Stress & Illness
Hans Selye (1936) was arguably the first theorist to carry out scientific research link illness to chronic stress.
Selye noted that the rats in his experiments and hospital patients showed a similar pattern which he termed the General Adaptation Syndrome (GAS) because it represented the body’s attempts to cope in an adaptive way with stress. GAS has 3 stages – see graphic below.
Stage 1 involves increased activity in both the SAM and the HPA systems. In the case of elongated stress, the Alarm reaction occurs 6-48 hours after the trigger of fight or flight and includes loss of muscle tone, drop in body temperature and decreases in size of the spleen and the liver.
Stage 2 involves the body adapting to the demands of the environment, with activity in the HPA. As this stage proceeds, the parasympathetic system requires more careful use of the body’s resources to cope. The system is being taxed to its limits, with an increase in the size of the adrenal glands and a decrease in certain pituitary activity such as the production of growth hormones. If the stress is not too great, the body may return to a near normal state of homeostasis.
Stage 3 sees the other physiological systems used in the previous 2 stages becoming ineffective due to very prolonged stress. The initial ANS fight or flight syndrome reoccurs. In extreme cases, the damage to the adrenal cortex leads to failure of the parasympathetic system and collapse of the immune system. Stress-related diseases – eg: high blood pressure, asthma, heart disease – become more likely. Anthony Curtis (2000) not only confirmed these links but added headaches, infectious illnesses (such as influenza) and rheumatoid arthritis to the list.
John Wayne Mason (1975) has heavily criticised Selye for claiming that stress always produces the same physiological pattern. Mason noted reactions to stressors producing different levels of fear, anger and/or uncertainty and, correspondingly, different patterns of adrenaline, noradrenaline and cortisol secretion. Mason also criticises Selye for assuming people always respond in a passive way to stressors. He argued that there is an active process of psychological assessment when people confront a stressor – fitting with Richard Lazarus’ (1976) concept of stress as a transaction. Joe Bosch et al (2001) state that ‘active stress’ better than ‘passive stress’because it produces more of the antibody IgA. Thomas Symington et al (1955) demonstrated the link between psychological stress and physiological symptoms by comparing a group of comatose dying patients who showed very few signs of physiological stress compared to a conscious group who knew only too well that they were dying and showed a wide and intense range of physiological stress symptoms. Selye has also been criticised for not fully differentiating between the SAM and HPA systems – although he was the first researcher to really focus on the HPA. His experiments on rats have been heavily criticised on ethical grounds for exposing them to ‘acute nocuous agents’ – namely cold, surgical injury (such as severing the spinal cord), excessive exercise and sub-lethal doses of various drugs.
For all the criticisms of Selye, GAS remains in large part applicable to many people’s experience of prolonged stress.
However, extended HPA activity can slow wound healing through the anti-inflammatory action of glucocorticoids.