Effect of secular trends on age-related trajectories of cardiovascular risk factors: the Whitehall II longitudinal study 1985-2009

Secular trends in cardiovascular risk factors have been described, but few studies have examined simultaneously the effects of both ageing and secular trends within the same cohort

Heart Rate and Heart Rate Variability Changes Are Not Related to Future Cardiovascular Disease and Death in People With and Without Dysglycemia: A Downfall of Risk Markers? The Whitehall II Cohort Study

OBJECTIVE: Higher resting heart rate (rHR) and lower heart rate variability (HRV) are associated with increased risk of cardiovascular disease (CVD) and all-cause mortality in people with and without diabetes. It is unknown whether temporal changes in rHR and HRV may contribute to this risk. We investigated associations between 5-year changes in rHR and HRV and risk of future CVD and death, taking into account participants' baseline glycemic state. RESEARCH DESIGN AND METHODS: In this prospective, population-based cohort study we investigated 4,611 CVD-free civil servants (mean [SD] age, 60 [5.9] years; 70% men). We measured rHR and/or six indices of HRV. Associations of 5-year change in 5-min rHR and HRV with fatal and nonfatal CVD and all-cause mortality or the composite of the two were assessed, with adjustments made for relevant confounders. Effect modification by glycemic state was tested. RESULTS: At baseline, 63% of participants were normoglycemic, 29% had prediabetes, and 8% had diabetes. During a median (interquartile range) follow-up of 11.9 (11.4; 12.3) years, 298 participants (6.5%) experienced a CVD event and 279 (6.1%) died of non-CVD-related causes. We found no association between 5-year changes in rHR and HRV and future events. Only baseline rHR was associated with all-cause mortality. A 10 bpm-higher baseline HR level was associated with a 11.4% higher rate of all-cause mortality (95% CI 1.0-22.9%; P = 0.032). Glycemic state did not modify associations. CONCLUSIONS: Changes in rHR and HRV and possibly also baseline values of these measures are not associated with future CVD or death in people with or without dysglycemia

Workplace bullying and the risk of cardiovascular disease and depression.

Occup Environ Med Aims: To examine exposure to workplace bullying as a risk factor for cardiovascular disease and depression in employees. Methods: Logistic regression models were related to prospective data from two surveys in a cohort of 5432 hospital employees (601 men and 4831 women), aged 18-63 years. Outcomes were new reports of doctor diagnosed cardiovascular disease and depression during the two year follow up among those who were free from these diseases at baseline. Results: The prevalence of bullying was 5% in the first survey and 6% in the second survey. Two per cent reported bullying experiences in both surveys, an indication of prolonged bullying. After adjustment for sex, age, and income, the odds ratio of incident cardiovascular disease for victims of prolonged bullying compared to non-bullied employees was 2.3 (95% CI 1.2 to 4.6). A further adjustment for overweight at baseline attenuated the odds ratio to 1.6 (95% CI 0.8 to 3.5). The association between prolonged bullying and incident depression was significant, even after these adjustments (odds ratio 4.2, 95% CI 2.0 to 8.6). Conclusions: A strong association between workplace bullying and subsequent depression suggests that bullying is an aetiological factor for mental health problems. The victims of bullying also seem to be at greater risk of cardiovascular disease, but this risk may partly be attributable to overweight. N o generally accepted definition of workplace bullying exists, but most definitions refer to aspects such as the persistence of bullying and the negative or detrimental effects perceived by the victim. 1 Examples of bullying include situations in which someone is subjected to social isolation or exclusion, the subject's work and work efforts are devalued, and the subject is threatened or otherwise worn down or frustrated. Thus, victimisation to workplace bullying may represent a social stressor related to a serious deficiency in perceived organisational justice and fairness. 2 7-9 However, the question whether workplace bullying predicts the onset of illness, such as cardiovascular disease and depression, has awaited longitudinal testing. Stress can contribute to the development of disease. Chronic overactivity or underactivity in cardiovascular and metabolic systems in relation to prolonged stress has been found to be an aetiological factor for cardiovascular disease and hypertension. 13 When representing a major chronic stressor, workplace bullying can be hypothesised to increase the victims' vulnerability to these stress related diseases. Testing this hypothesis requires repeated measurements of victimisation for the establishment of continuous bullying, a measurement strategy that has not been applied in prior occupational studies. We carried out a prospective study to examine whether exposure to workplace bullying is associated with new reports of cardiovascular disease and depression among hospital personnel. The study data on prolonged exposure to bullying were based on two surveys over two years. METHODS Study population A postal questionnaire was sent to all 10 969 employees (1712 men and 9257 women) aged 18-63 years, working in Finnish hospitals in 1998. Ten per cent of the employees were doctors, 47% nurses, 12% laboratory and x ray department staff, 12% administrative staff, and 19% maintenance, cleaners, and other workers. Respondents who were still working in the hospitals two years later, were sent a follow up questionnaire in 2000. The surveys gathered information on bullying, stress related diseases, and behavioural risks on both occasions. The approval of the Ethics Committee of the Finnish Institute of Occupational Health was obtained for the study. Measures Bullying was measured by the following question: ''Workplace bullying refers to a situation where someone is subjected to social isolation or exclusion, his or her work and efforts are devalued, he or she is threatened, derogatory comments are made about him or her in his or her absence, or other negative behaviour that is aimed to torment, wear down, or frustrate the victim occur. Have you been subjected to such bullying? ''. 5 Cardiovascular disease and depression were measured using a self administered checklist of common chronic diseases. 14 For each disease, the respondent was requested to indicate whether or not a medical doctor had diagnosed him or her as having the disease. Cardiovascular disease was identified if the respondent reported myocardial infarction, angina pectoris, cerebrovascular disease, or hypertension. Depression was identified if the respondent reported that a medical doctor had diagnosed him or her as having depression. Incident cases of cardiovascular disease and Other variables were: smoking (smoker versus nonsmoker, and the number of cigarettes smoked per day); alcohol consumption in grams of absolute alcohol per average week (cut offs for high consumption 280 and 190 g for men and women, respectively); weight and height for the calculation of body mass index (overweight indicated by BMI .29 kg/m 2 ); and demographics (sex, age, occupation, income, and job contract (permanent versus temporary) obtained from the employers' records). Statistical analysis We used logistic regression analysis to test predictive relations of bullying to cardiovascular disease and depression. The first step tested reversed causality. Baseline diseases and other baseline characteristics were set as predictors for incident caseness of bullying (bullied in the second survey) among employees who did not report being bullied at baseline. The second step examined whether prolonged bullying predicted incidence of cardiovascular disease and depression. Three exposure groups were formed: employees not reporting bullying in the first survey and in the second survey (the control group); employees who reported victimisation either in the first survey or the second survey (but not both); and victims of prolonged bullying (reporting victimisation in both surveys). Those with baseline diseases were excluded. Odds ratios and 95% confidence intervals (CI) for new cardiovascular disease and depression in the second survey were adjusted for sex, five year age categories, and income tertiles (calculated separately for men and women). The third step reported logistic models where the associations of bullying with cardiovascular disease and depression were additionally adjusted for those behavioural risk factors that showed significant differences between the levels of bullying. Finally, interactions between these behavioural risks and bullying on cardiovascular disease and depression were studied. All analyses were conducted using the SPSS 9.0 software package. RESULTS Response rates and sample attrition A total of 8104 employees (74%) responded to the first survey. The mean age of the respondents was 43.3 years, 88% were women, 77% had a permanent job contract, and the mean income was 1849 per month. The corresponding figures for the eligible population were 42.9 years, 84%, 75%, and 1884 per month, respectively. Thus, any differences between the respondents and all eligible employees were small. Of respondents to the first survey, 6674 were working in the target hospitals two years later at the time of the second survey. Of the 6674 eligible respondents of the first survey, 5432 (81%) responded to the second survey. Female, high income, non-depressive, and permanent employees were slightly overrepresented Reversed causality The prevalence of reported bullying was 5.2% in the first survey and 5.9% in the second survey. Bullying as a predictor of new disease Of the respondents, 1.7% reported bullying experiences in both surveys. As table 3 shows, prolonged bullying was associated with the onset of cardiovascular disease and depression. After adjustment for sex, age, and income, the odds ratio of incident cardiovascular disease for prolonged bullying, compared with no bullying, was 2.3. The corresponding odds ratio of new physician diagnosed depression was 4.8. For those who reported bullying only in one of the two surveys, the odds ratio of depression was 2.3. The role of behavioural risk factors Of the behavioural risk factors, overweight predicted the onset of new cardiovascular disease (OR 2.95, 95% CI 2.20 to 3.95). Smoking and high alcohol consumption at baseline were associated with an increased risk of depression (ORs 1.54 (95% CI 1.08 to 2.21) and 1.53 (95% CI 1.00 to 2.34), respectively). Examination of whether bullying contributes to behavioural risk factors shows that prolonged bullying, compared with no bullying, did not predict subsequent smoking (baseline adjusted OR 0.64, 95% CI 0.19 to 2.19), heavy alcohol consumption (OR 1.06, 95% CI 0.46 to 2.46), or overweight (OR 0.64, 95% CI 0.25 to 1.64). However, individuals who were bullied at both times were more often overweight at baseline than non-victims (OR 2.04, 95% CI 1.20 to 3.46). Adjustment for overweight in addition to demographic factors attenuated the association between bullying and new cardiovascular disease (OR 1.62, 95% CI 0.75 to 3.50 for bullying at both times versus at neither time), but did not affect the association between bullying and depression (OR 4.16, 95% CI 2.01 to 8.63). Interactions between bullying and overweight were not significant for cardiovascular disease (p = 0.902) and depression (p = 0.174). Main messages N There is a strong association between workplace bullying and subsequent depression. Exposure to bullying predicts the onset of depression in a doseresponse gradient. N There is also an association between bullying and incidence of cardiovascular disease. However, this association may partly be attributable to obesity. Policy implications N Evidence of depression implies that the problem of workplace bullying should be effectively treated in workplaces. N Early identification and prevention of workplace bullying may be a key factor in attempts to minimise its adverse effects on mental health

Parametric hazard rate models for long-term sickness absence

PURPOSE: In research on the time to onset of sickness absence and the duration of sickness absence episodes, Cox proportional hazard models are in common use. However, parametric models are to be preferred when time in itself is considered as independent variable. This study compares parametric hazard rate models for the onset of long-term sickness absence and return to work. METHOD: Prospective cohort study on sickness absence with four follow-up years of 53,830 employees working in the private sector in the Netherlands. The time to onset of long-term (>6 weeks) sickness absence and return to work were modelled by parametric hazard rate models. RESULTS: The exponential parametric model with a constant hazard rate most accurately described the time to onset of long-term sickness absence. Gompertz-Makeham models with monotonically declining hazard rates best described return to work. CONCLUSIONS: Parametric models offer more possibilities than commonly used models for time-dependent processes as sickness absence and return to work. However, the advantages of parametric models above Cox models apply mainly for return to work and less for onset of long-term sickness absence

Estimating sleep parameters using an accelerometer without sleep diary

This is the final version. Available from the publisher via the DOI in this record.Wrist worn raw-data accelerometers are used increasingly in large-scale population research. We examined whether sleep parameters can be estimated from these data in the absence of sleep diaries. Our heuristic algorithm uses the variance in estimated z-axis angle and makes basic assumptions about sleep interruptions. Detected sleep period time window (SPT-window) was compared against sleep diary in 3752 participants (range = 60–82 years) and polysomnography in sleep clinic patients (N = 28) and in healthy good sleepers (N = 22). The SPT-window derived from the algorithm was 10.9 and 2.9 minutes longer compared with sleep diary in men and women, respectively. Mean C-statistic to detect the SPT-window compared to polysomnography was 0.86 and 0.83 in clinic-based and healthy sleepers, respectively. We demonstrated the accuracy of our algorithm to detect the SPT-window. The value of this algorithm lies in studies such as UK Biobank where a sleep diary was not used.Medical Research Council (MRC)National Institute of Health (NIH

Reversion from prediabetes to normoglycaemia and risk of cardiovascular disease and mortality: the Whitehall II cohort study

AIMS/HYPOTHESIS: Reversion from prediabetes to normoglycaemia is accompanied by an improvement in cardiovascular risk factors, but it is unclear whether this translates into a reduction in risk of cardiovascular disease (CVD) events or death. Hence, we studied the probability of reversion from prediabetes to normoglycaemia and the associated risk of future CVD and death using data from the Whitehall II observational cohort study. METHODS: Three glycaemic criteria for prediabetes (fasting plasma glucose [FPG] 5.6-6.9 mmol/l, 2 h plasma glucose [2hPG] 7.8-11.0 mmol/l, and HbA1c 39-47 mmol/mol [5.7-6.4%]) were assessed in 2002-2004 and 2007-2009 for 5193 participants free of known diabetes at enrolment. Among participants with prediabetes in the first examination, we calculated the probability of reversion to normoglycaemia by re-examination according to each glycaemic criterion. Poisson regression analysis was used to estimate and compare incidence rates of a composite endpoint of a CVD event or death in participants with prediabetes who did vs did not revert to normoglycaemia. Analyses were adjusted for age, sex, ethnicity and previous CVD. RESULTS: Based on the FPG criterion, 820 participants had prediabetes and 365 (45%) of them had reverted to normoglycaemia in 5 years. The corresponding numbers were 324 and 120 (37%) for the 2hPG criterion and 1709 and 297 (17%) for the HbA1c criterion. During a median follow-up of 6.7 (interquartile range 6.3-7.2) years, 668 events of non-fatal CVD or death occurred among the 5193 participants. Reverting from 2hPG-defined prediabetes to normoglycaemia vs remaining prediabetic or progressing to diabetes was associated with a halving in event rate (12.7 vs 29.1 per 1000 person-years, p = 0.020). No association with event rate was observed for reverting from FPG-defined (18.6 vs 18.2 per 1000 person-years, p = 0.910) or HbA1c-defined prediabetes to normoglycaemia (24.5 vs 22.9 per 1000 person-years, p = 0.962). CONCLUSIONS/INTERPRETATION: Most people with HbA1c-defined prediabetes remained prediabetic or progressed to diabetes during 5 years of follow-up. In contrast, reversion to normoglycaemia was frequent among people with FPG- or 2hPG-defined prediabetes. Only reversion from 2hPG-defined prediabetes to normoglycaemia was associated with a reduction in future risk of CVD and death

Determinants of aortic stiffness: 16-year follow-up of the Whitehall II study.

Aortic stiffness is a strong predictor of cardiovascular disease endpoints. Cross-sectional studies have shown associations of various cardiovascular risk factors with aortic pulse wave velocity, a measure of aortic stiffness, but the long-term impact of these factors on aortic stiffness is unknown

Healthy obesity and risk of accelerated functional decline and disability

BACKGROUND/OBJECTIVES: Some obese adults have a normal metabolic profile and are considered 'healthy', but whether they experience faster ageing than healthy normal-weight adults is unknown. We compared decline in physical function, worsening of bodily pain, and likelihood of future mobility limitation and disability between these groups. SUBJECTS/METHODS: This was a population-based observational study using repeated measures over 2 decades (Whitehall II cohort data). Normal-weight (body mass index (BMI) 18.5-24.9 kg/m(2)), overweight (25.0-29.9 kg/m(2)), and obese (⩾30.0 kg/m(2)) adults were considered metabolically healthy if they had 0 or 1 of 5 risk factors (hypertension, low high-density lipoprotein cholesterol, high triacylglycerol, high blood glucose, and insulin resistance) in 1991/94. Decline in physical function and worsening of bodily pain based on change in Short Form Health Survey items using 8 repeated measures over 18.8 years (1991/94-2012/13) was compared between metabolic-BMI groups using linear mixed models. Odds of mobility limitation based on objective walking speed (slowest tertile) and of disability based on limitations in ⩾1 of 6 basic activities of daily living, each using 3 repeated measures over 8.3 years (2002/04-2012/13), were compared using logistic mixed models. RESULTS: In multivariable-adjusted mixed models on up to 6635 adults (initial mean age 50 years; 70% male), healthy normal-weight adults experienced a decline in physical function of -3.68 (95% CI=-4.19, -3.16) score units per decade; healthy obese adults showed an additional -3.48 (-4.88, -2.08) units decline. Healthy normal-weight adults experienced a -0.49 (-0.12, 1.11) score unit worsening of bodily pain per decade; healthy obese adults had an additional -2.23 (-0.69, -3.78) units worsening. Healthy obesity versus healthy normal-weight conferred 3.39 (2.29, 5.02) times higher odds of mobility limitation and 3.75 (1.94, 7.24) times higher odds of disability. CONCLUSIONS: Our results suggest that obesity, even if metabolically healthy, accelerates age-related declines in functional ability and poses a threat to independence in older age.International Journal of Obesity accepted article preview online, 21 February 2017. doi:10.1038/ijo.2017.51

Modifiable cardiovascular disease risk factors as predictors of dementia death: pooling of ten general population-based cohort studies

Background: With drug treatment for dementia being of limited effectiveness, the role of primary prevention, in particular the predictive value of modifiable cardiovascular disease risk factors, may warrant exploration. The evidence base is, however, characterised by discordant findings and is modest in size. Accordingly, we examined the association of modifiable cardiovascular disease risk factors with dementia death. / Design and methods: We pooled raw data from 10 UK general population-based prospective cohort studies within the context of an individual participant meta-analysis. / Results: A total of 103,764 men and women were followed up for a mean of 8 years giving rise to 443 dementia-related deaths and 2612 cardiovascular disease deaths. Cardiovascular disease mortality was, as anticipated, associated with the full range of risk factors under study, including raised blood pressure, smoking, diabetes, physical inactivity. By contrast, dementia death was related to very few of the cardiovascular disease risk factors: of those classified as modifiable, only smoking was associated with a raised risk and higher levels of non-HDL with a lower risk. / Conclusions: In the present individual participant meta-analysis, there was limited evidence that cardiovascular disease risk factors were related to dementia death

Endothelial Function: The Impact of Objective and Subjective Socioeconomic Status on Flow-Mediated Dilation

Although objective and subjective indicators of socioeconomic status (SES) are linked to cardiovascular disease (CVD), little is known about their relationship to endothelial dysfunction, which often precedes CVD. This study examined how objective and subjective SES relate to brachial artery flow-mediated dilation (FMD). FMD was assessed in 72 healthy adults (mean age 36 years). The MacArthur Scale of Subjective Social Status assessed perceived social standing in the USA (SSS-USA) and local community (SSS-Community). Objective SES measures included income and the Hollingshead Two-Factor Index of Social Position (education, occupation). Adjusted regressions revealed that SSS-Community positively correlated with FMD (p < 0.05) and explained 8% of the variance. No other SES measures were significant for FMD. The association between FMD and SSS-Community remained significant (p < 0.01) after adjustment for objective SES and other covariates. Lower subjective social status in one’s community may be linked to CVD via impaired vasodilation