Red meat intake, faecal microbiome, serum trimethylamine N-oxide and hepatic steatosis among Chinese adults.

BACKGROUND AND AIMS: Emerging evidence suggests a detrimental impact of high red meat intake on hepatic steatosis. We investigated the potential interplay between red meat intake and gut microbiome on circulating levels of trimethylamine N-oxide (TMAO) and hepatic steatosis risk. METHODS: This cross-sectional study was conducted in a representative sample of 754 community-dwelling adults in Huoshan, China. Diet was collected using 4 quarterly 3 consecutive 24-h dietary (12-day) recalls. We profiled faecal microbiome using 16S ribosomal RNA sequencing and quantified serum TMAO and its precursors using LC-tandem MS (n = 333). We detected hepatic steatosis by FibroScan. The adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated using logistic regression. RESULTS: TMAO levels but not its precursors were positively associated with the likelihood of hepatic steatosis (aOR per 1-SD increment 1.86, 95% CI 1.04-3.32). We identified 14 bacterial genera whose abundance was associated with TMAO concentration (pFDR < .05) belonging to the phyla Firmicutes, Bacteroidetes, Actinobacteria and Proteobacteria families. Per 10 g/day increase in red meat intake was positively associated with TMAO levels among participants who had higher red meat intake (>70 g/day) and higher TMAO-predicting microbial scores (TMS, ß = .045, p = .034), but not among others (pinteraction = .030). TMS significantly modified the positive association between red meat and steatosis (pinteraction = .032), with a stronger association being observed among participants with higher TMS (aOR 1.30, 95% CI 1.07-1.57). CONCLUSIONS: The bacterial genera that predicted TMAO levels may jointly modify the association between red meat intake and TMAO levels and the subsequent risk of hepatic steatosis.

Healthy plant-based diet might be inversely associated with gastric precancerous lesions: new evidence from a case-control study based on dietary pattern and fecal metabolic profiling.

Preventing the progression of gastric precancerous lesions (GPLs) can reduce the morbidity and mortality of gastric cancer (GC). The preventive effect of a plant-based diet on cancers has been widely recognised. In this case-control study, 1,130 subjects were included using 1:1 propensity score matching for age and sex. Dietary habits, anthropometry and sample collection were conducted using standard and effective methods. Plant-based diet indices (PDIs) were calculated using a previously reported method. Faecal samples were analysed by untargeted metabolomics. Our study found that adherence to a healthy plant-based diet was inversely associated with the occurrence of GPLs. Metabolomic analysis identified six different metabolites correlated with GPLs, among which luteolin-related metabolites may be used as biomarkers of the association between PDIs and GPLs. In addition, the difference in N-acyl amides found in PDIs needs further verification. Our findings suggest that a healthy plant-based diet may have a protective effect against GPLs.

Adequate Intake of Dietary Fiber May Relieve the Detrimental Impact of Blood Lead on Dyslipidemia among US Adults: A Study of Data from the National Health and Nutrition Examination Survey Database.

Lead (Pb) exposure is a well-established risk factor for dyslipidemia, and people are exposed to it in multiple ways daily. Dietary fiber is presumed to improve lipid metabolism disorders, but it is still unknown whether it can relieve the detrimental impact of Pb on dyslipidemia. We used publicly accessible data from the 2011-2016 cycles of the National Health and Nutrition Examination Survey (NHANES). A total of 2128 US adults were enrolled for the subsequent analysis. Heavy metal concentrations in blood were measured using inductively coupled plasma mass spectrometry (ICP-MS). A weighted logistic regression was conducted to calculate odds ratios (ORs) and 95% confidence intervals (CIs). The dose-response relationship between blood heavy metals and dyslipidemia was explored using a weighted restricted cubic spline (RCS) analysis. After fully adjusting for potential confounding factors (age, gender, race, education level, ratio of family income to poverty, marital status, body mass index, physical activity, waist circumference, smoke, alcohol drinking and history of metabolic syndrome, hypertension, and diabetes), a positive association between blood Pb levels and dyslipidemia risk was revealed (OR = 1.20, 95% CI: 1.03-1.40). Dietary fiber intake may significantly modify the association between blood Pb levels and dyslipidemia (p-interaction = 0.049), with a stronger association (OR = 1.26, 95% CI: 1.05-1.52) being revealed in individuals with an inadequate intake of dietary fiber (<14 g/1000 kcal/day), but a null association (OR = 1.01, 95% CI: 0.72-1.42) being observed in those with an adequate intake of dietary fiber (≥14 g/1000 kcal/day). Moreover, the weighted RCS analysis showed that compared with the average blood Pb exposure level (4.24 µg/dL), a lower blood Pb exposure level (3.08 µg/dL) may contribute to the risk of dyslipidemia in the group with an inadequate dietary fiber intake. Our findings suggest that Pb exposure in blood may be a risk factor for dyslipidemia. However, an adequate dietary fiber intake may offset the risk of dyslipidemia caused by blood Pb exposure. Since avoiding Pb exposure in daily life is difficult, increasing dietary fiber intake in the future might be a promising approach to alleviate dyslipidemia caused by Pb exposure.

Dietary inflammatory potential is associated with higher odds of hepatic steatosis in US adults: a cross-sectional study.

OBJECTIVE: Inflammation plays a critical role in the progression of chronic liver diseases, and diet can modulate inflammation. Whether an inflammatory dietary pattern is associated with higher risk of hepatic steatosis or fibrosis remains unclear. We aimed to investigate the associations between inflammatory dietary pattern and the odds of hepatic steatosis and fibrosis. DESIGN: In this nationwide cross-sectional study, diet was measured using two 24-h dietary recalls. Empirical dietary inflammatory pattern (EDIP) score was derived to assess the inflammatory potential of usual diet, which has been validated to highly predict inflammation markers in the study population. Controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) were derived from FibroScan to define steatosis and fibrosis, respectively. SETTING: US National Health and Nutrition Examination Survey. PARTICIPANTS: 4171 participants aged ≥18 years. RESULTS: A total of 1436 participants were diagnosed with S1 steatosis (CAP ≥ 274 dB/m), 255 with advanced fibrosis (LSM ≥ 9·7 kPa). Compared with those in the lowest tertile of EDIP-adherence scores, participants in the highest tertile had 74 % higher odds of steatosis (OR: 1·74, 95 % CI (1·26, 2·41)). Such positive association persisted among never drinkers, or participants who were free of hepatitis B and/or C. Similarly, EDIP was positively associated with CAP in multivariate linear model (P < 0·001). We found a non-significant association of EDIP score with advanced fibrosis or LSM (P = 0·837). CONCLUSIONS: Our findings suggest that a diet score that is associated with inflammatory markers is associated with hepatic steatosis. Reducing or avoiding pro-inflammatory diets intake might be an attractive strategy for fatty liver disease prevention.

Daytime napping, nighttime sleeping duration, and risk of hepatocellular carcinoma and liver disease-related mortality.

Background & Aims: Sleep duration has been linked to metabolic dysfunction and chronic inflammation, which may contribute to the development of liver cancer and chronic liver disease (CLD). However, little is known about the relationship between sleep or napping duration and hepatocellular carcinoma (HCC) risk and CLD mortality. Methods: We followed 295,837 individuals in the National Institutes of Health-American Association of Retired Persons (NIH-AARP) Diet and Health Study. We examined the associations of nighttime sleep duration and daytime napping duration with risk of HCC incidence and CLD mortality. Cox proportional hazards regression was used to calculate multivariable hazard ratios (HRs) and 95% confidence intervals (95% CIs). Results: A total of 357 incident HCC cases and 578 CLD deaths were identified after a median follow-up time of 15.5 years. After adjusting for confounder factors, we found U-shaped associations of nighttime sleep duration with the incidence of HCC (HR<5 vs. 7-8 h = 2.00, 95% CI: 1.22-3.26 and HR≥9 vs. 7-8 h = 1.63, 95% CI: 1.04-2.65) and CLD mortality (HR<5 vs. 7-8 h = 1.78, 95% CI: 1.18-2.69 and HR≥9 vs. 7-8 h = 1.91, 95% CI: 1.35-2.70). Daytime napping was associated with higher risk of HCC (HR≥1 vs. non-nappers = 1.46, 95% CI: 1.04-2.06) and higher CLD mortality (HR≥1 h vs. non-nappers = 1.54, 95% CI: 1.18-2.01) compared with no napping. Conclusions: We observed U-shaped associations for nighttime sleeping and risk of HCC and CLD mortality. Additionally, longer daytime napping duration was associated with higher risk of HCC and CLD death. Our study suggests that clinical follow up of individuals at risk for liver cancer or living with a liver disease should include information on nighttime and daytime sleep. Impact and implications: Sleep or napping duration may play a role in the development of liver cancer and chronic liver disease, but little is known about the relationship between them. In addition, abnormal sleep patterns in patients with chronic liver disease may further promote the development of liver disease, creating a vicious cycle. Our study suggests that clinical follow up of individuals at risk for liver cancer or living with a liver disease should include information on nighttime and daytime sleep, as they can be potentially important factors in the development and progression of liver disease.

Controlled oxidation and digestion of Pickering emulsions stabilized by quinoa protein and (-)-epigallocatechin-3-gallate (EGCG) hybrid particles.

In this study, we prepared Pickering emulsions stabilized by quinoa protein isolate (QPI) and (-)-epigallocatechin-3-gallate (EGCG) non-covalent hybrid particles using ultrasonic emulsification technique and demonstrated lipid oxidation and in vitro digestion process of Pickering emulsions. The interaction forces between QPI and EGCG were characterized using fluorescence spectroscopy, isothermal titration calorimetry, and Fourier transform infrared spectroscopy. Results indicated that the non-covalent QPI/EGCG hybrid particles were formed mainly via hydrophobic interactions, hydrogen bonds, and electrostatic interactions at pH 5. Then, the QPI/EGCG non-covalent hybrid particles were applied to modify the Pickering emulsion with ultrasonic homogenization. The rheological experimental results showed that the energy storage modulus (G') was higher than the loss modulus (G″), indicating that the emulsion had solid-like properties. As a physical barrier, interfacial layer fabricated by antioxidant QPI/EGCG hybrid particles limited lipid oxidation at 60 °C for 15 days. At 37 °C, the QPI/EGCG hybrid particles stabilized Pickering emulsions with robust antioxidant interfacial structure limited the lipid digestion under simulated gastrointestinal tract (gastric, small intestine phases). Thus, EGCG and quinoa proteins were more resistant to free radical oxidation and gastrointestinal digestion with the assistance of ultrasound. It provides a basis for better development of food and drug delivery systems by fully utilizing the antioxidant properties of plant polyphenols.

Metabolic and Risk Profiles of Lean and Non-Lean Hepatic Steatosis among US Adults.

Hepatic steatosis can occur in lean individuals, while its metabolic and risk profiles remain unclear. We aimed to characterize the clinical and risk profiles of lean and non-lean steatosis. This cross-sectional study included 1610 patients with transient elastography-assessed steatosis. The metabolic and risk profiles were compared. Compared to their non-lean counterparts, lean subjects with steatosis had a lower degree of fibrosis (F0-F1: 91.9% vs. 80.9%), had a lower prevalence of diabetes (27.9% vs. 32.8%), dyslipidemia (54.7% vs. 60.2%) and hypertension (50.0% vs. 51.3%), and had higher levels of high-density lipoprotein cholesterol while lower fasting insulin and homeostatic model assessment for insulin resistance (all p < 0.05). Of the 16 potential risk factors, being Hispanic was associated with higher odds of non-lean steatosis but not with lean steatosis (odds ratio (OR): 2.07 vs. 0.93), while excessive alcohol consumption had a different trend in the ratio (OR: 1.47 vs.6.65). Higher waist-to-hip ratio (OR: 7.48 vs. 2.45), and higher waist circumference (OR: 1.14 vs. 1.07) showed a stronger positive association with lean steatosis than with non-lean steatosis (all Pheterogeneity < 0.05). Although lean individuals with steatosis presented a healthier metabolic profile, both lean and non-lean steatosis had a significant proportion of metabolic derangements. In addition, the etiological heterogeneity between lean and non-lean steatosis may exist.

Synergistic effects of low-dose arsenic and N-methyl-N'-nitro-N-nitrosoguanidine co-exposure by altering gut microbiota and intestinal metabolic profile in rats.

Biological organisms are exposed to low-dose arsenic or N-nitro compounds (NOCs) alone or in combination worldwide, especially in areas with high cancer prevalence through drinking water or food exposure; however, information on their combined exposure effects is limited. Here, we conducted an in-depth study of the effects on the gut microbiota, metabolomics, and signaling pathways using rat models exposed to arsenic or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), one of the most active carcinogenic NOCs, separately or in combination with metabolomics and high-throughput sequencing. Compared to exposure alone, combined exposure to arsenic and MNNG exacerbated damage to gastric tissue morphology, interfered with intestinal microflora and substance metabolism, and exerted a stronger carcinogenic effect. This may be related to intestinal microbiota disorders, including Dyella, Oscillibacter, Myroides, and metabolic pathways such as glycine, serine, and threonine metabolism, arginine biosynthesis, central carbon metabolism in cancer, and purine and pyrimidine metabolism, thereby enhancing the cancer-causing effects of gonadotrophin-releasing hormone (GnRH), P53, and Wnt signaling pathways.

Co-exposure to iron, copper, zinc, selenium and titanium is associated with the prevention of gastric precancerous lesions.

Gastric cancer is the third leading cause of cancer death, and gastric precancerous lesions (GPLs) are an important stage in the transformation of normal gastric mucosa to gastric cancer. Matched for age and sex, a total of 316 subjects were eventually included from our prospective observation population (including 1007 patients with GPLs and 762 normal controls), and a questionnaire survey was conducted. In total, 10 plasma elements (iron, copper, zinc, selenium, rubidium, strontium, titanium, aluminum, vanadium and arsenic) were measured by applying inductively coupled plasma‒mass spectrometry (ICP‒MS). A multivariate conditional logistic regression model and Bayesian kernel logistic regression model (BKMR) were used to analyze the association between plasma element concentrations and GPLs. In the multimetal model, plasma titanium concentrations were significantly and positively associated with the prevalence of GPLs, with a fourth-quartile OR of 11.56 ([95% CI]: [2.78-48.13]). Plasma selenium and copper were negatively correlated with GPLs, with the highest quartiles of selenium and copper having an OR of 0.03 ([95% CI]: [0.01-0.15]; P < 0.001) and 0.24 ([95% CI]: [0.07-0.82]), respectively. In the BKMR model, there was a significant negative combined correlation of five metals on GPLs: iron, copper, zinc, selenium, and titanium. The results of this study showed that plasma concentrations of selenium and copper were negatively correlated with GPLs, while plasma concentrations of titanium were positively correlated with GPLs, and the combined action of the five elements was negatively correlated with GPLs.

Associations of healthful and unhealthful plant-based diets with plasma markers of cardiometabolic risk.

PURPOSE: Plant-based diets, particularly when rich in healthy plant foods, have been associated with a lower risk of type 2 diabetes and cardiovascular disease. However, the impact of plant-based diets that distinguish between healthy and unhealthy plant foods on cardiometabolic biomarkers remains unclear. METHODS: Dietary information was collected by two 24-h recalls among 34,785 adults from a nationwide cross-sectional study. Plasma levels of insulin, C-peptide, glucose, C-reactive protein (CRP), white blood cell (WBC) count, triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) were measured. Linear regression was used to evaluate the percentage difference in plasma marker concentrations by three plant-based diet indices, namely the overall plant-based diet index (PDI), the healthful PDI (hPDI), and the unhealthful PDI (uPDI). RESULTS: Greater hPDI-adherence scores (comparing extreme quartiles) were associated with lower levels of insulin, Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), TG/HDL-C ratio, CRP, WBC count, and TG, and higher levels of HDL-C, with the percentage differences of - 14.55, - 15.72, - 11.57, - 14.95, - 5.26, - 7.10, and 5.01, respectively (all Ptrend ≤ 0.001). Conversely, uPDI was associated with higher levels of insulin, C-peptide, HOMA-IR, TG/HDL-C ratio, CRP, WBC count, and TG, but lower HDL-C, with the percentage differences of 13.71, 14.00, 14.10, 10.43, 3.32, 8.00, and - 4.98 (all Ptrend ≤ 0.001), respectively. Overall PDI was only associated with lower levels of CRP and WBC count (all Ptrend ≤ 0.001). CONCLUSION: Our findings suggest that hPDI may have positive, whereas uPDI may have negative impacts on multiple cardiometabolic risk markers, and underscore the need to consider the quality of plant foods in future PDI studies.

Ultrasound-assisted multilayer Pickering emulsion fabricated by WPI-EGCG covalent conjugates for encapsulating probiotics in colon-targeted release.

This study demonstrated the influences of ultrasound-assisted multilayer Pickering double emulsion capsules on the pasteurization and gastrointestinal digestive viability of probiotic (L. plantarum) strain liquid. Firstly, the role of ultrasonic homogenization on the morphology of W1/O/W2 double emulsions were studied. The double emulsion formed by ultrasonic intensity at 285 W had a single and narrow distribution with smallest droplet size. The double emulsion particles were then coated with chitosan(Chi), alginate (Alg), and CaCl2(Ca). The multilayer emulsion after pasteurization and gastrointestinal digestion both had the highest viability at 5 coating layers, but its particle size (108.65 µm) exceeded the limit of human oral sensory (80 µm). It could be noted that the deposition of 3-4 layers of coating had similar activity after pasteurization/GIT digestion. And droplets with 3 layers of coating were the minimum and most available formulation for encapsulated probiotics (L. plantarum). Hence, the results suggest that the use of ultrasound-assisted multilayer emulsions encapsulated with probiotics in granular food and pharmaceutical applications is a promising strategy.

Association between time-restricted eating and non-alcoholic fatty liver disease in a nationwide cross-sectional study.

The association between time-restricted eating (TRE) and the risk of non-alcoholic fatty liver disease (NAFLD) is less studied. Moreover, whether the association is independent of physical exercise or diet quality or quantity is uncertain. In this nationwide cross-sectional study of 3813 participants, the timing of food intakes was recorded by 24-h recalls; NAFLD was defined through vibration-controlled transient elastography in the absence of other causes of chronic liver disease. OR and 95 % CI were estimated using logistic regression. Participants with daily eating window of ≤ 8 h had lower odds of NAFLD (OR = 0·70, 95 % CI: 0·52, 0·93), compared with those with ≥ 10 h window. Early (05.00-15.00) and late TRE (11.00-21.00) showed inverse associations with NAFLD prevalence without statistical heterogeneity (Pheterogeneity = 0·649) with OR of 0·73 (95 % CI: 0·36, 1·47) and 0·61 (95 % CI: 0·44, 0·84), respectively. Such inverse association seemed stronger in participants with lower energy intake (OR = 0·58, 95 % CI: 0·38, 0·89, Pinteraction = 0·020). There are no statistical differences in the TRE-NAFLD associations according to physical activity (Pinteraction = 0·390) or diet quality (Pinteraction = 0·110). TRE might be associated with lower likelihood of NAFLD. Such inverse association is independent of physical activity and diet quality and appears stronger in individuals consuming lower energy. Given the potential misclassification of TRE based on one- or two-day recall in the analysis, epidemiological studies with validated methods for measuring the habitual timing of dietary intake are warranted.

Dietary inflammatory and insulinemic potential, risk of hepatocellular carcinoma, and chronic liver disease mortality.

BACKGROUND: Diet modulates inflammation and insulin response and may be an important modifiable factor in the primary prevention of hepatocellular carcinoma (HCC) and chronic liver disease (CLD). We developed the empirical dietary inflammatory pattern (EDIP) and empirical dietary index for hyperinsulinemia (EDIH) scores to assess the inflammatory and insulinemic potentials of diet. We prospectively examined the associations of EDIP and EDIH at baseline with the following HCC risk and CLD mortality. DESIGN: We followed 485 931 individuals in the National Institutes of Health-American Association of Retired Persons Diet and Health Study since 1995. Cox proportional hazards regression was used to calculate multivariable hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: We confirmed 635 incident HCC cases and 993 CLD deaths. Participants in the highest compared with those in the lowest EDIP quartile had a 1.35 times higher risk of developing HCC (95% CI = 1.08 to 1.70, Ptrend = .0005) and a 1.70 times higher CLD mortality (95% CI = 1.41 to 2.04, Ptrend < .0001). For the same comparison, participants with the highest EDIH were at increased risk of HCC (HR = 1.53, 95% CI = 1.20 to 1.95, Ptrend = .0004) and CLD mortality (HR = 1.72, 95% CI = 1.42 to 2.01, Ptrend < .0001). Similar positive associations of scores with HCC risk and CLD mortality were observed for both women and men. Moreover, individuals in both the highest EDIP and EDIH tertiles had a 92% increased HCC risk (95% CI = 1.43 to 2.58) and 98% increased CLD mortality (95% CI = 1.27 to 3.08) compared with those in both lowest tertiles. CONCLUSIONS: Our findings suggest that inflammation and hyperinsulinemia are potential mechanisms linking diet to HCC development and CLD mortality.

A prospective cohort study of starchy and non-starchy vegetable intake and mortality risk.

Whether starchy and non-starchy vegetables have distinct impacts on health remains unknown. We prospectively investigated the intake of starchy and non-starchy vegetables in relation to mortality risk in a nationwide cohort. Diet was assessed using 24-h dietary recalls. Deaths were identified via the record linkage to the National Death Index. Hazard ratios (HR) and 95 % CI were calculated using Cox regression. During a median follow-up of 7·8 years, 4904 deaths were documented among 40 074 participants aged 18 years or older. Compared to those with no consumption, participants with daily consumption of ≥ 1 serving of non-starchy vegetables had a lower risk of mortality (HR = 0·76, 95 % CI 0·66, 0·88, Ptrend = 0·001). Dark-green and deep-yellow vegetables (HR = 0·79, 95 % CI 0·63, 0·99, Ptrend = 0·023) and other non-starchy vegetables (HR = 0·80, 95 % CI 0·70, 0·92, Ptrend = 0·004) showed similar results. Total starchy vegetable intake exhibited a marginally weak inverse association with mortality risk (HR = 0·89, 95 % CI 0·80, 1·00, Ptrend = 0·048), while potatoes showed a null association (HR = 0·93, 95 % CI 0·82, 1·06, Ptrend = 0·186). Restricted cubic spline analysis suggested a linear dose-response relationship between vegetable intake and death risk, with a plateau at over 300 and 200 g/d for total and non-starchy vegetables, respectively. Compared with starchy vegetables, non-starchy vegetables might be more beneficial to health, although both showed a protective association with mortality risk. The risk reduction in mortality plateaued at approximately 200 g/d for non-starchy vegetables and 300 g/d for total vegetables.

Healthy and unhealthy low-carbohydrate diets and plasma markers of cardiometabolic risk.

Previous studies have reported inconsistent associations between low-carbohydrate diets (LCD) and plasma lipid profile. Also, there is little evidence on the role of the quality and food sources of macronutrients in LCD in cardiometabolic health. We investigated the cross-sectional associations between LCD and plasma cardiometabolic risk markers in a nationwide representative sample of the US population. Diet was measured through two 24-h recalls. Overall, healthy (emphasising unsaturated fat, plant protein and less low-quality carbohydrates) and unhealthy (emphasising saturated fat, animal protein and less high-quality carbohydrate) LCD scores were developed according to the percentage of energy as total and subtypes of carbohydrate, protein and fat. Linear regression was used to estimate the percentage difference of plasma marker concentrations by LCD scores. A total of 34 785 participants aged 18-85 years were included. After adjusting for covariates including BMI, healthy LCD was associated with lower levels of insulin, homoeostatic model assessment for insulin resistance (HOMA-IR), C-reactive protein (CRP) and TAG, and higher levels of HDL-cholesterol, with the percentage differences (comparing extreme quartile of LCD score) of -5·91, -6·16, -9·13, -9·71 and 7·60 (all Ptrend < 0·001), respectively. Conversely, unhealthy LCD was associated with higher levels of insulin, HOMA-IR, CRP and LDL-cholesterol (all Ptrend < 0·001). Our results suggest that healthy LCD may have positive, whereas unhealthy LCD may have negative impacts on CRP and metabolic and lipid profiles. These findings underscore the need to carefully consider the quality and subtypes of macronutrients in future LCD studies.

Association between solid fuel use and nonfatal cardiovascular disease among middle-aged and older adults: Findings from The China Health and Retirement Longitudinal Study (CHARLS).

BACKGROUND: Few studies have been conducted on the association between domestic solid fuel combustion and incident nonfatal cardiovascular disease (CVD). We assessed the prospective association between domestic fuel type and incident nonfatal CVD among Chinese adults aged ≥45 years. METHODS: This was a prospective cohort study using data from the China Longitudinal Study of Health and Retirement (CHARLS) that recruited 8803 participants ≥45 years in 2013. Household fuel types were assessed based on self-reports, including solid fuel (coal, crop residue, or wood fuel) and clean fuel (central heating, solar power, natural gas, liquefied petroleum gas, electricity, or marsh gas). Nonfatal CVD was defined as self-reported physician-diagnosed nonfatal CVD. We established Cox proportional hazard regression models with age as the time scale and strata by sex to evaluate the hazard ratios (HRs) and 95 % confidence intervals (95 % CIs). RESULTS: After a median follow-up of five years, 970 (11.02 %) nonfatal CVD cases were documented, including 423 (9.96 %) in males and 547 (12.01 %) in females. Participants with exposure to solid fuel for cooking and clean fuel for heating [HR (95 % CI):2.01 (1.36-2.96)], solid fuel for heating and clean fuel for cooking [HR (95 % CI):1.45 (1.06-1.99)], and solid fuel for both heating and cooking [HR (95 % CI):1.43 (1.07-1.92)] had an elevated nonfatal CVD risk compared to users of cleaner fuel for both cooking and heating. Those whom self-reported switching from solid fuels to cleaner fuels for cooking had significantly decreased nonfatal CVD risk [HR (95 % CI):0.76 (0.58-0.99)] than participants who did not switch to cleaner fuels. CONCLUSIONS: Exposure to domestic solid fuel burning for cooking or heating is associated with an elevated nonfatal CVD risk. Notably, switching cooking fuels from solid to cleaner fuels is related to a reduced risk of nonfatal CVD.

Higher Adherence to Healthy Lifestyle Score Is Associated with Lower Odds of Non-Alcoholic Fatty Liver Disease.

Growing evidence supports that individual lifestyle factors contribute to the development of non-alcoholic fatty liver disease (NAFLD) without considering the coexistence and synergistic effect of lifestyle factors. Our aim is to derive a healthy lifestyle score (HLS) and estimate its association with NAFLD. In this nationwide cross-sectional study, we derived a five-item HLS including dietary pattern, body mass index, physical activity, cigarette smoking, and sleep duration. NAFLD and clinically significant fibrosis (CSF) were assessed based on vibration-controlled transient elastography (VCTE). Liver function parameters were also tested. Multivariable logistic and linear regressions were applied to investigate the association between HLS and liver diseases. Of the 3893 participants with VCTE examination, approximately 14.1% of participants possessed zero or one healthy lifestyle, 62.5% possessed two or three healthy lifestyles, and 23.4% possessed four or five healthy lifestyles. Compared with participants with a low HLS (0−1 score), the adjusted odds ratios and 95% confidence intervals for those with a high HLS (4−5 score) were 0.25 (0.19~0.33, Ptrend < 0.001) for NAFLD and 0.30 (0.18~0.50, Ptrend < 0.001) for CSF. HLS was positively associated with albumin, total protein, and total bilirubin (all Ptrend ≤ 0.001), and was inversely associated with globulin, alanine aminotransferase, and gamma-glutamyl transaminase (all Ptrend ≤ 0.003). Higher adherence to HLS is associated with lower odds of NAFLD and CSF and may improve liver function. Strategies for the promotion of a healthy lifestyle should be considered as part of NAFLD prevention.

A Healthful Plant-Based Diet Is Associated with Lower Odds of Nonalcoholic Fatty Liver Disease.

There is little evidence for the associations of the overall plant-based diet index (PDI), the healthful PDI (hPDI), and the unhealthful PDI (uPDI) with the odds of nonalcoholic fatty liver disease (NAFLD). We present a nationwide cross-sectional study among US adults aged 18 years or older. Diet was assessed by 24-h recalls. Overall PDI, hPDI, and uPDI were constructed based on 18 food groups. NAFLD was defined based on controlled attenuation parameter derived via transient elastography (TE) in the absence of other causes of chronic liver disease. Among 3900 participants with eligible TE examination, 1686 were diagnosed with NAFLD. The overall PDI was not associated with NAFLD prevalence (comparing extreme tertiles of PDI score OR = 1.03, 95% CI 0.76, 1.38, ptrend = 0.609). However, hPDI was inversely (OR = 0.50, 95% CI 0.35, 0.72, ptrend < 0.001), while uPDI was positively associated with odds of NAFLD (OR = 1.37, 95% CI 0.93, 2.02, ptrend = 0.009) in the multivariable-adjusted models without body mass index (BMI). After further adjustment for BMI, only the association of hPDI with NAFLD remained statistically significant (OR = 0.64, 95% CI 0.46, 0.87, ptrend = 0.006). Such inverse association appeared stronger in non-Hispanic whites, but not in other racial/ethnic groups (pinteraction = 0.009). Our findings suggest that a plant-based diet rich in healthy plant foods might be associated with lower odds of NAFLD, particularly among US non-Hispanic whites. Clinical trials and cohort studies to validate our findings are needed.

Associations between low-carbohydrate and low-fat diets and hepatic steatosis.

OBJECTIVE: This study assessed the cross-sectional associations of low-carbohydrate diets (LCDs) and low-fat diets (LFDs) with hepatic steatosis in the National Health and Nutrition Examination Survey. METHODS: Diet was measured using the 24-hour recalls. Hepatic steatosis was defined by vibration-controlled transient elastography. The odds ratios (OR) and 95% confidence intervals (CI) were estimated using logistic regression. Substitution analysis was performed using the leave-one-out model. RESULTS: Participants with higher adherence scores (comparing extreme tertiles) for an overall (OR = 0.76, 95% CI: 0.61-0.96, ptrend  = 0.049) or a healthful LCD (OR = 0.61, 95% CI: 0.43-0.87, ptrend < 0.001) exhibited lower odds of steatosis. Replacing 5% of the energy from carbohydrates with total fat and protein (OR = 0.91, 95% CI: 0.83-0.99) or unsaturated fat and plant protein (OR = 0.89, 95% CI: 0.84-0.94) was associated with lower steatosis prevalence. High overall (OR = 1.65, 95% CI: 1.13-2.40, ptrend  = 0.006) or unhealthful (OR = 1.41, 95% CI: 1.10-1.80, ptrend < 0.001) LFD scores were associated with increased likelihood of steatosis. CONCLUSIONS: These findings suggest that the associations between LCDs and LFDs and steatosis may depend on the quality and food sources of the macronutrients.

Association of handgrip strength with all-cause mortality: a nationally longitudinal cohort study in China.

OBJECTIVES: Handgrip strength is considered a vital and reliable measure of comprehensive physical assessments, whereas the association of handgrip strength with overall mortality risk among Chinese adults was less studied. We prospectively investigated the association between handgrip strength and all-cause mortality among Chinese middle-aged and older people based on data from the China Health and Retirement Longitudinal Study (CHARLS).3 DESIGN: Longitudinal cohort study. METHODS: Grip strength was assessed for both hands by a dynamometer. Odds ratios (ORs)4 and 95 % confidence intervals (CIs)5 were estimated applying logistic regression models with adjustments for age, body mass index, ethnicity, education level, annual household income, marital status, drinking, smoking, physical activity, and medical insurance among men and women. Deaths were ascertained by each follow-up survey in which the household member who lived with the participants were inquired. RESULTS: Over an average follow-up period of approximately 8 years among the screened 11,618 participants ≥45 years old, 1290 deaths were documented. The age range was 45-93 for men and 45-96 for women. Greater handgrip strength was associated with a lower overall mortality risk, with adjusted ORs (comparing with extreme tertiles) of 0.47 (95 % CI: 0.35-0.64; P-trend<0.001) in men and 0.51 (95 % CI: 0.24-1.08; P-trend = 0.059) in women. Such inverse association seemed stronger among younger men (OR = 0.29, 95 % CI: 0.18-0.45), compared with the older men (OR = 0.49, 95 % CI: 0.33-0.73; P-interaction = 0.023). CONCLUSIONS: Handgrip strength was inversely associated with all-cause mortality risk, especially among the younger men. Further investigations are warranted to elucidate the underlying mechanism.