The sympathomedullary (SAM) pathway is the immediate arm of the stress response. Trace its full pathway from stressor perception to the release of stress hormones into the bloodstream.

A: Hypothalamus → CRH → anterior pituitary → ACTH → adrenal cortex → adrenaline into bloodstream

B: Amygdala/hypothalamus → sympathetic nervous system → adrenal medulla → adrenaline (epinephrine) and noradrenaline (norepinephrine) into bloodstream

C: Prefrontal cortex → parasympathetic nervous system → adrenal cortex → cortisol into bloodstream

D: Hippocampus → CRH → posterior pituitary → oxytocin → adrenal medulla → adrenaline into bloodstream

Correct: Amygdala/hypothalamus → sympathetic nervous system → adrenal medulla → adrenaline (epinephrine) and noradrenaline (norepinephrine) into bloodstream

The sympathomedullary (SAM) pathway is the fast stress response axis. Pathway: (1) Amygdala detects threat and signals the hypothalamus. (2) Hypothalamus activates the sympathetic branch of the autonomic nervous system (ANS) via preganglionic fibres to the spinal cord. (3) Postganglionic sympathetic fibres reach multiple target organs — heart, lungs, blood vessels, sweat glands — producing the immediate fight-or-flight effects. (4) A specialised branch of the sympathetic system innervates the adrenal medulla (the inner part of the adrenal gland). The adrenal medulla is embryologically derived from neural crest tissue and functions as a modified ganglion; its chromaffin cells release adrenaline (~80%) and noradrenaline (~20%) directly into the bloodstream. This hormonal component amplifies and sustains the neural sympathetic response. The entire pathway activates within seconds — producing increased heart rate, elevated blood pressure, bronchodilation, pupil dilation, and mobilisation of glucose. The SAM response is distinct from the HPA axis (which releases cortisol and takes 15–30 minutes). Repeated SAM activation contributes to cardiovascular disease through endothelial damage, hypertension, and arterial plaque formation.

Through which physiological mechanisms does chronic psychological stress increase the risk of coronary heart disease (CHD)?

A: Chronic stress lowers heart rate variability, reducing cardiac demand; the risk comes from subsequent rebound tachycardia when stress resolves

B: Chronic stress elevates catecholamines and cortisol, raising blood pressure and LDL cholesterol, damaging arterial endothelium, promoting platelet aggregation and inflammation, and accelerating atherosclerosis

C: Chronic stress raises heart rate to high aerobic levels continuously, strengthening the cardiac muscle but causing arrhythmias over time

D: Chronic stress selectively damages the right ventricle by redirecting blood flow from the heart muscle to skeletal muscles, causing ischaemia

Correct: Chronic stress elevates catecholamines and cortisol, raising blood pressure and LDL cholesterol, damaging arterial endothelium, promoting platelet aggregation and inflammation, and accelerating atherosclerosis

Chronic stress increases CHD risk through multiple converging biological pathways: (1) Hypertension: repeated sympathetic activation raises blood pressure; sustained hypertension damages arterial walls. (2) Endothelial injury: catecholamines (especially noradrenaline) are directly toxic to arterial endothelium at high concentrations; damaged endothelium is the initiating lesion in atherosclerosis. (3) Lipid changes: cortisol raises LDL cholesterol and triglycerides, promoting plaque formation. (4) Inflammation: chronic stress activates inflammatory pathways (NF-κB → IL-6, CRP); inflammation promotes plaque instability and rupture. (5) Platelet aggregation: stress increases platelet stickiness, raising clotting risk and acute myocardial infarction vulnerability. (6) Behavioural pathways: stressed individuals often smoke more, exercise less, eat poorly, and sleep less — all independent CHD risk factors. Rozanski, Blumenthal, & Kaplan (1999) reviewed the literature and concluded that psychological stress constitutes an independent CHD risk factor, with effect sizes comparable to conventional risk factors like dyslipidaemia.

Friedman and Rosenman (1959) proposed the Type A behaviour pattern as a risk factor for coronary heart disease. What are the core characteristics of Type A, and what did the Western Collaborative Group Study (WCGS) find?

A: Type A = high neuroticism and introversion; the WCGS found Type A individuals had triple the rate of CHD compared to Type B over 8.5 years

B: Type A = a cluster of time urgency, competitive drive, achievement striving, and free-floating hostility; the WCGS found Type A men had approximately twice the rate of CHD compared to Type B men over 8.5 years

C: Type A = impulsive, extroverted, sensation-seeking; the WCGS found no significant difference in CHD rates between Type A and Type B after controlling for diet

D: Type A = perfectionism and obsessive attention to detail; the WCGS found Type A personality predicted CHD only in women

Correct: Type A = a cluster of time urgency, competitive drive, achievement striving, and free-floating hostility; the WCGS found Type A men had approximately twice the rate of CHD compared to Type B men over 8.5 years

Friedman and Rosenman (1959) described Type A behaviour pattern as a complex of: (1) time urgency / impatience (always rushing, finishing others' sentences); (2) competitive drive and achievement striving; (3) free-floating hostility (quick to anger, explosive); and (4) polyphasic activity (doing multiple things simultaneously). Type B is the contrasting pattern — relaxed, patient, non-competitive. The Western Collaborative Group Study (Rosenman et al., 1975) prospectively followed 3,154 California businessmen aged 39–59, assessed for Type A/B at baseline, over 8.5 years. Type A men had approximately twice the incidence of CHD compared to Type B men, even after controlling for conventional risk factors (smoking, BP, cholesterol, family history). This landmark result established personality as an independent CHD risk factor. However, subsequent research identified a problem: Type A as a global construct is not consistently predictive; the "toxic" component is hostility specifically (not time urgency or competitiveness).

Later research refined the Type A CHD link by identifying the specific "toxic ingredient." What did Dembroski, Williams, and others find was the active component?

A: Time urgency was the sole predictor; competitive drive and hostility were confounders rather than causal factors

B: Cynical hostility — characterised by angry, suspicious, contemptuous attitudes toward others — was the strongest predictor of CHD and mortality, independent of the other Type A components

C: Achievement striving predicted CHD in men, while free-floating hostility was the key risk factor only in women

D: The combination of time urgency and polyphasic activity (doing multiple things simultaneously) was the most reliable predictor, not hostility

Correct: Cynical hostility — characterised by angry, suspicious, contemptuous attitudes toward others — was the strongest predictor of CHD and mortality, independent of the other Type A components

Williams (1984) and subsequent meta-analyses (Dembroski & Costa, 1987; Miller et al., 1996) found that when the Type A components were disaggregated, cynical hostility emerged as the most consistent and strongest predictor of CHD outcomes. The MMPI Hostility scale (Ho scale) — measuring suspicion, resentment, and contempt toward others — predicted coronary events and mortality more reliably than the global Type A pattern. Possible mechanisms: (1) High-hostility individuals show exaggerated cardiovascular (BP, heart rate) and catecholamine responses to interpersonal provocations — greater cumulative endothelial damage. (2) Hostility predicts poorer social support (people find hostile individuals difficult to befriend), removing a known stress buffer. (3) Hostile individuals are more likely to engage in health-damaging behaviours (smoking, alcohol use, sleep disruption). This refinement matters because interventions targeting only time management in Type A individuals may miss the core risk; hostility-focused cognitive-behavioural approaches (e.g., anger management) are more likely to reduce CHD risk.

Kiecolt-Glaser et al. (1984) conducted a pivotal study on stress and immune function. What was the design, and what did it show?

A: They exposed healthy volunteers to a live cold virus under high vs low stress conditions and counted which group developed colds; the high-stress group had significantly more infections

B: They measured natural killer (NK) cell activity in 75 medical students at two time points — one month before exam period and during exams — and found significantly lower NK cell activity during exams

C: They compared NK cell activity in caregivers vs controls and found no significant difference, suggesting social role rather than stress determines immune function

D: They administered stress inoculation training to hospital patients and found it significantly improved post-operative immune markers compared to controls

Correct: They measured natural killer (NK) cell activity in 75 medical students at two time points — one month before exam period and during exams — and found significantly lower NK cell activity during exams

Kiecolt-Glaser et al. (1984) measured immune function in 75 first-year medical students at two points: one month before final examinations (lower-stress baseline) and during the exam period (high stress). Blood samples revealed significantly lower natural killer (NK) cell activity during exams compared to the baseline period. NK cells are a key component of innate immunity — they destroy virally infected cells and tumour cells without prior sensitisation. The repeated-measures design controlled for individual differences. The study also found that students who were lonely or who reported fewer social supports showed the most pronounced immune suppression. This was among the first human studies to directly link an everyday, naturalistic stressor to objectively measurable immune function changes — founding what became the field of psychoneuroimmunology (PNI). A related study (Kiecolt-Glaser et al., 1987) found that Alzheimer's caregivers — a chronically stressed group — showed substantially poorer immune function than matched controls, including slower wound healing.

Cohen et al. (1991) conducted a controlled study using deliberate viral exposure. What did they find, and why is this study methodologically stronger than correlational immune research?

A: They found that high-stress participants were 5× more likely to develop colds; the study was stronger because it used a randomised cross-over design eliminating all individual differences

B: They assessed psychological stress in 394 healthy volunteers, then deliberately exposed them to rhinovirus; participants with higher stress index scores were significantly more likely to develop a clinical cold, in a dose-dependent relationship

C: They found that stress did not independently predict cold incidence after controlling for prior immunity; the relationship was fully explained by health behaviours

D: They found that acute stress (within the past week) predicted cold incidence but chronic stress over 6+ months was protective due to immune system habituation

Correct: They assessed psychological stress in 394 healthy volunteers, then deliberately exposed them to rhinovirus; participants with higher stress index scores were significantly more likely to develop a clinical cold, in a dose-dependent relationship

Cohen, Tyrrell, and Smith (1991) assessed a composite stress index (including life events, perceived stress, negative affect) in 394 healthy volunteers and then deliberately exposed them to one of five respiratory viruses (or a control saline solution) via nasal drops, in a quarantine facility. Participants were then monitored for infection and clinical illness. After controlling for pre-existing antibody levels, health behaviours (smoking, alcohol, exercise, sleep), and demographic factors, those with higher stress index scores showed a significantly greater rate of both infection and clinical disease. The dose-response relationship was notable: risk increased with each increment of the stress index. This design — with controlled viral exposure, quarantine, and objective disease endpoints — was far stronger than the correlational studies showing stress-immune associations because it could establish that stress preceded illness onset, minimising reverse causation. A 1998 replication with 276 volunteers found that chronic stressors (lasting >1 month) were more strongly predictive than acute stressors, and that interpersonal stressors and work stressors were particularly potent.

Through which mechanisms does stress (specifically cortisol and catecholamines) suppress immune function?

A: Cortisol directly destroys immune cells by lysing their membranes; catecholamines prevent bone marrow from producing new immune cells

B: Cortisol binds glucocorticoid receptors on immune cells, suppressing production of pro-inflammatory cytokines (IL-1, IL-6, TNF-α), reducing T-cell proliferation, NK cell activity, and antibody production; catecholamines redistribute lymphocytes away from peripheral blood

C: Cortisol primarily suppresses the innate immune system by destroying neutrophils; catecholamines suppress only humoral (antibody) immunity

D: Cortisol raises body temperature, creating conditions inhospitable to immune cell function; catecholamines lower blood pH, acidifying the environment where immune cells operate

Correct: Cortisol binds glucocorticoid receptors on immune cells, suppressing production of pro-inflammatory cytokines (IL-1, IL-6, TNF-α), reducing T-cell proliferation, NK cell activity, and antibody production; catecholamines redistribute lymphocytes away from peripheral blood

Cortisol suppresses immune function through multiple cellular mechanisms: (1) Glucocorticoid receptors (GR) are expressed on virtually all immune cell types. When cortisol binds GR, it acts as a transcription factor, downregulating genes for pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, IFN-γ) and upregulating anti-inflammatory mediators. (2) Reduced cytokine production impairs communication between immune cells, slowing both innate and adaptive responses. (3) T-lymphocyte proliferation is suppressed (cortisol induces apoptosis in activated T-cells). (4) NK cell cytotoxicity is reduced. (5) B-cell antibody production is diminished. Catecholamines (adrenaline, noradrenaline) act through adrenergic receptors on immune cells, redistributing lymphocytes from secondary lymphoid tissues (spleen, lymph nodes) to peripheral blood in the short term (acute effect), but chronically suppressing NK cell activity and Th1 cytokine responses. Chronic stress also produces paradoxical proinflammatory effects (through sympathetic-neural–immune interactions and GR resistance in some cell types), contributing to inflammatory diseases.

True or False: The global Type A behaviour pattern (including time urgency, achievement striving, and hostility combined) has been confirmed as a reliable predictor of CHD in all major prospective studies since the WCGS.

Answer: False

False. The relationship between global Type A and CHD has been much less consistent than the original WCGS suggested. Several large prospective studies — including MRFIT (Multiple Risk Factor Intervention Trial) and the Framingham Heart Study re-analysis — did not find the global Type A pattern reliably predictive of CHD once conventional risk factors were controlled. Meta-analyses (e.g., Booth-Kewley & Friedman, 1987; Matthews, 1988) produced inconsistent results. The field largely concluded that Type A as a global construct was too heterogeneous: time urgency and achievement striving appear relatively benign or even health-protective, while cynical hostility (the "toxic core") is the active ingredient. Additionally, measurement issues were significant: the original Structured Interview method of assessing Type A (more valid but labour-intensive) predicted CHD better than questionnaire measures. The construct has been substantially refined; contemporary research focuses on hostility, anger expression, and vital exhaustion rather than global Type A.