Aims It is well known that a decline in physical activity is associated with an increase of all-cause death including cardiovascular events and cancer. Few studies have examined the association between occupational sitting time and mortality. Therefore, we investigated this issue in a general population. Methods Physical activity and occupational sitting time were measured using the Baecke physical activity questionnaire in 1999. The questionnaire generated indices in three physical activity categories: work, sport and leisure-time. A total physical activity index was calculated by adding these three indices. The Baecke physical activity questionnaire was able to evaluate occupational sitting time. Hazard ratios and 95% confidence intervals (CIs) were calculated using Cox's proportional hazard regression models. Results We enrolled a total of 1680 participants, who were followed up for 15.9 ± 3.8 years. The final follow-up rate was 93%. During the follow-up period, 397 subjects died. A significant inverse association ( p < 0.0001) was found between physical activity and mortality after adjustment for age and sex. Compared with lower levels of physical activity, the adjusted hazard ratio for mortality at higher levels of physical activity was 0.85 (95% CI: 0.78–0.92). Longer occupational sitting time was also significantly associated with higher mortality ( p < 0.01). The adjusted hazard ratio for mortality at longer occupational sitting time was 1.16 (95% CI: 1.05–1.27). These findings were observed in males, but not in females. Conclusions Our data demonstrated that higher levels of physical activity are associated with a reduced risk of cancer and cardiovascular death. Further, longer occupational sitting time is associated with increased mortality.

Serum urate levels have been shown to be correlated with risk for incident cardiovascular disease (CVD) events among middle-aged or older adults. However, serum urate trajectory during young adulthood and its association with CVD events has been understudied. Using serum urate measurements collected at baseline and 10, 15, 20 years after baseline from 3563 CARDIA (Coronary Artery Risk Development in Young Adults) participants (mean age 25.1±3.6 [18–30] years at baseline [year 0, 1985–1986]; 46.3% Black; 56.1% female), we determined sex-specific serum urate trajectories using SAS PROC TRAJ. We estimated hazard ratios for incident CVD events (coronary heart disease, heart failure, and stroke) occurring after the year 20 exam through 2017. We identified 3 serum urate trajectories by sex, including low-stable (n=1251), moderate-stable (n=1761), and high-increasing (n=551). Over a median 10.6 years of follow-up, 157 incident CVD events occurred. Participants among the high-increasing trajectory group had 2.89 (95% CI, 1.88–4.43) times greater risk for CVD compared with the low-stable trajectory group. The association was attenuated after adjustment for blood pressure levels during young adulthood. In conclusion, high-increasing serum urate trajectory during young adulthood was associated with incident CVD by middle age, and the association may be explained by blood pressure levels during the exposure period.

Background There is little data on the association between the lower nutrition represented by serum albumin levels and related factors in a general population. The present study aimed to determine whether the albumin level positioned as some kind of biomarker with frailty measures, trace elements, and an inflammation marker. Methods In 2018, we performed an epidemiological survey in 1368 subjects who resided in Tanushimaru, Japan, in which we examined the blood chemistry including albumin, trace elements, hormone levels, and carotid ultrasonography. Albumin levels were categorized into 4 groups (G1 [3.2–3.9 mg/dL], G2 [4.0–4.3 mg/dL], G3 [4.4–4.6 mg/dL], and G4 [4.7–5.3 mg/dL]). The participants underwent measurements of handgrip strength and were tested by asking to walk 5 m. Their cognitive functions were evaluated by the mini-mental state examination (MMSE). Results Multiple stepwise regression analysis demonstrated that albumin levels were significantly and independently associated with age (inversely), systolic blood pressures, estimated glomerular filtration rate (eGFR), MMSE score, frailty measures (handgrip strength), an inflammation marker (high-sensitivity C-reactive protein), hormones (growth hormone (inversely) and insulin-like growth factor-1), and trace elements (calcium, magnesium, iron, and zinc), with a linear trend. Conclusions Lower albumin levels, even in the normal range, were found to be related factors of frailty measures, trace elements, and an inflammation marker in a general population.

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Proprotein convertase subtilisin/kexin type 9 (PCSK9) has been identified as an important regulator of low-density lipoprotein (LDL) receptor processing. Evolocumab and alirocumab are PCSK9 inhibitors; however, little is known about the association between PCSK9 levels and lipid profiles in a general population. Because PCSK9 inhibitors have LDL-C lowering effects, we investigated whether there is a positive correlation between serum PCSK9 levels and LDL-C or lipoprotein(a) [Lp(a)]. Methods: In Uku town, 674 residents (mean age; 69.2 8.3 years) received health check-ups. The participants underwent a physical examination and blood tests, including PCSK9 and Lp(a). Serum PCSK9 and Lp(a) were measured by ELISA and Latex methods, respectively. HOMA-IR was calculated by fasting plasma glucose insulin levels/405. Results: The mean (range) of PCSK9 and Lp(a) were 211.2 (49-601) ng/mL and 60 (1-107) mg/dL, respectively. Because of a skewed distribution, the log-transformed values were used. With univariate linear regression analysis, PCSK9 levels were associated with Lp(a) (p 0.028), triglycerides (p 0.001), and HOMA-IR (p 0.001), but not with LDL-C (p 0.138) levels. Multiple stepwise regression analysis revealed that serum PCSK9 levels were independently associated with triglycerides (p 0.001), Lp(a) (p 0.033) and HOMA-IR (p 0.041). Conclusions: PCSK-9 is independently associated with triglycerides, Lp(a) levels, and HOMA-IR, but not LDL-C, in a relatively large general population sample.moting their degradation through the endosomal/ lysosomal pathway 1) .Data from clinical, in vivo, in vitro, and animal studies have associated PCSK9 with triglycerides 2) , triglycerides-rich lipoproteins 3) , high-density lipoprotein cholesterol (HDL-C) 4) , insulin, and insulin resistance 5,6) . Studies on the relationship between PCSK9 and the components of metabolic syndrome have been reported; however, the results are inconsistent 7,8) .

Objective There is little long-term data on the association between the serum albumin levels and mortality in community-based populations. We aimed to determine whether the serum albumin level is an independent risk factor for all-cause and cause-specific death in a community-based cohort study in Japan. Methods In 1999, we performed a periodic epidemiological survey over a 15-year period in a population of 1,905 healthy subjects (783 males, 1,122 females) who were older than 40 years of age and who resided in Tanushimaru, a rural community, in Japan. Over the course of the study, we periodically examined the blood chemistry of the study subjects, including their serum albumin levels. Their baseline serum albumin levels were categorized into quartiles. Results The baseline albumin levels were significantly associated with age (inversely), body mass index (BMI), diastolic blood pressure, lipid profiles [high density lipoprotein-cholesterol (HDL-c), low-density lipoprotein-cholesterol (LDL-c) and triglycerides] and estimated glomerular filtration rate (eGFR). After adjusting for confounders, a Cox proportional hazards regression analysis demonstrated that a low serum albumin level was an independent predictor of all-cause death [hazard ratio (HR): 0.39, 95% confidence interval (CI): 0.24-0.65], cancer death (HR: 0.43, 95% CI: 0.18-0.99), death from infection (HR: 0.21, 95% CI: 0.06-0.73) and cerebro-cardiovascular death (HR: 0.19, 95% CI: 0.06-0.63). The HRs for all-cause and cerebro-cardiovascular death in the highest quartile vs. the lowest quartile of albumin after adjusting for confounders were 0.59 (95%CI:0.39-0.88) and 0.15 (95%CI: 0.03-0.66), respectively. Conclusion The serum albumin level was thus found to be a predictor of all-cause and cerebro-cardiovascular death in a general population.

Accumulation of visceral fat leads to metabolic syndrome and increases risks of cerebro-cardiovascular diseases, which should be recognized and improved at the early stage in general population. Accurate measurement of visceral fat area (VFA) is commonly performed by the abdominal cross-sectional image measured by computed tomography scan, which is, however, limited due to the radiation exposure. The bioelectrical impedance analysis (OMRON, HDS-2000 DUALSCANR) has been recently developed to measure VFA, which is more easily accessible modality. In the present study, we investigated the clinical usefulness of DUALSCANR in 226 subjects who received health examination, including blood chemistries, electrocardiography, cardio, and carotid ultrasonography. VFA was measured within only just 5 min. Average of VFA was 83.5 ± 36.3 cm2 in men, and 64.8 ± 28.0 cm2 in women, which was correlated to weight (r = 0.7404, p < 0.0001), body mass index (BMI) (r = 0.7320, p < 0.0001), and waist circumstance (r = 0.7393, p < 0.0001). In multivariate analyses, VFA was significantly associated with weight (p < 0.0001), BMI (p < 0.0001), and waist circumstance (p < 0.0001). Compared to the group of smaller waist and normal BMI, VFA was significantly increased (p < 0.0001) in the group of larger waist and obese subjects. In conclusion, these results indicated that DUALSCANR is useful to measure VFA easily in general population, even in a large number of subjects.

This is the first report demonstrating the causal relationship between them. Elevated plasma TGF-β1 levels predicted the development of hypertension in normotensives in a population of community-dwelling Japanese.