The current epidemic of human obesity implies that whilst energy balance appears to be regulated, the extent of this regulatory process is being overwhelmed in large numbers of the population by environmental changes. Clearly, the shift towards positive energy balance reflects both alterations in energy intake and decreases in physical activity. Increased energy intake and, in particular, the rising proportion of energy from fat is linked with obesity. However, on a population level reduced levels of activity probably play the predominant role. It is apparent that individual susceptibility to weight gain varies enormously. The factors underlying this susceptibility are an area of intense research interest. Variations in BMR from that predicted appear to be linked to the propensity to gain weight. The genes responsible for this variation may include uncoupling proteins-2 and -3, with a number of studies showing a link with obesity. However, in vivo studies of these proteins have not yet demonstrated a physiological role for them that would explain the link with obesity. Non-exercise activity thermogenesis may also protect from weight gain, but the regulation of this type of thermogenesis is unclear, although the sympathetic nervous system may be important. A profusion of hormones, cytokines and neurotransmitters is involved in regulating energy intake, but whilst mutations in leptin and the melanocortin-3 receptor are responsible for rare monogenic forms of obesity, their wider role in common polygenic obesity is not known. Much current work is directed at examining the interplay between genetic background and environmental factors, in particular diet, that both lead to positive energy balance and seem to make it so hard for many obese subjects to lose weight.

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.

Energy balance is the difference between energy consumed and total energy expended. Over a given period of time it expresses how much the body stores of fat, carbohydrate and protein will change. For the critically-ill patient, who characteristically exhibits raised energy expenditure and proteolysis of skeletal muscle, energy balance information is valuable because underfeeding or overfeeding may compromise recovery. However, there are formidable difficulties in measuring energy balance in these patients. While energy intake can be accurately recorded in the intensive care setting, the measurement of total energy expenditure is problematic. Widely used approaches, such as direct calorimetry or doubly-labelled water, are not applicable to the critically ill patient. Energy balance was determined over periods of 5–10 d in patients in intensive care by measuring changes in the fat, protein and carbohydrate stores of the body. Changes in total body fat were positively correlated with energy balance over the 5 d study periods in patients with severe sepsis (n24, r 0.56, P=0.004) or major trauma (n 24, r 0.70, P<.0001). Fat oxidation occurred in patients whose energy intake was insufficient to achieve energy balance. Changes in body protein were independent of energy balance. These results are consistent with those of other researchers who have estimated total energy requirements from measurements of O2 consumption and CO2 production. In critically-ill patients achievement of positive non-protein energy balance or total energy balance does not prevent negative N balance. Nutritional therapy for these patients may in the future focus on glycaemic control with insulin and specialised supplements rather than on energy balance per se.

The need for an evidence base for human nutrition action is analysed in the context of human rights. Over the last 50 years the twin tracks of development, economical needs based and normative rights based, have come progressively closer in terms of goals and objectives, even if they do maintain different orientations and origins. The international human rights machinery is described, together with those parts that are of relevance to the right to food and nutrition. The role of the State in respecting, protecting and facilitating these rights is further described. The evidence base for the benefit of nutrition interventions during the fetal and infant period to the health and well-being of populations throughout life's course is briefly reviewed, and reasons why such a large body of evidence has not been acted upon are discussed. The power of nutrition is in prevention more than cure, and the prevention of nutritional deficiency is best suited to radical population-wide strategies rather than high-risk strategies targeted at individuals. The population-wide distribution of benefits of nutrition is in congruence with universality of human rights. In the UK much remains to be done to ensure that food and nutrition rights are realised, especially during the critical period of fetal and infant growth. What role the Nutrition Society might play in the realisation of these rights, including the creation of a robust evidence base for nutrition action, is further discussed.

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.

The present paper addresses the emergence and development of Nordic food and nutrition policies, with some reference to the types of nutrition policies characteristic of other North European countries. Nutrition programmes aimed at dietary change have a long history of public responsibility in several Nordic and North European countries. The extent of involvement, the orientation and (indication of) success have, however, varied considerably between countries. First, different types of policies are characterised by their choice of programmes and measures, e.g. information campaigns v. market regulation or catering and public services. Second, the distinctions are associated not only with programmes, but also with the status and validity of nutritional advice and dietary guidelines in public policy making. Third, when focusing on how and on what grounds the governments have developed nutrition policies, it is evident that while more or less the same participants and issues are involved, their roles and relationships may be different. In this case the role and involvement of nutritional expertise and scientific arguments in various countries will be discussed. Finally, nutrition policies may entail conflicts of interest, particularly when health concerns are confronted with food industry and agricultural interests. This situation is quite evident in the question of animal fat. The present paper addresses how these issues have been dealt with quite differently in various countries.

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.