The concept of prebiotic food ingredients is an important recent development in nutrition. The concept has attracted a great deal of attention, and many food ingredients (mainly dietary carbohydrates) have been claimed to be ‘prebiotic’. It is emphasised that in order to be called prebiotic, a compound should be: (1) non-digestible; (2) fermentable; (3) fermentable in a selective way. These properties should be demonstrated in human volunteers in at least two independent dietary intervention trials. On the basis of published and unpublished results, it is shown in the present paper that the way in which a prebiotic influences intestinal fermentation is the key to its physiological properties. This statement is illustrated mainly by considering an established group of prebiotics, the β(2–1) fructans. These linear molecules show a strong discontinuity in physicochemical properties as the chains become longer. The β(2–1) fructans with a chain length of up to ten monomer units are very soluble and are particularly ‘bifidogenic’. Longer chains (ten to sixty-five monomer units) are poorly soluble in water, they have less pronounced bifidogenic properties, and they are fermented more slowly. It was observed that a combination of short-chain and long-chain fructans (Synergy1) is physiologically (for example, increasing mineral absorption, suppressing carcinogenesis, modulating lipid metabolism, etc) more active than the individual fractions. A possible mechanism is described in the present review. From an in-depth overview of the literature it is confirmed that for prebiotic action, the ‘selectivity principle’ for intestinal fermentation is determinative for the type and for the efficiency of physiological activity. It is confirmed that prebiotics act through their influence on intestinal fermentation.

The human large intestine is recognised as a physiologically important organ responsible for the conservation of water and salts. Through its resident bacteria, it is also capable of complex, enzyme catalysed, hydrolytic-digestive functions that have a high biological impact on the host. These microorganisms metabolise dietary components, principally complex carbohydrates that are not hydrolysed or absorbed in the upper gastrointestinal tract, and in this way, sequester energy for the host, through fermentation. This process involves a series of anaerobic, energy-yielding, catabolic reactions which complete digestive processes in the gut, resulting in end products that in turn influence the distribution of microbial species present as well as having some systemic effects. Some of the bacteria are thought to possess important health-promoting activities, especially with respect to their influence on mucosal and systemic immune responses to disease. These bioactivities can be modulated by substrates that support and influence microbial development, growth and survival. For these reasons, it is necessary to review dietary factors that may delimit bacterial diversity, to be able to predict responses and sensitivities to various environmental pressures and manipulations that occur in this area of human microbiology.

Dietary polyunsaturated fatty acids (PUFA) reduce colonic proliferation and exert a mild laxative effect. We have studied the effect of the highly unsaturatede icosapentaenoic acid ethyl ester (EPA-EE) on the growth and metabolism of colonic bacteria in vitro, and in vivo. For the in vitro study, growth was assessed by viable counts. Bacteroides thetaiotaomicron was significantly inhibited in anaerobic media containing EPA-EE at concentrations > 7 g/I. Escherichia coli was apparently resistant even at 100 g/I. For the in vivo study, ten healthy volunteers ingested 18 g EPA-EE/d for 7 d. Stool frequency, 24 h stool weight and whole-gut transit time were assessed together with breath H2 and 14CO2 excretion following oral ingestion of 15 g lactitol labelled with 0·18 MBq [14C]lactitol. The area under the breath-H2-time curve was significantly reduced by EPA-EE, from a control value of 690·3 (SE 94·2) ppm.h to 449·5 (SE 91·7) ppm.h. Percentage dose of 14CO2 excreted, total stool weight and whole-gut transit time were unaltered, being respectively 24 (SE 2)%, 281 (SE 66) g and 45 (SE 4) h with EPA-EE v. control values of 27 (SE 1)%, 300 (SE 89) g and 42 (SE 5) h. It is concluded that dietary supplementation with EPA-EE reduces breath H2 excretion without apparently impairing overall colonic carbohydrate fermentation. The observed reduction may reflect utilization of H2 to hydrogenate the five double bonds of EPA-EE.