The relationship between dietary antioxidants and fatty liver disease remains a topic of debate. This study aimed to examine the association between the Composite Dietary Antioxidant Index (CDAI) and nonalcoholic fatty liver disease (NAFLD)/metabolic-associated fatty liver disease (MAFLD).

The study analyzed data from the 2003-2018 cycles of the National Health and Nutrition Examination Survey. The study included 16,321 individuals aged 20-85 years. Food and nutrient intake data were based on the 24-h recall method. Multivariate logistic regression models were employed to examine the relationship between CDAI and NAFLD/MAFLD.

In the fully adjusted multivariate logistic regression model, CDAI demonstrated a significant negative correlation with NAFLD and MAFLD. Mediation analysis showed that inflammatory factors partially mediated the relationship between CDAI and NAFLD/MAFLD prevalence. The combination of high CDAI levels with effective physical activity was associated with a greater reduction in NAFLD/MAFLD prevalence than high CDAI levels alone.

Our study highlighted a negative association between CDAI and NAFLD/MAFLD, mediated by inflammatory factors. Additionally, participants with characteristics of active physical activity and high levels of CDAI were more strongly correlated with the reduced prevalence of NAFLD/MAFLD. Further research in clinical cohorts should be conducted to comprehensively investigate the impact of CDAI on NAFLD/MAFLD prevalence.

There is limited and conflicting evidence on the association between selenium and non-alcoholic fatty liver disease (NAFLD). Therefore, the present population-based cross-sectional study aimed to explore the relationship between dietary selenium intake and the risk of NAFLD.

A total of 3026 subjects from the PERSIAN (Prospective Epidemiological Research Studies in IrAN) Kavar cohort study were included in the analysis. The daily selenium intake was evaluated using a semi-quantitative food frequency questionnaire, and energy-adjusted quintiles of selenium intake (µg/day) were calculated. NAFLD was defined as the fatty liver index (FLI) ≥ 60 or the hepatic steatosis index (HSI) > 36. The association between dietary selenium intake and NAFLD was evaluated using logistic regression analysis.

The prevalence rates of NAFLD were 56.4% and 51.9%, based on the FLI and HSI markers, respectively. The odds ratios (ORs) for FLI-defined NAFLD were 1.31 (95% confidence interval (CI): 1.01-1.70) and 1.50 (95% CI: 1.13-1.99) for the fourth and fifth quintiles of selenium intake, respectively, after adjustment for sociodemographic variables, smoking status, alcohol drinking, physical activity, and dietary factors (P trend = 0.002). There was also a similar association between selenium intakes and HSI-defined NAFLD (OR = 1.34 (95% CI: 1.03-1.75) for the fourth quintile and OR = 1.50 (95% CI: 1.12-2.01) for the fifth quintile of selenium intake) (P trend = 0.006).

In this large sample study, we observed a weak positive association between dietary selenium intake and NAFLD risk.

Little is known about the associations between healthy dietary patterns and metabolic dysfunction-associated fatty liver disease (MAFLD) in less-developed ethnic minority regions (LEMRs), where the prevalence of MAFLD is increasing rapidly and dietary habits are quite different from those in developed countries. Moreover, a significant subset of MAFLD individuals in LEMRs are nonobese, but the efficacy of dietary patterns on MAFLD individuals with different obese statuses is also unclear. We aimed to test the associations of two wildly recommended a priori dietary patterns-Alternate Mediterranean diet (AMED) and Dietary Approaches to Stop Hypertension (DASH)-with the risk of MAFLD in the total population, and further in nonobese and obese individuals.

We recruited 99,556 participants in the China Multi-Ethnic Cohort Study, an ongoing cohort study in less-developed southwest China. Using validated food frequency questionnaire, each participant was assigned an AMED score and a DASH score. MAFLD was ascertained as hepatic steatosis on ultrasound together with diabetes, overweight/obesity, or two other metabolic risk factors. We performed logistic regression with inverse probability of exposure weighting (IPEW) to examine associations between two dietary patterns and MAFLD, adjusting for potential confounders under the guidance of directed acyclic graphs. Further, analyses were stratified by body mass index.

We included 66,526 participants (age 49.5±11.0; 62.6% women), and the prevalence of MAFLD was 16.1%. Participants in the highest quintile of DASH score showed strong inverse associations with risks of MAFLD (OR = 0.85; 95% CI, 0.80-0.91; Ptrend < 0.001) compared with participants in the lowest quintile. The association between DASH and nonobese MAFLD (OR = 0.69; 95% CI, 0.61-0.78; Ptrend < 0.001) was stronger (I2 = 78.5 % ; Pheterogeneity = 0.001) than that with obese MAFLD (OR = 0.90; 95% CI, 0.83-0.98; Ptrend = 0.002). There was a null association between AMED and MAFLD risk.

In LEMRs, a DASH diet but not AMED was associated with MAFLD. The relationship appeared to be more pronounced in nonobese MAFLD individuals than in obese MAFLD individuals.

Herbal-induced liver injury (HILI) is an important and increasingly concerning cause of liver toxicity, and this study presents recent updates to the literature. An extensive literature review was conducted encompassing September 2019 through March 2021. Studies with clinically significant findings were analyzed and included in this review. We emphasized those studies that provided a causality assessment methodology, such as Roussel Uclaf Causality Assessment Method scores. Our review includes reports of individual herbals, including Garcinia cambogia, green tea extract, kratom as well as classes such as performance enhancing supplements, Traditional Chinese medicine, Ayurvedic medicine and herbal contamination. Newly described herbals include ashwagandha, boldo, skyfruit, and 'Thermo gun'. Several studies discussing data from national registries, including the United States Drug-Induced Liver Injury (DILI) Network, Spanish DILI Registry, and Latin American DILI Network were incorporated. There has also been a continued interest in hepatoprotection, with promising use of herbals to counter hepatotoxicity from anti-tubercular medications. We also elucidated the current legal conversation surrounding use of herbals by presenting updates from the Federal Drug Administration. The highlights of the literature over the past year indicate interest in HILI that will continue as the supplement industry in the United States grows.

Non-alcoholic fatty liver disease (NAFLD) was defined in 1980 and has the same histological characteristics as alcoholic liver disease except for alcohol consumption. After 40 years, the understanding of this disease is still imperfect. Without specific drugs available for treatment, the number of patients with NAFLD is increasing rapidly, and NAFLD currently affects more than one-quarter of the global population. NAFLD is mostly caused by a sedentary lifestyle and excessive energy intake of fat and sugar. To ameliorate or avoid NAFLD, people commonly replace high-fat foods with high-carbohydrate foods (especially starchy carbohydrates) as a way to reduce caloric intake and reach satiety. However, there are few studies that concentrate on the effect of carbohydrate intake on liver metabolism in patients with NAFLD, much fewer than the studies on fat intake. Besides, most of these studies are not systematic, which has made identification of the mechanism difficult. In this review, we collected and analysed data from studies on human and animal models and, surprisingly, found that carbohydrates and liver steatosis could be linked by inflammation. This review not only describes the effects of carbohydrates on NAFLD and body lipid metabolism but also analyses and predicts possible molecular pathways of carbohydrates in liver lipid synthesis that involve inflammation. Furthermore, the limitations of recent research and possible targets for regulating inflammation and lipogenesis are discussed. This review describes the effects of starchy carbohydrates, a nutrient signal, on NAFLD from the perspective of inflammation.