Source: Abnormal Psychology lecture notes, University of Florida
Difficulty: Intermediate | Prerequisites: Basic understanding of the nervous system and endocrine system. Familiarity with introductory abnormal psychology concepts (biopsychosocial models, what qualifies as "abnormal") is helpful.
This topic sits at the intersection of biological psychology and health psychology within an abnormal psych course. You need it to understand how the body's normal protective systems can turn pathological when stress becomes chronic. It connects directly to later material on anxiety disorders, depression, psychosomatic illness and the biopsychosocial model. If you are comfortable with basic neuroanatomy (hypothalamus, adrenal glands, sympathetic nervous system) you are ready for this.
Stress triggers two main hormonal systems: the SAM system (fast, adrenaline-based) and the HPA axis (slower, cortisol-based). Both are useful in short bursts but damaging when they stay switched on. Chronic activation leads to cardiovascular disease, immune suppression, metabolic problems and cognitive decline, a cumulative toll the field calls "allostatic load."
Stress
A physiological reaction to perceived aversive or threatening situations, involving behavioural, autonomic and endocrine responses. In simple terms, it is your body's alarm system firing up when it senses danger, whether or not the danger is physical.
Fight-or-flight response
The coordinated set of behavioural, autonomic and endocrine reactions that prepares an organism to confront or escape a threat. Think of it as the body's emergency mode: heart rate climbs, muscles get more blood, digestion pauses.
Sympathetic adrenal-medullary (SAM) system
The neuroendocrine pathway in which the hypothalamus activates the sympathetic nervous system, prompting the adrenal medulla to release catecholamines (epinephrine and norepinephrine). In simple terms, this is the fast-acting branch of the stress response, responsible for the immediate adrenaline rush.
Catecholamines
A class of stress hormones, chiefly epinephrine (adrenaline) and norepinephrine (noradrenaline), released by the adrenal medulla during sympathetic activation. Think of them as the chemical messengers that make your heart pound and your hands shake under pressure.
Hypothalamic-pituitary-adrenal (HPA) axis
The slower neuroendocrine cascade in which the hypothalamus secretes CRH, the pituitary releases ACTH, and the adrenal cortex releases glucocorticoids (primarily cortisol). In simple terms, this is the body's sustained stress circuit. Where the SAM system is the sprinter, the HPA axis is the marathon runner.
Corticotropin-releasing hormone (CRH)
A peptide hormone secreted by the hypothalamus that triggers the release of ACTH from the anterior pituitary gland. Think of it as the starting pistol for the HPA axis.
Adrenocorticotropic hormone (ACTH)
A hormone released by the pituitary gland in response to CRH. It travels through the blood to stimulate the adrenal cortex to produce cortisol. In simple terms, ACTH is the relay runner between the brain and the adrenal glands.
Glucocorticoids (cortisol)
Steroid hormones produced by the adrenal cortex that regulate glucose metabolism, protein breakdown, fat mobilisation and immune function. Cortisol is the one students need to know best. It is useful in a crisis but harmful when levels stay elevated for weeks or months.
Allostasis
The body's process of achieving stability through physiological change, including adjustments to set points for blood pressure, heart rate and hormone levels. Think of it as the body constantly recalibrating, rather than holding one fixed "normal."
Allostatic load
The cumulative wear and tear on the body produced by repeated or chronic activation of allostatic systems. In simple terms, this is what happens when the stress dial has been turned up for so long that the body starts breaking down.
Hypothalamus detects a threat and activates the sympathetic nervous system
Sympathetic nerves signal the adrenal medulla to release epinephrine and norepinephrine into the bloodstream
Effects are rapid, within seconds:
Glucose mobilisation: epinephrine triggers the liver to release stored glucose for immediate energy
Cardiovascular changes: heart rate and cardiac output increase, blood is redirected to skeletal muscles, blood pressure rises
Norepinephrine in the brain: acts as a neurotransmitter that sharpens attention and influences behavioural responses
This system is responsible for the immediate physical sensations of stress: racing heart, sweaty palms, heightened alertness
The hypothalamus secretes corticotropin-releasing hormone (CRH)
CRH travels to the anterior pituitary, which releases adrenocorticotropic hormone (ACTH)
ACTH circulates to the adrenal cortex, stimulating the release of glucocorticoids (mainly cortisol)
Effects take minutes to hours and last longer than SAM activation:
Metabolic effects: cortisol enhances glucose metabolism, promotes protein breakdown and mobilises fat stores to sustain energy supply
Blood flow and behaviour: increases blood flow to active tissues and affects behavioural responsiveness (vigilance, anxiety)
Reproductive suppression: cortisol reduces the sensitivity of gonads to reproductive hormones, which is why chronic stress can impair fertility
Immune modulation: short-term cortisol release is anti-inflammatory, but prolonged exposure suppresses immune function
SAM is the first responder: fast onset, short duration
HPA axis provides sustained backup: slower onset, longer-lasting effects
Both systems are controlled by the hypothalamus, and both can become dysregulated under chronic stress
When the stress response stays active for weeks or months, the same mechanisms that protect you in the short term begin to cause damage.
Cardiovascular disease: sustained high blood pressure, increased risk of heart disease and stroke
Endocrine and metabolic disorders: chronic cortisol exposure promotes insulin resistance, weight gain (particularly visceral fat), and metabolic syndrome, which in turn raises diabetes risk
Mental health: prolonged glucocorticoid exposure is linked to cognitive deficits (memory, concentration) and psychiatric conditions such as steroid psychosis
Immune suppression: the immune system is dampened, leading to greater susceptibility to infections and slower wound healing
Allostasis is the body's way of maintaining stability by adjusting physiological set points. Under normal conditions this is adaptive: your blood pressure rises when you stand up, for instance, and settles again.
Allostatic load is what accumulates when these adjustments are demanded too often or for too long. The body's regulatory systems wear out, set points drift, and the risk of stress-related disease climbs. This concept is central to understanding why two people can face similar stressors yet develop very different health outcomes: individual allostatic load accounts for much of the difference.
Physical activity: regular exercise helps recalibrate the HPA axis and reduces the physiological markers of chronic stress
Social support: strong social connections buffer the stress response, lowering cortisol output and cardiovascular reactivity
Psychological resilience: early nurturing experiences shape how effectively a person's stress systems respond later in life; resilience is partly built, not purely innate
This material explains why workplace burnout is a medical concern, not just a morale problem: chronic occupational stress drives measurable increases in cortisol, blood pressure and inflammatory markers. It is also the biological basis for prescribing exercise and social engagement as first-line interventions for stress-related conditions. Clinicians use the allostatic load framework to assess cumulative health risk in patients with histories of adverse childhood experiences (ACEs) or prolonged caregiving roles.
Students often confuse the SAM system with the HPA axis. Remember: SAM is fast (seconds, catecholamines, adrenal medulla) and the HPA axis is slow (minutes to hours, cortisol, adrenal cortex). They are two separate pathways, both starting at the hypothalamus but ending at different parts of the adrenal gland.
Students sometimes think cortisol is purely harmful. It is not. Short-term cortisol release is protective and anti-inflammatory. The damage comes from chronically elevated levels.
Allostasis and homeostasis are frequently mixed up. Homeostasis implies returning to a fixed set point. Allostasis means the set point itself can shift in response to demand. Allostatic load is the cost of those shifts accumulating over time.
"Fight or flight" is often treated as if it were only psychological. It is a full physiological cascade involving the endocrine, cardiovascular and immune systems.
⚠️ Be able to trace the full SAM pathway: hypothalamus → sympathetic nervous system → adrenal medulla → epinephrine and norepinephrine. Know the downstream effects on glucose and the cardiovascular system.
⚠️ Be able to trace the full HPA axis: hypothalamus → CRH → pituitary → ACTH → adrenal cortex → cortisol. Know the effects on metabolism, immunity and reproduction.
⚠️ Distinguish allostasis from allostatic load. Expect a question that asks you to explain how the same adaptive mechanism becomes pathological.
⚠️ Chronic stress health outcomes are a common exam theme: cardiovascular disease, metabolic syndrome, immune suppression, cognitive deficits. Be ready to link each back to either sustained SAM activation or chronic cortisol elevation.
⚠️ Know at least two evidence-based interventions (exercise, social support) and be able to explain the biological mechanism by which they help.
True or false: The SAM system releases cortisol. (False. The SAM system releases catecholamines. Cortisol comes from the HPA axis.)
Fill in the blank: The hypothalamus secretes ______, which triggers ACTH release from the pituitary. (CRH, corticotropin-releasing hormone.)
True or false: Allostatic load refers to the body's healthy adaptation to stress. (False. Allostatic load is the cumulative damage from excessive or prolonged stress. Allostasis is the adaptive process.)
Fill in the blank: Chronic cortisol elevation suppresses the ______ system, increasing susceptibility to infection. (Immune.)
True or false: Norepinephrine acts only as a hormone in the bloodstream. (False. It also acts as a neurotransmitter in the brain, influencing behaviour and attention.)
Q: Describe the two primary neuroendocrine pathways activated during the stress response and explain how they differ in speed and duration.
A: The SAM system is the fast pathway. The hypothalamus activates the sympathetic nervous system, which signals the adrenal medulla to release epinephrine and norepinephrine within seconds. Effects include increased heart rate, blood pressure and glucose mobilisation. The HPA axis is slower. The hypothalamus releases CRH, which causes the pituitary to release ACTH, which stimulates the adrenal cortex to produce cortisol. This takes minutes to hours and produces longer-lasting metabolic, immune and behavioural effects.
Q: What is allostatic load, and how does it differ from allostasis?
A: Allostasis is the body's normal process of maintaining stability by adjusting physiological set points in response to changing demands. Allostatic load is the cumulative physiological cost when these adjustments are required too frequently or for too long. High allostatic load is associated with cardiovascular disease, metabolic syndrome, immune dysfunction and cognitive decline.
Q: Explain how chronic stress affects the immune system.
A: Chronic stress keeps cortisol levels elevated. While short-term cortisol has anti-inflammatory effects, sustained high levels suppress immune function broadly, reducing the body's ability to fight infections and slowing wound healing. This is why chronically stressed individuals get ill more often.
Q: Name two evidence-based interventions for chronic stress and explain the biological mechanism behind each.
A: Physical activity helps recalibrate the HPA axis, reducing baseline cortisol levels and improving the body's ability to return to homeostasis after a stressor. Social support reduces cortisol output and cardiovascular reactivity during stressful events, buffering the physiological impact of the stress response.
Q: A student says "cortisol is the stress hormone that damages your body." What is incomplete or misleading about this statement?
A: Cortisol is one of several stress hormones (catecholamines are the others). In short bursts it is protective: it mobilises energy, reduces inflammation and enhances focus. The damage occurs only when cortisol remains elevated chronically, leading to immune suppression, metabolic disruption and cognitive impairment. Calling cortisol purely harmful ignores its essential adaptive role.
This material connects directly to anxiety disorders and depression, where HPA axis dysregulation is a well-documented biological finding. It also underpins the biopsychosocial model: stress is where biological vulnerability meets psychological appraisal and social context. If you go on to study health psychology or psychoneuroimmunology, allostatic load is a foundational concept you will encounter repeatedly.
Stress response, fight or flight, SAM system, sympathetic adrenal medullary system, HPA axis, hypothalamic pituitary adrenal axis, cortisol, epinephrine, adrenaline, norepinephrine, noradrenaline, catecholamines, CRH, corticotropin-releasing hormone, ACTH, adrenocorticotropic hormone, glucocorticoids, adrenal medulla, adrenal cortex, allostasis, allostatic load, chronic stress, cardiovascular disease and stress, immune suppression, metabolic syndrome, steroid psychosis, stress and fertility, stress resilience, psychoneuroimmunology, biopsychosocial model, abnormal psychology stress