Sauter, Christine
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The burden of overweight : Higher body mass index, but not vital exhaustion, is associated with higher DNA damage and lower DNA repair capacity
Background/Objectives
DNA damage and the capacity to repair damaged DNA has been associated with the pathogenesis of several diseases such as cancer. While it is well known that external mutagenic agents can induce DNA damage, less is known about endogenous contributors to genomic instability. The aim of this study was to investigate whether excess body weight as a physiological factor and vital exhaustion as a psychological factor would be associated with basal levels of DNA damage as well as DNA repair capacity.
Subjects/Methods
In a cross-sectional between-subject design we recruited 53 apparently healthy men within the normal to non-obese overweight range (mean BMI: 25.2±.5) who were either vitally exhausted (VE) (VE-score≥10) or non-exhausted (VE-score≤3). Vital exhaustion was assessed using the Maastricht Vital Exhaustion Questionnaire. We assessed DNA damage and repair in terms of strand breaks in PBMCs by means of the automated Fluorimetric Detection of Alkaline Unwinding (FADU) assay. DNA repair capacity was assessed by repeatedly measuring the amount of intact DNA up to 90 minutes after standardized X-irradiation of the cells.
Results
General linear models revealed that elevated levels of basal DNA damage (β=-.34,p=.013,f=0.33) as well as impaired capacity to repair damaged DNA (F(1/50)=5.40,p=.024,f=.33) with increasing BMI, but not with vital exhaustion (p’s≥.63).
Conclusion
Our findings point to DNA integrity impairments with increasing BMI, already in the overweight range, and suggest impaired DNA repair as a potential underlying molecular mechanism. In contrast, the psychological factor vital exhaustion was not associated with DNA damage or DNA repair capacity.
Aldosterone hyperreactivity to acute psychosocial stress induction in men with essential hypertension
Essential hypertension is a pivotal risk factor for the development of cardiovascular disease (CVD). Hypertensives exhibit greater stress-induced responses in various physiological systems considered to contribute to CVD progression. Whether this stress hyperreactivity extends to the adrenal hormone aldosterone has not yet been investigated in essential hypertension. Here, we investigated reactivity of plasma aldosterone to acute psychosocial stress induction in hypertensive and normotensive men. 21 hypertensive men and 25 normotensive controls underwent the standardized Trier-Social-Stress-Test (TSST). We repeatedly assessed plasma aldosterone before and up to 1 h after TSST cessation. Acute psychosocial stress induced significantly greater increases in hypertensives as compared to normotensives (F(3.60, 158.50) = 3.75; p = .008, f = 0.29). Our findings suggest stress-induced hyperreactivity of aldosterone in essential hypertension. Potential implications for stress-related cardiovascular risk remain to be elucidated.
Determinants and Mechanisms of the Renin Aldosterone Stress Response
Objective:
The renin-angiotensin-aldosterone system (RAAS) plays a relevant role in regulating blood pressure and thus maintaining cardiovascular homeostasis. While it was recently shown that RAAS parameters are responsive to acute psychosocial stress, the psychobiological determinants of the acute stress-induced RAAS activation have not yet been investigated so far. In a randomized placebo-controlled design, we investigated potential psychological and physiological determinants of the RAAS response and underlying mechanisms.
Methods:
57 young healthy male participants underwent either an acute standardized psychosocial stress test or a non-stress placebo task. We measured aldosterone in plasma and saliva, as well as renin, and the stress-reactive endocrine measures adrenocorticotropic hormone (ACTH), epinephrine, and norepinephrine in plasma at rest, immediately after the task and several times up to 3 h thereafter. Moreover, we assessed stress-reactive psychological (anticipatory cognitive stress appraisal, mood, physical discomfort) and basal demographic-physiological measures (age, BMI, blood pressure).
Results:
Acute psychosocial stress elicited changes in all assessed endocrine (p’s ≤ .028, ηp2‘s ≥ .07) and stress-reactive psychological measures (p’s ≤ .003, ηp2‘s ≥ .15). The basal parameter BMI, the stress-reactive endocrine parameters ACTH and norepinephrine, and the psychological parameter anticipatory stress appraisal were identified as determinants of higher RAAS parameter reactivity to acute psychosocial stress. The association between anticipatory cognitive stress appraisal and plasma RAAS measures was fully mediated by ACTH increases (p’s ≤ .044, ηp2‘s ≥ .05).
Conclusions:
Cognitive stress appraisal processes seem to modulate RAAS stress reactivity. This points to potential clinical implications for psycho-educative therapeutical interventions targeting stress appraisal processes in order to reduce endocrine stress reactivity.
Kinetics and interrelations of the renin aldosterone response to acute psychosocial stress : a neglected stress system
Context:
The Renin-Angiotensin-Aldosterone-System (RAAS) plays an important role in cardiovascular homeostasis and its dysfunction relates to negative health consequences. Acute psychosocial stress seems to activate the RAAS in humans, but stress kinetics and interrelations of RAAS parameters as compared to a non-stress control group remain inconclusive.
Objective:
We systematically investigated in a randomized placebo-controlled design stress kinetics and interrelations of the reactivity of RAAS parameters measured in plasma and saliva to standardized acute psychosocial stress induction.
Methods:
58 healthy young men were assigned to either a stress or a placebo-control group. The stress group underwent the Trier-Social-Stress-Test (TSST), while the control group underwent the placebo-TSST. We repeatedly assessed plasma renin, plasma and salivary aldosterone, before, and up to 3h after stress/placebo. We simultaneously assessed salivary cortisol to validate successful stress induction and to test for interrelations.
Results:
Acute psychosocial stress induced significant increases in all endocrine measures as compared to placebo-stress (p´s≤.041). Highest renin levels were observed 1min after stress, highest aldosterone and cortisol levels 10 and 20min after stress, with salivary aldosterone starting earlier at 1min after stress. Renin completed recovery at 10min, cortisol at 60min, salivary aldosterone at 90min, and plasma aldosterone at 180min after stress. Stress increase scores of all endocrine measures related to each other, as did renin and cortisol AUCi´s and salivary and plasma aldosterone AUCi´s (p´s≤.047).
Conclusions:
Our findings suggest that in humans acute psychosocial stress induces a differential and interrelated RAAS parameter activation pattern. Potential implications for stress-related cardiovascular risk remain to be elucidated.
Aldosterone secretion during the day : Salivary aldosterone awakening response and daytime levels
Background
The mineralocorticoid hormone aldosterone is a key regulator of the sodium–potassium balance and blood pressure. In excess, aldosterone relates to hypertension and cardiovascular disease (CVD). Here, we systematically investigated aldosterone secretion during the day in terms of salivary aldosterone awakening response (AldAR) and salivary aldosterone daytime levels (AldDay) under controlled conditions in participants’ natural environment including assessment of potential confounding variables.
Methods
In 40 healthy young men, saliva samples for AldAR were collected immediately after awakening and 15, 30, 45, and 60 min thereafter. AldDay levels were measured in 1 h intervals from 9:00–22:00 h. Analyses were complemented by salivary cortisol assessment. Fluid and food intake was standardized and as potential confounders, we assessed awakening time and sleep duration, age, BMI and MAP, as well as chronic stress.
Results
Awakening was followed by significant increases in salivary aldosterone (p = .004, f= 0.31), returning to baseline levels > 60 min later. Longer sleep duration was associated with lower AldAR (p < .001, f= 0.36). Over the course of the day we observed a continuous decrease of AldDay (p < .001, f= 0.45). Longer sleep duration (p = .097, f= .21), later time of awakening (p < .001, f= .29), and higher chronic stress (p = .041, f= .23) were associated with AldDay characteristics. Circadian aldosterone secretion was positively associated with most cortisol measures.
Conclusions
We observed an awakening response in salivary aldosterone and could confirm a decrease in aldosterone levels during the day, comparable to cortisol. Significant confounders were sleep-related variables and chronic stress. Clinical implications of circadian aldosterone secretion with respect to CVD risk remain to be elucidated.