Background: The triglyceride-glucose (TyG) index could serve as a convenient substitute of insulin resistance (IR), but epidemiological evidence on its relationship with the long-term risk of mortality is limited.Methods: Participants from the National Health and Nutrition Examination Survey during 1999–2014 were grouped according to TyG index (10). Cox regression was conducted to compute the hazard ratios (HRs) and 95% confidence interval (CI). Restricted cubic spline and piecewise linear regression were performed to detect the shape of the relationship between TyG index and mortality.Results: A total of 19,420 participants (48.9% men) were included. On average, participants were followed-up for 98.2 months, and 2,238 (11.5%) and 445 (2.3%) cases of mortality due to all-cause or cardiovascular disease were observed. After adjusting for confounders, TyG index was independently associated with an elevated risk of all-cause (HR, 1.10; 95% CI, 1.00–1.20) and cardiovascular death (HR, 1.29; 95% CI, 1.05–1.57). Spline analyses showed that the relationship of TyG index with mortality was non-linear (All non-linear P < 0.001), and the threshold value were 9.36 for all-cause and 9.52 for cardiovascular death, respectively. The HRs above the threshold point were 1.50 (95% CI, 1.29–1.75) and 2.35 (95% CI, 1.73–3.19) for all-cause and cardiovascular death. No significant difference was found below the threshold points (All P > 0.05).Conclusion: Elevated TyG index reflected a more severe IR and was associated with mortality due to all-cause and cardiovascular disease in a non-linear manner.

Cardiovascular disease (CVD) and environmental degradation are leading global health problems of our time. Recent studies have linked exposure to heavy metals to the risks of CVD and diabetes, particularly in populations from low‐ and middle‐income countries, where concomitant rapid development occurs. In this review, we 1) assessed the totality, quantity, and consistency of the available epidemiological studies, linking heavy metal exposures to the risk of CVD (including stroke and coronary heart disease); 2) discussed the potential biological mechanisms underlying some tantalizing observations in humans; and 3) identified gaps in our knowledge base that must be investigated in future work. An accumulating body of evidence from both experimental and observational studies implicates exposure to heavy metals, in a dose‐response manner, in the increased risk of CVD. The limitations of most existing studies include insufficient statistical power, lack of comprehensive assessment of exposure, and cross‐sectional design. Given the widespread exposure to heavy metals, an urgent need has emerged to investigate these putative associations of environmental exposures, either independently or jointly, with incident CVD outcomes prospectively in well‐characterized cohorts of diverse populations, and to determine potential strategies to prevent and control the impacts of heavy metal exposure on the cardiometabolic health outcomes of individuals and populations.