Dietary consumption and serum pattern of bioactive fatty acids in NAFLD patients.

INTRODUCTION AND OBJECTIVES: Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome. Some dietary fatty acids have showed different bioactive functions in metabolic syndrome. The aim of this study is to determine the dietary consumption patterns and serum percentage of bioactive fatty acids in NAFLD patients. PATIENTS AND METHODS: Cross-sectional study with NAFLD patients and non-NAFLD patients. Dietary consumption of bioactive fatty acids was assessed by a food frequency questionnaire. NAFLD and liver fibrosis were diagnosed by transient elastography. The identification of serum bioactive fatty acids was achieved by gas chromatography-mass spectrometry (%). Bioactive fatty acids consumption was correlated with NAFLD clinical characteristics with the Spearman correlation analysis. RESULTS: A total of 299 patients were included, whose mean of age and body mass index were 44.2±9.9 years and 25.9±3.8kg/m2, respectively. The consumption of bioactive fatty acids was no different regarding the presence of NAFLD; however, the consumption of stearic and linoleic fatty acids was higher in relation with NAFLD severity (p≤0.05). The consumption of myristic acid was higher in patients with fibrosis (p=0.02). Serum percentage and dietary consumption did not show correlations. CONCLUSION: Dietary consumption of bioactive fatty acids is different according to NAFLD severity. Individualized diets according to NAFLD severity could be successful in order to prevent liver injury-related outcomes.

Both alcoholic and non-alcoholic steatohepatitis association with cardiovascular risk and liver fibrosis.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is the most common cause of liver disease worldwide. Mortality in NAFLD is mainly related to cardiovascular disease (CVD) and cancer. NAFLD and its association with both CVD and liver disease risk have been well evaluated, but the association of NAFLD with alcohol, known as "both alcoholic and non-alcoholic steatohepatitis" (BASH), remains uncertain. The objective of this study was to assess the influence of alcohol and obesity in the development of liver and cardiovascular disease risk. METHODS: This was a case-control study that included patients from a regular check-up. Alcohol consumption was evaluated with MAST, AUDIT, and CAGE. Cardiovascular risk was evaluated using the Framingham score, and liver fibrosis was evaluated with APRI and NAFLD score. Patients were classified in five groups: healthy patients, steatosis with obesity, steatosis with alcoholism, BASH, and idiopathic steatosis. RESULTS: A total of 414 patients were included. The BASH group represented 16% of patients, and showed a greater proportion of patients with high cardiovascular risk with 17% (p = 0.001), and liver fibrosis with 9%, according to the APRI score (p = 0.10). A multivariate logistic regression showed that alcohol consumption >140 g/week (OR 2.546, 95% CI 1.11-5.81, p = 0.003) and BMI >25 kg/m2 (OR 12.64, 95% CI 1.66 96.20, p = 0.001) were related to high cardiovascular risk. Liver fibrosis according to APRI was only related to alcohol consumption >140 g/week (OR 2.74, 95% CI 1-7.48, p = 0.03). CONCLUSIONS: BASH remains an area not well explored, and of great implication given the increasing number of patients affected. We observed an additive effect of both etiologies in the development of high cardiovascular and liver disease risk.

Smoking is not associated with nonalcoholic fatty liver disease.

AIM: To analyze the relationship between smoking and nonalcoholic fatty liver disease (NAFLD). METHODS: This is a cross-sectional study of a healthy population, carried out in a check-up unit of a university hospital in Mexico City. We enrolled 933 subjects, 368 current smokers (cases) and 565 persons who had never smoked (controls). Demographic, metabolic and biochemical variables were measured in the two groups. NAFLD was determined by ultrasound and metabolic syndrome according to ATPIII. RESULTS: A total of 548 men (205 cases and 343 controls) and 337 women (114 cases and 223 controls) were included in the analysis. Statistical differences between cases and controls were observed only in high blood pressure prevalence (6.6% vs 11.3%, P < 0.05; cases and controls respectively), high-density lipoproteins (1.00 +/- 0.26 vs 1.06 +/- 0.28 mmol/L, P < 0.005), triglycerides (2.18 +/- 1.49 vs 1.84 +/- 1.1 mmol/L, P < 0.001), and erythrocyte sedimentation rate (11.3 +/- 9.3 vs 13.5 +/- 11.9 mm/h, P < 0.001). No differences were observed in the prevalence of NAFLD (22.27% vs 29.68%, P = NS) and metabolic syndrome (41.69% vs 36.74%, P = NS). Univariate analysis showed that smoking was not a risk factor for NAFLD (OR = 0.89, 95% CI 0.65-1.21). CONCLUSION: No differences in NAFLD prevalence were observed between current smokers and nonsmokers, and furthermore, no differences were observed in heavy smokers (more than 20 packs/year), indicating that there is no relationship between smoking and NAFLD.