Biomedical subjects

S R Kunz-Ebrecht

Publications and source records attributed to S R Kunz-Ebrecht.

3 recordsLinked to original sources

PubMed2005

Physiological correlates of cognitive functioning in an elderly population.

Cognitive decline in old age is not universal or inevitable. Associations have been observed with neuroendocrine function, but the relevance of other physiological processes is unclear. We predicted that impairment of memory in an ageing population would be related to the dysregulation of neuroendocrine and cardiovascular responses. One hundred and thirty-nine participants (65-80 years) were recruited from general practice in London. Two standardised verbal paired-associates recall tasks were administered in order to determine declarative memory performance, and a fluid intelligence task (matrix reasoning) was also performed. Salivary cortisol samples were collected every 10 min, while blood pressure and heart rate were measured before, during and after each task. Illness history and medication use were obtained from medical records. Multiple linear regression analysis, adjusted for age, gender, education, chronic illness, and medication use, revealed that cortisol responses were inversely related to memory performance. Additionally, superior memory was associated with more effective post-task recovery of heart rate (in both men and women) and diastolic blood pressure recovery in men. Cardiovascular recovery effects were independent of covariates, and of levels of heart rate and blood pressure measured during tasks themselves. These associations were also independent of subjective ratings of stress and perceived performance. Neither neuroendocrine nor cardiovascular responses were related to performance of the reasoning task. We conclude that memory in the elderly is associated both with hypothalamic-pituitary-adrenocortical function and cardiovascular regulation. Disturbances of neuroendocrine and hemodynamic function may be related to greater vulnerability to cognitive decline.

Aged↗

PubMed2004

Central adiposity and cortisol responses to waking in middle-aged men and women.

OBJECTIVE: Central obesity is associated with disturbances of hypothalamic-pituitary-adrenocortical (HPA) axis function. We investigated whether central adiposity indexed by waist/hip ratio is related to cortisol responses to waking and other measures of salivary cortisol over the working day. PARTICIPANTS: In total, 89 men and 83 women aged 47-59 y recruited from the British civil service. All were members of the Whitehall II epidemiological cohort. METHODS: Saliva samples were collected on waking, 30 min later, and then at 2-h intervals from 0800-0830 to 2200-2230. A strict procedure for excluding individuals who did not adhere to the sampling schedule was applied. RESULTS: Waist/hip ratio in men was positively correlated with the cortisol response to waking (30 min-waking value) after adjusting for age, socioeconomic position, smoking status, alcohol consumption, time of waking, and cortisol level on waking (r=0.29, P=0.009). The cortisol response to waking was negatively related to high-density lipoprotein (HDL) cholesterol (r=-0.25) and positively with total/HDL cholesterol ratio (r=0.25). Associations between the decline in cortisol over the day and waist/hip ratio, HDL cholesterol and total/HDL cholesterol ratios were also significant. No associations were significant in women, and body mass index was unrelated to cortisol. CONCLUSIONS: The cortisol response to waking is a dynamic indicator of HPA function that has previously been related to chronic psychological stress. These results confirm a recent Swedish study, and indicate that cortisol responses to waking may be indicative of neuroendocrine disturbance in central obesity.

Adipose Tissue↗

PubMed2003

Lack of association between depressive symptoms and markers of immune and vascular inflammation in middle-aged men and women.

BACKGROUND: Disturbed immune activity and vascular inflammation are associated both with clinical depression and coronary atherogenesis, and may constitute a mechanism through which depression contributes to coronary heart disease. If this is the case, then non-clinical depressive symptoms and psychological distress should be associated with immune activation and vascular inflammation. We tested this hypothesis in a healthy middle-aged sample. METHOD: Measures of depressive symptoms and hopelessness were obtained from 226 volunteers (122 men, 104 women) aged 47-59 years, drawn from the Whitehall II epidemiological cohort. C-reactive protein, fibrinogen, plasma interleukin-6, tumour necrosis factor alpha, interleukin-1 receptor antagonist, and T- and B-lymphocyte, and natural killer cells numbers and percentages were assessed. RESULTS: There were no associations between measures of depressive symptoms or hopelessness and markers of immune activation or inflammatory response. CONCLUSIONS: Factors such as the measures of depressive symptoms, the choice of inflammatory and immune indices, and sample size, are unlikely to be responsible for these null effects. Associations may be confined to clinically depressed or older age populations, but there are problems of confounding by co-morbidity and health compromising behaviours in this literature. We conclude that disturbances of immune function and inflammatory processes are unlikely to be primarily responsible for the associations between depressive symptoms and coronary heart disease described in the literature, and that other pathways are involved.

Biomarkers↗