Diverticular Disease: Diet Makes a Difference

JULY 10, 2011
Jeannette Y. Wick, RPh, MBA, FASCP

When patients are facing diverticulosis or diverticulitis, pharmacists can explain the pharmacological options and suggest lifestyle modification.

Diverticular disease (DD): it’s been known to undo a dictator and disable a musician—Fidel Castro allegedly vacated his position in Cuba due to diverticulitis, and Desi Arnaz’s career took a dip when his acted up. Like many other conditions that have grown in prevalence over the past few decades, DD seems to be related to our increasing affluence and changed diet. Rare at the turn of the 20th century, it now affects up to 70% of individuals living in industrialized nations by 60 years of age. 1,2 DD can present as diverticulosis (uninflamed diverticula) or diverticulitis (inflamed diverticula).

To understand what diverticula are, one needs to review how they occur. Diet is implicated in DD’s origin because, in general, fiber intake has decreased over time in the more prosperous countries. Decreased dietary fiber intake reduces fecal mass. Experts suggest this decreases the size of the lumen or causes fecal stasis; muscular contraction force or pressure is transferred from the lumen’s content to the colon’s wall. Pressure at the weakest point in the wall—the 3 sites where vessels deliver blood supply—causes diverticula formation. Diverticula are 0.5 to 1 cm herniations or out-pocketing through the muscular wall that some people describe as looking like weak spots in a tire. They can be “false” (penetrating some but not all of the musculature) or “true” (penetrating the complete wall). Even if the diverticula are “false,” stasis or obstruction in their narrow necks may lead to bacterial overgrowth and local tissue ischemia. This process is similar to that seen in appendicitis. 2-4

DD affects the sigmoid and descending colon in more than 90% of patients. Patients who have diverticula have diverticulosis; if they have symptoms, the most frequent complaints are cramping, bloating, and constipation. In about one-fourth of diverticulosis patients, the out-pocketing becomes inflamed and possibly infected, and the diagnosis progresses to diverticulitis. 2-4 Increasingly, experts believe that fiber deficiency also changes colon microecology, decreasing local immune response, creating a low-grade chronic inflammatory process, and inviting acute diverticulitis. 2 The Table5-14 describes risk factors related to DD. Risk Factors for Diverticular Disease


Many people who have DD have asymptomatic disease, but symptoms can vary, starting with fever, abdominal pain (usually on the left side), bowel habit changes, and local symptoms associated with leukocytosis. Diverticula can perforate through the wall of gut into the pericolic tissue, leading to microabscess and bleeding or a large abscess formation. Fistulization is possible, most often to the bladder. When patients present with possible DD, clinicians use computerized tomography scan to evaluate the extent of the disease without risk of iatrogenic perforation. 3,4


Once DD is diagnosed, treatment proceeds based on the patient’s symptoms and disease severity.

Acute diverticulitis may present with left-sided pain, abdominal tenderness, and possible ileus (stagnant bowel). Acute diverticulitis is often recurrent, and patients may volunteer that they have had it before. Perforation, if it occurs, frequently causes referred pain in the shoulder.

Complicated diverticulitis indicates that obstruction, mass, abscess, fistula, hemorrhage, or perforation may be present. Chronic diverticulitis is rare and atypical, and may occur in the transverse or ascending bowel. Pain may be its sole symptom. 4

In acute, uncomplicated, and mild DD, most prescribers will use a broad spectrum antibiotic that has activity against colonic bacteria, including bacteroides, peptostreptococcus, clostridium, and fusobacterium species. Oral regimens are prescribed for 7 to 14 days, with the assumption that infection has begun or will begin. After the episode resolves, follow-up is critical. Clinicians should rule out malignancy or other gastrointestinal complications. A colonoscopy should be performed 4 to 6 weeks after an acute episode. 4

If patients are febrile, cannot eat or drink, require narcotics, or have systemic symptoms, clinicians usually hospitalize them and administer antibiotics intravenously (often a third generation cephalosporin, aminoglycoside, or monobactam with an anaerobic agent). These patients are placed on hydration, and food is withheld. If abscess or blockage occurs, clinicians may try percutaneous drainage or move directly to surgical intervention. During surgery, surgeons clean the perotineal cavity and remove bleeding pouches and fistulas. They may need to perform colon resection, or a temporary or permanent colostomy. Complications from surgery are common. Once patients improve, they can switch to oral antibiotics. 4

In those patients for whom DD creates chronic discomfort and recurrent acute episodes, several strategies are under investigation. Some researchers have seen good results using nonabsorbable mesalamine and related compounds and/or rifaximin. 14-16 Others suggest that there is a role for probiotics, especially nonpathogenic Escherichia coli, because they seem to stabilize the intestinal mucosa and stimulate immune response. A few studies, most small, have documented improvement with probiotics in DD patients. Additional study is needed to support their use. 17-19 Immunocompromised patients (those on corticosteroids or chemotherapy, having autoimmune disease, or organ transplantation patients) are considered unique because they can present with a smoldering, indolent form of DD. Their disease is often complicated, and they are at high risk of perforation, abscess, or infection. Some surgeons advocate early surgery for these patients, whereas others believe a conservative approach is best because the rate of post-surgical complication is elevated. 20,21 Dietary advice flip-flops, depending on the patient’s progress. During symptomatic periods, clinicians direct patients to select a low-fiber, bland diet until the acute episode or highly symptomatic period has passed. After acute episodes are controlled or chronic disease is managed, patients should increase the fiber in their diet gradually to 20 to 30 g daily. 4 Patients who have trouble increasing dietary fiber may use bulk stimulants like psyllium. Patients should not use laxatives and should avoid enemas altogether, or use them only infrequently and under a physician’s care. In the past, clinicians warned patients to avoid high-residue foods—nuts, seeds, berries, or popcorn—with the thought being that such small, hard particles could become caught in diverticula and exacerbate the disease. Studies, however, have not proved this to be true. 22

Summary and Conclusion

Across the nation, most people only consume 11 to 13 g of fiber a day. That’s half of what we really need for optimal health. And it’s no surprise, considering that 53% of Americans think steak is a significant fiber source and 42% believe potato chips are. 23 There’s plenty of room to educate patients about fiber and its benefits. With the current national obsession with low-carb diets, many people are eschewing fruits and vegetables, and unwittingly decreasing their fiber intake to 7 or 8 g daily. Talk about fiber, and praise its benefits. In addition to preventing diverticulosis and its complications, increased fiber intake helps prevent or control many other health conditions. PT 

Ms. Wick is a senior clinical research pharmacist at the National Cancer Institute, National Institutes of Health, Bethesda, Maryland. 


1. Parks TG. Natural history of diverticular disease of the colon. Clin Gastroenterol. 1975;4:3-21.

2. Floch MH, Bina I. The natural history of diverticulitis: fact and theory. J Clin Gastroenterol. 2004;38(5 suppl 1):S2-S7.

3. Stollman NH, Raskin JB. Diverticular disease of the colon. J Clin Gastroenterol. 1999;29:241-252.

4. Hall J, Hammerich K, Roberts P. New paradigms in the management of diverticular disease. Curr Probl Surg. 2010;47:680-735.

5. Acosta JA, Grebenc ML, Doberneck RC, McCarthy JD, Fry DE. Colonic diverticular disease in patients 40 years old or younger. Am Surg. 1992;58:605-607.

6. Schauer PR, Ramos R, Ghiatas AA, Sirinek KR. Virulent diverticular disease in young obese men. Am J Surg. 1992;164:443-448.

7. Hall JF, Roberts PL, Ricciardi R, et al. Colonic diverticulitis: does age predict severity of disease on CT imaging? Dis Colon Rectum. 2010;53:121-125.

8. Munakata A, Nakaji S, Takami H, Nakajima H, Iwane S, Tuchida S. Epidemiological evaluation of colonic diverticulosis and dietary fiber in Japan. Tohoku J Exp Med. 1993;171:145-151.

9. Heaton KW, Thompson WG. Exercise and diverticular disease. BMJ. 1995;310:1332.

10. Aldoori WH, Giovannucci EL, Stampfer MJ, Rimm EB, Wing AL, Willett WC. A prospective study of alcohol, smoking, caffeine, and the risk of duodenal ulcer in men. Epidemiology. 1997;8:420-424.

11. Goh H, Bourne R. Non-steroidal anti-inflammatory drugs and perforated diverticular disease: a case-control study. Ann R Coll Surg Engl. 2002;84:93-96.

12. Piekarek K, Israelsson LA. Perforated colonic diverticular disease: the importance of NSAIDs, opioids, corticosteroids, and calcium channel blockers. Int J Colorectal Dis. 2008;23:1193-1197.

13. Strate LL, Liu YL, Aldoori WH, Syngal S, Giovannucci EL. Obesity increases the risks of diverticulitis and diverticular bleeding. Gastroenterology. 2009;136:115-122.

14. Di Mario F, Aragona G, Leandro G, et al. Efficacy of mesalazine in the treatment of symptomatic diverticular disease. Dig Dis Sci. 2005;50:581-586.

15. Humes DJ, Fleming KM, Spiller RC, West J. Concurrent drug use and the risk of perforated colonic diverticular disease: a population-based case-control study. Gut. 2011;60:219-224.

16. Tursi, A. New physiopathological and therapeutic approaches to diverticular disease of the colon. Expert Opin. Pharmacother. 2007;8:299-307.

17. Annibale B, Maconi G, Lahner E, De Giorgi F, Cuomo R. Efficacy of Lactobacillus paracasei sub. paracasei F19 on abdominal symptoms in patients with symptomatic uncomplicated diverticular disease: a pilot study. Minerva Gastroenterol Dietol. 2011;57:13-22.

18. Lamiki P, Tsuchiya J, Pathak S, et al. Probiotics in diverticular disease of the colon: an open label study. J Gastrointestin Liver Dis. 2010;19:31-36.

19. White JA. Probiotics and their use in diverticulitis. J Clin Gastroenterol. 2006;40(suppl 3):S160-S162.

20. Tyau ES, Prystowsky JB, Joehl RJ, Nahrwold DL. Acute diverticulitis: a complicated problem in the immunocompromised patient. Arch Surg. 1991;126:855-859.

21. Chapman J, Davies M, Wolff B, et al. Complicated diverticulitis: is it time to rethink the rules? Ann Surg. 2005;242:576-583.

22. Strate LL, Liu YL, Syngal S, Aldoori WH, Giovannucci EL. Nut, corn, and popcorn consumption and the incidence of diverticular disease. JAMA. 2008;300:907-914.

23. National Fiber Council. Are you getting your fill of fiber?www.nationalfibercouncil.org/af_are.shtml. Accessed May 1, 2011.


The Oncology Care Pharmacist in Health-System Pharmacy 
According to the National Cancer Institute, almost 40% of men and women will be given a diagnosis of some form of cancer in their lifetime.


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