The cumulative effect of unemployment on risks for acute myocardial infarction.
ABSTRACT Employment instability is a major source of strain affecting an increasing number of adults in the United States. Little is known about the cumulative effect of multiple job losses and unemployment on the risks for acute myocardial infarction (AMI).
We investigated the associations between different dimensions of unemployment and the risks for AMI in US adults in a prospective cohort study of adults (N = 13,451) aged 51 to 75 years in the Health and Retirement Study with biennial follow-up interviews from 1992 to 2010. Unadjusted rates of age-specific AMI were used to demonstrate observed differences by employment status, cumulative number of job losses, and cumulative time unemployed. Cox proportional hazards models were used to examine the multivariate effects of cumulative work histories on AMI while adjusting for sociodemographic background and confounding risk factors.
The median age of the study cohort was 62 years, and 1061 AMI events (7.9%) occurred during the 165,169 person-years of observation. Among the sample, 14.0% of subjects were unemployed at baseline, 69.7% had 1 or more cumulative job losses, and 35.1% had spent time unemployed. Unadjusted plots showed that age-specific rates of AMI differed significantly for each dimension of work history. Multivariate models showed that AMI risks were significantly higher among the unemployed (hazard ratio, 1.35 [95% CI, 1.10-1.66]) and that risks increased incrementally from 1 job loss (1.22 [1.04-1.42]) to 4 or more cumulative job losses (1.63 [1.29-2.07]) compared with no job loss. Risks for AMI were particularly elevated within the first year of unemployment (hazard ratio, 1.27 [95% CI, 1.01-1.60]) but not thereafter. Results were robust after adjustments for multiple clinical, socioeconomic, and behavioral risk factors.
Unemployment status, multiple job losses, and short periods without work are all significant risk factors for acute cardiovascular events.
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ABSTRACT: Aims: Atherosclerosis is latent precursor of clinical cardiovascular disease. The present study aimed to assess modifiable and non-modifiable atherogenic risk factors in both sexes. Study Design: Cross sectional design. Place and Duration of Study: It was conducted at Exservicemen Contributory Health Scheme (ECHS) Polyclinic, Sultanpur Lodhi, Kapurthala, Punjab, India from June, 2013 to Oct, 2013. Methodology: This study was undertaken to assess age, education, employment, socioeconomic status, physical activity, body mass index, dietary habits, family history, sleep, stress, dysglycaemia, hypertension and dyslipidemia as determinants of atherogenic risk factors. The level of significance was defined by P<.05 with Chi Square test. Results: All patients (N=351) were divided into male (49.58%) and female (50.42%) cohorts. A statistically significant males (45.41%; P<.001) were found >65 years old and females (43.51%; P<.001) in 51-65 years. Males had significant higher literacy (55.19%; P<.001) and employment status (55.75%; P<.001). Females were reported with significant positive family history (40.12%; P<.01), stress (25.99%), sleep inadequacy (28.82%; P<.001), sedentary lifestyle (83.62%; P<.001), and vegetarianism (74.02%; P<.01). Metabolic syndrome was more prevalent in females (19.78%) than males (14.95%). The higher prevalence of hypertension (females: 49.16%; males: 48.28%), obesity (females: 23.72%; males: 17.24%), dysglycaemia (females: 25.99%; males: 22.42%) was recorded in females; and dyslipidemia (males: 29.32%, females: 23.17%) in males. Conclusion: Females were reported with significantly higher frequencies of atherogenic risk factors which make them highly susceptible to cardiovascular events than males. Hence, sex should be considered to assess and differentiate atherogenic risk factors, and when health professionals recommend lifestyle modifications. Keywords: Atherosclerosis; cardiovascular disease; modifiable; non-modifiable; risk factors; sexesInternational Blood Research & Reviews. 09/2014; 2(5):247-261.
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ABSTRACT: Chronic stress is associated with morbidity and mortality from numerous conditions, many of whose pathogenesis involves persistent inflammation. Here, we examine how chronic stress influences signaling pathways that regulate inflammation in monocytes. The sample consisted of 33 adults caring for a family member with glioblastoma and 47 controls whose lives were free of major stressors. The subjects were assessed four times over eight months. Relative to controls, caregivers’ monocytes showed increased expression of genes bearing response elements for nuclear-factor kappa B, a key pro-inflammatory transcription factor. Simultaneously, caregivers showed reduced expression of genes with response elements for the glucocorticoid receptor, a transcription factor that conveys cortisol’s anti-inflammatory signals to monocytes. Transcript origin analyses revealed that CD14+/CD16 cells, a population of immature monocytes, were the predominate source of inflammatory gene expression among caregivers. We considered hormonal, molecular, and functional explanations for caregivers’ decreased glucocorticoid-mediated transcription. Across twelve days, the groups displayed similar diurnal cortisol profiles, suggesting that differential adrenocortical activity was not involved. Moreover, the groups’ monocytes expressed similar amounts of glucocorticoid receptor protein, suggesting that differential receptor availability was not involved. In ex vivo studies, subjects’ monocytes were stimulated with lipopolysaccharide, and caregivers showed greater production of the inflammatory cytokine interleukin-6 relative to controls. However, no group differences in functional glucocorticoid sensitivity were apparent; hydrocortisone was equally effective at inhibiting cytokine production in caregivers and controls. These findings may help shed light on the mechanisms through which caregiving increases vulnerability to inflammation-related diseases.Brain Behavior and Immunity 10/2014; 41:191-199. · 6.13 Impact Factor
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ABSTRACT: The aim of this research was to investigate the association between job loss and the development of stroke or cardiovascular disease among middle-aged to older individuals in Korea. We also examined how this relationship was modified by gender and the nature of the job loss. This study used samples from the first- to fourth-wave datasets from the Korean Longitudinal Study of Aging (KLoSA), which were collected in 2006, 2008, 2010, and 2012. The study collected data from a total of 10,254 subjects aged ≥45 years at baseline. After applying exclusion criteria, the final sample size for analysis consisted of 4,000 individuals. Information about employment status, development of stroke or cardiovascular disease, and covariates (age, income level, and behavioral factors) was obtained. Cox proportional hazards models were used to evaluate the association between voluntary/involuntary job loss and the development of stroke or cardiovascular disease. We performed these analyses separately according to disease, gender, and the nature of the job loss. Involuntary job loss significantly increased the risk of stroke or cardiovascular disease among males (adjusted hazard ratio [HR] = 3.560, 95% confidence interval [CI] = 2.055-6.168). Voluntary retirement also increased the risk of cardiovascular disease or stroke among males (adjusted HR = 2.879, 95% CI = 1.533-5.409). Job loss was more closely associated with stroke than with cardiovascular disease (stroke, adjusted HR = 6.208, 95% CI = 2.417-15.943; cardiovascular disease, adjusted HR = 2.768, 95% CI = 1.402-5.465). Our findings suggest that both voluntary retirement and involuntary job loss increase the risk for stroke or cardiovascular disease in middle-aged to older individuals, especially males.PLoS ONE 11/2014; 9(11):e113495. · 3.53 Impact Factor