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Previous research has shown an association between subjective wellbeing and incident diabetes. Less is known about the role of wellbeing for subclinical disease trajectories as captured via glycated hemoglobin (HbA1c). We aimed to explore the association between subjective wellbeing and future HbA1c levels, and the role of sociodemographic, behavioral and clinical factors in this association.
We used data from the English Longitudinal Study of Ageing for this study (N = 2161). Subjective wellbeing (CASP-19) was measured at wave 2 and HbA1c was measured 8 years later at wave 6. Participants were free from diabetes at baseline. We conducted a series of analyses to examine the extent to which the association was accounted for by a range of sociodemographic, behavioral and clinical factors in linear regression models.
Models showed that subjective wellbeing (CASP-19 total score) was inversely associated with HbA1c 8 years later after controlling for depressive symptoms, age, sex, and baseline HbA1c (B = −0.035, 95% CI −0.060 to –0.011, p = 0.005). Inclusion of sociodemographic variables and behavioral factors in models accounted for a large proportion (17.0% and 24.5%, respectively) of the relationship between wellbeing and later HbA1c; clinical risk factors explained a smaller proportion of the relationship (3.4%).
Poorer subjective wellbeing is associated with greater HbA1c over 8 years of follow-up and this relationship can in part be explained by sociodemographic, behavioral and clinical factors among older adults.
There is strong evidence linking adverse childhood experiences (ACEs) and poor outcomes in adulthood both in terms of mental and physical health. Gaps in both the evidence base and research priorities still exist. These include understanding how to identify and assess risk in children who have experienced ACEs, and also the development and, importantly, the evaluation of interventions. Outstanding gaps include whether there are sensitive periods during childhood, the role of resilience/protective factors, the causal relationships, biological mechanisms and relative risk of ACEs for particular negative outcomes. ACEs affect individual children differently and chronic exposure appears to increase the risk of poor outcomes in adulthood, meaning interventions should also be tailored to the individual children, families and communities. Generally, there needs to be better evaluation of interventions and dissemination of this information to ensure that their use is evidence based. More input from affected communities, clinicians, funding bodies and Government departments is required to identify research priorities and ensure gaps in the evidence base are addressed.
Depressive symptoms and inflammation are risk factors for cardiovascular disease (CVD) and mortality. We investigated the combined association of these factors with the prediction of CVD and all-cause mortality in a representative cohort of older men and women.
We measured C-reactive protein (CRP) and depressive symptoms in 5328 men and women aged 52–89 years in the English Longitudinal Study of Ageing. Depressive symptoms were measured using the eight-item Centre for Epidemiological Studies Depression Scale. CRP was analysed from peripheral blood. Mortality was ascertained from national registers and associations with depressive symptoms and inflammation were estimated using Cox proportional hazard models.
We identified 112 CVD related deaths out of 420 all-cause deaths in men and 109 CVD related deaths out of 334 all-cause deaths in women over a mean follow-up of 7.7 years. Men with both depressive symptoms and high CRP (3–20 mg/L) had an increased risk of CVD mortality (hazard ratio; 95% confidence interval: 3.89; 2.04–7.44) and all-cause mortality (2.40; 1.65–3.48) after adjusting for age, socioeconomic variables and health behaviours. This considerably exceeds the risks associated with high CRP alone (CVD 2.43; 1.59–3.71, all-cause 1.49; 1.20–1.84). There was no significant increase in mortality risk associated with depressive symptoms alone in men. In women, neither depressive symptoms or inflammation alone or the combination of both significantly predicted CVD or all-cause mortality.
The combination of depressive symptoms and increased inflammation confers a considerable increase in CVD mortality risk for men. These effects appear to be independent, suggesting an additive role.
Theories of cognitive reserve, disuse syndrome and stress have suggested that activities that are mentally engaging, enjoyable and socially interactive could be protective against the development of dementia. Using data from the English Longitudinal Study of Ageing, this study shows that for adults aged 50 and older visiting museums every few months or more was associated with a lower incidence rate of dementia over a 10-year follow-up period compared with less-frequent visiting. This association was independent of demographics, socioeconomic status, health-related variables including sensory impairment, depression, vascular conditions and other forms of community engagement. Visiting museums may be a promising psychosocial activity to support the prevention of dementia.
Parenting style is associated with offspring health, but whether it is associated with offspring mortality at older ages remains unknown.
We examined whether childhood experiences of suboptimal parenting style are associated with increased risk of death at older ages.
Longitudinal cohort study of 1964 community-dwelling adults aged 65–79 years.
The association between parenting style and mortality was inverse and graded. Participants in the poorest parenting style score quartile had increased risk of death (hazard ratio (HR) = 1.72, 95% CI 1.20–2.48) compared with those in the optimal parenting style score quartile after adjustment for age and gender. Full adjustment for covariates partially explained this association (HR = 1.49, 95% CI 1.02–2.18). Parenting style was inversely associated with cancer and other mortality, but not cardiovascular mortality. Maternal and paternal parenting styles were individually associated with mortality.
Experiences of suboptimal parenting in childhood are associated with increased risk of death at older ages.
An association between low levels of physical activity and impaired cognitive performance in schizophrenia has been proposed, but most studies have relied on self-report measures of activity. This study examined the association between actigraphy-derived physical activity and cognitive performance adjusting for multiple covariates in patients with schizophrenia.
Patients with schizophrenia (n = 199) were recruited from chronic psychiatric wards, and 60 age-, sex- and body mass index-matched comparison participants were recruited from the staff of two hospitals and universities. Physical activity was assessed objectively for 7 days using an ActiGraph. Cognitive performance was assessed with the Cognitrone test from the Vienna Test System and the Grooved Pegboard Test. Demographic variables, metabolic parameters, positive and negative symptoms, duration of illness and hospitalization, and medication use were included as covariates. Pearson correlations and multivariable linear regressions were conducted to examine the associations between physical activity levels and cognitive performance.
Patients with schizophrenia were less physically active and had poorer performance on attention/concentration and speed of processing than the comparison group. Patients with schizophrenia who spent more time in light physical activity showed better performance on attention/concentration (β = 0.198, p = 0.020) and speed of processing (β= −0.169, p = 0.048) tasks than those who were less active. Cognitive performance was also associated with moderate-vigorous physical activity, but the effect was no longer significant once light physical activity had been taken into account.
This study provides evidence for a positive association between objectively measured light physical activity and cognitive performance in people with schizophrenia, after adjustment for multiple confounders.
People with depression tend to have lower heart rate variability (HRV), but the temporal sequence is poorly understood. In a sample of the general population, we prospectively examined whether HRV measures predict subsequent depressive symptoms or whether depressive symptoms predict subsequent levels of HRV.
Data from the fifth (1997–1999) and ninth (2007–2009) phases of the UK Whitehall II longitudinal population-based cohort study were analysed with an average follow-up of 10.5 years. The sample size for the prospective analysis depended on the analysis and ranged from 2334 (644 women) to 2276 (602 women). HRV measures during 5 min of supine rest were obtained. Depressive symptoms were evaluated by four cognitive symptoms of depression from the General Health Questionnaire.
At follow-up assessment, depressive symptoms were inversely associated with HRV measures independently of antidepressant medication use in men but not in women. Prospectively, lower baseline heart rate and higher HRV measures were associated with a lower likelihood of incident depressive symptoms at follow-up in men without depressive symptoms at baseline. Similar but statistically insignificant associations were found in women. Adjustments for known confounders including sociodemographic and lifestyle factors, cardiometabolic conditions or medication did not change the predictive effect of HRV on incident depressive symptoms at follow-up. Depressive symptoms at baseline were not associated with heart rate or HRV at follow-up in either sex.
These findings are consistent with an aetiological role of the autonomic nervous system in depression onset.
Evidence suggests a link between sedentary behaviours and depressive
symptoms. Mechanisms underlying this relationship are not understood, but
inflammatory processes may be involved. Autonomic and inflammatory
responses to stress may be heightened in sedentary individuals
contributing to risk, but no study has experimentally investigated
To examine the effect of sedentary time on mood and stress responses
using an experimental design.
Forty-three individuals were assigned to a free-living sedentary
condition and to a control condition (usual activity) in a cross-over,
randomised fashion and were tested in a psychophysiology laboratory after
spending 2 weeks in each condition. Participants completed mood
questionnaires (General Health Questionnaire and Profile of Mood States)
and wore a motion sensor for 4 weeks.
Sedentary time increased by an average of 32 min/day (P
= 0.01) during the experimental condition compared with control. Being
sedentary resulted in increases in negative mood independent of changes
in moderate to vigorous physical activity (δGHQ= 6.23, δPOMS= 2.80). Mood
disturbances were associated with greater stress-induced inflammatory
interleukin-6 (IL-6) responses (β = 0.37).
Two weeks of exposure to greater free-living sedentary time resulted in
mood disturbances independent of reduction in physical activity.
Stress-induced IL-6 responses were associated with changes in mood.
Depressed mood and stress are associated with recurrent adverse outcomes following acute coronary syndrome (ACS), but the impact of psychological coping style has not been evaluated in detail.
We tested the relationship between task-oriented coping and event-free survival following ACS.
We followed 158 patients with ACS for an average of 59.8 months for major adverse cardiac outcomes. Psychological coping was assessed with the Coping Inventory of Stressful Situations.
Compared with patients in the lower half of the distribution, those reporting higher task-oriented coping had a reduced hazard of adverse cardiac events (hazard ratio (HR) = 0.28, 95% CI 0.11–0.68, P=0.005) independently of demographic, clinical and behavioural covariates. The combination of low task-oriented coping and high depressive symptoms showed a strong association with adverse outcomes (HR = 6.25, 95% CI 1.88–20.82, P=0.003).
The tendency to cope using task-oriented strategies may promote event-free survival following ACS.
Depression is associated with increased risk of several general medical conditions, including diabetes and cardiovascular disease. The nature of the association is complex and may involve bidirectional causation or a common pathophysiology.
To determine whether young people without depression but at increased familial risk have altered metabolic and blood pressure markers relative to matched controls.
We studied young people (n = 85), who had a parent with depression but no personal history of depressive illness (FH+) and healthy controls (n = 69). Cardiovascular risk profile was assessed by a fasting blood sample to measure insulin, glucose, lipids and high-sensitivity C-reactive protein (CRP) and blood pressure was measured centrally and peripherally. Arterial stiffness and waking cortisol concentration were also measured.
Compared with controls, the FH+ group demonstrated increased peripheral and central systolic blood pressure, increased arterial stiffness and diminished insulin sensitivity but they did not differ from controls in measures of lipids, CRP or waking cortisol.
Our data suggest that young people at increased familial risk of depression show evidence of altered cardiovascular risk profile in young adulthood even in the absence of depressive symptoms. It is possible therefore that vulnerability to conditions such as hypertension and diabetes may precede the onset of major depression and may share common risk factors.
Depressed mood following an acute coronary syndrome (ACS) is a risk factor for future cardiac morbidity. Hypothalamic–pituitary–adrenal (HPA) axis dysregulation is associated with depression, and may be a process through which depressive symptoms influence later cardiac health. Additionally, a history of depression predicts depressive symptoms in the weeks following ACS. The purpose of this study was to determine whether a history of depression and/or current depression are associated with the HPA axis dysregulation following ACS.
A total of 152 cardiac patients completed a structured diagnostic interview, a standardized depression questionnaire and a cortisol profile over the day, 3 weeks after an ACS. Cortisol was analysed using: the cortisol awakening response (CAR), total cortisol output estimated using the area under the curve method, and the slope of cortisol decline over the day.
Total cortisol output was positively associated with history of depression, after adjustment for age, gender, marital status, ethnicity, smoking status, body mass index (BMI), Global Registry of Acute Cardiac Events (GRACE) risk score, days in hospital, medication with statins and antiplatelet compounds, and current depression score. Men with clinically diagnosed depression after ACS showed a blunted CAR, but the CAR was not related to a history of depression.
Patients with a history of depression showed increased total cortisol output, but this is unlikely to be responsible for associations between depression after ACS and later cardiac morbidity. However, the blunted CAR in patients with severe depression following ACS indicates that HPA dysregulation is present.
The determinants of depression following acute coronary syndrome (ACS) are poorly understood. Triggering of ACS by emotional stress and low socio-economic status (SES) are predictors of adverse outcomes. We therefore investigated whether emotional triggering and low SES predict depression and anxiety following ACS.
This prospective observational clinical cohort study involved 298 patients with clinically verified ACS. Emotional stress was assessed for the 2 h before symptom onset and compared with the equivalent period 24 h earlier using case-crossover methods. SES was defined by household income and education. Depression was measured with the Beck Depression Inventory and the Hamilton Rating Scale for Depression and anxiety with the Hospital Anxiety and Depression Scale 3 weeks after ACS and again at 6 and 12 months. Age, gender, ethnicity, marital status, the Global Registry of Acute Coronary Events risk score, duration of hospital stay and history of depression were included as covariates.
Emotional stress during the 2-h hazard period was associated with increased risk of ACS (odds ratio 1.88, 95% confidence interval 1.01–3.61). Both low income and emotional triggering predicted depression and anxiety at 3 weeks and 6/12 months independently of covariates. The two factors interacted, with the greatest depression and anxiety in lower income patients who experienced acute emotional stress. Education was not related to depression.
Patients who experience acute emotional stress during their ACS and are lower SES as defined by current affluence and access to resources are particularly vulnerable to subsequent depression and anxiety.
Although a substantial body of research points to a link between psychological distress and inflammatory responses in middle-aged and older adults, particularly those with cardiovascular disease, the relationship between inflammation and distress in young, healthy individuals has not been established. This study was designed to investigate the cross-sectional association between psychological distress and inflammatory proteins in a young, healthy representative population of English adults.
Participants were 1338 individuals aged 16–34 years from the 2006 Health Survey for England (HSE). Blood samples to measure plasma fibrinogen and high sensitivity C-reactive protein (hsCRP), as well as measures of psychological distress (using the General Health Questionnaire 12-item scale, GHQ-12) and covariates, were collected during home visits. Linear regression was used to assess the relationship between psychological distress and fibrinogen and hsCRP.
Higher self-rated distress was positively associated with fibrinogen level in this young population, independently of age, sex, ethnicity, body mass index (BMI), high density lipoprotein (HDL) cholesterol, smoking, and alcohol and medication use (β=0.024, p<0.01). Psychological distress was not related to hsCRP.
Psychological distress may negatively impact inflammatory processes in young adulthood before the onset of chronic health problems such as hypertension and cardiovascular disease. Longitudinal research is needed to elucidate the relationship between distress and inflammation in young adults and its significance for later disease states.
Hypothalamic–pituitary–adrenocortical (HPA) regulation in adults is influenced by early psychosocial adversity, but the role of infectious disease history is poorly understood. We studied the association between cumulative pathogen burden and cortisol profile over the day in a sample of 317 healthy men and women aged 51–72 years. Cumulative pathogen burden was defined as positive serostatus for Chlamydia pneumoniae, cytomegalovirus (CMV) and herpes simplex virus 1 (HSV-1). Salivary cortisol was sampled repeatedly over the day. The cortisol slope was defined as the decrease across the day and evening. Age, gender, grade of employment, body mass index, smoking status, self-rated health, cardiovascular medication, depressed mood and time of waking were included as covariates. The pathogen burden averaged 1·76 (s.d.=0·92). The cortisol slope was inversely associated with pathogen burden after controlling for covariates. When individual pathogens were studied, only CMV was associated with flatter cortisol rhythms in isolation. We conclude that pathogen burden is independently associated with flatter cortisol slopes over the day, and may contribute to disturbed neuroendocrine regulation.
A lack of longitudinal studies has made it difficult to establish the direction of associations between circulating concentrations of low-grade chronic inflammatory markers, such as C-reactive protein and interleukin-6, and cognitive symptoms of depression. The present study sought to assess whether C-reactive protein and interleukin-6 predict cognitive symptoms of depression or whether these symptoms predict inflammatory markers.
In a prospective occupational cohort study of British white-collar civil servants (the Whitehall II study), serum C-reactive protein, interleukin-6 and cognitive symptoms of depression were measured at baseline in 1991–1993 and at follow-up in 2002–2004, an average follow-up of 11.8 years. Symptoms of depression were measured with four items describing cognitive symptoms of depression from the General Health Questionnaire. The number of participants varied between 3339 and 3070 (mean age 50 years, 30% women) depending on the analysis.
Baseline C-reactive protein (β=0.046, p=0.004) and interleukin-6 (β=0.046, p=0.005) predicted cognitive symptoms of depression at follow-up, while baseline symptoms of depression did not predict inflammatory markers at follow-up. After full adjustment for sociodemographic, behavioural and biological risk factors, health conditions, medication use and baseline cognitive systems of depression, baseline C-reactive protein (β=0.038, p=0.036) and interleukin-6 (β=0.041, p=0.018) remained predictive of cognitive symptoms of depression at follow-up.
These findings suggest that inflammation precedes depression at least with regard to the cognitive symptoms of depression.
The concept of stress is used in a variety of disciplines such as physiology, engineering and sociology. The concept originated in physics where stress is defined as external force applied to a system, and strain is the change in the system that is due to the applied force. In psychology and behavioural medicine the study of stress has moved beyond simple definitions towards identifying the processes of stress and mediating factors. Thus in psychology and medicine the term ‘stress’ covers a wide range of research that concentrates on different aspects of the stress process. For example, much medical stress research does not consider psychological factors and concentrates on physical stress responses, such as the impact of physical exercise on blood volume depletion. There are therefore conflicting views on how useful the concept of stress is. On the one hand some believe the concept is so widely misused and poorly defined that it is no longer useful and should be abandoned (e.g. Kasl, 1983). On the other hand, stress can be seen as an important construct that has the potential to unify different disciplines and help us understand the relationship between mind and body.
Stress is therefore a complex and multifaceted construct with many component parts. At a basic level, it is useful to distinguish between stressors, which are internal or external factors that cause ‘stress responses’, which can be physical, behavioural, cognitive or affective; and chronic strain, which is the negative impact of the stress process on the person.