The 'gold standard' method for the measurement of total dietary fibre is that of the Association of Official Analytical Chemists (2000; method 985.29). This procedure has been modified to allow measurement of soluble and insoluble dietary fibre, and buffers employed have been improved. However, the recognition of the fact that non-digestible oligosaccharides and resistant starch also behave physiologically as dietaryfibre has necessitated a re-examination of the definition of dietary fibre, and in turn, a re-evaluation of the dietary fibre methods of the Association of Official Analytical Chemists. With this realisation, the American Association of Cereal Chemists appointed a scientific review committee and charged it with the task of reviewing and, if necessary, updating the definition of dietary fibre. It organised various workshops and acceptedcomments from interested parties worldwide through an interactive website. More recently, the (US) Food and Nutrition Board of the Institute of Health, National Academy of Sciences, under the oversight of the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, assembled a panel to develop a proposed definition(s) of dietary fibre. Various elements of these definitions were in agreement, but not all. What was clear from both reviews is that there is an immediate need to re-evaluate the methods that are used for dietary fibre measurement and to make appropriate changes where required, and to find new methods to fill gaps. In this presentation, the 'state of the art' in measurement of total dietary fibre and dietary fibre components will be described and discussed, together with suggestions for future research.

The aim of our study was to investigate the relationship between dietary fibre intake and some clinical indices, blood biochemical variables and the incidence of cardiovascular disease and cancers in France, taking advantage of an ongoing cohort, the Supplementation en Vitamines et Minéraux AntioXydants (SU.VI.MAX) intervention study. This preliminary report provides data on dietary fibre intake in this French adult population group of 4080 subjects (2168 men and 1912 women) aged 45–65 years at inclusion. The data obtained for fibre intake indicate that most men and women have low to moderate intakes of total dietary fibre (mean 21·0 and 17·1 g/d respectively), with only 21% of the men and 7% of the women having total dietary fibre intakes at the recommended level (i.e. >25 g/d) and soluble fibre accounting for 19% of the total dietary fibre intake for both genders. The main food sources of dietary fibre are cereals (30–35% total), vegetables (20–24% total) and fruit (19–22% total). No marked regional differences were observed within France. The highest dietary fibre intakes have been found to be associated with a lower BMI, blood systolic pressure, plasma triacylglycerols and plasma glucose in men and lower BMI in women. Overall, these data support the concept of a beneficial effect of a high dietary fibre intake on cardiovascular disease risk.

There is very little evidence for the effects of dietary fibre in young children and current dietary guidelines are based on assumptions and data extrapolated from studies in adults. The first years of life may be critical for the establishment of a healthy colonic microflora, as well as good eating habits. The lack of clear and well-founded guidelines for the intake of dietary fibre in childhood may hinder both factors. The fears that a high-fibre diet in children <5 years of age will lead to growth faltering and mineral imbalance are not well supported in the literature, especially for children in the developed world. Indeed, with the rising levels of obesity, fibre intake may be of benefit in reducing energy intake. A low-fibre diet may also be implicated in the aetiology of childhood constipation and appendicitis. The latest proposals for the definition of dietary fibre include oligosaccharides, which may act as prebiotics. There are potential health benefits of including oligosaccharides in the diets of infants and children, but more research is needed to consider the long-term effects. The immature intestine of the infant may also result in a greater amount of starch entering the colon during weaning, and this starch would now be considered dietary fibre under the new definitions. Much new research is needed to allow adequate recommendations for the intake of dietary fibre in childhood based on data collected in appropriate age-groups.

The epidemiological data that directly examine whole grain v. refined grain intake in relation to weight gain are sparse. However, recently reported studies offer insight into the potential role that whole grains may play in body-weight regulation due to the effects that the components of whole grains have on hormonal factors, satiety and satiation. In both clinical trials and observational studies the intake of whole-grain foods was inversely associated with plasma biomarkers of obesity, including insulin, C-peptide and leptin concentrations. Whole-grain foods tend to have low glycaemic index values, resulting in lower postprandial glucose responses and insulin demand. High insulin levels may promote obesity by altering adipose tissue physiology and by enhancing appetite. The fibre content of whole grains may also affect the secretion of gut hormones, independent of glycaemic response, that may act as satiety factors. Future studies may examine whether whole grain intake is directly related to body weight, and whether the associations are primarily driven by components of the grain, including dietary fibre, bran or germ.

Diverticulosis is a condition that is associated with ageing. The older the individual the more likely they are to have diverticulosis, but this process is not necessarily inevitable. Diverticula are a herniation through the wall of the sigmoid colon and are likely to be a consequence of a weakness in the colonic wall or prolonged exposure to increased intracolonic pressure consequent on a low dietary fibre intake. The tensile strength of the colon declines with age and becomes least in the distal colon. Adult Africans living in Africa eat a high-fibre diet and are free from diverticulosis. Their colons are stronger, wider and thinner than those Scottish adults of the same age. The strength of the colon is in part dependent on collagen fibres and their diameter. The collagen fibrils on the left side of the colon are smaller and more tightly packed than those of the right side of the colon. Ageing and the presence of colonic diverticulosis are associated with smaller more-tightly-packed collagen fibrils. An animal model was established to investigate the effect of a lifelong high- and low-fibre diet on the development of colonic diverticulosis. The findings show that a high-fibre diet from birth, and preferably a maternal high-fibre diet, lessen the risk of diverticulosis with age.

Establishing a definition for dietary fibre has historically been a balance between nutrition knowledge and analytical method capabilities. While the most widely accepted physiologically-based definitions have generally been accurate in defining the dietary fibre in foods, scientists and regulators have tended, in practice, to rely on analytical procedures as the definitional basis in fact. As a result, incongruities between theory and practice have resulted in confusion regarding the components that make up dietary fibre. In November 1998 the president of the American Association of Cereal Chemists (AACC) appointed an expert scientific review committee and charged it with the task of reviewing and, if necessary, updating the definition of dietary fibre. The committee was further charged with assessing the state of analytical methodology and making recommendations relevant to the updated definition. After due deliberation, an updated definition of dietary fibre was delivered to the AACC Board of Directors for consideration and adoption (Anon, 2000; Jones 2000/7). The updated definition includes the same food components as the historical working definition used for approximately 30 years (a very important point, considering that the majority of the research of the past 30 years delineating the positive health effects of dietary fibre is based on that working definition). However, the updated definition more clearly delineates the make-up of dietary fibre and its physiological functionality. As a result, relatively few changes will be necessary in analytical methodology. Current methodologies, in particular AACC-approved method of analysis 32–05 (Grami, 2000), Association of Official Analytical Chemists' official method of analysis 985.29 (Horwitz, 2000a) or AACC 32–07 (Grami, 2000) Association of Official Analytical Chemists 991.43 (Horwitz, 2000a) will continue to be sufficient and used for most foods. A small number of additional methods will be necessary to quantify the dietary fibre levels in foods containing fibres such as fructans (polymers and oligomers of fructose, inulin), modified dextrins, and/or synthetic dietary fibre analogues.

The relationship between frequency of consumption of whole-grain foods and cancer risk has been analysed using data from an updated series of case-control studies conducted in Northern Italy between 1983 and 1997. The overall dataset included the following incident histologically-confirmed neoplasms: oral cavity and pharynx 524, oesophagus 410, stomach 745, colon 955, rectum 625, liver 435, gallbladder 65, pancreas 402, larynx 388, soft tissue sarcomas 217, breast 3412, endometrium 750, ovary 971, prostate 127, bladder 431, kidney 190, thyroid 428, Hodgkin's disease 201, non-Hodgkin's lymphomas 529, multiple myelomas 185. Controls were 10 058 patients admitted to hospital for acute non-neoplastic conditions unrelated to long-term modifications in diet, tobacco or alcohol use. The multivariate odds ratios for the highest category of whole-grain cereal consumption were 0.3–0.5 for upper digestive tract and respiratory neoplasms and colon, 0.6 for rectum and liver, 0.4 for gallbladder, 0.8 for pancreas, 0.2 for soft tissue sarcomas, 0.9 for breast and endometrium, 0.7 for ovary, 0.7 for prostate, 0.4 for bladder and kidney, 1.1 for thyroid and about 0.5 for lymphomas and 0.6 for myelomas. In this population whole-grain food consumption is an indicator of reduced risk of several neoplasms.

Loss of function of the adenomatous polyposis coli (APC) tumour suppressor gene through truncating mutations or other means is an early event in most colo-rectal cancer (CRC). The AFC gene encodes a large multifunctional protein that plays key roles in several cellular processes, including the wnt signalling pathway where an intact APC protein is essential for down regulation of β-catenin. The APC protein also plays a role in regulation of cell proliferation, differentiation, apoptosis, cell-cell adhesion, cell migration and chromosomal stability during mitosis. Acquisition of a non-functional APC gene can occur by inheritance (in the disease familial adenomatous polyposis (FAP)) or by a sporadic event in a somatic cell. Whilst there is strong epidemiological evidence that variation in diet is a major determinant of variation in CRC incidence, conventional adenoma recurrence trials in sporadic cases of the disease have been relatively unsuccessful in identifying potentially protective food components. Since the genetic basis of CRC in FAP and in sporadic CRC is similar, intervention trials in FAP gene carriers provide an attractive strategy for investigation of potential chemo-preventive agents, since smaller numbers of subjects and shorter time frames are needed. The Concerted Action Polyp Prevention (CAPP) 1 Study is using a 2×2 factorial design to test the efficacy of resistant starch (30 g raw potato starch-Hylon VII (1:1, w/w)/d) and aspirin (600 mg/d) in suppressing colo-rectal adenoma formation in young subjects with FAP. Biopsies of macroscopically-normal rectal mucosa are also being collected for assay of putative biomarkers of CRC risk.

Many studies have shown that overall dietary patterns, dietary components consumed, or mode of food preparation are all possibly relevant in either reducing or increasing the risk of cancer in animals or man. Yet, dietary intervention studies, stemming from laboratory and epidemiological observational studies have often failed to demonstrate the anticipated protection against cancer. One possible explanation for the discrepancy between the results of various observational and experimental chemo-prevention studies is the lack of control for biological diversity of the participants of these studies. It is suggested that future epidemiological studies provide evidence stratified by status of major metabolic polymorphisms pertinent to the study subject, and that future intervention studies take these differences into account in the design and analysis phases.

The relationship between intake of dietary fibre and risk of colon cancer has been studied for 30 years and still the data are inconclusive. There are many possible reasons for this outcome, and they include a failure to consider exposure to dietary fibre separately by source, or colon cancers separately by subsite. These potential confounders have been known for at least 20 years. However, the disease is normally considered by epidemiologists as a single entity. More recently, it has become clear that colon cancer can arise via various histological pathways, and by various genetic pathways. There is no reason at all for assuming that risk factors for these possible pathways are the same. There is a need, therefore, for a more detailed approach to the study of diet and colon cancer, with fibre source and cancer subsite, genetic pathway and histological pathway taken into account.

Short-chain fatty acid (SCFA) formation by intestinal bacteria is regulated by many different host, environmental, dietary and microbiological factors. In broad terms, however, substrate availability, bacterial species composition of the microbiota and intestinal transit time largely determine the amounts and types of SCFA that are produced in healthy individuals. The majority of SCFA in the gut are derived from bacterial breakdown of complex carbohydrates, especially in the proximal bowel, but digestion of proteins and peptides makes an increasing contribution to SCFA production as food residues pass through the bowel. Bacterial hydrogen metabolism also affects the way in which SCFA are made. This outcome can be seen through the effects of inorganic electron acceptors (nitrate, sulfate) on fermentation processes, where they facilitate the formation of more oxidised SCFA such as acetate, at the expense of more reduced fatty acids, such as butyrate. Chemostat studies using pure cultures of saccharolytic gut micro-organisms demonstrate that C availability and growth rate strongly affect the outcome of fermentation. For example, acetate and formate are the major bifidobacterial fermentation products formed during growth under C limitation, whereas acetate and lactate are produced when carbohydrate is in excess. Lactate is also used as an electron sink in Clostridium perfringens and, to a lesser extent, in Bacteroides fragilis. In the latter organism acetate and succinate are the major fermentation products when substrate is abundant, whereas succinate is decarboxylated to produce propionate when C and energy sources are limiting.

The mechanism of action of probiotics is largely unknown. A potential mechanism should be to increase the production of short-chain fatty acids (SCFA), known modulators of gut functions, by the bacterial ecosystem in the large intestine. The present paper reviews our recent studies in which the capacity of probiotic bacteria to increase the production of SCFA by pig caecal bacteria was investigated using batch-culture and continuous-culture techniques. All four commercial probiotic preparations and three strains of probiotic bacteria dose-dependently accelerated the net production of SCFA, succinic acid and lactic acid without changing the acid profile, and slowed the net production of NH4. Effects on organic acid production did not vary among different probiotic species. Neither probiotic preparations nor probiotic bacteria affected the organic acid production from glucose, gastric mucin, starch or lactose, or organic acids produced:added saccharide. Glucose abolished these effects of probiotic preparations. However, the capacity of probiotics to increase SCFA production was not modified by gastric mucin, starch or lactose. These results indicate that probiotic bacteria increase SCFA production by accelerating the breakdown of carbohydrates that are resistant to indigenous bacteria, and suggest that the concept of prebiotics in terms of SCFA production as a measure of probiotic function is arguable.

Butyrate is a C4 acid produced by microbial fermentation of carbohydrates and protein in the large intestine of all animal species. The factor of prime importance for the production rate of butyrate in the lower gut is type and levels of non-digestible carbohydrates entering the large intestine. It was previously believed that 85–90% of the butyrate produced in the gut was cleared when passing the gut epithelium, but recent studies with catheterised pigs have shown that the concentration of butyrate in the portal vein is strongly influenced by the production rate in the large intestine. Increased gut production of butyrate further raises the circulating level of butyrate. For good reason it is not possible with current technologies to perform direct measurements of the variation in the butyrate concentration in the portal vein of human subjects, but short-chain fatty acid levels in portal blood from sudden-death victims, subjects undergoing emergency surgery or planned surgery have indicated a higher gut production and absolute and relative concentration of butyrate in non-fasted as compared with fasted human subjects. However, despite an expected higher gut production of butyrate when feeding a high-fibre rye-bread-based diet as compared with a low-fibre wheat-bread-based diet, there was no difference in absolute or relative levels of butyrate in the peripheral blood of human subjects.

Short-chain fatty acids (SCFA; mainly acetate, propionate and butyrate) are largely produced in non-ruminants during the colonic bacterial fermentation of non-digestible carbohydrates. These intestinal exogenous SCFA pass in part through the splanchnic bed and reach the peripheral bloodstream, mixing with the endogenous circulating SCFA. The whole-body turnover of SCFA is thus composed of an endogenous peripheral turnover and an exogenous production that depends on dietary intake of non-digestible carbohydrates. In the present work methods were developed for determining the SCFA turnover in animals and in human subjects using stable isotopes. The original studies performed to determine endogenous and exogenous metabolism of SCFA in animals and in human subjects are summarised. Using intravenous infusion of 13C-labelled SCFA the whole-body turnover of acetate, propionate and butyrate was assessed in rats in a fasted state. The endogenous turnover of acetate and its oxidation were determined in healthy human subjects in the post-absorptive state, using intravenous infusion of[l-13C]acetate. Intragastric tracer infusions were performed to evaluate the splanchnic first-pass retention of acetate in adults. Finally, an original model was developed in healthy human subjects using intravenous infusion of[l-13C]acetate to determine in vivo the true colonic acetate production after ingestion of a non-digestible disaccharide. These present studies using stable isotopes provide the basis for a novel strategy to evaluate in vivo, in human subjects, the production of SCFA in the large intestine.

Short-chain fatty acids (SCFA) affect local and remote motility of the gastrointestinal tract by mechanisms that are not completely understood. In the large intestine where they are produced, they inhibit peristaltic activity and may stimulate tonic activity. When present in the terminal ileum as a result of reflux of colon contents, they elicit propulsive contractions. These local motor effects could involve a neuro-hormonal sensory mechanism located in the mucosa of the terminal ileum and proximal colon. Finally, through a humoral pathway probably involving polypeptide YY release, ileal and colonic SCFA modify upper motility by inducing relaxation of the proximal stomach and lower oesophageal sphincter and reducing gastric emptying. One characteristic feature of the SCFA effects is the dose-dependency of the gastrointestinal motor responses. Indeed, the effects occur only below or above a threshold of SCFA concentration in lumen contents. One putative physiological role of the motor effects of SCFA might be to maintain the physico-chemical balance of the lumen environment in the terminal ileum and proximal colon. Another role might be to co-regulate motility of the upper intestine. The clinical relevance of these effects is unclear. However, some recent findings suggest that excessive SCFA concentrations might induce adverse effects on gastrointestinal and colonic motility and sensitivity in certain diseases such as inflammatory bowel disease and gastro-oesophageal reflux disease.

Short-chain fatty acids (SCFA), particularly butyrate, were shown to regulate cell proliferation in vitro and in vivo. Indeed, butyrate is the major fuel for colonic epithelial cells, and it can influence cell proliferation through the release of growth factors or gastrointestinal peptides such as gastrin, or through modulation of mucosal blood flow. Lastly, SCFA can act directly on genes regulating cell proliferation, and butyrate is the main SCFA to display such an effect. Butyrate inhibits histone deacetylase, which will allow histone hyperacetylation. Such hyperacetylation leads to transcription of several genes, including p21/Cipl. Moreover, it will allow cyclin D3 hyper-expression by inhibiting its degradation. The induction of the cyclin-dependent kinase inhibitory protein p21/Cipl accounts for cell arrest in the Gl phase of the cell cycle. However, in the absence of p21 other mechanisms are initiated, leading to inhibition of cell proliferation.

Epidemiological evidence suggests that a high intake of resistant starch and NSP protects against colo-rectal cancer. The mechanisms underlying this protection are thought to be mediated by the short-chain fatty acid butyrate, which is present in the colonic lumen in millimolar concentrations as a result of bacterial fermentation of carbohydrates that have resisted digestion in the small intestine. In vitro studies have shown that butyrate displays a host of chemo-preventative properties including increased apoptosis, reduced proliferation, down regulation of angiogenesis, enhanced immunosurveillance and anti-inflammatory effects in colo-rectal cancer cell lines. However, the molecular mechanisms underlying the apparent chemo-preventative actions of butyrate are largely unknown. The evidence supporting the role of butyrate as an anti-cancer agent is reviewed, with particular emphasis on those studies that have attempted to elucidate the mechanism of action of butyrate. Our understanding of the mechanistic action of butyrate and its role in cancer prevention is likely to advance considerably in this post-genomic era with the application of genomic and proteomic technologies. Studies are described that have used gene array and proteomic techniques to investigate the response of colo-rectal cancer cells to butyrate. These pioneering studies illustrate the potential of these technologies to help characterise the molecular responses of the cancer cell to butyrate, and to define the role of butyrate (and other nutrients) in the prevention of colo-rectal cancer.

Manufacturing of healthy whole-grain foods demands knowledge of process-induced changes in macro-, micro- and non-nutrients. The high content of dietary fibre is a challenge in relation to good product texture and sensory quality. The stability and bioavailability of bioactive compounds have a marked influence on the health effects of cereal foods. It was confirmed that sterols, folates, tocopherols and tocotrienols, alkylresorcinols, lignans, phenolic acids and total phenolics are concentrated in the bran layers of the rye grain, and are only present at low levels in the flour endosperm. The levels of folate and easily-extractable phenolic compounds increase in germination and sourdough baking, but there are negligible changes in the levels of sterols, lignans and alk(en)ylresorcinols. The levels of tocopherols and tocotrienols are reduced during the sourdough fermentation. In conclusion, many of the bioactive compounds in whole-grain rye are stable during food processing, and their levels can even be increased with suitable processing.

Regular consumption of whole grain foods has been associated with a reduction in the incidence of cardiovascular disease and diabetes, reductions in cancer mortality at certain sites and an overall reduction in premature death. Although benefits are observed at relatively low levels of intake (between two and three servings per d), the consumption of whole grain foods in some Western countries is less than one serving per d. The main sources of whole grain are wholemeal and rye breads and whole grain breakfast cereals. Typical consumers of whole-grain foods tend to be older, from a high socio-economic group, are less likely to smoke and are more likely to exercise than non-consumers. Some of these attributes may contribute to the observed health benefits. However whole grain foods are an important source of a range of nutrients as part of a healthy eating plan. There is considerable scope for strategies to promote increased consumption of whole grain foods to reduce the risk of a variety of chronic diseases