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Smoking and cause of death in Korea: 11 years follow-up prospective study.
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Sun Ha Jee, Ji Eun Yun, Jung Yong Park, Jae Woong Sull, Il Soon Kim
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Korean J Epidemiol. 2005;27(1):182-190.
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Abstract
OBJECTIVE: In Korea, male smoking prevalence is among the world's highest and mortality rates from smoking-caused cancers, particularly lung cancer, are escalating. This cohort study examined the effects of cigarette smoking on the risk of mortality from all causes, cancers and cardiovascular diseases(CVD), and characterized the relationship of the risk with the amount and duration of cigarette smoking.METHOD A eleven-year prospective cohort study was carried out of on 1,207,592 Koreans, 30 to 95 years of age. The study population includes participants in a national insurance program, who completed a questionnaire on smoking and other risk factors. The main outcome measures were death from all causes, cancer and CVD, obtained through record linkage. At baseline, 482,997 men(60.0%) and 19,755(5.3%) women were current cigarette smokers.RESULTS In multivariate Cox proportional hazards models, controlling for age, alcohol drinking, exercise, and obesity, current smoking among men increased the risks of mortality from all cause death (relative risk[RR], 1.56; 95% confidence interval[CI], 1.52~1.59), all cancer (1.75, 1.68~1.82), and CVD(1.46, 1.38~1.55). Similar results were found for mortality among women. Smoking also increased the risks of mortality for cancer of the lung(4.60, 4.09~5.33) and other cancers, including larynx, bile duct, esophagus, liver, stomach, pancreas, bladder, and also leukemia.
Current smoking among women increased the risk of lung cancer mortality(RR=2.83, 95% CI 2.38~3.36).CONCLUSION In Korea, smoking is an independent risk factor for death from all causes, CVD and a number of major cancers. The findings affirm the need for aggressive tobacco control in Korea in order to minimize the epidemic of smoking-caused disease.
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Estimation of heritability attributable to single-locus effects with a regression of offspring on mid-parent (ROMP) method for cardiovascular risk factors.
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Sun Ha Jee, Jung Yong Park, Ji Eun Yoon, Minji Kim, Eun Young Cho, Yang soo Jang
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Korean J Epidemiol. 2003;25(1):24-31.
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PURPOSE
The objective of this study was to estimate the heritability attributable to single-locus effects with a regression of offspring on mid-parent (ROMP) method for cardiovascular risk factors.METHODS The regression of offspring on mid-parent is determined with and without the inclusion of a single-locus effect, and the difference between the slopes of these two regression is an estimate of the heritability attributable to the single-locus effect. The study population included 1,550 family members of 295 patients, derived from cardiovascular genome center. The risk factors considered were total serum cholesterol, triglyceride, LDL cholesterol, apoAI and apoB. Heritability was estimated from the slope of the linear regression of offspring on mid-parents.RESULTS Estimated heritability was 35 to 46% for total cholesterol with 6.2% attributable to polymorphism S128R.
For triglyceride, the estimated heritability was 47.6% with 2% attributable to polymorphism G-217A. The heritability was 36-46% for LDL-cholesterol. For LDL cholesterol, S128R specific effect was 8.7%. Estimated heritability was 62.2% for apoAI with 3.2% attributable to polymorphism G-217A and 58 to 75% for apoB with 5.4% attributable to polymorphism S128R.CONCLUSIONS These traits were significantly associated with polymorphism S128R. These results highlight the importance of considering genetic factors in studies of cardiovascular risk factors. Unlike traditional population-based tests of association, ROMP appears to be robust with respect to population stratification.
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Segregation Analysis of Serum LDL-cholesterol in Korean Families of Coronary Heart Disease Patients.
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Jung Yong Park, Sun Ha Jee, Kyung Soon Song, Won Heum Shim, Soo Jeong Kim
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Korean J Epidemiol. 2000;22(2):116-123.
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S: The aim of this study was to investigate the familial correlation of lipid profile and the mode of inheritance of LDL-cholesterol through segregation analysis.
The study population included 414 family members of 67 Probands who had a coronary heart disease.METHODS Gene frequency(qH) of the allele for high LDL-cholesterol levels, means of each genotypes, and other putative gene related parameters were estimated. Maximum likelihood methods were used to fit several genetic and nongenetic modes of inheritance to these data to determine if an unobserved Mendelian major gene could explain the familial distribution of LDL-cholesterol. LDL-cholesterol levels were adjusted for age, gender, body mass index, smoking and alcohol consumption.RESULTS LDL-cholesterol levels revealed familial correlation among spouses, parent-offsprings and siblings with correlations of 0.10, 0.22, and 0.32, respectively. The heritability of LDL-cholesterol was 53%. Two models of inheritance in LDL-cholesterol distribution, the Mendelian codominant model and the polygenic equal transmission model were found.
Comparison of these two models in each family among 67 families showed that thiry-six families favored the major gene model with Mendelian codominant and thirty-one families favored the polygenic model of equal transmission. In families favoring Mendelian codominant inheritance, means of each genotypes; LL, HL, HH were 102.1, 143.3, 248.4 mg/dl and gene frequency of H allele was 0.08. In families favoring equal transmission inheritance, means of each genotypes were 101.6, 122.7, 185.5 mg/dl and gene frequency of H allele was 0.14.CONCLUSIONS In conclusion, families of coronary heart disease patients of this study showed substantial familial correlation and results suggested that variation in LDL-cholesterol may be influenced by major gene effect.
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A Study of Major Gene Dominant Family for Factor VII Concentration: Segregation Analysis.
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Sun Ha Jee, Kyung Sooon Song, Won Heum Shim, Il Suh, Hyun Kyung Kim, Young Sup Yoon, Eunna Go, Jung Yong Park, Miyang Kim, Sujeong Kim
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Korean J Epidemiol. 1999;21(2):176-184.
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Elevated plasma level of factor VII is a risk factor for coronary artery disease. We investigated environmental, familial, and genetic influences on factor VII levels. We used maximum likelihood segregation analysis to fit several genetic and nongenetic modes of inheritance to the data to determine whether Mendelian inheritance of a major gene could best explain the familial distribution of factor VII.
The study population included 414 family members of 67 subjects who had undergone elective coronary arteriography.
The factor VII level was adjusted for age, gender, body mass index, smoking and alcohol drinking (R2=20.6%).
Factor VII levels revealed strong familial aggregation with estimated correlation spouse of 0.12, parent-offspring of 0.31, and siblings of 0.40. Regressive models were used to examine inter-individual variation in adjusted factor VII levels in these 67 families. This analysis strongly favored a major gene model with codominant transmission. Genotypic means were 111.6, 123.2, and 184.3% with relative frequencies of 59.4%, 35.4%, and 5.2%. This putative major gene explains 39.9% of the total variance of factor VII.
Likelihood was used to search for etiologic heterogeneity by sorting pedigrees into groups that favor one model over another. Compared to pedigrees less favoring Mendelian models, pedigrees favoring Mendelian codominant models have almost 8 times earlier onset of coronary heart disease.
These family data suggest that there are strong familial and genetic effects on the factor VII activity in these high risk families. Therefore, linkage studies in these families may be worthwhile to clarify the molecular basis of factor VII levels.
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