Diverticular disease AND/OR irritable bowel syndrome

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. https://bnf.nice.org.uk.

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.

Tags: , , , ,

Comments are closed.