scholarly journals Estimating Contributions of Social and Behavioral Factors to Cardiovascular Disease, Cancer, COPD, and Unintentional-Injury Mortality Disparities by Psychological Distress in the United States: A Blinder-Oaxaca Decomposition Analysis of the 1997-2014 NHIS-NDI Record Linkage Study

Author(s):  
Hyunjung Lee ◽  
Gopal K. Singh

Background: Previous research has shown a significant association between psychological distress (PD) and cause-specific mortality, but contributions of sociodemographic and behavioral characteristics to mortality differences by PD are not fully explored. Methods: The Blinder-Oaxaca decomposition analysis was used to quantify the contributions of individual sociodemographic and behavioral characteristics to the observed cardiovascular disease (CVD), cancer, chronic obstructive pulmonary disease (COPD), and unintentional-injury mortality disparities between United States (US) adults with no PD and those with serious psychological distress (SPD), using the pooled 1997-2014 data from the National Health Interview Survey prospectively linked to the National Death Index (N=263,825). Results: Lower levels of education and household income, and higher proportions of current smokers, former drinkers, non-married adults, US-born, and renters contributed to higher mortality for adults with SPD. The relative percentage of mortality explained by sociodemographic and behavioral factors was highest for cancer mortality (71.25%) and lowest for unintentional-injury mortality (20.19%). Enhancing education level among adults with SPD would decrease approximately 30% of cancer or CVD mortality disparity, and around 10% of COPD and unintentional-injury mortality disparities. Half of the cancer mortality disparity (47.4%) could be attributed to a single factor, smoking. Increasing income level will decrease 7 to 13% of the disparity in cause-specific mortality. Higher proportions of renters explained higher CVD and COPD mortality among adults with SPD by 7% and 3%, respectively. Higher proportions of former drinkers explained higher CVD, cancer, and COPD mortality among adults with SPD by 6%, 7%, and 3%, respectively. Younger age, higher proportion of females, and higher BMI among adults with SPD mitigated the mortality disparities. Conclusions and Implications for Translational Research: Improved education and income levels, and reduced smoking among US adults with SPD would eliminate around 90% of the cancer mortality disparity by SPD, and half of the CVD mortality disparity.   Copyright © 2021 Lee and Singh. Published by Global Health and Education Projects, Inc. This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY 4.0.

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Paulette D Chandler ◽  
Deirdre Tobias ◽  
Jule E Buring ◽  
I-Min Lee ◽  
Daniel Chasman ◽  
...  

Background: Given the increased prevalence of cancer survivors in the United States, it is imperative to define risk factors for potential reductions in total and cause-specific mortality. Physical activity (PA) represents a promising target for intervention. Design: We prospectively evaluated PA from questionnaires before and after cancer diagnosis with total and cause-specific mortality among 13,297 subjects diagnosed with invasive cancer combined from the Physicians’ Health Study (PHS) (n=6328), Physicians’ Health Study II (PHS II) (n=912), and Women's Health Study (WHS) (n=6057). WHS and PHS participants were free of baseline cancer; PHS II participants reported no active cancer at baseline. We ascertained PA before and after an incident cancer diagnosis based on reports on repeated follow-up questionnaires. Death was ascertained by medical records and death certificates. Cox regression estimated combined hazard ratios (HRs) of mortality by PA adjusted for age, randomized treatments, BMI, and other lifestyle/demographic factors. We evaluated the interaction between PA before and after cancer diagnosis by comparing PA ≤1 versus ≥2 times/wk. Results: The mean follow-up after cancer diagnosis was 8.0, 7.5, and 5.2 y for WHS, PHS, and PHS II, respectively, during which there were 5623 deaths (WHS, 2164; PHS, 3269; PHS II; 190). Higher PA before cancer diagnosis was associated with significantly lower mortality. Compared with PA ≤ once/wk, the HRs (95% CIs) associated with PA 2-4 and >4 times/wk were 0.87 (0.82-0.93) and 0.88 (0.82-0.94) for total mortality; 0.77 (0.63-0.95) and 0.79 (0.62-0.997) for CVD mortality, and 0.90 (0.83-0.98) and 0.90 (0.83-0.98) for cancer mortality. Higher PA after cancer diagnosis was associated with significantly lower total and cancer mortality and non-significantly lower CVD mortality, with HRs (95% CIs) of 0.65 (0.58-0.72) and 0.66 (0.59-0.73) for total mortality; 0.78 (0.59-1.03) and 0.82 (0.61-1.10) for CVD mortality, and 0.66 (0.57-0.77) and 0.64 (0.55-0.74) for cancer mortality. There was a significant interaction of PA before and after cancer diagnosis for total (p int =0.02) and cancer (p int =0.007) mortality, but not CVD mortality (p int =0.38). Conclusions: Greater PA both before and after cancer diagnosis were significantly associated with lower total and cancer mortality. Higher PA before cancer diagnosis was also associated with lower CVD mortality. PA may be an important target for lower mortality after cancer diagnosis.


2019 ◽  
Vol 29 (Supplement_4) ◽  
Author(s):  
H Pikhart ◽  
Q Liu ◽  
A Pajak ◽  
S Malyutina ◽  
R Kubinova ◽  
...  

Abstract Background Long working hours are common in countries of Central and Eastern Europe (CEE). A wide range of epidemiological studies have showed that long working hours had an adverse effect on health but the evidence mostly comes from Western Europe, East Asia and North America. This study aimed to assess the relationship between long working hours and the risk of mortality in employed people in three Eastern European countries. Methods Participants, aged 45-69 years at baseline, were from the Health, Alcohol and Psychosocial Indicators in Eastern Europe (HAPIEE) cohort study conducted in Russia, Poland and the Czech Republic. Baseline survey included a structured questionnaire and examination in the clinic during 2002-2005. Working hours were assessed by a self-reported questionnaire at baseline. Participants have been followed-up for all-cause mortality and cause-specific mortality for an average of 11 years. Impact of long working hours on mortality was analysed by Cox proportional hazards regression. In all-cause mortality analysis, a total of 10878 men and women were included, and 10399 participants were included in cause-specific mortality analysis. Results During the follow-up, there were 1187 deaths from all causes, 288 from CVD, and 251 from cancer. Those who worked 61 hours or more in a week showed higher risk of mortality compared to those working 36-45 hours per week: HR 1.32 (95%CI 1.01 to 1.74) for all-cause mortality and 1.73 (95% CI 1.03-2.93) for CVD mortality. There was no significant increase in risk of cancer mortality associated with working long hours. There was no significant association between working 46-60 hours a week and risk of mortality, including all-cause mortality and cause-specific mortality. Conclusions The risk of all-cause and CVD mortality in three CEE was significantly higher among employees working extensive hours. These findings suggest that more attention should be paid to shortening working hours for those who work extensively. Key messages Long working hours increase risk of all cause and CVD mortality. Cancer mortality is not related to long working hours.


2021 ◽  
Vol 8 ◽  
Author(s):  
Xin Xu ◽  
Shiqi Li ◽  
Yi Zhu

Evidence on the relationship between consumption of tomato or lycopene and mortality is limited. We investigated the associations of raw tomato, tomato catsup or lycopene intake with all-cause and cause-specific mortality using data from the Prostate, Lung, Colorectal, and Ovarian (PLCO) screening trial. A multivariate Cox proportional hazards model was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). During a total of 1,672,715 follow-up years, 24,141 all-cause deaths, 7,534 cardiovascular disease (CVD) deaths and 7,161 cancer deaths occurred. Total mortality was statistically significantly inversely associated with intake of raw tomato (Q5 vs. Q1; HR, 0.95 [95% CI, 0.91–0.99]), tomato catsup (Q5 vs. Q1; HR, 0.93 [95% CI, 0.89–0.97]), and moderate lycopene (Q4 vs. Q1; HR, 0.88 [95% CI, 0.85–0.93]). CVD mortality was significantly inversely related with intake of moderate raw tomato (Q4 vs. Q1; HR, 0.90 [95% CI, 0.83–0.97]), tomato catsup (Q5 vs. Q1; HR, 0.92 [95% CI, 0.85–0.99]), and moderate lycopene (Q4 vs. Q1; HR, 0.90 [95% CI, 0.83–0.98]). Dietary intake of raw tomato (Q5 vs. Q1; HR, 1.04 [95% CI, 0.96–1.14]) and tomato catsup (Q5 vs. Q1; HR, 1.00 [95% CI, 0.93–1.08]) were not related with cancer mortality. Moderate dietary intake of lycopene was significantly associated with a lower cancer mortality (Q4 vs. Q1; HR, 0.89 [95% CI, 0.82–0.96]). There was a non-linear J-shaped association between consumption of raw tomato, tomato catsup or lycopene and total mortality (P for non-linearity <0.001). In conclusion, in this large nationally representative sample of US adult population, tomato products, and lycopene intake were associated with lower risks of total and CVD mortality. Moderate consumption of lycopene was also related with a reduced cancer mortality. Further clinical studies and dietary intervention studies are warranted to confirm our premilitary findings.


2021 ◽  
Vol 8 ◽  
Author(s):  
Jiang-lin Wang ◽  
Wen-jun Yin ◽  
Ling-yun Zhou ◽  
Ya-feng Wang ◽  
Xiao-cong Zuo

Objectives: To examine the effect of smoking status, smoking intensity, duration of smoking cessation and age of smoking initiation on the risk of all-cause and cause-specific mortality among cardiovascular disease (CVD) patients.Design: A population-based prospective cohort study.Setting: The National Health Interview Survey (NHIS) in the U.S. that were linked to the National Death Index (NDI).Participants: 66,190 CVD participants ≥ 18 years of age who were interviewed between 1997 and 2013 in the NHIS linked to the NDI through December 31, 2015.Outcome Measures: The primary outcome was all-cause mortality and the secondary outcome was cause-specific mortality including CVD mortality and cancer mortality.Results: During the mean follow-up of 8.1 years, we documented 22,518 deaths (including 6,473 CVD deaths and 4,050 cancer deaths). In the overall CVD population, former and current smokers had higher risk of all-cause (Former smokers: hazard ratios (HRs), 1.26; 95% confidence interval (CI), 1.21–1.31, P < 0.001; Current smokers: HRs, 1.96; 95%CI, 1.86–2.07, P < 0.001), CVD (Former smokers: HRs, 1.12; 95%CI, 1.05–1.21, P = 0.001; Current smokers: HRs, 1.80; 95%CI, 1.64–1.97, P < 0.001) and cancer mortality (Former smokers: HRs, 1.49; 95%CI, 1.35–1.64, P < 0.001; Current smokers: HRs, 2.78; 95%CI, 2.49–3.09, P < 0.001) than never smokers. Furthermore, similar results were observed when the study subjects were stratified according to the type of CVD. Among current smokers, the risk for cancer mortality increased as the daily number of cigarettes increased, regardless of the specific type of CVD. However, the association of the risk for all-cause and CVD mortality with smoking intensity did not present a dose-response relationship. In participants with angina pectoris or stroke, smoking intensity was inversely associated with deaths from CVD. In addition, the risk for all-cause, CVD and cancer mortality declined as years of smoking cessation increased. Finally, the relative risk of all-cause mortality was not significantly different in individuals with a younger age of smoking initiation.Conclusions: CVD patients who are smokers have an increased risk of all-cause, CVD and cancer mortality, and the risk decreases significantly after quitting smoking. These data further provide strong evidence that supports the recommendation to quit smoking for the prevention of premature deaths among individuals with CVD.


2019 ◽  
Vol 75 (11) ◽  
pp. 2193-2199
Author(s):  
Xiong-Fei Pan ◽  
Yanping Li ◽  
Oscar H Franco ◽  
Jian-Min Yuan ◽  
An Pan ◽  
...  

Abstract Background To examine the impact of combined lifestyle factors on premature mortality and life expectancy in Chinese adults. Methods A total of 44,052 Chinese adults aged 45–74 years free of cardiovascular disease (CVD), cancer, and diabetes were followed from recruitment (1993–1998) to the end of 2016 in the Singapore Chinese Health Study. A composite score (0–5 scale) was calculated based on five baseline healthy lifestyle factors including healthy diet, nonsmoking status, light to moderate alcohol drinking, being physically active and optimal body mass index. Mortality cases were identified through linkage with the nationwide death registry. Results Adopting five healthy versus none was associated with a lower risk of all-cause and cause-specific mortality, and the hazard ratio (95% confidence interval [CI]) was 0.38 (0.29, 0.51) for all-cause mortality, 0.26 (0.13, 0.52) for CVD mortality, and 0.59 (0.37, 0.92) for cancer mortality. Nonadherence to 4–5 healthy lifestyle factors accounted for 34.9% (95% CI = 29.2, 40.2) in population attributable fraction for all-cause mortality, 35.1% (23.7, 44.9) for CVD mortality, and 18.0% (6.5, 28.0) for cancer mortality. Conversely, adherence to 4–5 healthy lifestyle factors versus none could achieve a gain of 8.1 years in women and 6.6 years in men for the life expectancy at 50 years. Conclusions A healthier lifestyle is associated with a substantially reduced risk of mortality and a longer life expectancy in the Chinese population. Our findings highlight the necessity of coordinated actions targeting combined lifestyle factors in reducing the overall burden of diseases and premature deaths.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Guo-dong He ◽  
Xiao-cong Liu ◽  
Lin Liu ◽  
Yu-ling Yu ◽  
Chao-lei Chen ◽  
...  

Abstract Background The link between total cholesterol (TC) and all-cause and specific mortality has not been elucidated. Herein, we aimed to evaluate the effect of TC levels on all-cause, cardiovascular disease (CVD), and cancer mortality. Methods All data analyzed were obtained from the National Health and Nutrition Examination Survey 1999–2014. The relationship between levels of TC and mortality was determined through Cox proportional hazard regression analysis coupled with multivariable adjustments. Two-piecewise linear regression models and Cox models with penalized splines were applied to explore nonlinear and irregular shape relationships. Kaplan–Meier survival curve and subgroup analyses were conducted. Results The sample studied comprised 14,662 men and 16,025 women, categorized as 25,429 adults aged 18–65 and 5,258 adults over 65 years old. A total of 2,570 deaths were recorded. All-cause, cardiovascular, and cancer mortality showed U-curve associations after adjusting for confounding variables in the restricted cubic spline analysis. Hazard ratios (HRs) of all-cause and cancer mortality were particularly negatively related to TC levels in the lower range < 200 mg/dL, especially in the range < 120 mg/dL (HR 1.97; 95% CI 1.38, 2.83, HR 2.39; 95% CI 1.21, 4.71, respectively). However, the HRs of cardiovascular disease mortality in the range < 120 mg/dL were the lowest (HR 0.60; 95% CI 0.15, 2.42). In the upper range, a TC range of ≥ 280 mg/dL was correlated with mortality as a result of CVD and cancer (HR 1.31; 95% CI 0.87, 1.97 and HR 1.22; 95% CI 0.82, 1.79). The lowest cumulative survival rate of all-cause mortality was recorded in the lowest TC-level group, while the lowest cumulative survival rate of CVD mortality was recorded in the highest TC-level group. Conclusions A nonlinear association of TC level with all-cause, cancer, and CVD mortality in the American population was observed, suggesting that too low or too high serum total cholesterol levels might correlate with adverse outcomes.


2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Saman Khalatbari-Soltani ◽  
Fiona Stanaway ◽  
Erin Cvejic ◽  
Fiona M. Blyth ◽  
Vasi Naganathan ◽  
...  

Abstract Background Among older people, the extent to which psychosocial factors explain socioeconomic inequalities in mortality is debated. We aimed to investigate the potential mediating effect of psychosocial factors on socioeconomic inequalities in mortality. Methods We used data from a prospective population-based cohort (the Concord Health and Ageing in Men Project; baseline recruitment in 2005–2007), in Sydney, Australia. The main outcomes were all-cause and cause-specific mortality. Socioeconomic status (SES; educational attainment, occupational position, source of income, housing tenure, and a cumulative SES score) was assessed at baseline. Measures of structural and functional social support, as well as depressive and anxiety symptoms were assessed three times during follow-ups. Associations were quantified using Cox regression. Mediation was calculated using “change-in-estimate method”. Results 1522 men (mean age at baseline: 77·4 ± 5·5 years) were included in the analyses with a mean (SD) follow-up time of 9·0 (3·6) years for all-cause and 8·0 (2·8) years for cause-specific mortality. At baseline, psychosocial measures displayed marked social patterning. Being unmarried, living alone, low social interactions, and elevated depressive symptoms were associated with higher risk of all-cause and cardiovascular disease (CVD) mortality. Psychosocial factors explained 35% of SES inequalities in all-cause mortality, 29% in CVD mortality, 12% in cancer mortality, and 39% in non-CVD, non-cancer mortality. Conclusion Psychosocial factors may account for up to one-third of SES inequalities in deaths from all and specific causes (except cancer mortality). Our findings suggest that interventional studies targeting social relationships and/or psychological distress in older men aiming to reduce socioeconomic inequalities in mortality are warranted.


2020 ◽  
Vol 11 (4) ◽  
pp. 790-814 ◽  
Author(s):  
Mei Chung ◽  
Naisi Zhao ◽  
Deena Wang ◽  
Marissa Shams-White ◽  
Micaela Karlsen ◽  
...  

ABSTRACT Tea flavonoids have been suggested to offer potential benefits to cardiovascular health. This review synthesized the evidence on the relation between tea consumption and risks of cardiovascular disease (CVD) and all-cause mortality among generally healthy adults. PubMed, EMBASE, Web of Science, Cochrane Central Register of Controlled Trials, Food Science and Technology Abstracts, and Ovid CAB Abstract databases were searched to identify English-language publications through 1 November 2019, including randomized trials, prospective cohort studies, and nested case-control (or case-cohort) studies with data on tea consumption and risk of incident cardiovascular events (cardiac or peripheral vascular events), stroke events (including mortality), CVD-specific mortality, or all-cause mortality. Data from 39 prospective cohort publications were synthesized. Linear meta-regression showed that each cup (236.6 mL)  increase in daily tea consumption (estimated 280 mg  and 338 mg  total flavonoids/d for black and green tea, respectively) was associated with an average 4% lower risk of CVD mortality, a 2% lower risk of CVD events, a 4% lower risk of stroke, and a 1.5% lower risk of all-cause mortality. Subgroup meta-analysis results showed that the magnitude of association was larger in elderly individuals for both CVD mortality (n = 4; pooled adjusted RR: 0.89; 95% CI: 0.83, 0.96; P = 0.001), with large heterogeneity (I2 = 72.4%), and all-cause mortality (n = 3; pooled adjusted RR: 0.92; 95% CI: 0.90, 0.94; P &lt; 0.0001; I2 = 0.3%). Generally, studies with higher risk of bias appeared to show larger magnitudes of associations than studies with lower risk of bias. Strength of evidence was rated as low and moderate (depending on study population age group) for CVD-specific mortality outcome and was rated as low for CVD events, stroke, and all-cause mortality outcomes. Daily tea intake as part of a healthy habitual dietary pattern may be associated with lower risks of CVD and all-cause mortality among adults.


Author(s):  
Hiromi Sugiyama ◽  
Munechika Misumi ◽  
Ritsu Sakata ◽  
Alina V. Brenner ◽  
Mai Utada ◽  
...  

AbstractWe examined the mortality risks among 2463 individuals who were exposed in utero to atomic bomb radiation in Hiroshima or Nagasaki in August 1945 and were followed from October 1950 through 2012. Individual estimates of mother’s weighted absorbed uterine dose (DS02R1) were used. Poisson regression method was used to estimate the radiation-associated excess relative risk per Gy (ERR/Gy) and 95% confidence intervals (CI) for cause-specific mortality. Head size, birth weight, and parents’ survival status were evaluated as potential mediators of radiation effect. There were 339 deaths (216 males and 123 females) including deaths from solid cancer (n = 137), lymphohematopoietic cancer (n = 8), noncancer disease (n = 134), external cause (n = 56), and unknown cause (n = 4). Among males, the unadjusted ERR/Gy (95% CI) was increased for noncancer disease mortality (1.22, 0.10–3.14), but not for solid cancer mortality (− 0.18, < − 0.77–0.95); the unadjusted ERR/Gy for external cause mortality was not statistically significant (0.28, < − 0.60–2.36). Among females, the unadjusted ERRs/Gy were increased for solid cancer (2.24, 0.44–5.58), noncancer (2.86, 0.56–7.64), and external cause mortality (2.57, 0.20–9.19). The ERRs/Gy adjusted for potential mediators did not change appreciably for solid cancer mortality, but decreased notably for noncancer mortality (0.39, < − 0.43–1.91 for males; 1.48, − 0.046–4.55 for females) and external cause mortality (0.10, < − 0.57–1.96 for males; 1.38, < − 0.46–5.95 for females). In conclusion, antenatal radiation exposure is a consistent risk factor for increased solid cancer mortality among females, but not among males. The effect of exposure to atomic bomb radiation on noncancer disease and external cause mortality among individuals exposed in utero was mediated through small head size, low birth weight, and parental loss.


2008 ◽  
Vol 43 (10) ◽  
pp. 1858-1864 ◽  
Author(s):  
Richard A. Falcone ◽  
Colin Martin ◽  
Rebeccah L. Brown ◽  
Victor F. Garcia

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