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. 2010;20(4):259-65.
doi: 10.2188/jea.je20100060. Epub 2010 Jun 19.

Dyslipidemia and cardiovascular disease: a series of epidemiologic studies in Japanese populations

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Dyslipidemia and cardiovascular disease: a series of epidemiologic studies in Japanese populations

Tomonori Okamura. J Epidemiol. 2010.

Abstract

Although the causal relationships of high serum levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) with coronary artery disease (CAD) are well established, there have been few community-based epidemiologic studies of these relations in Japan. Furthermore, even when analysis is restricted to ischemic stroke, the relationship between dyslipidemia and stroke is very weak. Accordingly, it is difficult to perform cohort studies of dyslipidemia and cardiovascular disease. A series of studies, such as the NIPPON DATA (National Integrated Project for Prospective Observation of Non-communicable Disease and Its Trends in the Aged) cohort study of a representative sample of Japanese, have greatly increased existing evidence. NIPPON DATA80 revealed a clear positive relationship between TC and CAD, and indicated that reverse causality between hypocholesterolemia and liver disease may increase all-cause mortality in hypocholesterolemic Japanese. NIPPON DATA90 showed that serum high-density lipoprotein cholesterol (HDL-C) was inversely associated with all-cause mortality, even when HDL-C was very high. NIPPON DATA80 revealed that low-normal levels of serum albumin and TC are associated with a decline in activity during old age, especially in women. The Suita study-a unique cohort study of urban residents-showed that LDL-C and non-HDL-C were equally accurate in predicting the incidence of myocardial infarction. Further research of this quality is needed to ascertain the public health burden of dyslipidemia in Japan.

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Figures

Figure 1.
Figure 1.. Multivariate-adjusted hazard ratios (HRs) for coronary artery disease mortality, grouped according to serum total cholesterol, after adjustment for age, serum albumin, body mass index, hypertension, diabetes, cigarette smoking, and alcohol intake. Black bars indicate HRs for men, and hatched bars indicate HRs for women. (*P < 0.05)
Figure 2.
Figure 2.. Multivariate-adjusted hazard ratios (HRs) for all-cause mortality, grouped according to serum total cholesterol, after adjustment for sex, age, serum albumin, body mass index, hypertension, diabetes, cigarette smoking, and alcohol intake. Black bars (model 1) indicate HRs for all-cause mortality among all participants. Hatched bars (model 2) indicate HRs for all-cause mortality after exclusion of deaths due to liver disease during the entire follow-up period and all-cause deaths within the first 5 years of follow-up. (*P < 0.05)
Figure 3.
Figure 3.. Multivariate-adjusted hazard ratios (HRs) for all-cause mortality, grouped according to serum high-density lipoprotein cholesterol (HDL-C), after adjustment for age, body mass index, triglyceride (log-transformed), non–HDL-C, hypertension, diabetes, cigarette smoking, and alcohol intake. Black bars indicate HRs for men, and hatched bars indicate HRs for women. (*P < 0.05)
Figure 4.
Figure 4.. Multivariate odds ratios (ORs) and 95% confidence intervals (CIs) for the composite outcome of low activities of daily living (ADL) or death, according to quartile of serum albumin, after stratification at median (200 mg/dl) serum total cholesterol (TC), in women. The model was adjusted for age, TC, diabetes, hypertension, body mass index, cigarette smoking, and alcohol intake.
Figure 5.
Figure 5.. Multivariate-adjusted hazard ratios (HRs) for the incidence of myocardial infarction, grouped according to serum low-density lipoprotein cholesterol (LDL-C) or non–high-density lipoprotein cholesterol (non–HDL-C), after adjustment for sex, age, body mass index, hypertension, diabetes, HDL-C, cigarette smoking, and alcohol intake. Black bars indicate HRs of LDL-C; the hatched bars indicate HRs of non–HDL-C. (*P < 0.05) ‘Q’ indicates quintile. The cutoff points for LDL-C were Q1: <98, Q2: 98–117, Q3: 118–132, Q4: 133–150, Q5: ≥151 mg/dl for men, and Q1: <106, Q2: 106–124, Q3: 125–141, Q4: 142–163, Q5: ≥164 mg/dl for women. The cutoff points for non–HDL-C were Q1: <123, Q2: 124–142, Q3: 143–159, Q4: 160–179, Q5: ≥180 mg/dl for men, and Q1: <125, Q2: 125–142, Q3: 143–164, Q4: 165–188, Q5: ≥189 mg/dl for women.

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