Independent Association Between Lower Level of Social Support and Higher Coagulation Activity Before and After Acute Psychosocial Stress

Department of Clinical Psychology and Psychotherapy, University of Zurich, Zurich, Switzerland.
Psychosomatic Medicine (Impact Factor: 3.47). 01/2009; 71(1):30-7. DOI: 10.1097/PSY.0b013e31818f6868
Source: PubMed


To investigate the relationship between social support and coagulation parameter reactivity to mental stress in men and to determine if norepinephrine is involved. Lower social support is associated with higher basal coagulation activity and greater norepinephrine stress reactivity, which in turn, is linked with hypercoagulability. However, it is not known if low social support interacts with stress to further increase coagulation reactivity or if norepinephrine affects this association. These findings may be important for determining if low social support influences thrombosis and possible acute coronary events in response to acute stress. We investigated the relationship between social support and coagulation parameter reactivity to mental stress in men and determined if norepinephrine is involved.
We measured perceived social support in 63 medication-free nonsmoking men (age (mean +/- standard error of the mean) = 36.7 +/- 1.7 years) who underwent an acute standardized psychosocial stress task combining public speaking and mental arithmetic in front of an audience. We measured plasma D-dimer, fibrinogen, clotting Factor VII activity (FVII:C), and plasma norepinephrine at rest as well as immediately after stress and 20 minutes after stress.
Independent of body mass index, mean arterial pressure, and age, lower social support was associated with higher D-dimer and fibrinogen levels at baseline (p < .012) and with greater increases in fibrinogen (beta = -0.36, p = .001; DeltaR(2) = .12), and D-dimer (beta = -0.21, p = .017; DeltaR(2) = .04), but not in FVII:C (p = .83) from baseline to 20 minutes after stress. General linear models revealed significant main effects of social support and stress on fibrinogen, D-dimer, and norepinephrine (p < .035). Controlling for norepinephrine did not change the significance of the reported associations between social support and the coagulation measures D-dimer and fibrinogen.
Our results suggest that lower social support is associated with greater coagulation activity before and after acute stress, which was unrelated to norepinephrine reactivity.

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    • "Here, we investigated for the first time in a placebocontrolled within-subjects design whether in healthy men NE-infusion induces sAA increases as commonly observed in reaction to acute psychosocial stress (Rohleder et al., 2006; Wirtz et al., 2009; Thoma et al., 2012), and whether these potential increases relate to alpha-adrenergic receptor mechanisms. We infused a NE-stress-reactivity mimicking dosage of NE with and without non-selective U. Kuebler et al. alpha-adrenergic blockade by phentolamine and repeatedly measured sAA levels before and several times after infusion procedures. "
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    Psychoneuroendocrinology 08/2014; 49C(1):290-298. DOI:10.1016/j.psyneuen.2014.07.023 · 4.94 Impact Factor
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    • "In a second step, we controlled for the cardiovascular risk factors age and body mass index (BMI) as covariates. In a third step, we additionally controlled for depression, neuroticism, and ΔNE as apriori defined set of potential confounders [31] [38] [39]. "
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    ABSTRACT: Objective Hypertension and an atherogenic lipid profile are known risk factors for coronary heart disease (CHD). Hypertensives show greater changes in atherogenic plasma lipids to acute stress than normotensives. In this study we investigated whether attribution of failure is associated with lipid stress reactivity in hypertensive compared with normotensive men. Methods 18 normotensive and 17 hypertensive men (mean ± SEM; 45 ± 2.2 years) underwent an acute standardized psychosocial stress task that can be viewed as a situation of experimentally induced failure. We assessed external-stable (ES), external-variable (EV), internal-stable (IS), and internal variable (IV) attribution of failure and psychological control variables (i.e. extent of depression and neuroticism). Moreover, total cholesterol (TC), low-density-lipoprotein cholesterol (LDL-C), and norepinephrine were measured immediately before and several times after stress. Results ES moderated TC- and LDL-C-stress reactivity in hypertensives as compared to normotensives (interaction mean arterial pressure [MAP]-by-ES for TC: F = 3.71, p = .015; for LDL-C: F = 3.61, p = .016). TC and LDL-C levels were highest in hypertensives with low ES immediately after stress (p ≤ .039). In contrast, hypertensives with high ES did not differ from normotensives in TC and LDL-C immediately after stress (p’s > .28). Controlling for norepinephrine, depression, and neuroticism in addition to age and BMI did not significantly change results. There were no significant associations between lipid baseline levels or aggregated lipid secretion and IS, IV, or EV (p’s > .23). Conclusion Our data suggest that ES may independently protect from elevated lipid stress reactivity in hypertensive individuals. ES thus might be a protective factor against CHD in hypertension.
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    • "of perceived stress management skills in different non - clinical populations . Psychoneuroendocrinology ( 2012 ) , http : / / dx . doi . org / 10 . 1016 / j . psyneuen . 2012 . 07 . 017 6 P . H . Wirtz et al . ISBF total score as continuous independent variable following previous methods while controlling for potential confounders as covariates ( Wirtz et al . , 2009 ) . To avoid overcontrolling given our sample sizes we restricted the number of covariates ( Babyak , 2004 ) . In the laboratory study we controlled for age , BMI , and MAP as covariates to rule out a potential confound - ing influence of these parameters ( Kudielka et al . , 2004a ; Wirtz et al . , 2006 ) . In the workplace study we co"
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