fibreandenteralnutrition - gut | gut delivers up-to-date...

Gut, 1989, 30, 246-264

Progress report

Fibre and enteral nutrition

Clinical experience during the last decade has confirmed that enteralnutrition is an efficient and cost effective means of providing nutritionalsupport to patients with normal or near normal gastrointestinal function.'Before and during this period the knowledge gained of the processesinvolved in the physiology of nutrient absorption has been applied to theformulation of enteral diets and if comparisons are made of the compositionof present day diets with those used 10 to 15 years ago several differences canbe seen. These relate mainly to the nitrogen and energy concentrations ofpolymeric diets and the sources of nitrogen and energy and electrolytecompositions of predigested chemically defined elemental diets.2

Until recently all the commercially produced liquid enteral diets con-tinued to have one thing in common, namely that they contained a low'residue' or 'fibre' content. Historically it must be remembered that the veryearliest low residue enteral diets were specifically designed not only toprovide balanced nutrition to astronauts in space but also to reduce theirstool weight and stool frequency.3 Subsequently it was realised that oneclinical advantage of low residue diets was that they had a low viscosity andcould be administered easily through 'fine bore' nasogastric or nasoentericfeeding tubes. Furthermore as it became clear that there could even be anumber of therapeutic advantages in administering low residue diets4 theirwidespread use became accepted without question.

Although the 1970s and early 1980s has been the time when advances havebeen achieved in the field of enteral nutrition the same period has seen alsosignificant advances in the field of fibre research and as a consequence therehas developed a belief that many of the diseases of Western civilisation suchas atherosclerosis, obesity, appendicitis, constipation, irritable bowelsyndrome, colon cancer, diverticular disease, diabetes mellitus, and gallstones were related to a deficiency in dietary fibre and that supplementingthe diet with fibre would prevent and might even cure these conditions.5Although not all recent studies6 have been in complete agreement theobservations made by Heaton and colleagues over 10 years ago78 thatingestion of bran accelerated slow intestinal transit and delayed rapidintestinal transit lead to suggestions that the ingestion of fibre produces amore regular bowel habit.9 Based largely on this premise, as well as on theabove doctrine that dietary fibre is good overall, suggestions are beginningto be made that there could be benefits to supplementing commerciallyproduced liquid enteral diets with fibre.

This article seeks to critically examine the premises on which the proposeduse of fibre supplemented enteral diets are based. In the ensuing text,attempts have been made to determine whether there is any substantiveevidence to support the use of fibre supplemented enteral diets clinically.Finally, potential areas of interest requiring further research have beenhighlighted. A proper understanding of the potential applications of fibre to

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enteral nutrition can only be achieved by taking into account recent progressthat has been made in the understanding of the physiological and bio-chemical processes that are involved in the intestinal assimilation of themajor components of dietary fibre - these are therefore reviewed beforeother discussions.

Definition of dietary fibre

One of the most confusing aspects of fibre and enteral nutrition has been thedifficulty in agreeing on a definition of the term 'fibre' or 'dietary fibre'. Thisproblem is by no means unique to enteral nutrition as many previousdiscussions testify.""'2 It is thus important to realise that fibre is not a singlesubstance, nor is it an inert, indigestible, 'unavailable' material which simplypasses through the gut.'0 Progress in understanding fibre has been slowbecause it is difficult material to handle in the laboratory, its action isdependent on its physical and chemical properties and adequate methods forits measurement are still being developed.For the purposes of the present discussion about the role of fibre in enteral

nutrition, the simple and precise definition proposed by Cummings'° will beused (Table 1). His proposal is to call the major fraction of fibre non-starchpolysaccharide (NSP). Non-starch polysaccharide is then divided intocellulose and non-cellulose polysaccharides (NCP).'3 1' Non-cellulose poly-saccharides includes those polysaccharides like inulin and guar and the plantgums and mucilages.

Lignin is not a carbohydrate, and Cummings suggests that if it is to beincluded as part of fibre, it must be considered separately.'" Chemicallylignin is reasonably well defined and comprises a group of polyphenoliccompounds of widely varying molecular weights. It contributes to thestructural rigidity of the plant cell wall and is an inhibitor of microbialcell wall digestion. As the amount of lignin in the human diet is so small(1 g/day), it is probably unjustifiable to single lignin out to be included underthe term 'dietary fibre'.

Assimilation of dietary fibre

As outlined above, the initial interest of fibre in the context of enteralnutrition has centred around its effect on bowel function. This in turn relatesto the undigestibility of fibre. It should be appreciated, however, that recentresearch has shown that there is striking variation in the apparentdigestibility of the different components of dietary fibre outlined in Table 1.

Table 1 Classification ofdietaryfibre*

Non-starch polysaccharide (NSP)

Cellulose non-cellulosic polysaccharide (NCP).hemicellulose.pectin.inulin.guar.plant gums and mucilages

*After Cummings.`"

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Fibre components

_____________ Intestinal microflora(anaerobic)

VFA (acetate, propionate, butyrate) gas (C02, H2, CH4)

and energy

345C6 H1206 --48CH3COOH + 11 CH3CH2COOH

+ 5 CH3(CH2) 2COOH + 23 75 CH4 + 34-25 C02

+ 105 H20Figure Digestion andfibre.

As the ensuing text will show, present day concepts about some of thepotential benefits of supplementing enteral diets with fibre relate as much tothe action of the products of colonic fibre digestion as to the stool bulkingeffect achieved by undigested fibre components. The Figure summarises theprocesses involved in the intestinal assimilation of the different componentsof dietary fibre.

Sites of fibre assimilation

Recent evidence overwhelmingly implicates the colon as the major site ofnon-starch polysaccharides (NSP) degradation.'" In three recent andimportant studies carried out in ileostomists, 87 9-100% of administeredfibre was recovered in ileostomy effluent. 16-18Two earlier studies also undertaken in ileostomy subjects, suggested that

some formentation of fibre occurs in the small. intestine. In the first,'9significant quantities of NCP were digested in the small intestine. Thisparticular study is open to some criticism, not only on methodologicalgrounds (vide infra) but also because ileostomy effluent may have beenpermitted to ferment for some hours during collection. In the second, inwhich "'C-labelled cellulose degradation was studied in man, a peak of'4C CO2 in expired air was noted as early as 30 minutes after the oralingestion of labelled cellulose.20 Quantitatively much smaller than the laterand main peak, its occurrence was thought to indicate a minor degree ofdegradation in the small intestine. An alternative explanation, however, asdiscussed by the authors20 is that there may have been some contaminationof the labelled cellulose with starch.As the Figure shows, volatile fatty acids (VFA's) are a major product of

fibre degradation. The virtual absence of VFA's in the ileostomy effluent oftwo of the ileostomy studies discussed above'6 17 provides supportiveevidence for the lack of fibre degradation in the small intestine. Finally, in arecent study in which jejunal ileal and colonic contents were obtained withinfour hours of sudden death2' the concentrations of VFA's were at least an

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order of magnitude greater in colonic as compared with small intestinalcontents, again implicating the former as the major site of degradation offibre components.

Microbial action

No luminal or mucosal enzymes have been identified in man that are capableof catalysing the hydrolysis of NSP, and there can be little doubt that thebreakdown of NSP is accomplished anaerobically by intestinal microflora(predominantly colonic). Available bacteriological data indicate that anumber of NSP-degrading bacteria are present in the human colon.Although some of the polysaccharidases produced by human colonicbacteria are extra cellular,2526 most of the enzymes studied appear to bebound to the bacterial cell wall.25 Potentially of great importance to enteralnutrition is the observation that many of the microbial polysaccharidedegrading enzymes are inducible.2526

Products of NSP degradation

VOLATILE FATTY ACIDS (VFA)Acetic, propionic, and butyric acids are the acids produced as a conse-quence of NSP degradation. Volatile fatty acids are avidly absorbed in thehuman colon27 and at the same time stimulate colonic sodium and waterabsorption.28 Their presence in the colon affects and indeed controls the pHof the colonic lumen,29 which in turn may indirectly affect transport of othersolutes such as ammonia.29 Once absorbed, VFA's are available for aerobicmetabolism in body tissues and as such are an energy source. In certaincircumstances VFA metabolism may make a significant contribution to dailyenergy balance. Lactitol, a synthetic disaccharide which is not absorbed inthe human small intestine,30 but extensively (>90%) metabolised to VFA3'in the colon, has been calculated to have a calorific value close to 2.5 kcallg.3'

GASMethane, carbon dioxide, and hydrogen are the gases produced during NSPdegradation. They are either absorbed and excreted in expired air or passedas flatus per rectum. A variety of abdominal symptoms such as colic, feelingsof distension and bowel disturbance have been attributed to colonic gasproduction, not always with justification. A recent study rather disappoint-ingly indicated that end alveolar breath hydrogen and methane analysisprovides no clear indication of fibre digestibility.32

BACTERIAL GROWTHThe third important end product of anaerobic colonic bacterial fermentationofNSP is energy which bacteria use for growth and maintenance. In man thepresence of fermentable polysaccharides in the diet has been shown tostimulate colonic microbial growth33 and the increased bacterial mass is oneof the mechanisms whereby NSP in the diet leads to an increase in humanfaecal output.10 Associated with stimulated microbial growth is increasednitrogen excretion as a result of the incorporation of nitrogen into microbialprotein.34 Theoretically other activities of colonic microflora, such as bileacid dehydroxylation, hydrolysis of glucuronide conjugates, and vitamin

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synthesis might also be affected by NSP degradation. As yet these have notbeen fully investigated.'0

Factors affecting the breakdown of non-starch polysaccharides (NSP)in man

As shown in Table 1, cellulose and non-cellulose polysaccharides (NCP) arethe two major components of NSP. Published evidence indicates that in manNCP digestion is more efficient than cellulose digestion, some componentsof NCP being very extensively degraded in the human gut. Data from eightstudies quoted by Cummings'° show that an average 80% NCP from varioussources was degraded. The cellulose component of the same fibre sourcesappears to be less well degraded. In 10 studies quoted by Cummings'0 onaverage 50% of the cellulose fraction from various fibre sources wasdegraded. This compares favourably with 42-8% digestibility found in oneof the more recent studies of cellulose degradation in man.20 A number ofimportant physical factors have now been identified that explain theobserved differences in the extent of colonic degradation of the differentcomponents of fibre.The pattern of absorption of digestible dietary carbohydrate is dependent

in part on the accessability of substrate to luminal a-amylase.35 Breakdownof NSP by bacterial polysaccharides is also dependent on these enzymesgaining access to its surface.6 The rate of breakdown of cellulose, being arelatively insoluble material, will be very much related to the form andparticle size that in turn will both determine the surface area that isaccessible to colonic bacterial polysaccharidases. Highly crystalline formspresent a relatively small surface area which is probably one of the reasonswhy pure cellulose isolated from wood is more poorly digested than the non-crytalline forms of cellulose in fruit and vegetables.3738 Particle size, which isdependent on the source and method of processing equally influences thedegree of digestibility.39 Reducing particle size increases available surfacearea, resulting for example in an increased digestibility of the cellulosecomponent of finely ground as compared with coarse bran."4'

Lignin, as mentioned above, is not a carbohydrate and comprises a groupof polyphenolic compounds of widely varying molecular weights. Althoughnot broken down to any extent in the gut,38 it does influence the extent ofNSP degradation. In general, the more lignified a cell wall of a plantstructure, the less liable it is to complete degradation in the gut. Thus theNSP in wheat bran is degraded much less than those present in the lesslignified cell walls such as cabbage and apples.37I3942

Cellulose digestion is a relatively slow process, studies in rumensindicating that it can proceed for up to 48 h.'34 Contact time betweensubstrate and enzyme will also clearly affect digestibility. Thus cellulosedigestion is more complete the slower the colonic transit time.45 Factors thataffect colonic transit such as treatment with codeine phosphate and senokotwill therefore influence cellulose digestibility.-'The majority of NSP in plant cell walls are in fact NCP.38 These are

chemically very different from cellulose in that they have a much more openchemical structure and many are water soluble at the pH of luminalcontents, which is the reason why these substances are metabolised to agreater extent by colonic bacterial polysaccharides than cellulose.?" Some of

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the water soluble NCP such as pectin are completely degraded in the normalhuman colon.45

Clearly one further factor that will affect the degradibility of NSP is theactivity of the colonic bacterial polysaccaridases themselves. Recent studiesof these enzymes have been reviewed.2" Many of the polysaccharidedegrading systems are complex, more than one enzyme being involved.None of the polysaccharide degrading species appears to be restricted to theproduction of one particular type of polysaccharide degrading system andgiven the number of enzymes that are needed to degrade any one of the NSPsubstrates, the versatility of these colonic organisms is remarkable. All ofthe polysaccharidases studied to date in human colonic bacteria have provedto be inducible - that is, an appreciable amount of enzyme is produced onlywhen the organism is exposed to the polysaccharide substrate. It followsfrom this discussion that the degree of digestibility of a single fibre sourcecould be expected to increase with time, a situation which might occurduring longterm administration of a fibre supplemented enteral diet. Incontrast, antibiotic therapy could be expected to reduce the activity ofcolonic bacterial polysaccharidases, reducing in turn the digestibility ofenterally administered NSP.


The two main areas of current interest are concerned with the possiblebenefits of fibre on bowel function during enteral feeding and its effects onsmall and large intestinal mucosal cell morphology and function. Beforeconsidering these, the pitfalls that exist in interpreting available clinical datashould be appreciated as well as the effects that fibre supplementation mayhave on nutrient absorption during enteral feeding.

Problems in interpretation of clinical data

Two major problems exist in interpreting much of the published clinicaldata. As mentioned above, it is clear that different components of NSP aredegraded to different extents in the human gut, and consequently theirphysiological properties will vary. Moreover, factors such as fibre source,particle size and lignin content all influence intestinal assimilation. Toachieve a full understanding of the significance of published data therefore,detailed information of the physiochemical characteristics and compositionof the fibre sources tested is required - this is, rarely, if ever, presented inclinical papers. As outlined by Southgate and Englyst46 as well as byCummings,10 problems with the methodology of fibre measurements areconsiderable. A satisfactory analytical method for dietary fibre mustmeasure all the NSP (cellulose, NCP, soluble and insoluble), and a methodsuch as described by Englyst et all7 appears to meet these criteria.Many authors quote values obtained by one of the Van Soest detergent

fibre methods."' Neutral detergent fibre (NDF) has often been used49 tosignify 'insoluble' dietary fibre. A proportion of NCP, such as the pectins, iswater soluble and therefore is not measured in the detergent fibremethods."4 I Thus although this method gives accurate values for somecereals, especially wheat products (which contain low proportions of solubleNCP), that are numerically of the same order as total dietary fibre values

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obtained by the summation of cellulose and NCP, direct analysis ofthe different fractions shows this is fortuitous.5' In fruits and veg-etables therefore, which contain significant water-soluble NCP, theneutral detergent fibre method will considerably underestimate dietaryfibre content very significantly.'4"- This discussion should help the readerto understand why there is often such a discrepancy between figures quotedfor neutral detergent fibre and total fibre contents (9-3 g versus30 g52).

Effects of added fibre on intestinal nutrient absorption

Recent research shows that the blood glucose response to the ingestion ofdifferent carbohydrate sources varies considerably.35 Although a number offactors such as the mono and disaccharide contents,53 as well as protein andfat contents,54 are thought to influence postprandial circulating bloodglucose levels, other experimental data indicate that the fibre content islikely to have an important effect on the pattern of absorption of glucosefrom different carbohydrate sources. Thus certain forms of purified dietaryfibre have been shown to modify carbohydrate absorption.55 Amongst these,the viscous predominantly NCP forms such as guar, pectin, and tragacanthhave the greatest modifying effects.5556 In contrast, wheat fibre has littlemodifying effect on the postprandial glucose response.55 The principlesgained from studying the modifying effects of the viscous forms of dietaryfibre on the patterns of glucose absorption from dietary carbohydrate havebeen applied to the treatment of diabetes57 and post gastrectomyhypoglycaemia.6' Interestingly the addition of guar to one liquid glucosemeal not only modified immediate plasma glucose concentrations and seruminsulin levels, but its effect persisted to modify the same responses after afibre free glucose meal administered four hours later.62

It follows from these discussions that the effects of fibre on intestinalnutrient assimilation will vary according to the physiochemical properties ofthe fibre source tested.'3 As the NCP forms such as guar, pectin andtragacanth have been shown to have the greatest modifying effect on glucoseabsorption,5556 these are the sources that have been most frequently used toinvestigate the mechanisms involved in the modifying effects of dietary fibreon nutrient assimilation. Thus, in different experiments fibre has beenshown to affect gastric emptying,'65 small intestinal flow and transit,P'pancreatic enzyme secretion67" the rate of nutrient digestion by pancreaticenzymes67 solute diffusion,'" the apparent Michaelis constant of amino acidand monosaccharide uptake,7' as well as postprandial gastrointestinalpolypeptide hormone responses.72-74

In patients with normal gastrointestinal function it would be difficult toenvisage on account of the large functional absorptive capacity of thegastrointestinal tract, that fibre supplementation of enteral diets would havea clinically significantly deleterious effect on the assimilation of the majorclasses of nutrients, carbohydrate, fat and protein. The situation with regardto mineral absorption is by no means as clear. Thus over 11 day feedingperiods the addition of 40 g soy fibre/d to a polymeric liquid enteral dietresulted in a significant decrease of absorption of iron and copper, and apattern of decreased absorption (not statistically significant) of calcium,magnesium, zinc, potassium, and phosphorous.75 Similar changes were not

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observed when 20 and 30 g soy fibre were added.75 Although fibresupplementation of enteral diets administered to diabetic patients wouldseem an attractive proposition, bearing in mind the results of work in thisfield"' no clinical data in enterally fed patients have been reported.As yet no studies have investigated the possible effects of fibre supple-

mentation on nutrient assimilation from predigested 'chemically defined'elemental diets administered to patients with severely impaired gastro-intestinal function. In such patients, particularly those with the nutritionallyinadequate short bowel syndrome, such factors as gastric emptying, smallintestinal motility and transit, unstirred water layer resistance, as well asmorphology are all likely to assume important roles in determining theextent of nutrient absorption. Because each may be affected by fibre, thereremains a clear indication to pursue investigations into the effects ofsupplementing the predigested 'chemically defined' elemental diets withfibre.

Effect of added fibre on bowel function

One of the main areas of interest of fibre enriched liquid enteral diets isbowel function. If one accepts that normal bowel function can be defined asabsence of diarrhoea or constipation with adequate nutrient absorption,52then the significant proportions of patients receiving low residue liquidenteral diets without added fibre who develop constipation of diarrhoea canbe considered to have abnormalities of bowel function.

CONSTIPATIONStudies of healthy volunteers have shown that the majority of the populationin the Western world pass one bowel movement per day with an averagedaily output of 120-130 g stool.76 Similar findings were reported in normalsubjects taking part in dietary studies and consuming metabolically control-led diets.77 Large individual variation is seen, however, both in frequencyand weight of bowel movements, without complaints of either constipationor diarrhoea.78 Such variability in normal bowel habit makes it difficult todefine an abnormal or constipated state and to date this somantic difficultyhas not been overcome.78 Clearly therefore the true incidence of constipa-tion during feeding of low residue liquid enteral diets is not known.

Fibre added to the diet affects bowel function in three ways. Faecal weightis increased, intestinal transit time is increased and frequency of bowelevacuation is increased.79 It is important to appreciate that different sourcesof fibre increase stool weights to different extents and by differentmechanisms.78 Thus cabbage and other vegetable fibre sources which arerapidly and extensively degraded stimulate growth of microflora within thecolon.8" Bacteria are 80% water8' and their increase in mass in stools withdegradable fibre materials largely accounts for the increase in faecalweights. On the other hand, poorly digestible bran stimulates bacterialgrowth to a lesser degree, but survives itself to hold water. There aretherefore, two water holding components in the stool with added bran, fibre,and bacteria and together these produce larger faecal weights thanequivalent supplements of the vegetable sources of fibre.78" Defecation isinitiated by mechanoreceptors in the anorectal area, by movements of therectal mucosa and by rectal distension."2 Sensory receptors respond to

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distension so that faecal bulk is an important determinant of the defecatorymechanism. The bulking effect of digestible and undigestible fibre is,therefore, associated with an increase in frequency of defecation.79

CLINICAL STUDIES IN ENTERAL NUTRITION (Table 2)The author is aware of five controlled crossover studies that have comparedbowel function in healthy volunteers5283I or patients85 receiving liquidenteral diets with and without added dietary fibre. The fibre sources used

Table 2 Bowelfunction in healthy volunteers and patients receiving liquid polymeric enteraldiets with and without added dietaryfibre

Duration of Fibre intake Faecal wet wt gid DailyAuthor Fibre source n study gid mean (SD) stoolfrequency

S16 10 0 67-3 (20-8) 0-7Slavl2 Soyfpbreo16 10 30 114.6(53. 1)* 0 9et at'2product ~~16 10 60 150-3 (78.4)* 1._0*

Labke Notstated 10 4 0 110(42) 0-9(0-4)etal' o a e 10 4 20 139(47) 14 (0.5)*

Matzkies Soya-bran f8 7 0 57 (15) 0-62&Webs S 8 14 30 86(4) 088

Fischer Soy- 13 30 0 241 (2.8) 0 45etal' polysaccharide 133 14 21.2(2-9) 40-3(19.1) 0-5

Patil Carrot- J 5 5 0 52(16) 0-64 (0.18)etal'P fibre 5 5 24 58(20) 0.81 (0.36)

Mean (SD). *p<0-05 v no added fibre.

were either not stated,' or described as a soy fibre product derived from thesoy coteleden high in the NCP hemicellulose,52 soya bran,83 soya poly-saccharide,85 and carrot fibre.' With the exception of 60 g/d of soy fibre and20 g/d undescribed fibre, both administered to healthy volunteers,52 nosignificant effect of fibre supplementation on stool frequency was seen. Theaddition of 30 and 60 g soy fibre to a polymeric diet administered to normalsubjects both resulted in significant increases in mean daily stool weights.52In four of the other five studies,8' however, no significant effect of fibresupplementation was seen on mean daily stool wet weights, range 24-1-110 g/24 h without added fibre: 40-4-139 g/24 h with added fibre. All wereshort term studies with the fibre supplements being administered forbetween four and 14 days. No longterm studies of fibre supplementation inpatients receiving liquid enteral diets have yet been reported.The most recent estimate of dietary fibre intake in the UK, based on the

analytical method of Englyst and Cummings,87 is 13-7 g/d.Y It is of interesttherefore that a range of fibre supplementation of 21 2-30 g/d produced suchmodest changes in stool weights. At first sight it would seem that the lack ofconsistent beneficial effects of added fibre in these studies is predictablyrelated to an inappropriate choice of fibre source. Thus the fibre supple-ments used contained a predominance of NCP.52 8 As discussed previouslythis is not the component of fibre that exerts maximal change in stoolweight.33 There is at least one study, however, that has shown thatsupplementing a normal diet with 20 g dietary fibre per day derived fromcarrot results in a significant increase in stool weight.89 As outlined above,the physical form of NSP affects digestibility. One does wonder thereforewhether acceptable viscosity of the fibre supplemented enteral diets used in

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these studies"2 was achieved by processing the fibre sources to very smallforms, thereby increasing digestibility and reducing water holding capacity,two factors known to mitigate against stool bulking.3"4"One is forced to conclude that on the basis of published data there is little

evidence to support the use of currently available fibre enriched diets as faras increasing stool frequency and weights of enterally fed patients isconcerned. It is clear that further research is still required to identify suitablyprocessed fibre sources that on the one hand result in significant increases instool frequency and weights of enterally fed patients and on the other handdo not have adverse effects on diet viscosity.

DIARRHOEADiarrhoea is a significant problem in enteral nutrition. According to basicphysiological principles, which take into account the capacity of the normalsmall and large intestine to assimilate fluid and electrolytes, diarrhoea canbe defined as the passage of more than 200 g of stool/24 h on an averageWestern diet.' It follows that the diagnosis of diarrhoea is dependent onaccurate measurements of stool outputs, hardly a feasable proposition inuncooperative enterally fed patients with faecal incontinence. For thepurposes of our clinical studies we have therefore defined enteral feedingrelated diarrhoea as the passage of too frequent stools or stools of too loosea consistency that are of inconvenience to the nursing staff and/or thepatient.992 In our experience, diarrhoea so defined, occurs in up to 25% ofpatients receiving enteral nutrition.93 A number of factors have beenimplicated in its pathogenesis.' These include use of infected feeds, lactoseintolerance, intolerance of high osmotic loads of nutrients administered,inapropriate release of gastrointestinal polypeptide hormones, concommit-ent antibiotic therapy, ingestion of laxatives, and hypoalbuminaemia.The role of lactose intolerance in the pathogenesis of the diarrhoea has

been discussed in some detail.' In brief, the deleterious effect of lactose inenterally fed patients with lactose intolerance will depend on the load(concentration x rate) of lactose administered. Bolus feeding in lactoseintolerant patients results in the production of stool volumes in excess of1 1/24 h.94 In contrast, when a low load of lactose is presented to the uppersmall intestine, as occurs during constant 24 hour intragastric infusion ofliquid lactose containing diets, diarrhoea does not occur.9' In a prospectivecontrolled trial of continuous 24 hour nasogastric infusion of polymeric dietsto patients with normal or near normal gastrointestinal function, thedevelopment of diarrhoea was not related to osmotic load of nutrientspresented for absorption but to concommitant antibiotic therapy.'3 Animalstudies carried out in our laboratory have not confirmed that the onset ofdiarrhoea is related to an inappropriate release of gastrointestinal poly-peptide hormones.95 Finally, hypoalbuminaemia has been related in onestudy to the development of diarrhoea.'6 No mention was made however, asto whether those patients with low serum albumins (who one could presumewere sicker) were receiving antibiotic therapy.'6As far as one can determine from these clinical studies, there appears to

be a link between concommitant antibiotic therapy and the development ofdiarrhoea during enteral feeding.' The incidence of diarrhoea in thesepatients on antibiotic therapy is higher than one would expect if they were onantibiotics alone, so it would seem possible that there is an interesting and

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deleterious synergistic effect between antibiotic therapy and the administra-tion of fibre free liquid enteral diets. ' As outlined previously, the absorptionof VFA's in the colon provides a powerful stimulus to colonic fluid andelectrolyte absorption.28 One explanation therefore which would explainthese associations is that antibiotic therapy reduces the bacterial enzymecatalysed production of VFA's within the colon, and in turn this reducesVFA stimulated water and electrolyte absorption in the colon, the end resultbeing the too frequent passage of watery stool.To prove this hypothesis it would be necessary first to ascertain colonic

inflows of substrate. Such information is currently not available. Further-more, it would then be necessary to investigate the effects of antibiotics oncolonic microflora and VFA production in an in vitro stool culture system.29A potential area of great interest would then be to determine if supple-mentation of enteral diets with an NCP such as pectin would result in adiminuation in the incidence of enteral nutrition associated diarrhoea andmoreover if diarrhoea occurs whether it can be reversed by NCP administra-tion.

Until such information is available, no firm recommendation can be madeas to the benefits of fibre supplementation of enteral diets in respect ofreducing the incidence of enteral feeding related diarrhoea.

Enteral diets and intestinal epithelial cell proliferation

EXPERIMENTAL STUDIESThe intestinal epithelium can respond to a wide variety of stimuli by alteringits proliferative rates.9798 There is now a large and interesting literature onthe effect of low residue liquid enteral diets on intestinal morphology, cellturnover kinetics and function. Almost all experiments have been per-formed in the rat and low residue chemically defined elemental diets andpolymeric diets have been studied. In general, in the jejunum, intestinalmass is maintained or increased,3'l° the specific activity of brush borderhydrolase activity maintained,' '1 or increased,'0' DNA synthesis ratesmaintained,' and absorptive function maintained.'02 In sharp contrast,administration of these low residue diets is associated with pronouncedatrophy in the ileum9;'02 and colon "03 as compared with the feeding of anormal fibre containing rat chow diet.As fibre has been shown experimentally to have a proliferative effect on

intestinal epithelium."'07 Suggestions have been made that the atrophy andreduced intestinal proliferation seen in rats fed on liquid enteral diets arisesbecause of the lack of fibre in these diets.'02103 '1 To prove this hypothesis itwould be necessary to compare the responses of ileal and colonic epithelia tothe same liquid enteral diet fed in the absence and presence of added fibre.Results of published studies in general are supportive. Ryan and colleaguesshowed that cellulose and petroleum jelly added to an oral liquid fibre freediet resulted in significant increases in colonic weight and DNA synthesisrates compared with values seen when the fibre free diet was fed."'3 Whenthe same liquid polymeric diet with and without 9% added bulk wasadministered orally to rats for four weeks, however, the total weight of ilealsegments were similar. 102 In the most comprehensive study to date, Goodladand colleagues"'8 have studied crypt cell production rate in starved rats refedwith a liquid elemental enteral diet supplemented with very large (1:1)

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quantities of different fibre sources, inert bulk (kaolin), a poorly digestiblefibre source (purified wood cellulose), a more readily digestible fibre source(purified wheat bran), and a soluble NSP (prepared from ispaghula husk).Crypt cell production rate in the terminal ileum and colon was unaffected bythe addition of inert bulk. Of the fibre sources, the most marked crypt cellproduction rates in terminal ileum and colon were seen when purified wheatbran was added to the diet."' Unfortunately, no firm conclusions could bereached as to the effect of soluble NSP as not all this diet was consumed.As outlined above (Figure) VFA's are the main products of colonic fibre

digestion. One of the implications of the study of Goodlad et al"' is that theproliferative effect of added fibre on the distal ileum and colon is related toits digestibility, and thence possibly VFA formation. It is of interesttherefore that other research shows that intraluminal VFA's stimulatecolonic mucosal proliferation.""°"' If the trophic effects of fibre are causedby VFA release, do they act directly or as a consequence of metabolitefunction or by some other systemic factor?Of the three VFA liberated during colonic fibre digestion, acetate,

propionate, and butyrate, butyrate is preferentially metabolised by isolatedcolonocytes."2 When butyrate (20 mmol/1) was infused for seven days intothe colon of caecectomised rats fed on fibre free elemental diets, colonicmucosal growth, as evidenced by changes in mucosal weight protein andDNA content, was stimulated as effectively as when a mixture of acetate 70mmolIl, propionate 25 mol/l, and butyrate 20 mmol/l was infused."3 Oneexplanation of these findings is that VFA's exert a direct trophic effect oncolonic epithelium, and that of the three, butyrate exerts the prominantrole.

Liberation of VFA's in the lumen of the right colon in man is associatedwith a lowering of luminal pH,29 and lowering of colonic luminal pHsimulates colonic mucosal proliferation.1"4 Other research shows that pectindiets115 and the intraluminal presence of VFA's"ll increase intestinal bloodflow, which may facilitate both small and large intestinal adaptation."7Finally, in the study of Goodlad etal,"0' crypt cell prolifeation rates at all sitesof the intestine correlated with plasma enteroglucagon concentrations.Enteroglucagon has been implicated in playing a role in promoting intestinalcell renewal.I""

Enteroglucagon secretory cells are localised predominantly in the colonand terminal ileum"' so it is possible that VFA's and specifically butyric acid,may exert their trophic effect by directly or indirectly stimulating release ofenteroglucagon.Rombeau and colleagues have recently moved forward to investigate the

effect of a pectin supplemented elemental diet on colonic anastomicintegrity'20 and on intestinal adaptation to massive small bowel resection,'2'both experiments being performed in the rat. In the colonic anastomosismodel, pectin significantly enhanced colonic mucosal cell proliferation andhigher pressures were required to disrupt the anastomosis in animals fed thepectin supplemented diet. 120 In the model of massive small bowel resection,clear evidence of enhanced intestinal adaptation was seen in animals fed thepectin supplemented diet.'2'

POTENTIAL AREAS OF CLINICAL APPLICATIONIn the animal studies discussed above the administration of fibre free enteral

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diets was generally associated with a maintenance or enhancement ofmucosal growth in the jejunum with a corresponding atrophy in the ileumand colon.0"' The addition of fibre appears to prevent the distal mucosalatrophy.'"" As yet no data are available concerning morphology, cellkinetics or function in the ileum and colon of normal subjects or patientswith normal gastrointestinal function receiving enteral nutrition. Althoughthere is a clear need to pursue this line of research, it would be premature toconclude in respect of ileal and colonic morphology and function that thereare clinically significant advantages of routinely prescribing fibre supple-mented enteral diets to patients with normal gastrointestinal function. Itshould be remembered that the small intestine and colon both havefunctional absorptive capacities far in excess of that normally required toassimilate nutrients, water and electrolytes. It would seem unlikely there-fore, that even if the administration of fibre free enteral diets to patients isfound to have a deleterious effect on morphology and function of the ileumand colon experimentally, that there will turn out to be any clinicallysignificant improvement of absorption or nutrients, water and electrolytes iffibre is added.Animal studies clearly show that when nutrition is provided solely by the

parenteral route intestinal atrophy occurs (see review 117). In the light ofthe experimental animal studies showing that supplementation of enteraldiets with fibre has a beneficial effect on ileal and colonic morphology'02-'08there would seem to be theoretical reasons for supposing that there might beadvantages to administering fibre supplemented enteral diets to patientswho have been receiving total parenteral nutrition. Again, however, moreresearch is needed before such a concept is applied in a wide clinical setting.In our experience it is actually rather unusual for patients who have receivedTPN to be fed enterally. This is so because when the decision is made to stopTPN, most patients have entered the anabolic phase of the metabolicresponse to the underlying injury,'22 gastrointestinal function is returning tonormal, and they are generally started on a normal diet.The experimental observation that pectin supplementation of a

chemically defined elemental diet has a beneficial effect on colonicanastomotic integrety'20 is certainly of interest, and has potential clinicalapplications in colonic surgery. At present, however, even the concept ofearly postoperative nutritional support is a controversial area.'23 Thus,although some benefits of routine early postoperative enteral feeding havebeen found, the clinical significance of these remains dubious.'23

Nutritionally inadequate short bowel syndrome

As discussed by Koretz,'23 nutritional support is required in patients with thenutritionally inadequate short bowel syndrome, and at least in the earlyphases of management, a predigested chemically defined 'elemental' diet isindicated.2 In the elegant animal study of Koruda et al'2' significantlyenhanced intestinal adaptation (1-3-2-fold) was seen in animals aftermassive small bowel resection who were fed on an elemental diet supple-mented with 2% citrus pectin as compared with a pectin free diet. Thenutritionally inadequate short bowel syndrome is a rare condition, and itmay be technically and practically impossible to confirm these experimentalfindings in patients. The management of these difficult cases demands that

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all possible steps be taken to manipulate the situation towards minimisingthe intestial loss of nutrients, fluid and electrolytes.'24 In the light of ourcurrent knowledge of the effects and mechanisms of action of pectin seriousconsideration could be given towards developing a pectin supplementedpredigested chemically defined elemental diet for these patients. Two pointsof caution are warranted, however: the first relates to the fact that in theanimal study discussed above'2' pectin supplementation was associated witha small but statistically significant diminution in nitrogen balance. This wascaused by increased faecal nitrogen losses probably as a consequence ofincreased excretion of bacteria or desquamated intestinal mucosal cells inthe faeces.34 Maintenance of body weight and serum albumin concentrationswere, however, unaffected.'2'The second point of caution relates to the fact that fibre supplementation

of enteral diets may have a deleterious effect on mineral absorption,7" and iffibre supplemented diets are to be developed for use in patients with thenutritionally inadequate short bowel syndrome, additional mineral supple-mentation may be required.

Enteral nutrition in Crohn's disease

Chemically defined 'elemental' diets have been shown to be as effectiveas corticosteroids in the treatment of acute exacerbations of Crohn'sdisease. 125 126 Various mechanisms as to how these diets influence the diseasehave been suggested. Improved nutritional status, exclusion of toxic dietaryfactors, the anergic properties of the diet and bowel rest have all beendiscussed.'2 126 The recent observation that atrophy of the ileal mucosaoccurs in animals fed Vivonex'02 raises an interesting possibility that thisproperty may in some way be beneficial in ileal Crohn's disease. Caution isrequired therefore before consideration is given to using fibre supplementedchemically defined elemental diets in patients with Crohn's disease.

Summary and conclusions

The recent launch of a number of fibre enriched polymeric diet in the UnitedStates and Europe has stimulated considerable interest in the topic of fibreand enteral nutrition, and several commercial concerns appear to be underconsiderable pressures from their consumers to produce similar products.As a means of identifying areas of potential application of fibre to enteral

nutrition some of the recent knowledge gained about the physical propertiesof dietary fibre and the processes involved in the intestinal assimilation offibre has been reviewed. Two areas of interest are identifiable. The firstrelates to the bulking properties of fibre and the application of this to theregulation of bowel function in enterally fed patients. It is clear from theclinical studies that have been reviewed that there remains a paucity ofcontrolled data, and a great deal more research is needed before widespreaduse of fibre supplemented diets can be supported. Perhaps of greater interestacademically is the potentially beneficial effects that appear to be exerted bythe VFA's, liberated as a consequence of colonic bacterial fermentation offibre, on morphology and function of ileal and colonic mucosa. Althoughthere are a number of potential applications of fibre supplemented enteraldiets in this area, more research is required before any firm recommenda-

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tions can be made about recommending their use. The one exceptionconcerns patients with the nutritionally inadequate short bowel syndrome.There does seem to be sufficient experimental evidence to suggest thatclinical studies should be commenced using a pectin supplemented pre-digested 'elemental' diet in these patients.

Overall therefore, one is forced to conclude that the increasing interestand use of fibre supplemented enteral diets is being driven more by marketthan scientific forces. Nevertheless, the promotion of these diets has alreadyprovided a powerful stimulus to the scientific community, and it remainsentirely possible that many of the potential applications of these diets will berealised in the near future.

D B A SILKCo-Director,Department of Gastroenterology and Nutrition,Central Middlesex Hospital,Acton Lane,London NWJO

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