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The stimulus

The stimulus. Self-efficacy: Sources of efficacy judgments. Feedback re: behavioral subgoals ( Cf : Karoly , Carver models) Sub-goals: concrete, specific  discernable feedback Attitude change: Behavior  attitude “Guided mastery” interventions Modeling Bandura & Walters:

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The stimulus

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  1. The stimulus

  2. Self-efficacy:Sources of efficacy judgments • Feedback re: behavioral subgoals(Cf: Karoly, Carver models) • Sub-goals: concrete, specific  discernable feedback • Attitude change: Behavior  attitude • “Guided mastery” interventions • Modeling • Bandura & Walters: • Coping model >> Mastery model • Controls resources > rewarded > simple performance • Similarity of model to participant: Peer-based interventions • Social persuasion • Normative / personal information • Social network mechanism? • Feedback post performance > simple attitude change • Interpretation of somatic information • E.g., “fear of fear” • Cognitive representation of disease • Miller C-SHIP model: Rx to “hot” disease or physical information

  3. Perceived control and stress • Averill, types of control: • Behavioral • Brown: Bereavement  stress  mortality • Learned helplessness • Decisional • Singer: stress Rx & perceived controllability • Interpretative • Taylor: “search for meaning” & coping w/cancer • “Hopelessness” & depression • Predictive • DV literature / Averill data: predictability >> aversiveness

  4. Efficacy training  immune system Immune parameters x Efficacy training stage x “Enhancer” v. “Suppressor” group

  5. Perceived control & stress, 2 • Bandura; • Consequences of low perceived control • Subjective stress & negative affect • Health risk behavior • Autonomic activation • HPA activation • Plasma catecholamine secretion • HPA activation decreased lymphocyte proliferation • Induced self-efficacy • Rapid efficacy gain  immuno-enhancing • High cortisol release  immuno-suppressant

  6. Self-discrepancies & affect Actual Ideal Ought Own Other Own Other Own Other Depression, disappointment Dejection, loss of esteem Fear, perceived threat Guilt, self-recrimination Anxiety, fear, social anxiety Depression, sadness, self-disappointment

  7. Self-discrepancy model of stress. Actual (self-rated) stressful events ? • Chronic availability of self-discrepancy • Ideal :: Actual • Ought :: Actual ? ? Acute negative self- appraisal • Negative affect • Depression • Anxiety Contextual activation of self-discrepancy Cortisol secretion NK suppression

  8. Primed self-discrepancies  NK activation • “Normal” Ss show immune enhancement after priming with yoked stimuli • Dysphoric Ss show immune suppression after self-priming with “ideal” stimuli • Anxious Ss show immune suppressionafter self-priming with “ought” stimuli

  9. Robles et al.: Balanced immune responses • Inflammation: • attracts immune cells to injury site • Induce adaptive “sickness behavior” • Activates HPA axis • HPA activation: • Stimulates cortisol production • Down-regulates pro-inflammatory cytokines Macrophages etc.

  10. Robles: Stress – modulated immune responses. A.Brain effects of stress: • Reduce glucocorticoid receptors • Disrupt receptor functioning • Dysregulate HPA axis • Decrease threshold for HPA arousal in response to stress • Possible chronic HPA arousal • Cortisol production Immune suppression

  11. Robles: Stress – modulated immune responses, 2. B. Cellular effects of stress: • Disrupt functioning of corticoid receptors on cytokine-producing cells • Less sensitive to the anti-inflammatory effects of cortisol

  12. Robles: Stress – modulated immune responses, 2. C. Immune suppression from stress / negative affect: • HPA activation  cortisol  immune suppression • Inhibits ability to fight off infection • Chronic infections • Inflammation

  13. Robles: Stress – modulated immune responses, 2. D.Proinflammatory cytokines • Reduce or disrupt glucocorticoid receptors in the brain • All four mechanisms • Chronic elevated production of proinflammatory cytokines • Direct effects on chronic disease and pathophysiology • Indirect via, e.g., production of C-reactive protein. CRP

  14. Behavioral intervention designs Not typical: direct affect regulation (DBT) skills. • Stress management • Education • Cognitive restructuring (simplified CBT) • Coping skills training • Support provision • Relaxation • Deep muscle • “Autogenic” • Mindfulness • Disclosure • Kemeny group: disclosure of sexual orientation • Pennebaker: systematic writing / “uplifting” language

  15. Stress & coping model of immune supression Mediating responses Unmeasured moderators Appraisal Catecholamine / corticosteroid / HPA  cellular & humoral immune cascade Perceived threat / vulnerability Subjective (dis)stress Chronic (?) stress Perceived control / self-efficacy Perceived Stress Life events Coping Approach / active coping Arousal & activity Ψ closeness Avoidant / affective coping Risk behavior: tobacco, etoh, drugs & sex…

  16. Alternate conceptualization Appraisal Negative affect Catecholamine / corticosteroid / HPA  cellular & humoral immune cascade Perceived threat / vulnerability • Depression • Neuroticism • Poor affect regulation • Affect or thought suppression Chronic (?) stress Perceived control / self-efficacy Perceived Stress Coping Approach / active coping Arousal & activity Avoidant / affective coping Risk behavior: tobacco, etoh, drugs & sex…

  17. Stress & coping intervention model Mediating responses Appraisal Perceived threat / vulnerability  • Cognitive reframing, • Basic CBT techniques Subjective (dis)stress  Perceived control / self-efficacy  • Bandura-esque self-efficacy training • Coping skills training Coping • Relaxation training • Depression treatment Approach / active coping Arousal & activity • Behavioral interventions  Avoidant / affective coping  Risk behavior: tobacco, etoh, drugs & sex…

  18. Thorton et al., Relaxation training  NA  inflammation • Study population • n = 45 breast cancer patients w / “clinically significant” depression scores on CES-D • (20% of patient population) • M = 45 days post-surgery • Intervention • Group-based (8-12 pt.) • 4 months of weekly 90 min. sessions, 8 months of monthly sessions • Targets: • reduce stress & emotional distress • enhance social adjustment, • improve compliance with cancer treatment • enhance health behaviors.

  19. Thorton et al., results • Clear effects on 3 core Ψ outcomes: • Depression • Fatigue • Pain tolerance • Asymptoteabout 8 months

  20. Thorton et al., results, 2 • More modest, but significant effects on immune / inflammation markers • WBC counts • T helper :: suppressor ratio • Δ in Ψ variables  less inflammation

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