ClinicalNutrition (1993) 12 tSuppl,1): 5106-5113©Longman Group UKLtd1993

Fibre and enteral nutrition

D.S.A. SILKDepartment of Gastroenterology and Nutrition, Central Middlesex Hospital NHS Trust, Acton Lane,London NW10 7NS, UK

Introduction

Clinical experience during the last decade has con­finned that enteral nutrition is an efficient and costeffective means of providing nutritional support topatients with normal or near normal gastro-intestinalfunction (1). Before and during this period the knowl­edge gained of the processes involved in the physiol­ogy of nutrient absorption has been applied to theformulation of enteral diets; and if comparisons aremade of the composition of present day diets withthose used 10-15 years ago several differences can beseen. These relate mainly to the nitrogen and energyconcentrations of polymeric diets, and the sources ofnitrogen and energy and electrolyte compositions ofpredigested chemically defined elemental diets (2).

Until recently all the commercially produced liquidenteral diets continued to have one thing in common,namely that they contained a low residue or low'fibre' content. The very earliest low residue enteraldiets were specifically designed not only to providebalanced nutrition to astronauts in space, but also toreduce their stool weight and stool frequency (3).Subsequently it was realised that one clinical ad­vantage of low residue diets was that they had a lowviscosity and could be administered easily through'fine bore' nasogastric or nasoenteric feeding tubes.Furthermore as it became clear that there could evenbe a number of therapeutic advantages in administer­ing low residue diets (4) their widespread use becameaccepted without question.

Although the 1970s and early 1980s has been thetime when advances have been achieved in the field ofenteral nutrition the same period has seen also signi­ficant advances in the field of fibre research and as aconsequence there has developed a belief that manyof the diseases of western civilisation such as athero­sclerosis, obesity, appendicitis, constipation, irritablebowel syndrome, colon cancer, diverticular disease,diabetes mellitus and gallstones were related to a de­ficiency in dietary fibre, and that supplementing thediet with fibre would prevent and might even curethese conditions (5). Although not all recent studies(6) have been in complete agreement the observations

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made by Heaton and colleagues over 10 years ago(7, 8) that ingestion of bran accelerated slow intes­tinal transit and delayed rapid intestinal transit, leadto suggestions that the ingestion of fibre produces amore regular bowel habit (9).

Based largely on the above premise as well as onthe fashionable doctrine that dietary fibre was goodoverall, suggestions began to be made in the secondhalf of the 1980s that there could be benefits to sup­plementing commercially produced liquid enteraldiets with fibre.

In 1989, our Unit published the first major reviewon fibre and enteral nutrition (10). Attempts weremade to critically examine the premises on which theproposed use of fibre supplemented enteral diets werebased. The definition of dietary fibre was discussed(11), the physiology of dietary fibre assimilation re­viewed and particular attention was paid to discussingthe factors affecting the breakdown of non starchpolysaccharide (NSP) in man. Of importance in re­lationship to the clinical applications of fibre sup­plementation in enteral feeding was the fact thatnon-cellulosic polysaccharide (NCP) components ofdietary fibre are known to be degraded more effi­ciently than cellulose (11). The influence of importantphysical properties such as solubility (12), particlesize (13) and surface area (14, 15) on the degree ofdigestibility was emphasised as was the influence thatthe substrate inducibility of the colonic bacterialpolysaccharidase enzyme systems would likely toexert on fibre degradation (16). As a consequence ofthese discussions it was suggested that the physicalcharacteristics of the fibre sources being used clini­cally in enteral feeding were likely to rapidly degrade,not only because most were predominantly NCP, butbecause particle size was small (in order to over­come viscosity problems), and since only single fibresources were being employed, digestibility would in­crease with time, a situation which was envisagedduring long term administration of fibre supplementedenteral diets (10).

Two main areas of interest in fibre and enteral nu­trition were identified, namely effect on bowel func­tion and effects on small and large intestinal mucosal

cell morphology (16). A particular area of interestthat developed later, concerned with the effects offibre supplementation on mucosal barrier functionhas arisen. This article seeks to update progress thathas been made in these areas.

Fibre and enteral nutrition - effect on bowelfunction

Constipation

Studies of healthy volunteers have shown that the ma­jority of the population in the Western World pass onebowel movement per day with an average daily output120-130 g stool (17). Similar findings were reportedin normal subjects taking part in dietary studies andconsuming metabolically controlled diets (18). Largeindividual variation is seen, however, both in fre­quency and weight of bowel movements, withoutcomplaints of either constipation or diarrhoea (19).Such variability in normal bowel habit makes it diffi­cult to define an abnormal or constipated state andto date this basic difficulty has not been overcome(19).

Clinical studies in which fibre free defined formulaenteral diets have been administered to normalhealthy volunteers suggest that wet stool weights inthe range of 40-70 g/d in the norm with a daily stoolfrequency of 0.5-0.7 (20-23). Based on the knowneffects that increasing the intake of dietary fibre hason bowel function (10) most investigations havesought to show that supplementing fibre free enteraldiets with fibre results in increases in daily stool wetweights and transit time. Certainly these have beenthe main goals of investigators who have carried outstudies in normal healthy subjects as well as in stablemedical patients and those with psychiatric or neuro­logical disorders.

Although Slavin and colleagues (20) showed thatthe addition of 30 and 60 gld soy fibre to a fibre freedefined formula diet administered to normal healthyvolunteers resulted in significant increases in dailywet stool weight (60 g/d) and daily stool frequencythe findings of other studies carried out in normalhealthy volunteers have been less impressive (21).Direct comparisons of data are unwarranted however,as experimental designs have not been standardised.In our Unit, we have been interested in investigatingthe differential effects of readily metabolised and re­latively poorly metabolised fibre sources on bowelfunction of normal human volunteers fed fibre freeand fibre supplemented diets (24, 25). Positive effectshave been minimal even where a poorly metabolisedoat fibre source was studied (26).

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One interesting recent study (27) has shown that theadministration of a fibre free chemically defined el­emental diet to normal human volunteers resulted inthe passage of liquid stools in 60% of subjects. Theaddition of pectin (range 14.5-31.5 gld) abolished theliquid stools (27). Two controlled studies have beenperformed in stable medical patients (23, 28). Neitherthe addition of 24 gld carrot fibre nor 12.4 gld and38.5 g/d of soy polysaccharide fibre to fibre free liq­uid formulae resulted in any significant change in theparameters of bowel function studied.

In a prospective crossover study performed in 28mentally retarded young individuals suffering fromchronic constipation as a consequence of fibre freeenteral feeding, the addition of soy polysaccharide(15.6-17.4 g/d) for 2 weeks was without effect onstool weight, stool frequency or transit time (22). Ina subsequent study from the same Unit (29) a 1 yeartrial in 11 mentally retarded patients showed that sup­plementation of a fibre free liquid diet administeredvia gastrostomy with 18-25 gld soy fibre resulted in asignificant increase in stool weights (30 ± SD 13 g/dvs 87 ± g/d) and bowel frequency 0.6 ± 0.2 vs 1.1 ±0.5).

One final study carried out in patients with neuro­logical disorders (30) is difficult to interpret as themean wet stool weights in the patients receiving longterm tube feeding with a fibre free diet were muchhigher (142.6 g/d) than one would have expected. Therequirements of laxatives were reported to be signifi­cantly less when the patients received the same dietsupplemented with 12.8 gIL soy fibre.

One is forced to conclude as a consequence of theabove studies that the supplementation of fibre freedefined formula diets with a single fibre source resultsin only marginal benefits in respect of bowel functionand that the positive benefits shown are of question­able clinical significance. Rapidly degraded fibresources increase faecal weight by virtue of the factthat they stimulate growth of microflora within thecolon (31, 32). Poorly digested fibre on the otherhand, stimulates bacterial growth to a lesser degree,but survives to hold water (33). Poorly degraded fibreproduces larger faecal weights than equivalent supple­ments of more rapidly degraded fibre (19, 31). It isperhaps hardly surprising therefore that the studiesdescribed above, most of which have employed theuse of well degradable small particle sized singlesources of predominantly non cellulosic polysaccha­ride containing fibre, have produced such modestimprovements in bowel function.

If in the future, there remains a demand to improvebowel function in patients receiving long term enteralfeeding then a different strategy will be required.

lOH FIBRE AND ENTERAL NUTRITION

Possibilities would seem to include the use of multi­ple fibre sources that in tum should be varied toovercome the problem of substrate inducibility ofthe colonic bacterial polysaccharidase enzyme sys­tems (16). Consideration might be given to the use ofmore poorly degraded fibre sources. Caution is re­quired though as the oat fibre studied by our group(26) was without effect on bowel function, and theuse of cellulose as a fibre supplement resulted in theproduction of hard pellety stools that were painfullydifficult to pass (34). Much innovative thinking andresearch will be required before the problems of slug­gish bowel function and low stool weights in patientson long term enteral feeding are overcome.

Diarrhoea

Diarrhoea is a significant problem in enteral nutrition.According to basic physiological principles, whichtake into account the capacity of the normal small andlarge intestine to assimilate fluid and electrolytes, di­arrhoea can be defined as the passage of more than200 g of stool/24 h on an average Western diet (35). Itfollows that the diagnosis of diarrhoea is dependenton accurate measurements of stool outputs, hardly afeasible proposition in uncooperative enterally fedpatients with faecal incontinence. For the purposes ofour clinical studies we have therefore defined enteralfeeding related diarrhoea as the passage of too fre­quent stools or stools of too loose a consistency thatare of inconvenience to the nursing staff and/or thepatient (36, 37). In our original experience, diarrhoeaso defined, occurred in up to 25% of patients receiv­ing enteral nutrition (38). A number of factors havebeen implicated in its pathogenesis (1). These includeuse of infected feeds, lactose intolerance, intoleranceof high osmotic loads of nutrients administered, in­appropriate release of gastro-intestinal polypeptidehormones, concomitant antibiotic therapy, ingestionof laxatives, and hypoalbuminaemia.

The role of lactose intolerance in the pathogenesisof the diarrhoea has been discussed in some detail (1).In brief, the deleterious effect of lactose in enterallyfed patients with lactose intolerance will depend onthe load (concentration x rate) of lactose adminis­tered. Bolus feeding in lactose intolerant patients re­sults in the production of stool volumes in excess of1 1/24 h (39). In contrast, when a low load of lactoseis presented to the upper small intestine, as occursduring constant 24-h intragastric infusion of liquidlactose containing diets, diarrhoea does not occur(36). In a prospective controlled trial of continuous24-h nasogastric infusion of polymeric diets to pa­tients with normal or near normal gastro-intestinal

function, the development of diarrhoea was not re­lated to osmotic load of nutrients presented for ab­sorption but to concomitant antibiotic therapy (37) anabservation that has subsequently been confirmed(40,41).

Animal studies carried out in our laboratory havenot confirmed that the onset of diarrhoea is relatedto an inappropriate release of gastro-intestinal poly­peptide hormones (42). Finally, hypoalbuminaemiahas been related to the development of diarrhoea (43).

Disappointed that so little progress was being madein achieving a greater understanding of the pathogen­esis of enteral feeding related diarrhoea, we haveundertaken a series of intubation studies in normalhuman subjects receiving continuous intragastric orintraduodenal enteral feeding. For the first series ofexperiments we devised and validated a multilumenorocaecal intubation technique that has permittedthe study of small intestinal motility responses to theenteral feeding as well as permitting quantitative ofcolonic inflows of nutrients, water and electrolytes(44,45). Intraduodenal infusion of different loads of apolymeric enteral diet evoked a normal post prandialsmall bowel motility response, and colonic inflowvolumes even during infusion of high nutrient loadsfell within the functional absorptive capacity of thecolon. In contrast, intragastric diet infusion was as­sociated with a persistence of fasting small intestinalmotility. Despite this, colonic inflow volumes werelow and not significantly greater than fasting values.A number of those subjects however, developed diar­rhoea during the course of the experiments (44, 45).Clearly, diarrhoea occurring in this experimental set­ting could not be explained on the basis of disturbedsmall intestinal physiology, and the findings pointedtowards a colonic basis to this important clinicalcomplication of enteral nutrition (46).

Further experiments are currently being undertakento investigate colonic function during enteral feeding.Preliminary results show evidence of water secretionin the ascending colon during intragastric enteralfeeding (47). This may tum out to be an importantfinding and even the clue to the pathogenesis of en­teral feeding related diarrhoea. The ascending colon isthe major site of fibre degradation (48). It is also themajor site of short chain fatty acid(SCFA) absorp­tion (49). SCFAs act as a powerful stimulus to colonicwater and electrolyte absorption (50).

Could it be therfore that diarrhoea occurs duringenteral feeding because the administration of fibrefree defined formula diets results in impaired colonicSCFA production which in some instances is somarked as to result in impaired colonic absorption offluid and electrolytes? If this was the case, there could

become an important basis to supplementing definedformula diets with a rapidly degradable fibre sourceto enhance colonic SCFA production. A number ofstudies have already been carried out to investigatewhether fibre supplementation of enteral diets resultsin a reduced incidence of enteral feeding relateddiarrhoea (40, 41, 51, 52). All were carried out in pa­tients in intensive care units, and none showed a sig­nificant benefit. Intensive care unit patients howeverare nearly always receiving concomitant antibiotictherapy and indeed in two of the studies (40, 41),there was a correlation between diarrhoea and theadministration of antibiotics.

Recently we have shown that antibiotics markedlyinhibit the bacterial fermentation of fibre (24). It re­mains possible therefore that enteral feeding relateddiarrhoea occurs as a consequence of impaired co­lonic SCFA production and that if this is the case fibresupplementation may have a very beneficial effectas long as the patients are not receiving concomitantantibiotic therapy. If future research confirms thishypothesis then a method other than fibre supplemen­tation of enteral diets will have to be devised toincrease colonic luminal SCFAs of patients on anti­biotic therapy.

Enteral diets and intestinal epithelial cellproliferation

Experimental studies

The intestinal epithelium can respond to a wide vari­ety of stimuli by altering its proliferative rates (53,54). There is now a large and interesting literature onthe effect of low residue liquid enteral diets on intes­tinal morphology, cell turnover kinetics and function.Almost all experiments have been performed in therat, and low residue chemically defined elemental di­ets and polymeric diets have been studied. In general,in the jejunum, intestinal mass is maintained or in­creased (55-58) the specific activity of brush borderhydrolase activity maintained (55, 56), or increased(57) DNA synthesis rates maintained (55) and absorp­tive function maintained (58). In shall) contrast, ad­ministration of these low residue diets is associatedwith pronounced atrophy in the ileum (55-58) andcolon (55, 59), compared with the feeding of a normalfibre containing rat chow diet.

As fibre has been shown experimentally to have aproliferative effect on intestinal epithelium (60, 63).Suggestions have been made that the atrophy and re­duced intestinal proliferation seen in rats fed on liquidenteral diets because of the lack of fibre in these diets(58, 59, 64). To prove this hypothesis it would be

CLINICAL NUTRITION 109

necessary to compare the responses of ileal and co­lonic epithelia to the same liquid enteral diet fed inthe absence and presence of added fibre. Results ofpublished studies in general are supportive. Ryan andcolleagues showed that cellulose and petroleum jellyadded to an oral liquid fibre free diet resulted in sig­nificant increases in colonic weight and DNA synthe­sis rates compared with values seen when the fibrefree diet was fed (59). When the same liquid poly­meric diet with and without 9% added bulk was ad­ministered orally to rats for 4 weeks, however, thetotal weight of ileal segments were similar (58). Inthe most comprehensive study to date, Goodlad andcolleagues (64) have studied crypt cell production ratein starved rats re-fed a liquid elemental enteral dietsupplemented with very large (1:1) quantities of dif­ferent fibre sources, inert bulk (kaolin), a poorly di­gestible fibre source (purified wood cellulose), a morereadily digestible fibre source(purified wheat bran),and a soluble NSP prepared from ispaghula husk).Crypt cell production rate in the terminal ileum andcolon was unaffected by the addition of inert bulk. Ofthe fibre sources, the most marked crypt cell produc­tion rates in terminal ileum and colon were seen whenpurified wheat bran was added to the diet (64). Un­fortunately, no firm conclusions could be reached asto the effect of soluble NSP as not all this diet wasconsumed.

One of the implications of the study of Goodlad etal (64) is that the proliferative effect of added fibre onthe distal ileum and colon is related to its digestibility,and thence SCFA formation. It is of interest thereforethat other research shows that intraluminal volatilefatty acids (VFAs) stimulate colonic mucosal pro­liferation (65, 67). Definitive proof that the trophiceffects of fibre are due to the products of fibre degra­dation rather than fibre per se was gained from studiesperformed in germ free rats, in whom no effect offibre on colonocyte proliferation was seen (68).

Of the three major SCFA liberated during colonicfibre digestion, acetate, propionate and butyrate, bu­tyrate is preferentially metabolised by isolated colo­nocytes (69). When butyrate (20 mmol/l) was infusedfor 7 days into the colon of caecectomised rats fed onfibre free elemental diets, colonic mucosal growth, asevidenced by changes in mucosal weight protein andDNA content, was stimulated as effectively as when amixture of acetate 70 mmol/l, propionate 25 mmol/l,and butyrate 20 mmol/l was infused (70).

These experimental animal findings suggest thatSCFAs exert a direct trophic effect on colonic epi­thelium, and that of the three major SCFAs, butyrateexerts the prominent role. These findings have re­cently been confirmed in man (71); in vitro incubation

110 FIBRE AND ENTERAL NUTRITION

studies showed that to mmol/l butyrate stimulatedDNA synthesis to the same extent as a SCFA mixture.

Effect of SCFA in experimental post-operativeconditions

Rambeau and colleagues have recently moved for­ward and undertaken a series of animal studies to in­vestigate the effects of fibre and SCFAs on colonicanasto~otic int~grity and an intestinal adaptationfollow ing massive small bowel resection (72-74) .In the colonic anastomosis model, pectin significantlyenhanced colonic mucosal cell proliferation andhigher pressures were required to disrupt the anasto­mosis in animals fed a pectin supplemented diet (72).Colonic infusion of SCFAs was then shown to ac­celerate wound healing after colonic transection andre-anastomosis (73). Spontaneous anastomotic dehis­cence was significantly less in the SCFA than in thecontrol group and, as with pectin, the suture line burstin fewer colons from the SCFA group when tensionwas applied to the bowel wall (73).

In their model of massive (80%) small bowel resec­tion , the addition of pectin to a fibre free chemicallydefined elemental diet significantly enhanced smallintestinal and colonic adaptation (74). Interestingly,~nder the same experimental conditions, parenterallymfusedSCFA led to a significant enhancement of theadaptive response only in the jejunum and ileum andnot in the colon (75). The most recent animal studiesreported by this group indicate that the trophic effectsof SCFAs on the colon are luminally and not pa­renterally mediated (76).

The evidence summarised above suggests thatthere could be advantages in incorporating a rapidlydegradable fibre source in defined formula enteraldiets. The proliferative effects of fibre are howeverrelated to the production of the end products offermentation, namely SCFAs. Clinicians should bewary therefore of assuming that advantages of fibresupplemented diets will accrue in patients receivingantibiotic therapy.

Fibre and gut barrier function

There is much evidence in the old literature that star­vation results in atrophy of the villous architecture.Similar findings have been described during long termparenteral nutrition in animals (77) and in the seg­ments o~ human small intestine surgically bypassedfor obesity (78). The lack of luminal nutrit ion plays a

pivotable role in producing these change, presumablyby inhibiting the production of hormones acting onthe gut.

Although the knowledge that depriv ing the gut ofluminal nutrition has a deleterious effect on intestinalmorphology has provided a powerful argument forproviding nutritional support where ever possible viathe enteral rather than the parenteral route the storydoes not end here. Changes in intestinal morphologyhave been shown to be associated with changes inbarrier function. Thus, not only does parenteral nutri­tion adversely affect the morphology of experimentalanimals but it is also associated with the pas sage ofviable bacteria from the gastro-intestinal tract tootherwise sterile tissue such as mesentery lymphnodes (MLN) liver and spleen (79), a phenomenonthat is known as bacterial translocation. Experimentalstudies show that bacterial translocation occurs to asignificantly lesser extent in animals receiving enteralrather than parenteral feeding (77).

Bacterial translocation has now been shown tooccurr in experimental animals submitted to a numberof stimuli including bums, trauma, sepsis, mesentericischaemia and intestinal bacterial overgrowth (80).Bacterial translocation can be potentiated by prote inm~lnutri.ti?n (81) and specifically by essential fattyacid deficiency (82). There is now experimental evi­dence to show that partial loss of intestinal barrierfunction may be reversed by luminal nutrition eitherin the form of oral nutrition (83) or as suggested insome experiments by glutamine alone (84).

Although the clinical significance of bacterialtranslocation is unclear, translocating bacteria havebeen hypothesised as a potential source of sepsis incritically ill patients. If this hypothesis is correct thenthe protective effects of luminal nutrition so far dem­onstrated may tum out to be of unparalled importancebecause it will elevate the status of enteral nutrition atleast in critically ill patients, from supportive to pri­mary therapy.

Clearly one important question that arises whenconsidering concepts of fibre and enteral nutrition iswh~ther there is any evidence that fibre or its degra­dation p~oducts ~ave any specific effects in madifyinggut barr ier funct ion. Experiments today prov ide inter­esting but conflicting data. The addition of celluloseto an orally administered total parenteral nutrition so­lution reduces the incidence of bacterial translocationin experimental animals (85). In a similar experimen­tal model citrus pectin exhibited no such effect (86).1.'he addition of corn cobs but not soy fibre to a de­fined fibre free formula diet in a further study reducedthe ~anslocation. rate significantly (87). Neither glu­tamme nor psyllium fibre when added to a fibre free

formula diet protected effectively against spontaneousor endotoxin induced bacterial translocation (88).

Clearly, therefore, much further work is needed inthis area, but there is much preliminary evidence tosuggest that the addition of fibre to fibre free definedformula diet may exert a beneficial effect an gut bar­rier function.

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