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Selye syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: Selye’s syndrome; general adaptation syndrome.

Overview

Overview

Selye syndrome Eponym used to indicate the sum of all reactions – physiological changes – that follow a prolonged exposure to intense stress. The typical pathologic findings are represented by adrenal cortical hyperplasia, thymic and lymphatic involution, gastrointestinal erosion or ulcers. The first two stages are the alarm reaction and the adaptation stage. If the stressor is not removed, the exhaustion stage and death will follow.

Historical Perspective

Historical Perspective

Selye first conceived this theory in 1936 after observing the reactions of animals exposed to a variety of non-specific damaging agents.

The non-specific response of the body to any demand made upon it.

Pathophysiology

Pathophysiology

This is a model on stress, researched mainly by Hans Selye[1][2] on rats and other animals. His research involved exposing animals to unpleasant or harmful stimuli such as injections, extreme cold and even vivisection.

He found that all animals showed a very similar series of reactions, broken into three stages. He describes this universal response to the stressors as the General Adaption Syndrome or GAS in 1936.

Stage one: alarm

When the threat or stressor is identified or realised, the body’s stress response is a state of alarm. During this stage adrenaline will be produced in order to bring about the fight-or-flight response. There is also some activation of the HPA axis, producing cortisol.

Stage two: resistance

If the stressor persists, it becomes necessary to attempt some means of coping with the stress. Although the body begins to try to adapt to the strains or demands of the environment, the body cannot keep this up indefinitely, so its resources are gradually depleted.

Stage three: exhaustion

In the final stage in the GAS model, all the body’s resources are eventually depleted and the body is unable to maintain normal function. At this point the initial autonomic nervous system symptoms may reappear (sweating, raised heart rate etc.). If stage three is extended, long term damage may result as the capacity of glands, especially the adrenal gland, and the immune system is exhausted and function is impaired resulting in decompensation. The result can manifest itself in obvious illnesses such as ulcers, depression or even cardiovascular problems, along with other mental issues.

References

References

  1. Seyle, Hans (1936). “A syndrome produced by diverse nocuous agents”. Nature.
  2. Selye, Hans (1950). “Diseases of adaptation”. Wisconsin medical journal. 49 (6): 515-6.

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