Association Between Triglyceride-Glucose Index-A Body Shape Index and Atherosclerotic Cardiovascular Disease, and the Modification Effect of Dietary Patterns

Why It Matters

TyG‑ABSI provides a more comprehensive metabolic‑obesity risk marker, enabling earlier detection and targeted prevention of ASCVD.

Key Takeaways

• TyG‑ABSI predicts ASCVD better than TyG alone
• Each unit increase doubles ASCVD odds
• Inflammatory and oxidative markers partially mediate risk
• Healthy dietary patterns weaken TyG‑ABSI‑ASCVD link
• Findings are exploratory due to cross‑sectional design

Pulse Analysis

Atherosclerotic cardiovascular disease remains the leading cause of mortality worldwide, driven by a complex interplay of metabolic dysfunction and excess adiposity. Traditional risk scores often treat lipid, glucose, and obesity metrics separately, which can obscure synergistic effects. The triglyceride‑glucose index (TyG) captures insulin resistance, while the a body shape index (ABSI) reflects visceral fat distribution; merging them into TyG‑ABSI creates a unified marker that aligns metabolic and anthropometric risk into a single, scalable measure.

The Nanchang University cohort demonstrated that TyG‑ABSI is not only statistically linked to ASCVD but also clinically useful. After adjusting for a broad set of confounders, a one‑unit rise in TyG‑ABSI more than doubled ASCVD odds, and the composite outperformed isolated TyG, TyG‑BMI, and related indices in ROC analysis (AUC 0.718). Mediation analyses revealed that systemic inflammation (CRP, SIRI, NLR, MLR) and oxidative stress (GGT, uric acid) explain roughly 15‑20 % of the association, underscoring biological pathways that could be targeted therapeutically. Moreover, participants with higher adherence to anti‑inflammatory dietary patterns—Mediterranean, DASH, or HEI‑2020—showed a blunted TyG‑ABSI‑ASCVD link, suggesting that diet can modify metabolic risk even in the presence of adverse biomarker profiles.

For clinicians and health systems, incorporating TyG‑ABSI into routine screening could refine cardiovascular risk stratification, especially in populations where obesity and insulin resistance co‑occur. The index’s moderate diagnostic performance makes it a practical adjunct to existing tools, while its sensitivity to dietary modification offers a tangible prevention lever. Nevertheless, the cross‑sectional design limits causal inference, and the single‑center Chinese sample may not generalize globally. Prospective, multi‑ethnic studies are needed to validate TyG‑ABSI’s predictive power and to explore intervention strategies that leverage its mechanistic ties to inflammation and oxidative stress.