Background Although accumulating evidence has demonstrated that consumption time of energy and macronutrients plays an important role in maintaining health, the association between consumption time of different foods and cardiovascular disease, cancer, and all‐cause mortalities is still largely unknown. Methods and Results A noninstitutionalized household population of the US 21 503 participants from National Health and Nutrition Examination Survey was included. Meal patterns and snack patterns throughout a whole day were measured using 24‐hour dietary recall. Principal component analysis was performed to establish dietary patterns. Cox proportional hazards models were used to evaluate the association between dietary patterns across meals and cardiovascular disease (CVD), cancer, and all‐cause mortalities. During the 149 875 person‐years of follow‐up, 2192 deaths including 676 deaths because of CVD and 476 because of cancer were documented. After adjusting for potential confounders, participants consuming fruit‐lunch had lower mortality risks of all‐cause (hazard ratio [HR], 0.82; 95% CI, 0.72–0.92) and CVD (HR, 0.66; 95% CI, 0.49–0.87); whereas participants who consumed Western‐lunch were more likely to die because of CVD (HR, 1.44; 95% CI, 1.10–1.89). Participants who consumed vegetable‐dinner had lower mortality risks of all‐cause, CVD, and cancer (HR all‐cause , 0.69; 95% CI, 0.60–0.78; HR CVD , 0.77; 95% CI, 0.61–0.95; HR cancer , 0.63; 95% CI, 0.48–0.83). For the snack patterns, participants who consumed fruit‐snack after breakfast had lower mortality risks of all‐cause and cancer (HR all‐cause , 0.78; 95% CI, 0.66–0.93; HR cancer , 0.55; 95% CI, 0.39–0.78), and participants who consumed dairy‐snack after dinner had lower risks of all‐cause and CVD mortalities (HR all‐cause , 0.82; 95% CI, 0.72–0.94; HR CVD , 0.67; 95% CI, 0.52–0.87). Participants who consumed a starchy‐snack after main meals had greater mortality risks of all‐cause (HR after‐breakfast , 1.50; 95% CI, 1.24–1.82; HR after‐lunch , 1.52; 95% CI, 1.27–1.81; HR after‐dinner , 1.50; 95% CI, 1.25–1.80) and CVD (HR after‐breakfast , 1.55; 95% CI, 1.08–2.24; HR after‐lunch , 1.44; 95% CI, 1.03–2.02; HR after‐dinner , 1.57; 95% CI, 1.10–2.23). Conclusions Fruit‐snack after breakfast, fruit‐lunch, vegetable‐dinner, and dairy‐snack after dinner was associated with lower mortality risks of CVD, cancer, and all‐cause; whereas Western‐lunch and starchy‐snack after main meals had greater CVD and all‐cause mortalities.

Background There is insufficient evidence for the ability of vitamin K2 to improve type 2 diabetes mellitus symptoms by regulating gut microbial composition. Herein, we aimed to demonstrate the key role of the gut microbiota in the improvement of impaired glycemic homeostasis and insulin sensitivity by vitamin K2 intervention. Methods We first performed a 6-month RCT on 60 T2DM participants with or without MK-7 (a natural form of vitamin K2) intervention. In addition, we conducted a transplantation of the MK-7-regulated microbiota in diet-induced obesity mice for 4 weeks. 16S rRNA sequencing, fecal metabolomics, and transcriptomics in both study phases were used to clarify the potential mechanism. Results After MK-7 intervention, we observed notable 13.4%, 28.3%, and 7.4% reductions in fasting serum glucose (P = 0.048), insulin (P = 0.005), and HbA1c levels (P = 0.019) in type 2 diabetes participants and significant glucose tolerance improvement in diet-induced obesity mice (P = 0.005). Moreover, increased concentrations of secondary bile acids (lithocholic and taurodeoxycholic acid) and short-chain fatty acids (acetic acid, butyric acid, and valeric acid) were found in human and mouse feces accompanied by an increased abundance of the genera that are responsible for the biosynthesis of these metabolites. Finally, we found that 4 weeks of fecal microbiota transplantation significantly improved glucose tolerance in diet-induced obesity mice by activating colon bile acid receptors, improving host immune-inflammatory responses, and increasing circulating GLP-1 concentrations. Conclusions Our gut-derived findings provide evidence for a regulatory role of vitamin K2 on glycemic homeostasis, which may further facilitate the clinical implementation of vitamin K2 intervention for diabetes management. Trial registration The study was registered at https://www.chictr.org.cn (ChiCTR1800019663).

To clarify the effects of dietary inflammatory and pro-oxidative potential, we investigated the impact of the Dietary Inflammation Index (DII) and the Dietary Oxidative Balance Score (DOBS) on all-cause and disease-specific mortality. For DII and DOBS, 17,550 and 24,527 participants were included. Twenty-six and seventeen dietary factors were selected for scoring. Cox proportional hazards regression models were used. DII and DOBS were significantly associated with all-cause, CVD, and cancer mortality in this nationally representative sample of American adults. Compared with the lowest DII, the multivariable-adjusted hazard ratios (95% CI) of all-cause, CVD, and cancer mortality for the highest were 1.49 (1.23–1.80), 1.58 (1.08–2.33), and 1.56 (1.07–2.25). The highest quartile of DOBS was associated with the risk of all-cause death (HR 0.71, 95% CI 0.59–0.86). Pro-inflammatory and pro-oxidative diets were associated with increased risk for all-cause (HR 1.59, 95% CI 1.28–1.97), and CVD (HR 2.29, 95% CI 1.33–3.94) death compared to anti-inflammatory and antioxidant diets. Similar results were observed among the stratification analyses. Inflammation-reducing and oxidative-balancing diets are linked to lower all-cause and CVD mortality. Diets impact health by regulating inflammation and oxidative stress.

BackgroundTryptophan and its metabolites have been found related to various cancers, but the direction of this relationship is still unclear. The purpose of this study is to explore the causal associations of tryptophan and kynurenine with multiple cancers based on the bidirectional Mendelian randomization analysis.MethodsThe data of a genome-wide association study meta-analysis on 7,824 individuals was used to explore the genetic variants strongly associated with tryptophan and kynurenine. Genetic instruments of four specific cancers were obtained from available summary-level data of 323,590 European participants. Bidirectional Mendelian randomization analysis was conducted to examine possible causality. Sensitivity analysis was performed to test heterogeneity and horizontal pleiotropy. COX regression analysis was conducted to explore associations between dietary tryptophan and cancer mortality in NHANES 1988-1994.ResultsNo evidence of any causal association of tryptophan and kynurenine with the risk of four specific cancers was shown, except for weak correlations were suggested between lung or prostate cancer and kynurenine. Multiple sensitivity analyses generated similar results. Our findings from COX regression analysis were consistent with the above results.ConclusionsOur study did not find any causal relationship between tryptophan and kynurenine and multiple cancers. The associations still need further research.

Dietary carbohydrate consumption was related to cognitive function. Whereas, there was no study investigate the association of dietary carbohydrate consumption with cognitive function modification by daily fasting duration. This study aims to examine the association between dietary carbohydrate consumption and cognitive function among participants with different daily fasting duration. In this cross-sectional study, 2485 adults aged over 60 years from the nationally representative data of the National Health and Nutrition Examination Survey (NHANES, 2011–2014) were enrolled. Percentage energy from carbohydrates was present in both quartiles and continuous forms. Daily fasting duration = 24 – (timing for dinner – breakfast). Cognitive function was assessed by the Consortium to Establish a Registry for Alzheimer’s Disease Word List Learning (CERAD-WL), CERAD Word List Delayed Recall (CERAD-DR), Animal Fluency (AF), and Digit Symbol Substitution (DSST) Test. Multiple logistic regression and linear regression models were developed to examine the association of dietary carbohydrates with cognitive function among participants with different daily fasting duration. Restricted cubic spline models were also applied. Compared with the lowest quartile of percentage energy from carbohydrates, the highest quartile had higher ORs of poor cognitive performance among total participants [(ORCERAD-WL 1.84 95% CI 1.25–2.71); (ORCERAD-DR 1.45 95% CI 1.10–1.91)] and participants with daily fasting duration fewer than 16 h [(ORCERAD-WL 2.14 95% CI 1.29–3.55); (ORCERAD-DR 1.51 95% CI 1.05–2.17)] but not in participants with daily fasting duration of more than 16 h. Further, the negative associations between percentage energy from carbohydrates and CERAD-WL score were still significant in addition to participants whose daily fasting duration was more than 16 h. Additionally, dose-response associations were detected between dietary carbohydrates and cognitive decline, while “U” curves were observed among participants whose daily fasting duration was more than 16 h. This study indicated that dietary carbohydrates consumption was associated with poor cognitive performance, but not in participants whose daily fasting duration was more than 16 h among US older adults. The current analysis provides evidence that a longer daily fasting duration may improve the harmful effect of dietary carbohydrates on cognitive function.