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GUMS | Nutritional Role of Guar Gum
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programmed with a time to die by a controlled process called apoptosis. It is probably the balance between the levels of proliferation and apoptosis that determine whether a cancer will or will not develop. Although butyrate has been shown to stimulate cell proliferation of normal colonic cells, it has been shown to stimulate apoptosis in cancer cells in vitro. It may also affect other important stages in carcinogenesis such as the promotion of cell differentiation and inhibition of histone deacetylase, which may promote DNA repair.
Gums as Prebiotics 0030
There has been much recent interest in the beneficial health effects of certain strains of lactic acid bacteria or probiotics believed to have various health benefits. These include reducing the duration of rotavirus diarrhea, reducing eczema in atopic infants, and potentially having protective actions against intestinal diseases, including colitis and cancer (See Microflora of the Intestine: Probiotics). These probiotics are usually bifidobacteria, lactobacilli or streptococci but may include certain strains of E. coli. The survival of these bacteria in the gut can be enhanced by the presence of certain fermentable carbohydrates. These are called ‘prebiotics,’ but to fulfill the definition, carbohydrates must selectively increase the populations of the probiotic organisms. The most accepted prebiotics are fructo-oligosaccharides and resistant starch, but some gums may also increase bacterial populations.
but is not used therapeutically. Other gums such as karaya and xanthan, which are slowly fermented, may increase stool wet weight and fecal SCFA without increasing stool solids. See also: Colon: Cancer of the Colon; Dietary Fiber: Properties and Sources; Energy Value; Microflora of the Intestine: Probiotics; Pectin: Properties and Determination; Food Use; Probiotics
Further Reading Blake DE, Hamblett CJ, Frost PG, Judd PA and Ellis PR (1997) Wheat bran supplemented with depolymerised guar gum, reduces the plasma cholesterol concentration in hypocholesterolemic human subjects. American Journal of Clinical Nutrition 65: 30–42. Bonfield C and Kritchevsky D (1997) Dietary Fiber in Health and Disease. New York: Plenum Press. Brown L, Rosner B, Willet WW and Sacks FM (1999) Cholesterol lowering effects of dietary fiber: a metaanalysis. American Journal of Clinical Nutrition 69: 30–42. Canovale E, Tomassi G and Cummings JH (eds) (1995) Topics in dietary fibre research. European Journal of Clinical Nutrition 49(Supplement 3). Eliasson AC (ed.) (1996) Carbohydrates in Foods, pp. 265– 319. New York: Marcel Dekker.
Nutritional Role of Guar Gum P Rayment* and P R Ellis, King’s College London, London, UK
Calories from Fermentation of Gums 0031
SCFA produced from fermentation can be used by the colonic cells and other body tissues for fuel. It is now recognized that dietary fibers, including gums, contribute energy, but the exact amount depends on the fermentability and any increased fecal nitrogen losses. After absorption, the SCFA have to be acylated before entering the major metabolic pathways, and this also has an energy cost. It is now estimated that, on average, fermentation provides 8.4 kJ (2 kcal) per gram of carbohydrate.
Constipation 0032
If a dietary gum is poorly fermented, it may have sufficient residual water-holding capacity to increase stool output. Ispaghula (psyllium), which has a waterholding capacity of approximately 7 g g1, has been used successfully to treat mild to moderate constipation for many years. Gellan, a bacterially produced gum, has also been shown to be a potent stool bulker
Copyright 2003, Elsevier Science Ltd. All Rights Reserved.
Introduction It has been recognized for many years that guar gum, a galactomannan-rich legume flour, has considerable potential as a therapeutic agent in the dietary management of diabetes and hyperlipidemia. For example, it is now well established that guar gum can reduce the postprandial rise in blood glucose and insulin concentrations in response to glucose drinks and starch-rich meals in both healthy and diabetic subjects. Furthermore, the addition of guar gum to a normal diet can elicit long-term improvements in metabolic control in people with type 1 (insulindependent) and type 2 (non-insulin-dependent) diabetes mellitus. The ease of isolation and purification of guar gum explains why it is frequently used as a *
Now at Unilever Research Colworth, UK.
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‘model’ non-starch polysaccharide in physiological and clinical studies. Also, the fact that it is well characterized with respect to other sources of dietary nonstarch polysaccharides makes it an ideal candidate for clinical use. This article highlights the nutritional and therapeutic role of guar gum, but mainly focuses on its blood glucose- and cholesterol-lowering actions. Also included is a brief discussion of the physicochemical properties of guar gum, including its rheological behavior in model systems and its influence on the properties of human and animal digesta in vivo,
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which has an important, if not crucial, influence on gut function and metabolism.
Extraction and Composition of Guar Gum Guar gum, a type of dietary fiber, is extracted from the seed endosperm of a leguminous plant (Cyamopsis tetragonoloba (L.) Taub.) indigenous to the Indian subcontinent. Figure 1 shows the pods, seeds, and endosperm extract of the guar plant. To recover guar gum from the seed, the endosperm halves (splits)
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Figure 1 (see color plate 81) Pictures of pods, seeds, and endosperm extract of the guar plant (Cyamopsis tetragonoloba (L.) Taub.), a member of the Leguminosae family. (a) Green pods, scale bar ¼ 1.3 cm. (b) Dried pods, scale bar ¼ 1.6 cm. (c) Seeds, scale bar ¼ 1 cm. (d) Endosperm halves (splits), scale bar ¼ 1 cm. (e) Guar gum flour, scale bar ¼ 1 cm. (f) Scanning electron micrograph of guar gum flour, scale bar ¼ 100 mm.
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sources. Table 1 lists the typical composition of a commercially available guar gum flour.
OH OH CH2OH
Potential Adverse Effects of Guar Gum
O
HO
O O OH
O
HO O
HO
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OH O CH2OH
O
Figure 2 Structure of guar galactomannan showing the mannose backbone and galactose side chains.
must be separated from the hull and the cotyledon. The splits are ground to a fine flour and may then be purified by repeated alcohol washings. In this way guar gum is commercially produced as a flour and is frequently used as an additive (E412) in the food industry for its thickening and stabilizing properties. Chemically, guar gum mainly consists of a highmolecular-weight polysaccharide, namely galactomannan, which is based on a mannan (M) backbone with galactose (G) side groups, as shown in Figure 2. The ratio of the two components (G:M) seems to vary slightly depending on the origin of the seed, but the gum is generally considered to contain approximately one galactose unit for every two mannose units. The linkages between the sugar groups cannot be hydrolyzed by human digestive enzymes in the small intestine but are fermented by bacterial enzymes in the large intestine. The products of this fermentation include short-chain fatty acids, mainly acetic, propionic, and butyric acids, which have important nutritional implications, notably in relation to colonic function. The Food Chemicals Codex specifies a standard of not less than 66% of galactomannan in food-grade guar gum in the USA, although generally most samples contain more than 80% (w/w). The other components of guar gum, including fat and protein, which are considered to be impurities, vary between different
In the food industry, guar gum is normally added to foods in concentrations of < 1 g 100 g1 to provide a thickening, binding, or stabilizing function. Since guar gum is derived from a normal food material, it is classified by the Food and Agricultural Organization/World Health Organization as a substance of low toxicity. The safety of guar gum is substantiated by the results of a number of long-term studies in human subjects. In general, adverse effects, observed in some but not all subjects, appear to be associated with gastrointestinal disturbances. These effects, which sometimes appear to diminish with regular consumption of guar gum, include flatulence, gastrointestinal pain or discomfort, nausea, and diarrhea. Some of these side-effects probably result from bacterial fermentation of guar gum in the large intestine. The extent of the problems is generally related to the dose given, with more adverse gastrointestinal effects occurring when guar gum consumption is excessive (*15–30 g day1). It has also been suggested that guar gum may reduce the bioavailability of a number of micronutrients (e.g., vitamins), although there is no evidence to indicate that this is of nutritional significance. There is more concern about the use of macroaggregates of guar gum that have the potential for causing obstruction in the esophagus and gastrointestinal tract. This concern has arisen from reported incidents of esophageal obstruction and rupture in patients ingesting guar granules. There have also been a number of cases of esophageal and small-bowel obstruction in patients ingesting a particular type of guar-containing diet pill. The USA and Australia have banned such products. In the European Community (EC), food additive legislation prohibits the use of guar gum and other gums for the production of ‘dehydrated foodstuffs that will rehydrate on ingestion.’ However, the selling of guar products as medicine under license and administered to patients under medical supervision is permitted under EC legislation.
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Table 1 Chemical composition of a commercially available guar gum flour Component
Concentration (g 100 g1)
Galactomannan Protein Crude fiber Ash (total minerals) Fat (petroleum ether extractables) Moisture Total impuritiesa
73.0–86.7 3.0–6.0 1.0–4.0 0.8–2.0 0.5–1.0 8.0–14.0 13.3–27.0
a
Calculated as total nongalactomannan components.
Physicochemical Properties of Guar Gum Solution Properties
The ability of the galactomannan component of guar gum to hydrate and increase the viscosity, or thickness, of the intestinal contents is an important determinant of its physiological effects. The majority of polysaccharides used in nutritional studies exist in solution as ‘random coils’ and the number and
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0.1% 0.2% 0.4% 0.6% 0.8% 1.0% 1.5% 2.0% 2.5%
Viscosity (Pa.s)
10 1 0.1
6 5 4 3 2
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Figure 3 Shear rate and concentration dependence of viscosity for guar galactomannan solutions. Data taken from Rayment P (1996) PhD thesis, University of London.
molecular size of the polymer chains are critical determinants of viscosity and thus physiological activity. The high levels of viscosity associated with watersoluble polysaccharides originate predominantly by interpenetration of individual polymer chains to form entangled networks. At low guar gum concentrations, the individual polymer coils occupy a separate domain within the solution with little or no interpenetration. These solutions are described as Newtonian because their viscosity is independent of the rate of stirring or mixing (i.e., related to shear rate). At higher concentrations, where the polymer coils begin to overlap, the system becomes nonNewtonian and viscosity then depends on the shear rate. The more common type of non-Newtonian flow in food systems is shear-thinning (or pseudoplastic) behavior, where viscosity decreases with increased mixing. Figure 3 shows the effect of shear rate and concentration on the viscosity of guar gum solutions. The viscosity or flow properties of guar gum can be determined by using various rheological techniques. Rheology (from the Greek word rheos, meaning stream) is a branch of physical science concerned with the study of the flow and deformation of materials under externally imposed forces. However, to predict the rheological behavior of guar gum in the human intestine, several factors require consideration. These factors include dependence on the mode of administration, the size of the dose and the physicochemical characteristics of the sample used as well as the physical state of the galactomannan in the gut lumen.
Hydration Kinetics of Guar Gum 0009
The realization that viscous polysaccharides can be used for therapeutic benefit has led to the
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Ultimate viscosity
Figure 4 Hydration rate profiles of guar gum samples presented as viscosity (Pa s) versus time. Experimental points are mean values from measurements on 4 replicate solutions of native guar gum flours M150 (—&—) and RG30 (- -d- -), pharmaceutical granule preparations Guarina (. . .!. . .), Guarem (—h—) and Lejguar (—s—), and Glucotard minitablets (—!—). The ‘ultimate viscosity’ is the measurement of viscosity taken after 24 hours of hydration following homogenisation of the guar solution with an ultra-turrax mixer. The final viscosity is taken only when a consistent maximum reading is recorded on the viscometer (usually after homogenising for 4–6 min). Data taken from Ellis PR & Morris ER (1991) Importance of the rate of hydration of pharmaceutical preparations of guar gum; a new in vitro monitoring method. Diabetic Medicine 8, 378–381.
development of various pharmaceutical preparations containing guar gum. These include capsules or macroaggregates of guar gum, such as granules and minitablets, which have been designed to hydrate slowly in the mouth to improve palatability. However, their beneficial effects have been reported to be extremely variable, most probably due to their lack of hydration in the stomach and small intestine. Consequently, the hydration rate of guar gum in the gut lumen is a critical factor. Figure 4 compares the hydration rate profiles of a range of commercially produced samples of guar gum. These samples were hydrated in water and viscosity was measured over a 5-h period. Unsurprisingly, the marked differences observed are mainly attributed to the physical nature of the guar gum preparations. Thus, samples with a smaller particle size (flours < 150 mm) hydrate much more quickly than those with a larger particle size (> 1 mm), e.g., Glucotard minitablets. The results of many clinical trials have shown that the latter types are often physiologically ineffective. Some research workers have also reported that the clinical efficacy of guar gum is improved when it is incorporated directly into a food rather than when taken as a pharmaceutical premeal supplement. Thus, a key factor in optimizing the glucose-lowering action
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of guar gum is to insure that the polymer is in intimate contact with the starch, the main source of dietary glucose.
Nutritional and Physiological Effects of Guar Gum 0011
Many research groups have reported the efficacy of guar gum in attenuating the postprandial rise in blood glucose and insulin concentrations in healthy and diabetic subjects (Figure 5). One reasonable explanation of these postprandial effects is that guar gum reduces the rate (and perhaps the extent) of digestion and absorption of available carbohydrate in the gastrointestinal tract. (Here available carbohydrate is defined as carbohydrate that is digested by a-amylase in the upper gastrointestinal tract and absorbed into the portal blood (mostly as glucose); this includes
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starch, dextrins and simple sugars (e.g., sucrose, lactose).) There are however problems with obtaining quantitative estimates of glucose absorption in humans; for example, access to the hepatic portal vein is very difficult. Nevertheless, studies in pigs, a useful animal model for studies on dietary polysaccharides, have provided the first direct evidence that guar gum decreases the rate of glucose absorption. In these types of experiment, glucose concentrations were measured simultaneously in the hepatic portal vein and peripheral blood (via the mesenteric artery) and the flow rate of the portal blood was measured also. Significant reductions in glucose absorption over 4 h were observed in the experimental animals given guar gum doses equivalent to those consumed by humans in clinical studies. In the same studies, insulin secretion was significantly decreased over the same period in response to the guar diet. This suggests that the attenuation in the plasma insulin levels seen in humans is attributed to a reduction in insulin secretion from the pancreatic islet b-cells in response to a lowered rate of glucose absorption. Also, a number of human studies have shown that guar gum decreases the postprandial rise in the insulinotropic hormones, plasma gastric-inhibitory polypeptide and glucagon-like peptide-1, which may partly explain the insulin-lowering action of guar gum. Another interpretation of data showing decreases in the peripheral blood insulin concentrations is that there has been an increase in hepatic extraction of insulin, a normal process by which insulin is removed from the blood circulation. Studies carried out to substantiate this have been largely contradictory, however. In relation to long-term studies of insulin action in experimental animals and humans, it has been reported that guar gum increases (improves) insulin sensitivity. A reduction in sensitivity to insulin (i.e., ‘insulin resistance’) is seen as a decrease in the response of tissues to insulin stimulation and is considered to be an important risk factor for both coronary heart disease (CHD) and type 2 diabetes.
Figure 5 Postprandial blood glucose and insulin concentrations of patients with type 2 (noninsulin-dependent) diabetes mellitus in response to control and test breakfast meals of bread and marmalade (total available carbohydrate, mainly starch and sugars, was 106 g). The test contained 16 g of guar gum (in the bread) and 10 g of pectin (in the marmalade). *Statistically significant differences between control and test meals at individual time points. Figure redrawn from data published by Jenkins DJA, Leeds AR, Gassull MA et al. (1976) Unabsorbable carbohydrates and diabetes: decreased post-prandial hyperglycaemia. Lancet 2: 172–174.
Mechanism of Action of Guar Gum There is little doubt that the consumption of guar gum, whether mixed in a drink or solid food, can significantly modify digesta properties at all sites of the gastrointestinal tract. One important feature is the capacity of guar gum at relatively low concentrations to form a highly viscous network in solution. As mentioned previously, the behavior of guar gum in a food material is highly complex. In such systems there is unlikely to be one mechanism to explain fully the effects of guar gum in the human gut. A number of physicochemical mechanisms may be
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involved, which are largely dependent on the type and form of the guar gum ingested. Much of the literature indicates that guar gum decreases the rate of glucose absorption into the hepatic portal vein by inhibiting the processes associated with digestion and absorption of available carbohydrates. These processes include gastric function, intestinal transit and mixing, a-amylase–starch interactions, and the movement of products of starch hydrolysis to the gut mucosa. A number of experiments in humans and animals have shown that guar gum reduces the rate of gastric emptying of a meal. However, there are also studies that have shown no effect or even sometimes an acceleration in gastric emptying after the ingestion of guar gum. These contradictory results probably arise from differences in the type of guar gum used, the way in which it was administered, the proportion of solids and liquids in the meals, and the techniques used to measure gastric emptying. In general, it is considered that guar gum may reduce the rate of gastric emptying under some conditions, but this action is unlikely to be the only mechanism. Other groups have shown guar gum has additional effects on gastric function. In studies in dogs, guar gum was reported to impair gastric trituration and sieving by increasing the viscosity of the stomach contents. It was shown that there was a significant increase in the proportion of larger particles of food entering the small intestine when guar gum was incorporated into the diets. Possible explanations for these findings include suggestions that the increased viscosity stabilizes the suspension of larger food particles, which are likely therefore to escape maceration in the antrum of the stomach, and/or that the guar gum alters the contractile pattern of the terminal antrum, thus impairing the ability of the stomach to retain large particles. There is evidence from human and animal studies that guar gum delays the transit of digesta in the small intestine. The postprandial pattern of gut motility also seems to be influenced by guar gum and other types of dietary fiber. Thus, whereas wheat bran and cellulose-supplemented diets were reported to produce prolonged bursts of intestinal contractions, guar consumption caused continuous contractions with a 50% reduction in amplitude compared with the other types of fiber. The effect of guar gum on the mixing behavior of digesta at different sites of the gastrointestinal tract has yet to be investigated, but it is likely to be extremely complex. It has been suggested that an increase in the viscosity of digesta will produce laminar or ‘streamline’ flow, rather than turbulent or disorderly flow, which is characteristic of less viscous fluids and facilitates efficient mixing of
digesta in the gut. An inhibition of the digesta flow rate will inhibit physical mixing of nutrients and enzymes (e.g., pancreatic amylase). Also, laminar flow behavior would almost certainly have an effect on the rate at which nutrients are exposed to the epithelial surface and then absorbed into the hepatic portal vein. However, an explanation of the precise mechanism by which guar gum modifies gut function is still elusive, despite the plethora of clinical and physiological studies that have been undertaken. The problem is that researchers understand little about the behavior of guar gum in the human gastrointestinal tract. Digesta is an extremely complex heterogeneous material and the effects of guar gum on this system have not been studied in great detail. Much of the work that has been done has involved investigating digesta in the stomach and small intestine, since it is assumed that guar gum has negligible effects on viscosity in the large intestine due to depolymerization by bacterial fermentation. There are a number of problems associated with measuring digesta rheology in vivo. In human subjects, there are obvious practical difficulties in gaining access to the sites of interest in the gut. Notwithstanding the initial problems involved with sampling intestinal contents, particularly in humans, the rheological properties of digesta will depend on the precise location of the sampling site. Thus, digesta is subjected to dilution by gastric secretions and then concentration by absorption of water, by both the intestine and the guar gum, at it passes further along the intestinal tract. Also the samples collected need to be tested quickly to prevent drying or dissolution of particulate materials. In the case of animal experiments, this requires access to rheometers or other measuring devices in the animal house. Many factors complicate the interpretation of the rheological behavior of digesta containing guar gum. These include a lack of information on the hydration kinetics of guar gum in vivo and the contribution of undissolved food particulates to viscosity. Therefore, to enhance our understanding of the physical properties of digesta it is important to study model systems of entangled networks filled with particulates, although in vivo other factors such as gastrointestinal motility and fluid secretion/absorption also play a crucial role. In recent years, the rheological properties of guar gum solutions with increasing particulate concentrations have been investigated. The particulates studies included materials that were essentially spherical and rod-like in shape (i.e., starch granules and microcrystalline cellulose, respectively). The effect of particulates or ‘fillers’ is primarily to increase the viscosity above that of the pure guar gum system, as shown in Figure 6. The initial Newtonian flow
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Figure 6 Effect of increasing rice starch concentration on the viscosity–shear rate flow curve of a 1% guar galactomannan solution. Data taken from Rayment P (1996) PhD thesis, University of London.
properties of the pure system at low shear rates become more rate-dependent on increasing particulate concentration – the so-called power-law behavior. The flow data have been fitted to mathematical equations, which incorporate parameters that describe the shear-thinning nature of guar gum and the increasing solid-like behavior of these filled systems. The model also seems to work well with a more heterogeneous food material containing wheat starch. The extrapolation of such models to real food systems and even digesta is fraught with difficulty, however. The inherent problems with studying digesta have been mentioned already, but to make any real progress in this area, at the very least, information is needed on the fractional volume of particulate material at different sites of the gastrointestinal tract. These data could be obtained by recovering ileal effluent from ileostomy patients and by the recovery of digesta from cannulated animals at appropriate sites of the gut. Further work on the development of more heterogeneous models and techniques to study such systems is crucial if we are to increase our understanding of how guar behaves in the gut environment. The mechanism by which guar gum reduces plasma cholesterol is still uncertain but, again, the discussion about the effects of guar gum on digesta viscosity and glucose absorption is important here also. The level of viscosity generated in the gut has been suggested as an important determinant of the hypocholesterolemic effect of guar gum in animal studies. The ingestion
of guar gum appears to enhance fecal bile acid and neutral sterol excretion, reduce the rate of digestion and absorption of lipids, and inhibit synthesis of cholesterol. In vitro, guar gum has been shown to reduce lipid emulsification and the rate of lipolysis of emulsified triacylglycerols, although these effects have not been substantiated in vivo. Also, guar gum has been shown to inhibit both the rate of diffusion of cholesterol mixed micelles and hepatic cholesterol synthesis; the latter has been attributed to propionic acid, one of the products of guar fermentation in the large intestine. However, the inconsistency between in vivo and in vitro studies prevents any conclusive statements being made about the precise mode of action of guar gum.
Dietary Management of Disease Although guar gum has frequently been used in clinical trials, interpretation of the results can be problematic. There are problems resulting from variable study design, lack of adequate controls, and heterogeneity of subject groups. Furthermore, many nutritional studies reporting the therapeutic effects of guar gum provide very limited information about the type and physicochemical properties of the sample tested, e.g., molecular weight and particle size. Moreover, sometimes it is not even known whether the guar was administered as a pre-meal supplement or incorporated directly into the subjects’ meal. Despite these problems, there is sufficient evidence to show that guar gum can be used effectively in the treatment of diabetes and hyperlipidemia, although its role in weight control management has yet to be defined.
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Diabetes Mellitus and Hyperlipidemia The plasma cholesterol-lowering properties of guar gum have been known since the 1960s. Most of the numerous clinical trials published since then have shown reductions in plasma concentrations of cholesterol, mainly the low-density lipoprotein (LDL) fraction, and occasionally triacylglycerols, in both healthy and hyperlipidemic individuals, in some studies for periods of up to 1–2 years. Similar results have been reported in people with diabetes, who are also likely to benefit from any improvements in lipid metabolism given their increased risk for CHD. Currently, although some pharmaceutical preparations are available in the UK, for the management of diabetes, no such products are available for the treatment of hyperlipidemia. In addition to evidence showing the blood glucose-lowering effect of guar gum in response to a starchy meal, long-term improvements have been demonstrated in patients with
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type 1 and type 2 diabetes. In one study of a group of type 2 diabetic patients, a 7-g daily dose of guar gum, which had been incorporated into wheat bread, improved glycemic control (as seen by a significant reduction in glycated hemoglobin) and lowered plasma total and LDL-cholesterol levels (Table 2). As discussed previously, some of the pharmaceutical preparations of guar gum, usually taken as a premeal drink, have been shown to be clinically ineffective due to impaired hydration. Moreover, when guar gum flour is incorporated directly into a meal, the clinically effective dose seems to be significantly lower than that recommended for the pharmaceutical preparations. This has led to the development of a number of everyday foods enriched with guar gum, such as bread, pasta, biscuits, and breakfast cereals. The recommended dose for pharmaceutical preparations of guar gum in diabetes therapy is usually 5 g with each meal (i.e., 15 g day1). However, it is not known what the precise dose and molecular weight of guar gum should be used in the diet to optimize clinical benefits. A lower and upper daily dose range of 6–15 g of native guar gum has been suggested for use in diabetes therapy. This has been suggested on the basis that doses of guar gum above 15 g day1
may cause side-effects, such as flatulence, and there is a lack of reliable long-term studies at doses of less than 6 g day1. The average molecular weights of guar galactomannan samples used in nutritional studies are in the range of 2.0–3.0 million. However, more recent studies have shown therapeutic benefits with samples of lower molecular weight (0.5–1 million), produced commercially by partial depolymerization. For example, one such product of approximately 1 million molecular weight has been used to lower plasma cholesterol levels in hypercholesterolemic human subjects (Table 3). Further work is required to define the lowest molecular weight and optimum dose that can be used without a loss in clinical efficacy. Such knowledge would have a number of advantages for any future product development, since low-molecular-weight grades are easier to incorporate into foods and are more palatable.
Obesity Obesity is associated with an increased risk of diabetes, insulin resistance, CHD, and hypertension. Most short-term studies (often single-meal tests) have shown that guar gum reduces feelings of hunger
Table 2 Mean values (+ SEM) of fasting plasma glucose, glycated hemoglobin (HbAlc), and plasma lipid concentrations in 16 patients with type 2 (noninsulin-dependent) diabetes after consuming control wheat bread and bread containing guar gum flour for two 6-week periods, respectively. Control and guar bread were taken by each patient in randomized order Controlperiod
1
Fasting glucose (mmol l ) HbA1c (%) Total cholesterol (mmol l1) LDL-cholesterol (mmol l1) HDL-cholesterol (mmol l1) Triacylglycerols (mmol l1)
Guar bread period
Start (0 weeks)
End (6 weeks)
Start (0 weeks)
End (6 weeks)
9.7 + 0.8 11.3 + 0.8 5.7 + 0.3 3.8 + 0.3 1.2 + 0.1 1.7 + 0.3
9.4 + 0.7 11.2 + 0.8 5.8 + 0.3 3.9 + 0.2 1.2 + 0.1 1.7 + 0.3
9.7 + 1.0 11.5 + 0.8 5.9 + 0.3 3.9 + 0.2 1.2 + 0.1 1.8 + 0.3
9.1 + 0.8 10.7a + 0.8 5.4b + 0.2 3.5c + 0.2 1.2 + 0.1 1.6 + 0.2
a,b,c Values after 6 weeks significantly different from control at P < 0.05, P < 0.02 and P < 0.01, respectively. LDL, low-density lipoprotein; HDL, high-density lipoprotein. Data taken from Peterson DB, Ellis PR, Baylis JM et al. (1987) Low dose guar in a novel food product: improved metabolic control in non-insulindependent diabetes. Diabetic Medicine 4: 111–115.
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Table 3 Mean values (+ SEM) of plasma lipid concentrations in 11 moderately hypercholesterolemic humans after consuming control wheat bread and bread containing depolymerized guar gum for two 3-week periods, respectively. Control and guar bread were taken by each patient in randomized order Controlperiod
Total cholesterol (mmol l1) LDL-cholesterol (mmol l1) HDL-cholesterol (mmol l1) Triacylglycerols (mmol l1) a
Guar bread period
Start (0 weeks)
End (3 weeks)
Start (0 weeks)
End (3 weeks)
6.37 + 0.21 4.18 + 0.15 1.26 + 0.05 1.84 + 0.25
6.53 + 0.16 4.31 + 0.14 1.31 + 0.06 1.86 + 0.32
6.52 + 0.17 4.28 + 0.19 1.33 + 0.05 1.96 + 0.27
5.89a + 0.8 3.81a + 0.12 1.23 + 0.05 1.85 + 0.25
Values after 3 weeks significantly different from control and baseline (start) values at P < 0.001. LDL, low-density lipoprotein; HDL, high-density lipoprotein. Data taken from Blake DE, Hamblett CJ, Frost PG et al. (1997) Wheat bread supplemented with depolymerised guar gum reduces plasma cholesterol concentration in hypercholesterolaemic human subjects. American Journal of Clinical Nutrition 65: 107–113.
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and appetite and increases feelings of satiety and satiation in all subjects, whether they be normalweight, overweight, or obese. However, there are problems in designing experiments to investigate feeding behavior, since it is very difficult to make the control food (placebo) look and taste like the test food. One study showed that breads containing high concentrations of guar gum were significantly less palatable than the control breads and this may explain why the subjects were less hungry after consuming the guar-containing bread meal. The energy value of the control and test meals should also be identical in such experiments. Despite the positive effects of guar gum in the short term, many of the long-term intervention studies are contradictory and suggest that a therapeutic role for guar gum in weight control management has yet to be established.
Conclusions and Final Comments 0024
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There is now overwhelming evidence to indicate that guar gum has therapeutic benefits for a range of metabolic disorders. At doses of guar gum that are likely to be consumed for therapeutic purposes, there is little evidence that it adversely affects human health. On the contrary, the cholesterol-lowering property of guar gum is of benefit to those who are at an increased risk of CHD, including people with hyperlipidemia and diabetes. Furthermore, the use of guar gum in decreasing postprandial glycemia and insulinemia and in improving long-term glycemic control in diabetic patients is now well established. Any improvement in glycemic control is likely to reduce the risk of microvascular complications (e.g., nephropathy), which are common in people with diabetes, and develop over a number of years. Recent epidemiological studies have also indicated that diets comprising low-glycemic-index foods may have a protective effect in the development of type 2 diabetes. Guar-containing foods could play an important role in such diets and should be tested in the future for their possible prophylactic benefits. In view of possible beneficial effects of guar gum on insulin resistance, which in itself is a risk factor for both CHD and type 2 diabetes, the role of guar foods needs to be evaluated here also. The effects of guar gum on weight reduction in the long term have yet to be demonstrated, although its use in maintaining weight in weight-reduced subjects merits further study. Obese individuals are likely to benefit however from the consumption of guar gum in terms of improvements in glycemic control, insulin sensitivity, and lipid metabolism. To assist in the development of new low-glycemicindex foods using guar gum as a major ingredient, it
would be advantageous to have a detailed understanding of its behavior in the gut environment. Fundamental information about the way in which guar galactomannan influences the rheological behavior of digesta, through its effects in solution, as an entangled network, or on the swelling of food particles, is of paramount importance. This would need to be closely linked to the effects of galactomannan on nutrient digestion and absorption, including, for example, starch and lipids. The initial attempts to produce palatable guar foods for the management of diabetes and hyperlipidemia were disappointing. However, the technological difficulties were exacerbated by the perceived need to use high doses of guar gum (15–30 g day1), since the results of early clinical trials suggested that such doses were needed to elicit metabolic benefits. More recent studies have shown that much lower doses (6– 12 g day1) and partially depolymerized guar gum are not only clinically effective, but have significantly less detrimental effects on sensory qualities of food. From a food technology perspective, it is now possible to produce guar-enriched foods that are both clinically effective and palatable. See also: Carbohydrates: Classification and Properties; Cholesterol: Factors Determining Blood Cholesterol Levels; Coronary Heart Disease: Prevention; Diabetes Mellitus: Treatment and Management; Dietary Fiber: Properties and Sources; Determination; Physiological Effects; Effects of Fiber on Absorption; Glucose: Maintenance of Blood Glucose Level; Glucose Tolerance and the Glycemic (Glycaemic) Index; Gums: Properties of Individual Gums; Food Uses; Dietary Importance
Further Reading Edwards CA and Read NW (1990) Fibre and small intestinal function. In: Leeds AR (ed.) Dietary Fibre Perspectives, vol. 2, pp. 52–75. London: John Libbey. Ellis PR (1999) The effect of fibre on diabetes. In: Hill M (ed.) The Right Fibre for the Right Disease, pp. 33–42. London: Royal Society of Medicine Press. Ellis PR, Rayment P and Wang Q (1996) A physicochemical perspective of plant polysaccharides in relation to glucose absorption, insulin secretion and the enteroinsular axis. Proceedings of Nutrition Society 55: 881–898. Ellis PR, Wang Q, Rayment P, Ren Y and Ross-Murphy SB (2001) Guar gum: agricultural and botanical aspects, physicochemical and nutritional properties, and its use in the development of functional foods. In: Cho SS and Dreher M (eds) Handbook of Dietary Fiber, pp. 613–657. New York: Marcel Dekker. Flourie B (1992) The influence of dietary fibre on carbohydrate digestion and absorption. In: Schweizer TF and Edwards CA (eds) Dietary Fibre – A Component
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GUMS/Nutritional Role of Guar Gum 3021 of Food. Nutritional Function in Health and Disease, pp. 295–332. London: Springer-Verlag. Gallaher DD and Hassel CA (1995) The role of viscosity in the cholesterol-lowering effect of dietary fiber. In: Kritchevsky D and Bonfield C (eds) Dietary Fiber, Health and Disease, pp. 106–114. St Paul, USA: Eagan Press. Leeds AR (1999) The effect of fibre on coronary heart disease and cholesterol. In: Hill M (ed.) The Right Fibre for the Right Disease, pp. 33–42. London: Royal Society of Medicine Press. Low AG (1990) Nutritional regulation of gastric secretion, digestion and emptying. Nutrition Research Reviews 3: 229–252. Maier H, Anderson M, Karl C, Magnuson K and Whistler RL (1993) Guar, locust bean, tara and fenugreek gums. In: Whistler RN and BeMiller JN (eds) Industrial Gums: Polysaccharides and their Derivatives, 3rd edn, pp. 181–226. London: Academic Press. Morgan LM (1992) Insulin secretion and the entero-insular axis. In: Flatt PR (ed.) Nutrient Regulation of Insulin Secretion, pp. 1–22. London: Portland Press.
Gut Hormones
Read NW and Eastwood M (1992) Gastro-intestinal physiology and function. In: Schweizer TF and Edwards CA (eds) Dietary Fibre – A Component of Food. Nutritional Function in Health and Disease, pp. 103–117. London: Springer-Verlag. Reid JSV and Edwards ME (1995) Galactomannans and other cell wall storage polysaccharides in seeds. In: Stephen AM (ed.) Food Polysaccharides and their Applications, pp. 155–186. New York: Marcel Dekker. Ross-Murphy SB (1994) Rheological methods. In: RossMurphy SB (ed.) Physical Techniques for the Study of Food Biopolymers, pp. 343–392. London: Blackie Academic & Professional. Todd PA, Benfield P and Goa KL (1990) Guar gum: a review of its pharmacological properties, and use as a dietary adjunct in hypercholesterolaemia. Drugs 39: 917–928. Truswell AS and Beynen AC (1992) Dietary fibre and plasma lipids: potential for prevention and treatment of hyperlipidaemias. In: Schweizer TF and Edwards CA (eds) Dietary Fibre – A Component of Food. Nutritional Function in Health and Disease, pp. 295–332. London: Springer-Verlag.
See Hormones: Adrenal Hormones; Thyroid Hormones; Gut Hormones; Pancreatic Hormones; Pituitary Hormones; Steroid Hormones
programmed with a time to die by a controlled process called apoptosis. It is probably the balance between the levels of proliferation and apoptosis that determine whether a cancer will or will not develop. Although butyrate has been shown to stimulate cell proliferation of normal colonic cells, it has been shown to stimulate apoptosis in cancer cells in vitro. It may also affect other important stages in carcinogenesis such as the promotion of cell differentiation and inhibition of histone deacetylase, which may promote DNA repair.
Gums as Prebiotics 0030
There has been much recent interest in the beneficial health effects of certain strains of lactic acid bacteria or probiotics believed to have various health benefits. These include reducing the duration of rotavirus diarrhea, reducing eczema in atopic infants, and potentially having protective actions against intestinal diseases, including colitis and cancer (See Microflora of the Intestine: Probiotics). These probiotics are usually bifidobacteria, lactobacilli or streptococci but may include certain strains of E. coli. The survival of these bacteria in the gut can be enhanced by the presence of certain fermentable carbohydrates. These are called ‘prebiotics,’ but to fulfill the definition, carbohydrates must selectively increase the populations of the probiotic organisms. The most accepted prebiotics are fructo-oligosaccharides and resistant starch, but some gums may also increase bacterial populations.
but is not used therapeutically. Other gums such as karaya and xanthan, which are slowly fermented, may increase stool wet weight and fecal SCFA without increasing stool solids. See also: Colon: Cancer of the Colon; Dietary Fiber: Properties and Sources; Energy Value; Microflora of the Intestine: Probiotics; Pectin: Properties and Determination; Food Use; Probiotics
Further Reading Blake DE, Hamblett CJ, Frost PG, Judd PA and Ellis PR (1997) Wheat bran supplemented with depolymerised guar gum, reduces the plasma cholesterol concentration in hypocholesterolemic human subjects. American Journal of Clinical Nutrition 65: 30–42. Bonfield C and Kritchevsky D (1997) Dietary Fiber in Health and Disease. New York: Plenum Press. Brown L, Rosner B, Willet WW and Sacks FM (1999) Cholesterol lowering effects of dietary fiber: a metaanalysis. American Journal of Clinical Nutrition 69: 30–42. Canovale E, Tomassi G and Cummings JH (eds) (1995) Topics in dietary fibre research. European Journal of Clinical Nutrition 49(Supplement 3). Eliasson AC (ed.) (1996) Carbohydrates in Foods, pp. 265– 319. New York: Marcel Dekker.
Nutritional Role of Guar Gum P Rayment* and P R Ellis, King’s College London, London, UK
Calories from Fermentation of Gums 0031
SCFA produced from fermentation can be used by the colonic cells and other body tissues for fuel. It is now recognized that dietary fibers, including gums, contribute energy, but the exact amount depends on the fermentability and any increased fecal nitrogen losses. After absorption, the SCFA have to be acylated before entering the major metabolic pathways, and this also has an energy cost. It is now estimated that, on average, fermentation provides 8.4 kJ (2 kcal) per gram of carbohydrate.
Constipation 0032
If a dietary gum is poorly fermented, it may have sufficient residual water-holding capacity to increase stool output. Ispaghula (psyllium), which has a waterholding capacity of approximately 7 g g1, has been used successfully to treat mild to moderate constipation for many years. Gellan, a bacterially produced gum, has also been shown to be a potent stool bulker
Copyright 2003, Elsevier Science Ltd. All Rights Reserved.
Introduction It has been recognized for many years that guar gum, a galactomannan-rich legume flour, has considerable potential as a therapeutic agent in the dietary management of diabetes and hyperlipidemia. For example, it is now well established that guar gum can reduce the postprandial rise in blood glucose and insulin concentrations in response to glucose drinks and starch-rich meals in both healthy and diabetic subjects. Furthermore, the addition of guar gum to a normal diet can elicit long-term improvements in metabolic control in people with type 1 (insulindependent) and type 2 (non-insulin-dependent) diabetes mellitus. The ease of isolation and purification of guar gum explains why it is frequently used as a *
Now at Unilever Research Colworth, UK.
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‘model’ non-starch polysaccharide in physiological and clinical studies. Also, the fact that it is well characterized with respect to other sources of dietary nonstarch polysaccharides makes it an ideal candidate for clinical use. This article highlights the nutritional and therapeutic role of guar gum, but mainly focuses on its blood glucose- and cholesterol-lowering actions. Also included is a brief discussion of the physicochemical properties of guar gum, including its rheological behavior in model systems and its influence on the properties of human and animal digesta in vivo,
fig0001
which has an important, if not crucial, influence on gut function and metabolism.
Extraction and Composition of Guar Gum Guar gum, a type of dietary fiber, is extracted from the seed endosperm of a leguminous plant (Cyamopsis tetragonoloba (L.) Taub.) indigenous to the Indian subcontinent. Figure 1 shows the pods, seeds, and endosperm extract of the guar plant. To recover guar gum from the seed, the endosperm halves (splits)
a
b
c
d
e
f
Figure 1 (see color plate 81) Pictures of pods, seeds, and endosperm extract of the guar plant (Cyamopsis tetragonoloba (L.) Taub.), a member of the Leguminosae family. (a) Green pods, scale bar ¼ 1.3 cm. (b) Dried pods, scale bar ¼ 1.6 cm. (c) Seeds, scale bar ¼ 1 cm. (d) Endosperm halves (splits), scale bar ¼ 1 cm. (e) Guar gum flour, scale bar ¼ 1 cm. (f) Scanning electron micrograph of guar gum flour, scale bar ¼ 100 mm.
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sources. Table 1 lists the typical composition of a commercially available guar gum flour.
OH OH CH2OH
Potential Adverse Effects of Guar Gum
O
HO
O O OH
O
HO O
HO
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0004
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OH O CH2OH
O
Figure 2 Structure of guar galactomannan showing the mannose backbone and galactose side chains.
must be separated from the hull and the cotyledon. The splits are ground to a fine flour and may then be purified by repeated alcohol washings. In this way guar gum is commercially produced as a flour and is frequently used as an additive (E412) in the food industry for its thickening and stabilizing properties. Chemically, guar gum mainly consists of a highmolecular-weight polysaccharide, namely galactomannan, which is based on a mannan (M) backbone with galactose (G) side groups, as shown in Figure 2. The ratio of the two components (G:M) seems to vary slightly depending on the origin of the seed, but the gum is generally considered to contain approximately one galactose unit for every two mannose units. The linkages between the sugar groups cannot be hydrolyzed by human digestive enzymes in the small intestine but are fermented by bacterial enzymes in the large intestine. The products of this fermentation include short-chain fatty acids, mainly acetic, propionic, and butyric acids, which have important nutritional implications, notably in relation to colonic function. The Food Chemicals Codex specifies a standard of not less than 66% of galactomannan in food-grade guar gum in the USA, although generally most samples contain more than 80% (w/w). The other components of guar gum, including fat and protein, which are considered to be impurities, vary between different
In the food industry, guar gum is normally added to foods in concentrations of < 1 g 100 g1 to provide a thickening, binding, or stabilizing function. Since guar gum is derived from a normal food material, it is classified by the Food and Agricultural Organization/World Health Organization as a substance of low toxicity. The safety of guar gum is substantiated by the results of a number of long-term studies in human subjects. In general, adverse effects, observed in some but not all subjects, appear to be associated with gastrointestinal disturbances. These effects, which sometimes appear to diminish with regular consumption of guar gum, include flatulence, gastrointestinal pain or discomfort, nausea, and diarrhea. Some of these side-effects probably result from bacterial fermentation of guar gum in the large intestine. The extent of the problems is generally related to the dose given, with more adverse gastrointestinal effects occurring when guar gum consumption is excessive (*15–30 g day1). It has also been suggested that guar gum may reduce the bioavailability of a number of micronutrients (e.g., vitamins), although there is no evidence to indicate that this is of nutritional significance. There is more concern about the use of macroaggregates of guar gum that have the potential for causing obstruction in the esophagus and gastrointestinal tract. This concern has arisen from reported incidents of esophageal obstruction and rupture in patients ingesting guar granules. There have also been a number of cases of esophageal and small-bowel obstruction in patients ingesting a particular type of guar-containing diet pill. The USA and Australia have banned such products. In the European Community (EC), food additive legislation prohibits the use of guar gum and other gums for the production of ‘dehydrated foodstuffs that will rehydrate on ingestion.’ However, the selling of guar products as medicine under license and administered to patients under medical supervision is permitted under EC legislation.
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Table 1 Chemical composition of a commercially available guar gum flour Component
Concentration (g 100 g1)
Galactomannan Protein Crude fiber Ash (total minerals) Fat (petroleum ether extractables) Moisture Total impuritiesa
73.0–86.7 3.0–6.0 1.0–4.0 0.8–2.0 0.5–1.0 8.0–14.0 13.3–27.0
a
Calculated as total nongalactomannan components.
Physicochemical Properties of Guar Gum Solution Properties
The ability of the galactomannan component of guar gum to hydrate and increase the viscosity, or thickness, of the intestinal contents is an important determinant of its physiological effects. The majority of polysaccharides used in nutritional studies exist in solution as ‘random coils’ and the number and
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0.1% 0.2% 0.4% 0.6% 0.8% 1.0% 1.5% 2.0% 2.5%
Viscosity (Pa.s)
10 1 0.1
6 5 4 3 2
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7
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0 0
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Figure 3 Shear rate and concentration dependence of viscosity for guar galactomannan solutions. Data taken from Rayment P (1996) PhD thesis, University of London.
molecular size of the polymer chains are critical determinants of viscosity and thus physiological activity. The high levels of viscosity associated with watersoluble polysaccharides originate predominantly by interpenetration of individual polymer chains to form entangled networks. At low guar gum concentrations, the individual polymer coils occupy a separate domain within the solution with little or no interpenetration. These solutions are described as Newtonian because their viscosity is independent of the rate of stirring or mixing (i.e., related to shear rate). At higher concentrations, where the polymer coils begin to overlap, the system becomes nonNewtonian and viscosity then depends on the shear rate. The more common type of non-Newtonian flow in food systems is shear-thinning (or pseudoplastic) behavior, where viscosity decreases with increased mixing. Figure 3 shows the effect of shear rate and concentration on the viscosity of guar gum solutions. The viscosity or flow properties of guar gum can be determined by using various rheological techniques. Rheology (from the Greek word rheos, meaning stream) is a branch of physical science concerned with the study of the flow and deformation of materials under externally imposed forces. However, to predict the rheological behavior of guar gum in the human intestine, several factors require consideration. These factors include dependence on the mode of administration, the size of the dose and the physicochemical characteristics of the sample used as well as the physical state of the galactomannan in the gut lumen.
Hydration Kinetics of Guar Gum 0009
The realization that viscous polysaccharides can be used for therapeutic benefit has led to the
4
5
Ultimate viscosity
Figure 4 Hydration rate profiles of guar gum samples presented as viscosity (Pa s) versus time. Experimental points are mean values from measurements on 4 replicate solutions of native guar gum flours M150 (—&—) and RG30 (- -d- -), pharmaceutical granule preparations Guarina (. . .!. . .), Guarem (—h—) and Lejguar (—s—), and Glucotard minitablets (—!—). The ‘ultimate viscosity’ is the measurement of viscosity taken after 24 hours of hydration following homogenisation of the guar solution with an ultra-turrax mixer. The final viscosity is taken only when a consistent maximum reading is recorded on the viscometer (usually after homogenising for 4–6 min). Data taken from Ellis PR & Morris ER (1991) Importance of the rate of hydration of pharmaceutical preparations of guar gum; a new in vitro monitoring method. Diabetic Medicine 8, 378–381.
development of various pharmaceutical preparations containing guar gum. These include capsules or macroaggregates of guar gum, such as granules and minitablets, which have been designed to hydrate slowly in the mouth to improve palatability. However, their beneficial effects have been reported to be extremely variable, most probably due to their lack of hydration in the stomach and small intestine. Consequently, the hydration rate of guar gum in the gut lumen is a critical factor. Figure 4 compares the hydration rate profiles of a range of commercially produced samples of guar gum. These samples were hydrated in water and viscosity was measured over a 5-h period. Unsurprisingly, the marked differences observed are mainly attributed to the physical nature of the guar gum preparations. Thus, samples with a smaller particle size (flours < 150 mm) hydrate much more quickly than those with a larger particle size (> 1 mm), e.g., Glucotard minitablets. The results of many clinical trials have shown that the latter types are often physiologically ineffective. Some research workers have also reported that the clinical efficacy of guar gum is improved when it is incorporated directly into a food rather than when taken as a pharmaceutical premeal supplement. Thus, a key factor in optimizing the glucose-lowering action
fig0004
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of guar gum is to insure that the polymer is in intimate contact with the starch, the main source of dietary glucose.
Nutritional and Physiological Effects of Guar Gum 0011
Many research groups have reported the efficacy of guar gum in attenuating the postprandial rise in blood glucose and insulin concentrations in healthy and diabetic subjects (Figure 5). One reasonable explanation of these postprandial effects is that guar gum reduces the rate (and perhaps the extent) of digestion and absorption of available carbohydrate in the gastrointestinal tract. (Here available carbohydrate is defined as carbohydrate that is digested by a-amylase in the upper gastrointestinal tract and absorbed into the portal blood (mostly as glucose); this includes
15
* *
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*
*
Blood glucose (mmol l−1)
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Control Test
0
50 40 30
*
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0012
10 0 0
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starch, dextrins and simple sugars (e.g., sucrose, lactose).) There are however problems with obtaining quantitative estimates of glucose absorption in humans; for example, access to the hepatic portal vein is very difficult. Nevertheless, studies in pigs, a useful animal model for studies on dietary polysaccharides, have provided the first direct evidence that guar gum decreases the rate of glucose absorption. In these types of experiment, glucose concentrations were measured simultaneously in the hepatic portal vein and peripheral blood (via the mesenteric artery) and the flow rate of the portal blood was measured also. Significant reductions in glucose absorption over 4 h were observed in the experimental animals given guar gum doses equivalent to those consumed by humans in clinical studies. In the same studies, insulin secretion was significantly decreased over the same period in response to the guar diet. This suggests that the attenuation in the plasma insulin levels seen in humans is attributed to a reduction in insulin secretion from the pancreatic islet b-cells in response to a lowered rate of glucose absorption. Also, a number of human studies have shown that guar gum decreases the postprandial rise in the insulinotropic hormones, plasma gastric-inhibitory polypeptide and glucagon-like peptide-1, which may partly explain the insulin-lowering action of guar gum. Another interpretation of data showing decreases in the peripheral blood insulin concentrations is that there has been an increase in hepatic extraction of insulin, a normal process by which insulin is removed from the blood circulation. Studies carried out to substantiate this have been largely contradictory, however. In relation to long-term studies of insulin action in experimental animals and humans, it has been reported that guar gum increases (improves) insulin sensitivity. A reduction in sensitivity to insulin (i.e., ‘insulin resistance’) is seen as a decrease in the response of tissues to insulin stimulation and is considered to be an important risk factor for both coronary heart disease (CHD) and type 2 diabetes.
Figure 5 Postprandial blood glucose and insulin concentrations of patients with type 2 (noninsulin-dependent) diabetes mellitus in response to control and test breakfast meals of bread and marmalade (total available carbohydrate, mainly starch and sugars, was 106 g). The test contained 16 g of guar gum (in the bread) and 10 g of pectin (in the marmalade). *Statistically significant differences between control and test meals at individual time points. Figure redrawn from data published by Jenkins DJA, Leeds AR, Gassull MA et al. (1976) Unabsorbable carbohydrates and diabetes: decreased post-prandial hyperglycaemia. Lancet 2: 172–174.
Mechanism of Action of Guar Gum There is little doubt that the consumption of guar gum, whether mixed in a drink or solid food, can significantly modify digesta properties at all sites of the gastrointestinal tract. One important feature is the capacity of guar gum at relatively low concentrations to form a highly viscous network in solution. As mentioned previously, the behavior of guar gum in a food material is highly complex. In such systems there is unlikely to be one mechanism to explain fully the effects of guar gum in the human gut. A number of physicochemical mechanisms may be
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involved, which are largely dependent on the type and form of the guar gum ingested. Much of the literature indicates that guar gum decreases the rate of glucose absorption into the hepatic portal vein by inhibiting the processes associated with digestion and absorption of available carbohydrates. These processes include gastric function, intestinal transit and mixing, a-amylase–starch interactions, and the movement of products of starch hydrolysis to the gut mucosa. A number of experiments in humans and animals have shown that guar gum reduces the rate of gastric emptying of a meal. However, there are also studies that have shown no effect or even sometimes an acceleration in gastric emptying after the ingestion of guar gum. These contradictory results probably arise from differences in the type of guar gum used, the way in which it was administered, the proportion of solids and liquids in the meals, and the techniques used to measure gastric emptying. In general, it is considered that guar gum may reduce the rate of gastric emptying under some conditions, but this action is unlikely to be the only mechanism. Other groups have shown guar gum has additional effects on gastric function. In studies in dogs, guar gum was reported to impair gastric trituration and sieving by increasing the viscosity of the stomach contents. It was shown that there was a significant increase in the proportion of larger particles of food entering the small intestine when guar gum was incorporated into the diets. Possible explanations for these findings include suggestions that the increased viscosity stabilizes the suspension of larger food particles, which are likely therefore to escape maceration in the antrum of the stomach, and/or that the guar gum alters the contractile pattern of the terminal antrum, thus impairing the ability of the stomach to retain large particles. There is evidence from human and animal studies that guar gum delays the transit of digesta in the small intestine. The postprandial pattern of gut motility also seems to be influenced by guar gum and other types of dietary fiber. Thus, whereas wheat bran and cellulose-supplemented diets were reported to produce prolonged bursts of intestinal contractions, guar consumption caused continuous contractions with a 50% reduction in amplitude compared with the other types of fiber. The effect of guar gum on the mixing behavior of digesta at different sites of the gastrointestinal tract has yet to be investigated, but it is likely to be extremely complex. It has been suggested that an increase in the viscosity of digesta will produce laminar or ‘streamline’ flow, rather than turbulent or disorderly flow, which is characteristic of less viscous fluids and facilitates efficient mixing of
digesta in the gut. An inhibition of the digesta flow rate will inhibit physical mixing of nutrients and enzymes (e.g., pancreatic amylase). Also, laminar flow behavior would almost certainly have an effect on the rate at which nutrients are exposed to the epithelial surface and then absorbed into the hepatic portal vein. However, an explanation of the precise mechanism by which guar gum modifies gut function is still elusive, despite the plethora of clinical and physiological studies that have been undertaken. The problem is that researchers understand little about the behavior of guar gum in the human gastrointestinal tract. Digesta is an extremely complex heterogeneous material and the effects of guar gum on this system have not been studied in great detail. Much of the work that has been done has involved investigating digesta in the stomach and small intestine, since it is assumed that guar gum has negligible effects on viscosity in the large intestine due to depolymerization by bacterial fermentation. There are a number of problems associated with measuring digesta rheology in vivo. In human subjects, there are obvious practical difficulties in gaining access to the sites of interest in the gut. Notwithstanding the initial problems involved with sampling intestinal contents, particularly in humans, the rheological properties of digesta will depend on the precise location of the sampling site. Thus, digesta is subjected to dilution by gastric secretions and then concentration by absorption of water, by both the intestine and the guar gum, at it passes further along the intestinal tract. Also the samples collected need to be tested quickly to prevent drying or dissolution of particulate materials. In the case of animal experiments, this requires access to rheometers or other measuring devices in the animal house. Many factors complicate the interpretation of the rheological behavior of digesta containing guar gum. These include a lack of information on the hydration kinetics of guar gum in vivo and the contribution of undissolved food particulates to viscosity. Therefore, to enhance our understanding of the physical properties of digesta it is important to study model systems of entangled networks filled with particulates, although in vivo other factors such as gastrointestinal motility and fluid secretion/absorption also play a crucial role. In recent years, the rheological properties of guar gum solutions with increasing particulate concentrations have been investigated. The particulates studies included materials that were essentially spherical and rod-like in shape (i.e., starch granules and microcrystalline cellulose, respectively). The effect of particulates or ‘fillers’ is primarily to increase the viscosity above that of the pure guar gum system, as shown in Figure 6. The initial Newtonian flow
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3018 GUMS/Nutritional Role of Guar Gum 100 0% 17% 26% 33% 41%
Viscosity (Pa.s)
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Figure 6 Effect of increasing rice starch concentration on the viscosity–shear rate flow curve of a 1% guar galactomannan solution. Data taken from Rayment P (1996) PhD thesis, University of London.
properties of the pure system at low shear rates become more rate-dependent on increasing particulate concentration – the so-called power-law behavior. The flow data have been fitted to mathematical equations, which incorporate parameters that describe the shear-thinning nature of guar gum and the increasing solid-like behavior of these filled systems. The model also seems to work well with a more heterogeneous food material containing wheat starch. The extrapolation of such models to real food systems and even digesta is fraught with difficulty, however. The inherent problems with studying digesta have been mentioned already, but to make any real progress in this area, at the very least, information is needed on the fractional volume of particulate material at different sites of the gastrointestinal tract. These data could be obtained by recovering ileal effluent from ileostomy patients and by the recovery of digesta from cannulated animals at appropriate sites of the gut. Further work on the development of more heterogeneous models and techniques to study such systems is crucial if we are to increase our understanding of how guar behaves in the gut environment. The mechanism by which guar gum reduces plasma cholesterol is still uncertain but, again, the discussion about the effects of guar gum on digesta viscosity and glucose absorption is important here also. The level of viscosity generated in the gut has been suggested as an important determinant of the hypocholesterolemic effect of guar gum in animal studies. The ingestion
of guar gum appears to enhance fecal bile acid and neutral sterol excretion, reduce the rate of digestion and absorption of lipids, and inhibit synthesis of cholesterol. In vitro, guar gum has been shown to reduce lipid emulsification and the rate of lipolysis of emulsified triacylglycerols, although these effects have not been substantiated in vivo. Also, guar gum has been shown to inhibit both the rate of diffusion of cholesterol mixed micelles and hepatic cholesterol synthesis; the latter has been attributed to propionic acid, one of the products of guar fermentation in the large intestine. However, the inconsistency between in vivo and in vitro studies prevents any conclusive statements being made about the precise mode of action of guar gum.
Dietary Management of Disease Although guar gum has frequently been used in clinical trials, interpretation of the results can be problematic. There are problems resulting from variable study design, lack of adequate controls, and heterogeneity of subject groups. Furthermore, many nutritional studies reporting the therapeutic effects of guar gum provide very limited information about the type and physicochemical properties of the sample tested, e.g., molecular weight and particle size. Moreover, sometimes it is not even known whether the guar was administered as a pre-meal supplement or incorporated directly into the subjects’ meal. Despite these problems, there is sufficient evidence to show that guar gum can be used effectively in the treatment of diabetes and hyperlipidemia, although its role in weight control management has yet to be defined.
0020
Diabetes Mellitus and Hyperlipidemia The plasma cholesterol-lowering properties of guar gum have been known since the 1960s. Most of the numerous clinical trials published since then have shown reductions in plasma concentrations of cholesterol, mainly the low-density lipoprotein (LDL) fraction, and occasionally triacylglycerols, in both healthy and hyperlipidemic individuals, in some studies for periods of up to 1–2 years. Similar results have been reported in people with diabetes, who are also likely to benefit from any improvements in lipid metabolism given their increased risk for CHD. Currently, although some pharmaceutical preparations are available in the UK, for the management of diabetes, no such products are available for the treatment of hyperlipidemia. In addition to evidence showing the blood glucose-lowering effect of guar gum in response to a starchy meal, long-term improvements have been demonstrated in patients with
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tbl0002
type 1 and type 2 diabetes. In one study of a group of type 2 diabetic patients, a 7-g daily dose of guar gum, which had been incorporated into wheat bread, improved glycemic control (as seen by a significant reduction in glycated hemoglobin) and lowered plasma total and LDL-cholesterol levels (Table 2). As discussed previously, some of the pharmaceutical preparations of guar gum, usually taken as a premeal drink, have been shown to be clinically ineffective due to impaired hydration. Moreover, when guar gum flour is incorporated directly into a meal, the clinically effective dose seems to be significantly lower than that recommended for the pharmaceutical preparations. This has led to the development of a number of everyday foods enriched with guar gum, such as bread, pasta, biscuits, and breakfast cereals. The recommended dose for pharmaceutical preparations of guar gum in diabetes therapy is usually 5 g with each meal (i.e., 15 g day1). However, it is not known what the precise dose and molecular weight of guar gum should be used in the diet to optimize clinical benefits. A lower and upper daily dose range of 6–15 g of native guar gum has been suggested for use in diabetes therapy. This has been suggested on the basis that doses of guar gum above 15 g day1
may cause side-effects, such as flatulence, and there is a lack of reliable long-term studies at doses of less than 6 g day1. The average molecular weights of guar galactomannan samples used in nutritional studies are in the range of 2.0–3.0 million. However, more recent studies have shown therapeutic benefits with samples of lower molecular weight (0.5–1 million), produced commercially by partial depolymerization. For example, one such product of approximately 1 million molecular weight has been used to lower plasma cholesterol levels in hypercholesterolemic human subjects (Table 3). Further work is required to define the lowest molecular weight and optimum dose that can be used without a loss in clinical efficacy. Such knowledge would have a number of advantages for any future product development, since low-molecular-weight grades are easier to incorporate into foods and are more palatable.
Obesity Obesity is associated with an increased risk of diabetes, insulin resistance, CHD, and hypertension. Most short-term studies (often single-meal tests) have shown that guar gum reduces feelings of hunger
Table 2 Mean values (+ SEM) of fasting plasma glucose, glycated hemoglobin (HbAlc), and plasma lipid concentrations in 16 patients with type 2 (noninsulin-dependent) diabetes after consuming control wheat bread and bread containing guar gum flour for two 6-week periods, respectively. Control and guar bread were taken by each patient in randomized order Controlperiod
1
Fasting glucose (mmol l ) HbA1c (%) Total cholesterol (mmol l1) LDL-cholesterol (mmol l1) HDL-cholesterol (mmol l1) Triacylglycerols (mmol l1)
Guar bread period
Start (0 weeks)
End (6 weeks)
Start (0 weeks)
End (6 weeks)
9.7 + 0.8 11.3 + 0.8 5.7 + 0.3 3.8 + 0.3 1.2 + 0.1 1.7 + 0.3
9.4 + 0.7 11.2 + 0.8 5.8 + 0.3 3.9 + 0.2 1.2 + 0.1 1.7 + 0.3
9.7 + 1.0 11.5 + 0.8 5.9 + 0.3 3.9 + 0.2 1.2 + 0.1 1.8 + 0.3
9.1 + 0.8 10.7a + 0.8 5.4b + 0.2 3.5c + 0.2 1.2 + 0.1 1.6 + 0.2
a,b,c Values after 6 weeks significantly different from control at P < 0.05, P < 0.02 and P < 0.01, respectively. LDL, low-density lipoprotein; HDL, high-density lipoprotein. Data taken from Peterson DB, Ellis PR, Baylis JM et al. (1987) Low dose guar in a novel food product: improved metabolic control in non-insulindependent diabetes. Diabetic Medicine 4: 111–115.
tbl0003
Table 3 Mean values (+ SEM) of plasma lipid concentrations in 11 moderately hypercholesterolemic humans after consuming control wheat bread and bread containing depolymerized guar gum for two 3-week periods, respectively. Control and guar bread were taken by each patient in randomized order Controlperiod
Total cholesterol (mmol l1) LDL-cholesterol (mmol l1) HDL-cholesterol (mmol l1) Triacylglycerols (mmol l1) a
Guar bread period
Start (0 weeks)
End (3 weeks)
Start (0 weeks)
End (3 weeks)
6.37 + 0.21 4.18 + 0.15 1.26 + 0.05 1.84 + 0.25
6.53 + 0.16 4.31 + 0.14 1.31 + 0.06 1.86 + 0.32
6.52 + 0.17 4.28 + 0.19 1.33 + 0.05 1.96 + 0.27
5.89a + 0.8 3.81a + 0.12 1.23 + 0.05 1.85 + 0.25
Values after 3 weeks significantly different from control and baseline (start) values at P < 0.001. LDL, low-density lipoprotein; HDL, high-density lipoprotein. Data taken from Blake DE, Hamblett CJ, Frost PG et al. (1997) Wheat bread supplemented with depolymerised guar gum reduces plasma cholesterol concentration in hypercholesterolaemic human subjects. American Journal of Clinical Nutrition 65: 107–113.
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3020 GUMS/Nutritional Role of Guar Gum
and appetite and increases feelings of satiety and satiation in all subjects, whether they be normalweight, overweight, or obese. However, there are problems in designing experiments to investigate feeding behavior, since it is very difficult to make the control food (placebo) look and taste like the test food. One study showed that breads containing high concentrations of guar gum were significantly less palatable than the control breads and this may explain why the subjects were less hungry after consuming the guar-containing bread meal. The energy value of the control and test meals should also be identical in such experiments. Despite the positive effects of guar gum in the short term, many of the long-term intervention studies are contradictory and suggest that a therapeutic role for guar gum in weight control management has yet to be established.
Conclusions and Final Comments 0024
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There is now overwhelming evidence to indicate that guar gum has therapeutic benefits for a range of metabolic disorders. At doses of guar gum that are likely to be consumed for therapeutic purposes, there is little evidence that it adversely affects human health. On the contrary, the cholesterol-lowering property of guar gum is of benefit to those who are at an increased risk of CHD, including people with hyperlipidemia and diabetes. Furthermore, the use of guar gum in decreasing postprandial glycemia and insulinemia and in improving long-term glycemic control in diabetic patients is now well established. Any improvement in glycemic control is likely to reduce the risk of microvascular complications (e.g., nephropathy), which are common in people with diabetes, and develop over a number of years. Recent epidemiological studies have also indicated that diets comprising low-glycemic-index foods may have a protective effect in the development of type 2 diabetes. Guar-containing foods could play an important role in such diets and should be tested in the future for their possible prophylactic benefits. In view of possible beneficial effects of guar gum on insulin resistance, which in itself is a risk factor for both CHD and type 2 diabetes, the role of guar foods needs to be evaluated here also. The effects of guar gum on weight reduction in the long term have yet to be demonstrated, although its use in maintaining weight in weight-reduced subjects merits further study. Obese individuals are likely to benefit however from the consumption of guar gum in terms of improvements in glycemic control, insulin sensitivity, and lipid metabolism. To assist in the development of new low-glycemicindex foods using guar gum as a major ingredient, it
would be advantageous to have a detailed understanding of its behavior in the gut environment. Fundamental information about the way in which guar galactomannan influences the rheological behavior of digesta, through its effects in solution, as an entangled network, or on the swelling of food particles, is of paramount importance. This would need to be closely linked to the effects of galactomannan on nutrient digestion and absorption, including, for example, starch and lipids. The initial attempts to produce palatable guar foods for the management of diabetes and hyperlipidemia were disappointing. However, the technological difficulties were exacerbated by the perceived need to use high doses of guar gum (15–30 g day1), since the results of early clinical trials suggested that such doses were needed to elicit metabolic benefits. More recent studies have shown that much lower doses (6– 12 g day1) and partially depolymerized guar gum are not only clinically effective, but have significantly less detrimental effects on sensory qualities of food. From a food technology perspective, it is now possible to produce guar-enriched foods that are both clinically effective and palatable. See also: Carbohydrates: Classification and Properties; Cholesterol: Factors Determining Blood Cholesterol Levels; Coronary Heart Disease: Prevention; Diabetes Mellitus: Treatment and Management; Dietary Fiber: Properties and Sources; Determination; Physiological Effects; Effects of Fiber on Absorption; Glucose: Maintenance of Blood Glucose Level; Glucose Tolerance and the Glycemic (Glycaemic) Index; Gums: Properties of Individual Gums; Food Uses; Dietary Importance
Further Reading Edwards CA and Read NW (1990) Fibre and small intestinal function. In: Leeds AR (ed.) Dietary Fibre Perspectives, vol. 2, pp. 52–75. London: John Libbey. Ellis PR (1999) The effect of fibre on diabetes. In: Hill M (ed.) The Right Fibre for the Right Disease, pp. 33–42. London: Royal Society of Medicine Press. Ellis PR, Rayment P and Wang Q (1996) A physicochemical perspective of plant polysaccharides in relation to glucose absorption, insulin secretion and the enteroinsular axis. Proceedings of Nutrition Society 55: 881–898. Ellis PR, Wang Q, Rayment P, Ren Y and Ross-Murphy SB (2001) Guar gum: agricultural and botanical aspects, physicochemical and nutritional properties, and its use in the development of functional foods. In: Cho SS and Dreher M (eds) Handbook of Dietary Fiber, pp. 613–657. New York: Marcel Dekker. Flourie B (1992) The influence of dietary fibre on carbohydrate digestion and absorption. In: Schweizer TF and Edwards CA (eds) Dietary Fibre – A Component
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GUMS/Nutritional Role of Guar Gum 3021 of Food. Nutritional Function in Health and Disease, pp. 295–332. London: Springer-Verlag. Gallaher DD and Hassel CA (1995) The role of viscosity in the cholesterol-lowering effect of dietary fiber. In: Kritchevsky D and Bonfield C (eds) Dietary Fiber, Health and Disease, pp. 106–114. St Paul, USA: Eagan Press. Leeds AR (1999) The effect of fibre on coronary heart disease and cholesterol. In: Hill M (ed.) The Right Fibre for the Right Disease, pp. 33–42. London: Royal Society of Medicine Press. Low AG (1990) Nutritional regulation of gastric secretion, digestion and emptying. Nutrition Research Reviews 3: 229–252. Maier H, Anderson M, Karl C, Magnuson K and Whistler RL (1993) Guar, locust bean, tara and fenugreek gums. In: Whistler RN and BeMiller JN (eds) Industrial Gums: Polysaccharides and their Derivatives, 3rd edn, pp. 181–226. London: Academic Press. Morgan LM (1992) Insulin secretion and the entero-insular axis. In: Flatt PR (ed.) Nutrient Regulation of Insulin Secretion, pp. 1–22. London: Portland Press.
Gut Hormones
Read NW and Eastwood M (1992) Gastro-intestinal physiology and function. In: Schweizer TF and Edwards CA (eds) Dietary Fibre – A Component of Food. Nutritional Function in Health and Disease, pp. 103–117. London: Springer-Verlag. Reid JSV and Edwards ME (1995) Galactomannans and other cell wall storage polysaccharides in seeds. In: Stephen AM (ed.) Food Polysaccharides and their Applications, pp. 155–186. New York: Marcel Dekker. Ross-Murphy SB (1994) Rheological methods. In: RossMurphy SB (ed.) Physical Techniques for the Study of Food Biopolymers, pp. 343–392. London: Blackie Academic & Professional. Todd PA, Benfield P and Goa KL (1990) Guar gum: a review of its pharmacological properties, and use as a dietary adjunct in hypercholesterolaemia. Drugs 39: 917–928. Truswell AS and Beynen AC (1992) Dietary fibre and plasma lipids: potential for prevention and treatment of hyperlipidaemias. In: Schweizer TF and Edwards CA (eds) Dietary Fibre – A Component of Food. Nutritional Function in Health and Disease, pp. 295–332. London: Springer-Verlag.
See Hormones: Adrenal Hormones; Thyroid Hormones; Gut Hormones; Pancreatic Hormones; Pituitary Hormones; Steroid Hormones