BACKGROUND & AIMS: Coffee has inverse relationships with both type 2 diabetes and hepatic fibrosis in patients with nonalcoholic fatty liver disease (NAFLD). Relationships were explored between coffee intake and insulin resistance (IR) with respect to NAFLD histologic severity. METHODS: We analyzed data from 782 adults (≥18 years) in the Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN) from 2004 to 2008. IR was assessed using the HOMA-IR. We modeled associations between coffee intake and NAFLD histologic severity using multiple logistic regression; and interactions between coffee and IR on NAFLD histology were explored. RESULTS: Among 782 participants, 38% (n = 295) were men, 12% (n = 97) were Latino, mean age (± standard deviation) was 48 ± 12 years. Median BMI was 33.5 kg/m(2) [interquartile range, 29.7-38.3] and median HOMA-IR was 4.3 [2.7-7.2]. Diabetes was present in 24% (n = 189). NASH was present in 79% (n = 616), and 25% (n = 199) had advanced fibrosis. The frequency of coffee intake (cups/day, cpd) was as follows: 0 cpd, n = 230 (29%); <1 cpd, n = 219 (28%); 1 to <2 cpd, n = 116 (15%); ≥2 cpd, n = 217 (28%). The effect of coffee on fibrosis varied with degree of IR (interaction P = 0.001). Coffee consumers with less IR, defined as HOMA-IR<4.3, had a lower odds of advanced fibrosis [OR = 0.64; 95% CI, (0.46-0.88), P = 0.001]. There was no protective effect of coffee on advanced fibrosis among individuals with higher HOMA-IR [OR = 1.06, 95% CI (0.87-1.28), P = 0.6]. CONCLUSIONS: Coffee intake is inversely associated with advanced fibrosis among NAFLD patients with lower HOMA-IR. Our findings warrant further investigation given the worldwide ubiquity of coffee intake.
BACKGROUND & AIMS: Coffee has inverse relationships with both type 2 diabetes and hepatic fibrosis in patients with nonalcoholic fatty liver disease (NAFLD). Relationships were explored between coffee intake and insulin resistance (IR) with respect to NAFLD histologic severity. METHODS: We analyzed data from 782 adults (≥18 years) in the Nonalcoholic Steatohepatitis Clinical Research Network (NASH CRN) from 2004 to 2008. IR was assessed using the HOMA-IR. We modeled associations between coffee intake and NAFLD histologic severity using multiple logistic regression; and interactions between coffee and IR on NAFLD histology were explored. RESULTS: Among 782 participants, 38% (n = 295) were men, 12% (n = 97) were Latino, mean age (± standard deviation) was 48 ± 12 years. Median BMI was 33.5 kg/m(2) [interquartile range, 29.7-38.3] and median HOMA-IR was 4.3 [2.7-7.2]. Diabetes was present in 24% (n = 189). NASH was present in 79% (n = 616), and 25% (n = 199) had advanced fibrosis. The frequency of coffee intake (cups/day, cpd) was as follows: 0 cpd, n = 230 (29%); <1 cpd, n = 219 (28%); 1 to <2 cpd, n = 116 (15%); ≥2 cpd, n = 217 (28%). The effect of coffee on fibrosis varied with degree of IR (interaction P = 0.001). Coffee consumers with less IR, defined as HOMA-IR<4.3, had a lower odds of advanced fibrosis [OR = 0.64; 95% CI, (0.46-0.88), P = 0.001]. There was no protective effect of coffee on advanced fibrosis among individuals with higher HOMA-IR [OR = 1.06, 95% CI (0.87-1.28), P = 0.6]. CONCLUSIONS: Coffee intake is inversely associated with advanced fibrosis among NAFLD patients with lower HOMA-IR. Our findings warrant further investigation given the worldwide ubiquity of coffee intake.
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