ScopeGTPs (green tea polyphenols) exert anti‐CRC (colorectal cancer) activity. The intestinal microbiota and intestinal colonization by bacteria of oral origin has been implicated in colorectal carcinogenesis. GT modulates the composition of mouse gut microbiota harmonious with anticancer activity. Therefore, the effect of green tea liquid (GTL) consumption on the gut and oral microbiome is investigated in healthy volunteers (n = 12).Methods and results16S sequencing and phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt) analysis of both fecal and saliva samples (collected before intervention, after 2 weeks of GTL (400 mL per day) and after a washout period of one week) in healthy volunteers show changes in microbial diversity and core microbiota and difference in clear classification (partial least squares‐discriminant analysis [PLS‐DA]). An irreversible, increased FIR:BAC (Firmicutes to Bacteroidetes ratio), elevated SCFA producing genera, and reduction of bacterial LPS synthesis in feces are discovered in response to GTL. GTL alters the salivary microbiota and reduces the functional pathways abundance relevance to carcinogenesis. Similar bacterial networks in fecal and salivary microbiota datasets comprising putative oral bacteria are found and GTL reduces the fecal levels of Fusobacterium. Interestingly, both Lachnospiraceae and B/E (Bifidobacterium to Enterobacteriacea ratio—markers of colonization resistance [CR]) are negatively associated with the presence of oral‐like bacterial networks in the feces.ConclusionThese results suggest that GTL consumption causes both oral and gut microbiome alterations.

Background At present, the beneficial effect of the ketogenic diet (KD) on weight loss in obese patients is generally recognized. However, a systematic research on the role of KD in the improvement of glycemic and lipid metabolism of patients with diabetes is still found scarce. Methods This meta-study employed the meta-analysis model of random effects or of fixed effects to analyze the average difference before and after KD and the corresponding 95% CI, thereby evaluating the effect of KD on T2DM. Results After KD intervention, in terms of glycemic control, the level of fasting blood glucose decreased by 1.29 mmol/L (95% CI: −1.78 to −0.79) on average, and glycated hemoglobin A1c by 1.07 (95% CI: −1.37 to −0.78). As for lipid metabolism, triglyceride was decreased by 0.72 (95% CI: −1.01 to −0.43) on average, total cholesterol by 0.33 (95% CI: −0.66 to −0.01), and low-density lipoprotein by 0.05 (95% CI: −0.25 to −0.15); yet, high-density lipoprotein increased by 0.14 (95% CI: 0.03−0.25). In addition, patients’ weight decreased by 8.66 (95% CI: −11.40 to −5.92), waist circumference by 9.17 (95% CI: −10.67 to −7.66), and BMI by 3.13 (95% CI: −3.31 to −2.95). Conclusion KD not only has a therapeutic effect on glycemic and lipid control among patients with T2DM but also significantly contributes to their weight loss.

Introduction Nonalcoholic fatty liver disease (NAFLD) was renamed metabolic dysfunction associated with fatty liver disease (MAFLD) recently. We aimed to explore the risk of all-cause deaths in MAFLD participants and compare it with NAFLD in Chinese adults. Materials and Methods We enrolled 152,139 participants with abdominal ultrasonography in the Kailuan Cohort from 2006 to 2012. We categorized the participants into MAFLD and non-MAFLD, NAFLD and non-NAFLD, and four groups of Neither-FLD, MAFLD-only, NAFLD-only, and MAFLD-NAFLD, respectively. We used Cox regression models to estimate the hazard ratios and 95% confidence interval (CI) of death. Results The prevalence of MAFLD and NAFLD was 31.5% and 27.3%, respectively. After a median follow-up of 12.7 years, MAFLD and NAFLD were both associated with increased mortality, especially in men aged <40, with HR (95% CI) of 1.51(1.19-1.93) and 1.37(1.06-1.78), respectively. The MAFLD-only group had higher mortality than the NAFLD-only in males aged ≥ 60 (adjusted HR=1.43; 95% CI, 1.00-2.03) and lower risk in males aged 40-59 (adjusted HR=0.65; 95% CI,0.48-0.90). MAFLD with overweight/obesity-only decreased, but those with diabetes and/or metabolic dysregulation increased the risk of death. MAFLD with positive HBsAg and/or excessive alcohol consumption further increased the risk of death, especially in men aged <40 years (HR, 9.86; 95% CI, 2.44-39.98). Conclusion MAFLD was associated with increased all-cause mortality among the Chinese population, which was different by the status of overweight/obesity, diabetes, other metabolic indicators, and second causes. MAFLD patients should be managed by metabolic indicators and second causes to fulfill precise treatment and management.

The ability to determine the prognosis of lean nonalcoholic fatty liver disease (NAFLD) is essential for decision making in clinical settings. Using a large community‐based Chinese cohort, we aimed to investigate NAFLD outcomes by body mass index (BMI). We used the restricted cubic splines method to investigate the dose–response relationship between BMI and outcomes in subjects with NAFLD and those without NAFLD. We included 73,907 subjects from the Kailuan cohort and grouped all subjects into four phenotypes by using NAFLD and BMI (<23 kg/m2). The probability of developing outcomes for individuals with lean NAFLD (LN), overweight/obese NAFLD (ON), overweight/obese non‐NAFLD (ONN), and lean non‐NAFLD (LNN) was estimated. We found a U‐shaped association between BMI and death but a linear positive association concerning cardiovascular disease (CVD) after adjusting for age and other covariates. Compared with the LNN group, the adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) of the LN, ON, and ONN groups were 1.30 (1.14–1.49), 0.86 (0.80–0.91), 0.84 (0.80–0.89) for all‐cause death, 2.61 (1.13–6.03), 0.74 (0.44–1.26), 1.10 (0.70–1.74) for liver‐related death, 2.12 (1.46–3.08), 1.23 (0.99–1.54), 1.19 (0.98–1.43) for digestive system cancers, and 2.04 (1.40–2.96), 1.30 (1.05–1.61), 1.21 (1.01–1.46) for obesity‐related cancers. Subjects with LN had a significantly higher risk of colorectal cancer and esophagus cancer. However, the ON group had the highest CVD risk (HR, 1.39; 95% CI, 1.27–1.52). The LN group with hypertension had a higher risk of adverse outcomes, and those without hypertension had a similar risk compared to LNN. Conclusion: Subjects with LN may experience a higher risk of all‐cause death, digestive system cancers, and obesity‐related cancers than the other three groups but a lower risk of CVD than ON subjects. LN with hypertension may be a high‐risk phenotype.