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Published on: November 10, 2015
Increased Risk of the APOB rs11279109 Polymorphism for CHD among the Kuwaiti Population
Suzanne A Al-Bustan1, Fatma G Ismael1, Ahmad Al-Serri2
1Department of Biological Sciences, Faculty of Science, Kuwait University, Kuwait City, Kuwait.
Insights
The APOB rs11279109 DD genotype is linked to a higher risk of coronary heart disease (CHD) in Kuwaitis. This genetic marker may aid in early diagnosis and prevention strategies for CHD.
Area of Science:
- Genetics
- Cardiovascular Disease Epidemiology
Background:
- Coronary heart disease (CHD) is a major cause of mortality in Kuwait.
- Investigating genetic factors contributing to CHD risk in the Kuwaiti population.
Purpose of the Study:
- To determine the association between the APOB rs11279109 polymorphism and CHD in Kuwaiti individuals.
- To explore the potential of APOB rs11279109 as a genetic marker for CHD risk.
Main Methods:
- A case-control study involving 734 Kuwaiti participants.
- Genotyping of the APOB rs11279109 polymorphism using direct amplification.
- Statistical analysis with genetic modeling to assess the association with CHD.
Main Results:
- A significant association was found between the rs11279109 DD genotype and CHD (P < 0.001).
- The DD genotype showed an odds ratio of 2.43 (CI: 1.34-4.41) for CHD.
- A codominant model indicated a 2.69 increased risk for the DD genotype (P = 0.009), independent of other risk factors.
Conclusions:
- The APOB rs11279109 DD genotype may be an indicator of increased CHD risk in Kuwaitis.
- This genotype might be involved in molecular mechanisms of increased LDL oxidation and atherosclerosis.
- Highlights the importance of identifying ethnic-specific genetic markers for improved CHD prognosis, diagnosis, and prevention.
Background:
Coronary heart disease (CHD) is among the leading causes of death in Kuwait. This case-control study investigated the genetic association of APOB rs11279109 with CHD in Kuwaitis.
Methods:
The polymorphism was genotyped in 734 Kuwaiti samples by direct amplification. Statistical analysis with genetic modeling was used to assess its association with CHD.
Results:
A statistically significant association (P < 0.001) between the rs11279109 DD genotype (OR: 2.43, CI: 1.34-4.41) with CHD was observed. A codominant genetic model revealed a 2.69 risk increase (CI: 1.57-4.61) for the DD genotype (P = 0.009) independent of age, sex, BMI, smoking, hypercholesterolemia, and ethnicity suggesting APOB rs11279109 as an indicator for the increased risk of CHD.
Conclusion:
The DD genotype may explain molecular mechanisms that underline increased LDL oxidation leading to arthrosclerosis. The findings emphasize the need to identify genetic markers specific to the CHD patient ethnic group in order to improve prognosis and help in early diagnosis and prevention.
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