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Dietary Fiber for Disease Prevention

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Mechanisms or Magic on Disease Prevention

As a nutrition graduate student in the mid-1970s, it was my good fortune to work in the field of dietary fiber. Dr. Denis Burkitt had been credited with discovering this new important dietary ingredient, and the race was on to study its important physiological effects. A few trips to the library revealed that dietary fiber was not new. Hippocrates wrote in 430 BC that “wholemeal bread clears out the gut and passes through as excrement,” suggesting that fiber’s role in maintaining bowel regularity had long been recognized. Graham, of graham cracker fame, and Dr. J. H. Kellogg, of cereal fame, also promoted dietary fiber in the early 1900s.

In the United States, from 1920 to 1943 although several reports on the laxative properties of fibers were published by Williams and Olmstead, the importance of dietary fiber in human nutrition was not accepted, and few scientific papers on dietary fiber were published in the 1950s and 1960s.

In South Africa in the late 1940s, Walter began work on the association of dietary fiber with a decreased incidence of certain diseases in rural blacks. Trowell also published articles on the diseases of civilization that were inversely related to intake of dietary fiber. In 1956 Surgeon Captain T. L. Cleave proposed the idea that the diseases of civilization were caused by overconsumption of sugar and a deficiency in dietary fiber intake. These epidemiological associations, popularized by Burkitt in the early 1970s, stimulated interest and research in dietary fiber that have gained momentum throughout the last two decades.

The essence of the fiber hypothesis can be summarized as follows.

1. Diets high in dietary fiber are protective against a wide variety of Westernized diseases;

2. Diets low in dietary fiber may be causative factors in the etiology of Westernized diseases.

Why the peaks of interest in dietary fiber followed by the valleys? Perhaps it is that the field of dietary fiber is a frustrating scientific field in which to work. Few other scientific fields are built around a compound that cannot be defined and therefore cannot be measured. This inability to characterize dietary fiber adequately and standardize it makes the field of dietary fiber challenging. The most accepted definition for dietary fiber is a physiological definition, not a chemical one. Dietary fiber is defined physiologically as “the sum of polysaccharides and lignin not digested by the endogenous secretions of the human gastrointestinal tract.” Dietary fiber may, however, be fermented by intestinal microflora. Such a definition brings up many interesting questions. Is starch resistant to digestion in the upper gastrointestinal tract actually dietary fiber? If so, then does processing of foods, either cooking, extruding, or other techniques, increase the dietary fiber in the food since as a result the starch may be less digestible? Is lactulose, a nondigestible disaccharide, dietary fiber? Does lactose function as dietary fiber in persons who lack adequate lactase activity?

According to the above definition of dietary fiber, resistant starch would be dietary fiber since it is a polysaccharide and is not digested in the upper gastrointestinal tract. Yet, lactulose or lactose would not be dietary fiber since they are not polysaccharides. A better definition for dietary fiber might be “the portion of plant cells that cannot be digested by human alimentary enzymes and therefore cannot be absorbed from human small bowels.” But, then are proteins from the cell wall that are not digested dietary fiber? As you see, defining dietary fiber quickly becomes a tiresome task. The most accepted definitions of dietary fiber, however, are physiological ones, which make fiber analysis problematic.

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COMPONENTS OF DIETARY FIBER Dietary fiber is not a homogeneous compound. It is a mixture of diverse compounds that are either polysaccharides or lignin. Methods to characterize the components of dietary fiber are not universally accepted. Historically, fiber was divided into chemical components, including cellulose, hemicellulose, pectins, gums, mucilages, and lignin. More recently, dietary fiber has been divided into structural polysaccharides (cellulose, hemicellulose), structural nonpolysaccharides (mainly lignin), and nonstructural polysaccharides (gums, mucilages). Currently, the popular trend is to divide dietary fiber into soluble and insoluble fiber, as a method to simplify fiber chemistry for the practitioner (Table 1). Dietary fiber is like a pie that can be cut in either ten or two pieces, depending on the interests of the person doing the cutting.

Part of the problem in describing the components of dietary fiber is deficiencies in fiber methodologies.

Progress in the study of dietary fiber has been slow because of our inability to design and support an “accepted” method for fiber and fiber component analysis. Data on crude fiber seriously underestimate the dietary fiber in human foods, and more recent procedures, such as the neutral detergent fiber procedure, only adequately measure insoluble dietary fiber, not the soluble fraction. The most accepted method for measuring dietary fiber in the United States (the method used in food labeling) is the approved method of the Association of Official Analytic Chemists (AOAC). This gravimetric procedure uses both enzymatic and chemical methods to isolate total dietary fiber. The procedure then isolates the soluble and insoluble fractions of the dietary fiber, although the methods to isolate soluble and insoluble fiber have not been officially approved by the AOAC. Since most fiber methods are gravimetric, they are inherently variable.


Epidemiological research supports the theory that high intakes of dietary fiber are protective against degenerative diseases. Are certain kinds of dietary fiber more protective against diseases? Research on dietary fiber during the past 20 years has shown that different dietary fibers have different physiological effects. Not all fiber is created equal. Insoluble dietary fiber is thought to be mainly a bulking agent, increasing stool weight and decreasing transit time. Soluble dietary fiber is associated with lowered serum cholesterol and improved serum glucose regulation in diabetics. For example, both cellulose and hemicellulose increase stool weight and have little effect on serum cholesterol, while gums and pectins decrease serum cholesterol yet have little effect on stool weight. Thus, it has become popular to simply divide dietary fiber into two fractions, soluble and insoluble, to help classify them according to their physiological effects.

Unfortunately the physiological effects of dietary fiber cannot be so neatly divided. Although it is generally true that soluble fibers such as oat bran lower cholesterol, other fibers such as rice bran, which is virtually devoid of soluble fiber, also have been shown to lower serum cholesterol. Psyllium seed has been shown to lower blood cholesterol and is thought to be highly soluble. On the other hand, many commercial laxatives are made from psyllium seed because it is also extremely effective in laxation, a property usually associated with insoluble fiber. Psyllium seed is a good example of why it is difficult to generalize about the physiological effects of a fiber based on its composition of soluble and insoluble dietary fiber. Currently, it is not possible to predict the physiological response of a particular fiber by knowing the chemical and physical structure of the fiber.


Before the science of dietary fiber can progress, its physiological effects must be more completely understood. If a particular dietary fiber lowers cholesterol, there must a physiological mechanism or series of mechanisms that explain the phenomenon. If we learn more about the mechanisms of the effects of dietary fiber in the body, we should be able to predict the physiological effects of a fiber source. Unfortunately, the current approach is to feed a large dose of a particular fiber to a group of hyper-cholesterolemic patients and look for a response in serum cholesterol. Little research is being done on the mechanisms by which fiber has its important physiological effects.

We can look at the effect of fiber on the gastrointestinal (GI) tract in two ways. First, how does dietary fiber affect the GI tract as it makes its way through the body? Second, what happens to dietary fiber as it passes through the GI tract? If we start with a complex carbohydrate and end with no trace of it in feces, the important changes that have taken place with the dietary fiber should relate to physiological effects

There are many limitations in ways to measure the fate of dietary fiber in the digestive tract of human subjects. We can first measure in and out-how much dietary fiber disappears as it makes its way through the tract? Some soluble dietary fibers such as pectin are completely degraded in the intestinal tract but insoluble fibers such as wheat bran also are degraded, although to a much lesser extent. Anyone who has conducted human feeding studies appreciates the problems with this type of gross” analysis.

Other indirect ways have been used to measure the fate of dietary fiber as it passes through the GI tract. Indirect measures of dietary fiber breakdown include intestinal gas production, such as hydrogen and methane, which can be collected in expired breath samples and easily measured. Our experience with breath gases in assessing fiber fermentation suggests that many other food components affect breath gases, such as resistant starch and unabsorbed sugars,

and it is difficult to estimate the fermentation of fiber by intestinal gas production alone.

Other indicators of fiber fermentation include fecal pH and fecal short chain fatty acids (SCFAs). Measures of wet and dry stool weight and gastrointestinal transit time have been used in fiber studies as indicators of the effect of fiber on the GI tract. From these it appears that the pentose content of the fiber, not its solubility, is the most important factor in increasing stool weight. Fibers known for their laxation ability, namely wheat bran and psyllium, are high in pentose sugars. Soluble fibers such as guar gum and oat bran have minimal effect on stool weight, suggesting that they are extensively fermented, leaving little fiber in feces. Since feces are predominantly water and bacteria, extensive fermentation of fiber may increase stool weight indirectly by increasing microbial mass.


As summarized by Heaton (Table 2), dietary fiber has a wide range of effects in the gastrointestinal tract. Mouth and Stomach. In the mouth, fiber stimulates the flow of saliva primarily by increasing the volume of food in the mouth. When dietary fiber reaches the stomach, it will dilute the contents and perhaps prolong storage. Pectin and guar gum generally increase gastric emptying time, while other fibers have no effect. Viscosity of the fiber source may be the important variable in gastric emptying, although these data are confusing.

Marlett et al. have postulated that dietary fiber could be altered chemically in the stomach. The pH of the stomach can get as low as 2.0, and acid treatment of dietary fiber can increase the soluble fiber fraction of the fiber. In the Marlett research, a modified Theander fiber method including a pepsin treatment increased recovery of soluble fiber, suggesting that the accepted notion that dietary fiber is not affected by stomach secretions needs to be reevaluated.

Small Intestine. Dietary fiber is thought to dilute the contents of the small intestine, and the most viscous dietary fibers may delay absorption of carbohydrates and fats in the small intestine. This is one potential mechanism to explain why viscous fibers (soluble) are usually more effective than insoluble fibers in lowering serum cholesterol and moderating glucose response. Changes in absorption of macronutrients seen with fiber feeding are of little practical significance in this country, but may be significant in countries where food supplies are scarce.

Fiber may affect pancreatic enzyme activity, although data are confusing. In vitro, insoluble fiber reduced the activity of amylase, lipase and typsin while pectin had no effect. It is generally accepted that dietary fiber in practical doses has little effect on mineral absorption in the small intestine. Persons on diets low in minerals may be at risk of mineral deficiencies, and additional fiber should not be recommended unless adequate minerals are consumed.

Fibers also may lower serum cholesterol by binding bile acids. If bile acids are bound to fiber, they may not be reabsorbed in the small intestine but will be lost in feces. Since the body can resynthesize bile acids, it is unlikely that binding of bile acids by certain fibers is a primary mechanism for the effect of fiber on serum cholesterol. Even if soluble fibers could effectively bind bile acids and therefore lower serum cholesterol, there is some concern that such therapy would be unwise. In the colon, bacteria convert primary bile acids into smaller, secondary, bile acids that may increase the risk of colon cancer. Insoluble fibers may dilute the concentration of secondary bile acids in the colon and therefore be protective against colon cancer.

Dietary fiber also affects small intestine morphology and epithelial cell regeneration. The intestinal villi of vegetarians are broad and leaf-shaped while jejunal villi in humans consuming usual American diets are fingerlike and regular. Animal studies have also shown that the level and type of dietary fiber consumed can alter the structure of the small intestine. Large Intestine. Most of the research on dietary fiber is directed to its metabolism in the large intestine. Most (>75%) dietary fiber in an average American diet is apparently digested in the large intestine with carbon dioxide, hydrogen, methane and SCFAs the result. SCFAs include butyrate, propionate and acetate. Propionate and acetate are thought to be metabolized in colonic epithelial cells or peripheral tissue. Butyrate may regulate colonic cell proliferation and serve as an energy source for colonic cells. Propionic acid is transported to the liver, and some research suggests that propionic acid may suppress cholesterol synthesis. This may be another potential explanation for how soluble dietary fiber lowers serum cholesterol. Fecal excretion of SCFAs may not reflect colonic levels, and other methods to quantitate SCFAs in the large intestine have not been well studied. Production of SCFAs will lower pH of the colon, which may be important in the role of fiber in the prevention of gastrointestinal diseases, including colon cancer. Dietary fiber has been shown to inhibit colonic cell proliferation and to influence its morphology, both of which may be related to the protective role of fiber in colon cancer and other large bowel diseases.


In our efforts to simplify a difficult topic, we have divided dietary fiber into two categories: insoluble and soluble fiber. Although some physiological effects of dietary fiber can be explained on the basis of this division, it is now clear that other chemical and physical attributes of dietary fiber need to be considered. The particle size of dietary fiber has important effects on its water-holding capacity and its effects on laxation. Finely ground wheat bran has less effect on stool weight than does coarse bran, suggesting that changes in the physical structure of a fiber source can change physiological effects. Very little is known about the effects of processing of dietary fiber on its physiological results. Some food-processing procedures can increase soluble fiber, which may change the physiological effect of a fiber. Yet, the solubility of a fiber may be altered within the GI tract, making the chemical enrichment of soluble fiber in the laboratory unnecessary.

Our current state of knowledge on the physiological effects of dietary fiber dictates that we must feed a dietary fiber to human subjects before we can claim that the fiber has any desirable attributes. Dietary fibers with little soluble fiber such as rice bran have been found to lower serum cholesterol while soluble fibers such as psyllium lower serum cholesterol, as expected, while also having significant effects on laxation. It is clear that the “solubility” of dietary fiber is not the all-important factor affecting physiological function.

Some of the potential mechanisms for the ability of dietary fiber to lower cholesterol may be related to increased risk of colon cancer. For example, soluble fibers may be important for their role in bile acid binding, yet these additional bound bile acids in the colon may be promoters for colon cancer. Animal studies show that soluble fibers are associated with the highest levels of cell proliferation, a precancerous event. The current interest in dietary fiber has allowed recommendations for fiber supplementation to outdistance the scientific research base. Until we have a better understanding of how fiber works its magic, we should recommend to American consumers only a gradual increase in dietary fiber from a variety of sources.


Anderson JW, Story L, Sieling B, Chen WJ, Petro MS, Story J. Hypercholesterolemic effects of oat-brain or bean intake for hypercholesterolemic men. Am J Clin Nutr 1984;40:1146-55.

Bell LP, Hectorne K, Reynolds RD, Balm TK, Hunninghake DB. Cholesterol-lowering effects of psyllium hydrophilic mucilloid, JAMA 1989;262: 3419-23.

Cleave TL. The neglect of natural principles in current medical practice. I R Nav Med Serv 1956;42:55-7.

Dreher ML. The concept of dietary fiber. In: Handbook of dietary fiber: an applied approach. New York: Marcel Dekker. Inc.. 1987: 1-15.

Dunaif G, Schneeman BO. The effect of dietary fiber on human pancreatic enzyme activity in vitro. Am J Clin Nutr 1981;34:1034-5.

Gordon DT. Functional properties vs physiological action of total dietary fiber. Cereal Foods World 1989;34:517-25.

Heaton KW. Dietary fibre in perspective. Human Nutr Clin Nutr 1980;37C:151-70.

Hegsted M, Windhauser, MM, Lesterand SB, Morris SK. Stabilized rice bran and oat bran lower cholesterol in humans. FASEB J 1990;4:368.

Kritchevsky D. Dietary fiber. Annu Rev Nutr 1988;8:301-28.

Lupton JR, Coder DM, Jacobs L. Long-term effects of fermentable fibers on rat colonic pH and epithelial cell cycle. I Nutr 1988;118:840 5.

Marlett JA, Chesters JG, Longacre ML, Bogdanske JJ. Recovery of soluble dietary fiber is dependent on the method of analysis. Am J Clin Nutr 1989;50:479-85.

McCance RD, Widdowson 0. Old thoughts and new work on breads white and brown. Lancet 1955;2:205-10.

McNamara EA, Levitt MD, Slavin JL. Breath hydrogen and methane: poor indicators of apparent digestion of soy fiber. Am J Clin Nutr 1986; 43:898-902.

Prosky L, Asp N, Schweizer TF, DeVries J, Furda I. Determination of insoluble, soluble, and total dietary fiber in foods and food products: Inter-laboratory study. J Assoc Off Anal Chem 1988; 71:1017-23.

Slavin, JL. Dietary fiber: Classification, chemical analyses, and food sources. J Am Diet Assoc 1987;87:1164-71.


The National Symposium and XIII International Vitamin A Consultative Group (IVACG) Meeting in November 1989 reviewed the evidence available to date on the relationship of vitamin A depletion and deficiency to childhood morbidity and mortality. Results from completed studies as well as preliminary findings of others underway were presented and discussed by experts from several disciplines. The IVACG Steering Committee realized the need for an interim statement summarizing the weight of evidence available because results from several large, randomized masked trials are unlikely to be available for 1 to 2 years. The following statement represents the steering committee’s careful consideration of the available evidence.

* An adequate vitamin A status prevents nutritional blindness and contributes significantly to child health and survival.

* The role of vitamin A in preventing nutritional blindness is well documented. Evidence is accumulating that it also reduces mortality. The mechanism(s) by which it has this effect is unclear.

* The impact of improved vitamin A nutrition will vary with the severity of vitamin A deficiency and the contributions of other ecological factors.

* It is therefore imperative to improve the diet and raise the level of vitamin A nutrition where a current intake is inadequate.

The IVACG Steering Committee hopes that this statement will be useful in the process of formulating country and regional policies and programs to control and combat vitamin A deficiency. The International Vitamin A Consultative Group was established in 1975 to guide international activities aimed at reducing vitamin A deficiency in the world.

Table 1 Soluble and insoluble Fiber Components in Total Dietary Fiber Insoluble Soluble Cellulose Soluble gums (including [beta]-glucan) Lignin Soluble pectins Hemicellulose Soluble hemicellulose Insoluble pectins Polysaccharides (not Pentosans susceptible to enzyme digestion) Table 2 Effects of Dietary Fiber in the Gastrointestinal Tract Site Activity Mouth Stimulates saliva Stomach Dilutes contents, prolongs storage Small intestine Dilutes contents, delays absorption Large intes- Dilutes contents, bacterial substrate, tine traps water, binds cations Stool Softens, enlarges, prevents straining
COPYRIGHT 1990 Lippincott/Williams & Wilkins
COPYRIGHT 2004 Gale Group

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This entry was posted on Monday, October 13th, 2008 at 3:46 pm and is filed under Health Food Articles. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.

5 Responses to “Dietary Fiber for Disease Prevention”

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