Archive for the ‘Diverticular disease information’ 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.

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.

Diverticular Disease: Genetics and Collagen

Thursday, July 9th, 2015

Compared with other diseases, advancements in science and technology left diverticular disease (DD) behind decades ago. Worldwide occurrence, poor quality of life, level of mortality and healthcare costs should have generated far more research effort. Preoccupation with dietary fibre levels, constipation and ageing has and still is stunting research. Fibre levels have benefits for constipation and symptoms but research into cause, prevention and other treatments has been overtaken by the necessary investigations into the surgical rescue of DD effects. Recently valid trials and surveys have disputed traditional thinking about a dietary cause and revealed a genetic factor. (more…)

Diverticular Disease And Colon Cancer

Thursday, April 3rd, 2014

Does having diverticular disease (DD) increase the risk of colon cancer (CC)?  One expert would say “yes” and another would answer “no”. Much depends on the design of studies, choice of patients, what data is fed into the computer for statistical analysis, interpretation of the results and what opinions and conclusions are made.

Research can be based on the occurrence of the two separate diseases, how many people with DD have CC and how many people with CC have DD (1). Comparison can be made with the levels of CC and DD which would be expected in the general population. Information can be expanded by including different types of cancerous lesions and their position in the colon. The diagnosis of DD is not so stable. Diverticulitis but not diverticulosis was indicated to be in a long-term causal relationship with increased risk of left-sided CC (2). However, these conditions at diagnosis can change. Diverticulitis can revert to diverticulosis with few further problems, or, diverticulosis can later progress to diverticulitis or even further to serious complications. This is a basic problem in DD research. (more…)

Diverticulitis: a wind of change

Sunday, December 2nd, 2012

There have been many changes over the years in the approach to diverticular disease (DD), even in the names used. Diverticular disease is the overall name. The presence of the grape-like diverticula on the outside of the colon results in a diagnosis of diverticulosis. Diverticulitis occurs when there is infection and inflammation of the diverticula but is often used when there are any symptoms caused by the disease.

Diverticulosis can have episodes of diverticulitis or complicated diverticulitis when problems such as bleeding, abscess, fistula or blockage need surgical treatment. This is a simplistic explanation of what might happen in DD in decreasing numbers, so that only a small fraction of people with DD ever need surgery. Any progression in the disease can stop and revert to symptomless diverticulosis at any time, some people with diverticulosis do not even know that they have it.

There has been confusion over many years about the symptoms with DD. (more…)

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…)

Diverticular Disease: Updated Epidemiology

Thursday, May 3rd, 2012

“Ideas, like living organisms, have their natural history, growing from conception through a more or less tumultuous adolescence and reproductive maturity to an old age, when they act as a bar to further progress. During this time they become so modified that their origin is obscured” Sir Richard Doll (1)

Looking at the occurrence of a disease in time and place, and assessing what might have influenced changes, is known as the science of epidemiology. The theory, that diverticular disease (DD) was caused by low levels of fibre in the diet, has been prominent for about 40 years. This was based on the rarity of DD in Uganda compared with Western countries such as Great Britain or the USA. It was assumed that high levels of fibre in the Ugandan diet protected people from DD and that an increase in dietary fibre would prevent DD and its symptoms would be eliminated. This was a conclusion too far. It ignored the rarity of DD in people eating very little fibre (2,3) and that vegetarians can get DD (4,5). There is no evidence that a high fibre diet prevents DD. The theory is so entrenched that if DD appears in a country then it is assumed that its inhabitants have changed from their normal to a low fibre western diet. This is particularly incongruous when applied to right-sided DD in the caecum and ascending colon. Even the theory’s originators thought low fibre levels could not be relevant to this area (6)

Data from post-mortems, mortality statistics and surveys can provide information on the occurrence of DD, each aspect contributing to the overall picture. Song et al. (7) showed how colonoscopy findings, over time, could plot a rising prevalence of DD in Korea. Jun and Stollman in 2002 (8) collected results from research papers on the % of patients with DD in series of examinations by colonoscopy or barium enema Xray. They used these results to show that changes in the prevalence of DD varied greatly in time and between countries. Searching through later research reports mainly in the PubMed website gives this type of information for many more countries. (References to these sources are too numerous to include here). The results fall into 4 distinct patterns of when DD appeared and how numbers have changed over time until 2010. (more…)

How many people have diverticular disease and symptoms

Wednesday, January 12th, 2011

Nearly every review of diverticular disease (DD) and some research papers begin with statistics about how many people have DD at different ages. Figures regularly quoted for Western countries are 5% of the population by the age of 40, 25% by the age of 60 and 65% at 85 years. Variations are also described such as 50% of the population over 60 years, or 1/3 to 1/2 of the population will get the disease. In England and Wales this works out at over 5 million people which would rise with the aging population.

Trying to find the sources of these figures (more…)

All in a name – medical terms

Thursday, September 9th, 2010


Diverticular disease is an umbrella term which covers the physical changes in the colon wall and the effects from diagnosis to life-threatening complications and all the different symptoms which result from the disease. The muscular deformity with the characteristic bulging hernia or pouches called diverticula is known as diverticulosis. This definition is of a visible physical abnormality and does not indicate the extent of damage to the colon or describe its effects. Some people do not know that they have diverticulosis but after diagnosis about ¾ of patients have some type of symptoms. (more…)

What is Diverticular Disease

Thursday, August 5th, 2010

What is diverticular disease

 The large bowel becomes deformed in diverticular disease. The muscles appear to be permanently contracted so that the colon can be shortened and more corrugated. The bowel wall becomes ruptured particularly next to it’s blood vessels and pressure forces the inner layers to protrude through the wall to produce the characteristic grape-like pouches on the outside of the colon. There can be few of these pouches – called diverticula – or the whole colon can be affected. Similarly there can be a wide range of symptoms, but nobody knows how to stop the possible progression of the disease from symptomless, to a chronic, debilitating and recurring syndrome and on to life-threatening complications. Death rates in this country started at nil and have risen throughout the 20th century. With any other complaint, this statistic alone would prompt an outcry for research into causes, prevention and treatment. (more…)