Relationship between circadian eating behavior (daily eating frequency and nighttime fasting duration) and cardiovascular mortality.

BACKGROUND: Knowledge regarding the health impacts of daily eating frequency (DEF) and nighttime fasting duration (NFD) on mortality is very limited. OBJECTIVE: This study aimed to examine whether DEF and NFD are associated with CVD and all-cause mortality. METHODS: This was a prospective cohort study of a nationally representative sample from the United States, including 30,464 adults who participated in the National Health and Nutrition Examination Survey 2003-2014. Using 24-h dietary recall, DEF was assessed by the number of eating episodes, and NFD was calculated by the first and last eating time across a day. Death information was obtained from the National Death Index up to 2019. Weighted Cox proportional hazards regression models were used to assess survival relationships of DEF and NFD with mortality. RESULTS: During 307,686 person-years of follow-up, 4560 deaths occurred, including 1824 CVD cases. After adjustment for confounders, compared to DEF at 4-6 times, participants whose DEF was less than 3 times had greater CVD [hazard-ratio (HR) = 1.33, 95% confidence-interval (CI): 1.06-1.67] and all-cause (HR = 1.16, 95% CI: 1.01-1.33) mortality risks. Furthermore, compared to NFD of 10 to 11 h, participants whose NFD was shorter than 10 h had HRs of 1.30 (95% CI: 1.08-1.55) for CVD mortality and 1.23 (95% CI: 1.08-1.39) for all-cause mortality. NFD longer than 14 h was also related to CVD mortality (HR = 1.37, 95% CI: 1.12-1.67) and all-cause mortality (HR = 1.36, 95% CI: 1.19-1.54). Similar results for the association of NFD and DEF with heart-specific and stroke-specific mortality were observed. CONCLUSION: This study found that DEF less than 3 times and NFD shorter than 10 h or longer than 14 h were independently associated with greater cardiovascular and all-cause mortality.

Maternal smoking, nutritional factors at different life stage, and the risk of incident type 2 diabetes: a prospective study of the UK Biobank.

BACKGROUND: This study aims to investigate potential interactions between maternal smoking around birth (MSAB) and type 2 diabetes (T2D) pathway-specific genetic risks in relation to the development of T2D in offspring. Additionally, it seeks to determine whether and how nutritional factors during different life stages may modify the association between MSAB and risk of T2D. METHODS: This study included 460,234 participants aged 40 to 69 years, who were initially free of T2D from the UK Biobank. MSAB and breastfeeding were collected by questionnaire. The Alternative health eating index(AHEI) and dietary inflammation index(DII) were calculated. The polygenic risk scores(PRS) of T2D and pathway-specific were established, including ß-cell function, proinsulin, obesity, lipodystrophy, liver function and glycated haemoglobin(HbA1c). Cox proportion hazards models were performed to evaluate the gene/diet-MSAB interaction on T2D. The relative excess risk due to additive interaction (RERI) were calculated. RESULTS: During a median follow-up period of 12.7 years, we identified 27,342 cases of incident T2D. After adjustment for potential confounders, participants exposed to MSAB had an increased risk of T2D (HR=1.11, 95%CI:1.08-1.14), and this association remained significant among the participants with breastfeeding (HR= HR=1.10, 95%CI: 1.06-1.14). Moreover, among the participants in the highest quartile of AHEI or in the lowest quartile of DII, the association between MSAB and the increased risk of T2D become non-significant (HR=0.94, 95%CI: 0.79-1.13 for AHEI; HR=1.09, 95%CI:0.99-1.20 for DII). Additionally, the association between MSAB and risk of T2D became non-significant among the participants with lower genetic risk of lipodystrophy (HR=1.06, 95%CI:0.99-1.14), and exposed to MSAB with a higher genetic risk for ß-cell dysfunction or lipodystrophy additively elevated the risk of T2D(RERI=0.18, 95%CI:0.06-0.30 for ß-cell function; RERI=0.16, 95%CI:0.04-0.28 for lipodystrophy). CONCLUSIONS: This study indicates that maintaining a high dietary quality or lower dietary inflammation in diet may reduce the risk of T2D associated with MSAB, and the combination of higher genetic risk of ß-cell dysfunction or lipodystrophy and MSAB significantly elevate the risk of T2D in offspring.

The association between blue light exposure and incidence of type 2 diabetes: A prospective study of UK biobank.

BACKGROUND: Type 2 diabetes (T2D) is the most common type of diabetes. However, research on the relationship between blue light exposure and diabetes development is limited. OBJECTIVE: The present study aimed to investigate the relationship between blue light exposure and T2D incidence and whether it is affected by sleep duration, physical activity, outdoor activity time, and genetic susceptibility. METHODS: A total of 471,686 participants without diabetes were recruited from the UK Biobank cohort. T2D incidence was assessed using hospital inpatient records. Blue light exposure was calculated based on the time spent watching TV, using a computer, and playing computer games, which was determined using an online questionnaire. Cox proportional hazards regression models were used to assess the survival relationship between blue light exposure and T2D, as well as the potential modification effects. RESULT: A total of 18,738 cases of T2D were documented during the median follow-up of 13.04 years. After adjusting for potential confounders, the participants with heavy blue light exposure had a greater risk of T2D compared to those with mild blue light exposure (hazard ratio (HR) = 1.17, 95% confidence interval (CI): 1.12-1.23). A significant association between blue light exposure and T2D risk was observed among the participants with heavy physical activity (HR = 1.39, 95%CI: 1.25-1.55), healthy sleep habits (HR = 1.23, 95%CI: 1.10-1.36), higher outdoor activity time (HR = 1.14, 95%CI: 1.07-1.22), or high genetic susceptibility (HR = 1.24, 95%CI: 1.14-1.35). However, this association became non-significant among the participants with low genetic susceptibility (HR = 1.05, 95%CI: 0.97-1.15). CONCLUSION: The present study showed that blue light exposure is associated with a greater risk of T2D independent of classical T2D risk factors.

The rest-activity rhythm, genetic susceptibility and risk of type 2 diabetes: A prospective study in UK Biobank.

AIMS: This study aims to examine the association between the rest-activity rhythm (RAR) and the incidence of type 2 diabetes (T2D). MATERIALS AND METHODS: In total, 97 503 participants without diabetes in the UK Biobank cohort were recruited. Wearable accelerometry was used to monitor circadian behaviour. The parameters of RAR including inter-daily stability, intra-daily variability, relative amplitude (RA), most active continuous 10 h period (M10), and least active continuous 5 h period (L5) were calculated to evaluate the robustness and regularity of the RAR. The weighted polygenic risk score for T2D (T2D-PRS) was calculated. Cox proportion hazards models were used to evaluate the survival relationship and the joint and interaction effects of RAR parameters and T2D-PRS on the occurrence of T2D. RESULTS: During 692 257 person-years follow-ups, a total of 2434 participants were documented. After adjustment for potential confounders, compared with participants in the highest quartile of RA and M10, the participants in the lowest quartile had a greater risk of T2D (HRRA = 2.06, 95% CI: 1.76-2.41; HRM10 = 1.33, 95% CI: 1.19-1.49). Meanwhile, the highest quartile of L5 was related to a higher risk of T2D (HR = 1.78, 95% CI: 1.55-2.24). The joint analysis showed that the high T2D-PRS with the lowest quartile of RA and M10, or highest quartile of L5 jointly increased the risk of T2D (HRRA = 4.46, 95% CI: 3.36-6.42; HRM10 = 3.15, 95% CI: 2.29-4.32; HRL5 = 3.09, 95% CI: 2.40-3.99). No modification effects of T2D-PRS on the association between the RAR parameters and risk of T2D were observed (p > .05). CONCLUSION: The unbalanced RAR are associated with a greater risk of T2D, which are independent of known risk factors of T2D.

The Association of Food Groups and Consumption Time with Hyperuricemia: The U.S. National Health and Nutrition Examination Survey, 2005-2018.

Hyperuricemia (HUA) is associated with a wide range of diseases and increases the public health burden on society as a whole. In addition to genetic variation, diet plays a crucial role in the prevention and treatment of HUA as an important modifiable behavior. The purpose of this study is to investigate whether food groups and consumption time are associated with HUA. A total of 41,230 participants from the National Health and Nutrition Examination Survey between 2005 and 2018 were included in the study. All meals, including breakfast, lunch, and dinner, were obtained according to their corresponding Food Patterns Equivalents Database dietary data. The binary logistic regression model was used to analyze the relationship between food groups, food consumption time and HUA. We found that the intake of fruit (mixed in various forms) (OR = 0.942, 95% CI: 0.909-0.976) or freshly squeezed juices (OR = 0.915, 95% CI: 0.859-0.975), milk (OR = 0.839, 95% CI: 0.808-0.872), and eggs (OR = 0.881, 95% CI: 0.839-0.924), poultry (OR = 1.055, 95% CI: 1.033-1.077) and seafood high in n-3 fatty acids (OR = 1.068, 95% CI: 0.1.018-1.120) at dinner, eating refined grains at breakfast (OR = 0.954, 95% CI: 0.924-0.985) and dinner (OR = 0.962, 95% CI: 0.944-0.980), eating whole grains (OR = 0.908, 95% CI: 0.845-0.976) at lunch, consuming alcoholic beverages or foods at breakfast (OR = 0.748, 95% CI: 0.564-0.990)/lunch (OR = 1.118, 95% CI: 1.008-1.240)/dinner (OR = 1.127, 95% CI: 1.073-1.185) were associated with HUA. Eating particular meals at particular times of the day was related to a lower risk of HUA.

Association of 24 h Behavior Rhythm with Non-Alcoholic Fatty Liver Disease among American Adults with Overweight/Obesity.

Emerging evidence suggests that in addition to metabolic, genetic and environmental factors, circadian rhythm also plays a role in non-alcoholic fatty liver disease (NAFLD). This study aimed to explore the association of 24 h behavior rhythm (activity-rest and feeding-fasting rhythm) with NAFLD. A total of 4502 adult participants with overweight/obesity from the National Health and Nutrition Examination Survey (NHANES) 2011-2014 were included in the current study. The behavior rhythm indices were calculated and divided into quintiles for logistic regression models. Compared to those in the lowest quintile, participants in the highest quintile of relative amplitude (RA) had a lower risk of NAFLD (OR = 0.71, 95% CI, 0.55-0.91); participants in the highest quintile of the average activity of the least active continuous 5 h period (L5) were associated with a higher risk of NAFLD (OR = 1.35, 95% CI, 1.07-1.71). Additionally, participants in the highest quintile of fasting duration and feeding rhythm score were associated with a lower risk of NAFLD relative to those in the lowest quintile (OR = 0.76, 95% CI, 0.59-0.98 for fasting duration, OR = 0.74, 95% CI, 0.58-0.95 for feeding rhythm score). The associations were stronger among participants with obesity. No significant associations were found in the relationship of other behavior rhythm indices with NAFLD. This study indicated a significant association of 24 h behavior rhythm with NAFLD among American adults with overweight/obesity.

Inhibition of MAOB Ameliorated High-Fat-Diet-Induced Atherosclerosis by Inhibiting Endothelial Dysfunction and Modulating Gut Microbiota.

In this study, monoamine oxidase B (MAOB) was activated under pathological conditions, and was the novel source of cardiovascular reactive oxygen species (ROS). ROS-induced endothelial dysfunction results in sustained and chronic vascular inflammation, which is central to atherosclerotic diseases. However, whether MAOB regulates endothelial oxidative stress and its related mechanism and whether gut microbiota mediates the anti-atherosclerosis effect of MAOB inhibitor remains unclear. In our study, MAOB expressions were elevated in high-fat diet (HFD) fed mice aortas, but only in vascular endothelial cells (not in smooth muscle cells). MAOB small interfering RNA significantly attenuated the palmitic-acid (PA)-induced endothelial oxidative stress and dysfunction. Furthermore, RNA-sequencing data revealed that MAOB knockdown decreased the levels of proinflammatory and apoptotic gene induced by PA. Microarray analysis and qPCR assay showed that miR-3620-5p was significantly decreased under the HFD condition. The dual-luciferase reporter, Western blot and qPCR assay confirmed that miR-3620-5p directly regulated MAOB by binding to its mRNA 3'UTR. Moreover, inhibition of MAOB by selegiline significantly ameliorated endothelial dysfunction and reduced atherosclerotic burden in HFD-fed ApoE-/- mice. Finally, 16S rRNA sequencing showed that selegiline significantly altered the community compositional structure of gut microbiota. Specifically, selegiline treatment enriched the abundance of Faecalibaculum and Akkermansia, decreased the abundance of unclassified_f__Lachnospiraceae, Desulfovibrio, and Blautia, and these genera were significantly correlated with the serum biochemical indices. Taken together, our findings showed that MAOB controlled endothelial oxidative stress homeostasis, and revealed the anti-atherosclerotic effect of selegiline by ameliorating endothelial dysfunction and modulating the composition and function of gut microbiota.

Selegiline ameliorated dyslipidemia and hepatic steatosis in high-fat diet mice.

Certain monoamine oxidase (MAO) inhibitors exhibit beneficial effects, such as reducing adiposity and metabolic disorders; however, their effects on hepatic lipid metabolism have not been revealed. This study aimed to investigate the effects of a selective MAO-B inhibitor, selegiline, on dyslipidemia and hepatic steatosis in mice induced by a high-fat diet (HFD). Administration of selegiline (0.6 mg/kg body weight) by intraperitoneal injection was found to reduce HFD-induced body weight gain and increases in liver and adiposity coefficients, blood lipids and fatty acid levels. Furthermore, selegiline dramatically reduced the total triglyceride (TG) and cholesterol (TC) levels and lipid accumulation in the livers of HFD-fed mice and palmitic acid (PA)-treated AML-12 hepatocytes. In vivo and in vitro results indicated that selegiline protects against HFD- and PA-induced hepatic inflammation by reducing the expression of proinflammatory cytokines, namely IL-6, TNF-α, IL-1ß, and IL-1α. Additionally, selegiline exhibited antioxidative effects on HFD and PA exposure in mouse liver and AML-12 cells by decreasing the levels of reactive oxygen species (ROS) and malonaldehyde (MDA) and increasing superoxide dismutase (SOD) activity. Further study showed that selegiline administration mitigated the expression of Srebf-1, Fasn, and Acaca and downregulated the expression of Cpt-1 and Pparα in HFD-fed mouse livers and PA-treated AML-12 cells. In conclusion, our findings suggest that selegiline exerts protective effects against HFD-induced dyslipidemia and hepatic steatosis, which may be related to an improved inflammatory response, oxidative stress, and hepatic lipid metabolism.

Prognostic value of gut microbiota-derived metabolites in patients with ST-segment elevation myocardial infarction.

BACKGROUND: Studies about the prognostic role of gut microbiota-derived metabolites including phenylacetyl glutamine (PAGln), indoxyl sulfate (IS), lithocholic acid (LCA), deoxycholic acid (DCA), trimethylamine (TMA), trimethylamine N-oxide (TMAO), and its precursor trimethyllysine (TML) are limited in patients with ST-segment elevation myocardial infarction (STEMI). OBJECTIVES: To examine the relationship between plasma metabolite levels and major adverse cardiovascular events (MACEs), including nonfatal MI, nonfatal stroke, all-cause mortality, and heart failure in patients with STEMI. METHODS: We enrolled 1004 patients with STEMI undergoing percutaneous coronary intervention (PCI). Plasma levels of these metabolites were determined by targeted liquid chromatography/mass spectrometry. The associations of metabolite levels with MACEs were assessed with the Cox regression model and quantile g-computation. RESULTS: During a median follow-up of 360 d, 102 patients experienced MACEs. Higher plasma PAGln (hazard ratio [HR], 3.17 [95% CI: 2.05, 4.89]; P < 0.001), IS (2.67 [1.68, 4.24], P < 0.001), DCA (2.36 [1.40, 4.00], P = 0.001), TML (2.66 [1.77,3.99], P < 0.001), and TMAO (2.61 [1.70, 4.00], P < 0.001) levels were significantly associated with MACEs independent of traditional risk factors. According to quantile g-computation, the joint effect of all these metabolites was 1.86 (95% CI: 1.46, 2.27). PAGln, IS and TML had the greatest proportional positive contributions to the mixture effect. Additionally, plasma PAGln and TML combined with coronary angiography scores including the Synergy between PCI with Taxus and cardiac surgery (SYNTAX) score (area under the curve [AUC]: 0.792 vs. 0.673), Gensini score (0.794 vs. 0.647) and Balloon pump-assisted Coronary Intervention Study (BCIS-1) jeopardy score (0.774 vs. 0.573) showed better prediction performance for MACEs. CONCLUSIONS: Higher plasma PAGln, IS, DCA, TML, and TMAO levels are independently associated with MACEs suggesting that these metabolites may be useful markers for prognosis in patients with STEMI.

Dysregulation of the microbiota-brain axis during long-term exposure to polystyrene nanoplastics in rats and the protective role of dihydrocaffeic acid.

Polystyrene nano-plastics (PS-NPs) can be accumulated in the food chain and can penetrate biological barriers to affect multiple physiological functions. However, the adverse effects of nano-plastics on mammals and the underlying mechanism still remain unknown. To fill the gaps, our study administrated low-dose PS-NPs (50 and 100 µg/L) for 24 consecutive weeks in rats. Behavioral and morphological evaluations were performed to assess the neurobehavoirs. A combined analysis of multiple omics was used to evaluate the dysfunctions of the gut-microbe-brain axis. After dihydrochalcone(NHDC) treatment in the PS-NPs rat model, the inflammation response and apoptosis process were assessed and proteomics was used to explore the underlying mechanism. Our results indicated that long-term exposure to low-dose PS-NPs could induce abnormal neurobehaviors and amygdaloid nucleus impairment, and stimulate inflammatory responses and apoptosis. Metagenomics results revealed that four microbial phyla including Proteobacteria, Firmicutes, Defferibacteres, and Bacteroidetes changed significantly compared to the control. Targeted metabolomics analysis in the feces showed alteration of 122 metabolites induced by the PS-NPs exposure, among which the content of dihydrocaffeic acid was significantly associated with the different microbial genera and pivotal differential metabolites in the amygdaloid nucleus. And NHDC treatment significantly alleviated PS-NP-induced neuroinflammation and apoptosis and the cyclic adenosine monophosphate(cAMP)/protein kinase A(PKA)/phosphorylated cAMP-response element binding protein(p-CREB)/plasma membrane calcium-transporting ATPase 2(Atp2b2) signaling pathway was identified in the proteomics. In conclusion, long-term exposure to low-dose PS-NPs has adverse effects on emotion through the dysregulation of the gut-brain axis, and dihydrocaffeic acid can alleviate these effects via the cAMP/PKA/p-CREB/Atp2b2 signaling pathway.

Association of meal timing of energy, macronutrients and foods with hypercholesterolaemia in the US adults.

Few studies examined the association of energy, macronutrients and food consumption at dinner v. breakfast with hypercholesterolaemia. A total of 27 911 participants from the National Health and Nutrition Examination Survey (2003-2016) were included in the cross-sectional study. Energy, macronutrients and food consumption at breakfast, dinner and the difference at dinner v. breakfast (Δratio) were calculated. Multiple logistic regression models and substitution effects of foods at dinner with breakfast were also performed. After adjustment for potential covariates, compared with the lowest quintile, participants in the highest quintile of Δratio in terms of energy had a higher risk of prevalent hypercholesterolaemia (ORΔratio of energy 1·16, 95 % CI (1·01, 1·33)) mainly due to Δratio of low-quality carbohydrates and plant protein (ORΔratio of low-quality carbohydrates 1·19; 95 % CI (1·05, 1·35)); ORΔratio of plant protein 1·13; 95 % CI (1·01, 1·28)). ΔAdded sugars and Δnuts were associated with hypercholesterolaemia (ORΔadded sugars 1·01; 95 % CI (1·00, 1·02)); ORΔnuts 1·08; 95 % CI (1·01, 1·16)). Furthermore, the substitution of added sugars, nuts and processed meat at dinner with breakfast could reduce the OR of hypercholesterolaemia. This study indicated that among US adults, overconsumption of energy, macronutrients including low-quality carbohydrates and plant protein at dinner than breakfast was significantly associated with a higher risk of prevalent hypercholesterolaemia. The replacing of added sugar, nuts and processed meat at dinner with breakfast reduced the risk of prevalent hypercholesterolaemia. This study emphasised the importance of meal timing in the prevention of hypercholesterolaemia.

Association of Urinary Nitrate With Diabetes Complication and Disease-Specific Mortality Among Adults With Hyperglycemia.

CONTEXT: The hyperglycemia condition disrupts metabolism of nitrate/nitrite and nitric oxide, and dietary nitrate intake can restore nitric oxide homeostasis. OBJECTIVE: This study aims to examine whether urinary nitrate is associated with diabetes complications and long-term survival among people with hyperglycemia. METHODS: A total of 6208 people with hyperglycemia who participated in the National Health and Nutrition Examination Survey from 2005 to 2014 were enrolled. Diabetes complications included congestive heart failure, coronary heart disease, angina, stroke, myocardial infarction, diabetic retinopathy, and nephropathy. Mortality was obtained from the National Death Index until 2015. Urinary nitrate was measured by ion chromatography coupled with electrospray tandem mass spectrometry, which was log-transformed and categorized into tertiles. Logistic regression models and Cox proportional hazards models were respectively performed to assess the association of urinary nitrate with the risk of diabetes complications and disease-specific mortalities. RESULTS: After adjustment for potential confounders, including urinary perchlorate and thiocyanate, compared with the participants in the lowest tertile of nitrate, the participants in the highest tertile had lower risks of congestive heart failure (odds ratio [OR] 0.41; 95% CI, 0.27-0.60) and diabetic nephropathy (OR 0.50; 95% CI, 0.41-0.62). Meanwhile, during a total follow-up period of 41 463 person-years, the participants in the highest tertile had lower mortality risk of all-cause (hazard ratio [HR] 0.78; 95% CI, 0.62-0.97), cardiovascular disease (CVD) (HR 0.56; 95% CI, 0.37-0.84), and diabetes (HR 0.47; 95% CI, 0.24-0.90), which showed dose-dependent linear relationships (P for nonlinearity > 0.05). Moreover, no association between nitrate and cancer mortality was observed (HR 1.13; 95% CI, 0.71-1.80). CONCLUSION: Higher urinary nitrate is associated with lower risk of congestive heart failure and diabetic nephropathy, and lower risk of all-cause, CVD, and diabetes mortalities. These findings indicate that inorganic nitrate supplementation can be considered as a supplementary treatment for people with hyperglycemia.

Associations between the timing of different foods' consumption with cardiovascular disease and all-cause mortality among adults with sleep disorders.

Introduction: People with sleep disorders are under disrupted biological rhythms. Whether changing the timing of specific food consumption contributes to decreasing cardiovascular and all-cause risk is unknown. Methods: A total of 8,005 participants with sleep disorders were selected from the U.S. National Health and Nutrition Examination Survey (NHANES) from 2005 to 2014. Cox proportional hazards regression models were used to analyze the relationship between the consumption time of foods and cardiovascular disease (CVD) and all-cause death. Moreover, equivalent food substitution models were carried out to evaluate the alterations in the risk of CVD mortality for the changed food intake time. Results: After adjusting for multiple confounders, participants who consume red and orange vegetables, starchy vegetables, and fermented dairy in the morning (hazard ratio (HR) red and orange vegetables = 0.45, 95% CI: 0.26-0.81; HR starchy vegetables = 0.47, 95% CI: 0.25-0.88; HR fermented dairy = 0.57, 95% CI: 0.36-0.89) and milk and eggs in the evening contribute to reducing the likelihood of death from CVD (HR milk = 0.65, 95% CI: 0.43-0.96; HR eggs = 0.72, 95% CI: 0.53-0.98). Iso-calorically switching 0.1 serving of starchy vegetable and fermented dairy and milk intake from one period to another does significantly reduce the mortality risk of CVD. Conclusion: Higher intake of red and orange vegetables, starchy vegetables, and fermented dairy in the morning and milk and eggs in the evening confers a lower risk of CVD among individuals with sleep disorders.

The association of diet carbohydrates consumption with cognitive function among US older adults modification by daily fasting duration.

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.

The association of dietary spermidine with all-cause mortality and CVD mortality: The U.S. National Health and Nutrition Examination Survey, 2003 to 2014.

Background: Current studies on the protective effects of dietary spermidine (SPD) on cardiovascular disease (CVD) are mainly limited to animal studies, and the relationship between dietary SPD and CVD mortality remains inconclusive. Objective: This study aims to evaluate the association between dietary SPD intake and CVD and all-cause mortality. Methods: A total of 23,894 people enrolled in the National Health and Nutrition Examination Survey (NHANES) from 2003 to 2014 were recruited for this study. The dietary intake of SPD from 11 specific food origins and total SPD was categorized into tertiles or quartiles. Cox proportional hazard regression models were developed to evaluate the association of SPD intake with CVD and all-cause mortalities. Results: Among the 23,894 participants, 2,365 deaths, including 736 deaths due to CVD, were documented. After adjustment for potential confounders, compared with participants in the lowest quartile, participants in the highest quartile of total SPD had a significantly lower risk of CVD mortality (HR = 0.68, 95% CI: 0.51-0.91) and all-cause mortality (HR = 0.70, 95% CI: 0.60-0.82); participants in the highest tertiles or quartiles of vegetable-derived SPD, cereal-derived SPD, legume-derived SPD, nut-derived SPD, and cheese-derived SPD had a lower risk of CVD mortality (HR vegetable - derivedSPD = 0.68, 95% CI: 0.54-0.86; HR cereal - derivedSPD = 0.75, 95% CI: 0.57-0.97; HR legume - derivedSPD = 0.68, 95% CI: 0.52-0.88; HR nut - derivedSPD = 0.66, 95% CI: 0.53-0.80; HR cheese - derivedSPD = 0.68, 95% CI: 0.52-0.88) and all-cause mortality (HR vegetable - derivedSPD = 0.73, 95% CI: 0.64-0.84; HR cereal - derivedSPD = 0.80, 95% CI: 0.69-0.93; HR legume - derivedSPD = 0.70, 95% CI: 0.60-0.80;HR nut - derivedSPD = 0.72, 95% CI: 0.64-0.81; HR cheese - derivedSPD = 0.70, 95% CI: 0.61-0.81) than those in the lowest tertiles or quartiles. Moreover, subgroup analysis showed consistent associations among the people with hypertension and hyperlipidemia. Conclusion: Higher intake of dietary SPD is associated with decreased risk of CVD and all-cause mortality, and among specific food origin SPD, SPD derived from vegetables, cereals, legumes, nuts, and cheese was associated with reduced CVD and all-cause mortality.

Relationship Between Carbohydrate Intake (Quantity, Quality, and Time Eaten) and Mortality (Total, Cardiovascular, and Diabetes): Assessment of 2003-2014 National Health and Nutrition Examination Survey Participants.

OBJECTIVE: In this study we investigated the association of the quantity, quality, and timing of carbohydrate intake with all-cause, cardiovascular disease (CVD), and diabetes mortality. RESEARCH DESIGN AND METHODS: This secondary data analysis included use of National Health and Nutrition Examination Survey (2003-2014) and National Death Index data from adults (n = 27,623) for examination of the association of total daily and differences in carbohydrate intake with mortality. Participants were categorized into four carbohydrate intake patterns based on the median values of daily high- and low-quality carbohydrate intake. The differences (Δ) in carbohydrate intake between dinner and breakfast were calculated (Δ = dinner - breakfast). Cox regression models were used. RESULTS: The participants who consumed more high-quality carbohydrates throughout the day had lower all-cause mortality risk (hazard ratio [HR] 0.88; 95% CI 0.79-0.99), whereas more daily intake of low-quality carbohydrates was related to greater all-cause mortality risk (HR 1.13; 95% CI: 1.01-1.26). Among participants whose daily high- and low-quality carbohydrate intake were both below the median, the participants who consumed more high-quality carbohydrates at dinner had lower CVD (HR 0.70; 95% CI 0.52-0.93) and all-cause mortality (HR 0.82; 95% CI 0.70-0.97) risk; an isocaloric substitution of 1 serving low-quality carbohydrates intake at dinner with high-quality reduced the CVD and all-cause mortality risks by 25% and 19%. There was greater diabetes mortality among the participants who consumed more low-quality carbohydrates at dinner (HR 1.78; 95% CI 1.02-3.11), although their daily high-quality carbohydrate intake was above the median. CONCLUSIONS: Consuming more low-quality carbohydrates at dinner was associated with greater diabetes mortality, whereas consuming more high-quality carbohydrates at dinner was associated with lower all-cause and CVD mortality irrespective of the total daily quantity and quality of carbohydrates.

The Association Between Exposure to Acrylamide and Mortalities of Cardiovascular Disease and All-Cause Among People With Hyperglycemia.

Background: Acrylamide is a common environmental volatile organic compound that humans are frequently exposed to in their daily lives. However, whether exposure to acrylamide is associated with long-term survival in patients with hyperglycemia remains largely unknown. Methods and Results: A total of 3,601 hyperglycemic people were recruited in this study, including 1,247 people with diabetes and 2,354 people with pre-diabetes, who enrolled in the National Health and Nutrition Examination survey (2003-2004, 2005-2006, and 2013-2014). The acrylamide exposure was measured by the serum hemoglobin adduct of acrylamide (HbAA) and glycidamide (HbGA), and the ratio of HbAA and HbGA (HbAA/HbGA) was calculated, which were all categorized into quintiles. The National Death Index was used to identify the participants' death information until 2015. Cox proportional hazards (CPHs) regression models were performed to examine the survival relationship between these biomarkers and mortality. During the 28,652 person-year follow-up, 268 deaths due to the cardiovascular disease (CVD) were documented. After adjustment for multiple confounders, compared with participants in the lowest quintile of HbAA/HbGA, the participants in the highest quintile were more likely to die due to CVD (hazard ratio [HR] = 1.61, 95% CI: 1.09-2.39) and all-cause (HR = 1.59, 95% CI: 1.25-2.01). Moreover, subgroup analysis showed that the highest quintile of HbAA/HbGA in the people with diabetes or pre-diabetes was related to mortalities risk of CVD (HR diabetes = 1.92, 95% CI: 1.11-3.31; HR pre-diabetes = 1.78, 95% CI: 1.01-3.14) and all-cause mortality (HR diabetes = 1.81, 95% CI: 1.27-2.58; HR pre-diabetes = 1.59, 95% CI: 1.14-2.20). Additionally, no significant association between the levels of HbAA or HbGA and CVD mortality was observed among people with diabetes or pre-diabetes. Conclusion: Higher levels of HbAA/HbGA are associated with greater mortalities of CVD and all-cause among hyperglycemic people.

Association of phthalate exposure with all-cause and cause-specific mortality among people with hypertension: The U.S. National Health and Nutrition Examination Survey, 2003-2014.

There is growing evidence that phthalate exposure results in a deteriorated effect on human health, while very few studies directly investigate the relationship of phthalate metabolites with mortality among people with hypertension. We aimed to explore whether exposure to phthalates is associated with all-cause and cause-specific mortality among people with hypertension. This study included 4012 people with hypertension from the National Health and Nutrition Examination Survey from 2003 to 2014. Death information was obtained from the National Death Index until 2015. A total of 577 deaths including 196 deaths due to cardiovascular disease (CVD) and 119 deaths due to cancer were documented. Cox proportional hazards regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI). After adjustment for potential covariates, participants exposed to mono-ethyl phthalate (MEP) had a higher risk of cancer mortality (HR, 2.06; 95% CI, 1.07-3.95). Participants exposed to mono-n-butyl phthalate (MnBP) had higher risks of all-cause (HR, 1.83; 95% CI, 1.28-2.60), CVD (HR, 2.19; 95% CI, 1.21-3.95), and cancer (HR, 2.35; 95% CI, 1.07-5.17) mortality. Participants exposed to mono-benzyl phthalate (MBzP) had higher risks of all-cause (HR, 2.19; 95% CI, 1.58-3.05) and CVD (HR, 2.36; 95% CI, 1.35-4.13) mortality. Participants exposed to di-2-ethylhexylphthalate (DEHP) had a higher risk of all-cause mortality (HR, 1.69; 95% CI, 1.19-2.39). Our findings suggested that higher levels of specific phthalates were significantly associated with increased risks of all-cause, CVD, and cancer mortality among people with hypertension. Further studies are needed to confirm these findings and identify the underlying mechanisms.

The Association of Dietary Fiber Intake in Three Meals with All-Cause and Disease-Specific Mortality among Adults: The U.S. National Health and Nutrition Examination Survey, 2003-2014.

The timing of food intake can significantly alter the body's metabolism of nutrient intake and affect the occurrence of chronic diseases. However, whether and how the intake time of dietary fiber could influence mortality risks is largely unknown. This study aims to reveal the association between total dietary fiber intake and fiber intake at different times with all-cause, cancer, and cardiovascular disease (CVD) mortality rates. A total of 31,164 adults who enrolled in the National Health and Nutrition Examination Survey from 2003 to 2014 are included in this study. Dietary fiber intake was measured using 2-day, 24 h dietary recall. The main exposures in this study were the intake of dietary fiber at breakfast, lunch, and dinner via regression analysis of the residual method. The main outcomes were the all-cause, cancer, and CVD mortality rates. Cox proportional hazards regression models were used to evaluate the survival relationship between dietary fiber intake at different times and mortality rates. Among the 31,164 adults, 2915 deaths, including 631 deaths due to cancer and 836 deaths due to CVD, were documented. Firstly, after adjusting for potential confounders, compared to the participants in the lowest quintile of total dietary fiber intake, the participants in the highest quintile of fiber intake had lower all-cause (HR = 0.686, 95% CI: 0.589−0.799, p for trend <0.001) and cancer (HR = 0.606, 95% CI: 0.446−0.824, p for trend = 0.015) mortality risks. Secondly, compared to the participants in the lowest quintile of dietary fiber intake at dinner, the participants in the highest quintile of fiber intake had lower all-cause (HR = 0.796, 95% CI: 0.668−0.949, p for trend = 0.009) and cancer (HR = 0.564, 95% CI: 0.388−0.822, p for trend = 0.005) mortality risks. Furthermore, equivalently replacing each standard deviation of dietary fiber consumed at breakfast with that at dinner was associated with lower cancer mortality risks (HR = 0.846, 95% CI: 0.747−0.958). In conclusion, this study demonstrates that, in the NHANES (2003−2014) cohort, to reduce all-cause and cancer mortality risks, the optimal dietary fiber intake time is in the evening.

The Association of Dietary Vitamin Intake Time Across a Day With Cardiovascular Disease and All-Cause Mortality.

Background: Chrono-nutrition emphasized the importance of the intake time; however, less is known about the impact of dietary vitamin intake time on health. This study aimed to examine our hypothesis about which vitamin intake time could influence the natural course of cardiovascular disease (CVD). Methods: A total of 27,455 adults enrolled in the National Health and Nutrition Examination Survey (NHANES) during 2003-2014 were recruited. The 12 dietary vitamin intakes in the morning, afternoon, and evening were categorized into tertiles or quartiles. Cox-proportional hazard regression models were developed to evaluate the association of vitamin intake time with CVD and all-cause mortalities. Results: Compared with participants in the lowest quartile, participants in the highest quartile of dietary VB2 intake in the morning had significantly lowest mortality risk of CVD [hazard ratio (HR)VB2 = 0.75, 95% CI: 0.60-0.94, p = 0.017]; whereas, participants in the highest quartile of dietary-vitamin B6 (VB6), vitamin C (VC), vitamin E (VE), and folate-equivalent consumed in the evening showed the lowest risks of CVD (HRVB6 = 0.77, 95% CI: 0.60-0.99, p = 0.103; HRVC = 0.80, 95% CI: 0.65-0.98, p = 0.050; HRVE = 0.75, 95% CI: 0.56-0.99, p = 0.032; HRfolate-equivalent = 0.78, 95% CI: 0.63-0.97, p = 0.116) and all-cause mortalities (HRVB6 = 0.81, 95% CI: 0.71-0.93, p = 0.006; HRVC = 0.85, 95% CI: 0.76-0.95, p = 0.004; HRVE = 0.84, 95% CI: 0.72-0.97, p = 0.011; HRfolate-equivalent = 0.80, 95% CI: 0.71-0.90, p = 0.001). Moreover, equivalently replacing 10% intake of dietary VB6, VC, VE, and folate-equivalent in the morning with evening were associated with 4% (HRVB6 = 0.96, 95% CI: 0.92-0.99), 5% (HRVC = 0.95, 95% CI: 0.92-0.99), 4% (HRVE = 0.96, 95% CI: 0.91-0.99), and 5% (HRfolate-equivalent = 0.95, 95% CI: 0.92-0.99) lower risk of CVD mortality. Conclusion: This study found that the optimal intake time of dietary VB2 was in the morning, and the optimal intake times of dietary VB6, VC, VE, and folate-equivalent were in the evening.