Independent association between lower level of social support and higher coagulation activity before and after acute psychosocial stress.
ABSTRACT 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.
- SourceAvailable from: Jürgen Barth[show abstract] [hide abstract]
ABSTRACT: To conduct a systematic review and meta-analysis on the relevance of low social support for the development and course of coronary heart disease (CHD). Three electronic databases were searched (MEDLINE, PsycINFO/PSYNDEX, and Web of Science 2007/03). More than 1700 papers were screened in a first step. We included prospective studies assessing the impact of social support in either an initially healthy study population (etiologic studies) or in a study population with preexisting CHD (prognostic studies). Outcomes: Myocardial infarction in etiologic studies; cardiovascular mortality and all-cause mortality in prognostic studies. Effects were reported as relative risk (RR) or hazard ratio (HR). There is some evidence for an impact of low functional social support on the prevalence of CHD in etiologic studies (RR, range, 1.00-2.23). In contrast, there is no evidence of an impact of low structural social support on the prevalence of myocardial infarction in healthy populations (RR, range, 1.01-1.2). In prognostic studies, results consistently show that low functional support negatively affects cardiac and all-cause mortality (pooled RR, range, 1.59-1.71). These results were also confirmed in analyses adjusted for other risk factors for disease progression (pooled HR, 1.59). It remains unclear whether low structural social support increases mortality in patients with CHD (pooled RR, between 1.56; pooled HR, 1.12, NS). Because the perception of social support seems important for CHD prognosis, monitoring of functional social support is indicated in patients with CHD, and interventions to increase the perception of positive social resources are warranted.Psychosomatic Medicine 03/2010; 72(3):229-38. · 4.08 Impact Factor
Article: Verhaltensmedizinische Grundlagen[show abstract] [hide abstract]
ABSTRACT: Es stellt sich die Frage, warum ausgerechnet in einem Lehrbuch der Klinischen Psychologie und Psychotherapie der Begriff Verhaltensmedizin auftauchen muss. Verhaltensmedizin ist ein, wie heute alle Wissenschaftler dieses Arbeitsgebietes einmütig feststellen, etwas unglücklich gewählter Begriff für einen interdisziplinären Wissenschaftsbereich, der historisch gesehen die Anwendung der Verhaltenstherapie in der Medizin bedeutet. Die Begriffswahl ist sicherlich als Ausdruck einer Gegenbewegung zur Psychosomatik zu sehen. Ähnlich wie in der Verhaltensmedizin spiegeln sich auch im Begriff der Psychosomatik ihre therapeutischen Wurzeln wider, denn dort wurde und wird primär die Psychoanalyse zur Behandlung ausgewählter somatischer Krankheitsbilder eingesetzt. Beiden Disziplinen, der Verhaltensmedizin und der Psychosomatik, ist die Grundannahme gemeinsam, dass psychische Prozesse einen wichtigen Einfluss auf die Entstehung und/ oder Aufrechterhaltung von Störungen und Krankheiten nehmen können und dies nicht nur für psychische Störungen im engen Sinn gilt, sondern auch für körperliche Krankheiten, die üblicherweise in den verschiedenen medizinischen Fächern behandelt werden. Aus diesem Grund ist es wichtig, dass in einem Lehrbuch der Klinischen Psychologie und Psychotherapie auch dieser Forschungsbereich aufgeführt wird.
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ABSTRACT: Both the size and diversity of an individual's social network are strongly and prospectively linked with cardiovascular morbidity and mortality. Social relationships may influence cardiovascular outcomes, at least in part, via their impact on physiologic pathways influenced by stress, such as daytime blood pressure (BP) levels. However, scant research has examined whether social relationships influence key nocturnal pathways, such as nocturnal BP dipping. The current study examined the degree to which social integration, as measured by participants' reported engagement in a range of different types of social relationships, and the frequency of daily social contacts influence the ratio of night/day mean arterial pressure (MAP) in a community sample of African-American and white men and women (N = 224). In addition, we examined the degree to which observed associations persisted after statistical adjustment for factors known to covary with nocturnal BP, including objective measures of sleep, catecholamines, health behaviors, and comorbidities. In fully adjusted models, there was a significant association between both social integration and frequency of social contacts and the ratio of night/day MAP, indicating that socially isolated individuals were more likely to have blunted nocturnal BP-dipping profiles. There was also a significant interaction between social contact frequency and ethnicity, suggesting that the benefits of social relationships were particularly evident in African-Americans. These findings contribute to our understanding of how social integration or conversely, social isolation, influences cardiovascular risk.Journal of hypertension 02/2010; 28(2):265-71. · 4.02 Impact Factor