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Diverticulosis and Dietary Fiber: Rethinking the Relationship
Editorials Diverticulosis and Dietary Fiber: Rethinking the Relationship See “A high-fiber diet does not protect against asymptomatic diverticulosis,” by Peery AF, Barrett PR, Park D, et al, on page 266.
F
or more than a half century, the development of diverticulosis has been largely attributed to insufficient fiber intake and aging. In seminal work, Painter and Burkitt described marked differences in the prevalence of diverticular disease in Africa and Asia compared with Western countries, as well as pre- and postindustrialization in Europe and the United States.1 Western diets tended to be lower in fiber than African and Asian diets, and, in the West, the steady decline in fiber consumption mirrored the increase in diverticular disease. Furthermore, individuals living in Africa had shorter stool transit times and greater stool weights than those residing in England, and patients with diverticulosis were noted to have altered colonic motility particularly after pharmacologic stimuli.2,3 Based on these observations, they hypothesized that low-fiber diets resulted in the development of diverticulosis via small-caliber stools and high colon pressures.1 Despite the logic of this theory and its subsequent widespread acceptance, the data on which it is based have a number of potential shortcomings. Notably, regional dietary habits were broadly assumed to be uniform and to reflect the intake of individual patients, and geographical differences in lifespan as well as other potential confounding factors were not accounted for. Subsequent evidence in support of Painter and Burkitt’s fiber hypothesis is limited and conflicting (Table 1). Rodents that, under normal circumstances are free of diverticulosis, develop the condition when fed extremely lowfiber diets.4 In a study of 264 nonvegetarians and 56 long-time vegetarians, Gear et al found that diverticulosis was significantly more prevalent in the nonvegetarian group who on average consumed significantly less fiber.5 Nonetheless, there was substantial overlap in fiber consumption between patients with and without diverticulosis (eg, vegetarians with diverticulosis consumed more fiber than nonvegetarians without diverticulosis), and age and other potential differences between the 2 groups were not addressed. In contrast, 2 studies of patients with predominantly right-sided diverticulosis found no difference in fiber intake between individuals with and without diverticulosis.6,7 However, the pathogenesis of right-sided diverticulosis may be different from left-sided disease and, in these studies, assessment of dietary fiber was limited to fruit and vegetable intake. Other studies linking fiber intake with diverticulosis have focused on populations with symptomatic uncomplicated diverticular disease (ie, chronic gastrointestinal symptoms in the setting of diver-
ticulosis).8 –12 In general, these studies demonstrate that fiber can ameliorate a number of symptoms in individuals with diverticulosis, but tell us little about its effect on the development of diverticulosis or its complications.8 –12 In this issue of GASTROENTEROLOGY, Peery et al report the results of an observational cross-sectional study of 2104 patients undergoing outpatient colonoscopy as part of 3 successive studies of environment and lifestyle and colorectal adenomas.13 Patients reported by the endoscopists to have diverticulosis were considered cases (42% of patients), and were compared with patients without note of diverticulosis. Diet and lifestyle information were collected via phone interview within 3 months after the endoscopy using validated instruments. The authors found that contrary to long-standing dogma, low dietary fiber was not associated with the presence of diverticulosis. In fact, surprisingly, high fiber intake was positively related to diverticulosis after adjustment for body mass index, age, and race (adjusted prevalence ratio 1.30, 95% confidence interval [CI], 1.13–1.50 when comparing individuals in the highest quartile of fiber to those in the lowest). In support of these findings, there was a dose–response relationship, and the association was stronger in individuals with more marked diverticulosis (⬎3 vs ⬍3 diverticula). In addition, individuals with more frequent bowel movements seemed to be at greater risk for diverticulosis. There were no associations between fat and red meat intake or physical activity and diverticulosis. Consistent with prior work, the prevalence of diverticulosis increased with age. These data are the most convincing to date regarding the association between fiber and diverticulosis. Nonetheless, the results should be interpreted in the context of the crosssectional study design. Dietary and lifestyle exposures were ascertained after the colonoscopic diagnosis of diverticulosis, and years, if not decades, after the onset of the condition. Therefore, a causal relationship between fiber and diverticulosis cannot be established. Knowledge of the findings at colonoscopy as well as the prevailing association between fiber and diverticulosis may have led to differential recall of dietary intake by diverticulosis cases compared with controls. There may also be a potential bias attributable to changes in fiber intake owing to a prior diagnosis of diverticular disease. Indeed, it is likely that individuals diagnosed with diverticulosis or its complications were instructed to increase fiber consumption. However, in a secondary analysis, the authors excluded the subset of individuals with a prior colonoscopy (n ⫽ 680), and the results were largely unchanged, suggesting that this did not account for the findings. Finally, given that diverticulosis had been longstanding in most patients, the validity of the results depends on the stability of diet over long periods of time, and diet in GASTROENTEROLOGY 2012;142:205–210
Editorials, continued Table 1. Dietary Fiber and Risk of Asymptomatic Diverticulosis Study
Year
Diverticulosis cases (n)
Findings
Case control
95
2000
Case control
86 (100% right sided)
Song7
2010
Cross-sectional
103 (85% right sided)
Peery13
2011
Cross-sectional
878
Diverticulosis less prevalent in vegetarians who on average consumed more fiber No significant association between fruit and vegetable intake and diverticulosis in high vs low comparison of 3 categories. Vegetable: OR, 0.55 (95% CI, 0.19–1.61) Fruit: OR, 0.56 (95% CI, 0.18–1.72) No significant difference in mean dietary fiber score in cases vs controls (mean score 7.0 vs 7.1, respectively) Increased risk of diverticulosis in high vs low quartile of fiber intake. OR, 1.30 (95% CI, 1.13–1.50)
Gear5
1979
Lin6
Design
the distant past may be difficult to capture with a single current measure. It is also possible that increased fiber consumption in response to symptoms of undiagnosed diverticular disease led to the apparent positive association. Chronic symptoms in the setting of diverticulosis (symptomatic uncomplicated diverticular disease) are known to respond to fiber supplementation.8,10 –12 The prevalence of symptomatic uncomplicated diverticular disease is unknown, but is likely underappreciated.14 In a population-based study by Jung et al of ⬎2000 patients in Olmstead County who had undergone ⱖ1 relevant diagnostic test for diverticulosis, 25% of patients with diverticulosis reported abdominal pain or altered bowel habits, which was a significantly greater proportion than those without diverticulosis.15 In addition, irritable bowel syndrome, particularly diarrhea predominant, was predictive of the presence of diverticulosis.15 Currently, chronic gastrointestinal symptoms in diverticulosis are often attributed to coexisting irritable bowel syndrome, but there is increasing interest in defining and treating symptomatic uncomplicated diverticular disease as a unique disorder.14,16 The fact that most colonoscopies in this study were screening examinations reduces the possibility of functional symptoms and their influence on dietary preferences. Additional information on symptoms or diagnoses predating colonoscopy is not reported, but laxative use, and therefore presumably constipation, was more common among patients without diverticulosis. Also contrary to the tenets of the fiber hypothesis, bowel movement frequency was positively associated with diverticulosis in the Peery study. Similarly, Jung et al noted that diarrhea-predominant irritable bowel syndrome, although not functional diarrhea, was positively related to diverticulosis.15 In addition, patients with constipation who did not take laxatives or bulking agents were at a 40% decreased risk of diverticulosis compared with those without constipation.15 Increased bowel movement frequency could provide a mechanistic link between fiber intake and diverticulosis, although fiber and bowel movement frequency were not associated in the Peery study. Colonic pressures increase with defecation, and it has been postulated that the excessive straining required for defecation in the sitting versus squatting position, and not diet, explains the geographical disparities in diverticular disease.17 It is also possible that divertic206
ulosis results in increased colonic motility and therefore increased bowel movement frequency. Studies have noted faster colon transit times in individuals with diverticulosis.18 The results of the Peery study do not undermine the potential benefit of fiber on diverticular complications. The biological mechanisms underlying the development of diverticulosis versus subsequent diverticulitis and diverticular bleeding are probably quite different. Furthermore, a number of studies, including 2 large prospective cohorts, have observed an inverse association between dietary fiber intake and diverticular complications. In the Health Professionals Follow-up Study of 47,888 men followed over 4 years, the adjusted relative risk was 0.58 (95% CI, 0.41– 0.83) for symptomatic diverticular disease when comparing highest with the lowest quintiles of fiber intake.19 A strikingly similar result was seen in the Oxford cohort of European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford study), a cohort of 47,033 men and women followed for an average of 12 years.20 The adjusted relative risk of hospitalization for diverticular disease was 0.59 (95% CI, 0.46 – 0.78) in individuals in the highest category of fiber intake compared with those with the lowest fiber intake. A potential drawback with these studies is the inability to distinguish between diverticulitis, diverticular bleeding, and symptomatic uncomplicated diverticular disease although patients in the EPIC study were hospitalized or died as a result of diverticular disease and were therefore more likely to have had complicated disease. It is unclear how to translate the findings from Peery et al into dietary recommendations for patients. As noted, evidence from large prospective cohorts suggests that fiber may prevent diverticular complications, and these complications, and not diverticulosis itself, result in the bulk of the health and economic burden of this disease. Although the prevention of diverticulosis would in turn prevent its downstream consequences, this strategy would require knowledge of its absence. Importantly, the beneficial effects of fiber on many other chronic diseases such as cardiovascular disease, obesity, diabetes, and cancer need to be considered because it appears that the amount of fiber required to increase the risk of diverticulosis is below current dietary recommendations. For these reasons, it seems premature to tell patients without divertic-
Editorials, continued ulosis to cut down on the consumption of fiber-containing foods. In patients with diverticulosis, the evidence suggests that a high-fiber diet is beneficial. The important and provocative paper by Peery et al calls into question the long-standing but poorly proven fiber theory of the pathogenesis of diverticulosis. In this study, high, not low, fiber intake was associated with an increased risk of diverticulosis in a dose-dependent fashion and the association was stronger in individuals with more marked disease. These results open the door for new avenues of thought regarding the pathogenesis of and risk factors for this common yet understudied disease. A future study of individuals with detailed data on diet and gastrointestinal symptoms before the diagnosis of diverticulosis, or ideally before its onset, would be welcomed to confirm these findings. Given the other health benefits of dietary fiber, further evidence is needed before altering dietary recommendations in patients without diverticulosis.
LISA L. STRATE Division of Gastroenterology Harborview Medical Center University of Washington Medical School Seattle, Washington References 1. Painter NS, Burkitt DP. Diverticular disease of the colon: a deficiency disease of Western civilization. Br Med J 1971;2:450 – 454. 2. Burkitt DP, Walker AR, Painter NS. Effect of dietary fibre on stools and the transit-times, and its role in the causation of disease. Lancet 1972;2:1408 –1412. 3. Painter NS TS. The intraluminal pressure patterns in diverticulosis of the colon. Gut 1964;5:201–213. 4. Carlson AJ, Hoelzel F. Relation of diet to diverticulosis of the colon in rats. Gastroenterology 1949;12:108 –115. 5. Gear JS, Ware A, Fursdon P, et al. Symptomless diverticular disease and intake of dietary fibre. Lancet 1979;1:511–514. 6. Lin OS, Soon MS, Wu SS, et al. Dietary habits and right-sided colonic diverticulosis. Dis Colon Rectum 2000;43:1412–1418. 7. Song JH, Kim YS, Lee JH, et al. Clinical characteristics of colonic diverticulosis in Korea: a prospective study. Korean J Intern Med 2010;25:140 –146.
8. Brodribb AJ. Treatment of symptomatic diverticular disease with a high-fibre diet. Lancet 1977;1:664 – 666. 9. Ornstein MH, Littlewood ER, Baird IM, et al. Are fibre supplements really necessary in diverticular disease of the colon? Br Med J (Clin Res Ed) 1981;282:1629 –1630. 10. Hodgson WJ. The placebo effect. Is it important in diverticular disease? Am J Gastroenterol 1977;67:157–162. 11. Smits BJ, Whitehead AM, Prescott P. Lactulose in the treatment of symptomatic diverticular disease: a comparative study with highfibre diet. Br J Clin Pract 1990;44:314 –318. 12. Taylor I, Duthie HL. Bran tablets and diverticular disease. Br Med J 1976;1:988 –990. 13. Peery AF, Barrett PR, Park D, et al. A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology 2012;142:266 –272. 14. Simpson J, Scholefield JH, Spiller RC. Origin of symptoms in diverticular disease. Br J Surg 2003;90:899 –908. 15. Jung HK, Choung RS, Locke GR 3rd, et al. Diarrhea-predominant irritable bowel syndrome is associated with diverticular disease: a population-based study. Am J Gastroenterol 2010;105:652– 661. 16. Bianchi M, Festa V, Moretti A, et al. Meta-analysis: long-term therapy with rifaximin in the management of uncomplicated diverticular disease. Aliment Pharmacol Ther 2011;33:902–910. 17. Sikirov BA. Etiology and pathogenesis of diverticulosis coli: a new approach. Med Hypotheses 1988;26:17–20. 18. Manousos ON, Truelove SC, Lumsden K. Transit times of food in patients with diverticulosis or irritable colon syndrome and normal subjects. Br Med J 1967;3:760 –762. 19. Aldoori WH, Giovannucci EL, Rimm EB, et al. A prospective study of diet and the risk of symptomatic diverticular disease in men. Am J Clin Nutr 1994;60:757–764. 20. Crowe FL, Appleby PN, Allen NE, et al. Diet and risk of diverticular disease in Oxford cohort of European Prospective Investigation into Cancer and Nutrition (EPIC): prospective study of British vegetarians and non-vegetarians. BMJ 2011;343:d4131.
Reprint requests Address requests for reprints to: Lisa L. Strate, MD, MPH, Division of Gastroenterology, University of Washington Medical School, Harborview Medical Center, 325 Ninth Avenue, Box 359773, Seattle, Washington 98104. e-mail: [email protected] Conflicts of Interest The authors disclose no conflicts. © 2012 by the AGA Institute 0016-5085/$36.00 doi:10.1053/j.gastro.2011.12.019
Outcomes Among Living Liver Donors See “Estimates of early death, acute liver failure, and long-term mortality among live liver donors,” by Muzaale AD, Dagher NN, Montgomery RA, et al, on page 273.
M
anagement of donor risk is the most important consideration in the decision to perform a living donor liver transplantation (LDLT). Counseling potential donors on operative morbidity and mortality requires a comprehensive understanding of the available data on
outcomes. Ideally, an individual potential living donor should be informed of the potential complications based on an objective analysis of a center’s own results. At present, this ideal has not been obtained. Instead, potential donors and their physicians must rely on outcome data from numerous single-center and a few multicenter studies. Reports from the three largest series from North America found that 28%– 40% of donors developed ⱖ1 complication.1–3 Perhaps the most comprehensive of these studies, the 9-center Adult-to-Adult Living Donor Liver Transplant Cohort Study (A2ALL) noted that most com207
F
or more than a half century, the development of diverticulosis has been largely attributed to insufficient fiber intake and aging. In seminal work, Painter and Burkitt described marked differences in the prevalence of diverticular disease in Africa and Asia compared with Western countries, as well as pre- and postindustrialization in Europe and the United States.1 Western diets tended to be lower in fiber than African and Asian diets, and, in the West, the steady decline in fiber consumption mirrored the increase in diverticular disease. Furthermore, individuals living in Africa had shorter stool transit times and greater stool weights than those residing in England, and patients with diverticulosis were noted to have altered colonic motility particularly after pharmacologic stimuli.2,3 Based on these observations, they hypothesized that low-fiber diets resulted in the development of diverticulosis via small-caliber stools and high colon pressures.1 Despite the logic of this theory and its subsequent widespread acceptance, the data on which it is based have a number of potential shortcomings. Notably, regional dietary habits were broadly assumed to be uniform and to reflect the intake of individual patients, and geographical differences in lifespan as well as other potential confounding factors were not accounted for. Subsequent evidence in support of Painter and Burkitt’s fiber hypothesis is limited and conflicting (Table 1). Rodents that, under normal circumstances are free of diverticulosis, develop the condition when fed extremely lowfiber diets.4 In a study of 264 nonvegetarians and 56 long-time vegetarians, Gear et al found that diverticulosis was significantly more prevalent in the nonvegetarian group who on average consumed significantly less fiber.5 Nonetheless, there was substantial overlap in fiber consumption between patients with and without diverticulosis (eg, vegetarians with diverticulosis consumed more fiber than nonvegetarians without diverticulosis), and age and other potential differences between the 2 groups were not addressed. In contrast, 2 studies of patients with predominantly right-sided diverticulosis found no difference in fiber intake between individuals with and without diverticulosis.6,7 However, the pathogenesis of right-sided diverticulosis may be different from left-sided disease and, in these studies, assessment of dietary fiber was limited to fruit and vegetable intake. Other studies linking fiber intake with diverticulosis have focused on populations with symptomatic uncomplicated diverticular disease (ie, chronic gastrointestinal symptoms in the setting of diver-
ticulosis).8 –12 In general, these studies demonstrate that fiber can ameliorate a number of symptoms in individuals with diverticulosis, but tell us little about its effect on the development of diverticulosis or its complications.8 –12 In this issue of GASTROENTEROLOGY, Peery et al report the results of an observational cross-sectional study of 2104 patients undergoing outpatient colonoscopy as part of 3 successive studies of environment and lifestyle and colorectal adenomas.13 Patients reported by the endoscopists to have diverticulosis were considered cases (42% of patients), and were compared with patients without note of diverticulosis. Diet and lifestyle information were collected via phone interview within 3 months after the endoscopy using validated instruments. The authors found that contrary to long-standing dogma, low dietary fiber was not associated with the presence of diverticulosis. In fact, surprisingly, high fiber intake was positively related to diverticulosis after adjustment for body mass index, age, and race (adjusted prevalence ratio 1.30, 95% confidence interval [CI], 1.13–1.50 when comparing individuals in the highest quartile of fiber to those in the lowest). In support of these findings, there was a dose–response relationship, and the association was stronger in individuals with more marked diverticulosis (⬎3 vs ⬍3 diverticula). In addition, individuals with more frequent bowel movements seemed to be at greater risk for diverticulosis. There were no associations between fat and red meat intake or physical activity and diverticulosis. Consistent with prior work, the prevalence of diverticulosis increased with age. These data are the most convincing to date regarding the association between fiber and diverticulosis. Nonetheless, the results should be interpreted in the context of the crosssectional study design. Dietary and lifestyle exposures were ascertained after the colonoscopic diagnosis of diverticulosis, and years, if not decades, after the onset of the condition. Therefore, a causal relationship between fiber and diverticulosis cannot be established. Knowledge of the findings at colonoscopy as well as the prevailing association between fiber and diverticulosis may have led to differential recall of dietary intake by diverticulosis cases compared with controls. There may also be a potential bias attributable to changes in fiber intake owing to a prior diagnosis of diverticular disease. Indeed, it is likely that individuals diagnosed with diverticulosis or its complications were instructed to increase fiber consumption. However, in a secondary analysis, the authors excluded the subset of individuals with a prior colonoscopy (n ⫽ 680), and the results were largely unchanged, suggesting that this did not account for the findings. Finally, given that diverticulosis had been longstanding in most patients, the validity of the results depends on the stability of diet over long periods of time, and diet in GASTROENTEROLOGY 2012;142:205–210
Editorials, continued Table 1. Dietary Fiber and Risk of Asymptomatic Diverticulosis Study
Year
Diverticulosis cases (n)
Findings
Case control
95
2000
Case control
86 (100% right sided)
Song7
2010
Cross-sectional
103 (85% right sided)
Peery13
2011
Cross-sectional
878
Diverticulosis less prevalent in vegetarians who on average consumed more fiber No significant association between fruit and vegetable intake and diverticulosis in high vs low comparison of 3 categories. Vegetable: OR, 0.55 (95% CI, 0.19–1.61) Fruit: OR, 0.56 (95% CI, 0.18–1.72) No significant difference in mean dietary fiber score in cases vs controls (mean score 7.0 vs 7.1, respectively) Increased risk of diverticulosis in high vs low quartile of fiber intake. OR, 1.30 (95% CI, 1.13–1.50)
Gear5
1979
Lin6
Design
the distant past may be difficult to capture with a single current measure. It is also possible that increased fiber consumption in response to symptoms of undiagnosed diverticular disease led to the apparent positive association. Chronic symptoms in the setting of diverticulosis (symptomatic uncomplicated diverticular disease) are known to respond to fiber supplementation.8,10 –12 The prevalence of symptomatic uncomplicated diverticular disease is unknown, but is likely underappreciated.14 In a population-based study by Jung et al of ⬎2000 patients in Olmstead County who had undergone ⱖ1 relevant diagnostic test for diverticulosis, 25% of patients with diverticulosis reported abdominal pain or altered bowel habits, which was a significantly greater proportion than those without diverticulosis.15 In addition, irritable bowel syndrome, particularly diarrhea predominant, was predictive of the presence of diverticulosis.15 Currently, chronic gastrointestinal symptoms in diverticulosis are often attributed to coexisting irritable bowel syndrome, but there is increasing interest in defining and treating symptomatic uncomplicated diverticular disease as a unique disorder.14,16 The fact that most colonoscopies in this study were screening examinations reduces the possibility of functional symptoms and their influence on dietary preferences. Additional information on symptoms or diagnoses predating colonoscopy is not reported, but laxative use, and therefore presumably constipation, was more common among patients without diverticulosis. Also contrary to the tenets of the fiber hypothesis, bowel movement frequency was positively associated with diverticulosis in the Peery study. Similarly, Jung et al noted that diarrhea-predominant irritable bowel syndrome, although not functional diarrhea, was positively related to diverticulosis.15 In addition, patients with constipation who did not take laxatives or bulking agents were at a 40% decreased risk of diverticulosis compared with those without constipation.15 Increased bowel movement frequency could provide a mechanistic link between fiber intake and diverticulosis, although fiber and bowel movement frequency were not associated in the Peery study. Colonic pressures increase with defecation, and it has been postulated that the excessive straining required for defecation in the sitting versus squatting position, and not diet, explains the geographical disparities in diverticular disease.17 It is also possible that divertic206
ulosis results in increased colonic motility and therefore increased bowel movement frequency. Studies have noted faster colon transit times in individuals with diverticulosis.18 The results of the Peery study do not undermine the potential benefit of fiber on diverticular complications. The biological mechanisms underlying the development of diverticulosis versus subsequent diverticulitis and diverticular bleeding are probably quite different. Furthermore, a number of studies, including 2 large prospective cohorts, have observed an inverse association between dietary fiber intake and diverticular complications. In the Health Professionals Follow-up Study of 47,888 men followed over 4 years, the adjusted relative risk was 0.58 (95% CI, 0.41– 0.83) for symptomatic diverticular disease when comparing highest with the lowest quintiles of fiber intake.19 A strikingly similar result was seen in the Oxford cohort of European Prospective Investigation into Cancer and Nutrition (EPIC-Oxford study), a cohort of 47,033 men and women followed for an average of 12 years.20 The adjusted relative risk of hospitalization for diverticular disease was 0.59 (95% CI, 0.46 – 0.78) in individuals in the highest category of fiber intake compared with those with the lowest fiber intake. A potential drawback with these studies is the inability to distinguish between diverticulitis, diverticular bleeding, and symptomatic uncomplicated diverticular disease although patients in the EPIC study were hospitalized or died as a result of diverticular disease and were therefore more likely to have had complicated disease. It is unclear how to translate the findings from Peery et al into dietary recommendations for patients. As noted, evidence from large prospective cohorts suggests that fiber may prevent diverticular complications, and these complications, and not diverticulosis itself, result in the bulk of the health and economic burden of this disease. Although the prevention of diverticulosis would in turn prevent its downstream consequences, this strategy would require knowledge of its absence. Importantly, the beneficial effects of fiber on many other chronic diseases such as cardiovascular disease, obesity, diabetes, and cancer need to be considered because it appears that the amount of fiber required to increase the risk of diverticulosis is below current dietary recommendations. For these reasons, it seems premature to tell patients without divertic-
Editorials, continued ulosis to cut down on the consumption of fiber-containing foods. In patients with diverticulosis, the evidence suggests that a high-fiber diet is beneficial. The important and provocative paper by Peery et al calls into question the long-standing but poorly proven fiber theory of the pathogenesis of diverticulosis. In this study, high, not low, fiber intake was associated with an increased risk of diverticulosis in a dose-dependent fashion and the association was stronger in individuals with more marked disease. These results open the door for new avenues of thought regarding the pathogenesis of and risk factors for this common yet understudied disease. A future study of individuals with detailed data on diet and gastrointestinal symptoms before the diagnosis of diverticulosis, or ideally before its onset, would be welcomed to confirm these findings. Given the other health benefits of dietary fiber, further evidence is needed before altering dietary recommendations in patients without diverticulosis.
LISA L. STRATE Division of Gastroenterology Harborview Medical Center University of Washington Medical School Seattle, Washington References 1. Painter NS, Burkitt DP. Diverticular disease of the colon: a deficiency disease of Western civilization. Br Med J 1971;2:450 – 454. 2. Burkitt DP, Walker AR, Painter NS. Effect of dietary fibre on stools and the transit-times, and its role in the causation of disease. Lancet 1972;2:1408 –1412. 3. Painter NS TS. The intraluminal pressure patterns in diverticulosis of the colon. Gut 1964;5:201–213. 4. Carlson AJ, Hoelzel F. Relation of diet to diverticulosis of the colon in rats. Gastroenterology 1949;12:108 –115. 5. Gear JS, Ware A, Fursdon P, et al. Symptomless diverticular disease and intake of dietary fibre. Lancet 1979;1:511–514. 6. Lin OS, Soon MS, Wu SS, et al. Dietary habits and right-sided colonic diverticulosis. Dis Colon Rectum 2000;43:1412–1418. 7. Song JH, Kim YS, Lee JH, et al. Clinical characteristics of colonic diverticulosis in Korea: a prospective study. Korean J Intern Med 2010;25:140 –146.
8. Brodribb AJ. Treatment of symptomatic diverticular disease with a high-fibre diet. Lancet 1977;1:664 – 666. 9. Ornstein MH, Littlewood ER, Baird IM, et al. Are fibre supplements really necessary in diverticular disease of the colon? Br Med J (Clin Res Ed) 1981;282:1629 –1630. 10. Hodgson WJ. The placebo effect. Is it important in diverticular disease? Am J Gastroenterol 1977;67:157–162. 11. Smits BJ, Whitehead AM, Prescott P. Lactulose in the treatment of symptomatic diverticular disease: a comparative study with highfibre diet. Br J Clin Pract 1990;44:314 –318. 12. Taylor I, Duthie HL. Bran tablets and diverticular disease. Br Med J 1976;1:988 –990. 13. Peery AF, Barrett PR, Park D, et al. A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology 2012;142:266 –272. 14. Simpson J, Scholefield JH, Spiller RC. Origin of symptoms in diverticular disease. Br J Surg 2003;90:899 –908. 15. Jung HK, Choung RS, Locke GR 3rd, et al. Diarrhea-predominant irritable bowel syndrome is associated with diverticular disease: a population-based study. Am J Gastroenterol 2010;105:652– 661. 16. Bianchi M, Festa V, Moretti A, et al. Meta-analysis: long-term therapy with rifaximin in the management of uncomplicated diverticular disease. Aliment Pharmacol Ther 2011;33:902–910. 17. Sikirov BA. Etiology and pathogenesis of diverticulosis coli: a new approach. Med Hypotheses 1988;26:17–20. 18. Manousos ON, Truelove SC, Lumsden K. Transit times of food in patients with diverticulosis or irritable colon syndrome and normal subjects. Br Med J 1967;3:760 –762. 19. Aldoori WH, Giovannucci EL, Rimm EB, et al. A prospective study of diet and the risk of symptomatic diverticular disease in men. Am J Clin Nutr 1994;60:757–764. 20. Crowe FL, Appleby PN, Allen NE, et al. Diet and risk of diverticular disease in Oxford cohort of European Prospective Investigation into Cancer and Nutrition (EPIC): prospective study of British vegetarians and non-vegetarians. BMJ 2011;343:d4131.
Reprint requests Address requests for reprints to: Lisa L. Strate, MD, MPH, Division of Gastroenterology, University of Washington Medical School, Harborview Medical Center, 325 Ninth Avenue, Box 359773, Seattle, Washington 98104. e-mail: [email protected] Conflicts of Interest The authors disclose no conflicts. © 2012 by the AGA Institute 0016-5085/$36.00 doi:10.1053/j.gastro.2011.12.019
Outcomes Among Living Liver Donors See “Estimates of early death, acute liver failure, and long-term mortality among live liver donors,” by Muzaale AD, Dagher NN, Montgomery RA, et al, on page 273.
M
anagement of donor risk is the most important consideration in the decision to perform a living donor liver transplantation (LDLT). Counseling potential donors on operative morbidity and mortality requires a comprehensive understanding of the available data on
outcomes. Ideally, an individual potential living donor should be informed of the potential complications based on an objective analysis of a center’s own results. At present, this ideal has not been obtained. Instead, potential donors and their physicians must rely on outcome data from numerous single-center and a few multicenter studies. Reports from the three largest series from North America found that 28%– 40% of donors developed ⱖ1 complication.1–3 Perhaps the most comprehensive of these studies, the 9-center Adult-to-Adult Living Donor Liver Transplant Cohort Study (A2ALL) noted that most com207