Stress response and allostatic load
The stress response mobilises the body (cortisol, adrenaline, heart rate) to meet demands; allostatic load is the cumulative wear when that response is triggered too often, lasts too long, or fails to switch off.
What drives it
Explains why chronic pressure that seems manageable day to day shows up months later as illness, poor sleep, irritability and cognitive decline.
How it shows
Work
Months into a high-stakes period: frequent colds, back pain, sleep problems, short temper, forgetting things, needing alcohol to wind down, 'I'll rest after this quarter'. Performance holds until it suddenly does not.
Relationships
Less patience at home, less interest in sex, weekends spent recovering, conflict over small things. Partners notice before the person does.
Self
Can't switch off at night, wake in the early hours thinking about work, holidays take a week before you can relax, minor illnesses pile up.
What tells it apart
Burnout: Allostatic load is the physical cost of chronic stress in any domain; burnout is a work-specific syndrome with exhaustion, cynicism and lower efficacy. A person can carry high load and still be engaged.
Generalised anxiety: Allostatic load tracks real, sustained demands; generalised anxiety generates stress from worry even when demands are light.
Hyperarousal and hypoarousal: Hyperarousal is a state you can see in the moment; allostatic load is the slow cumulative cost that shows in health and sleep over months.
A test
Map sleep, illness and recovery time over the last six months against workload; if symptoms track demand and recovery has lengthened, load is building.
Questions to carry
- Over the last six months, how have sleep, illness and recovery time tracked the workload?
- Which pressure have I called manageable for so long that I’ve stopped counting what it costs my body?
How strong the research is
moderate. The stress response is well established; allostatic load is supported as a concept linking chronic stress to illness, but it is measured with varying biomarker sets that are not standardised.
Where it comes from
Hans Selye, 1936 and 1956; Peter Sterling and Joseph Eyer, 1988 (allostasis); Bruce McEwen and Eliot Stellar, 1993
Sources
- Bruce S. McEwen, Protective and Damaging Effects of Stress Mediators (1998)
- Robert M. Sapolsky, Behave: The Biology of Humans at Our Best and Worst (2017)