10.2 Recorded Lecture - Stress Response and Health

• Western culture's work ethic, rooted in a 16th-century Protestant philosophy, combined with constant connectivity demands, leads to stress-related disorders.
• Stress occurs when the psychological perception of a stimulus exceeds an individual's coping capacity.
• Acute stress is generally immune enhancing while chronic stress is immune suppressive.

Brain Response

• Stress activates the limbic system, which then activates neural pathways and causes norepinephrine release and slower-acting cortisol release.
• Various other hormones also influence the stress response.

Adrenal Medulla Activation

• Stress triggers the release of epinephrine and norepinephrine from the adrenal medulla.
• This causes physiological effects like gluconeogenesis, increased cardiac output, increased blood pressure, and increased venous return, preparing the body for fight or flight.

HPA Axis

• The hypothalamus secretes corticotropin-releasing hormone (CRH), which stimulates the anterior pituitary to produce adrenocorticotropic hormone (ACTH).
• ACTH is transported to the adrenal glands, causing the release of glucocorticoid hormones, primarily cortisol.
• Cortisol enhances immunity during acute stress, but suppresses it during chronic stress.
• Cortisol easily diffuses into tissues and exerts significant adverse actions.
• Cortisol stimulates a negative feedback mechanism in the pituitary hypothalamus to decrease production.
• Cortisol causes gluconeogenesis and inhibits glucose uptake, resulting in overall increased blood glucose.

Metabolic Effects of Cortisol

• Cortisol increases protein synthesis in the liver but causes metabolism in other tissues.
• This increases circulating amino acid levels, but chronic exposure depletes protein stores in muscle, bone, connective tissue, and skin.
• Chronic cortisol secretion, combined with catecholamines and immune system response, contributes to metabolic syndrome and obesity.
• Over time, it leads to increased visceral fat and loss of muscle and bone mass.

Inflammatory and Immune Response

• Acutely, cortisol inhibits initial inflammatory effects.
• Cortisol suppresses the activity of TH1 cells, decreasing innate immunity and the pro-inflammatory response.
• At the same time, TH2 cell activity is stimulated, increasing adaptive immunity and the anti-inflammatory response.
• This TH1 to TH2 shift increases the likelihood of allergic responses, infections, and temporary worsening of autoimmune conditions.
• Corticotropin-releasing hormone (CRH) secreted by the hypothalamus acts at sites of inflammation.
• Peripheral CRH is pro-inflammatory, stimulating mast cells, which causes vasodilation and increased vascular permeability.
• Systemic stress responses decrease innate immunity and enhance adaptive immunity.
• Local stress responses may induce pro-inflammatory activities that cause infections, autoimmune, allergic, and neoplastic diseases.

Hormonal Influences

• Stress generally inhibits the female reproductive system via the HPA axis.
• Endorphins and enkephalins decrease pain and may play a role in excitement.
• Prolactin influences immune cells and has a positive influence on B-cell activation and differentiation.
• Oxytocin modulates fear and anxiety and attenuates the HPA stress response.
• Testosterone levels decrease after stressful stimulation, potentially increasing susceptibility to sepsis and mortality in males.

Stress and Coping

• Psychological distress involves a state of unpleasant arousal after exposure to life events, manifesting as psychological, emotional, cognitive, and behavioral changes.
• A situation that is a stressor for one person may not be for another, but the affected person still has the same physiological responses to stress.
• Effective coping strategies are typically problem focused and encourage seeking social support.
• Intervention can result in greater stress resilience and improve psychological than physiologic outcomes.