Posts Tagged ‘Faeces’

Diverticular Disease: The Fibre Story

Thursday, September 14th, 2017

In the early part of the 20th century constipation was not generally related to any individual illness. The idealised achievement of daily defaecation meant constipation was common particularly in the elderly. Treatment was not free until the NHS came along and natural and herbal laxatives were well used medications. Diverticular disease (DD) became recognised more before WW11. The distinguishing symptoms were pain, fever and diarrhoea. A low residue diet was recommended to reduce diarrhoea and give the bowel rest. Serious pain sometimes resulted in surgery. Infection and inflammation (diverticulitis) were not always present but pieces of food and faeces were trapped in diverticula. Avoidance of coarse fruit and vegetables, seeds and pips was recommended.

Hospital diet sheet for diverticulitis 1961………”forbidden foods – all fried foods, pips and skins of fruits, pastry, suet puddings, coarse stalky vegetables, salads, onions and celery, chunky marmalade, jam with pips or skins, wholemeal or brown bread, coarse biscuits-Ryvita, digestive, Allbran, oatmeal, Weetabix, Shredded Wheat, fruitcake or scones, nuts, dried fruit.”

A significant change in diet started about 1970 when treatment for diverticular disease (DD) was suddenly reversed.

Hospital diet sheet for diverticulis 1982………..”you can eat a normal varied diet but include…… (all of the forbidden foods from 1961 except fried food)….SUPPLEMENT meals with 2 teaspoonfuls of unprocessed bran twice daily. EAT LESS white flour in any form and white and other sugars. DIETARY FIBRE ….by helping to restore normal function of the digestive tract, fibre can be useful in the treatment of constipation and diarrhoea”

  • Who persuaded health professionals that wheat bran was good for diarrhoea?
  • What was the evidence for this complete reversal of treatment?
  • Did anyone ask patients if this helped them?
  • Who was behind this change?


The individual who had the greatest influence on the treatment of DD in the last 100 years was surgeon Denis Parsons Birkitt. One biography title calls him ‘The Fibre Man’ another ‘How a Humble Surgeon Changed the World’. These volumes describe a one eyed Northern Irish man whose Christian beliefs were greatly impassioned by a group at university. Religious practice and fervour were the engine and steering wheel of his life and medical practice. After surgical qualification, a position as ships doctor and war time service with the Royal Army Medical Corps followed, then employment by the Colonial Office meant he practiced overseas for about 30 years.

Birkitt became well known in Uganda. Using the network of Christian missions and hospitals and extended safaris, he became interested in what he called ‘geographical medicine’. He found that hydrocelle cases occurred in particular areas and were caused by a microscopic worm carried by mosquitos.The same type of investigation eventually uncovered the cause of a cancer in children which became known as Birkitt’s lymphoma. An insect vector he proposed was not to blame, but the Epstein-Barr virus was discovered. The cancer/virus connection became the platform for intensive research into cancer causes by specialists worldwide. Birkitt’s fame spread, aided by his brilliant, charismatic oratory and invitations to preach and lecture worldwide on cancer.

Ugandan independence affected medical services and Birkitt’s surgical practice finished. He was employed by the Medical Research Council External Scientific Staff in London in 1964. His African travels continued collecting ‘geographical’ data on cancers and diseases. Writing, lecturing and preaching tours continued.


The fibre story only started in 1967 in London. At the age of 56, Birkitt was introduced to a retired naval physician Captain T.L. Cleave. Cleave was one of several doctors who had used wheat bran to treat constipation. Cleave thought that excessive sugar and refined carbohydrates were behind the diseases in Western countries which were not found inAfrica. Birkitt considered meeting Cleave was one of the most important occasions of his professional life. He had been introduced to the concept of ‘Western diseases’ and ‘one cause’ of different diseases and that cause was considered to be diet. In 1969 he used his network to obtain samples of faeces to weigh and with the time taken for them to pass through the body. He used groups of people who had different diets. He had contact with Dr Alec Walker, Dr Hugh Trowell and Dr Ted Dimock in Africa who had previously carried out such studies, and Dr George Campbell who had worked with Cleave. Burkitt thought Providence had brought these contacts into his life in perfect order. He was convinced that the Lord was calling him to a wider, more important commitment in medicine. He was determined to step even more wholeheartedly into popularising not only the neglected field of nutrition but preventative medicine as well. Medical researchers who had previously produced articles and books on this theme had not managed to change traditional medical opinions on dietary fibre. The role of dietary fats was then fashionable. Birkitt had the gift of oratory, the contacts and the clout from his cancer work to become the spokesman for his colleagues and previous investigators.

People who attended Birkitt’s messianic talks write mostly about the slides showing the voluminous heaps of the stools of Ugandan rural villagers. He certainly knew how to get their attention. His biographers describe how he used slides and stories to get his points across. Biblical parables come to mind. He could demonstrate that increased weight of stools was generally associated with quicker passage of food through the body. This was the basis of his opinions and conclusions. His subjects did not include the old or infirm but were predominantly young and healthy with different lifestyles and diets. There was much overlap between diets and individuals, the amount of fibre in the different diets was  perversely assumed according to the size of stools. It was obvious that the stools of the rural villagers were in a class of their own in size. At the sides of paths in the bush a squatting position was inevitable. The location suggests some urgency. Is this the model the western world should achieve by increasing dietary fibre levels to the 150g per day? This figure was calculated from a “personal communication” which said that men eat at least 1Kg of plantain at each main meal. Plantain is 6g fibre per 100g therefore the total dietary fibre intakes are 150g/day. Similar calculations gave fibre levels of 130g/day for the Kikuyu tribe and 100g/day for Venda males in South Africa. These levels are equivalent to about 50 portions/day of porridge oats! Vegetarians in the West have about 40g/day of fibre. The claim that diverticular disease is caused by not using a squatting position on Western toilets is also based on the rural Ugandans habits. This is used to promote sales of devices to modify water closets. Birkitt himself did not comply with this claim. Helping constipation should not be confused with causing disease


There are reports that Ugandans have large, wide bowels and a common surgical emergency is twisting of the colon (volvulus). Widespread use of herbal laxatives to meet African defaecation ideals has been mentioned. We didn’t hear much about the ‘African’ problems. Earlier missionaries and doctors were aware that some diseases becoming common in the Western world were not found in Africa. Birkitt’s information from his networks and travels agreed. Coronary heart disease, gallstones, appendicitis, diverticular disease (DD), diabetes, varicose veins, haemorroids, hiatus hernia, peptic ulcer and colon cancer were the Western diseases. They were only occasionally found in African individuals who had adopted an urban, Western lifestyle, but not necessarily a Western diet as found by other researchers. Also noted was that a Western individual could have more than one of these typical diseases.

Apart from the Inuit, who Birkitt described as one hiatus in his dietary research, there was no mention of any peoples who had little dietary fibre but no Western diseases. The Massai, Chewya and Watus tribes were noted by other African missionaries. Mormons and Seventh Day Adventist had Western diets but low levels of Western diseases; no smoking was offered as a possible explanation. Birkitt knew that coronary heart disease was linked to cigarette smoking but persisted with a low dietary fibre explanation of its cause.


  1. The distribution (epidemiology) of Western diseases found in the 1960s/70s was distinctive, suggesting a lifestyle and possibly single cause.
  2. Wheat bran can help relieve constipation in some people.
  3. Increased dietary fibre will in general pass through the body faster with speedier evacuation and softer stools.


  1. The rural African diet protects against Western diseases
  2. The change in disease patterns when individuals emigrated to Western countries was due to a change in diet.
  3. Increase in prevalence of Western diseases in countries which were previously low was caused by the adoption of a Western diet.
  4. Western diseases are caused by insufficient fibre in the diet. Copious amounts of wheat bran would prevent, treat and cure the ailments of the Western world.

There is no evidence, biological link or possible extrapolation between the facts and conclusions. There are many lifestyle differences to account for individual and regional variations in disease patterns and colon function. Choosing assumed dietary fibre levels and ignoring examples which do not conform is not valid epidemiological evidence. There are many food ingredients which promote bowel movement, not just wheat bran. For example, Birkitt found in Ireland, that plenty of potatoes matched the effects of bran; or was it an effect of the national beverage? It is an essential physiological mechanism that more undigested food residues will give quicker passage and larger stools, just like drinking more fluids results in increase urination. If disease affects these mechanisms, can they be overloaded?


Neil S Painter was a surgeon at the Manor House Hospital in London. He had spent most of the 1960s studying diverticular disease. Unlike Birkitt he had patients to treat. He was responsible for insight into the mechanisms of diverticula formation and researched the effects of drugs on the diseased colon. Segmentation in the sigmoid colon resulted in pockets of high internal pressure which forced hernia through the colon wall to give diverticula on the outside.

Cleave persuaded Painter to use unprocessed wheat bran in his medical practice and for the treatment of constipation in uncomplicated diverticular disease. The trial took place between 1967 and 1971, involved 70 patients, replacing previous laxative use and an assessment of symptoms at 1 and 2 months. Many of the aged, 70 patients had other western diseases whose treatment may not have helped their bowel problems. The results were presented by how many of the 12 symptoms were relieved or abolished, not by how many patients had been helped. It is possible that the 17% of the patients with repeated problems could have produced a majority of the symptoms in this type of presentation. Some patients could not tolerate bran, some still required occasional laxatives. Some symptoms were not relieved by bran, some were reduced and just over half disappeared during the trial period. Stools were softer and passed with less straining thus helping constipation. Painter emphasised that the bran regime did not prevent attacks of painful diverticular disease or acute diverticulitis. 3 patients were admitted to hospital. The amount of bran added to the diet varied to meet the trial end point of daily defaecation and varied between 6 teaspoons/day to several tablespoons daily. 3 patients had frequent passage of small hard stools with diarrhoea episodes attributed to laxatives, these became more regular with bran. This type of constipation appears to be the basis of treating diarrhoea with bran. That diarrhoea might be a symptom of irritation, infection or inflammation was not considered.

Painter asked Trowell to write a letter to the British Medical Journal to support the use of bran for intestinal conditions. A mutually beneficial collaboration with Birkitt published a paper on fibre and diverticular disease in 1971. Although headed ‘for debate’ it transformed treatment of diverticular disease by previously sceptical health professionals. Painter had got on board the bran wagon.


Medical research for decades tried to find evidence to support Birkitt, his colleagues and Painter. Trials did not consider anything but dietary fibre, involved small numbers of subjects and no controls. Effects of bran and high fibre diets were always balanced by a change in proportion of other foodstuffs. This was particularly relevant in animal tests which attempted to produce diverticula by reducing fibre in their natural diets. Publications which did not agree with the fibre theory were counteracted. The letters pages of medical journals were the equivalent of today’s Twitter and Facebook. Opinions were divided but Birkitt welcomed the disagreement as publicity.

How did the fibre gospel achieve such worldwide publicity? Described as a human dynamo obsessed with fibre, Birkitt’s charisma and lecturing prowess were reasons that attracted the media and publishers. Increased sales of breakfast cereals were another. Kellogg sponsorship of lecture tours, worldwide medical symposia on the fibre content of diet and paying for the publication if a bibliography by Trowell, gave medical backing for promotion of cereal products. For patients, bran could be a useful cheap medication in the absence of any other treatment on offer for diverticular disease. There was also an element that patients could be blamed for their problems because of their choice of diet.

The fibre message was far more effective in the USA than in the UK. Particularly controversial was Birkitt’s opinion that colon cancer could be prevented by a high fibre diet. Medical journals were reluctant to publish the idea of many diseases having a common cause. However in 1972 the British Medical Journal agreed to publish a lecture beforehand. This was Birkitt’s breakthrough in getting into print his opinions on diseases which were increasing in Western countries in the 20th century. He theorised the relationship of dietary fibre as the cause of the various diseases.

The voluminous flow of articles by Birkitt and his colleagues in medical journals had slowed down considerably by 1976. Now he felt that he could only write about fibre and not medical conditions he had no involvement in. He had no new personal research to report on and maybe exhausted usable medical journals. He did continue involvement in collaborative books on dietary fibre.

At the age of 65, Birkitt had to retire from the Medical Research Council resulting in reduced income. He believed that the Lord would provide, as he had done in the past, if he wanted the work to continue. His friends found him an appointment as Honorary Senior Research Fellow and a room at St Thomas’s hospital. Kellogg, who had sponsored lecturing tours since 1972, provided an honorarium, secretary and expense account for lectures “on the understanding that their cereal products would not be promoted”. Kellogg sponsorship of symposia and speaking appointments continued.

Other authors had jumped on the fibre bandwagon with popular publications. Birkitt had been unable to find a publisher for a book for the general public. After several rejections, in 1977, a 28 year old Martin Dunitz approached Birkitt about producing a book. A property company registered in 1977 changed its name to Martin Dunitz Ltd in 1978. The book ‘Don’t forget fibre in your diet’ appeared in 1979 to be the first from this publisher. There was emphasis that readers should look for the word “bran” in cereal products.


A means of continually controlling constipation would be preferable to the stop/start regime of laxative use. Daily wheat bran can achieve this in many people but not all. Concerns arose about wheat bran’s ability to reduce absorption of minerals such as iron from food. Bran could provoke urgency which the less mobile and elderly could not cope with. Painter’s trial showed that a standard dosage, taken like a medicine, did not take into account the fibre present in a person’s normal diet. Wheat intolerance and gluten sensitivity were not considered at that time and a requirement for daily defaecation is now outdated.  One patient was satisfied by a sterculia product. Nowadays, regular supplementation with an ispaghula preparation is popular to keep stools soft. So many foods and lifestyles affect bowel function as well as health, age and disease. Exercise and hydration are important. DD can have such variable effects that only an individual can find by trial and error what is best for them.

Dietary fibre can increase comfort and reduce symptoms but it does not follow that reduced levels are the cause of disease. In bowel complaints characterised by pain and diarrhoea such as IBD (Crohn’s and ulcerative colitis) and IBS (irritable bowel syndrome) wheat bran is far from helpful. Bran is not appropriate when there is diarrhoea with diverticular disease (DD).The problem with DD is to distinguish the reason for pain and symptoms. Are there muscle spasms, strictures or narrowing of the colon, chronic inflammation or age-related dysfunction compounded by the structural damage to the colon? Increasing numbers of research publications disprove the dietary fibre theory of the cause and treatment of DD and suggest other relevant factors, yet after half a century there are still some believers to be found. Maybe this is because medicine still has little else to offer patients.


Colon cancer was probably the first of the western diseases to be successfully disputed as a dietary fibre deficiency disease, others have followed over the decades, diverticular disease is hopefully the last. Fibre can have varied sources and bran is less fashionable now, fats and sugar wax and wane in popularity and publicity. Research into the relationship between diet and disease however has not faltered. Surveys and computers programs produce data which often disagrees and confuses. The popular headlines present results as risk levels which may or may not be relevant to actual numbers. There are fashions in recommendation of superfoods, supplements etc. Regional differences in diet are still used to claim reduced risk of western diseases. We have Mediterranian, Japanese, Eskimo etc. diets. Currently emphasis is on fermented foods from Eastern Asia to counteract western diseases through effects on gut microorganisms. Are omnivore humans so sensitive to small changes in diet? Should more emphasis be placed on how food is produced and treated before it is eaten? Diet is not the only way noxious substances can get into the body, we breathe as well as eat.

An overlooked but important work by Birkitt, Painter and their colleagues was the value of their epidemiology research. For DD in particular was the look at its early appearance in the 20th century. The suggestion that there could be one cause of western diseases was not appreciated at the time. Was it a mistake to choose the level of dietary fibre? At that time only lung cancer and heart attacks were considered the effects of smoking. Epidemiology is not static and other cancers and the western diseases including DD, follow a same pattern of prevalence and mortality during the 20th century. That pattern follows the worldwide use of cigarettes. Western diseases appear when and where Western cigarettes are smoked, diet can only modify their effects.

© Mary Griffiths 2017


The Fibre Man by Brian Kellock , 1985, Lion Publishing plc, ISBN 0 85648 583 7

Burkitt, Cancer, Fibre. How a humble surgeon changed the world. By Ethel R. Nelson, 1998, TEACH Services Inc, ISBN 1-57258-093-3

Diverticular disease of the colon, A deficiency disease of western civilisation. By Neil S Painter. 1975, William Heinemann Medical Books Ltd, ISBN 0 433 24660 x

Don’t Forget Fibre In Your Diet. To help avoid many of our commonest diseases. By Dennis Burkitt. 1979, Martin Dunitz Ltd, IBSN 0 906348 07 2 Pbk

Dietary Fibre, Fibre-depleted Foods And Disease, Edited by H. Trowell, D. Birkitt and K. Heaton, 1985, Academic Press, ISBN 0-12-701160-9.

Nutrition and Killer Diseases. Edited by J Rose. 1982, Noyes. Diseases of affluence, DP Birkitt, Pp 1-7. Essential fatty acids and chronic degenerative diseases, HM Sinclair, Pp 69-83.

The Saccharine Disease, Conditions caused by the taking of refined carbohydrates such as sugar and white flour. By T.L. Cleave. 1974, John Wright & Sons Ltd. ISBN 0 7236 0368 5.

Out of Africa. What Drs Price and Burkitt discovered in their studies of Sub-Saharan Tribes. By The Weston A Price Foundation.

Medical Aspects of Dietary Fibre. A report of the Royal College of Physicians of London, 1980, Pitman Medical, ISBN 0-272-79609-3.

Some Diseases Characteristic of Modern Western Civilisation (Crookshank lecture 19.5.72) By DP Burkitt. Br med J. 1973, 1, 274.

Diverticular Disease of the Colon: A Deficiency Disease of Western Civilization. NS Painter & DP Burkitt. Br Med J. 1971, 2, 450.

The Diet Delusion. By Gary Taubes. 2007, Vermilion. ISBN 9780091891411.

Trick and Treat. By Barry Groves. 2008, Hammersmith Press Ltd. ISBN 978-1-905140-22-0.

The Microbiome in Diverticular Disease

Thursday, November 10th, 2016

New techniques which identify individual species have lead to an explosion of research into the role of bacteria in the colon. The terms ‘microbiota’ (the bacteria) and ‘microbiome’ (the collection of bacteria) are widely used. Some researchers consider the microbiome as equivalent to a body organ. It is certainly a significant, integral and specific part of the digestive system in man and animals. In protein-eating humans the microbiome is in the caecum, the first bag-like part of the large intestine which receives the residues of digestion and has enzymes which degrade amino acids from proteins. In herbivores the microbiome is in an earlier part of the digestive system to deal with large quantities of plant material to extract maximum nutrients for its host with enzymes to synthesise amino acids (1). The microbiome in humans can have both beneficial and unhelpful effects. Its position in the human body and the role of an associated appendix had not been considered apart from the letter on this website (2). The appendix is no longer considered a vestigial organ (3), contains extremely variable bacteria (4) and may be involved in microbiome changes (5).

Differences in the bacteria present in the microbiome have been found in conditions  such as obesity, autoimmune diseases, autism and bowel disease including diverticular disease (DD). The microbiome and its surrounding immune system are linked (6).

  • Is the microbiome content a cause or an effect of a disease?
  • Is the presence of a specific organism significant?
  • Could the microbiome be changed to treat a disease?

These are the questions research is trying to answer. Bacteria will only survive and flourish if the conditions and nutrients are right for the species. There is great variation both between and within people, with age and even with geographical location. So far only diet appears to make a difference (1, 7). Does the microbiome match dietary residues and the disease affect diet?

Probiotics and prebiotics are tools to add particular species of bacteria to the microbiome (8).and are basically a dietary adjustment. Like the bacteria in food, probiotic bacteria may not reach or persist in the microbiome  unless they are taken continuously and survive stomach acid. A review of probiotics in the treatment of DD (9) found poor quality studies which gave insufficient data to reach a conclusion on effectiveness and could not be recommended for DD (10). Most bacteria in the colon are anaerobic i.e. do not need oxygen for growth. Popular ‘probiotic’ products are bacterial species which grow in dairy-based medium for factory production.

The relationship between DD and gut bacteria has been examined in the past and some organisms appeared to be associated (11, 12). New techniques have identified Proteobacteria as a species with sufficient prominence to suggest a way to diagnose diverticulitis (13). Previous studies found bacteria which produced raised levels of methane from the microbiome (11). Changes in the breath gasses when food residues reached the caecum confirmed methane production which could predict a finding of diverticulosis from colonoscopy (14).

Deleting a particular bacterial species from the microbiome would be a challenge. Antibiotics which kill a wide range of bacteria can have a devastating effect, sometimes leaving resistant organisms to flourish e.g. C. difficile. The production or recycling of substances useful to the body, also the deactivation of toxic by-products could be determined by the overall activity of the microbiome. Gut bacteria are used to release drugs to act directly in the colon, they can also inactivate drugs and influence their side-effects (15).

Early research has made use of faeces as the source of gut bacteria in experiments on germ-free mice. These have no microbiome. Faeces from humans with diseases have been given to mice and the effects observed The organisms  present in faeces will have already been selected by dietary residue composition. Mice are different from humans in digestive system anatomy, physiology, colon function and genetics and might not reflect real live humans (16). There has been some success in using human transplanted faeces to treat Ulcerative Colitis (UC) and persistent C. difficile colon infection. Why UC might be helped by added bacteria was discussed in the PJ 1999 letter on this web site (2).

Interest in the micrbiome has resurrected research into bacteriophages which are viruses to target and kill specific bacterial species. These have been used with success against other resistant bacteria in humans (17) and can work in the microbiome against C. difficile (18). Bacteriophages might be a way of dealing with specific disease-causing bacteria in the microbiome. Researchers are also considering antibiotics with a narrow spectrum of activity to target specific bacteria (19). The broad spectrum antibiotic “Rifaximin” which is not absorbed and passes unchanged into the colon is now used to reduce the activity of the microbiome in a disease which compromises liver activity and in traveller’s diarrhoea. Rifaximin in DD has received attention in Italy (20, 21, 22) The design of trials has made it difficult to separate the effects of Rifaximin from Mesalazine and dietary fibre levels. There is evidence and promise the Rifaximin can help reduce symptoms in uncomplicated DD but does not prevent relapse of diverticulitis. Rifaximin is not approved for treatment of DD in the UK.

The difference in the microbiome between people with DD and those without are producing speculation on how this might produce symptoms (23). Reviews are linking changes in the microbiome with gut inflammation and the development of conditions such as acute and chronic diverticulitis (24). However, linking microbiome changes to pre 1970s low fibre diets is an outdated approach to the cause of symptoms with DD (25).Recent research compared faeces from patients with and without symptoms against healthy controls who did not have diverticula. The number of bacteria did not differ between the three groups nor did the presence of many species of bacteria. Amounts of Akkermansia muciniphila species did differ between the groups and were associated with different levels of metabolic compounds in faeces between the groups, distinguishing the presence of diverticula and the presence of symptoms (26). Clinical trials are planned to examine the microbiomes of people with no symptoms from their diverticulosis for comparison with diverticulitis patients. What changes diverticulosis into diverticulitis has been a mystery for decades. The first episode of diverticulitis may have a different cause and risk factors than recurrent episodes (27). Hopefully microbiome research will illuminate these problems.

DD and other diseases must wait for research results but this has not stopped commercial exploitation and ‘health’ books and articles about the microbiome. Often there is no differentiation between mice and man. We are urged to get a good, rich and optimum microbiota but does this mean variety, high numbers and/or specific species of bacteria? How do we know what we have inside us? One popular advice is to increase the variety of bacteria in the gut by eating fermented foods from East Asia countries such as Korea or Japan. The old adage reappears that ‘Western’ diseases (eg DD) are less prevalent in those countries. ‘Eastern’ diseases, such as the world’s highest levels of stomach cancer are not mentioned.

© Mary Griffiths 2016


1        Muegge BD et al. Diet drives convergence in gut microbiome functions across mammalian phylogeny and within humans. Science, 2011, 332, 970.

2        Griffiths M Pharmaceutical Journal letter 1999, and the article ‘The colons little helpers’on this website.

3        Bollinger RR et al. Biofilms in the large bowel suggest an apparent function of the human vermiform appendix. Journal of Theoretical Biology, 2007, 249, 826.

4        Guinane CM et al. Microbial composition of human appendices from patients following appendectomy. MBio, 2013, 4, pii: e00366-12 doi: 10.1128/mBio. 00366-12 (PubMed 23322636)

5        Sanders NL et al. Appendectomy and Clostridium difficile colitis: Relationships revealed by clinical observations and immunology. World J Gastroenterol. 2013, 19, 5607.

6        Wu HJ, Wu E. The role of gut microbiota in immune homeostasis and autoimmunity. Gut Microbes, 2012, 3, 4.

7        Wu GD et al. Linking long-term dietary patterns with gut microbial enterotypes. Science, 2011, 334, 105.

8        Marchesi JR et al. The gut microbiota and host health: a new clinical frontier. Gut, 2016, 65, 330.

9        Lahner E et al. Probiotics in the treatment of diverticular disease. A systematic review. J Gastrointestin Liver Dis, 2016, 25, 79.

10    Scarpignato C et al. Probiotics for the treatment of symptomatic uncomplicated diverticular disease: rationale and current evidence. J Clin Gastroenterol, 2016, 50 Suppl 1, S70.

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

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

13    Daniels L et al. Fecal microbiome analysis as a diagnostic test for diverticulitis. Eur J Clin Microbiol Infect Dis, 2014, 33, 1927.

14    Yazici C et al. Breath methane levels are increased among patients with diverticulosis. Dig Dis Sci, 2016, 61, 2648.

15    Deweerdt S. Drug metabolism: manipulating the microbiome. Pharm J, 2015, 294, 377.

16    Thi LAN et al. How informative is the mouse for human gut microbiota research. Dis Model Mech, 2015, 8, 1.

17    Ryan EM et al. Recent advances in bacteriophage therapy: how delivery routes, formulation, concentration and timing influence the success of phage therapy. J Pharm Pharmacol, 2011, 63, 1253.

18    Hargreaves KR, Clokie MRJ. Clostridium difficile phages: still difficult? Front Microbiol. 2014, 5, 184.

19    Yao J et al. A pathogen-selective antibiotic minimizes disturbance to the microbiome. Antimicrob Agents Chemother. 2016, 60, 4264.

20    Bianchi M et al. Meta-analysis: long-term therapy with rifaximin in the management of uncomplicated diverticular disease. Aliment Pharmacol Ther. 2011, 33, 902.

21    Moretti A et al. Role of rifaximin in the treatment of colonic diverticular disease. Clin Ter. 2012, 163, 33.

22    Koch M et al. Diverticular disease: towards 2020. An evidence-based approach. Recenti Prog Med. 2016, 107, 309.

23    Scaioli E et al. Pathophysiology and therapeutic strategies for symptomatic uncomplicated diverticular disease of the colon. Dig Dis Sci. 2016, 61, 673.

24    Spiller RC Changing views on diverticular disease: impact of aging, obesity, diet, and microbiota. Neurogastroenterol Motil. 2015, 27, 305.

25    Tursi A. Diverticulosis today: unfashionable and still under-researched. Therap Adv Gastroenterol. 2016, 9, 213.

26    Tursi A et al. Assessment of fecal microbiota and fecal metabolome in symptomatic uncomplicated diverticular disease of the colon. J Clin Gastroenterol. 2016, 50 Suppl 1, S9.

27    Peery AF. Colonic diverticula and diverticular disease: 10 facts clinicians should know. N C Med J. 2016, 77, 220.

Colon Wall Muscles in Diverticular Disease

Sunday, September 2nd, 2012


Between the mucus producing lining and the outer layer of the colon wall, there are two major muscle systems. The inner circular muscles surround the colon, contraction can close the colon or they can act in waves to propel contents along. Between the appendix at the beginning and the rectum at the end of the colon, longitudinal muscles are gathered into three bands known as taenia. This arrangement allows contractions to shorten the colon and propel faeces without compressing them. Coordination between the two types of muscle can produce a variety of movements. An earthworm moving along soil is a good example to observe a similar system.


In the caecum, repeated circular muscle contractions mix the liquid contents (chyme). These change into backwards and forwards segmenting and propulsive movements to dry and move the mushy contents along the ascending and transverse lengths of the colon. Longitudinal muscles become more involved as faeces become more solid in the second, left side, of the colon. Occasional powerful contractions sweep faeces into the descending and sigmoid areas. Faeces are stored with the sigmoid area acting as a vertical warehouse with supporting arcs of circular muscle. Strong contractions of longitudinal muscles produce a concertina effect to push out colon contents on defaecation. The first half of the colon is controlled automatically by the vagus nerve from the brain. The left side has some local nerve reflexes and a person can have some influence such as when to defaecate.


Changes in the colon musculature in diverticular disease (DD) were described even before the early 20th century when DD was rare, (1) and in many reports since. Muscle abnormality and dysfunction persisted in the colon after resection of the areas with diverticula (2). Long sections of the left colon can change in appearance without any diverticula which may only occur years later. The muscular abnormalities are the primary pathogenic mechanisms of DD (3). DD is only diagnosed when diverticula are observed, changes in muscles have had little attention especially in areas without diverticula. (more…)

Keeping Moving

Thursday, August 26th, 2010

  African schoolchildren 33 English schoolboys 70

 This is not the result of a rugby match but the start of the revolution in the treatment of diverticular disease (DD) in the 1970s. The figures are the average times in hours for food to pass through the digestive system (1) a measurement known as ‘transit time’ The difference in the two figures was attributed to the amount of fibre in the children’s diets. Researchers then tested this theory in adults, for example, adding fibre to a standard diet of five healthy young men reduced the mean transit time from 2.4 days to 1.6 days(2). People with DD had very little fibre in their diets and long transit times (3) (this was the medical treatment at the time so this finding was not surprising) Thus the fibre theory of cause, prevention and treatment of DD was born and dietary fibre has become an institution which has spread throughout medical research. As Dr le Fanu pointed out (4) it has never been demonstrated that those who get diseases eat more or less fibre than those who don’t, nor has it been demonstrated that eating more fibre will prevent diseases.

 There is another way of reducing transit time. (more…)

What is Constipation, Diarrhoea and Normal

Thursday, August 12th, 2010


Scientists desperately try to put values on body functions to measure and classify symptoms. This enables statistical comparisons to evaluate the effects of diseases and treatments. Defaecation is a good example of this and also of the influence of history, fashions and personal opinions. (more…)