The historical perspective on the aetiology of diverticular disease can be recognized as far back as 1853 when Virchow (Rankin and Brown, 1930) described inflammatory areas, particularly in the sigmoid colon flexures, as 'isolated circumscribed adhesive peritonitis' and in 1869 when Klebs investigated the relationship of diverticula and their associated blood vessels in the intestinal wall.
In 1930, Rankin and Brown were describing diverticula and their aetiology as a controversial subject, whereas Erdmann (1932) postulated that the presence of diverticula in the intestine was of no more importance than diverticula in other organs. Bell (1929) considered that multiple diverticula, i.e. diverticulosis, was mainly of academic interest. Mayo (1930) suggested that muscular weakness of the colon and not constipation or obesity was the underlying cause of diverticular disease.
Lockhart-Mummery and Hodgson (1931) suggested that after a certain age (45 years) the muscle sheath of the colon could lose its tone and diverticula result from the muscle weakness. Even at the beginning of the twentieth century there was wide divergence of opinion as to whether diverticula occur more frequently at the area of the intestinal wall where the bowel is weak, as previously described, or whether they are associated with the openings between blood vessels coming in from the mesenteric side, because, in the colon, diverticula present at any point along the circumference of the colon wall have added confusion to the understanding of the aetiology of diverticular disease (Rankin and Brown, 1930).
It was initially supposed that a weakened colonic muscle wall in obese people resulted in fat being deposited around the blood vessels, so making a potential defect in the muscle coat, although it was also observed that people who were thin and people who were wasted had colonic diverticula (Klebs, 1869; Edel, 1894). As no hard evidence could be found to support this hypothesis, obesity has been rejected as an aetiological factor in diverticular disease.
There have been many reasons postulated for weakening of the intestinal wall, among which are old age, muscular atrophy, fatty atrophy and even bacterial damage of the intestine (Henderson, 1994). Thinness of the colon muscle coat, enabling the mucosa and serosa to be in close approximation, is thought to be caused by excessive segmentation which is an acquired defect and not nascent.
In observing the history of dietary change and diverticular disease, Painter and Burkitt (1975) suggest that the British diet started to change from 1870. White flour with little fibre in it was available as early as 1800 and was taken daily mixed with rye and oatmeal, making a fibre intake of 600 g. As the development of transport and the migration of the work force spread around the country, and refrigeration became available, refined sugars within the diet became more freely available for all classes together with meat as a regular meal. Between the years 1860 and 1890 the intake of bread in the diet decreased and refined sugar intake doubled. Other than the periods of the two world wars, when there was food rationing, this trend has continued. If diverticulosis is caused by the move from a high-residue to a low-residue diet, it would follow that, about 40 years after 1880 and these dietary changes, diverticular disease would be noted to become more widespread, as in fact it did in the UK.
In looking at the cultural prevalence of diverticular disease, it has been found that there is a relationship between a population and its economic development (see Chapter 9) and industrialization. Painter and Burkitt (1975) suggest that it takes about 40 years for diverticular disease to develop within a community, after that community departs from its traditional eating habits, and that 'consequently the disease will not be found in a population until its diet and hence the quality of the faecal stream that its colons have to propel have been altered for about forty years'.
Painter et al. (1972), in researching historical and epidemiological studies on diverticular disease, found that they contained much circumstantial evidence to suggest that economically developed countries with altered dietary intake at the turn of the nineteenth century were more prone to diverticular disease. If diverticular disease is considered to be a deficiency disease, a deficiency of high fibre in the population's food intake, the answer must be to retrace our dietary footsteps.
The word 'diverticula' is the plural of the Latin word diverticulum, meaning a wayside house of ill repute. It was in 1916 that diverticular disease was first mentioned in textbooks in the UK and diverticulosis was first mentioned in 1914 (Painter and Burkitt, 1975). Although diverticular disease was little documented or seen in the nineteenth century, the few cases that were documented were accurately described by today's knowledge of the disease. In addition radiographic diagnosis did not become available until a century later. Painter and Burkitt (1975), in their historical overview of diverticular disease, suggest that the term 'divertikel' was used as early as 1815 by Fleischman (in Spriggs and Marxer, 1925). In 1859 in the Transactions of the Pathological Society of London, Sidney Jones describes a colovesicular fistula that was caused by diverticulitis and in 1870 Loomis (cited in Hartwell and Cecil, 1910) noted a case of peritonitis as the outcome of diverticulitis.
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