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

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

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

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

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

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

Sarcopenic obesity and risk of new onset depressive symptoms in older adults: English Longitudinal Study of Ageing

Background: 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. Methods: 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 greater than or equal to4 on the 8-item Centre of Epidemiological Studies Depression scale. Sarcopenic obesity was defined as obese individuals (body mass index greater than or equal to30 kg m−2) in the lowest tertile of sex-specific grip strength (<35.3 kg men; <19.6 kg women). Results: 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. Conclusions: 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

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

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

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

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.

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