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.

Background: There have been reports linking branched-chain amino acids (BCAAs) to the hazard of various cardiovascular diseases (CVDs); however, the causal role of this relationship is still unclear. We conducted a study using bi-directional two-sample Mendelian randomization (MR) with the aim of investigating the possible causal correlation between BCAAs and 13 types of cardiovascular diseases. Methods: The study analyzed data of the largest genome-wide association studies (GWAS) published for the total BCAAs, encompassing isoleucine, leucine, and valine, which were obtained from the UK Biobank, as well as data for 13 cardiovascular endpoints from the MRC-IEU, the FinnGen consortium, and the EBI database. The approach of the primary dissection used became the inverse-variance-weighted (IVW) approach, with additional analyses using the MR-PRESSO global test as well as MR-Egger regression with a view to determining horizontal pleiotropy. Heterogeneity was evaluated by means of Cochran’s Q test. The study also conducted logistic regression dissection for the sake of investigating the correlation between cardiovascular events and serum BCAAs in the UK biobank cohort study. Results: In this study, it was found that individuals with a genetic predisposition to more elevated levels for circulating total BCAAs had a higher hazard of peripheral arterial disease (OR 1.400, 95% CI 1.063, 1.844; p = 0.017) in addition to stroke (OR 1.266, 95% CI 1.012, 1.585; p = 0.039); circulating valine casually increased the risk of intracerebral hemorrhage (OR 1.760, 95% CI 1.116, 2.776; p = 0.015), along with stroke (OR 1.269, 95% CI 1.079, 1.492; p = 0.004); genetically predicted isoleucine showed a positive association with peripheral arterial disease (OR 1.466, 95% CI 1.044, 2.058; p = 0.027), along with cardioembolic stroke (OR 1.547, 95% CI 1.126, 2.124; p = 0.007); furthermore, leucine causally associated with stroke (OR 1.310, 95% CI 1.031, 1.663, p = 0.027). In the UK Biobank cohort study, we detected that total BCAAs (OR: 1.285; 95% CI: 1.009, 1.636), valine (OR: 1.287; 95% CI: 1.009, 1.642), and isoleucine (OR: 1.352; 95% CI: 1.064, 1.718) were independently linked to stroke, but not leucine (OR: 1.146; 95% CI: 0.901, 1.458). No such association was found for BCAAs with peripheral arterial disease and intracerebral hemorrhage in the cohort study. Conclusions: In summary, circulating total BCAAs and valine may be causally associated with stroke. The association of BCAAs with other CVD events needs further study.