705 research outputs found

    Hemodynamic profiles of functional and dysfunctional forms of repetitive thinking

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    Background: The ability of the human brain to escape the here and now (mind wandering) can take functional (problem solving) and dysfunctional (perseverative cognition) routes. Although it has been proposed that only the latter may act as a mediator of the relationship between stress and cardiovascular disease, both functional and dysfunctional forms of repetitive thinking have been associated with blood pressure (BP) reactivity of the same magnitude. However, a similar BP reactivity may be caused by different physiological determinants, which may differ in their risk for cardiovascular pathology. Purpose: To examine the way (hemodynamic profile) and the extent (compensation deficit) to which total peripheral resistance and cardiac output compensate for each other in determining BP reactivity during functional and dysfunctional types of repetitive thinking. Methods: Fifty-six healthy participants randomly underwent a perseverative cognition, a mind wandering, and a problem solving induction, each followed by a 5-min recovery period while their cardiovascular parameters were continuously monitored. Results: Perseverative cognition and problem solving (but not mind wandering) elicited BP increases of similar magnitude. However, perseverative cognition was characterized by a more vascular (versus myocardial) profile compared to mind wandering and problem solving. As a consequence, BP recovery was impaired after perseverative cognition compared to the other two conditions. Conclusions: Given that high vascular resistance and delayed recovery are the hallmarks of hypertension the results suggest a potential mechanism through which perseverative cognition may act as a mediator in the relationship between stress and risk for developing precursors to cardiovascular disease

    Editorial: Can't get you out of my head: brain-body interactions in perseverative cognition

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    Perseverative cognition represents a prototypical example of how our internal thoughts can impact our psychological and physical health, as if we were facing an actual environmental stressor (Brosschot et al., 2006). The mechanisms involved—together with other emblematic examples like the placebo effect—provide clear evidence for brain-body interaction. This collection of articles presents recent advances in our understanding of perseverative cognition that have arisen from the integration of multidisciplinary approaches encompassing cognitive and clinical psychology, affective neuroscience, and autonomic physiology. These advances carry with them the promise of more effective treatments to mitigate the negative consequences of maladaptive perseverative cognition on health and well-being

    Piekeren en rumineren en fysieke gezondheid: Een meta-analyse

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    FSW - Self-regulation models for health behavior and psychopathology - ou

    Exposed to events that never happen: Generalized unsafety, the default stress response, and prolonged autonomic activity

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    FSW - Self-regulation models for health behavior and psychopathology - ou

    Metabolically exaggerated cardiac reactions to acute psychological stress revisited

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    The reactivity hypothesis postulates that large magnitude cardiovascular reactions to psychological stress contribute to the development of pathology. A key but little tested assumption is that such reactions are metabolically exaggerated. Cardiac activity, using Doppler echocardiography, and oxygen consumption, using mass spectrometry, were measured at rest and during and after a mental stress task and during graded submaximal cycling exercise. Cardiac activity and oxygen consumption showed the expected orderly association during exercise. However, during stress, large increases in cardiac activity were observed in the context of modest rises in energy expenditure; observed cardiac activity during stress substantially exceeded that predicted on the basis of contemporary levels of oxygen consumption. Thus, psychological stress can provoke increases in cardiac activity difficult to account for in terms of the metabolic demands of the stress tas

    Enteric helminths promote Salmonella co-infection by altering the intestinal metabolome

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    Intestinal helminth infections occur pre dominantly in regions where exposure to enteric bacterial pathogens is also common. Helminth infections inhibit host immunity against microbial pathogens, which has largely been attributed to the induction of regulatory or type 2 (Th2) immune responses. Here we demonstrate an additional three-way interaction in which helminth infection alters the metabolic environment of the host intestine to enhance bacterial pathogenicity. We show that an ongoing helminth infection increased colonization by Salmonella independently of T regulatory or Th2 cells. Instead, helminth infection altered the metabolic profile of the intestine, which directly enhanced bacterial expression of Salmonella pathogenicity island 1 (SPI-1) genes and increased intracellular invasion. These data reveal a novel mechanism by which a helminth-modified metabolome promotes susceptibility to bacterial co-infection

    The effects of perseverative cognition on diverse physiological responses: an integrative view

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    FSW - Self-regulation models for health behavior and psychopathology - ou
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