ObjectiveThe objectives of this study were to develop a coronary heart disease (CHD) risk model among the Korean Heart Study (KHS) population and compare it with the Framingham CHD risk score.DesignA prospective cohort study within a national insurance system.Setting18 health promotion centres nationwide between 1996 and 2001 in Korea.Participants268 315 Koreans between the ages of 30 and 74 years without CHD at baseline.Outcome measureNon-fatal or fatal CHD events between 1997 and 2011. During an 11.6-year median follow-up, 2596 CHD events (1903 non-fatal and 693 fatal) occurred in the cohort. The optimal CHD model was created by adding high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol and triglycerides to the basic CHD model, evaluating using the area under the receiver operating characteristic curve (ROC) and continuous net reclassification index (NRI).ResultsThe optimal CHD models for men and women included HDL-cholesterol (NRI=0.284) and triglycerides (NRI=0.207) from the basic CHD model, respectively. The discrimination using the CHD model in the Korean cohort was high: the areas under ROC were 0.764 (95% CI 0.752 to 0.774) for men and 0.815 (95% CI 0.795 to 0.835) for women. The Framingham risk function predicted 3–6 times as many CHD events than observed. Recalibration of the Framingham function using the mean values of risk factors and mean CHD incidence rates of the KHS cohort substantially improved the performance of the Framingham functions in the KHS cohort.ConclusionsThe present study provides the first evidence that the Framingham risk function overestimates the risk of CHD in the Korean population where CHD incidence is low. The Korean CHD risk model is well-calculated alternations which can be used to predict an individual's risk of CHD and provides a useful guide to identify the groups at high risk for CHD among Koreans.

Recently, it was reported that reduction in serum adiponectin levels is correlated with the incidence of breast cancer. As an effort to explain this, we screened various human breast cancer cell lines to identify those in which proliferation is directly controlled by adiponectin. Among the five tested cell lines, proliferation of MDA-MB-231 cancer cell was significantly suppressed by adiponectin within the range of physiological concentration. Furthermore, prolonged adiponectin treatment caused cell growth arrest and even apoptosis of MDA-MB-231. This result is the first to show that adiponectin can directly control cancer cell growth and provides a rationale for the theory that reduction in plasma adiponectin levels could be a risk factor for breast cancer.

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Data from the present sample, based on data linkage, show close agreement with South Korea-wide surveys (for risk factor prevalence) and the extant literature (for risk factor associations). These findings gives confidence in future results anticipated from this cohort study of east Asians - a group that has been traditionally under-researched.

The principal objective of this study was to determine whether visceral fat or liver fat is a more relevant risk factor for metabolic syndrome. A total of 98 subjects aged 18-65 yr, who visited a health promotion center in a university hospital, were enrolled in this study. Metabolic syndrome was diagnosed based on the modified National Cholesterol Education Program's Adult Treatment Panel III report (NCEP-ATPIII) criteria. We defined the visceral obesity as a visceral fat area of ≥ 100 cm2 which was acquired by CT at the L4-5 level. To evaluate fatty liver, we applied a liver-to-spleen attenuation ratio ≤ 1.1 as measured by CT at the T12 level. We employed binary logistic regression models that used the presence or absence of metabolic syndrome as a dependent variable and age, sex, and the presence or absence of visceral obesity and fatty liver as independent variables. Visceral obesity was not found to be an independent variable as a risk factor of metabolic syndrome (odds ratio 2.7; 95% confidence interval 0.55-13.30), but fatty liver was found to be significant in this model (odds ratio 71.3; 95% CI 13.04-389.53). Our study suggests that liver fat may be a more important risk factor than visceral fat in terms of its association with metabolic syndrome.