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Understanding Self-Efficacy, Stress, and Immune Response: The Interconnection of Behavior and Health

This text delves into the complex relationships between self-efficacy, stress, and immune system functions. It discusses how perceived control and coping strategies influence stress and health outcomes. Key concepts include guided mastery interventions, feedback mechanisms, and the impact of self-discrepancies on mental well-being. It also explores how cognitive representations of stressors affect immune responses, and the role of interventions like mindfulness and cognitive restructuring in managing stress. By combining behavioral theories and psychological insights, this work aims to illuminate pathways for improving health through enhanced self-efficacy and coping skills.

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Understanding Self-Efficacy, Stress, and Immune Response: The Interconnection of Behavior and Health

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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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