The colon’s little helpers


A report in 2007 by doctors at Duke University USA (1) proposed that the appendix functioned as a safe house for beneficial bacteria in the human gut. Rather than assessing the significance of this proposal for human biology, news agencies and internet sites seemed more concerned with the creation v evolution argument. The appendix had previously thought to be a relic of evolution even though its structure suggested otherwise.

The authors were unaware that I had come to the same conclusion in 1999 (2). Their literature search had not picked this up. Their proposal was based on observations of bacteria and immune system activity in the film of mucus lining the appendix and colon. My conclusion followed the realisation of why there was a symbiotic relationship with bacteria in the colon


The body produces enzymes in the digestive system to break down food into nutrients which can be absorbed. These enzymes (biological catalysts) are not used up in the process. They have finished their work in a short time while they speed to the end of the small intestine. They are not reabsorbed back into the bloodstream with the digested food. Some researchers consider that if the enzymes do escape from the digestive tract then they trigger inflammation in other parts of the body (3). Enzymes from the pancreas which attack proteins are particularly relevant. The question is, where and how does the body in health protect itself from these aggressive chemicals it has created?

When the end of the small intestine is surgically brought to the surface of the skin to form an ileostomy, the digestive enzymes in the discharge can cause problems attacking the surrounding skin. A colostomy formed after the caecum does not have the same problem. Patients with cystic fibrosis need to take pancreatic enzymes by mouth in large doses. Some patients were found to have damage to the ascending colon, suggesting that an enzyme deactivation system in the caecum might be exceeded.


The caecum is the bag-like first part of the colon where there is an immense increase in the number of bacteria and a surrounding of immune system tissues to keep them in their place. The development of the gut immune system follows the colonisation of the gut with bacteria in babies (4). In the caecum there is mingling of residues from different meals and muscular movement to mix all its contents before they proceed along the colon. This enables bacteria to grow and do their work.

Employing lesser species to deal with waste disposal is a natural phenomenon. It appears that humans encourage a symbiotic relationship with bacteria in the caecum to destroy aggressive enzymes. It follows that there must be a method of continuity of this vital process. The appendix provides a culture chamber and inoculating system to sustain and replenish the caecum bacteria. Inoculating with an actively growing culture is the best way to get fermentation off to a good start and is available from the appendix even if the colon is emptied by diarrhoea.

There should be some effects of appendectomy for this theory of the role of colon bacteria to be considered. Not much research has been done in this area. There is evidence that the removal of the appendix increases the risk of Crohn’s disease (5) and Small Intestine Bacterial Overgrowth (SIBO) i.e. colon bacteria migrating into the end of the small intestine (6). IBS risk is not increased (7) and Ulcerative Colitis may or may not benefit (8). In a Swedish study there were frequent readmissions due to non-specific abdominal pain within a ten year period after appendectomy (9).

There should also be some effects if caecum activity is reduced or prevented. My suggestion (2) that mixing movements are reduced in ulcerative colitis has been confirmed in animal tests (10) and a patent for a potential new treatment (11). Depletion of colon bacteria by antibiotics can result in diarrhoea. This and diarrhoea from other causes benefits from probiotics (12). The caecum and colon are removed and replaced with a pouch fashioned from the small intestine in a surgical treatment for Ulcerative Colitis. Many patients develop pouchitis, but the effects of digestion enzymes have not been considered as a reason for effectiveness of added bacteria from probiotics. No information was found on the effects of digestion enzymes or appendectomy on diverticular disease.


Over 90% of bacteria in the colon are anaerobic, i.e. they need little or no oxygen, and the fermentation in the caecum results in gasses such as methane or hydrogen. Bacteria injested as probiotics may not survive in these conditions unless they are taken regularly and frequently. Over 400 species of bacteria are living on unwanted food residues and repaying their host with vitamins, bowel wall nutrients and disposal of unwanted products. These are “good guys” working for you. The balance of species will vary according to the food provided for them. “Bad guys” and “strangers” are recognised and are got rid of by speeding up evacuation i.e. diarrhoea. Some advertised probiotics appear to do their work in this way.

There is a lot of interest in gut bacteria at the present time. Different bacteria are found in different bowel diseases – is this a cause or effect? Some pharmaceuticals use gut bacteria to release a drug only in the large intestine and there is interest in using this route for oral vaccines. Can the manipulation of bowel flora by probiotics be standardised to give predictable benefits or will there always be too much biodiversity?


Research some time ago (13) showed that people with diverticular disease (DD) had the same total numbers of anaerobic bacteria as in other colon diseases or healthy controls. However, far more DD patients had high concentrations of a methane- producing bacteria Methanobrevibacter smithii in enema samples. Other researchers (14) compared levels of Bifdobacter in patients with colon cancer, inflammatory bowel disease (IBD) and diverticulitis. All patients with DD or IBD had these organisms, but there were significantly higher counts of B. longnum and B. animalis with DD. Sometimes differences with DD have been attributed to the growth conditions inside diverticula favouring anaerobes. Maybe diet and fibre treatments for DD act as prebiotics to support the growth of particular organisms.


There has not been enough research on probiotics for DD to demonstrate clear benefits or recommendations (15). Trials will always be difficult because of wide variation in the effects of DD and no consistent patterns of progression (16). A non-pathogenic strain of E. coli as a probiotic improved symptoms and prolonged remission from diverticulitis (17). A similar result was obtained using a polymicrobial lysate (killed bacteria) as an oral vaccine (18). Probiotics appear to be beneficial for antibiotic-related diarrhoea, but different bacteria have been used in different trials. 59% of DD patients were found to have small intestine bacterial overgrowth (SIBO). This could be eliminated and symptoms reduced by treatment with Rifaximin (antibiotic) and mesalazine (anti-inflammatory) drugs (19). A probiotic product (Yakult ®) showed promise in reducing SIBO and improving the passage of wind in a pilot study of SIBO in IBS patients (20).


Some therapies are neither complementary nor alternative to encouraging bowel micro-organisms in their work. Colon irrigation is promoted for DD and other colon diseases but is in effect artificial diarrhoea with a risk of perforation. It does give a feeling of instant weight loss until the colon recovers its function and complement of bacteria. (No I have not tried it – it was used pre- barium enema x-ray in the good old days). Another therapy is advertised to introduce oxygen into the colon. This is not logical when colon bacteria work mainly by anaerobic fermentation. Achieving “better digestion” by taking extra enzymes with meals when there is no known deficiency, might not be helpful if it results in the absorption into the system of excess nutrients such as fats. If the enzymes are not the same as normally present in the body, there is potential for the absorption of alien compounds. It must surely be better to eat a varied and balanced diet.

© Mary Griffiths 2009


1 Bollinger R R et al. Biofilms in the large bowel suggest an apparent function of the human vermiform appendix. J Theor Biol 2007,249, 826.

2 Griffiths M. Ulcerative colitis. More pieces for the jigsaw please. Pharm J. 1999, 263, 569.

3 Schmid-Schonbein G W. Biomechanical aspects of the auto-digestion theory. Mol Cell Biomech. 2008, 5, 83.

4 Gebbers J O et al. Bacterial translocation in the normal human appendix parallels the development of the local immune system. Ann N Y Acad Sci. 2004, 1029, 337.

5 Kaplan G G et al. The risk of developing Crohn’s disease after an appendectomy: a meta-analysis. Am J Gastroenterol. 2008 103, 2925.

6 Lauritano E C et al. Small intestinal bacterial overgrowth recurrence after antibiotic therapy. Am J Gastroenterol. 2008, 103, 2031.

7 Minocha A et al. Prevalence of abdominal and pelvic surgeries in patients with irritable bowel syndrome: comparison between Caucasians and African Americans. Am J Med Sci. 2008, 335, 82.

8 Frisch M et al. Appendectomy and subsequent risk of inflammatory bowel disease. Surgery. 2001, 130, 121.

9 Tingstedt B et al. Late abdominal complaints after appendectomy- readmissions during long-term follow-up. Dig Surg. 2004, 21, 23.

10 Miceli P C et al. Cholinergic pathways modulate experimental dinitrobenzine sulphonic acid colitis in rats. Autonomic Neuroscience 2003, 105, 16.

11 Ester Neurosciences LTD et al. Antisense oligonucleotides against acetylcholinesterase for treating inflammatory diseases. Patent WO/2007/116395.

12 Abdelrazeq A S et al. Predictors for acute and chronic pouchitis following restorative proctocolectomy for ulcerative colitis. Colorectal Dis. 2008, 10, 805.

13 Weaver G A et al. Incidence of methanogenic bacteria in a sigmoidoscopy population: an association of methanogenic bacteria and diverticulosis. Gut, 1986, 27,698.

14 Gueimonde M et al. Qualitative and quantitative analyses of the bifidobacterial microbiota in the colonic mucosa of patients with colorectal cancer, diverticulitis and inflammatory bowel disease. World J Gastroenterol. 2007, 13, 3985.

15 White J A. Probiotics and their use in diverticulitis. J Clin Gastroenterol. 2006, 40, S160.

16 Frattini J et al. Diagnosis and treatment of chronic and recurrent diverticulitis. J Clin Gastroenterol. 2006, 40, S145.

17 Fricu P et al. The effect of non-pathogenic Escherichia coli in symptomatic uncomplicated diverticular disease of the colon. Eur J Gastroenterol Hepatol. 2003, 15, 313.

18 Dughera L et al. Acute recurrent diverticulitis is prevented by oral administration of a polybacterial lysate suspension. Minerva Gastroenterol Dietol. 2004, 50, 149.

19 Tursi A et al. Assessment of small intestinal bacterial overgrowth in uncomplicated acute diverticulitis if the colon. World J Gastroenterol. 2005, 11, 2773.

20 Barrett J S et al. Probiotic effects on intestinal fermentation patterns in patients with irritable bowel syndrome. World J Gastroenterol. 2008, 14, 5020.

Note This article appeared in the Summer 2009 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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