Key result
Prothrombin F2 rs1799963 GG genotype shows no significant association with atherosclerosis in non-smokers.
Why the study?
The genetic and environmental factors contributing to atherosclerosis in non-smoking populations remain poorly understood, prompting an investigation into the association between the prothrombin F2 gene rs1799963 G/A polymorphism and atherosclerotic risk in non-smoking Pakistani adults.
Case-Control (n=62)
No
In this small cohort of non-smoking Pakistani adults, the prothrombin F2 rs1799963 polymorphism was not significantly associated with atherosclerosis, whereas family history of cardiovascular disease, high stress, and physical activity levels showed significant associations.
Answers are grounded in this paper and cite their sources.
Should not guide genetic risk stratification in non-smokers; leaves open contributions of other variants or gene-environment interactions.
Background Atherosclerosis is a leading cause of cardiovascular related morbidity and mortality worldwide. Although smoking is a well-established risk factor, the genetic and environmental factors contributing to atherosclerosis in non-smoking populations remain less understood. This study aimed to investigate the association between the prothrombin F2 gene rs1799963 G/A polymorphism and atherosclerotic risk in non-smoking Pakistani adults. Results Family history of cardiovascular diseases (p < 0.001), high stress level (p = 0.001) and low physical activity (p = 0.002) showed significant association with atherosclerosis. The rs1799963 GG genotype (90% vs. 74%, p = 0.213) and G allele (95% vs 85%, p = 0.126) were more prevalent in patient group as compare to healthy controls. However, association between atherosclerosis and rs1799963 G/A in non-smokers was not significant. Discussion The findings suggest that family history, stress level, and lifestyle-related factors may contribute more strongly to atherosclerotic risk in non-smoking individuals than the studied F2 rs1799963 polymorphism. Although a higher frequency of the GG genotype and G allele was observed among patients, the lack of statistical significance may be due to the small sample size. Further studies with larger cohorts and multiple genetic markers are required to better understand genetic and environmental interactions in non-smoking populations. Conclusion In summary, risk of atherosclerosis increases in subjects with family history of cardiovascular diseases, high stress level and low physical activity. However, no influence of F2 rs1799963 polymorphism for the risk of atherosclerosis was found in non-smokers in the studied cohort.
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Abbas et al. (2026) conducted a case-control in Atherosclerosis (n=62). Prothrombin F2 gene rs1799963 G/A polymorphism vs. Healthy non-smoking controls was evaluated on Prevalence of F2 rs1799963 GG genotype (p=0.213). Prothrombin F2 rs1799963 GG genotype was not significantly associated with atherosclerosis in non-smokers (90% in patients vs. 74% in controls, p=0.213).
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