Epidemiological studies find that whole-grain intake is protective against cancer, cardiovascular disease, diabetes and obesity. Potential mechanisms for this protection are diverse since whole grains are rich in nutrients and phytochemicals. First, whole grains are concentrated sources of dietary fibre, resistant starch and oligosaccharides, carbohydrates that escape digestion in the small intestine and are fermented in the gut, producing short-chain fatty acids (SCFA). SCFA lower colonic pH, serve as an energy source for the colonocytes and may alter blood lipids. These improvements in the gut environment may provide immune protection beyond the gut. Second, whole grains are rich in antioxidants, including trace minerals and phenolic compounds, and these compounds have been linked to disease prevention. Additionally, whole grains mediate insulin and glucose responses. Although lower glycaemic load and glycaemic index have been linked to diabetes and obesity, risk of cancers such as colon and breast cancer have also been linked to high intake of readily-available carbohydrate. Finally, whole grains contain many other compounds that may protect against chronic disease. These compunds include phytate, phyto-oestrogens such as lignan, plant stanols and sterols, and vitamins and minerals. As a consequence of the traditional models of conducting nutrition studies on isolated nutrients, few studies exist on the biological effects of increased whole-grain intake. The few whole-grain feeding studies that are available show improvements in biomarkers with whole-grain consumption, such as weight loss, blood lipid improvement and antioxidant protection.

Atherosclerotic cardiovascular disease (ASCVD) is the most common cause of death in most Western countries. Nutrition factors contribute importantly to this high risk for ASCVD. Favourable alterations in diet can reduce six of the nine major risk factors for ASCVD, i.e. high serum LDL-cholesterol levels, high fasting serum triacylglycerol levels, low HDL-cholesterol levels, hypertension, diabetes and obesity. Wholegrain foods may be one the healthiest choices individuals can make to lower the risk for ASCVD. Epidemiological studies indicate that individuals with higher levels (in the highest quintile) of whole-grain intake have a 29% lower risk for ASCVD than individuals with lower levels (lowest quintile) of whole-grain intake. It is of interest that neither the highest levels of cereal fibre nor the highest levels of refined cereals provide appreciable protection against ASCVD. Generous intake of whole grains also provides protection from development of diabetes and obesity. Diets rich in whole-grain foods tend to decrease serum LDL-cholesterol and triacylglycerol levels as well as blood pressure while increasing serum HDL-cholesterol levels. Whole-grain intake may also favourably alter antioxidant status, serum homocysteine levels, vascular reactivity and the inflammatory state. Whole-grain components that appear to make major contributions to these protective effects are: dietary fibre; vitamins; minerals; antioxidants; phytosterols; other phytochemicals. Three servings of whole grains daily are recommended to provide these health benefits.

The epidemic of type 2 diabetes among children, adolescents and adults is increasing along with the increasing prevalence of overweight and obesity. Overweight is the most powerful modifiable risk factor for type 2 diabetes. Intake of whole-grain foods may reduce diabetes risk. Three prospective studies in 160 000 men and women examined the relationship of whole-grain or cereal-fibre intake with the risk of type 2 diabetes. Each study used a mailed Willett food-frequency questionnaire and similar methods of quantifying whole-grain foods and cereal fibre. The self-reported incident diabetes outcome was more reliably determined in the two studies of health-care professionals than in the study of Iowa women. Risk for incident type 2 diabetes was 21–27% lower for those in the highest quintile of whole-grain intake, and 30–36% lower in the highest quintile of cereal-fibre intake, each compared with the lowest quintile. Risk reduction persisted after adjustment for the healthier lifestyle found among habitual whole-grain consumers. Observations in non-diabetic individuals support an inverse relationship between whole-grain consumption and fasting insulin levels. In feeding studies in non-diabetic individuals insulin resistance was reduced using whole grains or diets rich in whole grains. Glucose control improved with diets rich in whole grains in feeding studies of subjects with type 2 diabetes. There is accumulating evidence to support the hypothesis that whole-grain consumption is associated with a reduced risk of incident type 2 diabetes; it may also improve glucose control in diabetic individuals.

In response to the 1990 Nutrition Labeling and Education Act, the Food and Drug Administration approved seven health claims that addressed the relationship between broad food categories and risk of certain chronic diseases. These claims are based on scientific consensus that includes epidemiological, animal and clinical research. The Food and Drug Administration also established a process to petition for new health claims that address substance-disease relationships supported by adequate scientific and specific regulatory requirements. The whole grain-cancer and heart disease authoritative statement health claim approved in July 1999 followed a completely different process mandated by the Food and Drug Administration Modernization Act of 1997. It is based on an authoritative statement made by a government body that represents scientific consensus and is supported by other scientific agencies and organizations. The scientific basis for the claim published in Diet and Health reflects a comprehensive and deliberative review of epidemiological, animal and human studies by the National Academy of Sciences Committee on Diet and Health. Health claims used on whole-grain products can attract the attention of health-conscious consumers and are important tools in communicating health messages. However, the US public consumes substantially fewer whole-grain servings than recommended by US dietary guidance. Reasons given by consumers for not purchasing whole-grain foods include colour, price, softness, texture, moisture content and taste. Developing tastier value-added whole-grain foods along with simple coordinated messages from industry, the scientific community, public health experts and government will help consumers identify, purchase and consume more whole-grain products.

Wholegrain foods are important sources of nutrients and phyto-protective components, which are in short supply in many member states of the EU, including the UK. Encouraging the public to increase consumption of whole-grain foods is a positive health message that has critical public health implications. In February 2002 the UK Joint Health Claims Initiative (JHCI) published its authoritative endorsement that whole-grain foods are associated with a healthy heart (Joint Health Claims Initiative, 2002). This new health claim reflects a similar one in the USA based on the accumulation of epidemiological evidence between 1996 and 2001 from several very large cohort studies in the USA, Finland and Norway, which show a consistent protective effect of whole grain and reduced risk of CHD. The JHCI code of practice on health claims requires that the claimed benefit must be scientifically valid, with evidence supporting efficacy of the food in human consumers, under typical conditions of use. The evidence-based approach consists of the identification of studies, an evaluation of individual references, a critical evaluation of the totality of the evidence and a statement that there is significant scientific agreement to establish the validity of the claim. The studies suggest that an intake of three servings per d may have an important cardio-protective effect. The development of a process for the substantiation of health claims in the UK and in the EU is important to underpin regulatory developments, which should protect the consumer, promote fair trade and encourage innovation in the food industry. The present paper sets out the format of the scientific dossier that was presented to the JHCI and includes a call to promote further research to identify the important protective components in the whole grain ‘package’ and the biological mechanisms behind the observed beneficial effects on health. The major sources of whole grain in the UK are bread and breakfast cereals, and >90% of adults in the UK consume less than three servings per d. Increasing the variety and availability of acceptable whole-grain foods could lead to greater consumption levels, which has important public health implications and offers an attractive and food-based dietary strategy for targeting the whole population.

Non-infectious diseases such as CHD and certain cancers have become major causes of death and disability in affluent countries. Probiotics (principally lactic acid bacteria; LAB) may assist in lowering the risk of these diseases. Experimental studies with probiotics have given generally inconclusive outcomes for infectious disease and for biomarkers for non-infectious disease. In part this situation may reflect their inability to colonise the adult human gut effectively. Prebiotics can assist in promoting colonisation, and resistant starch (RS), as a high-amylose starch, is a prebiotic and synbiotic. This starch exerts its synbiotic action through adhesion of the bacteria to the granule surface. Consumption of RS assists in recovery from infectious diarrhoea in man and animals. A rice porridge, high in RS, appears to modify the autochthonous porcine large-bowel microflora favourably through lowering Escherichia coli and coliform numbers. Many of the beneficial effects of RS on large-bowel function appear to beexerted through short-chain fatty acids (SCFA) formed by bacterial fermentation. In man LAB are found in relatively highest numbers in milk-fed infants where theprofile of fermentation products differs quite markedly from that in adults. It appearsunlikely that ingestion of current probiotics will alter either total SCFA or the proportions of the major acids. More emphasis needs to be given to the investigation of the effects of complex carbohydrates, including RS, on the autochthonous microflora of the human large bowel.

Oligosaccharides, consisting of a mixture of hexose oligomers with a variable extent of polymerisation, are food products with interesting nutritional properties. They may be naturally present in food, mostly in fruits, vegetables or grains, or produced by biosynthesis from natural sugars or polysaccharides and added to food products because of their nutritional properties or organoleptic characteristics. The dietary intake of oligosaccharides is difficult to estimate, but it may reach 3–13 g/d per person (for fructo-oligosaccharides), depending on the population. The extent of resistance to enzymic reactions occurring in the upper part of the gastrointestinal tract allows oligosaccharides to become ‘colonic nutrients’, as some intestinal bacterial species express specific hydrolases and are able to convert oligosaccharides into short-chain fatty acids (acetate, lactate, propionate, butyrate) and/or gases by fermentation. Oligosaccharides that selectively promote some interesting bacterial species (e.g. lactobacilli, bifidobacteria), and thus equilibrate intestinal microflora, are now termed prebiotics. The pattern of short-chain fatty acid production in the caeco-colon, as well as the prebiotic effect, if demonstrated, are dynamic processes that vary with the type of oligosaccharide (e.g. extent of polymerisation, nature of hexose moieties), the duration of the treatment, the initial composition of flora or the diet in which they are incorporated. Experimental data obtained in vitro and in vivo in animals, and also recent data obtained in human subjects, support the involvement of dietary oligosaccharides in physiological processes in the different intestinal cell types (e.g. mucins production, cell division, immune cells function, ionic transport) and also outside the gastrointestinal tract (e.g. hormone production, lipid and carbohydrates metabolism). The present paper gives an overview of the future development of oligosaccharides, newly recognised as dietary fibre.

Prebiotics have the potential to promote immediate and long-term effects on the health and well-being of infants. They have been added to infant formulas in Japan for 20 years and have only recently been used in Europe. The objective is to change the intestinal microflora in order to mimic the bacteriological effect and, thus, the functional effects of human milk. There is, however, a potential risk of long-term effects of the use of these infant formulas. The consequences of using prebiotics in infants, during the first months of life, on the composition and development of the intestinal microflora, and on the resulting bacterial–bacterial and bacterial–host interactions are not known. Attempts have been made to improve infant and follow-on formulas by prebiotic supplementation, but intervention studies are needed to evaluate their immediate and long-term beneficial effects and demonstrate the absence of harmful consequences from their use.

There is considerable loss of DM during wet heat treatment of vegetables, leading to an increase in dietary fibre. Correction for the loss of DM indicates that the effects on total dietary fibre are minor. There is, however, depolymerization of the dietary fibre polysaccharides. The degradation is related to the severity of the heat treatment. Souring, freezing and mild microwave treatment have no effects. The viscosity is in general related to the extent of polymerisation. Microwave treatment has different effects on various cultivars of green beans, and the addition of salt (NaCl and CaCl2) to the boiling water changes the physico-chemical properties of soluble fibre in carrots, depending on the cation. The higher viscosity of the soluble fibre in raw carrots may partly explain the lower glucose and hormonal responses observed in healthy subjects when compared with blanched and microwave-cooked carrots. In studies on rats the amount of butyric acid in the distal colon has been shown to be higher with dietary components containing high amounts of resistant starch. Further, the fermentability is lower and the butyric acid concentration higher with composite foods than with the corresponding purified fibre fractions. In human studies the faecal concentration of butyric acid has been shown to increase in patients with ulcerative colitis when β-glucan-enriched oat bran (20 g fibre) is added to the diet for 12 weeks. Also, an improvement of symptoms was reported.

Rye bran contains a high content not only of dietary fibre, but also of plant lignans and other bioactive compounds in the so-called dietary fibre complex. Blood concentrations of lignans such as enterolactone have been used as biomarkers of intake of lignan-rich plant food. At present, evidence from studies in human subjects does not warrant the conclusion that rye, whole grains or phyto-oestrogens protect against cancer. Some studies, however, have pointed in that direction, especially in relation to cancers of the upper digestive tract. A number of prospective epidemiological studies have clearly shown a protective effect of whole-grain cereals against myocardial infarctions. A corresponding protective effect against diabetes and ischaemic stroke (brain infarct) has also been demonstrated. It seems reasonable to assume that these protective effects are associated with one or more factors in the dietary fibre complex.

An increasing body of evidence suggests that a low-glycaemic-index (GI) diet has a therapeutic as well as a preventive potential in relation to the insulin resistance syndrome. The implementation of a low-GI diet, however, will require an extended list of low-GI foods to be available on the market. The tailoring of low-GI bread products offers a particular challenge due to their generally high GI and abundance in the diet. Low-GI bread products can be tailored by, for example, enclosure of cereal kernels, sourdough fermentation and/or addition of organic acids, or use of cereal genotypes with elevated contents of amylose or β-glucans. Low-GI cereal foods appear to vary in effect on ‘second-meal’ glucose tolerance in healthy subjects. In addition to the slow release properties of such foods, the content of dietary fibre appears to play a role. The low glycaemia to starch in a pasta breakfast (GI 54) promoted a higher glucose tolerance and lowered triacylglycerol levels at a standardized lunch ingested 4 h later, compared with a white-wheat bread breakfast (GI 100). The metabolic benefits of the low GI properties per se have been demonstrated also in the longer term. Thus, a reduction in dietary GI improved glucose and lipid metabolism and normalized fibrinolytic activity in type 2 diabetics, while maintaining a similar amount and composition of dietary fibre. However, the higher dietary fibre content frequently associated with low-GI foods may add to the metabolic merits of a low-GI diet. Consequently, a low-GI barley meal rich in dietary fibre (GI 53) improved glucose tolerance from evening meal to breakfast, whereas an evening meal with pasta had no effect (GI 54). The exchange of common high-GI bread for low-GI high-fibre bread, as the only dietary modification, improved insulin economy in women at risk of type 2 diabetes. These results are in accordance with epidemiological evidence of a reduced risk of type 2 diabetes with a low-GI diet rich in cereal fibre. It is concluded that low-GI cereal foods developed should preferably be rich in dietary fibre.

A series of experiments and evaluations of fractions isolated from psyllium seed husk (PSH) were used to test the overall hypothesis that a gel-forming component of PSH is not fermented and that it is this component that is responsible for the laxative and cholesterol-lowering properties of PSH. A gel is isolated from human stools collected during a controlled diet study when PSH is consumed but not when the control diet only is consumed. Evaluations of three fractions isolated from PSH suggest that gel-forming fraction B, which is about 55% of PSH, is poorly fermented and is the component that increases stool moisture and faecal bile acid excretion, the latter leading to lower blood cholesterol levels. Fraction C, representing <15% of PSH, is viscous, but is rapidly fermented. Fraction A is alkali-insoluble material that is not fermented. In concentrations comparable with their presence in PSH, fractions A and C do not alter moisture and bile acid output. The active fraction of PSH is a highly-branched arabinoxylan consisting of a xylose backbone and arabinose- and xylose-containing side chains. In contrast to arabinoxylans in cereal grains that are extensively fermented, PSH possesses a structural feature, as yet unidentified, that hinders its fermentation by typical colonic microflora.

Molecular variables, using aqueous and alkaline extracts, of the polysaccharide from ispaghula husk (IH) were examined using gel-permeation chromatography linked to multi-angle laser light scattering. Progressive extraction can yield a component with a molecular weight (MW) value up to about 7×106 Da, and gels, which accompany the extraction, have MW ranging from 10–20× 106 Da. To mimic the polysaccharide degradation, particularly in the colon, the solid IH was degraded progressively using ionising radiation. A chain break occurs every 7.5 kGy in NaOH and every 15 kGy in water. The solid-state matrix is opened by the radiation to yield increased visco-elasticity of the aqueous extracts at critical radiation doses, before further degradation occurs after about 12 kGy. Differential scanning calorimetry is used to study the mechanism of interaction of water with IH. The first water to be taken up is non-freezing water and represents about twelve water molecules/disaccharide unit of the polysaccharide. As the water content is increased, the water becomes bound to the polysaccharide and freezes and melts at a temperature different from free water. This water is thermodynamically distinguishable from free water. It forms amorphous ice on cooling which crystallises exothermically and subsequently melts endothermically. Saturation occurs at a water content of 2–3 g water/g polymer, showing that about 60% of the water in the system is ‘bound’. The most surprising conclusion is that despite the fact that the IH swells in water to form a solid and stiff gel, the greater part of that water in the gel is still free and behaves like liquid water.

he primary structures of ispaghula husk and wheat bran were investigated in order to determine how and why these fibres are among the most beneficial dietary fibres. To this end, the polysaccharide preparations have been subjected to enzymic hydrolysis and methylation analysis. The results have shown ispaghula husk and wheat bran to be very-highly-branched arabinoxylans consisting of linear Β-D-→l(4)-linked xylopyranose →Xylp) backbones to which a-L-arabinofuranose →Araf) units are attached as side residues via α-→1(3) and a-→l(2) linkages. Other substituents identified as present in wheat bran include Β-D-glucuronic acid attached via the C→O)-2 position, and arabinose oligomers, consisting of two or more arabinofuranosyl residues linked via 1–2, 1–3, and 1–4 linkages. Ispaghula-husk arabinoxylan is more complex having additional side residues which include a-D-glucuronopyranose →GalAp)-→l→2(-linked-α-L-rhamnopyranose-(1→4)-β-D-Xylp, α-D-GalA/>-→l→3(-linked-a-L-Araf-→1)4(-p-D-Xylp, and <x-L-Araf-→1→3(-linked-p-D-Xylp-→1→4(-β-D-Xylp. The beneficial effects of increased faecal bulk and water-holding capacity are undoubtedly related to the structures of the arabinoxylans, with differences in their efficacy to treat various functional bowel disorders due to their specific structural features

The range of interactions between fibre and water and the consequential properties of the bound water are modelled and examined. Dietary fibre may interact with water by means of polar and hydrophobic interactions, hydrogen bonding and enclosure. The results of these interactions vary with the flexibility of the fibre surface. When the fibre is insoluble or junction zones are formed, this may result in profound changes in the surrounding water. Such interactions are capable of affecting the structuring and solvation properties of water well away from the immediate surfaces involved. In particular, the specific properties of water enclosed by dietary fibre are examined, an area of investigation previously receiving scant attention. The way this enclosure may affect the properties of water is exemplified by modelling the colon to show how fibre may exert a beneficial action by the preferential partitioning of hydrophobic carcinogens. Unfermented dietary fibre has a tendency to form low-density expanded water that acts as a preferential solvent for hydrophobic molecules when compared with the less-structured denser water within the much more hydrophilic mucus layer.

β-Catenin is a multifunctional protein originally identified as a component of the cadherin cell-cell adhesion complex. It also binds the adenomatous polyposis coli (APC) tumour suppressor which controls β-catenin cellular levels through its degradation. β-Catenin and/or APC mutations result in increased cytoplasmic β-catenin and nuclear translocation. The aim of the present study was to examine the expression and cellular localisation of α- and β-catenin, pi20 and E-cadherin in a chemically-induced mouse model of colo-rectal cancer using 1,2-dimethylhydrazine (DMH). Female Balb/C mice were injected subcutaneously with a solution providing 25 mg DMH base/kg body weight for 17 weeks. Animals were killed and tumours identified in the intestine with a dissecting microscope. Formalin-fixed paraffin-embedded sections of normal and dysplastic colonic mucosa were stained by an indirect avidin-biotin immunohistochemical technique using mouse monoclonal antibodies, and membranous, cytoplasmic and nuclear cellular localisation was assessed by light microscopy. Staining distribution scored as follows: 3, >90% positive epithelial cells; 2, >50% positive epithelial cells; 1, <50% positive epithelial cells. Non-dysplastic colonic epithelial cells revealed p-catenin expression at the membrane (33/41 scored 3), areas of cytoplasmic expression (24/41 scored 1) and no nuclear staining. Dysplastic colonic epithelium revealed increased membranous and cytoplasmic p-catenin immunoreactivity (39/41 and 38/41 both scored 3) with focal nuclear staining (14/41). Expression patterns for a-catenin, pi20, and E-cadherin were similar to β-catenin with increased membranous and cytoplasmic immunoreactivity in dysplastic mucosa, although no nuclear staining was observed. Increased cytoplasmic expression and nuclear localisation of β-catenin are consistent with a possible mutation in its gene, and this finding was in keeping with the mutational analysis of exon 3 by single-strand conformational polymorphism. Increased immunoreactivity of the other catenins also suggests further disruption in catenin regulation. In summary, alterations in the β-catenin expression and cellular localisation in the DMH-induced tumours are similar to those seen in human sporadic colo-rectal tumours. The DMH is therefore a useful model for studying the abnormalities of the E-cadherin-catenin pathway in colo-rectal carcinogenesis.

Mucus is a water-insoluble gel secreted by the gastrointestinal tract. It exists as a protective gel layer adherent to the epithelial surface of the stomach, small intestine and colon. The mucus gel is composed of 1–10% (w/v) mucin glycoprotein in a plasma-like fluid. Since the mucus gel is predominantly water, standard histological techniques dehydrate the mucus, making visualisation of the functional barrier difficult. Specialist techniques have been developed to enable visualisation of the intact mucus layer. A simple histological method using snap-frozen tissue, sectioned with a cryostat and stained with modified periodic acid-Schiff s/Alcian blue in mucus-preserving conditions will be described. A second powerful in vivo animal model is described which enables measurement of mucus secretion over time. The use of these two methods has allowed the characterisation of the normal mucus layer in the colon and the determination of how it is affected by disease and dietary intervention, in particular the effect of dietary fibre, and evidence that fibre deficiency results in colonic mucosal fragility is presented.

The colon is subjected to a myriad of potentially damaging agents that may reside within the lumen for 1–2 d. Its first line of defence against these agents is the protective mucus bilayer that lines the entire colonic mucosa. This bilayer acts as a physical barrier to mucosal aggressors and also reduces shear stress to the mucosa. These actions are dependent on the unstimulated (‘resting’) colonic mucus thickness, and also on the rate that this layer can be replenished. The colonic mucus layer is altered in a number of colonic diseases that have been linked to a deficiency of fibre in the diet. The action of fibre intake on colonic mucus thickness and secretion is unknown. Using an in vivo rat model it has been demonstrated that: (1) fibre deficiency leads to a decreased protective potential of the mucus layer (e.g. the mean resting mucus thickness of the fibre-deficient group (429 μm) was significantly lower than its respective control (579 μm; P< 0.001), as was its total mucus secretion over 6 h (270 μm v. 541 μm; P<0.01); (2) specific fibre types in the diet alter the secretion dynamics of colonic mucus (e.g. a cellulose-based diet reduces total mucus secretion over 6 h compared with its control (175 μm v. 463 μm). Analysis of the diets suggested a necessity for both soluble and insoluble fibre types in the diet to increase mucosal protection.