Archive for the ‘Treatments’ Category

Diverticular disease AND/OR irritable bowel syndrome

Friday, June 29th, 2018

Information about diverticular disease (DD) is available in fact sheets on many internet sites, but these should be assessed. Is it up to date, does it help day-to-day problems, is it a charity or a business? Discussions on forums show a variety of experiences of DD and no general approach on what can be done to help. DD is sometimes mentioned by charities which support younger people with, for example, Crohn’s and ulcerative colitis (IBD) or Irritable Bowel Syndrome (IBS). In the last few years some people with DD have been told that they also have IBS. This can be very confusing because DD and IBS are different complaints sometimes with conflicting treatments and certainly different potential outcomes. Some researchers propose that any symptoms without diverticulitis must be IBS. This ignores or denies the colon damage which resulted in diverticula forming. Sources of information about IBS do not cover an IBS/DD diagnosis, never mind any differences which should be considered.

There are a range of symptoms produced by the bowel which show that it is not working properly. Some or all of these can be caused by any bowel complaint. IBS is not a ‘disease’ in itself but a spectrum of pain, diarrhoea, constipation, bloating etc. which cannot be explained. It is in essence an interim diagnosis, because if a cause is found it can become endometriosis, coeliac disease, lactose intolerance, etc. and can be better controlled. IBS is also excluded if colon damage is observed in scans or internal examinations which can account for the symptoms, for example, damage to the internal bowel surface in IBD. DD is in this category. The presence of grape-like hernia, (diverticula), on the outside of the colon is the easily recognised manifestation of the disease and the diagnostic criterion, but are not the only colon changes present (1).

Colon nerves are not sensitive to the damage which causes diverticula formation. DD can be diagnosed without any symptoms. However, changes in colon collagen and structure have been observed before diverticula are formed (2,3,4) The sigmoid colon walls become thickened and shortened, giving a corrugated appearance, These changes are permanent and cannot be reversed. The seratogenic, cholinergic and nitric oxide nerves, which control muscle contraction and relaxation for normal movements, are damaged. Whereas the sympathetic nerves giving “flight and fight” responses are not affected (5,6,7) This might be the reason for apparent exaggerated constipation and diarrhoea responses. Such effects might get worse over the years if the damage progresses. The number of diverticula may or may not increase but their presence is a continuous risk for the infection and inflammation of diverticulitis. A bout of this is sometimes a path to recurring symptoms and complications. Alternatively, the disease may never change after diagnosis.


Many older people become more constipated because of changes in lifestyle, age-related colon changes and perhaps side effects of their common drugs. DD is often described as a disease of old age, caused by constipation, because it’s symptoms, problems, complications and risks can increase with ageing (8). When such problems lead to barium enema examinations it was assumed that diverticula only appeared at retirement age. Screening colonoscopies about the age of 50 can show diverticula earlier in life without symptoms, Diet, obesity, lack of exercise, constipation etc. are often described as the cause or risk factors for DD, but they are risk factors for symptoms of DD and the investigations leading to diagnosis (9). These IBS-like symptoms in older people are different in cause to the IBS problems which beset young adults. IBS does not lead to DD, A survey of people with DD found that only 7.5% thought they had IBS earlier in life. A follow–up of IBS patients in America found only 6.7% had DD (10). Fewer IBS patients had diverticulosis than the controls in one survey (11).


The Rome criteria are used to standardise IBS symptoms to select patients for research. Patients are divided according to the predominance of constipation, diarrhoea or alternating effects. When the IBS standards were applied to DD patients only 14% fitted them, DD was distinguished by episodes of pain lasting over 24 hours. In DD research, patients are divided into five categories, no symptoms, symptoms of dysfunction, bleeding, infection and inflammation of diverticulitis and complications needing hospital admission or surgery (12). It is the dysfunction which has been relabelled IBS by some researchers. This used to be called “painful DD” decades ago, now “symptomatic uncomplicated DD” (SUDD). Patients’ problem is deciding which category their pain is in. A person with DD can unpredictably move between these categories in a short time, or may not change, nor progress to chronic symptoms. This gives problems in symptom treatments (13).There is no known diet or treatment to prevent diverticulitis. IBS does not progress or have a mortality risk or give raised temperatures but more side-effects from drugs have been noted (14).

The symptoms of DD are specific to the colon whereas IBS can be associated with gastric or bladder symptoms and other body conditions. Both complaints reduce the quality of life, but, traditionally with IBS, the quality of life is thought to have an effect on the complaint and is an area of potential treatment.

Data can be collected for DD on the proportion of people with diverticula, hospital admissions or mortality. Differences in age of patients, differences between countries and changes over a century, put DD into the “Western” diseases collection. In some countries surveys found more than 50% of the population were affected.  IBS levels are difficult to assess because it is a clinical diagnosis and secondary care level is not needed and there can be self diagnosis. IBS appears to have a global prevalence of 11%. (15). DD and IBS are different bowel conditions. A dual diagnosis might be convenient but is confusing and unhelpful for DD patients.

“That which separates seemingly similar conditions in a majority of patients may be more important than what apparently links them in a minority” (16).


Having DD does not preclude difficulties with other conditions which alone have been associated with IBS. Small intestine bacterial overgrowth (SIBO) has been found in 60% of people with DD (17) and between 4% and 78% With IBS. The levels of migraine sufferers with DD and IBS are greater than the general population. Changes in serotonin levels which affect gut motility are found in both DD and IBS and might be part of the migraine spectrum of effects. A case has been reported where “IBS” in a migraine patient was prevented by using a triptan migraine drug when needed (18). Could this approach be useful for IBS compared with continuous treatment with gut serotonin drugs? Drugs affecting serotonin activity have not been considered for DD. As well as gas producers and irritants, it is interesting to find common problem foods triggering DD, IBS and migraine.

The guts of even healthy people are affected by stress and gastroenteritis or food poisoning can have lasting effects which have been recognised with both IBS and DD. Trying to find food triggers of symptoms is common to both complaints, also using diet to try and control symptoms. Over half a century ago, wheat bran and high-fibre diets were promoted for  most bowel diseases. Unlike IBS, it has taken decades for this theory on the cause and treatment of DD to be disproved. Increased dietary fibre may help some people with constipation but not others. A good fluid intake and exercise are also important.


IBS research has lead to new laxative drugs, serotonin regulation treatments, low dose antidepressant drugs in addition to traditional antispasmodic and anti-diarrhoea drugs. DD research rightly emphasises the surgical treatment of complications. There is not enough evidence from trials to recommend any overall treatment for DD including high fibre diets (19,20,21,22). Dietary fibre does not prevent diverticulosis and what changes diverticulosis into diverticulitis is still unknown. There is always a caution in the treatment of chronic DD because of the possibility of colon narrowing and strictures.


The gut/brain axis is important in health and disease. The two way nerve system accounts for some people feeling more pain than others from their gut problems. In the opposite direction, lifestyle effects on gut function can be helped hypnosis, cognitive behavioural therapy (CBT) or relaxation techniques. The nervous systems work by using neurotransmitters to relay messages between nerves or between nerves and muscles. These are present in both the gut brain and the head brain, acetylcholine and serotonin are examples. Different organs can selectively respond to the same neurotransmitter through their receptors. Drugs or chemicals in foods can mimic, change or block neurotransmitters. Some problem foodstuffs which feature in lists for DD, IBS and migraine are those which contain biologically active chemicals. Though not confined to plants, particularly the nightshade family, examples of these are nicotine which disturbs gut function and the possible cause of DD, and caffeine taken for brain stimulation which affects the gut. Hyoscine and atropine are used medically for their effects on the gut. Such “natural drugs” are broken down by liver enzymes for excretion but there is a wide range of activity of this function between individuals. Is it possible that some people are less able to metabolise and inactivate food chemicals? Are the “safe” levels of insecticides and environmental chemicals not safe for everybody? Is this an area where genetics interacting with environment might be a factor in symptoms (14,23,24) like genetics can modify activity and side effects of drugs?

© Mary Griffiths 2018


1        Barrenschee M. et al. No neuronal loss, but alterations of the GDNF system in asymptomatic diverticulosis. PLoS One, 2017, 12, e0171416.

2        Spriggs E.I. Lantern Demonstration, Internal Diverticula. B.M. J. 1925, Dec 5, 1061.

3        Janes S.E.J. et al. Management of diverticulitis. B.M.J. 2006, 332, 271.

4        Painter N.S. Diverticular disease of the colon. B.M.J. 1968, 3, 475.

5        Yun A.J. et al. A new mechanism for diverticular disease: aging-related vagal withdrawal. Medical Hypotheses, 2005, 64, 252.

6        Bottner M. et al. The enteric serotonergic  system is altered in patients with diverticular disease. Gut, 2013, 62, 1753.

7        Espin F. et al. Nitrergic neuro-muscular transmission is up-regulated in patients with diverticulosis. Neurogastroenterol Motil. 2014, 26, 1458.

8        Peery A.F. et al. Constipation and a low-fibre diet are not associated with diverticulosis. Clin Gastroenterol Hepatol. 2013, 11, 1622.

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

10    Adeniji O.A. et al. Durability of the diagnosis of irritable bowel syndrome based on clinical criteria. Dig Dis Sci, 2004, 49, 572.

11    Chey W.D. et al. The yield of colonoscopy in patients with non-constipated irritable bowel syndrome: results from a prospective, controlled US trial. Am J Gastroenterol. 2010, 105, 859.

12    Wedel T. et al. Morphological basis for developing diverticular disease, diverticulitis, and diverticular bleeding. Viszeralmedizin, 2015, 31, 76.

13    Wensaas K.A. & Hungin A.P. Diverticular disease in the primary care setting. J Clin Gastroenterol. 2016,  50 Suppl 1, S86.

14    Poltras P. et al. Extra digestive manifestations of irritable bowel syndrome: intolerance to drugs?  Dig Dis Sci,  2008, 53, 2168.

15    Canavan C. et al. The epidemiology of irritable bowel syndrome. Clin Epidemiol. 2014, 6, 71.

16    Shanahan F. Editorial, The neglected spectrum of diverticular-related disorders. Clin Gastroenterol Hepatol. 2013, 11, 1620.

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

18    Cheyette B.N. and Cheyette S.N. Acute exacerbation of irritable bowel syndrome prevented by prn oral triptan. Clin J Gastroenterol. 2016, 9, 375.

19    Smith J. Should we treat uncomplicated symptomatic diverticular disease with fibre? BMJ, 2011, 342, d2951.

20    Tursi A. Dietary pattern and colonic diverticulosis. Curr Opin Clin Nutr Metab Care. 2017, 20, 409.

21    NICE Diverticular disease treatment.

22    Peery A.F. et al. A high-fibre diet does not protect against asymptomatic diverticulosis. Gastroenterology, 2012, 142, 266.

23    Makker J. et al. Genetic epidemiology of irritable bowel syndrome. World J Gastroenterol. 2015, 21, 11353.

24    Reichert M.C. and Lammert F. The genetic epidemiology of diverticulosis and diverticular disease: emerging evidence. United European Gastroenterol J. 2015, 3, 409.

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.

Expert Patient Programme

Tuesday, October 11th, 2011

Nearly two years ago I wrote to the Secretary of State for Health asking why diverticular disease (DD) was not included with all the other diseases in the National Service Framework (NSF) for long term conditions or the NSF for older people or the ‘Expert Patient’ initiative. The government thought that both NSFs should ensure that all older people receive improved services based around their own individual needs, and in this way DD may well be covered but not specifically. 

The Expert Patient initiative is a new approach to the management of chronic diseases. (more…)

RIFAXIMIN – a potential treatment for diverticular disease

Thursday, July 7th, 2011


Rifaximin is a synthetic antibiotic, a modification of rifamycin which was originally produced by the  microbe Streptomyces mediterranei. Rifaximin should not be confused with rifampicin which is used under brand names and in combined treatments particularly for Tuberculosis infections.

Rifaximin passes through the digestive system virtually unabsorbed and unchanged so retaining its antimicrobial activity and concentration level inside the colon. (more…)

Diverticular Disease in Healthcare Systems, part 2, community

Monday, December 6th, 2010

 The impact of diverticular disease (DD) in the hospital situation was discussed in the Winter 2006/2007 issue of the magazine. This area is well researched to update and optimise the diagnosis of DD and the expert treatment of complications on an individual basis. This research also shows that DD is an increasing burden on hospitals in terms of number of admissions and costs. Better management in the community is critical in reducing this burden. Prevention of complications of DD would benefit both NHS budgets and patients. (more…)

Diverticular Disease in Healthcare Systems, part 1 hospitals

Monday, December 6th, 2010

Diverticular disease (DD) is not the sort of complaint where a distinct diagnosis is obvious without investigation. Nor is there a well established treatment regime which prevents or slows down a foreseeable progression. DD is not predictable in its effects, it may or may not progress and there is no treatment which is universally successful. The place of DD in the healthcare system is not clear-cut. (more…)