Position of the American Dietetic Association: health ...
Position of the American Dietetic Association:
Health Implications of Dietary Fiber
Journal of the American Dietetic Association, Oct 1997 v97 n10 p1157(3)
Judith A. Marlett and Joanne L. Slavin
Abstract: The American Dietetic Assn (ADA) is calling on the public to consume sufficient amounts of dietary fiber from various plant foods. Dietary fiber is mostly the storage and cell wall polysaccharides of plants that human digestive enzymes cannot hydrolyze. It greatly benefits the gastrointestinal tract, and may offer protection against colon cancer. Fiber-rich foods may help prevent breast cancer and may be valuable in prevention of obesity. The ADA proposes to health professionals to help promote consumption of fiber-rich foods.
Dietary fiber has demonstrated benefits for health maintenance, disease prevention, and as a component of medical nutrition therapy. Except in certain therapeutic situations, dietary fiber should be obtained through consumption of foods. In addition to fiber, minimally processed fruits, vegetables, grains, and legumes provide micronutrients that are essential components of healthful diets. Plant foods also contain many other nonnutritive components (eg, xenobiotics, antioxidants, phytoestrogens) that have implications for health.
POSITION STATEMENT
It is the position of The American Dietetic Association (ADA) that the public should consume adequate amounts of dietary fiber from a variety of plant foods.
DIETARY FIBER
Recommended Fiber Intakes Through the Life Cycle
Recommendations for dietary fiber intake for adults generally fall in the range of 20 to 35 g/day or 10 to 13 g dietary fiber per 1,000 kcal (1,2). Nutrition Facts labels use 25 g dietary fiber per day for a 2,000 kcal/day diet or 30 g/day for a 2,500 kcal/day diet as goals for American intake. However, dietary fiber intake continues to be at less-than-recommended levels in the US population, with usual intakes averaging only 14 to 15 g/day (3). Most popular American foods are not high in dietary fiber. Servings of commonly consumed grains, fruits, and vegetables contain only 1 to 3 g dietary fiber (4,5). Legumes and high-fiber cereal products supply more dietary fiber but are not commonly consumed.
Recently, attempts have been made to define recommended dietary fiber intakes for children and adolescents. Although based on limited clinical data, the recommendation for children older than 2 years is to increase dietary fiber intake to an amount equal to or greater than their age plus 5 g/day (7), to achieve intakes of 25 to 35 g/day after age 20 years. To our knowledge, no studies have defined desirable fiber intakes for infants and children younger than 2 years. Until there is more information about the effects of dietary fiber in the very young, a rational approach would be to introduce a variety of fruits, vegetables, and easily digested cereals as solid foods are brought into the diet. Specific recommendations for the elderly have not been published, although a safe recommendation would be to encourage intake of 10 to 13 g dietary fiber per 1,000 kcal. All recommendations need to recognize the importance of adequate fluid intake and caution should be used when recommending fiber to those with gastrointestinal diseases, including constipation.
Benefits of Adequate Fiber Intake
The primary action of fiber in the body is in the gastrointestinal tract, but not all fiber sources have the same physiological effects. Generally, concentrates of water-soluble fibers delay transit through the stomach and small intestine (8). Soluble fibers are rapidly broken down (fermented) by bacteria in the large intestine and do not promote laxation (1). Fibers that are predominantly water insoluble promote laxation and are either slowly or not fermented (1,9). Two notable exceptions to these general guidelines are oats, which contain up to 50% soluble fiber (primarily as 1 [approaches] 3, 1 [approaches] 4 [Beta]-glucans) and psyllium seed husks (10), which also analyze as a soluble fiber. Both of these fiber sources promote laxation and modulate gastric and small intestine physiology.
Some soluble fiber sources slow the appearance of glucose in the blood. For a soluble fiber to be effective, it also must be viscous. Viscosity slows transit of chyme in the upper gastrointestinal tract, resulting in slower absorption rates, lower blood concentrations of nutrients, and altered hormonal responses to these absorbed nutrients (8). Viscosity also appears to be a requirement for fiber to lower blood cholesterol concentrations (11). Most of these effects of soluble fibers were demonstrated using fiber concentrates (8,9). There is no evidence that the soluble fiber in a mixed-food diet would have the same effect on upper gastrointestinal tract physiology.
Stool weight, an important measure of the laxative effect of fiber, increases with fiber intake, although the addition of insoluble fiber sources modulates other measures of large-bowel physiology. Defecation frequency is increased only when there is less than the normal one bowel movement daily. Consuming more food fiber decreases gastrointestinal transit time (the time required for the residue from an ingested meal to be excreted) only when it is longer than about 2 1/2 to 3 days. The concentration of water in stools is not usually affected by larger fiber intakes.
More than 75% of the dietary fiber in an average American's diet is broken down in the large intestine, where carbon dioxide, hydrogen, methane, short-chain fatty acids, butyrate, propionate, and acetate are produced by bacterial fermentation. In some studies short-chain fatty acids have been shown to promote growth and healing of the mucosa (12). Research using isolated human coloncytes suggests that butyrate is a major energy source for the colonic mucosa, while acetate and propionate enter the portal circulation (13,14). In healthy adults, about 60% of the produced short-chain fatty acids is acetate and only 10% to 20% is butyrate (14).
Definition and Sources of Fiber
Dietary fiber is primarily the storage and cell wall polysaccharides of plants that cannot be hydrolyzed by human digestive enzymes (1). Lignin, which is a complex molecule of polyphenylpropane units and present only in small amounts in the human diet, is also included as a component of dietary fiber (1,15). Soluble fiber is that fraction of the total fiber that is suspended in water during analysis (16). Soluble dietary fiber may vary 15% to 50% of the total fiber using different analytic methods (16). Nearly all fiber-containing foods have more insoluble than soluble dietary fiber. About two-thirds to three fourths of the dietary fiber in typical mixed-food diets is water insoluble (1). Most fruits and vegetables contain less than 2 g/serving total fiber and most refined grain products contain less than 1 g/serving (5). Only legumes, whole grains, and concentrated grain products typically have more fiber (5).
Resistant starch (the sum of starch and starch-degradation products not absorbed in the small intestine [17]) contributes to the pool of dietary fiber when the starch is undigested in the small intestine. The amount of resistant starch in a typical Western diet is not known. Legumes appear to be the single most important source of resistant starch, with as much as 35% of legume starch escaping digestion (18). No meaningful tables of the resistant starch content of foods are available, although in vitro measures of this starch fraction that has been defined by its in vivo behavior are being developed (19).
Fiber concentrates are frequently not all dietary fiber. Fiber concentrates such as pectins and gums (eg, gum arabic, carob bean gum, guar gum), wood pulp cellulose, psyllium seed husk, and oat hull fiber are more than 90% fiber (10). In contrast, citrus fiber, pea fiber, corn bran, and soy polysaccharide are 60% to 85% fiber (10). Oat bran is about 15% to 20%; wheat bran, 40% to
50%; barley, 15%; and rice bran, 20% to 30% dietary fiber (10,20).
A variety of low molecular carbohydrates are not digested by human digestive enzymes (sugar alcohols such as sorbitol and mannitol, polydextroses, and fructooligosaccharides). The US Food and Drug Administration (21) states that because these materials do not analyze as dietary fiber in the official Association of Official Analytical Chemists methods they are not to be reported on nutrition labels as dietary fiber, but as "other carbohydrate."
Disease Risk Reduction and Therapeutic Uses of Fiber
Correlation studies that compare colorectal cancer incidence or mortality rates among countries with estimates of national dietary fiber consumption suggest that fiber intake may be protective against colon cancer (22). When results of 13 case-control studies of colorectal cancer rates and dietary practices were pooled, it was concluded that the results provided substantive evidence that intake of fiber-rich foods is inversely related to risks of both colon and rectal cancer (23). It is estimated that the risk of colorectal cancer in the US population could be reduced by about 31% if fiber intake from food sources were increased by an average of about 13 g/day (23). Clinical trials using the incidence of adenomatous polyps as a marker for colon cancer risk have not supported these epidemiologic associations (24), although studies have not measured fiber intake adequately.
Limited epidemiologic evidence has been published on fiber intake and risk of breast cancer in human beings. International comparisons show an inverse correlation between breast cancer death rates and the consumption of fiber-rich foods (25). A meta-analysis of 12 case-control studies of dietary factors and risk of breast cancer revealed that high dietary fiber intake was associated with a reduced breast cancer risk (26). Not all studies, however, including a prospective cohort study (27) find a relationship between dietary fiber intake and breast cancer incidence. Foods high in fiber, namely vegetables and fruits (28) and whole grains (29), have been linked to decreased risk of developing cancer at other sites. Fiber may also protect against prostate cancer (30).
No clear relationship has been demonstrated between treatment for obesity and dietary fiber. However, a diet with adequate amounts of fiber-containing foods is usually less energy dense and its greater bulk has a short-term satiety effect.
A low-fiber diet may increase the risk for diabetes because such diets are usually more energy dense and promote obesity (1). Fiber has a role in the treatment of diabetes because it slows the absorption of glucose from the small intestine. If postprandial blood glucose levels are elevated, incorporating soluble viscous fibers into the diet will minimize this abnormal glucose spike (8).
The role of fiber in the prevention and treatment of cardiovascular disease is related to its effect on blood cholesterol levels. Typically, viscous, soluble fiber sources lower blood cholesterol levels by 5% or more (31). Greater decreases are attainable when initial blood cholesterol concentrations are elevated. A variety of measurements indicate that the major mechanism by which fiber drains cholesterol from the body pool is through the interference of viscous fibers in the absorption of bile acids, not the absorption of cholesterol in the diet (11). Most of the cholesterol in the body is synthesized in the liver, not supplied by the diet. Measuring fetal bile acids does not always detect this decrease in bile acid absorption. Other compounds in fiber sources may also affect sterol balance. For example, the gamma analog of tocotrienol found in oats, barley, and rice bran (11) is a potent inhibitor of endogenous cholesterol biosynthesis and will lower blood cholesterol concentrations (32). Fatal and nonfatal myocardial infarctions have been inversely associated with total fiber retakes m some studies (33).
Dietary fiber has been used to treat constipation and promote laxation for thousands of years. The gastrointestinal tract is remarkably sensitive to dietary fiber. Foods and other sources of insoluble fiber have demonstrated positive effects on laxation. Fiber in wheat bran and oat bran have comparable effects on stool weight. These two brans are more effective at increasing stool weights than the same amounts of fiber provided from fruits and vegetables, mixed-food diets, or purified cellulose (8,9,34).
Long-term animal feeding studies indicate that diverticular disease of the colon is an outgrowth of a lifelong pattern of low fiber intake (35). Although the diverticula remain anatomically intact, a higher fiber diet eliminates exacerbation of diverticulitis. Because they may become trapped in one of the diverticula, whole pieces of fiber (hulls of nuts and corn and seeds such as those of tomato and cucumber) may be excluded from a high-fiber diet to treat diverticulosis. To our knowledge, no controlled studies have been conducted to demonstrate that skins and seeds are harmful (36).
Two types of enteral formulas that contain dietary fiber are currently marketed: blenderized formulas made from whole foods and formulas supplemented with purified fiber sources. Purified fiber sources used in enteral products include soy, oat, pea, hydrolyzed guar gum, and sugar beet fibers. Some formulas use a mixture of fiber sources. In healthy subjects, dietary fiber normalizes bowel function, and success stories exist in which diarrhea in enterally fed patients was reduced using fiber-containing liquid formulas. Perhaps because studying the physiologic effects of dietary fiber in a sick population is extremely difficult, no convincing data have been published to document that fiber-containing enteral formulas prevent diarrhea in tube-fed patients. The results of clinical studies with dietary fiber also have been disappointing (37).
Despite lack of compelling clinical data, dietary fiber is the treatment of choice for many enterally fed patients with many bowel disorders (38). In the enterally nourished population, increased dietary fiber has been recommended for therapy for constipation and diarrhea and as a treatment for diverticular disease. Fiber-containing formulas tend to be more expensive than standard formulas, which makes them a difficult choice without compelling clinical data to support their use.
SUMMARY: ACHIEVING ADEQUATE DIETARY FIBER INTAKE
ADA recommends that health professionals:
• promote food intake patterns consistent with the Food Guide Pyramid (39) that make use of a wide variety of plant foods to achieve adequate fiber intakes in healthy children and adults. Include at least 2 to 3 servings of whole grains as part of the daily 6 to 11 servings of grains (40), 5 servings of fruits and vegetables daily, and legumes at least once or twice a week;
• recognize that diets containing excess bulk may not contain sufficient energy to support normal growth in children;
• recognize that 1 to 2 servings daily of higher fiber foods leg, legumes, whole grains, cereal brans) or concentrated fiber sources may be necessary to achieve adequate intakes in those persons whose energy needs are low relative to body mass, such as the elderly, hospitalized or ill patients, or those in long-term-care facilities;
• consider the use of concentrated sources of dietary fiber (9) to treat chronic constipation when a limited variety of food is consumed or the amount of food consumed is inadequate;
• incorporate new sources of dietary fiber into diet plans for specific diseases only when benefit claims are documented and the overall diet is consistent with the medical nutrition therapy appropriate for the disease;
• recognize that viscous concentrated fiber sources with documented health benefits do have demonstrated blood cholesterol-lowering effects and can be part of lifestyle that includes a heart-healthy diet and exercise;
• use a diet pattern for persons with diabetes mellitus that is moderate in fat and contains a wide variety of fiber-containing foods to lower abnormal elevations in postprandial blood glucose levels and promote body weight normalization;
• Use enteral feedings containing dietary fiber to promote normal enterocyte function, but recognize that clinical benefits may be modest.
References
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4. Slavin JL. Dietary fiber: classification, chemical analyses, and food sources. JAm Diet Assoc. 1987; 87:1164-1171.
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7. Williams CL. Importance of dietary fiber in childhood. J Am. Diet Assoc. 1995;95:1146-1149.
8. Wolever TMS, Jenkins DJA. Effect of dietary fiber and foods on carbohydrate metabolism. In: Spiller GA, ed. CRC Handbook of Dietary Fiber in Human Nutrition. 2nd ed. Boca Raton, Fla: CRC Press; 1993:111-152.
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10. Marlett JA. Comparisons of dietary fiber and selected nutrient compositions of oat and other grain fractions. In: Wood PJ, ed. Oat Bran. St Paul, Minn: American Association of Cereal Chemists;1993:49-82.
11. Mariett JA. Sites and mechanisms for the hypocholesterolemic actions of soluble dietary fiber sources. In: Kritchevsky D, Bonfield C, eds. Dietary Fiber in Health and Disease. New York, NY: Plenum Press; 1997:109-121.
12. Scheppach W, Muller UG, Boxberger F, Dusel G, Richter F, Bartram HP, Christi SU, Dempfle CE, Kasper H. Histological changes in the colonic mucosa following irrigation with short cram fatty acids. Eur J Gastroenterol and Hepatol. 1997;9:163-168.
13. Palacio J, Rolandelli R, Settle R, Rombeau JL. Dietary fiber's physiological effects and potential applications to enteral nutrition. In: Rombeau JL, Caldwell MD, eds. Clinical Nutrition: Enteral and Tube Feeding. 2nd ed. Philadelphia, Pa: WB Saunders; 1990:556-574.
14. Valazquez OC, Lederer HM, Rombeau JL. Butyrate and the colonocyte: implications for neoplasia. Dig Dis Sci. 1996;14:727-739.
15. Marlett JA. Analysis of dietary fiber in human foods. In: Kritchevsky D, Bonfield C, Anderson JW, eds. Dietary Fiber: Chemistry, Physiology and Health Effects. New York, NY: Plenum Press; 1990:31-48.
16. Marlett JA. Soluble dietary fiber workshop. In: Kritchevsky D, Bonfield C, eds. Dietary Fiber in Health and Disease. New York, NY: Plenum Press; 1997:311-313.
17. Asp N-G. Nutritional classification and analysis of food carbohydrates. Am J Clin Nutr. 1994;59(suppl):6798-681S.
18. Marlett JA, Longacre MJ. Comparisons of in vitro and in vivo measures of resistant starch in selected grain products. Cereal Chem. 1996;73:63-68.
19. Asp N-G, van Amelsvoort JMM, Hautvast JGAJ, eds. Proceedings of the Concluding Plenary Meeting of EURESTA: Physiological Implication of the Consumption of Resistant Starch in Man. Wageningen, The Netherlands: EURESTA; 1995:1-204.
20. Saunders RM. The properties of rice bran as a foodstuff. Cereal Foods World. 1990;35:632-636.
21. Food labeling: mandatory status of nutrition labeling and nutrient content revision, format for nutrition label. Federal Register. January 6, 1993;58:2079-2173.
22. Bingham SA. Mechanisms and experimental and epidemiological evidence relating dietary fibre (nonstarch polysaccharides) and starch to protection against large bowel cancer. Proc Nutr Soc. 1990;49:153-171.
23. Howe GR, Benito E, Castelleto R, Cornee J, Esteve J, Gallagher RP, Iscovich JM, Deng-ao J, Kaaks-Kune GA. Dietary intake of fiber and decreased risk of cancers of the colon and rectum: evidence from the combined analysis of 13 case-control studies. J Natl Cancer Inst. 1992;84:1887-1896.
24. McKeowyn-Eyssen GE, Bright-See E, Bruce WR, Jazmaji V. A randomized trial of a low fat high fibre diet in the recurrence of colorectal polyps. Toronto Polyp Prevention Group. J Clin Epidemiol. 1994;47:525-536.
25. Rose DP. Dietary fiber, phytoestrogens, and breast cancer. Nutrition. 1992;8:47-51.
26. Howe GR, Hirohata T, Hislop TG, Iscovich JM, Yuan JM, Katsouyanni K, Lubin F, Marubini E, Modan B, Rohan T. Dietary factors and risk of breast cancer: combined analysis of 12 case-control studies. J Natl Cancer Inst. 1990;82:561-569.
27. Willett WC, Hunter DJ, Stampfer MJ, Colditz G, Manson JE, Spiegelman D, Rosner B, Hennekens CH, Speizer FE. Dietary fat and fiber in relation to risk of breast cancer: An 8-year follow-up. JAMA. 1992;268:2037-2044.
28. Steinmetz KA, Potter JD. Vegetables, fruit, and cancer. 1. Epidemiology. Cancer Causes Control. 1991;2:325-357.
29. Jacobs DR, Slavin J, Marquart L. Whole grain intake and cancer: a review of the literature. Nutr Cancer. 1995;24:221-229.
30. Rohan TE, Howe GR, Burch JD, Jam M. Dietary factors and the risk of prostate cancer: a case-control study in Ontario, Canada. Cancer Causes Control. 1995;6:145-154.
31. Shinnick FL, Mathews R, Ink S. Serum cholesterol reduction by oats and other fiber sources. Cereal Foods World. 1991;36:815-821.
32. Parker RA, Pearce BC, Clark RW, Gordon DA, Wright JJK. Tocotrienols regulate cholesterol production in mammalian cells by post-transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. J Biol Chem. 1993;268:11230-11238.
33. Rimm EB, Ascherio A, Giovannucci E, Spiegelman D, Stampfer MJ, Willet WC. Vegetable, fruit and cereal fiber intake and risk of coronary heart disease among men. JAMA. 1996;275:447-451.
34. Hosig KB, Shinnick FL, Johnson MD, Stow JA, Mariett JA. Comparison of large bowel function and calcium balance during wheat bran and oat bran consumption. Cereal Chem. 1996;73:392-398.
35. Fisker N, Berry CS, Fearn T, Gregory JA, Hardy J. Cereal dietary fiber consumption and diverticular disease: a lifespan study in rats. Am J Clin Nutr. 1985;42:788-804.
36. Nelson JK, Moxness KE, Jensen MD. Gastineau CF. Mayo Clinic Diet Manual. 7th ed. St Louis, Mo: Mosby; 1994:235.
37. Evans MA, Shronts EP. Intestinal fuels: glutamine, short-chain fatty acids, and dietary fiber. J Am Diet Assoc. 1992;92:1239-1246.
38. Scheppach WM, Bartram HP. Experimental evidence for and clinical implications of fiber and artificial/enteral nutrition. Nutrition. 1993;9:399-405.
39. The Food Guide Pyramid. Washington, DC: US Dept of Agriculture;1992. Home and Garden Bulletin No. 252.
40. Schwartz NE. Narrowing the gap: practical strategies for increasing whole-grain consumption. Crit Rev Food Sci Nutr. 1994;34:513-516.
* ADA Position adopted by the House of Delegates on October 18, 1987, and reaffirmed on September 12, 1992, and September 6, 1996. This position will be in effect until December 31, 2001. ADA authorizes republication of the position statement/support paper, in its entirety, provided full and proper credit is given. Requests to use portions of the position must be directed to ADA Headquarters at 800/877-1600, ext 4896, or hod@
* Recognition is given to the following for their contributions:
Authors:
Judith A. Marlett, PhD, RD, and Joanne L. Slavin, PhD, RD
Reviewers:
James W. Anderson, MD; Barbara F. Harland, PhD, RD; David J. A. Jenkins, MD, PhD; Joanne R. Lupton, PhD; Oncology Nutrition dietetic practice group (Barbara L. Eldridge, RD; Karen P. Kulakowski, MA, RD); Public Health Nutrition dietetic practice group (Laura Kruse, MS, RD)
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