Few studies have examined both the relative magnitude of association and the discriminative capability of multiple indicators of obesity with cardiovascular disease (CVD) mortality risk. We conducted ...an individual‐participant meta‐analysis of nine cohort studies of men and women drawn from the British general population resulting in sample of 82 864 individuals. Body mass index (BMI), waist circumference (WC) and waist‐to‐hip ratio (WHR) were measured directly. There were 6641 deaths (1998 CVD) during a mean of 8.1 years of follow‐up. After adjustment, a one SD higher in WHR and WC was related to a higher risk of CVD mortality (hazard ratio 95% CI): 1.15 (1.05–1.25) and 1.15 (1.04–1.27), respectively. The risk of CVD mortality also increased linearly across quintiles of both these abdominal obesity markers with a 66% increased risk in the highest quintile of WHR. In age‐ and sex‐adjusted models only, BMI was related to CVD mortality but not in any other analyses. No major differences were revealed in the discrimination capabilities of models with BMI, WC or WHR for cardiovascular or total mortality outcomes. In conclusion, measures of abdominal adiposity, but not BMI, were related to an increased risk of CVD mortality. No difference was observed in discrimination capacities between adiposity markers.
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 cardiometabolic 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 years, 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 m(-2). Based on blood pressure, high-density lipoprotein 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% confidence interval (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.
The hypothesis of metabolically healthy obesity posits that adverse health effects of obesity are largely avoided when obesity is accompanied by a favorable metabolic profile. We tested this ...hypothesis with depressive symptoms as the outcome using cross-sectional data on obesity, metabolic health and depressive symptoms. Data were extracted from eight studies and pooled for individual-participant meta-analysis with 30,337 men and women aged 15-105 years (mean age=46.1). Clinic measures included height, weight and metabolic risk factors (high blood pressure, high triglycerides, low high-density lipoprotein cholesterol, high C-reactive protein and high glycated hemoglobin). Depressive symptoms were assessed using clinical interview or standardized rating scales. The pooled sample comprised 7673 (25%) obese participants (body mass index ⩾30 kg m(-2)). Compared to all non-obese individuals, the OR for depressive symptoms was higher in metabolically unhealthy obese individuals with two or more metabolic risk factors (1.45; 95% confidence interval (CI)=1.30, 1.61) and for metabolically healthy obese with ⩽1 metabolic risk factor (1.19; 95% CI=1.03, 1.37), adjusted for sex, age and race/ethnicity. Metabolically unhealthy obesity was associated with higher depression risk (OR=1.23; 95% CI=1.05, 1.45) compared with metabolically healthy obesity. These associations were consistent across studies with no evidence for heterogeneity in estimates (all I(2)-values<4%). In conclusion, obese persons with a favorable metabolic profile have a slightly increased risk of depressive symptoms compared with non-obese, but the risk is greater when obesity is combined with an adverse metabolic profile. These findings suggest that metabolically healthy obesity is not a completely benign condition in relation to depression risk.
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 authors aggregated the results of observational studies examining the association between long working hours and coronary heart disease (CHD). Data sources used were MEDLINE (through January 19, ...2011) and Web of Science (through March 14, 2011). Two investigators independently extracted results from eligible studies. Heterogeneity between the studies was assessed using the I(2) statistic, and the possibility of publication bias was assessed using the funnel plot and Egger's test for small-study effects. Twelve studies were identified (7 case-control, 4 prospective, and 1 cross-sectional). For a total of 22,518 participants (2,313 CHD cases), the minimally adjusted relative risk of CHD for long working hours was 1.80 (95% confidence interval (CI): 1.42, 2.29), and in the maximally (multivariate-) adjusted analysis the relative risk was 1.59 (95% CI: 1.23, 2.07). The 4 prospective studies produced a relative risk of 1.39 (95% CI: 1.12, 1.72), while the corresponding relative risk in the 7 case-control studies was 2.43 (95% CI: 1.81, 3.26). Little evidence of publication bias but relatively large heterogeneity was observed. Studies varied in size, design, measurement of exposure and outcome, and adjustments. In conclusion, results from prospective observational studies suggest an approximately 40% excess risk of CHD in employees working long hours.
We examined the role of sarcopenic obesity as a risk factor for new-onset depressive symptoms over 6-year follow-up in a large sample of older adults.
The sample comprised 3862 community dwelling ...participants (1779 men, 2083 women; mean age 64.6±8.3 years) without depressive symptoms at baseline, recruited from the English Longitudinal Study of Ageing. At baseline and 4-year follow-up, handgrip strength (kg) of the dominant hand was assessed using a hand-held dynamometer, as a measure of sarcopenia. The outcome was new onset depressive symptoms at 6-year follow-up, defined as a score of ⩾4 on the 8-item Centre of Epidemiological Studies Depression scale. Sarcopenic obesity was defined as obese individuals (body mass index ⩾30 kg m(-)(2)) in the lowest tertile of sex-specific grip strength (<35.3 kg men; <19.6 kg women).
Using a multivariable logistic regression model, the risk of depressive symptoms was greatest in obese adults in the lowest tertile of handgrip strength (odds ratio (OR), 1.79, 95% confidence interval (CI), 1.10, 2.89) compared with non-obese individuals with high handgrip strength. Participants who were obese at baseline and had a decrease of more than 1 s.d. in grip strength over 4-year follow-up were at greatest risk of depressive symptoms (OR=1.97, 95% CI, 1.22, 3.17) compared with non-obese with stable grip strength.
A reduction in grip strength was associated with higher risk of depressive symptoms in obese participants only, suggesting that sarcopenic obesity is a risk factor for depressive symptoms.
High levels of excess mortality (i.e. that not explained by deprivation) have been observed for Scotland compared with England & Wales, and especially for Glasgow in comparison with similar ...post-industrial cities such as Liverpool and Manchester. Many potential explanations have been suggested. Based on an assessment of these, the aim was to develop an understanding of the most likely underlying causes.
Note that this paper distils a larger research report, with the aim of reaching wider audiences beyond Scotland, as the important lessons learnt are relevant to other populations.
Review and dialectical synthesis of evidence.
Forty hypotheses were examined, including those identified from a systematic review. The relevance of each was assessed by means of Bradford Hill's criteria for causality alongside—for hypotheses deemed causally linked to mortality—comparisons of exposures between Glasgow and Liverpool/Manchester, and between Scotland and the rest of Great Britain. Where gaps in the evidence base were identified, new research was undertaken. Causal chains of relevant hypotheses were created, each tested in terms of its ability to explain the many different aspects of excess mortality. The models were further tested with key informants from public health and other disciplines.
In Glasgow's case, the city was made more vulnerable to important socioeconomic (deprivation, deindustrialisation) and political (detrimental economic and social policies) exposures, resulting in worse outcomes. This vulnerability was generated by a series of historical factors, processes and decisions: the lagged effects of historical overcrowding; post-war regional policy including the socially selective relocation of population to outside the city; more detrimental processes of urban change which impacted on living conditions; and differences in local government responses to UK government policy in the 1980s which both impacted in negative terms in Glasgow and also conferred protective effects on comparator cities. Further resulting protective factors were identified (e.g. greater ‘social capital’ in Liverpool) which placed Glasgow at a further relative disadvantage. Other contributory factors were highlighted, including the inadequate measurement of deprivation.
A similar ‘explanatory model’ resulted for Scotland as a whole. This included: the components of the Glasgow model, given their impact on nationally measured outcomes; inadequate measurement of deprivation; the lagged effects of deprivation (in particular higher levels of overcrowding historically); and additional key vulnerabilities.
The work has helped to further understanding of the underlying causes of Glasgow's and Scotland's high levels of excess mortality. The implications for policy include the need to address three issues simultaneously: to protect against key exposures (e.g. poverty) which impact detrimentally across all parts of the UK; to address the existing consequences of Glasgow's and Scotland's vulnerability; and to mitigate against the effects of future vulnerabilities which are likely to emerge from policy responses to contemporary problems which fail sufficiently to consider and to prevent long-term, unintended social consequences.
•High levels of excess mortality in Scotland & Glasgow compared with elsewhere in UK.•We investigate 40 previously proposed hypotheses to identify the underlying causes.•Glasgow made more vulnerable to key socio-economic and political exposures.•Vulnerability caused by a series of adverse historical factors and decisions.•Findings re-emphasise the importance of political economy for population health.
Anecdotal and biographical reports have long suggested that bipolar disorder is more common in people with exceptional cognitive or creative ability. Epidemiological evidence for such a link is ...sparse. We investigated the relationship between intelligence and subsequent risk of hospitalisation for bipolar disorder in a prospective cohort study of 1,049,607 Swedish men. Intelligence was measured on conscription for military service at a mean age of 18.3 years and data on psychiatric hospital admissions over a mean follow-up period of 22.6 years was obtained from national records. Risk of hospitalisation with any form of bipolar disorder fell in a stepwise manner as intelligence increased (P for linear trend <0.0001). However, when we restricted analyses to men with no psychiatric comorbidity, there was a 'reversed-J' shaped association: men with the lowest intelligence had the greatest risk of being admitted with pure bipolar disorder, but risk was also elevated among men with the highest intelligence (P for quadratic trend=0.03), primarily in those with the highest verbal (P for quadratic trend=0.009) or technical ability (P for quadratic trend <0.0001). At least in men, high intelligence may indeed be a risk factor for bipolar disorder, but only in the minority of cases who have the disorder in a pure form with no psychiatric comorbidity.
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