# Association of CETP, APOA5, IL6, and PON1 Gene Variants with Dyslipidemia and Cardiovascular Risk in a Population from Cauca Department, Colombia

## TL;DR

This study explores how specific gene variants are linked to dyslipidemia and cardiovascular risk in a Colombian population.

## Contribution

The study identifies the APOA5 rs662799 variant as a potential genetic biomarker for cardiovascular risk in this population.

## Key findings

- Individuals with dyslipidemia had higher total cholesterol and VLDL levels and lower HDL levels.
- The APOA5 rs662799 variant was significantly associated with increased VLDL levels.
- The study highlights the role of genetic variants in cardiovascular risk stratification.

## Abstract

Background: Cardiovascular disease remains the leading cause of death worldwide, and dyslipidemia is a critical, modifiable risk factor. Aim: We sought to evaluate the relationship between polymorphisms in CETP (rs3764261), APOA5 (rs662799), IL6 (rs1800796), and PON1 (Q192R) and lipid parameters, and to assess their contribution to dyslipidemia and overall cardiovascular risk in an urban cohort from Cauca, Colombia. Methods: In this cross-sectional observational study, 304 participants aged 40–69 years were enrolled. Clinical, anthropometric, and biochemical data were collected, and genotyping was performed for the four target polymorphisms. We used descriptive statistics to characterize the sample, non-parametric tests to compare lipid levels by genotype, and multivariable logistic regression to identify independent predictors of dyslipidemia. Results: Individuals with dyslipidemia exhibited significantly higher total cholesterol and VLDL levels, lower HDL levels, and an elevated Castelli II index compared with the non-dyslipidemia group. Although CETP genotype frequencies differed between groups, only the APOA5 rs662799 variant was significantly associated with increased VLDL levels, suggesting its potential role as a genetic biomarker of cardiovascular risk. Conclusions: Our findings underscore the interplay between metabolic factors and genetic variants in the pathogenesis of dyslipidemia. Notably, the APOA5 rs662799 polymorphism emerged as a key determinant of VLDL concentration, highlighting its promise for personalized cardiovascular risk stratification and management in this population.