Despite the almost universal clinical observation that inflammation of the gut is frequently associated with inflammation of the joints and vice versa, the nature of this relationship remains elusive. In the present review, we provide evidence for how the interaction of dietary lectins with enterocytes and lymphocytes may facilitate the translocation of both dietary and gut-derived pathogenic antigens to peripheral tissues, which in turn causes persistent peripheral antigenic stimulation. In genetically susceptible individuals, this antigenic stimulation may ultimately result in the expression of overt rheumatoid arthritis (RA) via molecular mimicry, a process whereby foreign peptides, similar in structure to endogenous peptides, may cause antibodies or T-lymphocytes to cross-react with both foreign and endogenous peptides and thereby break immunological tolerance. By eliminating dietary elements, particularly lectins, which adversely influence both enterocyte and lymphocyte structure and function, it is proposed that the peripheral antigenic stimulus (both pathogenic and dietary) will be reduced and thereby result in a diminution of disease symptoms in certain patients with RA.

Since the food habits of many elderly people are inadequate, the first experiment of the present study tested whether flavour amplification induces changes in preferences for and consumption of food and thus might result in a nutritional benefit. Two panels, one of 260 and one of 120 subjects, aged 19–98 years, took part in the study in which preferences for flavour-amplified yoghurt and Quorn® were measured. For both products, only a few of the young subjects (20 %) preferred the high flavour level; the percentage of subjects preferring the high flavour levels increased with age. These changes were highly significant. In a second experiment, participants received, under ad libitum conditions over 2 d in random order, a dish of yoghurt with either a high or a low flavour level. When adjusted for total consumption quantity, consumption of the highly flavoured yoghurt was not significantly correlated with age (r -0·03, P = 0·35). In a third experiment, odour perception was measured by determining the detection threshold for isoamylacetate. BMI values were obtained and the relationships between BMI and odour perception, age, preference and consumption were assessed in the age group 40–65 years. A significant correlation was observed between age and BMI (r 0·51, P < 0·0005). No significant correlation was observed between BMI and relative consumption of highly flavoured yoghurt (r -0·14, P = 0·14). A significant correlation was observed between BMI and preference for flavour-amplified yoghurt (r 0·35, P < 0·001). However, no significant correlation was observed between BMI and odour perception (r 0·07, P = 0·32). With increasing age, a combined influence of age, sex, BMI and odour perception on food preference is to be expected. According to our multiple regression analysis, BMI showed a significant partial regression coefficient (standardized β 0·36, P = 0·03). In conclusion, flavour amplification of food for older adults deserves attention, but specific approaches, which are tailored to the candidate food systems and older adult target groups, are needed.

The purpose of the present study was to estimate whole-body fatty acid and cholesterol synthesis in weight-stable adults and to determine the likely effect on the doubly-labelled water (DLW) method for measuring energy expenditure. Synthesis was measured by 2H incorporation over 14 d in six adult males in approximate energy balance following noradrenaline infusion to maximize mobilization of free fatty acid from adipose tissue. The inter-individual variation in synthesis rates was large and in one subject the proportion of free fatty acid synthesized was ten times that of the mean of the rest of the group; the fasting concentration of esterified fatty acid in this subject was five times that of the rest of the group indicating likely violation of the assumptions underlying the calculation of whole-body synthesis. After 14 d of labelling in the other five subjects, 0·9 (SEM 0·3) % OF THE CIRCULATING FREE FATTY ACID, 9·3 (sem 3·0) % of the esterified fatty acid, 14·6 (sem 2·4) % of the free cholesterol and 28·3 (sem 3·7) % of esterified cholesterol had been synthesized de novo. A high rate of synthesis correlated with a low pre-dose 2H abundance both within and between lipid classes suggesting that natural 2H abundance variations in some lipid classes may be used to determine their metabolic origin. Whole-body synthetic rates were 8 g/d for fatty acid and 0·3–0·5 g/d for cholesterol. These values correspond to very small errors on DLW-derived estimates of CO2 production; -2·5 litres/d for fatty acid and -0·1 to -0·2 litres/d for cholesterol. These results, obtained in subjects typically consuming a diet with a lower fat and cholesterol content that the typical Western diet, suggest that the DLW method is unlikely to be affected by fatty acid and cholesterol synthesis in subjects in energy balance consuming a typical Western diet.

The main Fe storage organ in the body is the liver. In patients with chronic liver disease, secondary Fe overload is common. Phlebotomy, often used in the West to reduce Fe overload to improve the efficacy of interferon therapy, is not socially acceptable in India. We assessed the efficacy of a low-Fe diet in reducing serum Fe levels. Nineteen patients with hepatitis B- and C-related chronic liver disease, ten with normal (< 25 μmol/l) baseline serum Fe levels (group A) and nine with high (> 25 μmol/l) serum Fe levels (group B) were included. All the subjects were advised to eat a low-Fe diet. The daily Fe intake was reduced approximately 50 % by consumption of the rice-based diet. Haemoglobin, serum Fe, transferrin saturation index (TSI), ferritin and alanine transaminase (EC 2.6.1.2) levels were studied at 1 and 4 months. Dietary Fe intake and body weight were closely monitored. All patients complied with the dietary regimen and at 4 months significant (P < 0·001) reductions from baseline were seen in serum Fe (20 (SD 3) V. 12 (sd 4) μmol/l group A; 30 (sd 3) v. 19 (sd 7) μmol/l group B) and TSI (38 (sd 8) v. 23 (sd 9) % group A; 53 (sd 15) v. 34 (sd 13) %, group B) in both the groups, albeit earlier in group B subjects. Serum ferritin levels, however, reduced only in group A (112 (sd 62) v. 43 (sd 25) ng/ml, P < 0·05) and not in group B. Non-significant reductions in haemoglobin levels were seen in both groups. Alanine transaminase levels reduced significantly (P < 0·05) in both the groups (95 (sd 49) v. 44 (sd 25) IU/l, group A; 82 (sd 16) v. 51 (sd 14) IU/l group B). Thus, a low-Fe diet results in significant reductions in serum Fe and TSI levels, irrespective of baseline Fe levels. This diet should be evaluated to improve the efficacy of interferon therapy in patients with hepatitis B- and C-related chronic liver disease.

Trehalose is a disaccharide, the main dietary source being mushrooms. It has been approved as an additive in the preparation of dried food. Isolated intestinal trehalase deficiency is found in 8 % of Greenlanders, but is rare elsewhere. The normal range of trehalase activity and the incidence of isolated trehalase deficiency in the UK have not been reported. Patients (n 400) were investigated for suspected malabsorption. Endoscopic distal duodenal biopsies were taken for histological assessment and maltase, sucrase, lactase and trehalase estimation. Disaccharidase activities were determined by Dahlqvist's technique (). Most patients (n 369) had normal duodenal histology. In these, square root transformation of trehalase activity produced a normal distribution. The normal range (mean ± 2 SD) was 4·79–37·12 U/g protein. One patient had an isolated borderline trehalase deficiency. The thirty-one patients with villous atrophy had significantly reduced disaccharidase activities. With ingestion of a gluten-free diet, maltase, sucrase and trehalase activities recovered to normal in most patients, whereas lactase activity did not. The normal range and very low incidence of isolated enzyme deficiency is comparable with that described in populations from the USA and mainland Europe. Activity is significantly reduced in untreated coeliac disease and recovers with treatment with a gluten-free diet. There is no place for routine determination of trehalase activity in the UK population and there should be no concern over the introduction of trehalose-containing dried foods.

Anaerobic batch culture fermenters were used for a preliminary screening of the in vitro utilization by human gut microflora of dextran and novel oligodextrans (I, II and III) produced in the University of Reading (UK). Glucose and fructooligosaccharides (FOS) were used as reference carbohydrates. As expected, FOS acted as a good prebiotic in that it selectively increased numbers of bifidobacteria in the early stages of the fermentation. Dextran and oligodextrans each resulted in an enrichment of bifidobacteria in the batch cultures, with high levels of persistence up to 48 h. They also produced elevated levels of butyrate ranging from 5 to 14·85 mmol/l. To more effectively simulate conditions that prevail in different regions of the large intestine, a three-stage continuous culture cascade system was used to study further the fermentation of dextran, a low-molecular-mass oligodextran (IV) and maltodextrin. Oligodextran IV was shown to be the best substrate for bifidobacteria and lactobacilli with steady-state populations of bifidobacteria and lactobacilli being higher in all three vessels of the gut model than the respective populations resulting from dextran and maltodextrin. A maximum difference of 1·9 log was observed in vessel 1 for both bifidobacteria and lactobacilli in the case of dextran fermentation, while 1·4 log and 0·8 log in vessel 3 were the maximum differences for bifidobacteria and lactobacilli when maltodextrin was used as the carbohydrate source. Moreover, dextran and oligodextran appeared to stimulate butyrate production, with a maximum production up to 25·39 mmol/l in vessel 3 when fermenting dextran, followed by 21·70 mmol/l in the case of oligodextran IV and only 12·64 mmol/l in the case of maltodextrin.

Previous epidemiological studies have demonstrated relationships between individual nutrients and glucose intolerance and type 2 diabetes, but the association with the overall pattern of dietary intake has not previously been described. In order to characterize this association, 802 subjects aged 40–65 years were randomly selected from a population-based sampling frame and underwent a 75 g oral glucose-tolerance test. Principal component analysis was used to identify four dietary patterns explaining 31·7 % of the dietary variation in the study cohort. These dietary patterns were associated with other lifestyle factors including socio-economic group, smoking, alcohol intake and physical activity. Component 1 was characterized by a healthy balanced diet with a frequent intake of raw and salad vegetables, fruits in both summer and winter, fish, pasta and rice and low intake of fried foods, sausages, fried fish, and potatoes. This component was negatively correlated with central obesity, fasting plasma glucose, 120 min non-esterified fatty acid and triacylglycerol, and positively correlated with HDL-cholesterol. It therefore appears to be protective for the metabolic syndrome. Component 1 was negatively associated with the risk of having undiagnosed diabetes, and this association was independent of age, sex, smoking and obesity. The findings support the hypothesis that dietary patterns are associated with other lifestyle factors and with glucose intolerance and other features of the metabolic syndrome. The results provide further evidence for the recommendation of a healthy balanced diet as one of the main components of chronic disease prevention.

Type 2 diabetes is commoner in Asians than Caucasians. Many nitrosamines are diabetogenic, causing both type 2 and type 1 diabetes. Of CD1 mice fed with betel-nut or associated nitrosamines 8·5 % develop glucose intolerance with marked obesity. Glycaemia and anthropometric risk markers for type 2 diabetes were therefore examined in relation to betel usage in 993 ‘healthy’ Bangladeshis by one bilingual research-worker (N.M.). Of these, 12 % had known diabetes. A further 145 of 187 subjects ‘at-risk’ of diabetes (spot glucose >6·5 mmol/l <2 h after food, or >4·5 mmol/l >2 h after food) had a second blood glucose sample taken; sixty-one were confirmed as ‘at-risk’, and had an oral glucose tolerance test; nine new diabetics were identified. Multiple regression analysis showed that spot blood glucose values decreased with time after eating (P = 0·0005) and increased independently with waist size (P = 0·0005) and age (P = 0·0005) without relationships to other aspects of the diet, season or smoking. Waist size was strongly related to betel usage independent of other factors such as age. Betel use interacted with sex, relating to increasing glycaemia only in females. Since waist and age were the major markers of increasing glycaemia we suggest that betel chewing, a habit common to about 10 % of the world population (more than 200 million people) may contribute to the risk of developing type 2 diabetes mellitus.

To gain an understanding of UK consumer attitudes and beliefs regarding starchy foods and their dietary role, a questionnaire based on the theory of planned behaviour was developed and sent out to a UK consumer sample (n 800). The content focused on attitudes and beliefs towards starchy foods, perceived barriers towards increasing their intake (e.g. cost, habit, social influences), perceptions of personal and recommended starchy food intake, intention to increase starchy food intakes in the future and socio-demographic information. Responses (n 414) indicated that consumers have highly divergent attitudes and beliefs regarding starchy foods. These foods are seen as nutritious and good for one's health, but also as high in energy and not helping to control weight, and the overall intention to increase starchy food intake was extremely low. Possible barriers towards increasing starchy food intake were the perceptions that personal starchy food intakes were already high, beliefs that starchy food intakes should be reduced to achieve a healthier diet, and the view that personal starchy food intakes did not need to be changed any further, because (depending on attitude) individual's intakes had already been increased or reduced. The model including attitude and subjective norm had the best fit for predicting reported intention to increase starchy food consumption, with attitude being the strongest contributor. Addition of the factor ‘family's liking of starchy foods’ significantly improved the model. For reported starch intake, the model including attitude had the best fit, and addition of other factors did not improve the model. These findings indicate that health promotion strategies aimed at increasing complex carbohydrate intakes should take these perceptions into consideration; however, further work is required to examine how these potential barriers can best be addressed in practice.

There have been many attempts to characterize day-to-day variation in nutrient intake. This variation has a fixed component, associated with particular days of the week, and a random component. Both components were studied for a range of nutrients, using 4 d weighed diary data from a large, nationally representative survey of people aged 65 years or over. Since day-to-day variation may distort the characterization of the population distribution of habitual nutrient intakes, especially when diets are studied over only a small number of days, a statistical method was developed to correct for this distortion. Results suggested that population distributions of habitual nutrient intake could be accurately constructed from 4 d weighed diary data and that the method might be successfully applied to studies based on as little as 2 d of observation. The method is particularly valuable for correcting estimates of extreme nutrient intakes for biases induced by uneven representation of days of the week and by within-person variation.

An experiment was conducted to investigate the compartmental mean residence time, (CMRT) of feed residues in segments of gastrointestinal digesta of mature Holstein steers. The objective was to evaluate assumptions that feed residues flow through ruminal digesta as sequential mixing pools having age-dependent (GN) and age-independent (G1) distributed residence times respectively (GN → G1 flow). The basal diet was a semi-tropical hay containing 98 g crude protein and 503 g apparently digestible DM per kg DM. The hay was consumed and feed residues of different size and/or previous digestion from the hay were inserted into the reticulo-rumen (rumen) and abomasum. Marker profiles appearing at the duodenum and faeces were fitted to various compartment models to estimate CMRT. Post-abomasal CMRT did not differ among solutes or feed residues of different size and previous digestion and constituted only 5·8 % of the CMRT for the entire gastrointestinal tract. Markers initially applied to orally or ruminally dosed feed residues exhibited profiles in duodenal digesta and faeces conforming to GN → G1 flow. Previously undigested, masticated feed residues inserted into the dorsal rumen digesta had longer ruminal CMRT in the GN pool but not the G1 pool than did similarly inserted faecal small particles or normally ingested hay. These results support model assumptions of GN → G1 flow within rumen digesta. The results support mechanisms proposed for the GN pool as the ‘lag-rumination pool’ and the G1 pool as the ‘mass action turnover pool’. If further validated, rumen CMRT in cattle could be estimated from marker profiles in more easily obtained faeces to estimate ruminal CMRT required for feed evaluation systems.

The mass transfers of O2, glucose, NH3, urea and amino acids across the portal-drained viscera (PDV) and the liver were quantified, by arterio–venous techniques, during the last 4 h of a 100 h infusion of 0 (basal), 150 or 400 μmol NH4HCO3/min into the mesenteric vein of three sheep given 800 g grass pellets/d and arranged in a 3 × 3 Latin-square design. Urea irreversible loss rate (ILR) was also determined by continuous infusion of [14C]urea over the last 52 h of each experimental period. PDV and liver movements of glucose, O2 and amino acids were unaltered by NH4HCO3 administration, although there was an increase in PDV absorption of non-essential amino acids (P = 0·037) and a trend for higher liver O2 consumption and portal appearance of total amino acid-N, glucogenic and non-essential amino acids at the highest level of infusion. PDV extraction of urea-N (P = 0·015) and liver removal of NH3 (P < 0·001), release of urea-N (P = 0·002) and urea ILR (P = 0·001) were all increased by NH4HCO3 infusion. Hepatic urea-N release (y) and NH3 extraction(x) were linearly related (R2 0·89), with the slope of the regression not different from unity, both for estimations based on liver mass transfers (1·16; SE 0·144; PB ≠ 1 = 0·31) AND [14C]UREA (0·97; se 0·123; Pb ≠ 1 = 0·84). The study indicates that a sustained 1·5 or 2·4-fold increase in the basal NH3 supply to the liver did not impair glucose or amino acid supply to non-splanchnic tissues; nor were additional N inputs to the ornithine cycle necessary to convert excess NH3 to urea. Half of the extra NH3 removed by the liver was, apparently, utilized by periportal glutamate dehydrogenase and aspartate aminotransferase for sequential glutamate and aspartate synthesis and converted to urea as the 2-amino moiety of aspartate.

Leptin is a 167-amino acid protein that is secreted from adipose cells and expressed in placental tissues. It is important nutritionally in the regulation of energy balance, but also has other functions such as a role in reproduction. To investigate the function of the leptin system in fetal development we examined, primarily by in-situ hybridization and immunohistochemistry, the expression (both mRNA and protein) of leptin and its receptor (including the signalling splice variant) in tissues from 11·5, 13·5, 16·5 and 18·5 d postcoitus murine fetuses and associated placentas. We detected leptin mRNA (at low levels) and protein predominantly in the cytotrophoblasts of the labyrinth part of the placenta, an area of nutrient exchange between the developing fetus and the placenta, and in the trophoblast giant cells situated in the junctional zone at the maternal interface. In addition, leptin was strongly expressed in the fetal cartilage–bone and at a lower level in the hair follicles, heart, and liver of the murine fetus at differing stages of development. The leptin receptor, including the signalling splice variant, was also identified in specific fetal tissues. The physiological importance of expression of both leptin and the leptin receptor (OB-R and OB-Rb) in the placenta remains to be determined. In addition, the high levels of expression of leptin and its receptor in discrete areas of the murine fetus suggest that leptin has a critical role in fetal development.

The effects of dietary lipids on the fatty acid composition, activation and proliferation of lymphocytes were investigated. Weanling male Wistar rats were fed for 8 weeks on one of two low-fat diets which contained 50 g lipid/kg, or one of two high-fat diets containing 200 g lipid/kg, from either coconut oil or soyabean oil. The fatty acid composition of phospholipids from splenocyte membranes was affected by dietary lipid manipulation, and these differences influenced lymphocyte functions. Increased levels of linoleic acid in spleen lymphocytes correlated negatively with interleukin-2 receptor α-chain expression determined either by measuring the mean fluorescence or by the proportion of cells staining positive for CD25, and with the cell proliferation index. However, we found a positive correlation between interleukin-2 receptor α-chain expression determined by measuring the mean fluorescence and the cell proliferation index with the oleic acid concentration of spleen lymphocytes. Since phospholipid hydrolysis occurs early in lymphocyte activation, immunosuppressive effects induced by polyunsaturated fatty acids, described in the literature, could be due to an increase of linoleic acid or a decrease of oleic acid affecting many components of plasma-membrane-associated events involved in lymphocyte activation.