Stress-related prolonged cardiovascular activity: The impact and changeability of stressful cognition without awareness
The research question is that unconscious perseverative cognition (UPC) is responsible for a considerable part of cardiovascular (CV) activity that occurs even in the absence of threats and other stressors that one may encounter in one’s daily life.
- ZONMW TOP grant
Prof. Julian F. Thayer (Dept Psychology; The Ohio State University, OH, US (collaborator)
Jürgen Stumpp;. Jörg Ottenbacher, Movisens GmbH, Karlsruhe (D) (collaborator)
Markus R. Quirin (Inst Psychology, University of Osnabrück, D (collaborator)
Ph. Spinhoven (Clinical Psychology, Dept Psychology, Leiden University (collaborator & promotor)
William Gerin (Dept Biobehavioral Health; Dept Psychology, Penn State University, PA, US (collaborator)
Richard Lane (Dept Psychiatry, University of Arizona, Tucson, AZ, US (collaborator)
Psychosocial stress is a risk factor for cardiovascular disease (CVD), but the underlying mechanisms remain poorly specified. Researchers have focused mainly on the magnitude of the cardiovascular (CV) response to stressors as they are occurring (often over a period of minutes), but have neglected the duration of the exposure. The latter often outlasts the stressful events themselves, because the effects of a stressor, including the resultant thoughts and negative affect, often do not end when the stressful situation ends and indeed, the effect may last minutes or hours or in some cases years. Moreover, one may anticipate, or worry, about future events, and such thoughts and affect do not necessarily wait for the stressor to begin: the cognitive and affective processes may be activated long before the event ever occurs. We have referred to this process as “perseverative cognition” (PC). Thus, stressful events can continuously exert effects on the CV and other biological systems, through PC, which over time will result in dysregulation of those systems (e.g., higher blood pressure (BP) resting levels) and, ultimately, will result in poor clinical outcomes.
Our prior research suggests that individuals tend to be unaware of most PC, although such thoughts and feelings still can increase CV activity. Developments in unconscious cognition research allow us to study unconscious PC (UPC) with scientific rigor. Researchers have suggested that indeed most cognition is “unconscious thought” which means that it occurs while one’s attention cannot be directed toward it or is directed elsewhere. It is possible, therefore, that most of the stress research has missed the essential phenomena by focusing solely on the conscious “tip of the iceberg”. We propose to test the hypothesis that UPC is responsible for a considerable part of CV activity that occurs even in the absence of threats and other stressors that one may encounter in one’s daily life.
Our data support a role for UPC. First, in daily life, we found that worry was linked to cardiac activity, and this activity persisted for hours after the worry itself had ended. Second, we found that that these effects occurred during sleep. Neither result is explained by conscious PC. We also found evidence that BP can be increased by threatening stimuli that are presented subliminally, an accepted experimental model of unconscious cognition.
We propose three projects that, taken together, will provide insight into the question of the mechanisms by which psychosocial stress is linked to CVD:
Project 1 comprises a series of controlled experiments to be conducted in our psychophysiology laboratory, in which we will test the hypothesis that UPC causes changes in three biological measures that are linked to CVD: Heart rate variability (HRV), which will be the primary parameter, and BP and total peripheral resistance (TPR). To induce UPC we will use four approaches: (1) subliminal threatening stimuli; (2) subliminal conditioned threat stimuli (i.e. neutral stimuli that are previously coupled to mild electric shocks); preventing conscious PC using a distracting task following (3) a laboratory stressor, and following (4) worry induction.
Project 2 (which will occur in the natural environment) will assess whether and to what extent low HRV in daily life is explained by UPC. During several days, in volunteers, we will detect all periods of decreased HRV that are not explained by physical activity, called ‘additional HRV decrease’, and lasting longer than 15 min. By comparing these measures to random periods that are characterized by normal or high HRV from the same volunteer, we will be able to examine whether ‘additional HRV decrease’ is associated with UPC. We will also examine whether decreased HRV during sleep is associated with UPC.
Project 3 will test whether interventions that reduce UPC also decrease CV activity. We will test and compare two short, internet-assisted interventions that reduce two cognitive biases that are prevalent under stress and of which people are generally not aware: The tendency to attend to threatening information at the cost of neutral and positive information, and the tendency to negatively evaluate oneself. The interventions will train volunteers’ brains to automatically attend more to neutral and positive information, or to automatically evaluate themselves more positively. We hypothesize that one or both of these interventions by reducing UPC will in turn reduce BP, TPR and increase HRV in the lab and in daily life.
The proposed projects will show whether UPC causes increased CV activity and explains a considerable part of increased CV activity in daily life. If so, this result will stimulate an entirely new area of CV risk research, and general stress research, and potentially yield methods that reduce CVD risk in the future.
The proposed research will be performed as part of the research program "Self-regulation models for health, behavior and psychopathology", of the Institute of Psychology of Leiden University.