Objective To examine whether overall lifestyles mediate associations of socioeconomic status (SES) with mortality and incident cardiovascular disease (CVD) and the extent of interaction or joint relations of lifestyles and SES with health outcomes. Design Population based cohort study. Setting US National Health and Nutrition Examination Survey (US NHANES, 1988-94 and 1999-2014) and UK Biobank. Participants 44 462 US adults aged 20 years or older and 399 537 UK adults aged 37-73 years. Exposures SES was derived by latent class analysis using family income, occupation or employment status, education level, and health insurance (US NHANES only), and three levels (low, medium, and high) were defined according to item response probabilities. A healthy lifestyle score was constructed using information on never smoking, no heavy alcohol consumption (women ≤1 drink/day; men ≤2 drinks/day; one drink contains 14 g of ethanol in the US and 8 g in the UK), top third of physical activity, and higher dietary quality. Main outcome measures All cause mortality was the primary outcome in both studies, and CVD mortality and morbidity in UK Biobank, which were obtained through linkage to registries. Results US NHANES documented 8906 deaths over a mean follow-up of 11.2 years, and UK Biobank documented 22 309 deaths and 6903 incident CVD cases over a mean follow-up of 8.8-11.0 years. Among adults of low SES, age adjusted risk of death was 22.5 (95% confidence interval 21.7 to 23.3) and 7.4 (7.3 to 7.6) per 1000 person years in US NHANES and UK Biobank, respectively, and age adjusted risk of CVD was 2.5 (2.4 to 2.6) per 1000 person years in UK Biobank. The corresponding risks among adults of high SES were 11.4 (10.6 to 12.1), 3.3 (3.1 to 3.5), and 1.4 (1.3 to 1.5) per 1000 person years. Compared with adults of high SES, those of low SES had higher risks of all cause mortality (hazard ratio 2.13, 95% confidence interval 1.90 to 2.38 in US NHANES; 1.96, 1.87 to 2.06 in UK Biobank), CVD mortality (2.25, 2.00 to 2.53), and incident CVD (1.65, 1.52 to 1.79) in UK Biobank, and the proportions mediated by lifestyle were 12.3% (10.7% to 13.9%), 4.0% (3.5% to 4.4%), 3.0% (2.5% to 3.6%), and 3.7% (3.1% to 4.5%), respectively. No significant interaction was observed between lifestyle and SES in US NHANES, whereas associations between lifestyle and outcomes were stronger among those of low SES in UK Biobank. Compared with adults of high SES and three or four healthy lifestyle factors, those with low SES and no or one healthy lifestyle factor had higher risks of all cause mortality (3.53, 3.01 to 4.14 in US NHANES; 2.65, 2.39 to 2.94 in UK Biobank), CVD mortality (2.65, 2.09 to 3.38), and incident CVD (2.09, 1.78 to 2.46) in UK Biobank. Conclusions Unhealthy lifestyles mediated a small proportion of the socioeconomic inequity in health in both US and UK adults; therefore, healthy lifestyle promotion alone might not substantially reduce the socioeconomic inequity in health, and other measures tackling social determinants of health are warranted. Nevertheless, healthy lifestyles were associated with lower mortality and CVD risk in different SES subgroups, supporting an important role of healthy lifestyles in reducing disease burden.
OBJECTIVE The evidence regarding vitamin D status and mortality among people with diabetes is scarce. This study aimed to examine the association of serum 25-hydroxyvitamin D [25(OH)D] concentrations with all-cause and cause-specific mortality among adults with diabetes. RESEARCH DESIGN AND METHODS This study included 6,329 adults with diabetes from the Third National Health and Nutrition Examination Survey (NHANES III) and NHANES 2001–2014. Death outcomes were ascertained by linkage to National Death Index records through 31 December 2015. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% CIs for mortality from all causes, cardiovascular disease (CVD), and cancer. RESULTS The weighted mean (95% CI) level of serum 25(OH)D was 57.7 (56.6, 58.8) nmol/L, and 46.6% had deficient vitamin D (<50 nmol/L [20 ng/mL]). Higher serum 25(OH)D levels were significantly associated with lower levels of glucose, insulin, HOMA of insulin resistance, HbA1c, blood lipids, and C-reactive protein at baseline (all Ptrend < 0.05). During 55,126 person-years of follow-up, 2,056 deaths were documented, including 605 CVD deaths and 309 cancer deaths. After multivariate adjustment, higher serum 25(OH)D levels were significantly and linearly associated with lower all-cause and CVD mortality: there was a 31% reduced risk of all-cause mortality and a 38% reduced risk of CVD mortality per one-unit increment in natural log-transformed 25(OH)D (both P < 0.001). Compared with participants with 25(OH)D <25 nmol/L, the multivariate-adjusted HRs and 95% CI for participants with 25(OH)D >75 nmol/L were 0.59 (0.43, 0.83) for all-cause mortality (Ptrend = 0.003), 0.50 (0.29, 0.86) for CVD mortality (Ptrend = 0.02), and 0.49 (0.23, 1.04) for cancer mortality (Ptrend = 0.12). CONCLUSIONS Higher serum 25(OH)D levels were significantly associated with lower all-cause and CVD mortality. These findings suggest that maintaining adequate vitamin D status may lower mortality risk in individuals with diabetes.
Background The aim of this study was to identify associations between dietary intakes of eggs and cholesterol and all‐cause and heart disease mortality in a US population. Methods and Results Data from the National Health and Nutrition Examination Survey 1999–2014 were used in this study, which included 37 121 participants ≥20 years of age. Dietary information was assessed via 24‐hour dietary recalls at baseline. Mortality status was documented until December 31, 2015. Cox proportional hazards models were used to examine the associations between dietary intakes of eggs and cholesterol and all‐cause and heart disease mortality. During a median follow‐up of 7.8 years, 4991 deaths were documented, including 870 deaths from heart disease. No significant association was observed between additional daily consumption of half an egg and all‐cause mortality (multivariable‐adjusted hazard ratio, 1.04; 95% CI, 0.96–1.13), or heart disease mortality (0.96; 0.80–1.14). Each 50‐mg/day increase of cholesterol intake was inversely associated with all‐cause mortality among participants with daily intake <250 mg (0.87; 0.77–0.98), but positively associated with all‐cause mortality among participants with daily intake ≥250 mg (1.07; 1.01–1.12). No significant association was found between dietary cholesterol intake and heart disease mortality. Conclusions No significant association was found between egg consumption and mortality in US adults. The association between dietary cholesterol intake and all‐cause mortality depended on the baseline intake levels, with an inverse association in those with lower intake levels (<250 mg/day) but a positive association in those with higher intake levels (≥250 mg/day).
Water chlorination can lead to the formation of disinfection byproducts, including trihalomethanes (THMs). However, few epidemiologic studies have explored associations between THM exposure and mortality. This study included 6720 adults aged ≥40 years from the National Health and Nutrition Examination Survey 1999−2012 who had blood THM concentrations quantified. A higher risk of all-cause mortality was found across increasing quartile concentrations of blood chloroform (TCM) and total THMs (TTHMs; sum of all four THMs) (both p for trend = 0.02). Adults in the highest quartile of TCM and TTHM concentrations had hazard ratios (HRs) of 1.35 (95% confidence intervals: 1.05−1.74) and 1.37 (1.05−1.79), respectively, for all-cause mortality, compared with adults in the lowest quartile. When cause-specific mortality was evaluated, a positive relationship was found between blood bromodichloromethane (BDCM), dibromochloromethane (DBCM), bromoform (TBM), total brominated THMs (Br-THMs; sum of BDCM, DBCM, and TBM), and TTHM concentrations and risk of cancer death and between blood TCM and TTHMs and risk of other cause (noncancer/nonheart disease) mortality. Our findings suggest that higher exposure to Br-THMs was associated with increased cancer mortality risk, whereas TCM was associated with a greater risk of noncancer/nonheart disease mortality.
Introduction: Estimating trends in long-term outcomes after stroke is important for long-term planning of health resources. Data on trends in long-term post-stroke outcomes are not available among Hispanics. Whether race-ethnic disparities exist and how trends in these outcomes have changed over time comparing non-Hispanic Whites (NHWs) with Mexican Americans (MAs) are also unknown. Thus, we aimed to estimate ethnic-specific trends in risk of 5-year all-cause mortality and recurrence after initial stroke in MAs and NHWs. Methods: We included 3308 patients who had first-ever ischemic stroke ascertained between January 1, 2000 and December 31, 2012 from the Brain Attack Surveillance in Corpus Christi (BASIC) project in Texas. Data on recurrent stroke and death were available through December 31, 2017. Fine-Gray subdistribution hazard models including covariates and an interaction term between calendar year and ethnicity were used to calculate 5-year cumulative incidence of recurrence and death in both ethnic groups in each year. Results: Among the 3308 index stroke patients, 402 (12.15%) recurrences and 1420 (37.61%) deaths were observed during the 5-year follow-up. Adjusted 5-year cumulative incidence of recurrence among MAs declined from 15.76% to 11.28%. Among NHWs, a slight decline from 12.49% to 10.46% was observed. An ethnic disparity in 5-year recurrence was not apparent in 2000 (risk difference 3.27%, [95% CI, -10.41, 9.10]) or during the study duration (Figure). The greatest ethnic disparity in 5-year mortality risk was observed in 2000 but disappeared in 2012, which was driven by the increasing trend in MAs from 23.11% in 2000 to 24.28% in 2012 and the decreasing trend in NHWs from 31.09% to 27.19% accordingly. Conclusions: No apparent ethnic disparity in long-term stroke recurrence was found and long-term survival advantage in MAs presented early in the study gradually disappeared over the 13 years.
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