The physiological basis of stress as an adaptive response
Copyright David Tierney 1998
The stress response is a mechanism used by organisms to adapt to and overcome a stress stimulus in order to preserve homoeostasis. Whilst facilitating survival, the stress response has become associated with a plethora of maladies for modern man suggesting it has maladaptive qualities. In considering the physiological process and its contribution to survival this essay will argue that stress response cannot be considered a single response to a single system. It needs to be viewed as different variables in different systems with complex interactions between the physiological and psychological. The stress response may be modified by subjective perception of a real or imagined stimulus. This may offer a means of intervening in the stress response to mitigate against adverse consequences.
Glucocorticoids are a group of steroids that promote mobilisation of energy resources, combat inflammation and assist in healing. Increases in levels of glucocorticoids are also associated with psychological stressors (Burns, 1990). Glucocorticoids are released from the adrenal cortex in response to stimulation by adrenocorticotropic hormone (ACTH) which is, in turn, elicited by corticotropin releasing hormone (CRH) in response to a stressor. The binding sites for CRH are widespread throughout the pituitary, cortical and limbic areas of the brain and peripheral nervous system. This suggests CRH and glucocorticoids have a role as mediators of both the endocrine and autonomic nervous system in the stress response (Haugel, Millan, Harwood, Lorang, Catt, Aguilera). Their overarching importance is suggested by the fact that blood levels of glucocorticoids is now the most common method of measuring physiological stress (Pinel).
Catecholamines, epinephrine and norepinephrine, also have a major role in the stress response. They are released by the adrenal medulla in response to stimulation by the sympathetic nervous system (Tortora). They respond to stress by inducing bodily responses that characterise the effects of the sympathetic nervous system - an increase in heart-rate, deeper breathing and increased levels of blood sugar. This response to stress facilitates 'fight or flight' from the threat (Cannon).
The sympathetic nervous system prepares the body to deal with an emergency by facilitating the pumping of glucose, simple proteins and fats together with oxygen into muscles dealing with the threat. The transportation of these emergency resources is hastened by an increase in heart and breathing rate and blood pressure. The organism is then prepared to either fight or flee the threatening stimuli.
The physiological response mechanism is efficient at adapting to short term physical emergencies. In addition to the rapid mobilisation of energy the stress response can also decrease perception of physical pain by triggering the release of beta-endorphins from the pituitary gland (Guillemin et al), increase sensory perception and selectively improve memory (Sapolsky). These are usefully adaptive when it is necessary to recall an escape route fleeing a threat whilst injured. The concept of threat includes hunger as well as danger. Enhanced sensory perception is adaptive in seeking out prey whilst a surge in energy is needed to catch it.
Short term stress responses enable organisms to adapt to and overcome short term stress stimuli. The stress response enables the organism to mobilise energy to fight or flee from a threat thereby enhancing its chances of survival. Stressors and the stress response may, however, become prolonged with maladaptive consequences (Selye). A prolonged stress response may result from a relatively long term stressor or inappropriately extend the response to a short term stressor. Moreover, a stress response, prolonged or otherwise, may be induced even by the expectation of a stressor, whether or not the perceived threat is real or imagined (Sapolsky). Maladaptive responses result from a combination of overwork by the sympathetic nervous system and prolonged inactivity of the parasympathetic nervous system. Prolonged activity by the sympathetic nervous system in response to stress can cause excessive wear and tear on the heart, blood vessels and organs adversely affected by persistent high blood pressure. It can also induce enlarged adrenal glands, gastric ulcers and a shrunken thymus gland.
Mobilising resources to fight or flee a perceived threat results in the direction of resources away from areas not immediately involved in overcoming the threat. The organisim therefore decreases activity in body tissue repair, digestion, immunity, reproduction and other tasks concerning energy conservation and restoration normally handled by the parasympathetic nervous system. This is adaptive in that the first priority is to overcome life threatening emergencies and all resources need to be directed to this end. Adaptation to normal circumstances is efficiently resumed as the parasympathetic nervous system becomes especially active when the stressful stimuli is removed (Pinel). This diversion of resources during an emergency can be damaging and maladaptive if the threat and the subsequent stress response is chronic (Pinel, 1993). A longer term reduction in the activities of the parasympathetic nervous system will have adverse consequences for physical growth, tissue repair, energy storage and reproduction. It may also induce psychological depression and reduce the effectiveness of the immune system (Sapolsky).
During infection the immune system releases interleukin - 1 which stimulates the hypothalamus to release CRF. CRF stimulates the pituitary to release ACTH which causes the adrenal glands to release glucocorticoids which, in turn suppress the immune system. They do so by destroying or reducing the effect of lymphocytes and impairing their production by shrinking the thymus gland. In effect the immune system, upon infection, asks the body to secrete hormones that ultimately suppress the immune system. A possible adaptive explanation to this paradox is the immune system may become over active in response to infection and glucocorticoids are employed to calm it down (Sapolsky).
Depression as a stress response would appear to be a significant failure of adaptation. However it may be argued the purpose of mood, and by implication depression, is part of a mechanism whereby the brain can register rewards and punishment (Barondes). Rewards induce good feelings and punishment induces bad feelings. Mood is thereby a socialising agent. Mother and child or mating couples are distressed when parted. This is adaptive as it is biological expedient that mother and child or mating couples remain together. Parting induces depression therefore the avoidance of depression by maintaining the pair bond is adaptive.
Chronic or repeated stressors only potentially and not automatically lead to illness. Indeed some organisms thrive in stressful situations relishing physically and psychologically demanding challenges. It is therefore more accurate to state that "stress increases your risk of getting diseases that make you sick or increase the risk of your defences being overwhelmed by the disease" (Sapolsky). It may therefore be pertinent to consider studies suggesting intervening factors between stressors and sickness. These include genetics, previous experience, training, information and perception.
Murray-Parkes argues the reaction of an organism to stress is a function of genetic inheritance. The biological root of human behaviour is the survival of the gene. This might explain the apparent over-reaction of some parts of an organism to stress to the detriment of other parts of the organism - each cell is concerned more with its own survival than with events elsewhere. The stress response, genetically determined or otherwise, may, however, be modified by environmental experiences in early life (Heim et al; Francis et al.). Experiments with mice suggests that physical training in early years modifies the response to stressors in later life (Reznick et al.) although the stress response varies between species (Sapolsky). Information and knowledge of the intensity and duration of an impending stressor can have modifying effects on the stress response (Schome, Breznitz, Wolfe) Perception and mood also serve to modify the intensity of the stress response (Frankenhaesur).
There are, however, limitations and complications to these modifying influences. An organism will respond physiologically to a physiological stressor whether or not it perceives the stressor. It will, for example, respond to an incision under anaesthetic (Selye). It is also possible for an organism to exhibit signs of psychological arousal associated with anxiety but not feel anxious and vice versa (Gatchel et al). Within these limitations it is possible for individuals to employ coping strategies that reduce the stress response (Katz, 1970). Physiological non cognitive coping strategies include relaxation techniques (Lavey & Taylor, 1975), meditation (Shapiro, 1995), tranquillisers and physical exertion. Psychological cognitive approaches include behaviour modification, counselling and psychodrama (Burchfield, Stein, Hamilton) which, if successful, feed back to influence the physiological basis of the stress response.
In conclusion, the stress response can be adaptive by preserving homoeostasis and survival of the organism. It can prove maladaptive if it has an intensity or endurance beyond that required to overcome the stress stimulation or if the stressor is chronic. The stress response is both physiological and psychological with both qualities interacting with mutual feedback. Cognitive and non-cognitive techniques may be employed to modify the stress response facilitating adaptation to the stress stimuli.
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25 November 1998