Dietary Fibre and Prebiotics

April 2013

Dietary fibre intake is asso­ciated with a myriad of health benefits. (Scott et al., 2008, Maayan Elad & Lesmes, 2012) Among others, their fer­men­tation by the micro­biota results in the for­mation of short chain fatty acids, which protect against patho­genic bac­teria. Tog­ether with dietary fibres, pre­biotics are colonic nut­rients but pre­biotics are degraded and uti­lized only by bene­ficial bac­teria, namely bifi­do­bac­teria and/​or lac­to­ba­cilli. (S. Mac­farlane, 2010)

Ger­linda Bellei, Alex­ander Haslberger*

It is becoming incre­asingly accepted that the colonic micro­biota is of key importance to health and well-​being of the host. (Wallace et al., 2011)The growth and meta­bolism of the indi­vidual bac­terial species resident in the large intestine, espe­cially in the large bowel, depends pri­marily on the sub­strates available to them, which come from the diet. (G. T. Mac­farlane & Cum­mings, 1999) The human adult colon is the most densely popu­lated region where at least 50 genera of bac­teria, com­prised of about 400 to 500 dif­ferent species, reside. In a healthy gut there is a balance between poten­tially harmful and bene­ficial bac­teria. (Gibson & Rober­froid, 1995) (Wallace et al., 2011) (Patel & Goyal, 2012) Lac­to­ba­cilli and bifi­do­bac­teria are con­sidered to be bene­ficial with many health pro­moting pro­perties which can be modu­lated by sub­strates obtained from diet. (Rabiu & Gibson, 2002)

Dietary fibre

Today, there is no single defi­nition for dietary fibre that is accepted worldwide. (Lunn & Buttriss, 2007) Dietary fibre includes polys­ac­cha­rides, oli­gos­ac­cha­rides, lignin and asso­ciated plant sub­s­tances. Dietary fibre pro­motes bene­ficial phy­sio­lo­gical effects including laxation, and/​or blood cho­le­sterol atte­nuation, and/​or blood glucose atte­nuation. (Buttriss & Stokes, 2008) Fibres occur with dif­ferent degrees of poly­me­rization which is usually defined as the number of mono­meric units. (Gibson & Rober­froid, 1995) Dietary fibre as for example cel­lulose, hemic­el­lulose, pectin, lignin, inulin or oli­go­fructose, which are natu­rally occurring in many foods like fresh vege­tables and fruits, whole grains, legumes and nuts, reach the large bowel and are prin­cipal sub­strates for fer­men­tation by dif­ferent bac­terial species. Fur­thermore they can be clas­sified in terms of soluble/​insoluble, fermentable/​non-​fermentable, and viscous/​non-​viscous, which form the bases of the phy­sio­lo­gical benefits. (Li & Uppal, 2010) Soluble fibres (e.g. Inulin, oli­go­fructose, pectin) dis­solve in water, forming viscous gels and in general are more readily fer­mented and are earlier in the colon. (Blackwood et al., 2000); (Lat­timer & Haub, 2010) Inso­luble fibres (e.g. Cel­lulose, hemic­el­lulose, lignin) are not water soluble, do not form gels and their fer­men­tation is severely limited. (Lat­timer & Haub, 2010) The phy­sio­lo­gical effects of fibres depend on the type (par­tially or highly fer­men­table), the dose of a spe­cific fibre con­sumed and the indi­vidual phy­sio­lo­gical profile of the subject con­suming the fibre-​containing meal. (Tungland & Meyer, 2002)


The two main types of anae­robic fer­men­tation that are carried out in the gut are pro­te­olytic and sac­cha­ro­lytic, the latter being more dominant. Some meta­bolites resulting from protein breakdown (e.g. NH3, indol, cresol, H2S) may be con­sidered as poten­tially adverse to health. (Blaut, 2002) The process of fer­men­tation can be described as an inter­action where bac­teria obtain the sub­strates that they need for growth from the host and return their by-​products of their meta­bolism. (Gibney et al., 2009) Fibre par­ticle size and degree of solu­bility have a con­siderable effect on sus­cep­ti­bility of fibres to bac­terial fer­men­tation. (Gibson, 2004) The bac­teria in the colon can syn­thesize many dif­ferent types of sac­cha­ro­lytic enzymes (e.g. polys­ac­cha­ri­dases, glu­co­si­dases) and are able to degrade poly­me­rized car­bo­hy­drates. (Bernalier-​Donadille, 2010) The end-​product of fer­men­tation is pyruvate, which is further con­verted to short chain fatty acids (SCFA), prin­ci­pally acetate, pro­pionate and butyrate. (Gibney et al., 2009) Between 10 and 60 g of dietary car­bo­hy­drates reach the colon every day. The major con­tri­bution comes from non-​digested polys­ac­cha­rides (resistant starch). (Rabiu & Gibson, 2002)

Short-​chain fatty acids (SCFA)

The health pro­moting SCFA´s are acetate, pro­pionate and butyrate which all act to lower the colonic pH. The impact of each of them differs, but all of them play a vital role in the main­tenance of colonic inte­grity and meta­bolism. (Scott et al., 2008) Acetate, pro­pionate and butyrate are rapidly absorbed in dif­ferent regions in the colon into the portal blood and about 10–15% are excreted with feces. Acetate, the prin­cipal SCFA in the colon, is used as a fuel for muscle tissues, the heart and the brain. (Olm­stead et al., 2008) Pro­pionate is a primary pre­cursor for glu­co­neo­ge­nesis but the exact meta­bolism of pro­pionate in humans is less understood. (Hijova & Chme­larova, 2007) Butyrate is accepted as the most important SCFA in the colo­nocyte meta­bolism because it pro­vides the cells of the intestine with a meta­bolic fuel and may be a pro­tective factor for the health of these cells. (Cook & Sellin, 1998) Further it has been shown to induce apo­ptosis in colonic cancer cell lines and exert a level of control over the cell cycle. This sug­gests that butyrate might play a necessary role in pre­venting the uncon­trolled pro­li­fe­ration of abnormal cells that occurs in the early stages of colo­rectal cancer. Increased dietary fibre intake and thus enhanced butyrate pro­duction is asso­ciated with a reduced risk of colon cancer. (Lunn & Buttriss, 2007) Aci­di­fi­cation of the gut by SCFA´s may modify the meta­bolism of bile acids. The con­version of primary bile acids to secondary bile acids, as these are believed to be asso­ciated with increased risk of colon cancer, may be reduced. (Tungland & Meyer, 2002)

The reduced pH creates an unfa­vourable envi­ronment (Lunn & Buttriss, 2007) that impedes the growth of certain harmful bac­terial species, par­ti­cu­larly ente­ro­bac­te­riacae, while encou­raging the growth of health-​promoting genres. (Gibson & Rober­froid, 1995)

Signi­ficant amounts of minerals may be absorbed throughout the length of the gut. (Venter, 2007) Studies indicate that highly fer­men­table car­bo­hy­drates (e.g. pectin, inulin, oli­go­fructose) have resulted in improved meta­bolic absorption of certain minerals, such as calcium, magnesium and iron. Pre­do­mi­nantly butyrate enlarges the absorption surface by pro­moting pro­li­fe­ration of ente­ro­cytes and in addition the low pH dis­solves inso­luble mineral salts and increases their dif­fusive absorption via the paracel­lular route. (Tungland & Meyer, 2002)

Definition of prebiotics and its Origins

Even though all non-​digestible car­bo­hy­drates can all be clas­sified as “colonic foods”, not all are pre­biotics. (Gibson & Rober­froid, 1995) The terms dietary fibre and pre­biotics are often used inter­ch­an­geably but what distin­gu­ishes pre­biotics from other fibres is that pre­biotics sel­ec­tively sti­mulate the growth of only bene­ficial micro­floral micro­or­ga­nisms. Pre­biotics the­r­efore are unique dietary fibres that pref­en­tially promote the growth and/​or meta­bolic activity of species that con­tribute to health benefits. (Olm­stead et al., 2008) They highly sti­mulate bac­terial fer­men­tation, resulting in the repli­cation and sti­mu­lation of bifi­do­bac­teria and lac­to­ba­cilli and the for­mation of SCFA. (Venter, 2007) Bifi­do­bac­teria are a part of a stable adherent micro­biota that helps to maintain the mucosal barrier. (Fahey, 2010) When bifi­do­bac­teria grow on pre­biotic sub­strates they see­mingly do so at the expense of bac­te­roides, clos­tridia and coli­forms. (Gibson & Rober­froid, 1995)

The term “pre­biotic” was first coined and intro­duced in 1995 by Glenn Gibson and Marcel Rober­froid, who exch­anged “pro” to “pre” which means “before”. (Aida et al., 2009) The defi­nition was updated in 2004 when pre­biotics were defined as “sel­ec­tively fer­mented ingre­dients that allow spe­cific changes, both in the gas­tro­in­testinal micro­flora that confer benefits upon host well-​being and health.” The defi­nition con­siders micro­flora changes in the whole gas­tro­in­testinal tract and as such extra­po­lates the defi­nition into other areas that may benefit from a sel­ective tar­geting of bifi­do­bac­teria and lactobacilli.

The cri­teria used for clas­si­fi­cation of a food ingre­dient as a pre­biotic are as follows:

  • Resis­tance to digestive pro­cesses in the upper gas­tro­in­testinal tract
  • Fer­men­tation by gas­tro­in­testinal microbiota
  • Sel­ective sti­mu­lation of growth and/​or activity of bene­ficial bac­teria which are asso­ciated with health and well-being.

Established prebiotics

According to Gibson and Rober­froid only the inulin-​type fructans, namely inulin and oli­go­fructose, are proven pre­biotics which fulfill all three cri­teria, notably the last cri­teria. The final demons­tration of pre­biotic attri­butes should of course not only include in vitro tests but also in vivo nut­ri­tional feeding trials in tar­geted species (humans, animals) using vali­dated metho­do­logies that are sup­ported by sound science. Other can­di­dates (e.g. resistant starch, pectin, cel­lulose, β‑glucan) have the potential to act as pre­biotics, but current con­fir­matory evi­dence in humans is scant or even absent and more studies are required. (Gibson & Rober­froid, 2008) However, oligo­ga­lactose and lac­tulose are regarded as estab­lished pro­biotics as well as sum­ma­rized in table 1.

Inulin and oli­go­fructose are members of a larger group called “fructans”. Fructans are linear or branched oligo- or polys­ac­cha­rides com­posed of fructose moities linked by β-(2→1) gly­co­sidic bonds. (Kelly, 2008) Inulin is com­posed of a mixture of oligo- and polymers in which the degree of poly­me­rization varies from 2 to 60. For the inulin content of various plants see table 2. Oli­go­fructose is defined as having a chain length no longer than 9 fructose mole­cules. (Rober­froid, 2007) Fruc­tooli­gos­ac­cha­rides (FOS) and olig­fructose are often used inter­ch­an­geably but FOS are syn­thetic oli­gos­ac­cha­rides. (Olm­stead et al., 2008) The spe­ci­ficity of bifi­do­bac­teria for inulin and oli­go­fructose are likely due to the pro­duction of several enzymes that are par­ti­cu­larly suited to meta­bo­lizing oli­gos­ac­cha­rides, including β‑fructofuranosidases. (Gibson & Rastall, 2004)

The volume of the increase in bifi­do­bac­teria numbers is related to the size of the person´s intestinal bifi­do­bac­teria popu­lation prior to pre­biotic tre­atment. The daily dose is thus, by itself, not a deter­minant for its pre­biotic effect. (Gibson & Rober­froid, 2008) A recom­mended daily dose for pre­biotics has not been estab­lished. Some results of cli­nical trials suggest an optimal and well-​tolerated daily dose of 7–10 g/​day that increases bifi­do­bac­teria and lac­to­ba­cilli popu­la­tions, but bifido­genic effects have also been observed at lower doses (e.g. 4 g/​day). (Olm­stead et al., 2008)


Today only inulin and oli­go­fructose are proven pre­biotics. (Gibson & Rober­froid, 2008) They have the potential to elevate indi­genous bifi­do­bac­teria and lac­to­ba­cilli levels in the colon and thus influence the whole body´s phy­siology and con­se­quently health and well-​being. (Conway, 2001) Inulin and oli­go­fructose are found in a number of vege­tables and plants. Most of the eaten food-​stuffs like wheat, onions, garlic, leeks, artichokes or bananas have tiny amounts of inulin and oli­go­fructose, thus ade­quate con­sumption of vege­tables, fruits and whole-​grains should be war­ranted. (Gibson & Rober­froid, 2008) The concept of pre­biotics is 17 years old and is still a rela­tively new field of study. (S. Mac­farlane et al., 2006) There are still great defi­ci­encies in our know­ledge of the exact mecha­nisms of pre­biotic action and their invol­vement in disease pro­cesses. (Sandra Mac­farlane, 2010) New deve­lo­p­ments in mole­cular tech­niques for micro­bio­lo­gical ana­lysis will allow the acqui­sition of defi­nitive infor­mation on species rather than genera that are influenced by a test car­bo­hy­drate. Maybe then the picture will become clearer for clas­si­fying certain car­bo­hy­drates where evi­dence is curr­ently sparse or absent (e.g. RS) (Gibson & Rober­froid, 2008)


* Univ.-Doz. Dr. Alex­ander Hasl­berger, Department for Nut­ri­tional Sci­ences, Uni­versity of Vienna,


Aida, F. M. N. A., Shuhaimi, M., Yazid, M., & Maaruf, A. G. (2009). Mushroom as a potential source of pre­biotics: a review. Trends in Food Science & Tech­nology, 20(11–12), 567–575.

Bernalier-​Donadille, A. (2010). Fer­men­tative meta­bolism by the human gut micro­biota. Gas­troen­té­ro­logie Cli­nique et Bio­lo­gique, 34, Sup­plement 1(0), S16-​S22

Blackwood, A. D., Salter, J., Dettmar, P. W., & Chaplin, M. F. (2000). Dietary fibre, phy­si­co­che­mical pro­perties and their rela­ti­onship to health. The Journal of the Royal Society for the Pro­motion of Health, 120(4), 242–247

Blaut, M. (2002). Rela­ti­onship of pre­biotics and food to intestinal micro­flora. European Journal of Nut­rition, 41(0), 11–16.

Buttriss, J. L., & Stokes, C. S. (2008). Dietary fibre and health: an overview. Nut­rition Bul­letin, 33(3), 186–200

Conway, P. L. (2001). Pre­biotics and human health: The state-​of-​the-​art and future per­spec­tives. 2001, 45, 7–451.

Cook, S. I., & Sellin, J. H. (1998). Review article: short chain fatty acids in health and disease. Ali­mentary Phar­ma­cology & The­ra­peutics, 12(6), 499–507.

Elia, M., & Cum­mings, J. H. (2007). Phy­sio­lo­gical aspects of energy meta­bolism and gas­tro­in­testinal effects of car­bo­hy­drates. Eur J Clin Nutr, 61(S1), S40-​S74.

Fahey, G. C. (2010). The effects of Inulin on Gut Health and Bifi­do­bac­terial Popu­la­tions in the Colon. US Gas­tro­en­te­rology & Hepa­tology Review, 6, 58–63.

Gibney, M., Vorster, H., & Kok, F. (2009). Intro­duction to Human Nut­rition Digestion and meta­bolism of car­boyh­drates (pp. 384).

Gibson, G. R. (2004). Fibre and effects on pro­biotics (the pre­biotic concept). Cli­nical Nut­rition, Sup­plement, 1(2), 25–31.

Gibson, G. R., & Rastall, R. A. (2004). When we eat, which bac­teria should we be feeding? Ame­rican Society for Micro­biology News, 70(5), 224–231.

Gibson, G. R., & Rober­froid, M. (2008). Handbook of pre­biotics: CRC Press, Taylor and Francis Group. 7–451

Gibson, G. R., & Rober­froid, M. B. (1995). Dietary Modu­lation of the Human Colonic Micro­biota: Intro­ducing the Concept of Pre­biotics. The Journal of Nut­rition, 125(6), 1401–1412.

Hijova, E., & Chme­larova, A. (2007). Short chain fatty acids and colonic health. Bratisk Lek Listy, 108(8), 354–358.

Kelly, G. (2008). Inulin-​Type Pre­biotics – A Review: Part 1. 13(4), 15.

Lat­timer, J. M., & Haub, M. D. (2010). Effects of Dietary Fiber and Its Com­ponents on Meta­bolic Health. Nut­rients, 2(12), 1266–1289.

Li, C., & Uppal, M. (2010). Canadian Dia­betes Asso­ciation National Nut­rition Com­mittee Cli­nical Update on Dietary Fibre and Diabete: Food sources to phy­sio­lo­gical effects. [Review]. Canadian Journal of Dia­betes, 34(4), 355–361.

Lunn, J., & Buttriss, J. L. (2007). Car­bo­hy­drates and dietary fibre. Nut­rition Bul­letin, 32(1), 21–64

Maayan Elad, A. & Lesmes, U. (2012) Nut­ri­tional Pro­gramming of Pro­biotics to Promote Health and Well-​Being, Everlon Cid Rigobelo (Ed.), Chapter 2, 37–54

Mac­farlane, G. T., & Cum­mings, J. H. (1999). Pro­biotics and pre­biotics: can regu­lating the acti­vities of intestinal bac­teria benefit health? BMJ, 318(7189), 999‑1003.

Mac­farlane, S. (2010). Chapter 10 – Pre­biotics in the Gas­tro­in­testinal Tract. In W. Ronald Ross & R. P. Victor (Eds.), Bio­active Foods in Pro­moting Health (pp. 145–156). Boston: Aca­demic Press.

Mac­farlane, S., Mac­farlane, G. T., & Cum­mings, J. H. (2006). Review article: pre­biotics in the gas­tro­in­testinal tract. Ali­mentary Phar­ma­cology & The­ra­peutics, 24(5), 701–714.

Olm­stead, S., Wolfson, D., Meiss, D., & Ralston, J. (2008). Under­standing pre­biotics. 1–8

Patel, S., Goyal, A. (2012) The current trends and future per­spec­tives of pre­biotics research: a review, 3 Biotech, Vol. 2(2), 115–125

Rabiu, B. A., & Gibson, G. R. (2002). Car­bo­hy­drates: A limit on bac­terial diversity within the colon. Bio­lo­gical Reviews of the Cam­bridge Phi­lo­so­phical Society, 77(3), 443–453.

Rober­froid, M. (2007). Pre­biotics: The Concept Revi­sited. The Journal of Nut­rition, 137(3), 830–837.

Scott, K. P., Duncan, S. H., & Flint, H. J. (2008). Dietary fibre and the gut micro­biota. Nut­rition Bul­letin, 33(3), 201–211.

Tungland, B. C., & Meyer, D. (2002). Non­di­ges­tible Oligo- and Polys­ac­cha­rides (Dietary Fiber): Their Phy­siology and Role in Human Health and Food. Com­pre­hensive Reviews in Food Science and Food Safety, 1(3), 90–109.

Venter, C. S. (2007). Pre­biotics: un update. Journal of Family Ecology and Con­sumer Sci­ences, 35, 17–25.

Wallace, T.C., Guarner, F., Madsen, K., Cabana, M.D., Gibson, G.R., Hentges, E., Sanders, M.E. (2011) Human gut micro­biota and its rela­ti­onship to health and disease, Nut­rition Reviews Vol. 69(7), 392–403