106 research outputs found

    Longitudinal patterns in physical activity and sedentary behaviour from mid-life to early old age: a substudy of the Whitehall II cohort

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    Background 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. Methods 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 891668 min/day). Results 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 (2.0e16.0) 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. Conclusion 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

    Obesity, metabolic health, and history of Cytomegalovirus infection in the general population

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    Context:Commoncommunity-acquired infections, such as cytomegalovirus (CMV),maycontribute to the development of obesity and metabolic dysfunction, but empirical evidence is scarce. Objective: We examined the associations between CMV, obesity and metabolic characteristics in a large, general population-based sample of adults. Design and setting: An observational study in community dwelling adults from the general population, ‘Understanding Society – the UK Household Longitudinal Study’. Participants: 9,517 men and women (aged 52.4 ± 16.4 yrs; 55.3% female). Measures: CMV infection was measured using Immunoglobulin G (IgG) from serum. Obesity was defined as body mass index ≥30 kg/m2. Based on blood pressure, HDL-cholesterol, triglycerides,glycated haemoglobin A1c, and C-reactive protein, participants were classified as ‘healthy’ (0 or 1 metabolic abnormality) or ‘unhealthy’ (≥2 metabolic abnormalities). Results: A positive CMV test was recorded in 47.5% of the sample. There was no association between CMV and obesity. Of the individual metabolic risk factors, CMV was positively associated with glycated haemoglobin and HDL-cholesterol. In combination, only ‘unhealthy non-obese’ participants had modestly increased odds of CMV (odds ratio compared to healthy normal weight = 1.12, 95% confidence interval 1.00 – 1.26) after adjusting for a range of variables. CMV was associated with an increased prevalence of cardiovascular diseases (odds ratio=1.67; 1.07 – 2.60) independently of obesity, metabolic risk factors, and other covariates. Conclusion: Our findings suggest a weak but statistically significant association between CMV and metabolic dysfunction in non-obese adults. This relationship appears to be masked in the obese, possibly by the effects of excess adiposity on metabolism

    Pulse rate reactivity in childhood as a risk factor for adult hypertension: the 1970 Birth Cohort Study

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    Purpose: Cardiovascular reactivity to mental stress has been used as a tool to predict short-term hypertension risk in adults but the impact of cardiovascular reactivity in childhood on hypertension in adulthood is unknown. Using the 1970 British Cohort study, we examined the association between pulse rate reactivity in childhood and risk of hypertension in adulthood. Methods: A total of 6,507 participants (51.6% female) underwent clinical examination at 10 years of age that involved measurement of blood pressure, body mass index, and pulse rate pre- and post-examination. Hypertension was ascertained by self-reported doctor diagnosis 32 years later at age 42. Results: On average, there was a reduction in pulse rate after the medical examination (-1.2±8.2 bpm), although nearly a third of the sample recorded an increase in pulse rate of ≥3bpm. A total of 488 (7.5%) study members developed hypertension at follow-up. After adjustment for a range of covariates including resting blood pressure and body mass index in childhood, a heightened pulse rate response to the examination (≥3bpm) was associated with greater risk of hypertension in adulthood (odds ratio = 1.30, 95% CI, 1.02, 1.67). The association persisted whether we modelled pulse rate as an absolute measure (post examination) or a change score. Conclusion: These observational data suggest that elevated childhood cardiovascular reactivity could increase risk for hypertension in adulthood

    Pulse rate reactivity in childhood as a risk factor for adult hypertension: the 1970 Birth Cohort Study

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    Purpose: Cardiovascular reactivity to mental stress has been used as a tool to predict short-term hypertension risk in adults but the impact of cardiovascular reactivity in childhood on hypertension in adulthood is unknown. Using the 1970 British Cohort study, we examined the association between pulse rate reactivity in childhood and risk of hypertension in adulthood. Methods: A total of 6,507 participants (51.6% female) underwent clinical examination at 10 years of age that involved measurement of blood pressure, body mass index, and pulse rate pre- and post-examination. Hypertension was ascertained by self-reported doctor diagnosis 32 years later at age 42. Results: On average, there was a reduction in pulse rate after the medical examination (-1.2±8.2 bpm), although nearly a third of the sample recorded an increase in pulse rate of ≥3bpm. A total of 488 (7.5%) study members developed hypertension at follow-up. After adjustment for a range of covariates including resting blood pressure and body mass index in childhood, a heightened pulse rate response to the examination (≥3bpm) was associated with greater risk of hypertension in adulthood (odds ratio = 1.30, 95% CI, 1.02, 1.67). The association persisted whether we modelled pulse rate as an absolute measure (post examination) or a change score. Conclusion: These observational data suggest that elevated childhood cardiovascular reactivity could increase risk for hypertension in adulthood

    Metabolically healthy obesity and risk of incident type 2 diabetes: a meta-analysis of prospective cohort studies

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    The risk of type 2 diabetes among obese adults who are metabolically healthy has not been established. We systematically searched Medline (1946–August 2013) and Embase (1947–August 2013) for prospective studies of type 2 diabetes incidence (defined by blood glucose levels or self-report) among metabolically healthy obese adults (defined by body mass index [BMI] and normal cardiometabolic clustering, insulin profile or risk score) aged ≥18 years at baseline. We supplemented the analysis with an original effect estimate from the English Longitudinal Study of Ageing (ELSA), with metabolically healthy obesity defined as BMI ≥ 30 kg m−2 and <2 of hypertension, impaired glycaemic control, systemic inflammation, adverse high-density lipoprotein cholesterol and adverse triglycerides. Estimates from seven published studies and ELSA were pooled using random effects meta-analyses (1,770 healthy obese participants; 98 type 2 diabetes cases). The pooled adjusted relative risk (RR) for incident type 2 diabetes was 4.03 (95% confidence interval = 2.66–6.09) in healthy obese adults and 8.93 (6.86–11.62) in unhealthy obese compared with healthy normal-weight adults. Although there was between-study heterogeneity in the size of effects (I2 = 49.8%; P = 0.03), RR for healthy obesity exceeded one in every study, indicating a consistently increased risk across study populations. Metabolically healthy obese adults show a substantially increased risk of developing type 2 diabetes compared with metabolically healthy normal-weight adults. Prospective evidence does not indicate that healthy obesity is a harmless condition

    Long working hours, socioeconomic status, and the risk of incident type 2 diabetes: a meta-analysis of published and unpublished data from 222 120 individuals

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    Background Working long hours might have adverse health effects, but whether this is true for all socioeconomic status groups is unclear. In this meta-analysis stratified by socioeconomic status, we investigated the role of long working hours as a risk factor for type 2 diabetes. Methods We identified four published studies through a systematic literature search of PubMed and Embase up to April 30, 2014. Study inclusion criteria were English-language publication; prospective design (cohort study); investigation of the effect of working hours or overtime work; incident diabetes as an outcome; and relative risks, odds ratios, or hazard ratios (HRs) with 95% CIs, or sufficient information to calculate these estimates. Additionally, we used unpublished individual-level data from 19 cohort studies from the Individual-Participant-Data Meta-analysis in Working-Populations Consortium and international open-access data archives. Effect estimates from published and unpublished data from 222 120 men and women from the USA, Europe, Japan, and Australia were pooled with random-effects meta-analysis. Findings During 1·7 million person-years at risk, 4963 individuals developed diabetes (incidence 29 per 10 000 personyears). The minimally adjusted summary risk ratio for long (≥55 h per week) compared with standard working hours (35–40 h) was 1·07 (95% CI 0·89–1·27, difference in incidence three cases per 10 000 person-years) with signifi cant heterogeneity in study-specific estimates (I²=53%, p=0·0016). In an analysis stratified by socioeconomic status, the association between long working hours and diabetes was evident in the low socioeconomic status group (risk ratio 1·29, 95% CI 1·06–1·57, diff erence in incidence 13 per 10 000 person-years, I²=0%, p=0·4662), but was null in the high socioeconomic status group (1·00, 95% CI 0·80–1·25, incidence diff erence zero per 10 000 person-years, I²=15%, p=0·2464). The association in the low socioeconomic status group was robust to adjustment for age, sex, obesity, and physical activity, and remained after exclusion of shift workers. Interpretation In this meta-analysis, the link between longer working hours and type 2 diabetes was apparent only in individuals in the low socioeconomic status groups

    Psychological distress as a risk factor for death from cerebrovascular disease

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    Background: 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. Methods: 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. Results: 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 disress (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. Interpretation: 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

    Psychological distress and infectious disease mortality in the general population

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    There is a paucity of studies examining the relation between high psychological distress and infectious disease in the general population. We examined this association in a large multi-cohort study drawn from the general population. The analytic sample comprised 104,923 men and women (age, 47.3 ± 17.4 year; 45.7% men) in which psychological distress symptoms was assessed using the 12-item version of the General Health Questionnaire. There were 1535 deaths attributed to infectious diseases during 971,220 person-years of follow up (mean 9.3; range 0.1–17.1 years). A dose-response association between GHQ-12 score and all infectious disease mortality was observed after adjusting for age, sex, survey year, occupational social class, longstanding illness, smoking, alcohol, and physical activity (per SD increase, hazard ratio = 1.24; 95% CI, 1.20–1.28). A similar pattern was apparent for viral infections (1.23; 1.14, 1.33) and pneumonia (1.20; 1.13, 1.28), but weaker for bacterial infections (1.09; 1.00, 1.19). In conclusion, psychological distress is associated with higher risk of infectious disease

    Stability of metabolically healthy obesity over 8 years: the English Longitudinal Study of Ageing.

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    Objective Metabolically healthy obesity possibly reflects a transitional stage before the onset of metabolic dysfunction, but few studies have characterised this transition. We examined the behavioural and biological characteristics of healthy obese adults that progressed to an unhealthy state over 8 years follow-up. Methods Participants were 2422 men and women (aged 63.3±7.7 years, 44.2% men) from the English Longitudinal Study of Ageing. Obesity was defined as BMI ≥30 kg/m2. Based on blood pressure (BP), HDL-cholesterol, triglycerides, HbA1c and C-reactive protein (CRP) participants were classified as ‘healthy’ (0 or 1 metabolic abnormality) or ‘unhealthy’ (≥2 metabolic abnormalities). Results Over 8 years follow-up, 44.5% of healthy obese subjects had transitioned into an unhealthy state, compared to only 16.6 and 26.2% of healthy normal-weight and overweight adults respectively. Compared with healthy obese adults who remained stable, those who progressed to an unhealthy state were more likely to have high BP (75.0% vs 37.0%, age- and sex-adjusted odds ratio (OR) 8.9, 95% CI 4.7–17.0), high CRP (53.7% vs 17.0%, OR=8.6, 95% CI 4.1–18.0), high HbA1c (46.3% vs 5.9%, OR=13.8, 95% CI 6.1–31.2) and high triglycerides (45.4% vs 11.9%, OR=5.9, 95% CI 2.9–12.0) at follow-up, with excess risk remaining independent of lifestyle factors including self-reported physical activity. Progression to an unhealthy state was also linked with significant gains in waist circumference (B=2.7, 95% CI, 0.5–4.9 cm). Conclusion These data show that a healthy obesity phenotype is relatively unstable. Transition to an unhealthy state is characterised by multiple biological changes that are not fully explained by lifestyle risk factors

    Combined effect of physical activity and leisure time sitting on long-term risk of incident obesity and metabolic risk factor clustering

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    Aims/hypothesis Our study aimed to investigate the combined effects of moderate-to-vigorous physical activity and leisure time sitting on the long-term risk of obesity and clustering of metabolic risk factors. Methods The duration of moderate and vigorous physical activity and of leisure time sitting was assessed by questionnaire between 1997 and 1999 among 3,670 participants from the Whitehall II cohort study (73% male; mean age 56 years). Multivariable-adjusted logistic regression models examined associations of physical activity and leisure time sitting tertiles with odds of incident obesity (BMI ≥ 30 kg/m2) and incident metabolic risk factor clustering (two or more of the following: low HDL-cholesterol, high triacylglycerol, hypertension, hyperglycaemia, insulin resistance) at 5 and 10 year follow-ups. Results Physical activity, but not leisure time sitting, was associated with incident obesity. The lowest odds of incident obesity after 5 years were observed for individuals reporting both high physical activity and low leisure time sitting (OR = 0.26; 95% CI 0.11, 0.64), with weaker effects after 10 years. Compared with individuals in the low physical activity/high leisure time sitting group, those with intermediate levels of both physical activity and leisure time sitting had lower odds of incident metabolic risk factor clustering after 5 years (OR 0.53; 95% CI 0.36, 0.78), with similar odds after 10 years. Conclusions/interpretation Both high levels of physical activity and low levels of leisure time sitting may be required to substantially reduce the risk of obesity. Associations with developing metabolic risk factor clustering were less clear
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