Abstract

Abstract Background: Mexican-origin (MO) Hispanic adults have the highest rates of non-alcoholic fatty liver disease (NAFLD) in the United States (US), which places them at high risk of hepatocellular carcinoma (HCC). Diet plays a significant role in the development and treatment of NAFLD given the lack of pharmacological treatment. Nutritional components hypothesized to influence NAFLD risk include an imbalance in the consumption of omega-6 (n-6) relative to omega-3 (n-3) polyunsaturated fatty acids (PUFAs). However, data on the relationship between dietary intake of fatty acids (FA) and liver steatosis and fibrosis is limited for MO adults. Purpose: This study examined FA intake among overweight and obese Mexican-origin (MO) Hispanic adults and evaluated its association to liver steatosis and fibrosis. Methods: Overweight and obese participants (n=285, MO Hispanic adults) completed three 24-hour dietary recalls on two week days and one weekend day, to estimate dietary FA intake. Liver steatosis was defined by continuous attenuation parameter (CAP) scores that can range from 100 to 400 dB/m. Fibrosis was defined by kilopascals (kPa) and can range from 2 to 75 kPa. Liver steatosis and fibrosis were quantified using non-invasive transient elastography (Fibroscan®). Multiple regression analyses tested relationships between FA intakes and liver steatosis or fibrosis, adjusting for sex, BMI, and total energy intake. Results: Among MO Hispanic adults, mean CAP score was 289.5 ± 48.9 dB/m, equivalent to approximately 67% hepatic steatosis, and a mean fibrosis of 5.67± 2.83 kPa. The mean intake of n-6 and n-3 was 12.0 ± 6.5 g/day and 1.50 ± 1.01 g/day, respectively, with a ratio of 8.9 (range: 2.46 - 19.8). The most commonly consumed n-6 and n-3 FAs were linoleic acid (LA) (12 ± 6.5 g/day) and alpha-linoleic acid (ALA) (1.50 g/day ± 1.01), respectively. Overall, no associations were observed between the ratio of n-6 to n-3 and liver steatosis. However, LA-to-ALA ratio and the n-6 to n-3 ratio were positively associated with liver fibrosis such that a one point increase in the LA-to-ALA ratio resulted in a 1.01-point increase in fibrosis (95% CI: [1.00, 1.03]; p=0.029), and a one point increase in the n-6 to n-3 resulted in a 1.02-point increase in fibrosis (95% CI: [1.01, 1.03]; p=0.005). Conclusion: Intake and ratios of n-6 and n-3 PUFAs were comparable to what is observed in general US populations and were not associated with liver steatosis. However, n-6 and n-3 ratios were associated with liver fibrosis. These findings highlight the need for a more rigorous examination of the association between n-PUFAS and liver fibrosis and their potential as a therapeutic strategy for more severe liver disease such as non-alcoholic steatohepatitis (NASH) and cirrhosis in this high-risk population. Citation Format: Melissa Lopez-Pentecost, Brian Hallmark, Cynthia Thomson, Floyd Chilton, David Garcia. Relationship between fatty acid intake and liver steatosis and fibrosis among overweight and obese Mexican-origin adults [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5956.

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