Abstract
A model is presented which links social change, stress and disease as a series of interacting variables. The mechanisms underlying Cannon and Selye stress are discussed and it is suggested that neither response properly meets the coping needs induced by current stressful experiences. Evidence from this Symposium and elsewhere suggests that coronary heart disease (CHD) has psychosocial stress as one of its major predisposing factors. Two key hypotheses are developed: that all psychosocial stresses may be reduced to a small number of categories, and that pathology arises when the stress responses are inappropriate to the problem in hand. Both of these hypotheses, if validated, could have practical value in assessing an individual's risk of contracting stress induced disease, and in demonstrating at a very early stage whether interventions were improving the situation or making it worse.
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