Key result
Higher lipid accumulation product linked to ~12% higher stroke odds per SD.
Why the study?
Lipid accumulation product and visceral adiposity index are surrogate markers of visceral adiposity-related metabolic dysfunction, but their associations with stroke prevalence were not well established.
Cross-Sectional (n=21,146)
Odds Ratio: 1.115 (95% CI 1.061–1.171)
p-value: p=<0.001
Higher lipid accumulation product and visceral adiposity index are associated with an increased prevalence of stroke in US adults, suggesting their potential utility as markers for visceral adiposity-related cerebrovascular risk.
Higher LAP associated with prevalent stroke; hypothesis-generating for visceral adiposity markers in cerebrovascular risk pending prospective validation.
Aims Lipid accumulation product (LAP) and visceral adiposity index (VAI) are surrogate markers of visceral adiposity‐related endocrine and metabolic dysfunction, including insulin resistance, rather than simple obesity indices. This study aimed to evaluate their associations with stroke prevalence using nationally representative data. Materials and Methods This cross‐sectional study analyzed data from the National Health and Nutrition Examination Survey (NHANES) 1999–2018. Stroke status was determined through standardized questionnaires. LAP and VAI were calculated using established gender‐specific formulas. Analyses used the fasting subsample weights with strata and primary sampling units, and missing covariates were multiply imputed. Weighted logistic regression, restricted cubic spline (RCS), subgroup and incremental discrimination analyses were performed. Results Among 21,146 participants, 721 reported a prior stroke (weighted prevalence 2.64%). Both indices were higher in stroke cases (median LAP 54 vs 42; VAI 1.72 vs 1.46, both p < 0.001). In the primary model (Model 3), each 1‐SD increment was associated with higher stroke odds for LAP (OR = 1.115, 95% CI 1.061–1.171, p < 0.001) and VAI (OR = 1.073, 95% CI 1.020–1.129, p = 0.007), and the highest quartile exceeded the lowest (LAP: OR = 1.557, 95% CI 1.117–2.170; VAI: OR = 1.381, 95% CI 1.026–1.858). Both were attenuated after additional adjustment for metabolic mediators (HbA1c, systolic blood pressure, eGFR and medication use), consistent with partial mediation. RCS analyses showed significant overall associations (LAP p < 0.001; VAI p = 0.041) without significant nonlinearity ( p = 0.177 and 0.143). Only race/ethnicity modified the LAP‐stroke association ( p for interaction = 0.009; non‐Hispanic Black OR = 1.427, 95% CI 1.231–1.654). Adding either index did not materially improve discrimination. Conclusions Higher LAP and VAI values are associated with a greater prevalence of stroke after adjustment for demographic, socioeconomic, and lifestyle factors, and their attenuation after adjustment for metabolic variables is consistent with partial mediation through insulin resistance and its hemodynamic consequences. Both indices are inexpensive endocrine‐metabolic markers of visceral adipose tissue dysfunction and insulin resistance that warrant prospective evaluation.
No takes yet. Share an insight, caveat, or question.
Zhou et al. (2026) conducted a cross-sectional in Stroke (n=21,146). Lipid accumulation product (LAP) vs. Lower LAP values (per 1-SD increment or lowest quartile) was evaluated on Prevalent stroke (OR 1.115, 95% CI 1.061-1.171, p=<0.001). Each 1-SD increment in lipid accumulation product (LAP) was associated with higher odds of prevalent stroke (OR 1.115, 95% CI 1.061–1.171, p<0.001) after adjusting for demographic and lifestyle factors.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: