Animal, Human and Fibre Trials

Animals do get diverticula and hence ‘diverticulosis’. Like mankind, such diverticula can be found in several organs such as oesophagus, ureter, bladder, jejunum or small intestine. This condition is rarely encountered in veterinary gastroenterology (1), there are only occasional case reports. Animals do not get the kind of colon diverticular disease (DD) that began to increase in humans in the western world from the beginning of the 20th century. Questions about human DD were inevitably directed towards diet. What changed around the 1900s and would a human diet produce colon DD in animals?

There are many differences between animals in the structure and function of their digestive systems and colons. For example, dog’s and rat’s colons have a tube-like continuous surrounding of longitudinal muscle which in humans, rabbits, guinea pigs and horses is gathered into bands (taenia) (2). When the taenia contract it produces haustra (rounded segmented compartments). Some animals do not store faeces but continually expel pellets.

Many animal experiments varied the level of fibre in their diets. As in humans, this alters the level of other ingredients, usually replacing fibre by fat. Humans worldwide can be healthy on a variety of diets, including those with little fibre. Feeding herbivores with fat is not a good experimental basis and can cause deterioration in health (3). Coprophagia (eating faeces) is common in rats, rabbits and dogs, so that the amount of recycled fibre is unknown as is the amount of animal fibre in fur balls. Animals can be selective, Fisher and colleagues (4) found rats left the bran flakes in their food.

The presence of tumours (4,5), a salmonella epidemic (6), widespread virus infection (4) and ‘pathological abnormalities’ (5) have complicated animal experiments. Information is not always available in reports on how many animals examined post-mortem had died from disease, old age or were euthanized. Microscopic examination of ‘diverticula’ was not always mentioned. Some trials were poorly controlled and experimental numbers e.g. 6 rabbits (3), groups of 20 rats (7), or 6 monkeys (8) were too small for statistical evaluation and are hardly a basis for extrapolation to profound opinion and advice on human diet.

Trials of the effects of dietary fibre levels in humans in the last century sometimes also had low numbers of participants (9,10,11) and like animal tests, showed variable results. The vast differences in the effects of diverticular disease in individuals will always complicate trials. Other illnesses, the effects of drugs and lifestyle were not considered in animals or humans in the effort to support the theory that diverticular disease was caused by low levels of fibre in the diet. Tunnel vision excluded the effects of substances reaching the colon in its blood supply. The collective evidence from animal tests is poor and the role of other factors in the cause of diverticular disease remains unexplored (12 ). Trials with humans are carried out on people who already have DD and relate to treatment not the cause of the condition.

What animal and human trials do confirm is that there are reduced amounts of faeces, a longer transit time and sometimes increased internal pressure when there is not much fibre in the diet. Increasing dietary fibre will keep things moving and give bulkier, softer stools. This is a normal physiological effect like drinking more fluid increases the frequency and amount of urination. Increasing dietary fibre will reduce straining and ‘constipation’ symptoms such as pain. This is not peculiar to DD sufferers, but is the first and often successful treatment to try for constipation. It is not so simple for people with DD which can give a degree of obstruction, and age which can slow down the gut. The level of fibre should be determined by personal comfort and symptom relief. Whole-grains, fruit, vegetables and perhaps soluble-fibre supplements provide more variety of nutrients necessary for health than wheat bran. High amounts of dietary fibre are not appropriate when there is diarrhoea, infection and inflammation (ie diverticulitis) or obstruction.

Animal tests in general now use isolated tissues from colons. Human tissue, available after colectomy, has been used to find differences between healthy and diseased parts of organs. There is still little evidence about what causes these changes. Animal studies may yet prove useful. Mice have been genetically modified so that the protein smoothelin-A was no longer produced in intestinal smooth muscle. This resulted in over-contracted longitudinal and circular muscle. There were irregular and impared contractions leading to less movement of faeces, obstructions, diverticulosis and colon perforation(13). There was no difference in diet between test and control animals. So far, this research has not been followed up for DD but it does suggest similarity between human and animal colon effects.


  1. Christodoulopoulos G. et al. Rectal and colonic diverticulosis in a fallow deer (Dama dama) Veterinary Record 2005,156,115.
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  4. Fisher N. et al.Cereal dietary fibre consumption and diverticular disease: a lifespan study in rats. Am J Clin Nut. 1985, 42, 788.
  5. Wess L et al. Collagen alteration in an animal model of colonic diverticulosis. Gut 1996, 38, 701.
  6. Lubbock DM. et al. Epithelial overgrowths and diverticula in the gut of rats fed on a human diet. Brit Med J 1937, June 19, 1252.
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  9. Brodribb AJ. Treatment of symptomatic diverticular disease with a high-fibre diet. Lancet 1977, Mar 26, 664. (18 patients)
  10. Thorburn HA. et al. Does ispaghula husk stimulate the entire colon in diverticular disease. Gut 1992, 33, 352. (10 patients)
  11. Hodgson J. The effect of methylcellulose on rectal and colonic pressures in treatment of diverticular disease. Brit Med J 1972, 3, 729. (6 patients)
  12. Commane DM. et al. Diet, ageing and genetic factors in the pathogenesis of diverticular disease. World J Gastroenterol 2009, 15, 2479.
  13. Niessen P. et al. Smoothelin-A is essential for functional intestinal smooth muscle contractility in mice. Gastroenterology 2005, 129, 1592.

© Mary Griffiths 2011



On a low fibre diet ‘diverticula’ in rats were found to be beads of glandular tissue which also occurred in 29% of rats on the control diet(1). Other trials produced a few diverticular-like abnormalities mainly around the caecum (2,3). The rats used by Fisher et al. (4) had gaps in the cylindrical longitudinal muscle of the colon before tests on diet. Small blips on the outside of the colon in control stock rats became bigger bulges in those fed a low fibre diet and 10% of those on a normal diet. Some trials have produced no evidence of diverticula in rats fed a low fibre diet (5,6,7 ). Colons from rats eating various levels of fibre have been closely examined in many trials relating to diet and colon cancer (8,9,10 ). No diverticula were reported. One study found atrophy of the end of the colon of rats fed a fibre-free diet but one of the authors has personally confirmed that their rats do not get diverticular disease.


Diverticular disease is not a significant feature of canine veterinary problems (11 ). There was no effect on the colon wall or pressure inside the colon, and diverticula were not reported in a trial of low residue diets by Havia (12 ). A low fibre diet is recommended for dogs if they suffer from too much gas, diarrhoea or colon inflammation. Low fibre food products also have benefits for poop-scooping owners.


Hodgson (13) found 2 reviews of diseases in the domestic rabbit which did not mention divertivula. He fed 6 rabbits on a diet of white bread, butter, milk, Complan and sugar which represented (?) the diet of old people. Individual rabbits had different levels of added fibre. The rabbits put on weight and their condition deteriorated. The colon examinations and internal pressure tests were done with the rabbits anaesthetised with a stoma to the caecum. This surgery was repeated after 4 months on test diets. Some temporary ‘diverticula’ appeared in areas replacing haustra. In this experiment there was an anaesthetic which stimulates feeding (14) and reduces smooth muscle contractions, surgery which can stop bowel movements and injections of physostigmine to get the bowel moving. Were the results really an effect of diet?


There are reports of diverticula in the small or large intestines of individual primates (eg.15 ). These were captive, caged animals, fed laboratory diets appropriate for the species. Any differences in diet from companions was not mentioned nor were any experiments these animals had been subjected to. Some diverticulosis was found in an examination of the small and large intestines of female vervet monkeys. This was not confined to those on a low fibre diet. The authors concluded that there were changes ‘suggestive’ of the development of intestinal disease due to a low fibre diet (16 ). Brodribb et al. (17 ) also examined the effects of dietary fibre intake on the bowel function of 6 monkeys. No diverticula were found.


1 Lubbock DM et al. Brit Med J. 1937, June 19, 1252

2 Carlson AJ et al. Gastroenterology. 1949, 12, 108

3 Wierda JL. Arch Pathology. 1943, 36, 621 (cited by ref 5)

4 Fisher N et al. Am J Clin Nut. 1985 42 788

5 Morgan MN et al. Brit Med J. 1969, April 5, 53

6 Ellis H. Brit Med J. 1970, Sept 5, 565

7 Murakami H et al. Dig Dis Sci. 2001, 46, 1247

8 Wong CS et al. Carcinogenesis. 2003, 24, 343

9 Jacobs LR. Cancer Research. 1983, 43, 4057

10 Malville-Shipan K et al. J Nutr. 1992, 122, 37

11 Simson JW. J Nutr. 1998, 128, 2717s

12 Havia T. Acta Chir Scand Suppl. 1971, 415, 1 (cited by Parks TG Ulster Med J 1971 41 45)

13 Hodgson WJB. Gut. 1972, 13, 802

14 Blackburn JG. Physiology & Behaviour. 1972, 8, 791

15 Bunton TE et al. Vet Pathol. 1989, 26, 351

16 Jaskiewicz K et al. Br J Exp Pathol. 1986, 67, 361

17 Brodribb J et al. Dig Dis Sci. 1980, 25, 260

©Mary Griffiths 2011

NOTE This article appeared in the July, 2011 issue of the Journal of the Bladder and Bowel Foundation and is available in the professional resources section of their website.

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