There is mounting evidence for associations between sedentary behaviours and adverse health outcomes, although the data on occupational sitting and mortality risk remain equivocal. The aim of this study was to determine the association between occupational sitting and cardiovascular, cancer and all-cause mortality in a pooled sample of seven British general population cohorts.
The sample comprised 5380 women and 5788 men in employment who were drawn from five Health Survey for England and two Scottish Health Survey cohorts. Participants were classified as reporting standing, walking or sitting in their work time and followed up over 12.9 years for mortality. Data were modelled using Cox proportional hazard regression adjusted for age, waist circumference, self-reported general health, frequency of alcohol intake, cigarette smoking, non-occupational physical activity, prevalent cardiovascular disease and cancer at baseline, psychological health, social class, and education.
In total there were 754 all-cause deaths. In women, a standing/walking occupation was associated with lower risk of all-cause (fully adjusted hazard ratio [HR] = 0.68, 95% CI 0.52–0.89) and cancer (HR = 0.60, 95% CI 0.43–0.85) mortality, compared to sitting occupations. There were no associations in men. In analyses with combined occupational type and leisure-time physical activity, the risk of all-cause mortality was lowest in participants with non-sitting occupations and high leisure-time activity.
Sitting occupations are linked to increased risk for all-cause and cancer mortality in women only, but no such associations exist for cardiovascular mortality in men or women.
Depressive symptoms and physical performance are inversely associated, but it is unclear whether their association is bidirectional. We examined whether the association between depressive symptoms and physical performance measured using gait speed is bidirectional.
We used a national sample of 4,581 community-dwelling people aged 60 years and older from the English Longitudinal Study of Ageing (from 2002–03 to 2008-09). We fitted Generalized Estimating Equation (GEE) regression models to analyse repeated measurements of gait speed (m/sec) and elevated depressive symptoms (defined as a score of ≥4 on the eight-item Center for Epidemiological Studies-Depression scale).
Slower gait speed was associated with elevated depressive symptoms both concurrently and two years later. After adjustment for previous depressive symptoms and sociodemographic, clinical, lifestyle, psychosocial, and cognitive factors the concurrent association was partially explained (Odds Ratio [OR] 0.42, 95% confidence interval [CI], 0.30 to 0.59, per 1m/sec increase in gait speed) and the two-year lagged association fully (OR 0.75, 95% CI, 0.56 to 1.00). Elevated depressive symptoms were associated with slower gait speed. Full adjustment for covariates (including previous gait speed) partially explained both the concurrent (β regression coefficient [β] -0.038, 95% CI, -0.050 to -0.026, for participants with elevated depressive symptoms compared with those with no or one symptom) and the two-year lagged associations (β -0.017, 95% CI, -0.030 to -0.005). Subthreshold depressive symptoms (defined as a score of two or three on the eight-item Center for Epidemiological Studies-Depression scale) were also associated with slower gait speed. Full adjustment for covariates partially explained both the concurrent (β -0.029, 95% CI, -0.039 to -0.019, for participants with subthreshold symptoms compared with those with no or one symptom) and the two-year lagged associations (β -0.011, 95% CI, -0.021 to -0.001).
The inverse association between gait speed and depressive symptoms appears to be bidirectional.
Although research productivity in the field of frailty has risen exponentially in recent years, there remains a lack of consensus regarding the measurement of this syndrome. This overview offers three services: first, we provide a comprehensive catalogue of current frailty measures; second, we evaluate their reliability and validity; third, we report on their popularity of use.
In order to identify relevant publications, we searched MEDLINE (from its inception in 1948 to May 2011); scrutinized the reference sections of the retrieved articles; and consulted our own files. An indicator of the frequency of use of each frailty instrument was based on the number of times it had been utilized by investigators other than the originators.
Of the initially retrieved 2,166 papers, 27 original articles described separate frailty scales. The number (range: 1 to 38) and type of items (range of domains: physical functioning, disability, disease, sensory impairment, cognition, nutrition, mood, and social support) included in the frailty instruments varied widely. Reliability and validity had been examined in only 26% (7/27) of the instruments. The predictive validity of these scales for mortality varied: for instance, hazard ratios/odds ratios (95% confidence interval) for mortality risk for frail relative to non-frail people ranged from 1.21 (0.78; 1.87) to 6.03 (3.00; 12.08) for the Phenotype of Frailty and 1.57 (1.41; 1.74) to 10.53 (7.06; 15.70) for the Frailty Index. Among the 150 papers which we found to have used at least one of the 27 frailty instruments, 69% (n = 104) reported on the Phenotype of Frailty, 12% (n = 18) on the Frailty Index, and 19% (n = 28) on one of the remaining 25 instruments.
Although there are numerous frailty scales currently in use, reliability and validity have rarely been examined. The most evaluated and frequently used measure is the Phenotype of Frailty.
Frailty; Frail elderly; Measure; Overview; Reliability; Validity
Job strain is associated with an increased coronary heart disease risk, but few large-scale studies have examined the relationship of this psychosocial characteristic with the biological risk factors that potentially mediate the job strain – heart disease association.
Methodology and Principal Findings
We pooled cross-sectional, individual-level data from eight studies comprising 47,045 participants to investigate the association between job strain and the following cardiovascular disease risk factors: diabetes, blood pressure, pulse pressure, lipid fractions, smoking, alcohol consumption, physical inactivity, obesity, and overall cardiovascular disease risk as indexed by the Framingham Risk Score. In age-, sex-, and socioeconomic status-adjusted analyses, compared to those without job strain, people with job strain were more likely to have diabetes (odds ratio 1.29; 95% CI: 1.11–1.51), to smoke (1.14; 1.08–1.20), to be physically inactive (1.34; 1.26–1.41), and to be obese (1.12; 1.04–1.20). The association between job strain and elevated Framingham risk score (1.13; 1.03–1.25) was attributable to the higher prevalence of diabetes, smoking and physical inactivity among those reporting job strain.
In this meta-analysis of work-related stress and cardiovascular disease risk factors, job strain was linked to adverse lifestyle and diabetes. No association was observed between job strain, clinic blood pressure or blood lipids.
It is unclear whether a healthy lifestyle mitigates the adverse effects of job strain on coronary artery disease. We examined the associations of job strain and lifestyle risk factors with the risk of coronary artery disease.
We pooled individual-level data from 7 cohort studies comprising 102 128 men and women who were free of existing coronary artery disease at baseline (1985–2000). Questionnaires were used to measure job strain (yes v. no) and 4 lifestyle risk factors: current smoking, physical inactivity, heavy drinking and obesity. We grouped participants into 3 lifestyle categories: healthy (no lifestyle risk factors), moderately unhealthy (1 risk factor) and unhealthy (2–4 risk factors). The primary outcome was incident coronary artery disease (defined as first nonfatal myocardial infarction or cardiac-related death).
There were 1086 incident events in 743 948 person-years at risk during a mean follow-up of 7.3 years. The risk of coronary artery disease among people who had an unhealthy lifestyle compared with those who had a healthy lifestyle (hazard ratio [HR] 2.55, 95% confidence interval [CI] 2.18–2.98; population attributable risk 26.4%) was higher than the risk among participants who had job strain compared with those who had no job strain (HR 1.25, 95% CI 1.06–1.47; population attributable risk 3.8%). The 10-year incidence of coronary artery disease among participants with job strain and a healthy lifestyle (14.7 per 1000) was 53% lower than the incidence among those with job strain and an unhealthy lifestyle (31.2 per 1000).
The risk of coronary artery disease was highest among participants who reported job strain and an unhealthy lifestyle; those with job strain and a healthy lifestyle had half the rate of disease. A healthy lifestyle may substantially reduce disease risk among people with job strain.
Sarcopenia is associated with loss of independence and ill-health in the elderly although the causes remain poorly understood. We examined the association between two screen-based leisure time sedentary activities (daily TV viewing time and internet use) and muscle strength.
Methods and Results
We studied 6228 men and women (aged 64.9±9.1 yrs) from wave 4 (2008-09) of the English Longitudinal Study of Ageing, a prospective study of community dwelling older adults. Muscle strength was assessed by a hand grip test and the time required to complete five chair rises. TV viewing and internet usage were inversely associated with one another. Participants viewing TV ≥6hrs/d had lower grip strength (Men, B = −1.20 kg, 95% CI, −2.26, −0.14; Women, −0.75 kg, 95% CI, −1.48, −0.03) in comparison to <2hrs/d TV, after adjustment for age, physical activity, smoking, alcohol, chronic disease, disability, depressive symptoms, social status, and body mass index. In contrast, internet use was associated with higher grip strength (Men, B = 2.43 kg, 95% CI, 1.74, 3.12; Women, 0.76 kg, 95% CI, 0.32, 1.20). These associations persisted after mutual adjustment for both types of sedentary behaviour.
In older adults, the association between sedentary activities and physical function is context specific (TV viewing vs. computer use). Adverse effects of TV viewing might reflect the prolonged sedentary nature of this behavior.
The impact of diet on specific age-related diseases has been studied extensively, but few investigations have adopted a more holistic approach to determine the association of diet with overall health at older ages. We examined whether diet, assessed in midlife, using dietary patterns and adherence to the Alternative Healthy Eating Index (AHEI), is associated with aging phenotypes, identified after a mean 16-year follow-up.
Data were drawn from the Whitehall II cohort study of 5350 adults (age 51.3 ± 5.3 years, 29.4% women). Diet was assessed at baseline (1991-1993). Mortality, chronic diseases, and functioning were ascertained from hospital data, register linkage, and screenings every 5 years and were used to create 5 outcomes at follow-up: ideal aging (free of chronic conditions and high performance in physical, mental, and cognitive functioning tests; 4%), nonfatal cardiovascular event (7.3%), cardiovascular death (2.8%), noncardiovascular death (12.7%), and normal aging (73.2%).
Low adherence to the AHEI was associated with an increased risk of cardiovascular and noncardiovascular death. In addition, participants with a “Western-type” diet (characterized by high intakes of fried and sweet food, processed food and red meat, refined grains, and high-fat dairy products) had lower odds of ideal aging (odds ratio for top vs bottom tertile: 0.58; 95% confidence interval, 0.36-0.94; P = .02), independently of other health behaviors.
By considering healthy aging as a composite of cardiovascular, metabolic, musculoskeletal, respiratory, mental, and cognitive function, the present study offers a new perspective on the impact of diet on aging phenotypes.
Aging; Cognitive functioning; Dietary patterns; Diet quality indices; Mortality; Nutritional epidemiology; Overall diet; Physical functioning
There is some evidence to suggest that obesity is a risk factor for the development of depression, although this is not a universal finding. This discordance might be ascribed to the existence of a ‘healthy obese phenotype’– that is, obesity in the absence of the associated burden of cardio-metabolic risk factors. We examined whether the association of obesity with depressive symptoms is dependent on the individual’s metabolic health. Participants were 3851 men and women (aged 63.0 ± 8.9 yrs, 45.1% men) from the English Longitudinal Study of Ageing, a prospective study of community dwelling older adults. Obesity was defined as body mass index ≥ 30 kg/m2. Based on blood pressure, HDL-cholesterol, triglycerides, glycated haemoglobin, and C-reactive protein, participants were classified as ‘metabolically healthy’ (0 or 1 metabolic abnormality) or ‘unhealthy’ (≥ 2 metabolic abnormalities). Depressive symptoms were assessed at baseline and at 2 years follow up using the 8-item Centre of Epidemiological Studies Depression (CES-D) scale. Obesity prevalence was 27.5%, but 34.3% of this group was categorized as metabolically healthy at baseline. Relative to non-obese healthy participants, after adjustment for baseline CES-D score and other covariates, the metabolically unhealthy obese participants had elevated risk of depressive symptoms at follow-up (odds ratio [OR] = 1.50, 95% CI, 1.05–2.15), although the metabolically healthy obese did not (OR = 1.38, 95% CI, 0.88–2.17). The association between obesity and risk of depressive symptoms appears to be partly dependent on metabolic health, although further work is required to confirm these findings.
C-reactive protein (CRP) is associated with the risk of cardiovascular disease (CVD); whether the effects are modified by diabetes status still is unclear. This study investigated these issues and assessed the added value of CRP to predictions.
RESEARCH DESIGN AND METHODS
Participants were drawn from representative samples of adults living in England and Scotland. Cox proportional hazards regression models were used to relate baseline plasma CRP with all-cause and CVD mortality during follow-up in men and women with and without diabetes. The added value of CRP to the predictions was assessed through c-statistic comparison and relative integrated discrimination improvement.
A total of 25,979 participants (4.9% with diabetes) were followed for a median of 93 months, during which period there were 2,767 deaths (957 from CVD). CRP (per SD loge) was associated with a 53% (95% CI 43–64) and 43% (38–49) higher risk of cardiovascular and all-cause mortality, respectively. These associations were log linear and did not differ according to diabetes status (both P ≥ 0.08 for interaction), sex, and other risk factors. Adding CRP to conventional risk factors improved predictions overall and separately by diabetes status but not for CVD mortality, although such improvements only were marginal based on several discrimination statistics.
The association between CRP and CVD was similar across diabetes status, and the effects are broadly similar across levels of other conventional risk factors.
There are few longitudinal data on physical activity patterns from mid-life into older age. The authors examined associations of self-reported physical activity, adiposity and socio-demographic factors in mid-life with objectively assessed measures of activity in older age.
Participants were 394 healthy men and women drawn from the Whitehall II population-based cohort study. At the baseline assessment in 1997 (mean age 54 years), physical activity was assessed through self-report and quantified as metabolic equivalent of task hours/week. At the follow-up in 2010 (mean age 66 years), physical activity was objectively measured using accelerometers worn during waking hours for seven consecutive days (average daily wear time 891±68 min/day).
Self-reported physical activity at baseline was associated with objectively assessed activity at follow-up in various activity categories, including light-, moderate- and vigorous-intensity activity (all ps<0.04). Participants in the highest compared with lowest quartile of self-reported activity level at baseline recorded on average 64.1 (95% CI 26.2 to 102.1) counts per minute more accelerometer-assessed activity at follow-up and 9.0 (2.0–16.0) min/day more moderate-to-vigorous daily activity, after adjusting for baseline covariates. Lower education, obesity and self-perceived health status were also related to physical activity at follow-up. Only age and education were associated with objectively measured sedentary time at follow-up.
Physical activity behaviour in middle age was associated with objectively measured physical activity in later life after 13 years of follow-up, suggesting that the habits in adulthood are partly tracked into older age.
Actigraph; ageing; education; epidemiology; obesity; physical activity; health behaviour; psychological stress; prevention; coronary heart disease
Shorter telomere length and poor sleep are more prevalent at older ages, but their relationship is uncertain. This study explored associations between sleep duration and telomere length in a sample of healthy middle and early old age people.
Participants were 434 men and women aged 63.3 years on average drawn from the Whitehall II cohort study. Sleep duration was measured by self-report.
There was a linear association between sleep duration and leukocyte telomere length in men but not in women (P = 0.035). Men reporting shorter sleep duration had shorter telomeres, independently of age, body mass index, smoking, educational attainment, current employment, cynical hostility scores and depressive symptoms. Telomeres were on average 6% shorter in men sleeping 5 hours or fewer compared with those sleeping more than 7 hours per night.
This study adds to the growing literature relating sleep duration with biomarkers of aging, and suggests that shortening of telomeres might reflect mechanisms through which short sleep contributes to pathological conditions in older men.
Published work assessing psychosocial stress (job strain) as a risk factor for coronary heart disease is inconsistent and subject to publication bias and reverse causation bias. We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies.
We used individual records from 13 European cohort studies (1985–2006) of men and women without coronary heart disease who were employed at time of baseline assessment. We measured job strain with questions from validated job-content and demand-control questionnaires. We extracted data in two stages such that acquisition and harmonisation of job strain measure and covariables occurred before linkage to records for coronary heart disease. We defined incident coronary heart disease as the first non-fatal myocardial infarction or coronary death.
30 214 (15%) of 197 473 participants reported job strain. In 1·49 million person-years at risk (mean follow-up 7·5 years [SD 1·7]), we recorded 2358 events of incident coronary heart disease. After adjustment for sex and age, the hazard ratio for job strain versus no job strain was 1·23 (95% CI 1·10–1·37). This effect estimate was higher in published (1·43, 1·15–1·77) than unpublished (1·16, 1·02–1·32) studies. Hazard ratios were likewise raised in analyses addressing reverse causality by exclusion of events of coronary heart disease that occurred in the first 3 years (1·31, 1·15–1·48) and 5 years (1·30, 1·13–1·50) of follow-up. We noted an association between job strain and coronary heart disease for sex, age groups, socioeconomic strata, and region, and after adjustments for socioeconomic status, and lifestyle and conventional risk factors. The population attributable risk for job strain was 3·4%.
Our findings suggest that prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking.
Finnish Work Environment Fund, the Academy of Finland, the Swedish Research Council for Working Life and Social Research, the German Social Accident Insurance, the Danish National Research Centre for the Working Environment, the BUPA Foundation, the Ministry of Social Affairs and Employment, the Medical Research Council, the Wellcome Trust, and the US National Institutes of Health.
Predictive power, for total and vascular mortality, of selected indices measured at baseline in the British National Diet and Nutrition Survey (community-living subset) of People Aged 65 Years and Over was tested. Mortality status and its primary and underlying causes were recorded for 1100 (mean age 76·7 (SD 7·5) years, 50·2 % females) respondents from the baseline survey in 1994–5 until September 2008. Follow-up data analyses focussed especially on known predictors of vascular disease risk, together with intakes and status indices of selected nutrients known to affect, or to be affected by, these predictors. Total mortality was significantly predicted by hazard ratios of baseline plasma concentrations (per SD) of total homocysteine (tHcy) (95 % CI) 1·19 (1·11, 1·27), pyridoxal phosphate 0·90 (0·81, 1·00), pyridoxic acid 1·10 (1·03, 1·19), α1-antichymotrypsin 1·21 (1·13, 1·29), fibrinogen 1·14 (1·05, 1·23), creatinine 1·20 (1·10, 1·31) and glycosylated Hb 1·23 (1·14, 1·32), and by dietary intakes of energy 0·87 (0·80, 0·96) and protein 0·86 (0·77, 0·97). Prediction patterns and significance were similar for primary-cause vascular mortality. The traditional risk predictors plasma total and HDL cholesterol were not significant mortality predictors in this age group, nor were the known tHcy-regulating nutrients, folate and vitamin B12 (intakes and status indices). Model adjustment for known risk predictors resulted in the loss of significance for some of the afore-mentioned indices; however, tHcy 1·34 (1·04, 1·73) remained a significant predictor for vascular mortality. Thus, total and primary vascular mortality is predicted by energy and protein intakes, and by biochemical indices including tHcy, independent of serum folate or vitamin B12.
British National Survey of older adults; Mortality prediction; Intakes and biochemical indices; Plasma homocysteine; B-vitamins and inflammatory indices
Little is known about psychological risk factors in cerebrovascular disease. We examined the association between psychological distress and risk of death due to cerebrovascular disease.
We obtained data from 68 652 adult participants of the Health Survey for England (mean age 54.9 [standard deviation 13.9] yr, 45.0% male sex) with no known history of cardiovascular diseases at baseline. We used the 12-item General Health Questionnaire (GHQ-12) to assess the presence of psychological distress. We followed participants for eight years for cause-specific death using linkage to national registers.
There were 2367 deaths due to cardiovascular disease during follow-up. Relative to participants with no symptoms of psychological distress (GHQ-12 score 0) at baseline, people with psychological distress (GHQ-12 score ≥ 4, 14.7% of participants) had an increased risk of death from cerebrovascular disease (adjusted hazard ratio [HR] 1.66, 95% confidence interval [CI] 1.32–2.08) and ischemic heart disease (adjusted HR 1.59, 95% CI 1.34–1.88). There was also evidence of a dose–response effect with increasing GHQ-12 score (p for trend < 0.001 in all analyses). Associations were only marginally attenuated after we adjusted for possible confounders, including socioeconomic status, smoking and use of antihypertensive medications.
Psychological distress was associated with increased risk of death due to cerebrovascular disease in a large population-representative cohort. These data suggest that the cardiovascular effects of psychological distress are not limited to coronary artery disease.
Both anaemia and cardiovascular disease (CVD) are common in people with diabetes. While individually both characteristics are known to raise mortality risk, their combined influence has yet to be quantified. In this pooling project, we examined the combined impact of baseline haemoglobin levels and existing CVD on all-cause and CVD mortality in people with diabetes. We draw comparison of these effects with those apparent in diabetes-free individuals.
A combined analyses of 7 UK population-based cohorts resulted in 26,480 study members. There were 946 participants with physician-diagnosed diabetes, 2227 with anaemia [haemoglobin<13 g/dl (men) or <12 (women)], 2592 with existing CVD (stroke, ischaemic heart disease), and 21,396 with none of the conditions. Across diabetes and anaemia subgroups, and using diabetes-free, non-anaemic participants as the referent group, the adjusted hazard ratios (HR) were 1.46 (95% CI: 1.30–1.63) for anaemia, 1.67 (1.45–1.92) for diabetes, and 2.10 (1.55–2.85) for diabetes and anaemia combined. Across combined diabetes, anaemia and CVD subgroups, and compared with non-anaemic, diabetes-free and CVD-free participants, HR (95% CI) for all-cause mortality were 1.49 (1.32–1.69) anaemia, 1.60 (1.46–1.76) for existing CVD, and 1.66 (1.39–1.97) for diabetes alone. Equivalents were 2.13 (1.48–3.07) for anaemia and diabetes, 2.68 (2.14–3.36) for diabetes and existing CVD, and 3.25 (1.88–5.62) for the three combined. Patterns were similar for CVD mortality.
Individually, anaemia and CVD confer similar mortality risks in people with diabetes, and are excessively fatal in combination. Screening for anaemia would identify vulnerable diabetic patients whose outcomes can potentially be improved.
Objective To quantify the link between lower, subclinically symptomatic, levels of psychological distress and cause-specific mortality in a large scale, population based study.
Design Individual participant meta-analysis of 10 large prospective cohort studies from the Health Survey for England. Baseline psychological distress measured by the 12 item General Health Questionnaire score, and mortality from death certification.
Participants 68 222 people from general population samples of adults aged 35 years and over, free of cardiovascular disease and cancer, and living in private households in England at study baseline.
Main outcome measures Death from all causes (n=8365), cardiovascular disease including cerebrovascular disease (n=3382), all cancers (n=2552), and deaths from external causes (n=386). Mean follow-up was 8.2 years (standard deviation 3.5).
Results We found a dose-response association between psychological distress across the full range of severity and an increased risk of mortality (age and sex adjusted hazard ratio for General Health Questionnaire scores of 1-3 v score 0: 1.20, 95% confidence interval 1.13 to 1.27; scores 4-6: 1.43, 1.31 to 1.56; and scores 7-12: 1.94, 1.66 to 2.26; P<0.001 for trend). This association remained after adjustment for somatic comorbidity plus behavioural and socioeconomic factors. A similar association was found for cardiovascular disease deaths and deaths from external causes. Cancer death was only associated with psychological distress at higher levels.
Conclusions Psychological distress is associated with increased risk of mortality from several major causes in a dose-response pattern. Risk of mortality was raised even at lower levels of distress.
The predictive power, for total, vascular, cancer and respiratory mortality, of selected redox-modulatory (vitamin and mineral nutrient) indices measured at baseline, was studied in the British National Diet and Nutrition Survey (community-living subset) of people aged 65 years and over. Mortality status and its primary and underlying causes were recorded for 1054 (mean age 76·6 (SD 7·4) years and 49·0 % female) participants, from the baseline survey in 1994–5 until September 2008. During this interval, 74 % of the male and 62 % of the female participants died. Total mortality was significantly predicted by baseline plasma concentrations (per SD) of vitamin C (hazard ratio (HR) 0·81; 95 % CI 0·74, 0·88), α-carotene (HR 0·90; 95 % CI 0·81, 0·99), Se (HR 0·76; 95 % CI 0·69, 0·84), Zn (HR 0·79; 95 % CI 0·72, 0·87), Cu (HR 1·27; 95 % CI 1·14, 1·42) and Fe (HR 0·81; 95 % CI 0·74, 0·89). Total mortality was also significantly predicted by baseline dietary intakes (per SD) of food energy (HR 0·86; 95 % CI 0·79, 0·94), vitamin C (HR 0·88; 95 % CI 0·80, 0·94), carotenoids (HR 0·89; 95 % CI 0·83, 0·96), Zn (HR 0·89; 95 % CI 0·82, 0·96) and Cu (HR 0·91; 95 % CI 0·84, 1·00). Prediction patterns and significance for primary vascular, cancer and respiratory mortality differed in certain respects, but not fundamentally. Model adjustment for known disease or mortality risk predictors resulted in loss of significance for some of the indices; however, plasma Se and Zn, and food energy remained significant predictors. We conclude that total and primary vascular, cancer and respiratory mortality in older British people of both sexes is predicted by several biochemical indices of redox-modulatory nutrients, some of which may reflect the respondents’ acute-phase status at baseline, whereas others may reflect the healthiness of their lifestyle.
British National Survey of Older Adults; Mortality prediction; Intakes and biochemical indices; Plasma vitamins C and E; carotenoids; selenium; zinc; copper; iron
Hostility is associated with a significantly increased risk of age-related disease and mortality, yet the pathophysiological mechanisms involved remain unclear. Here we investigated the hypothesis that hostility might impact health by promoting cellular aging.
We tested the relationship between cynical hostility and two known markers of cellular aging, leukocyte telomere length (TL) and leukocyte telomerase activity (TA), in 434 men and women from the Whitehall II cohort.
High-hostile men had significantly shorter leukocyte TL than their low-hostile counterparts. They also had elevated leukocyte TA, with a significantly increased likelihood of having both short TL and high TA, compared with low-hostile individuals.
Because telomerase is known to counteract telomere shortening by synthesizing telomeric DNA repeats, particularly in the context of shortened telomeres, heightened TA might represent a compensatory response in high-hostile individuals. The relationship between hostility and disease is stronger in men than in women, and men generally have a shorter life expectancy than women. Our findings suggest that telomere attrition might represent a novel mechanism mediating the detrimental effects of hostility on men's health.
Aging; gender; hostility; psychological stress; telomerase activity; telomere length
To examine the association between objectively measured second–hand-smoke (SHS) exposure and incident CVD death, and assess the extent to which this association can be explained through novel circulating markers of inflammation and haemostasis.
Existing evidence suggests there is an association between SHS and cardiovascular disease (CVD) risk, although the mechanisms remain poorly understood.
In a prospective study of 13,443 participants living in England and Scotland [aged 53.5, (SD 12.6 yrs), 52.3% women] we measured salivary cotinine (an objective marker of SHS exposure) and novel CVD biomarkers (C-reactive protein, fibrinogen) at baseline.
20.8% of the sample had high SHS exposure based on elevated levels of salivary cotinine (0.71 – 14.99 ng/mL). During a mean follow-up of 8 years, there were 1221 all-cause deaths and 364 CVD deaths. High SHS was associated with all-cause (age adjusted HR= 1.25, 95% CI, 1.02 – 1.53) and CVD death (age adjusted HR= 1.21, 95% CI, 0.85 – 1.73). High SHS was also associated with elevated CRP, which explained 48% of the association between SHS and CVD death. The excess risk of CVD associated with active smoking was exaggerated in relation to self report (age adjusted HR= 3.27, 95% CI, 2.48 – 4.31) compared with objective assessment (age adjusted HR= 2.44, 95% CI, 1.75 – 3.40).
Among a large representative sample of British adults we observed elevated levels of low grade inflammation in otherwise healthy participants exposed to high SHS, and this partly explained their elevated risk of CVD death.
cotinine; inflammation; nicotine; passive smoke; mortality; epidemiology
There is conflicting evidence regarding the association of hypertension with psychological distress, such as anxiety and depressive symptoms. The association may be due to a direct effect of the raised blood pressure; side effects of treatment; or the consequences of labelling. In a representative study of 33,105 adults (aged 51.7 ±12.1 yrs, 45.8% men) we measured levels of psychological distress using the 12-item General Health Questionnaire and collected blood pressure, data on history of hypertension diagnosis, and medication usage. Awareness of hypertension was confirmed through a physician’s diagnosis or the use of anti-hypertensive medication and unaware hypertension was defined by elevated clinic blood pressure (systolic/diastolic ≥140/90 mm Hg) without prior treatment or diagnosis. In comparison with normotensive participants, an elevated risk of distress (General Health Questionnaire score ≥4) was observed in aware hypertensive participants (multivariable adjusted odds ratio [OR]=1.57, 95% CI, 1.41 – 1.74), although not in unaware hypertensives (OR = 0.91, 95% CI, 0.78 – 1.07). Anti-hypertensive medication and co-morbidity was also associated with psychological distress although this did not explain the greater risk of distress in aware hypertensives. We observed a weak curvilinear association between systolic blood pressure and distress which suggested that distressed participants were more likely to have low or highly elevated blood pressure. These findings suggest that labelling individuals as hypertensive, rather than elevated blood pressure per se, may partially explain the greater levels of distress in patients treated for hypertension.
depression; anxiety; blood pressure; medication; cardiovascular risk; labelling
Tooth loss is associated with increased cardiovascular disease (CVD) mortality risk. This association may however be due to residual confounding. We aimed to assess whether tooth loss is associated with specific CVD mortality endpoints in a national population sample adjusting for potential confounders.
Methods and Results
We used a prospective cohort design and data from the Scottish Health Survey. We combined data from surveys in 1995, 1998, 2003 and linked this to mortality records. Dental status was classified through self-reports as natural teeth only, natural teeth and dentures, and no natural teeth (edentate). Cox proportional hazards models were used to estimate risk of CVD mortality by dental status adjusting for potential confounders. The sample consisted of 12871 participants. They were followed for 8.0 (SD: 3.3) years. During 103173 person-years, there were 1480 cases of all-cause mortality, 498 of CVD, and 515 of cancer. After adjusting for demographic, socio-economic, behavioural and health status, edentate subjects had significantly higher risk of all-cause (HR, 1.30; 95% CI, 1.12,1.50) and CVD mortality (HR, 1.49; 95% CI, 1.16,1.92) compared to subjects with natural teeth only. Dental status was not significantly associated with cancer mortality in fully adjusted analysis. Further analysis for CVD mortality showed that in the fully adjusted model, edentate subjects had 2.97 (95% CI, 1.46, 6.05) times higher risk for stroke-related mortality.
In a national population sample of Scottish adults, being edentate was an independent predictor of total CVD mortality, although this was mainly driven by fatal stroke events.
The Mendelian randomization approach exploits genetic variants to improve causal inference when using observational data. The authors examined the relation between long-term obesity and common mental disorders (CMD) by utilizing the known relation between fat mass and obesity-associated (FTO) genotype and body mass index (BMI; weight (kg)/height (m)2). Data collection in 2,981 men and 1,164 women (mean age at baseline = 44 years) from the Whitehall II Study (London, United Kingdom) included 4 repeated examinations of BMI and CMD over a 19-year follow-up period (1985–2004), plus an assessment of FTO polymorphism rs1421085. In men, there was an association of FTO genotype with all measures of adiposity (mean BMI, number of times obese, and, in nonobese persons, number of times overweight). FTO was also associated with CMD in men. This was independent of adiposity, thus potentially violating the exclusion restriction assumption. According to both conventional and FTO-instrumented regression analysis, measurement of obesity was associated with an increased occurrence of CMD. In the FTO-instrumented analysis only, higher BMI and overweight were also associated with CMD. In women, there was no link between FTO and adiposity. Mendelian randomization analyses supported the status of long-term obesity as a risk factor for CMD in men—a finding that should be interpreted cautiously because the function of the FTO gene is unknown.
anxiety; body mass index; depression; Mendelian randomization analysis; mental health; obesity; risk factors