Hui Ting Chan

Minimum amount of physical activity for reduced mortality and extended life expectancy: A prospective cohort study

BACKGROUND The health benefits of leisure-time physical activity are well known, but whether less exercise than the recommended 150 min a week can have life expectancy benefits is unclear. We assessed the health benefits of a range of volumes of physical activity in a Taiwanese population. METHODS In this prospective cohort study, 416,175 individuals (199,265 men and 216,910 women) participated in a standard medical screening programme in Taiwan between 1996 and 2008, with an average follow-up of 8·05 years (SD 4·21). On the basis of the amount of weekly exercise indicated in a self-administered questionnaire, participants were placed into one of five categories of exercise volumes: inactive, or low, medium, high, or very high activity. We calculated hazard ratios (HR) for mortality risks for every group compared with the inactive group, and calculated life expectancy for every group. FINDINGS Compared with individuals in the inactive group, those in the low-volume activity group, who exercised for an average of 92 min per week (95% CI 71-112) or 15 min a day (SD 1·8), had a 14% reduced risk of all-cause mortality (0·86, 0·81-0·91), and had a 3 year longer life expectancy. Every additional 15 min of daily exercise beyond the minimum amount of 15 min a day further reduced all-cause mortality by 4% (95% CI 2·5-7·0) and all-cancer mortality by 1% (0·3-4·5). These benefits were applicable to all age groups and both sexes, and to those with cardiovascular disease risks. Individuals who were inactive had a 17% (HR 1·17, 95% CI 1·10-1·24) increased risk of mortality compared with individuals in the low-volume group. INTERPRETATION 15 min a day or 90 min a week of moderate-intensity exercise might be of benefit, even for individuals at risk of cardiovascular disease. FUNDING Taiwan Department of Health Clinical Trial and Research Center of Excellence and National Health Research Institutes.

All-cause mortality attributable to chronic kidney disease: a prospective cohort study based on 462 293 adults in Taiwan

BACKGROUND Both end-stage renal disease and chronic kidney disease are increasing worldwide; however, the full effect of chronic kidney disease is unknown because mortality risks for all five stages are unavailable. We assessed prevalence and mortality risks for all stages of chronic kidney disease and quantified its attributable mortality in Taiwan. METHODS The cohort consisted of 462 293 individuals aged older than 20 years who participated in a standard medical screening programme since 1994. As of Dec 31, 2006, we identified 14 436 deaths. Chronic kidney disease was determined by glomerular filtration rate and urinary protein. We estimated national prevalence in Taiwan from the cohort by adjusting age and educational levels. Hazard ratios (HRs) were calculated with Cox proportionate hazards model. We calculated mortality attributable to chronic kidney disease for national population and for low socioeconomic status. FINDINGS The national prevalence of chronic kidney disease was 11.93% (95% CI 11.66-12.28), but only 3.54% (3.37-3.68) of participants in the cohort were aware of their disorder. Prevalence was substantially higher in the group with low socioeconomic status than in the high status group (19.87% [19.84-19.91] vs 7.33% [7.31-7.35]). 56 977 (12%) of cohort participants had chronic kidney disease; those with disease had 83% higher mortality for all cause (HR 1.83 [1.73-1.93]) and 100% higher for cardiovascular diseases (2.00 [1.78-2.25]), in a cohort that was observed for 13 years with median follow-up of 7.5 years (IQR 4.0-10.1). 10.3% (95% CI 9.57-11.03) of deaths in the entire population were attributable to chronic kidney disease, but 17.5% (16.27-18.67) of deaths in the low socioeconomic status population. 2350 (39%) deaths occurred before 65 years of age in those with chronic kidney disease. Regular users of Chinese herbal medicines had a 20% (odds ratio 1.20 [1.16-1.24]) increased risk of developing chronic kidney disease. INTERPRETATION The high prevalence of chronic kidney disease and its associated all-cause mortality, especially in people with low socioeconomic status, make reduction of this disorder a public-health priority. Promotion of its recognition through the general public knowing their glomerular filtration rate and testing their urine is crucial to reduce premature deaths from all causes and to attenuate this global epidemic.

Is high serum uric acid a risk marker or a target for treatment? Examination of its independent effect in a large cohort with low cardiovascular risk.

BACKGROUND Cohort studies evaluating increased uric acid level as a cardiovascular disease (CVD) risk factor have shown variable results; studies are particularly lacking in lower risk populations. STUDY DESIGN Prospective cohort study. SETTING & PARTICIPANTS 484,568 adults participating in a medical screening program in Taiwan since 1994 were followed up for a median of 8.5 years. Two subgroups were constructed: the first (n = 246,697; 51%) excluded participants with either overt CVD or overt CVD risk factors (including hypertension, diabetes, obesity, and hypertriglyceridemia) and the second (n = 157,238; 32%) further excluded individuals with early-stage CVD risk factors (including prehypertension, prediabetes, overweight, and borderline hypertriglyceridemia). PREDICTOR Serum uric acid. OUTCOMES & MEASUREMENTS All-cause and CVD mortality risk assessed using Cox proportional hazards models for categorical and continuous serum uric acid levels. As applicable, models adjusted for 14 variables. Population-attributable fraction was applied to compare contributions to mortality between high uric acid level and other CVD risk factors. RESULTS In the total cohort, mean age was 41.4 +/- 14.0 years and 26.2% had serum uric acid levels >or=7 mg/dL. Through 2007, there were 16,246 deaths (3.4% of all participants), with 35.2% of deaths occurring in individuals with hyperuricemia. Adjusted HRs associated with serum uric acid levels >or=7 mg/dL for all-cause and CVD mortality were 1.10 (95% CI, 1.04-1.17) and 1.38 (95% CI, 1.20-1.58), respectively. In individuals with hyperuricemia, 64.3% had overt CVD risk factors and 82.5% had either overt or early-stage CVD risk factors. Individuals with serum uric acid levels >or=8 mg/dL without overt CVD risk factors constituted 13.5% of the total study population with hyperuricemia; in analyses excluding those with overt CVD risk factors, serum uric acid level >or=8 mg/dL was significantly associated with all-cause and CVD mortality, with HRs of 1.37 (95% CI, 1.18-1.60) and 2.30 (95% CI, 1.51-3.49), respectively. In the subgroup of those with serum uric acid levels >or=8 mg/dL but who lacked both overt and early-stage CVD risk factors, the HRs for all-cause and CVD mortality were also significant and were 1.39 (95% CI, 1.08-1.78) and 2.38 (95% CI, 1.24-4.54), respectively. HRs for individuals with the same risk profiles but with serum uric acid of 7.0-7.9 mg/dL were not significant. In all groups, inclusion of proteinuria and glomerular filtration rate in models substantially attenuated the association between uric acid level and outcomes. High uric acid levels contributed a relatively insignificant portion to mortality (1.2%) and CVD deaths (4.5%) in this population. LIMITATIONS A single measurement of uric acid was used. CONCLUSION Increased serum uric acid level is a minor, but significant, risk factor for all-cause and CVD mortality. However, except for a small proportion (13.5%), increased serum uric acid level is more a risk marker than a target for treatment and is not an independent risk. Determining appropriate groups to target in clinical trials for uric acid-lowering therapy is critical.

Excess injury mortality among smokers: a neglected tobacco hazard

Objective: To assess the mortality risks from injuries for smokers and ex-smokers and to quantify the mortality burden of smoking from injury in Taiwan. Methods: Smokers’ (and ex-smokers’) mortality risks from injuries were compared with that of non-smokers in a merged cohort from Taiwan. A total of 64 319 male subjects were followed up for 12–18 years. Relative risks (RR) (adjusted for age and alcohol use) and 95% confidence intervals (CI) for cause specific injury deaths were calculated using the Cox proportional hazard model. Relative risks of injury mortality were also calculated to assess the presence of dose–response relations with daily smoking quantity. Results: Alcohol use adjusted relative mortality risks for all injuries (RR 1.69, 95% CI 1.39 to 2.05) including those from motor vehicle accidents (RR 1.88, 95% CI 1.44 to 2.45) and non-motor vehicle accidents (RR 1.48, 95% CI 1.11 to 1.99) were significantly higher for smokers than non-smokers. Mortality was also increased for most subtypes of non-motor vehicle injuries including falls, fires, and job related injuries. Furthermore, these increases were dose dependent, with the heaviest smokers having the highest risk and the lightest smokers the lowest risk, and ex-smokers, no increase. In 2001, over one fifth (23%) of all male injury deaths in Taiwan was associated with smoking. Conclusion: This study demonstrated the significant association between fatal injuries and smoking. This relation adds further weight to smoking cessation campaigns.

Making hypertensive smokers motivated in quitting: Developing 'blood pressure equivalence of smoking'

Objective To express the increased risk from smoking in terms of ‘blood pressure’ so that hypertensive smokers are motivated into quitting. Methods Mortality risks of smokers were compared with nonsmokers in a large worker cohort in Taiwan (n = 23 755 with a 17-year follow-up) for all-cause and for cardiovascular diseases. The blood pressure equivalence of smoking was then identified by the difference in mortality risks between smokers and nonsmokers. Results Some interaction between hypertension and smoking was found to be synergistic. When hypertension and smoking co-existed, the all-cause mortality outcome [relative risk (RR) = 4.25] was larger than the sum or product of each individual risk for hypertension (RR = 2.16) or for smoking (RR = 1.97). The excess mortality risks of smoking for smokers were converted into a ‘blood pressure equivalence’. The results demonstrate that the addition of smoking was similar to an increase of mortality risk approximately equivalent to an increase in blood pressure of 40 mmHg. Conclusions Smoking cessation in hypertensive patients could provide a reduction of mortality risks similar to a permanent reduction of 40 mmHg in blood pressure, over and above any antihypertensive medications. Appreciating this relationship enables physicians to bridge the clinical disconnection and motivates hypertensive smokers to seek smoking cessation. The use of a ‘blood pressure equivalence of smoking’ can link the two separate risk factors and may lead to a paradigm shift in overcoming an existing clinical challenge.

Abstract B135: Mortality risks and life‐shortening effect of hepatitis C virus infection: A prospective cohort study of 487,369 adults in Taiwan

Background: There has been emerging knowledge on the serious burden of diseases attributable to Hepatitis C carriers (HCV). However, the extent of the life time risk of HCV, when independently assessed, is as yet fully understood, particularly regarding associated risk factors that are amenable to reductions. Objectives: We assessed the mortality risks and life‐shortening effect of HCV, along with its associated risk factors, based on following up a large healthy cohort in Taiwan. Methods: The cohort, consisting of 487,369 subjects, participated in a standardized medical screening program since 1994. Based on the hepatitis carrier status (either HBV or HCV or both), three sub‐cohorts were created. As of 2007, 16,920 deaths were identified, including 1,383 liver cancer and 631 cirrhosis, with average follow up of 8.5 years. Hazard ratio (RR) was calculated using Cox proportionate hazard model. National prevalence was arrived at by standardizing age and educational status, a surrogate for socioeconomic status (SES) to those in Taiwan. Glomerular Filtration Rate (GFR) was calculated by MDRD equation. Results: National Prevalence for HCV: 3.6% above age 20, and 6.6% above age 40 (male 6.0% and female 7.3%) increased with age and with lower SES. Rates of diabetes, hypertension, obesity, and HDL among HCV+ participants were significantly higher, but total cholesterol and triglycerides were lower. They had 35% more chronic kidney disease (CKD), with 54% more proteinuria and 13% more reduced GFR (13%). Cohort mortality results: HCV+ male participants had 7.37 years shorter than the total cohort at age 20, compared to 3.36 years for HBV+. In contrast to one out of 7 deaths (13.7%) in the total cohort was liver related, one out of two in the HCV+ sub‐cohort. With HR for all‐cause being 2.42, 58.7% of the deaths were HCV‐related, larger than HBV counterparts (36.7%). The number of HCV related cirrhosis was 1/4 (28%) that of HCC, and HCV related risk, 10.74, was slightly smaller than that for HCC, 14.56. Nearly one out of 10 HCV+ coexisted with HBV (8.9%), and the risk became synergistic, with 2/3 of them dying from liver‐related causes. Kidney cancer (5.46), diabetes (2.31), and stroke (1.91) were also significantly increased. In the order of ranking All Cause mortality risks among HCV+ subjects, diabetes (4.5), proteinuria (4.1), smoking (3.5), obesity (3.3), drinking (3.2) and hypertension (2.9) were all significantly increased. Conclusion: The life expectancy of HCV+ carriers was shortened by 7.37–8.45 years. While the main effect was liver cancer and cirrhosis, HCV also involved kidney damage, producing proteinuria and reduced GFR, and led to an increased mortality from diabetes and stroke. The ranking order of reducible HCV risks were diabetes, CKD including proteinuria, smoking, obesity, drinking and hypertension. Citation Information: Cancer Prev Res 2010;3(1 Suppl):B135.