Non-alcoholic fatty liver disease (NAFLD) has recently become the most common liver disease with a global prevalence of over 25% and is expected to increase. Recently, experts have reached a consensus that “fatty liver disease associated with metabolic dysfunction or MAFLD” may be a more appropriate and inclusive definition than NAFLD. Like the former name NAFLD, MAFLD, as a manifestation of multiple system metabolic disorders involving the liver, has certain heterogeneity in its pathogenesis, clinical manifestations, pathological changes and natural outcomes. We found that there is a delicate dynamic balance among intestinal microflora, metabolites and host immune system to maintain a healthy intestinal environment and host health. On the contrary, this imbalance is related to diseases such as MAFLD. However, there are no clear studies on how dietary nutrients affect the intestinal environment and participate in the pathogenesis of MAFLD. This review summarizes the interactions among dietary nutrients, intestinal microbiota and MAFLD in an attempt to provide evidence for the use of dietary supplements to regulate liver function in patients with MAFLD. These dietary nutrients influence the development and progression of MAFLD mainly through the hepatic-intestinal axis by altering dietary energy absorption, regulating bile acid metabolism, changing intestinal permeability and producing ethanol. Meanwhile, the nutrients have the ability to combat MAFLD in terms of enriching abundance of intestinal microbiota, reducing Firmicutes/Bacteroidetes ratio and promoting abundance of beneficial gut microbes. Therefore, family therapy with MAFLD using a reasonable diet could be considered.

Background: The association between renal impairment (RI) and stroke outcome after endovascular thrombectomy (EVT) remains unclear, which limits the estimation of patient prognosis by clinicians involved in EVT decision-making. Purpose: This study aimed to investigate the association between RI and acute ischemic stroke (AIS) outcomes in patients treated with EVT. Methods: Studies involving the association between RI at admission and AIS outcomes after EVT were retrieved from the PubMed and Embase databases from their inception to 17 January 2022. A fixed-effects model was used to synthesize the data of the included studies. Sensitivity analysis was performed to identify the source of heterogeneity. Results: Overall, 11 studies, including 5053 patients with stroke receiving EVT, were included in the full analysis. In unadjusted analyses, RI was associated with 3-month poor functional outcome and mortality; the odds ratios (ORs) were 2.13 [10 studies; 95% confidence interval (CI), 1.77–2.56; I2 = 45%] and 2.42 (8 studies; 95% CI, 2.02–2.90; I2 = 58%), respectively. In adjusted analyses, the above associations remained significant; the OR of the 3-month poor functional outcome was 1.49 (5 studies; 95% CI, 1.17–1.90; I2 = 58%), and the OR of the 3-month mortality was 1.84 (6 studies; 95% CI, 1.45–2.33; I2 = 74%). Similar results were obtained in sensitivity analyses. Conclusion: Our results suggest that in patients with AIS who underwent EVT, RI at admission was associated with 3-month poor functional outcome and mortality.

Obesity is closely related with diet, including the regularity of meals and inflammation in the diet. No previous study focused on the associations among eating breakfast, which is regarded the most important meal, dietary inflammation, and obesity. This study analyzed data from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2018, with 23,758 participants involved. Obesity and dietary inflammation were measured by body mass index (BMI) and dietary inflammatory index (DII), respectively. Eating breakfast was defined by two days of dietary recalls based on NHANES dietary data. Pro-inflammatory diet and skipping breakfast were positively associated with obesity in the whole population. Compared with eating breakfast in both recalls, skipping breakfast had the higher OR of obesity, especially for individuals who reported no recall. Participants with diabetes were the sensitive population of these associations. Compared with participants who reported breakfast in both recalls, the mediated proportion of participants reported breakfast in one recall and in no recall were 24.71% and 27.34%, respectively. The association between eating breakfast and obesity was partly mediated by DII. We recommended eating breakfast regularly to reduce dietary inflammation, as well as further obesity, especially for diabetic populations.

Objective: Dietary inflammatory index (DII) and handgrip strength (HGS) were correlated, and both were associated with cardiovascular disease (CVD). However, the role of the 10-year CVD risk in the relationship between DII and grip strength remains uncertain. Methods: This study involved 5691 adults from the National Health and Nutrition Examination Survey (NHANES) in 2011–2014. Dietary inflammation, 10-year CVD risk and relative grip strength were assessed by the Dietary Inflammation Index, the Framingham Risk Score (FRS) and handgrip strength adjusted BMI. Linear regression analyses and mediation analysis were used to explore these associations. Results: Both DII and 10-year CVD risk were negatively associated with relative handgrip strength, and DII was positively associated with 10-year CVD risk. Additionally, 10-year CVD risk partially mediated the association between DII and relative handgrip strength by a 11.8% proportion. Specifically, the mediating effect of the 10-year risk of CVD varied by gender and age. Conclusions: Reducing the 10-year risk of CVD attenuates the effect of an inflammatory diet on relative grip strength impairment. Therefore, we recommend reducing the effect of inflammatory diet on grip strength impairment by controlling any of the FRS parameters, such as lowering blood pressure and smoking cessation, especially with targeted measures for different populations.

The underlying mechanism in both cognitive impairment and depression was chronic inflammation, which could be reflected by the dietary inflammatory index (DII). However, the effect of cognitive impairment on the association between DII and depression was not clear. Therefore, in this study, we hypothesized that cognitive impairment could mediate the association between dietary inflammation and depressive symptoms. A total of 2550 participants aged ≥60 from the National Health and Nutrition Examination Survey (NHANES) in 2011–2014 were involved in the serial, cross-sectional study. Proinflammatory and anti-inflammatory diets were measured by DII. Cognitive impairment was measured by four dimensions, CERAD-immediate, CERAN-delayed, animal fluency test, and DSST. Depressive symptoms were measured by PHQ-9 scores. We found that a proinflammatory diet and cognitive impairment were both risk factors for depressive symptoms. An interaction between an inflammatory diet and cognitive impairment was detected (P-interaction = 0.060). In addition, all four dimensions of cognition mediated the association between DII and depressive symptom scores. Part of the association between DII and depressive symptoms scores could be explained by different dimensions of cognitive function, and the proportion of mediation ranged from 10.0% to 36.7%. In conclusion, cognitive impairment levels partly mediated the association between DII and depressive symptoms.