Health Psychology Stress & Stressors (Part IV)
Measuring Stress
Self-Report Inventories
Life events inventories
Daily hassles scales
Ecological Momentary Assessment (EMA):
Self-reports made closer in time to the events being investigated
Signal-contingent recording (ambulatory diary record): captures stressors as they occur
Physiological Measures
Changes in physiological measures as a response to:
Stress-induced activation
Emotion-induced activation of the sympathetic division of the autonomic nervous system
Hormonal association: levels of epinephrine and norepinephrine during or immediately after stress
Limitations of physiological measures in assessing stress:
Potential variability in physiological responses.
Cardiovascular Reactivity (CVR)
Individual’s characteristic reaction to stress
Measured changes in:
Heart rate
Blood pressure
Hormonal levels
Vascular responses: peripheral resistance
Reactivity Hypothesis:
Individuals showing large changes in blood pressure and vascular resistance to stress have an increased risk of developing heart disease.
Identifies individuals termed as hyperreactors.
Respiratory Sinus Arrhythmia (RSA)
Variability in heart rate in synchrony with breathing (vagal tone)
High RSA is linked to better emotional well-being
Low RSA is correlated with poor health outcomes including:
Cardiovascular disease
Obesity
Diabetes
How Does Stress Make You Sick?
Ader and Cohen (1985): Demonstrated that the immune system could be conditioned
Natural stimulus paired with an unconditioned stimulus leads to nausea reaction.
Another unconditioned stimulus resulting in death.
Pert's Findings:
Identified brain receptors for immune molecules.
Indicates how the brain can influence immune system activity.
Solomon's Contribution:
Published a landmark article on psychoneuroimmunology (PNI):
Explores links among emotions, immunity, and disease.
Emphasizes the interaction of:
Psychological (psycho)
Neuroendocrine (neuro)
Immunological processes in the context of stress and illness.
Research Themes in Psychoneuroimmunology:
Short-term stressors can:
Trigger up-regulation of immune response.
Long-term, chronic stressors can:
Have damaging effects by suppressing immunity.
Pathways from Stress to Disease
Direct Effect Hypothesis:
States that immunosuppression is part of the body's natural response to stress.
Involves the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic-adrenal-medullary (SAM) system.
Involves T cells and B cells (types of lymphocytes).
Highlights the cortisol awakening response.
Stress and Blood Clotting:
Activation of SAM and HPA influences blood clotting processes.
Overcommitment, overload, and job-related stress linked to hypercoagulable states.
Indirect Effect Hypothesis:
Suggests that immunosuppression occurs as an aftereffect of the stress response.
States that stress may lead to maladaptive behaviors that disrupt immune functioning.
Duration of Stress:
The ability to recover after a stressful experience is critical in determining the total burden on an individual.
Allostatic Load:
Refers to the cumulative long-term effects of the body's physiological responses to stress.
Classifies stressors as:
Acute stressors
Chronic stressors