was ascertained using an established, food-based empirical dietary inflammatory pattern score. Cox proportional hazard models were used to estimate multivariable-adjusted hazard ratios and 95% CIs for incident NAFLD and cirrhosis.
Results: Over 2,085,947 person-years of follow-up, we documented 4389 cases of incident NAFLD and 102 cases of incident cirrhosis. Increasing cumulative average empirical dietary inflammatory pattern (EDIP) score was significantly and positively associated with incident NAFLD (multivariable-adjusted HR 1.31 per each 1-U increase in EDIP score, p-trend < 0.0001) and cirrhosis (p-trend of 0.034). Our findings also were consistent when examining recent diets using simple updated EDIP scores. In analyses of specific EDIP components, we observed an increased risk of incident NAFLD and cirrhosis with higher consumption of certain proinflammatory components of the EDIP score.
Conclusions: Dietary patterns with a higher proinflammatory potential may be associated with a higher risk of developing both NAFLD and cirrhosis. Reducing the inflammatory potential of diet may potentially provide an effective strategy for preventing the development of NAFLD and progression to cirrhosis.