Exhaustive Study Notes on COM-B, Metabolism, Stress, and Psychosocial Health Factors in Health

The COM-B Model of Behavior

• The COM-B model posits that behavior arises from the convergence of Capability, Opportunity, and Motivation. A deficit in any of these components can lead to health disparities.

• Capability (Can I):

  • Physical: Refers to physical strength and dexterity.

  • Psychological: Refers to knowledge and skills.

• Opportunity (External):

  • Social: Influences from groups, social circles, cultural norms, and accepted behaviors.

  • Physical: The availability of time, money, and resources.

• Motivation (Should I):

  • Reflective: Conscious beliefs about health, such as skepticism about a treatment's efficacy (e.g., "this won't help me").

  • Automatic: Habits, emotions, and behaviors that have been reinforced over time.

Metabolic Adaptations to Energy Depletion

• Energy balance is determined by:

  • Energy intake: Fat, carbohydrates, and protein.

  • Energy expenditure: Calculated as the sum of Basal Metabolic Rate (BMR), digestion, physical activity, and exercise.

• Central Nervous System (CNS) Regulation: The CNS is critical in regulating metabolism through two primary processes:

  • Anabolic Processes: Increasing energy intake and reducing energy expenditure.

    • Scenario: Increasing calorie intake from $2000\,kcal$ to $2300\,kcal$ while maintaining the usual level of physical activity.

  • Catabolic Processes: Reducing energy intake and increasing energy expenditure.

    • Scenario: During a busy exam week, maintaining usual physical activity but skipping meals to study.

• Biological Response to Low Energy Stores: When stores are low, the body shifts towards energy conservation through the following changes:

  • Decreased: Insulin, leptin, and metabolic rate.

  • Increased: Hunger.

• Weight Maintenance: Maintaining weight loss is biologically challenging, with a high likelihood of weight regain due to these intrinsic metabolic shifts.

Social Norms and Health Behaviors

• Injunctive Norms: Beliefs about what society should do or what society approves of.

• Descriptive Norms: Observations of what people actually do.

  • Descriptive norms are a stronger predictor of health behaviors than injunctive norms.

Stress Physiology: Systems and Pathways

• Stress is understood through two lenses: exposure (external events or demands) and response (the internal reaction).

• Hypothalamic-Pituitary-Adrenal (HPA) Axis: Regulates the immune system and manages long-term stress responses.

  • Pathway: The Hypothalamus releases Corticotropin-Releasing Hormone ($CRH$) $\rightarrow$ the Pituitary gland releases Adrenocorticotropic Hormone ($ACTH$) $\rightarrow$ the Adrenal glands release $Cortisol$.

  • Characteristics: This system is slower than the autonomic response but has a longer-lasting effect. It is most strongly activated by uncontrollable, unpredictable, or socially evaluative situations (e.g., public speaking). This effect is robust regardless of individual experience.

  • Functions of $Cortisol$: Raising blood glucose, providing energy, maintaining body temperature, suppressing immunity, and sustaining the stress response.

• Autonomic Nervous System (ANS):

  • Sympathetic Nervous System: Triggers the "fight or flight" response, increasing Heart Rate ($HR$) and Blood Pressure ($BP$) while releasing adrenaline.

  • Parasympathetic Nervous System: Engages the "rest and digest" state for recovery. It is always active, decreasing $HR$ and $BP$ and increasing digestion to maintain physiological balance.

Impact of Stress on Physiological Systems

• Cardiovascular System: Prolonged increases in $BP$ and $HR$ due to chronic stress can lead to hypertension.

• Immune System: The transcript notes that "Stress is always bad!" regarding its link to inflammation and the innate immune response.

  • Acute Stress: Can temporarily boost the immune system by mobilizing immune cells (an adaptive response for injury/infection). It specifically boosts humoral immunity but decreases cell-mediated immunity.

  • Chronic Stress: Suppresses the immune system and promotes an inflammatory response, impairing healing. This results in decreased overall immunity and increased inflammation. It decreases both humoral and cell-mediated immunity.

• Specific Immune Responses:

  • Innate Immunity (Inflammation): Both acute and chronic stress increase pro-inflammatory cytokines, such as interleukin-6 ($IL-6$).

  • Adaptive Immunity: Generally dampened by stress. A key exception is the humoral response (antibodies), which can increase during acute stress due to the dysregulation of latent viruses like Epstein-Barr.

Social Connectedness and Support

• Social Connectedness: Defined by the number of meaningful relationships an individual has. It influences stress levels, coping mechanisms, and health behaviors.

• Benefits and Risks: Social support reduces stress and improves adherence to health behaviors, whereas social isolation is a strong predictor of mortality.

• Perceived vs. Received Support:

  • Perceived Support: The belief that support would be available if needed. This is more salient over time than received support.

  • Received Support: The support that was actually provided to the individual.

• Measurements of Social Support:

  • Structure: The number of people in a social network.

  • Function: The perceived quality and helpfulness of support.

  • Subjective: Self-reported satisfaction with relationships.

  • Social Integration: The degree of participation in various social roles (e.g., marriage, employment, religious groups).

  • Social Networks: The web of ties surrounding an individual, characterized by size, density, frequency of contact, and reciprocity.

  • Social Support Resources: Emotional (care/empathy), Informational (advice), Instrumental (tangible help), and Appraisal (feedback on self-worth or situation).

  • Loneliness vs. Isolation: Loneliness is the subjective feeling of lacking connection; social isolation is the objective absence of ties. These are distinct; one can be isolated without feeling lonely.

Atherosclerosis: Mechanisms and Progression

• Definition: The process of inflammation and plaque buildup within arteries, causing "hardening of the arteries" that supply oxygen and nutrients.

• Developmental Steps:

  1. Endothelial Damage: Injury to the inner lining of the artery.

  2. Oxidation of LDL: High levels of low-density lipoprotein ($LDL$) cholesterol become oxidized.

  3. Inflammation: Immune cells are recruited to the damage site.

  4. Macrophage Engulfment: Macrophages engulf oxidized $LDL$, forming foam cells and triggering further immune activation.

  5. Plaque Formation: Foam cells accumulate, leading to plaque and arterial blockage.

• Plaque Types:

  • Stable Plaque: Thick fibrous cap; surface erosion leads to gradual narrowing (chronic).

  • Unstable Plaque: Thin cap; prone to rupture, resulting in clot formation, heart attacks ($HA$), or strokes ($S$).

Psychosocial Risk Factors and Disease Outcomes

• Chronic Stress: Increases $Cortisol$ (and inflammation) and norepinephrine. Animal studies show increased Vascular Endothelial Growth Factor ($VEGF$), promoting angiogenesis (vessel formation) which may enhance tumor growth through beta-adrenergic activation.

• Depression: Associated with poor treatment adherence and increased inflammation.

• Social Isolation: Eliminates the buffering effect of support; strongly predicts mortality.

• Hostility and Cynicism: Linked to increased $BP$, sympathetic activity, and $CVD$ risk.

• Disease Outcome Definitions:

  • Incidence: First-time development of a disease.

  • Recurrence: Return of disease after treatment/remission.

  • Progression: Worsening of disease over time.

  • Survival: Length of time lived after diagnosis.

Adjustment to Illness and Interventions

• Adjustment Trajectories:

  • Resilient: Low distress maintained (majority).

  • Recovery: Initial high distress followed by reduction (moderate group).

  • Chronic: High distress maintained throughout (minority group).

• Predictors of Poor Adjustment: Low social support, Low Socioeconomic Status ($SES$), avoidant coping, advanced cancer stage, longer treatment, specific illness beliefs, being non-married, and unemployment.

• Psychosocial Interventions: Strong evidence for mental health improvement; mixed evidence for physical survival.

  • Types: Cognitive Behavioral Therapy ($CBT$), Stress Management, Behavioral Interventions, Social Support Interventions, Mindfulness, and Psychoeducation.

• ENRICHD Study: $CBT$ helped with depression but did not improve overall mortality. Effects were larger for patients starting with high distress and larger for white men, highlighting health disparities in the current medical system.

Research Methodology and Causality

• Bradford Hill Causality Criteria:

  • Temporality: Cause precedes effect.

  • Strength of Association: Measured by effect size (Relative Risk ($RR$) or Hazard Ratio ($HR$)).

    • $RR \approx 1.0$: No effect.

    • $RR \in [1.1, 1.3]$: Weak/small effect.

    • $RR \in [1.3, 2.0]$: Moderate effect.

    • RR > 2.0: Strong effect.

    • Note: A Confidence Interval ($CI$) including $1.0$ suggests confounding or chance.

  • Biological Plausibility: Known mechanism exists.

  • Dose-Response: Increased exposure leads to increased risk.

  • Experimental Evidence: Evidence from controlled trials.

  • Consistency: Repeatable across studies.

  • Coherence: Doesn't conflict with existing knowledge.

  • Specificity: Specific exposure leads to specific outcome.

  • Analogy: Similar established relationships exist.

• Study Design Strength:

  1. Prospective: Follows people over time (Strong).

  2. Case-control: Retrospective comparisons (Medium).

  3. Cross-sectional: One time point only (Weak).