We aimed to examine the effect of natto and red yeast rice (NR) supplementation on lipid and lipoprotein profiles, gene expressions of cholesterol metabolism, and the composition of gut microbiota in ApoE^-/- mice. Forty-one male ApoE^-/- mice aged 7–8 wks old were randomly fed a control diet (CD), CD + NR (oral gavage at 0.3 g/kg BW/day), high-fat and high-cholesterol diet (HFD), or HFD + NR for 12 wks. Fasting blood samples, liver and intestine tissues and fecal samples were collected at week 12. Biochemical parameters, gene expressions in cholesterol metabolism and gut microbiota composition and diversity were measured using standard methods. NR supplementation had no significant effect on lipid and lipoprotein profiles. Compared with the HFD group, HFD + NR resulted in higher mRNA expressions of HMGCR and CYP7A1 (both P-NR < 0.05) and ABCA1 (P-diet*NR = 0.0134, P-NR = 0.0407), lower mRNA expression of PCSK9 (P-diet*NR = 0.0002), lower fasting glucose concentrations (P-diet*NR = 0.0011), and lower relative abundance of genera Bacteroides and Lactococcus (both P-NR < 0.01) and Coriobacteriaceae_UCG-002 (P-diet*NR = 0.0007). The relative abundance of Lactococcus was inversely correlated with HMGCR and CYP7A1, and the relative abundance of Coriobacteriaceae_UCG-002 was positively correlated with PCSK9 and inversely correlated with ABCA1 (all P < 0.05). These findings suggest that NR supplementation may regulate gene expressions in cholesterol metabolism via changes in the gut microbiota in HFD-fed ApoE^-/- mice.

Background: Environmental and cardiometabolic impacts of adherence to plant-based dietary patterns with different quality are unclear. Objectives: To investigate the associations between adherence to the overall, healthy, and unhealthy plant-based dietary patterns, as assessed by the plant-based diet index (PDI), healthy PDI (hPDI), and unhealthy PDI (uPDI), respectively, and risk of myocardial infarction (MI), type 2 diabetes (T2D), stroke, and all-cause mortality and greenhouse gas (GHG) emissions. Methods: Data from adults (N = 14,652 for cardiometabolic diseases and 15,318 for all-cause mortality) in the China Health and Nutrition Survey (1997–2015 wave) were analyzed. PDI, hPDI, and uPDI scores were calculated with dietary intake data. The total GHG emissions were calculated by summing the amount of emissions from all food groups included in the index. Cox proportional hazard regression models and linear regression models were used for statistical analysis. Results: Greater adherence to an unhealthy plant-based dietary pattern, as reflected by higher uPDI scores, was positively associated with risk of MI (Q5 vs. Q1: HR = 5.90; 95% CI: 2.59–13.48), T2D (Q5 vs. Q1: HR = 2.18; 95% CI: 1.75–2.73), stroke (Q5 vs. Q1: HR = 5.96; 95% CI: 2.86–12.42) and all-cause mortality (Q5 vs. Q1: HR = 6.87; 95% CI: 4.70–10.03). PDI scores were inversely associated with the risk of MI, T2D, and all-cause mortality, and hPDI scores were inversely and positively associated with the risk of T2D and stroke, respectively. All scores were inversely associated with GHG emissions (all p-trends < 0.001). Conclusions: Long-term adherence to unhealthy plant-based dietary patterns guided by higher uPDI scores may be a risk factor for new-onset cardiometabolic diseases and all-cause death in Chinese adults. Food-based dietary guidelines, clinicians, and dietitians should consider the quality of plant-based dietary patterns prior to making recommendations for both healthy individuals and those with elevated cardiometabolic disease risk.

Background: Current research inadequately substantiates the impacts of dietary inflammatory potential based on the dietary inflammatory index (DII) on population health and environmental sustainability in Chinese adults. Objectives: We aimed to investigate the associations between the DII with the risk of all-cause mortality and greenhouse gas (GHG) emissions in Chinese adults. Methods: Data from adults (N = 15,318) in the China Health and Nutrition Survey 1997–2015 wave were included in the analysis. DII and energy-adjusted DII (E-DII) were calculated using dietary intake data collected with a combination of 3-day consecutive 24-h dietary recalls and the food weighing method. The total GHG emissions were calculated by summing the amount of emissions from all the food groups consumed by the participants. Cox proportional hazards regression models and linear regression models were conducted for statistical analysis. Results: A pro-inflammatory diet, as reflected by higher DII and E-DII scores was associated with an increased risk of all-cause mortality (DII: Q5 vs. Q1: HR = 1.82; 95% CI: 1.45–2.30; p-trend < 0.0001; E-DII: Q5 vs. Q1: HR = 1.86; 95% CI: 1.38–2.52; p-trend < 0.0001) and higher amounts of GHG emissions (both p-trend < 0.0001). Conclusions: These findings demonstrated positive associations between pro-inflammatory potentials with an increased risk of all-cause mortality and higher GHG emissions among Chinese adults, suggesting dual adverse impacts of a pro-inflammatory diet on health and environmental sustainability.