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Journal of the Korean Geriatrics Society 2006;10(4):301-305.
Published online December 31, 2006.
Angiotensin-converting Enzyme Deletion Polymorphism is Associated with Essential Hypertension in Men with Higher Salt Intake
Jun Hyun Yoo
Department of Family Medicine, Samsung Medical Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul, Korea. drjohn.yoo@samsung.com
Abstract
Background
Hypertension is etiologically associated with lifestyles and genetic factors. A number of investigations in various populations have shown discordant evidence on the association of the insertion-deletion (I/D) polymorphism of angiotensin-converting enzyme (ACE) gene with hypertension. However, there is no population study on hypertension, ACE gene and salt. This study explored whether the ACE I/D polymorphism is associated with essential hypertension in relation to dietary salt intake.
Methods
A cross-sectional study was conducted on a total of 4,588 healthy male subjects aged 20 to 79 years. ACE genotypes were determined using polymerase chain reaction. Semi-quantitative questionnaire using weekly recall method was used to assess dietary salt intake. With regard to level of salt intake, subjects were divided into tertile groups.
Results
The overall OR of ACE DD genotype for hypertension showed 29% increased risk (OR=1.29, 95% CI, 1.08 - 1.56) (p=0.003), with adjustment for age, body mass index, and impaired fasting glucose. According to salt intake, only a group consuming higher salt (more than 17 gram/day) showed that DD genotype was at increased risk for hypertension, having 48% increased risk in DD genotype than ID/II genotype (OR 1.48, 95% CI 1.06-2.05).
Conclusions
Among Korean men studied, ACE DD genotype was at increased risk of hypertension in men consuming higher dietary salt. Finding suggests that ACE polymorphism may be one of the factors involved in the predisposition of hypertension, in men consuming high salt.
Key Words: Angiotensin, Gene, Polymorphism, Hypertension, Sodium, Salt
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