ABSTRACT
BACKGROUND: population ageing challenges the sustainability of healthcare provision. OBJECTIVE: to investigate occupational class differences in hospital use in women aged 80+ years. METHODS: a total of 8,353 female residents, aged 45-64, took part in the Renfrew and Paisley prospective cohort study in 1972-76. Information on general and mental health hospital discharges was provided from computerised linkage with the Scottish Morbidity Records data to 31 December 2012. Numbers of admissions and bed-days after the 80th birthday were calculated for all and specific causes. Rate ratios by occupational class were calculated using negative binomial regression analysis, adjusting for age and a range of risk factors. RESULTS: four thousand and four hundred and seven (56%) women survived to age 80 and had 17,563 general admissions thereafter, with a mean stay of 19.4 days. There were no apparent relationships with occupational class for all general admissions, but lower occupational class was associated with higher rate ratios for coronary heart disease and stroke and lower rate ratios for cancer. Adjustment for risk factors could not fully explain the raised rate ratios. Bed-day use was higher in lower occupational classes, especially for stroke. There were strong associations with mental health admissions, especially dementia. Compared with the highest occupational class, admission rate ratios for dementia were higher for the lowest occupational class (adjusted rate ratio = 2.60, 95% confidence interval 1.79-3.77). CONCLUSION: in this population, there were no socio-economic gradients seen in hospital utilisation for general admissions in old age. However, occupational class was associated with mental health admissions, coronary heart disease, stroke and cancer.
Subject(s)
Hospitalization/statistics & numerical data , Occupations/statistics & numerical data , Aged , Aged, 80 and over , Coronary Disease/epidemiology , Female , Humans , Length of Stay/statistics & numerical data , Middle Aged , Neoplasms/epidemiology , Prospective Studies , Risk Factors , Scotland/epidemiology , Social Class , Stroke/epidemiologyABSTRACT
IMPORTANCE: The prevalence of cardiometabolic multimorbidity is increasing. OBJECTIVE: To estimate reductions in life expectancy associated with cardiometabolic multimorbidity. DESIGN, SETTING, AND PARTICIPANTS: Age- and sex-adjusted mortality rates and hazard ratios (HRs) were calculated using individual participant data from the Emerging Risk Factors Collaboration (689,300 participants; 91 cohorts; years of baseline surveys: 1960-2007; latest mortality follow-up: April 2013; 128,843 deaths). The HRs from the Emerging Risk Factors Collaboration were compared with those from the UK Biobank (499,808 participants; years of baseline surveys: 2006-2010; latest mortality follow-up: November 2013; 7995 deaths). Cumulative survival was estimated by applying calculated age-specific HRs for mortality to contemporary US age-specific death rates. EXPOSURES: A history of 2 or more of the following: diabetes mellitus, stroke, myocardial infarction (MI). MAIN OUTCOMES AND MEASURES: All-cause mortality and estimated reductions in life expectancy. RESULTS: In participants in the Emerging Risk Factors Collaboration without a history of diabetes, stroke, or MI at baseline (reference group), the all-cause mortality rate adjusted to the age of 60 years was 6.8 per 1000 person-years. Mortality rates per 1000 person-years were 15.6 in participants with a history of diabetes, 16.1 in those with stroke, 16.8 in those with MI, 32.0 in those with both diabetes and MI, 32.5 in those with both diabetes and stroke, 32.8 in those with both stroke and MI, and 59.5 in those with diabetes, stroke, and MI. Compared with the reference group, the HRs for all-cause mortality were 1.9 (95% CI, 1.8-2.0) in participants with a history of diabetes, 2.1 (95% CI, 2.0-2.2) in those with stroke, 2.0 (95% CI, 1.9-2.2) in those with MI, 3.7 (95% CI, 3.3-4.1) in those with both diabetes and MI, 3.8 (95% CI, 3.5-4.2) in those with both diabetes and stroke, 3.5 (95% CI, 3.1-4.0) in those with both stroke and MI, and 6.9 (95% CI, 5.7-8.3) in those with diabetes, stroke, and MI. The HRs from the Emerging Risk Factors Collaboration were similar to those from the more recently recruited UK Biobank. The HRs were little changed after further adjustment for markers of established intermediate pathways (eg, levels of lipids and blood pressure) and lifestyle factors (eg, smoking, diet). At the age of 60 years, a history of any 2 of these conditions was associated with 12 years of reduced life expectancy and a history of all 3 of these conditions was associated with 15 years of reduced life expectancy. CONCLUSIONS AND RELEVANCE: Mortality associated with a history of diabetes, stroke, or MI was similar for each condition. Because any combination of these conditions was associated with multiplicative mortality risk, life expectancy was substantially lower in people with multimorbidity.
Subject(s)
Diabetes Mellitus , Life Expectancy , Mortality , Myocardial Infarction , Stroke , Adult , Aged , Comorbidity , Diabetes Mellitus/epidemiology , Female , Humans , Male , Middle Aged , Myocardial Infarction/epidemiology , Risk Factors , Stroke/epidemiologyABSTRACT
A long-term cohort study of working men in Israel found that smokers who reduced their cigarette consumption had lower subsequent mortality rates than those who did not. We conducted comparable analyses in 2 populations of smokers in Scotland. The Collaborative Study included 1,524 men and women aged 40-65 years in a working population who were screened twice, in 1970-1973 and 1977. The Renfrew/Paisley Study included 3,730 men and women aged 45-64 years in a general population who were screened twice, in 1972-1976 and 1977-1979. Both groups were followed up through 2010. Subjects were categorized by smoking intensity at each screening as smoking 0, 1-10, 11-20, or ≥21 cigarettes per day. At the second screening, subjects were categorized as having increased, maintained, or reduced their smoking intensity or as having quit smoking between the first and second screenings. There was no evidence of lower mortality in all reducers compared with maintainers. Multivariate adjusted hazard ratios of mortality were 0.91 (95% confidence interval (CI): 0.75, 1.10) in the Collaborative Study and 1.08 (95% CI: 0.97, 1.20) in the Renfrew/Paisley Study. There was clear evidence of lower mortality among quitters in both the Collaborative Study (hazard ratio = 0.66, 95% CI: 0.56, 0.78) and the Renfrew/Paisley Study (hazard ratio = 0.75, 95% CI: 0.67, 0.84). In the Collaborative Study only, we observed lower mortality similar to that of quitters among heavy smokers (≥21 cigarettes/day) who reduced their smoking intensity. These inconclusive results support the view that reducing cigarette consumption should not be promoted as a means of reducing mortality, although it may have a valuable role as a step toward smoking cessation.
Subject(s)
Smoking/mortality , Adult , Aged , Female , Humans , Male , Middle Aged , Prospective Studies , Risk Factors , Scotland/epidemiology , Smoking/epidemiologyABSTRACT
BACKGROUND: High cholesterol may be a modifiable risk factor for prostate cancer but results have been inconsistent and subject to potential "reverse causality" where undetected disease modifies cholesterol prior to diagnosis. METHODS: We conducted a prospective cohort study of 12,926 men who were enrolled in the Midspan studies between 1970 and 1976 and followed up to 31st December 2007. We used Cox-Proportional Hazards Models to evaluate the association between baseline plasma cholesterol and Gleason grade-specific prostate cancer incidence. We excluded cancers detected within at least 5 years of cholesterol assay. RESULTS: 650 men developed prostate cancer in up to 37 years' follow-up. Baseline plasma cholesterol was positively associated with hazard of high grade (Gleason score≥8) prostate cancer incidence (n = 119). The association was greatest among men in the 2nd highest quintile for cholesterol, 6.1 to < 6.69 mmol/l, Hazard Ratio 2.28, 95% CI 1.27 to 4.10, compared with the baseline of < 5.05 mmol/l. This association remained significant after adjustment for body mass index, smoking and socioeconomic status. CONCLUSIONS: Men with higher cholesterol are at greater risk of developing high-grade prostate cancer but not overall risk of prostate cancer. Interventions to minimise metabolic risk factors may have a role in reducing incidence of aggressive prostate cancer.
Subject(s)
Cholesterol/blood , Prostatic Neoplasms/blood , Prostatic Neoplasms/epidemiology , Adult , Age Factors , Aged , Follow-Up Studies , Humans , Incidence , Male , Middle Aged , Neoplasm Grading , Proportional Hazards Models , Prospective Studies , Prostatic Neoplasms/pathology , Risk Factors , Scotland/epidemiology , Young AdultABSTRACT
Tea may be a potentially modifiable and highly prevalent risk factor for the most common cancer in men, prostate cancer. However, associations between black tea consumption and prostate cancer in epidemiological studies have been inconsistent, limited to a small number of studies with small numbers of cases and short follow-up periods and without grade-specific information. We conducted a prospective cohort study of 6,016 men who were enrolled in the Collaborative Cohort Study between 1970 and 1973 and followed up to December 31, 2007. We used Cox proportional hazards models to investigate the association between tea consumption and overall as well as grade-specific risk of prostate cancer incidence. Three hundred and eighteen men developed prostate cancer in up to 37 years of follow-up. We found a positive association between consumption of tea and overall risk of prostate cancer incidence (P = 0.02). The association was greatest among men who drank ≥ 7 cups of tea per day (HR: 1.50, 95% CI: 1.06 to 2.12), compared with the baseline of 0-3 cups/day. However, we did not find any significant association between tea intake and low- (Gleason <7) or high-grade (Gleason 8-10) prostate cancer incidence. Men with higher intake of tea are at greater risk of developing prostate cancer, but there is no association with more aggressive disease. Further research is needed to determine the underlying biological mechanisms for the association.
Subject(s)
Prostatic Neoplasms/epidemiology , Prostatic Neoplasms/etiology , Tea , Adult , Aged , Cohort Studies , Follow-Up Studies , Humans , Male , Middle Aged , Proportional Hazards Models , Prospective Studies , Prostatic Neoplasms/mortality , Prostatic Neoplasms/pathology , Risk Factors , Scotland , Surveys and Questionnaires , Young AdultABSTRACT
The relationship between parental BMI and that of their adult offspring, when increased adiposity can become a clinical issue, is unknown. We investigated the intergenerational change in body mass index (BMI) distribution, and examined the sex-specific relationship between parental and adult offspring BMI. Intergenerational change in the distribution of adjusted BMI in 1,443 complete families (both parents and at least one offspring) with 2,286 offspring (1,263 daughters and 1,023 sons) from the west of Scotland, UK, was investigated using quantile regression. Familial correlations were estimated from linear mixed effects regression models. The distribution of BMI showed little intergenerational change in the normal range (<25 kg/m(2)), decreasing overweightness (25-<30 kg/m(2)) and increasing obesity (≥30 kg/m(2)). Median BMI was static across generations in males and decreased in females by 0.4 (95% CI: 0.0, 0.7) kg/m(2); the 95th percentile increased by 2.2 (1.1, 3.2) kg/m(2) in males and 2.7 (1.4, 3.9) kg/m(2) in females. Mothers' BMI was more strongly associated with daughters' BMI than was fathers' (correlation coefficient (95% CI): mothers 0.31 (0.27, 0.36), fathers 0.19 (0.14, 0.25); P = 0.001). Mothers' and fathers' BMI were equally correlated with sons' BMI (correlation coefficient: mothers 0.28 (0.22, 0.33), fathers 0.27 (0.22, 0.33). The increase in BMI between generations was concentrated at the upper end of the distribution. This, alongside the strong parent-offspring correlation, suggests that the increase in BMI is disproportionally greater among offspring of heavier parents. Familial influences on BMI among middle-aged women appear significantly stronger from mothers than fathers.
Subject(s)
Body Mass Index , Family , Overweight/etiology , Adult , Cohort Studies , Environment , Female , Health Surveys , Heredity , Humans , Linear Models , Male , Middle Aged , Obesity/epidemiology , Obesity/etiology , Overweight/epidemiology , Regression Analysis , Scotland/epidemiology , Sex Factors , Surveys and QuestionnairesABSTRACT
In the absence of a 'gold standard' to estimate the economic burden of disease, a decision about the most appropriate costing method is required. Researchers have employed various methods to cost hospital stays, including per diem or diagnosis-related group (DRG)-based costs. Alternative methods differ in data collection and costing methodology. Using data from Scotland as an illustrative example, costing methods are compared, highlighting the wider implications for other countries with a publicly financed healthcare system. Five methods are compared using longitudinal data including baseline survey data (Midspan) linked to acute hospital admissions. Cost variables are derived using two forms of DRG-type costs, costs per diem, costs per episode-using a novel approach that distinguishes between variable and fixed costs and incorporates individual length of stay (LOS), and costs per episode using national average LOS. Cost estimates are generated using generalised linear model regression. Descriptive analysis shows substantial variation between costing methods. Differences found in regression analyses highlight the magnitude of variation in cost estimates for subgroups of the sample population. This paper emphasises that any inference made from econometric modelling of costs, where the marginal effect of explanatory variables is assessed, is substantially influenced by the costing method.
Subject(s)
Data Collection/methods , Hospital Charges/statistics & numerical data , Hospitalization/economics , Models, Economic , Age Factors , Aged , Costs and Cost Analysis , Diagnosis-Related Groups/economics , Female , Humans , Length of Stay/economics , Longitudinal Studies , Male , Middle Aged , Regression Analysis , Scotland , Sex Factors , Socioeconomic FactorsABSTRACT
OBJECTIVE: This study investigated the association between long-term exposure to black smoke (BS) air pollution and mortality in two related Scottish cohorts with 25 years of follow-up. METHODS: Risk factors were collected during 1970-1976 for 15331 and 6680 participants in the Renfrew/Paisley and Collaborative cohorts respectively. Exposure to BS during 1970-1979 was estimated by inverse-distance weighted averages of observed concentrations at monitoring sites and by two alternative spatial modelling approaches which included local air quality predictors (LAQP). RESULTS: Consistent BS-mortality associations (per 10 µg m(-3) increment in 10-year average BS) were observed in the Renfrew/Paisley cohort using LAQP-based exposure models (all-cause mortality HR 1.10 (95% CI 1.04 to 1.17); cardiovascular HR 1.11 (1.01 to 1.22); ischaemic heart disease HR 1.13 (1.02 to 1.25); respiratory HR 1.26 (1.02 to 1.28)). The associations were largely unaffected by additional adjustment for area-level deprivation category. A less consistent and generally implausible pattern of cause-specific BS-mortality associations was found for inverse-distance averaging of BS concentrations at nearby monitoring sites. BS-mortality associations in the Collaborative cohort were weaker and not statistically significant. CONCLUSIONS: The association between mortality and long-term exposure to BS observed in the Renfrew/Paisley cohort is consistent with hypotheses of how air pollution may affect human health. The dissimilarity in pollution-mortality associations for different exposure models highlights the critical importance of reliable estimation of exposures on intraurban spatial scales to avoid potential misclassification bias.
Subject(s)
Air Pollution/adverse effects , Cardiovascular Diseases/mortality , Cause of Death , Environmental Exposure/adverse effects , Respiratory Tract Diseases/mortality , Smoke/adverse effects , Adult , Cohort Studies , Female , Humans , Male , Middle Aged , Scotland/epidemiology , Time FactorsABSTRACT
BACKGROUND: Higher consumption of coffee intake has recently been linked with reduced risk of aggressive prostate cancer (PC) incidence, although meta-analysis of other studies that examine the association between coffee consumption and overall PC risk remains inconclusive. Only one recent study investigated the association between coffee intake and grade-specific incidence of PC, further evidence is required to understand the aetiology of aggressive PCs. Therefore, we conducted a prospective study to examine the relationship between coffee intake and overall as well as grade-specific PC risk. METHODS: We conducted a prospective cohort study of 6017 men who were enrolled in the Collaborative cohort study in the UK between 1970 and 1973 and followed up to 31st December 2007. Cox Proportional Hazards Models were used to evaluate the association between coffee consumption and overall, as well as Gleason grade-specific, PC incidence. RESULTS: Higher coffee consumption was inversely associated with risk of high grade but not with overall risk of PC. Men consuming 3 or more cups of coffee per day experienced 55% lower risk of high Gleason grade disease compared with non-coffee drinkers in analysis adjusted for age and social class (HR 0.45, 95% CI 0.23-0.90, p value for trend 0.01). This association changed a little after additional adjustment for Body Mass Index, smoking, cholesterol level, systolic blood pressure, tea intake and alcohol consumption. CONCLUSION: Coffee consumption reduces the risk of aggressive PC but not the overall risk.
Subject(s)
Coffee/adverse effects , Coffee/chemistry , Prostatic Neoplasms/epidemiology , Prostatic Neoplasms/physiopathology , Adult , Aged , Alcohol Drinking , Blood Pressure , Body Mass Index , Cholesterol/blood , Follow-Up Studies , Humans , Incidence , Male , Middle Aged , Neoplasm Grading , Proportional Hazards Models , Prospective Studies , Prostatic Neoplasms/etiology , Risk Factors , Smoking , Social Class , Surveys and Questionnaires , Tea/chemistry , Young AdultABSTRACT
AIMS: To examine the association of physiological, behavioural and social characteristics in pre-middle age with future total and cardiovascular disease (CVD) mortality. METHODS AND RESULTS: Risk factor data on 1503 individuals aged 16-35 years at baseline were collected in two prospective cohort studies using standard protocols. Their association with total and CVD mortality ascertained during 40 years of follow-up was summarized using Cox proportional hazards regression. A median follow-up of 39.6 years gave rise to 255 deaths (103 from CVD). In age-adjusted and sex-adjusted analyses, impaired lung function [one standard deviation increases in forced expiratory volume in 1 s: hazards ratio 0.69; 95% confidence interval 0.55, 0.86; and in forced vital capacity: 0.76; 0.59, 0.98], current cigarette smoking (4.16; 2.22, 7.80) and higher alcohol consumption (one standard deviation increase in standard units consumed: 1.20; 1.02, 1.41) were associated with CVD. In fully adjusted analyses associations generally held. For total mortality, these factors and obesity and socioeconomic disadvantage were predictive. CONCLUSION: A range of risk factors measured before middle age were related to risk of total and CVD mortality up to four decades later, indicating that public health interventions should be implemented earlier in the life course than is currently the case.
Subject(s)
Cardiovascular Diseases/etiology , Cardiovascular Diseases/mortality , Adolescent , Adult , Age Factors , Alcohol Drinking/adverse effects , Alcohol Drinking/mortality , Cardiovascular Diseases/physiopathology , Cardiovascular Diseases/prevention & control , Cause of Death , Female , Forced Expiratory Volume , Health Promotion , Humans , Lung/physiopathology , Male , Obesity/complications , Obesity/mortality , Predictive Value of Tests , Preventive Health Services , Proportional Hazards Models , Prospective Studies , Risk Assessment , Risk Factors , Scotland/epidemiology , Smoking/adverse effects , Smoking/mortality , Socioeconomic Factors , Time Factors , Vital Capacity , Young AdultABSTRACT
BACKGROUND: Smoking and consuming alcohol are both related to increased mortality risk. Their combined effects on cause-specific mortality were investigated in a prospective cohort study. METHODS: Participants were 5771 men aged 35-64, recruited during 1970-73 from various workplaces in Scotland. Data were obtained from a questionnaire and a screening examination. Causes of death were all cause, coronary heart disease (CHD), stroke, alcohol-related, respiratory and smoking-related cancer. Participants were divided into nine groups according to their smoking status (never, ex or current) and reported weekly drinking (none, 1-14 units and 15 or more). Cox proportional hazards models were used to obtain relative rates of mortality, adjusted for age and other risk factors. RESULTS: In 30 years of follow-up, 3083 men (53.4%) died. Compared with never smokers who did not drink, men who both smoked and drank 15+ units/week had the highest all-cause mortality (relative rate = 2.71 (95% confidence interval 2.31-3.19)). Relative rates for CHD mortality were high for current smokers, with a possible protective effect of some alcohol consumption in never smokers. Stroke mortality increased with both smoking and alcohol consumption. Smoking affected respiratory mortality with little effect of alcohol. Adjusting for a wide range of confounders attenuated the relative rates but the effects of alcohol and smoking still remained. Premature mortality was particularly high in smokers who drank 15 or more units, with a quarter of the men not surviving to age 65. 30% of men with manual occupations both smoked and drank 15+ units/week compared with only 13% with non-manual ones. CONCLUSIONS: Smoking and drinking 15+ units/week was the riskiest behaviour for all causes of death.
Subject(s)
Alcohol Drinking/mortality , Cause of Death/trends , Smoking/mortality , Adult , Cohort Studies , Female , Humans , Male , Middle Aged , Proportional Hazards Models , Scotland/epidemiology , Surveys and QuestionnairesABSTRACT
AIMS: The aim of this study was to investigate relationships between alcohol consumption and social mobility in a cohort study in Scotland. METHODS: 1040 sons and 1298 daughters aged 30-59 from 1477 families reported their alcohol consumption from which was derived: weekly units (1 UK unit being 8 g ethanol), exceeding daily or weekly limits, binge drinking and consuming alcohol on 5+ days per week. Own and father's social class were available enabling social mobility to be investigated. RESULTS: More downwardly mobile men exceeded the weekly limit, the daily limit, were defined as binge drinkers and drank the most units per week of the four social mobility groups. Stable non-manual women were more likely to consume alcohol on 5+ days a week but very few were binge drinkers. Stable non-manual and upwardly mobile men and women were more likely to drink wine, and downwardly mobile men to drink beer. CONCLUSIONS: Downward mobility was associated with less favourable alcohol behaviours, especially in men. Wine consumption was more closely related to the social mobility groups than beer and spirits consumption. Drinking patterns could both influence and be influenced by social mobility.
Subject(s)
Alcohol Drinking/epidemiology , Family , Social Mobility , Adult , Alcohol Drinking/economics , Cohort Studies , Female , Humans , Male , Middle Aged , Prospective Studies , Social Class , Socioeconomic FactorsABSTRACT
We investigate the association between psychological stress and breast cancer and, as oestrogen may provide a common mechanism, the association between stress and prostate cancer. A prospective study of 991 women and 5743 men employed in Scotland in the 1970s provided data. Risk exposure was measured by questionnaire and physical examination, routine data collection provided cancer outcomes over the subsequent 30 years. There was weak evidence of elevated incidences in those reporting moderate (breast cancer: hazard ratio [HR] 2.16, 95% CI 1.00-4.71; prostate cancer: HR 1.65, 95% CI 1.20-2.27) and high stress (breast cancer: HR 1.92, 95% CI 0.81-4.55; prostate cancer: HR 1.35, 95% CI 0.87-2.10) compared to those reporting low stress. These estimates are adjusted for socioeconomic circumstances and health-related behaviours. With no dose-response relationship and no established mechanism linking stress with breast and prostate cancer, confounding is the parsimonious explanation of these findings.
Subject(s)
Breast Neoplasms/psychology , Prostatic Neoplasms/psychology , Stress, Psychological/complications , Adult , Breast Neoplasms/mortality , Epidemiologic Methods , Female , Humans , Male , Middle Aged , Prostatic Neoplasms/mortality , Scotland/epidemiology , Stress, Psychological/mortalityABSTRACT
OBJECTIVE: To assess the value of psychosocial risk factors in discriminating between individuals at higher and lower risk of coronary heart disease, using risk prediction equations. DESIGN: Prospective observational study. SETTING: Scotland. PARTICIPANTS: 5191 employed men aged 35 to 64 years and free of coronary heart disease at study enrollment MAIN OUTCOME MEASURES: Area under receiver operating characteristic (ROC) curves for risk prediction equations including different risk factors for coronary heart disease. RESULTS: During the first 10 years of follow up, 203 men died of coronary heart disease and a further 200 were admitted to hospital with this diagnosis. Area under the ROC curve for the standard Framingham coronary risk factors was 74.5%. Addition of "vital exhaustion" and psychological stress led to areas under the ROC curve of 74.5% and 74.6%, respectively. Addition of current social class and lifetime social class to the standard Framingham equation gave areas under the ROC curve of 74.6% and 74.9%, respectively. In no case was there strong evidence for improved discrimination of the model containing the novel risk factor over the standard model. CONCLUSIONS: Consideration of psychosocial risk factors, including those that are strong independent predictors of heart disease, does not substantially influence the ability of risk prediction tools to discriminate between individuals at higher and lower risk of coronary heart disease.
Subject(s)
Coronary Artery Disease/etiology , Psychology , Social Class , Adult , Coronary Artery Disease/prevention & control , Forecasting , Humans , Logistic Models , Male , Middle Aged , Prospective Studies , ROC Curve , Risk Assessment/statistics & numerical data , Risk Factors , ScotlandABSTRACT
OBJECTIVES: To investigate how loss of a spouse affects mortality risk in the bereaved partner. DESIGN AND SETTING: Prospective cohort study in Renfrew and Paisley in Scotland. PARTICIPANTS: 4395 married couples aged 45-64 years when the study was carried out between 1972 and 1976. METHODS: The date of bereavement for the bereaved spouse was the date of death of his or her spouse. Bereavement could occur at any time during the follow-up period, so it was considered as a time-dependent exposure variable and the Cox proportional hazards model for time-dependent variables was used. The relative rate (RR) of mortality was calculated for bereaved versus non-bereaved spouses and adjusted for confounding variables. MAIN OUTCOME MEASURES: Causes of death to 31 March 2004. RESULTS: Bereaved participants were at higher risk than non-bereaved participants of dying from any cause (RR 1.27; 95% CI 1.2 to 1.35). These risks remained but were attenuated after adjustment for confounding variables. There were raised RRs for bereaved participants dying of cardiovascular disease, coronary heart disease, stroke, all cancer, lung cancer, smoking-related cancer, and accidents or violence. After adjustment for confounding variables, RRs remained higher for bereaved participants for all these causes except for mortality from lung cancer. There was no strong statistical evidence that the increased risks of death associated with bereavement changed with time after bereavement. CONCLUSIONS: Conjugal bereavement, in addition to existing risk factors, is related to mortality risk for major causes of death.
Subject(s)
Bereavement , Death , Marriage , Aged , Cause of Death , Female , Humans , Male , Middle Aged , Proportional Hazards Models , Risk , Scotland , Time FactorsABSTRACT
BACKGROUND: This study examined whether psychological distress might be a predictor of chronic obstructive pulmonary disease (COPD). METHOD: The relation between psychological distress at baseline, measured by the general health questionnaire (GHQ), and chronic bronchitis three years later, as measured by the Medical Research Council (MRC) bronchitis questionnaire and forced expiratory flow in one second (FEV(1)), was examined in 1682 men and 2203 women from the Renfrew and Paisley (MIDSPAN) study. The analyses were run on men and women separately and adjustments were made for age, socioeconomic position, and lung function at baseline (FEV(1)). People with chronic diseases at baseline were then excluded to give a "healthy" baseline cohort. The effect of psychological distress on individual components of the MRC bronchitis questionnaire and FEV(1) was also assessed. RESULTS: In multivariate analyses of the whole cohort baseline psychological distress in women was associated with reduced FEV(1) at follow up (OR 1.31 95% CI 1.0 to 1.73) after adjustment. In women, in the healthy cohort, psychological distress was associated with chronic bronchitis (OR 2.00, 95% CI 1.16 to 3.46), symptoms of bronchial infection (OR 2.14, 95% CI 1.44 to 3.19), symptoms of breathlessness (OR 3.02, 95% CI 1.99 to 4.59), and reduced FEV(1) (OR 1.62, 95% CI 1.13 to 2.32). In men psychological distress predicted symptoms of bronchial infection (OR 2.09, 95% CI 1.28 to 3.42). CONCLUSION: This study supports research suggesting that psychological distress is associated with COPD and shows that psychological distress predicts COPD in women. The robustness of the association and the exact mechanism requires further investigation.
Subject(s)
Pulmonary Disease, Chronic Obstructive/epidemiology , Stress, Psychological/epidemiology , Bronchial Diseases/epidemiology , Dyspnea/epidemiology , Female , Forced Expiratory Flow Rates/physiology , Humans , Longitudinal Studies , Male , Middle Aged , Pulmonary Disease, Chronic Obstructive/psychology , Risk Factors , Scotland/epidemiology , Sex FactorsABSTRACT
We tested the predictive ability of cardiac biomarkers N-terminal pro B-type natriuretic peptide (NT-proBNP), high-sensitivity troponin T, and midregional pro adrenomedullin for cardiovascular disease (CVD) events using the British Regional Heart Study (BRHS) of men aged 60 to 79 years, and the MIDSPAN Family Study (MFS) of men and women aged 30 to 59 years. They included 3757 and 2226 participants, respectively, and during median 13.0 and 17.3 years follow-up the primary CVD event rates were 16.6 and 5.3 per 1000 patient-years, respectively. In Cox models adjusted for basic classical risk factors, 1 SD increases in log-transformed NT-proBNP, high-sensitivity troponin T, and midregional pro adrenomedullin were generally associated with increased primary CVD risk in both the studies (P<0.006) except midregional pro adrenomedullin in MFS (P=0.10). In BRHS, QRISK2 risk factors yielded a C-index of 0.657, which was improved by 0.017 (P=0.005) by NT-proBNP, but not by other biomarkers. Using 28% 14-year risk as a proxy for 20% 10-year risk, NT-proBNP improved risk classification for primary CVD cases (case net reclassification index, 5.9%; 95% confidence interval, 2.8%-9.2%), but only improved classification of noncases at a 14% 14-year risk threshold (4.6%; 2.9%-6.3%). In MFS, ASSIGN risk factors yielded a C-index of 0.752 for primary CVD; none of the cardiac biomarkers improved the C-index. Improvements in risk classification were only seen using NT-proBNP and high-sensitivity troponin T among cases using the 28% 14-year risk threshold (4.7%; 1.0%-9.2% and 2.6%; 0.0%-5.8%, respectively). In conclusion, the improvement in treatment allocation gained by adding cardiac biomarkers to risk scores seems to depend on the risk threshold chosen for commencing preventative treatments.
Subject(s)
Biomarkers/blood , Cardiovascular Diseases/epidemiology , Disease Management , Risk Assessment , Adult , Aged , Cardiovascular Diseases/blood , Cardiovascular Diseases/therapy , Female , Follow-Up Studies , Humans , Incidence , Male , Middle Aged , Prognosis , Proportional Hazards Models , Retrospective Studies , Risk Factors , United Kingdom/epidemiologyABSTRACT
Both subjective and objective measures of lower social position have been shown to be associated with poorer health. A psychosocial, as opposed to material, aetiology of health inequalities predicts that subjective social status should be a stronger determinant of health than objective social position. In a workplace based prospective study of 5232 Scottish men recruited in the early 1970s and followed up for 25 years we examined the association between objective and subjective indices of social position, perceived psychological stress, cardiovascular disease risk factors and subsequent health. Lower social position, whether indexed by more objective or more subjective measures, was consistently associated with an adverse profile of established disease risk factors. Perceived stress showed the opposite association. The main subjective social position measure used was based on individual perceptions of workplace status (as well as their actual occupation, men were asked whether they saw themselves as "employees", "foremen", or "managers"). Compared to foremen, employees had a small and imprecisely estimated increased risk of all cause mortality, whereas managers had a more marked decreased risk. The strongest predictors of increased mortality were father's manual as opposed to non-manual occupation; lack of car access and shorter stature, (an indicator of material deprivation in childhood). In the fully adjusted analyses, perceived work-place status was only weakly associated with mortality. In this population it appears that objective material circumstances, particularly in early life, are a more important determinant of health than perceptions of relative status. Conversely, higher perceived stress was not associated with poorer health, presumably because, in this population, higher stress was not associated with material disadvantage. Together these findings suggest that, rather than targeting perceptions of disadvantage and associated negative emotions, interventions to reduce health inequalities should aim to reduce objective material disadvantage, particularly that experienced in early life.
Subject(s)
Health Status Indicators , Occupational Health/statistics & numerical data , Occupations/classification , Social Class , Administrative Personnel/statistics & numerical data , Adult , Aged , Cardiovascular Diseases/epidemiology , Humans , Hypertension/epidemiology , Male , Middle Aged , Observer Variation , Prospective Studies , Risk Factors , Scotland/epidemiology , Social Perception , Stress, Psychological/epidemiologyABSTRACT
BACKGROUND: The primary prevention of cardiovascular disease involves using the Framingham risk score to identify high risk patients and then prescribe preventive treatments. AIM: To examine the performance of the Framingham risk score in different socioeconomic groups in a population with high rates of cardiovascular disease. DESIGN OF STUDY: A prospective study. SETTING: West of Scotland. METHOD: The observed 10-year cardiovascular disease and coronary heart disease mortality rates in 5626 men and 6678 women free from cardiovascular disease from the Renfrew/Paisley Study were compared with predicted rates, stratified by socioeconomic class and by area deprivation score. RESULTS: The ratio of predicted to observed cardiovascular mortality rate in the 12 304 men and women with complete risk factor information was 0.56 (95% confidence interval [CI] = 0.52 to 0.60), a relative underestimation of 44%. Cardiovascular disease mortality was underestimated by 48% in manual participants (predicted over observed = 0.52, 95% CI = 0.48 to 0.56) compared to 31% in the non-manual participants (predicted over observed = 0.69, 95% CI = 0.60 to 0.81, P = 0.0005). Underestimation was also worse in participants from deprived areas (P = 0.0017). Only 4.8% of individuals had a 10-year cardiovascular risk of >40% (equivalent to >30% 10-year coronary risk), and 81% of deaths occurred in the rest. If the Framingham score had been recalibrated for manual and non-manual members of this population, an additional 3611 individuals mainly from manual social classes would have reached the treatment threshold. CONCLUSION: Currently recommended risk scoring methods underestimate risk in socioeconomically deprived individuals. The likely consequence is that preventive treatments are less available to the most needy.
Subject(s)
Cardiovascular Diseases/prevention & control , Mass Screening/methods , Adult , Female , Health Status Indicators , Humans , Male , Middle Aged , Predictive Value of Tests , Prospective Studies , Risk Assessment/standards , Risk Factors , Sensitivity and Specificity , Socioeconomic FactorsABSTRACT
OBJECTIVE: To investigate the associations of childhood IQ and adult social factors, and smoking behaviour, lung function (forced expiratory volume in one second; FEV(1)), and smoking-related outcomes in adulthood. DESIGN: Retrospective cohort study. METHOD: Participants were from the Midspan prospective studies conducted on Scottish adults in the 1970s. The sample consisted of 938 Midspan participants born in 1921 who were successfully matched with their cognitive ability test results on the Scottish Mental Survey 1932. RESULTS: Structural equation modelling showed that age 11 IQ was not directly associated with smoking consumption, but that IQ and adult social class had indirect effects on smoking consumption via deprivation category. The influence of IQ on FEV(1) was partly indirect via social class. Gender influenced smoking consumption and also IQ and social class. There was a 21% higher risk of having a smoking-related hospital admission, cancer, or death during 25 years of follow-up for each standard deviation disadvantage in IQ. Adjustment for adult social class, deprivation category, and smoking reduced the association to 10%. CONCLUSION: Childhood IQ was associated with social factors which influenced lung function in adulthood, but was not associated directly with smoking consumption. In future studies, it is important to consider other pathways which may account for variance in the link between childhood IQ and health in later life.