An-Chun Hwang1, Li-Ning Peng1, Yu-Wen Wen2, Yi-Wen Tsai3, Li-Chuan Chang4, Shu-Ti Chiou5, Liang-Kung Chen6. 1. Aging and Health Research Center, National Yang Ming University, Taipei, Taiwan; Institute of Public Health, National Yang Ming University, Taipei, Taiwan; Center for Geriatrics and Gerontology, Taipei Veterans General Hospital, Taipei, Taiwan. 2. Clinical Informatics and Medical Statistics Research Center, Chang-Gung University, Taoyuan, Taiwan. 3. Aging and Health Research Center, National Yang Ming University, Taipei, Taiwan; Institute of Health Welfare and Policy, National Yang Ming University, Taipei, Taiwan. 4. Institute of Health Welfare and Policy, National Yang Ming University, Taipei, Taiwan. 5. Institute of Public Health, National Yang Ming University, Taipei, Taiwan; Health Promotion Administration, Ministry of Health and Welfare, Taipei, Taiwan. 6. Aging and Health Research Center, National Yang Ming University, Taipei, Taiwan; Clinical Informatics and Medical Statistics Research Center, Chang-Gung University, Taoyuan, Taiwan. Electronic address: lkchen2@vghtpe.gov.tw.
Abstract
OBJECTIVE: To evaluate the role of allostatic load (AL), either static or dynamic measurements, in predicting all-cause and cause-specific mortality of older people in Taiwan. DESIGN: A prospective cohort study. SETTING: Population-based community study. PARTICIPANTS: One thousand twenty-three community-dwelling older people. MEASUREMENTS: Allostatic load (calculated by systolic blood pressure, diastolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, triglyceride, glycosylated hemoglobin, fasting glucose, waist-to-hip ratio, body mass index, dehydroepiandrosterone sulfate, insulin-like growth factor-1, 12-hour urine cortisol, 12-hour urine epinephrine, 12-hour urine norepinephrine, 12-hour urine dopamine, white blood cell count, neutrophils, interleukin-6, albumin, creatinine) and all-cause and cause-specific mortality from national death registry. INTERVENTION: None. RESULTS: Adjusted for age and sex, each 1-point increase in AL score was associated with 20% incremental risk of mortality [hazard ratio 1.20, 95% confidence interval (CI) 1.09-1.31]. This association can be extended to cause-specific mortality in both sexes in general. In addition, the higher AL score quintile was significantly associated with higher risk of 10-year all-cause mortality (P < .0001). This association was consistent across different cause-specific mortality (ie, malignant neoplasm (P = .008), cardiometabolic diseases (P < .0001), infectious diseases (P < .0001), respiratory diseases (P < .0001), and others (P = .0002), respectively. Compared with AL score decliners, adjusted for age, sex, and baseline AL score in 2000, participants with fast increase had significantly higher mortality (HR 2.68, 95% CI 1.23-5.84, P = .01). The effect was stronger in men (HR 2.83, 95% CI 1.1-7.29, P = .03 in slow increase; HR 4.06, 95% CI 1.56-10.6, P = .001 in fast increase group), but it was insignificant in female participants. CONCLUSIONS: Higher AL score or rapid increase of AL score significantly increased subsequent mortality risk in older adults, either measured statically or dynamically. AL is predictive of 10-year mortality regardless of cause of death, and rapid increase in AL score is associated with higher subsequent mortality.
OBJECTIVE: To evaluate the role of allostatic load (AL), either static or dynamic measurements, in predicting all-cause and cause-specific mortality of older people in Taiwan. DESIGN: A prospective cohort study. SETTING: Population-based community study. PARTICIPANTS: One thousand twenty-three community-dwelling older people. MEASUREMENTS: Allostatic load (calculated by systolic blood pressure, diastolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, triglyceride, glycosylated hemoglobin, fasting glucose, waist-to-hip ratio, body mass index, dehydroepiandrosterone sulfate, insulin-like growth factor-1, 12-hour urine cortisol, 12-hour urine epinephrine, 12-hour urine norepinephrine, 12-hour urine dopamine, white blood cell count, neutrophils, interleukin-6, albumin, creatinine) and all-cause and cause-specific mortality from national death registry. INTERVENTION: None. RESULTS: Adjusted for age and sex, each 1-point increase in AL score was associated with 20% incremental risk of mortality [hazard ratio 1.20, 95% confidence interval (CI) 1.09-1.31]. This association can be extended to cause-specific mortality in both sexes in general. In addition, the higher AL score quintile was significantly associated with higher risk of 10-year all-cause mortality (P < .0001). This association was consistent across different cause-specific mortality (ie, malignant neoplasm (P = .008), cardiometabolic diseases (P < .0001), infectious diseases (P < .0001), respiratory diseases (P < .0001), and others (P = .0002), respectively. Compared with AL score decliners, adjusted for age, sex, and baseline AL score in 2000, participants with fast increase had significantly higher mortality (HR 2.68, 95% CI 1.23-5.84, P = .01). The effect was stronger in men (HR 2.83, 95% CI 1.1-7.29, P = .03 in slow increase; HR 4.06, 95% CI 1.56-10.6, P = .001 in fast increase group), but it was insignificant in female participants. CONCLUSIONS: Higher AL score or rapid increase of AL score significantly increased subsequent mortality risk in older adults, either measured statically or dynamically. AL is predictive of 10-year mortality regardless of cause of death, and rapid increase in AL score is associated with higher subsequent mortality.
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