Hypertension remains a major contributor to the global disease burden and mortality, representing a critical public health challenge. While the cumulative lipid accumulation product (LAP), a marker of abdominal and visceral fat deposition, has shown cross-sectional associations with hypertension, existing studies inadequately address the impact of long-term cumulative LAP exposure on hypertension risk. Furthermore, causal relationships between cumulative LAP and incident hypertension remain underexplored.

To evaluate the association between cumulative LAP and hypertension risk and assess its predictive capacity for incident hypertension.

Data were derived from the Guizhou Natural Population Cohort Study database. Participants were enrolled from November 20, 2010, to December 19, 2012, and followed up from April 2016 to October 2020. A total of 3 548 subjects were ultimately included in the analysis. Participants were divided into four quartiles based on cumulative LAP (Q1-Q4 groups) : Q1 (cumulative LAP ≤14.54, n=887), Q2 (14.54<cumulative LAP≤24.35, n=887), Q3 (24.35<cumulative LAP≤39.21, n=887), and Q4 (cumulative LAP >39.21, n=887). Subjects were further categorized into non-hypertension group (n=2 696) and hypertension group (n=852) based on the development of new-onset hypertension. The relationship between cumulative LAP and hypertension was evaluated using the Cox proportional hazards regression model. The dose-response relationship between cumulative LAP and hypertension risk was assessed using restricted cubic splines. Time-dependent receiver operating characteristic (ROC) curves were constructed to evaluate the predictive ability of cumulative LAP for hypertension. Participants with follow-up duration <3 years and those with pre-hypertension were excluded.

Among the 3 548 adults included, 1 607 (45.3%) were men and 1 941 (54.7%) were women, with a mean age of (42.5±14.1) years. During the follow-up period, 852 (11.2%) subjects were newly diagnosed with hypertension. Significant differences were observed between the non-hypertension and hypertension groups in terms of gender, age, education level, family history of hypertension, excessive intake of oil, excessive intake of salt, insufficient intake of fresh fruits, proportion of inadequate sleep, BMI, diastolic blood pressure, fasting plasma glucose (FPG), and cumulative LAP (P<0.05). The results of the Cox proportional hazards regression model showed that, compared with the Q1 group, the risk of hypertension increased progressively in the Q2 group (aHR=1.330, 95%CI=1.053-1.681), Q3 group (aHR=1.706, 95%CI=1.364-2.134), and Q4 group (aHR=2.339, 95%CI=1.869-2.928) after adjusting for potential confounders (P<0.05). The restricted cubic spline analysis revealed a non-linear dose-response relationship between cumulative LAP and hypertension risk (P_{non-linearity}<0.01), with the risk of new-onset hypertension increasing with cumulative LAP but stabilizing after cumulative LAP >65. The time-dependent ROC curves for predicting hypertension incidence showed that the area under the ROC curve (AUC) for the overall population was 0.617, 0.590, 0.603, and 0.634 for continuous average exposure of 6, 7, 8, and 9 years, respectively. The AUC for men was 0.600, 0.561, 0.571, and 0.558, and for women, it was 0.638, 0.629, 0.647, and 0.711. For urban populations, the AUC was 0.596, 0.565, 0.602, and 0.621, while for rural populations, it was 0.629, 0.592, 0.594, and 0.635.

Cumulative LAP is an independent risk factor for the onset of hypertension, but it is not an ideal indicator for predicting the onset of hypertension, and its predictive value for the onset of hypertension is relatively limited.