Cortisol has a legitimate and essential physiological function. Acutely elevated cortisol mobilises glucose from liver glycogen and muscle protein, sharpens sensory processing, temporarily suppresses immune function and inflammation, and prepares the body to respond to a physical threat. All of this is adaptive in an acute context. The problem that characterises modern chronic stress is not that cortisol is produced. It is that it remains elevated long after the triggering event has passed and the physiological response it produces, designed to be short-term, creates sustained damage when it runs continuously.
Muscle: The Cortisol Tax
Cortisol promotes gluconeogenesis, the conversion of protein to glucose. The protein it preferentially harvests is skeletal muscle. Chronically elevated cortisol is therefore directly catabolic: it breaks down muscle tissue to provide glucose even when dietary glucose is available. Studies of adults with Cushing's syndrome, a condition of extreme cortisol excess, show profound muscle wasting as the primary physical manifestation. The same process operates at lower magnitudes in chronically stressed adults, contributing to the muscle loss and physical decline often attributed to ageing alone.
Fat: Visceral Redistribution
Cortisol preferentially promotes fat storage in visceral adipose tissue, the fat that surrounds the abdominal organs, rather than subcutaneous fat. Visceral fat tissue has higher densities of cortisol receptors than subcutaneous fat, and chronic cortisol elevation drives fat relocation from peripheral stores to the abdomen. This is why chronically stressed adults often gain abdominal fat even without any increase in caloric intake, and why the classic chronic stress body composition is accompanied by the metabolic risk profile of visceral obesity.
The Hippocampus
The hippocampus, the brain region central to memory formation, contains high densities of cortisol receptors and is exquisitely sensitive to cortisol excess. Sustained high cortisol reduces hippocampal volume, reduces neurogenesis in the dentate gyrus, and impairs long-term potentiation, the synaptic mechanism underlying memory formation. This is why people under chronic stress consistently report poor memory and cognitive fog, and it is why the neurological effects of chronic stress parallel the early stages of Alzheimer's pathology in some respects.
Sources
- Sapolsky, R.M. (2004). Why Zebras Don't Get Ulcers. Henry Holt and Company.
- Bjorntorp, P. (2001). Do stress reactions cause abdominal obesity and comorbidities? Obesity Reviews, 2(2), 73-86.
- McEwen, B.S., & Sapolsky, R.M. (1995). Stress and cognitive function. Current Opinion in Neurobiology, 5(2), 205-216.