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

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

Association of objectively measured physical activity with brain structure: UK Biobank study

Background Physical activity may be beneficial for cognition but mechanisms are unclear. We examined the association between objectively assessed physical activity and brain volume, with a focus on the hippocampus region. Methods We used data from UK Biobank (n=5,272; aged 55.4±7.5 yrs; 45.6% men) collected through 2013‐2016. Participants wore the Axivity AX3 wrist‐worn triaxial accelerometer for seven days to assess habitual physical activity. Structural magnetic resonance imaging was performed using a standard Siemens Skyra 3T running VD13A SP4 to obtain images of the brain. Results There was an association between physical activity (per SD increase) and grey matter volume after adjustment for a range of covariates, although this association was only detected in older adults (>60 yrs old). We also observed associations of physical activity with both left (B=0.52, 95% CI, 0.01, 1.03; p=0.046) and right hippocampal volume (B=0.59, 95% CI, 0.08, 1.10; p=0.024) in covariate adjusted models. Conclusion In summary, physical activity may play a role in the prevention of neurodegenerative diseases

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

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

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

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

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

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

Overweight, obesity and risk of cardiometabolic multimorbidity: pooled analysis of individual-level data for 120,813 adults from 16 cohort studies from the USA and Europe

Background Although overweight and obesity have been studied in relation to individual cardiometabolic diseases, their association with risk of cardiometabolic multimorbidity is poorly understood. Here we aimed to establish the risk of incident cardiometabolic multimorbidity (ie, at least two from: type 2 diabetes, coronary heart disease, and stroke) in adults who are overweight and obese compared with those who are a healthy weight. Methods We pooled individual-participant data for BMI and incident cardiometabolic multimorbidity from 16 prospective cohort studies from the USA and Europe. Participants included in the analyses were 35 years or older and had data available for BMI at baseline and for type 2 diabetes, coronary heart disease, and stroke at baseline and follow-up. We excluded participants with a diagnosis of diabetes, coronary heart disease, or stroke at or before study baseline. According to WHO recommendations, we classified BMI into categories of healthy (20·0–24·9 kg/m²), overweight (25·0–29·9 kg/m²), class I (mild) obesity (30·0–34·9 kg/m²), and class II and III (severe) obesity (≥35·0 kg/m²). We used an inclusive definition of underweight (<20 kg/m²) to achieve sufficient case numbers for analysis. The main outcome was cardiometabolic multimorbidity (ie, developing at least two from: type 2 diabetes, coronary heart disease, and stroke). Incident cardiometabolic multimorbidity was ascertained via resurvey or linkage to electronic medical records (including hospital admissions and death). We analysed data from each cohort separately using logistic regression and then pooled cohort-specific estimates using random-effects meta-analysis. Findings Participants were 120 813 adults (mean age 51·4 years, range 35–103; 71445 women) who did not have diabetes, coronary heart disease, or stroke at study baseline (1973–2012). During a mean follow-up of 10·7 years (1995–2014), we identified 1627 cases of multimorbidity. After adjustment for sociodemographic and lifestyle factors, compared with individuals with a healthy weight, the risk of developing cardiometabolic multimorbidity in overweight individuals was twice as high (odds ratio [OR] 2·0, 95% CI 1·7–2·4; p<0·0001), almost five times higher for individuals with class I obesity (4·5, 3·5–5·8; p<0·0001), and almost 15 times higher for individuals with classes II and III obesity combined (14·5, 10·1–21·0; p<0·0001). This association was noted in men and women, young and old, and white and non-white participants, and was not dependent on the method of exposure assessment or outcome ascertainment. In analyses of different combinations of cardiometabolic conditions, odds ratios associated with classes II and III obesity were 2·2 (95% CI 1·9–2·6) for vascular disease only (coronary heart disease or stroke), 12·0 (8·1–17·9) for vascular disease followed by diabetes, 18·6 (16·6–20·9) for diabetes only, and 29·8 (21·7–40·8) for diabetes followed by vascular disease. Interpretation The risk of cardiometabolic multimorbidity increases as BMI increases; from double in overweight people to more than ten times in severely obese people compared with individuals with a healthy BMI. Our findings highlight the need for clinicians to actively screen for diabetes in overweight and obese patients with vascular disease, and pay increased attention to prevention of vascular disease in obese individuals with diabetes