Reading: Kiecolt-Glaser, Renna, Shrout & Madison (2020) - Stress Reactivity Flashcards

1
Q

Adaptive Stress Response

A
  • When response aligns with magnitude of the stressor
  • And when the body can return to resting rate soon afterwards
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2
Q

Exaggerated Stress Response

A
  • Needlessly taxes the body i.e. preparing for action that might not be appropriate e.g. social evaluation mobilizes energy reserves even though this serves no function.
  • Not appropriate in length i.e. worry provokes an anticipatory stress response and post-stressor rumination hinders a return to baseline.
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3
Q

Depression as a factor effecting stress reactivity

A
  • Individual level factor
  • Reciprocal relationship between depression and stress reactivity
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4
Q

Stress reactivity —> depression

A
  • Larger responses to stressors increase the likelihood of heightened depressive symptoms and inflammation as well as the possibility of clinically significant depression.

-Inflammation can increase depression vulnerability by heightening amygdala reactivity to threat, reducing ventral striatal reward responding, and reducing serotonin availability within the brain

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5
Q

Depression —> stress reactivity

A
  • Could be current or past depression
  • The scarring hypothesis suggests that depression can result in cognitive, emotional, and behavioral changes. These “scars” result in someone being more vulnerable to depressive symptoms at times of high stress
  • Even mild depressive symptoms have been shown to heighten and prolong inflammatory activity during the TSST.
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6
Q

Worry + Rumination

A
  • Individual level factors
  • Collective termed preservation
  • Raise baseline levels of physiological arousal and facilitate ongoing reactivity even in the absence of imminent threat.
  • Rumination promoted larger and more long-lasting cortisol, blood pressure, heart rate, and HRV responses
  • Worry predicted lower HRV and diastolic and systolic blood pressure reactivity
  • Anticipatory cortisol in the TSST test explained 67% of the variance in cortisol reactivity during the stressor (i.e. when they actually had to do the speech).
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7
Q

Early Life Aversity

A
  • Individual level factor
  • Adaptive-calibration model emphasizes the plastic nature of stress-response systems by positing that they can recalibrate even after birth to align with unique environmental demands
  • Biological-embedding model suggests that stressful experiences early in life are programmed into cells that regulate inflammation, thus promoting greater psychological and biological stress reactivity throughout the life span as primed immune cells are more reactive to stress and unrestrained because of deficient inhibitory signalling.

-IL-6 levels were 2.35 times greater in individuals with a history of childhood abuse who experienced multiple stressors in the prior day compared with participants who experienced the same number of prior day stressors but had no abuse history

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8
Q

Social evaluation

A
  • Individual level factor

-Cortisol levels rise in response to evaluation in the TSST test and when receiving negative feedback.

-Stress recovery after completing the task was prolonged when individuals felt it was uncontrollable, slowing the return to baseline cortisol levels.

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9
Q

Interpersonal stress process

A
  • Dyadic level factor
  • Couples share each other’s stress reactivity
  • Partners response to external experiences becomes more similar over time.
  • Stress can be contagious
  • Partners can themselves be the cause of stress e.g. hostility argument and their response (further hostility) can sink their stress reactivity to their partner —> leading to worse outcomes.
  • Couples regulate each other’s emotional responses to stress e.g. can share positive emotions and become less stressed. But can also be a bad thing if constantly discussion negative emotions with each other (i.e. co rumination then this can heighten stress reactivity for both of the pair).
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10
Q

Relationship Quality

A
  • Dyadic level factor
  • Positive relationship perceptions and interactions including support and validation can lessen stress responses, whereas frequent conflict and hostile interactions (e.g. eye rolling, sarcasm) exacerbate stress responses.
  • Not surprising that unhappy marriages provide grounds for increasing risk of depressive symptoms + clinical depression.
  • Newlyweds who use more hostile behaviours during discussion have acute increases in stress hormones as well as bigger negative changes in immune function 24hrs later compare with less hostile couples.
    —-> sustained SNS responsiveness
    —-> predicted divorce/ unhappy marriages years later
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11
Q

Altering Stress Reactivity: Yoga + Mediation

A
  • Yoga + Mediation = “reboot” the SNS-dominated nervous system by increasing PNS activity.
  • Participants who were randomly assigned to meditation interventions had lower levels of inflammatory markers, cortisol, resting heart rate, triglycerides, and blood pressure after the intervention compared with control participants.
  • Seasoned meditators also had smaller cortisol rises in response to the TSST than nonmeditators.
  • Mindfulness meditation can hasten recovery from stressors; when viewing stressful images, participants’ amygdala activation levels were lower when they were instructed to use a mindfulness skill than when they were intentionally distracted
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12
Q

Altering Stress Reactivity: Health Behaviours

A
  • Growing evidence suggests that exercise, a healthy diet low in sugar and saturated fats, and regular high-quality sleep may also reduce stress reactivity as well as depressive symptoms
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13
Q

Altering Stress Reactivity: CBT

A
  • Cognitive reappraisal seeks to better align a person’s stress appraisals with the stressor’s actual threat.
  • Research addressing CBT’s ability to reduce physiological stress reactivity has been mixed.
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