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.

The question of whether or not intermittent fasting diets improve the clinical indicators of glycolipid metabolism remains unclear. This study systematically reviewed the relevant clinical trials to evaluate the effects of intermittent fasting diet on glucose and lipid metabolism and insulin sensitivity in patients with metabolic syndrome. To evaluate the effect of intermittent fasting diet intervention on patients with disorders of glucose and lipid metabolism, random-effect or fixed-effect meta-analysis models were used to calculate the average difference before and after intermittent fasting diet intervention and the corresponding 95% confidence intervals (CIs). After intermittent fasting diet intervention, in terms of glucose metabolism, fasting blood glucose reduced by 0.15 mmol/L (95% CI: −0.23; −0.06), glycosylated hemoglobin reduced by 0.08 (95% CIs: −0.25; −0.10), insulin plasma levels reduced by 13.25 uUI (95% CIs: −16.69; −9.82), and HOMA-IR decreased by 0.31 on an average (95% CIs: −0.44; −0.19). In addition, BMI decreased by 0.8 kg/m2 (95% CIs: −1.32; −0.28), body weight reduced by 1.87 kg (95% CIs: −2.67; −1.07), and the waist circumference decreased by 2.08 cm (95% CIs: −3.06; −1.10). Analysis of lipid metabolism showed that intermittent fasting diet intervention effectively reduced the total cholesterol level by 0.32 mmol/L (95% CIs: −0.60; −0.05), low-density lipoprotein level by 0.22 mmol/L (95% CIs: −0.37; −0.07), and triglyceride level by 0.04 mmol/L (95% CIs: −0.15; −0.07). Intermittent fasting diets have certain therapeutic effects on blood glucose and lipids in patients with metabolic syndrome and significantly improve insulin resistance. It may be considered as an auxiliary treatment to prevent the occurrence and development of chronic diseases.

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Background: Lifestyles generally change across the life course yet no prospective study has examined direct associations between healthy lifestyle trajectories and subsequent cardiovascular disease (CVD) or all-cause mortality risk.Methods: Healthy lifestyle score trajectories during 2006–2007, 2008–2009, and 2010–2011 were collated through latent mixture modeling. An age-scale based Cox proportional hazard regression model was implemented to calculate hazard ratios (HR) with corresponding 95% confidence intervals (CI) for developing CVD or all-cause mortality across healthy lifestyle trajectories.Results: 52,248 participants were included with four distinct trajectories identified according to healthy lifestyle scores over 6 years i.e., low-stable (n = 11,248), high-decreasing (n = 7,374), low-increasing (n = 7,828), and high-stable (n = 25,799). Compared with the low-stable trajectory, the high-stable trajectory negatively correlated with lower subsequent risk of developing CVD (HR, 0.73; 95% CI, 0.65–0.81), especially stroke (HR, 0.70; 95% CI, 0.62–0.79), and all-cause mortality (HR, 0.89; 95% CI, 0.80–0.99) under a multivariable-adjusted model. A protective effect for CVD events was observed only in men and in those without diabetes, while a reduced risk of all-cause mortality was observed only in those older than 60 years, though interactions were not statistically significant. Marginally significant interactions were observed between the changing body mass index (BMI) group, healthy lifestyle score trajectories and stratified analysis. This highlighted an inverse correlation between the high-stable trajectory and CVD in BMI decreased and stable participants as well as all-cause mortality in the stable BMI group. The low-increasing trajectory also had reduced risk of CVD only when BMI decreased and in all-cause mortality only when BMI was stable.Conclusions: Maintaining a healthy lifestyle over 6 years corresponds with a 27% lower risk of CVD and an 11% lower risk in all-cause mortality, compared with those engaging in a consistently unhealthy lifestyle. The benefit of improving lifestyle could be gained only after BMI change is considered further. This study provides further evidence from China around maintaining/improving healthy lifestyles to prevent CVD and early death.

Background: No study has explored the modification effect of ideal cardiovascular health metrics (ICVHMs) on the association between famine exposure and risk of cardiovascular disease (CVD) so far. We aim to examine the effect of ICVHMs on the association between exposure to famine early in life and the risk of CVD in adulthood.Methods: A total of 61,527 participants free of CVD were included in this study from the Kailuan Study. All participants were divided into three groups, included nonexposed, fetal-exposed, and childhood-exposed groups. Cox regression was used to estimate the effect of famine exposure and ICVHMs on CVD risk.Results: After a median of 13.0 (12.7–13.2) years follow-up, 4,814 incident CVD cases were identified. Compared with nonexposed participants, the CVD risk increased in participants with fetal famine exposure (hazard ratio [HR]: 1.21; 95% CI: 1.07–1.37), but not in childhood famine-exposed participants. After stratifying by the number of ICVHMs, the increased CVD risk associated with fetal famine exposure was only observed in participants with less ICVHMs ( ≤ 2) (HR: 1.30; 95% CI: 1.11–1.52, P for interaction=0.008), but disappeared in those with three or more ICVHMs. The modified effect of ICVHMs was sex specific (P for sex interaction = 0.031).Conclusions: Exposing to famine in the fetal period could increase the risk of CVD in late life; however, ICVHMs might modify the effect of famine exposure on CVD risk, especially in men.