The correlation of increased incidence of diverticular disease with age is well documented. Such a correlation results from the development of a structural change in the taeniae coli, a progressive elastosis. The consequences of this elastosis are a shortening of the taeniae coli and a subsequent change in the circular muscle layer secondary to this. This type of structural alteration takes time to develop and thus explains the time lag experienced between a change in diet and an altered incidence of the disease. Eastwood et al (1982) have suggested that diverticular disease is merely a normal concomitant of ageing which is degenerative in nature. However, the changes in structure in this condition appear to be dynamic, being associated with an altered intraluminal environment. Such a concept is crucial to our understanding of the pathology of ageing in general. Atherogenesis is associated with muscle cell hypertrophy, another dynamic change, which also leads to elastin formation. This suggests that treatment of such conditions should not just be limited to the control of an inevitable deterioration but should be directed to the investigation of the stimuli that may trigger such conditions. For example, it is interesting to speculate exactly when the changes that lead to diverticular disease begin: not only is a high fibre diet eaten in Africa, but breast-feeding may continue until the age of two years. The greatest increase in thickness in the normal colon occurs in this period and it may be that early weaning distorts this proliferation. The initiating factor in the aetiology of elastogenesis could be the small stools produced on a 'Western' diet which only intermittently distend the colon. Arterial smooth muscle cells increase their uptake of elastin precursors (particularly proline) when subjected to intermittent distension (Leung et al, 1976) and this may form a common link in the changes generated in vascular and colonic muscle tissue with time. This type of change is independent of alterations in motility and thus explains why asymptomatic patients have a normal motility index (Weinreich and Anderson, 1976). The muscular thickening in uncomplicated diverticular disease can therefore be explained in terms of elastosis and contracture of the taeniae coli in the presence of normal muscle cells. This does not exclude the possibility that hypertrophy and hyperplasia of these cells can develop in response to subsequent pericolic inflammation and fibrosis.