In this population-based cross-sectional study, the TyG index was positively associated with the increment in BP. Note that the study participants were apparently healthy individuals with no history of HTN or CVD and were not taking anti-diabetic or antihyperlipidemic medications. Even after adjusting for conventional risk factors, the significant association between the TyG index and BP was maintained. These findings suggest that the TyG index can predict HTN early.
IR has been implicated in the pathogenesis of diseases related to metabolic syndrome, including HTN, diabetes mellitus, obesity, and CVD3,21,22. The gold standard for assessing IR is hyperinsulinemic-euglycemic clamp analysis23. However, it is difficult to perform in real-world settings because it is time-consuming and labor-intensive. HOMA-IR has been suggested as a simpler method and its results correlated well with those assessed by the clamp analysis24. However, it also has limited value because serum insulin is not measured routinely in clinical settings. More recently, the TyG index has been proposed for evaluating IR5. In previous studies, the TyG index correlated well with HOMA-IR5,7−9. Because triglycerides and FPG can be assessed simply and easily, it is more suitable as a mass screening test to predict IR-related diseases, such as in our study.
Although the mechanisms underlying IR in the development of HTN have not been fully elucidated, several have been suggested. Hyperinsulinemia caused by IR may increase the activity of the renin-angiotensin-aldosterone system, which can induce renal sodium retention25,26. It can indirectly cause water-sodium retention and increase vascular activity via angiotensin II, resulting in HTN27. IR may also stimulate sympathetic nervous system activity, inducing the secretion of adrenaline and norepinephrine, leading to increased cardiac output and peripheral vascular resistance via vascular smooth muscle cell hypertrophy and endothelial dysfunction28–30.
Several studies have evaluated the relationship between the TyG index and IR-related disease, especially in HTN. In a 9-year longitudinal study, a higher TyG index was associated with an increased risk of subsequent incident HTN14. A large epidemiological study of the temporal relationship between BMI and the TyG index and its impact on the incidence of HTN found that a higher BMI at baseline was significantly associated with a higher TyG index and an increased risk of HTN31. In addition, a higher TyG index was significantly associated with a higher BMI at the 2-year follow-up and an increased risk of HTN. These results provide direct evidence for a temporal relationship between BMI and IR. A more recent study demonstrated that an increased TyG index was significantly associated with a higher risk of pre-HTN and HTN.15 Furthermore, obesity parameters such as the waist-to-hip ratio and percent body fat have additive effects on the HTN risk with the TyG index. Our results also showed a positive correlation between the TyG index and BP and prevalence of HTN in alignment with these previous studies.
This study examined subjects who had low risks for IR. Individuals who had previously been diagnosed with HTN, diabetes mellitus, dyslipidemia, or CVD were excluded. Nevertheless, a significant relationship was observed between the TyG index and BP; SBP in the lowest and highest quartiles was 109.1 ± 13.0 and 121.3 ± 15.3 mmHg, respectively (p for trend < 0.001) and DBP in the lowest and highest quartiles was 71.7 ± 8.5 and 80.0 ± 10.1 mmHg (p for trend < 0.001). In the subgroup analysis according to BMI, the TyG index was significantly associated with the prevalence of elevated BP, pre-HTN, and HTN, even in the non-obese subjects (BMI < 25 kg/m2). Furthermore, the associations between the TyG index and the prevalence of pre-HTN and HTN were more prominent in younger subjects (p interaction < 0.001). Overall, these results suggest that the TyG index might be an early marker to identify patients with HTN.
This study has several advantages. It included relatively large number of subjects from a national health survey. We were able to analyze various confounding factors potentially influencing HTN (demographic, lifestyle, and laboratory parameters). In addition, the analysis examined categories of BP and subgroups by subject characteristics. However, our study also has some limitations that need to be considered. First, because of its cross-sectional design, it cannot show a causal relationship between the TyG index and HTN. Second, as KNHANES did not include fasting insulin, we could not compare the TyG index with the HOMA-IR as an independent risk factor. Third, although we tried to adjust for confounding risk factors, there might be some confounding factors that we did not include.
In conclusion, a higher TyG index significantly correlated with the risk of increased BP in healthy individuals after adjusting for conventional risk factors of HTN. Considering its simplicity of measurement and good functionality, the TyG index might be an early marker for identifying patients at risk of HTN.