The study aimed to examine dietary changes and their associations with demographic, lifestyle and health variables in a random sample of British adults. The Health and Lifestyle Survey of 1984–5 (HALS1) identified four main dietary components by principal component analysis from food frequency data. Comparison of the HALS1 dietary component scores with those of the follow-up survey of 1991–2 (HALS2) for the same individuals revealed increases on component 1 (high weightings for fresh fruit, salads, ‘brown’ bread, fruit juice and green vegetables but low weightings for chips, fried food and processed meat). There were substantial decreases on component 2 (high weightings for puddings/pies, cake, potatoes, biscuits, preserves, pulses and meat), small increases on component 3 (high weightings for crisps, soft drinks and chips) and increases on component 4 (high weightings for confectionery, biscuits and cake and low weightings for vegetables of all kinds). Except for women on component 3 the changes were all significant, P < 0·001. Unadjusted score changes were smallest in elderly respondents for all components. Differences in score changes between groups were based on an analysis of covariance adjusting for the HALS1 score. On component 1 the largest score increases were associated with non-manual groups, improvements in lifestyle and good health. For component 2 the greatest changes in score were associated with changes in household size, smoking habit and heavy drinking. Score increases on component 3 were also associated with heavy drinking, whilst the largest rises on component 4 were amongst the non-manual, the non-drinkers and the non-smokers and, for women only, those who had few malaise symptoms or who lived in Scotland. The results show that there have been overall dietary changes and that changes have been associated with longitudinal alterations in socio-demographic, lifestyle and health circumstances.

Increasing the precision of measurements of total energy expenditure in population-based epidemiological studies is important for accurately quantifying the relationship between this exposure and disease. Current questionnaire-based methods cannot accurately quantify total energy expenditure, although they may provide an estimate of the frequency of vigorous activities. Heart rate monitoring with individual calibration has been advocated as a method for assessing energy expenditure in field studies and has been compared with the ‘gold standard’ techniques of doubly-labelled water and indirect calorimetry. However the method has previously only been used on small and selected populations. This study was, therefore, established to test the feasibility of using heart rate monitoring in a population-based study of adults. A total of 167 individuals aged 30–40 years were randomly selected and underwent 4 d heart-rate monitoring. Only three individuals could not complete the protocol. The mean physical activity level (PAL) measured over 4 d was 1.89 (sd 0.40) in men and 1.76 (sd 0.31) in women. There was no difference between mean PAL on weekend days compared with weekdays (mean paired difference 0.0008, 95% CI −0.06 to + 0.06). The estimate of mean PAL was not correlated with BMI, percentage body fat or the waist:hip ratio. It was, however, correlated with cardio-respiratory fitness as measured by VO2max per kg (Spearman rank correlation coefficient 0.50 in men and 0.42 in women). The pattern of energy expenditure was assessed by calculating the percentage of daytime hours in which PAL was greater than five times basal energy expenditure. This measure was strongly correlated with the mean PAL in both men (Spearman correlation coefficient 0.77) and women (0.71). We conclude that heart-rate monitoring is a feasible method for assessing the pattern and total level of energy expenditure in medium-sized epidemiological studies. It may also prove useful as the reference technique for calibrating questionnaires to estimate energy expenditure in larger scale studies.

The aims of this study were (1) to compare various measures of I status, and (2) to assess urinary I and thyroid hormone status of residents of two areas of New Zealand where, before the iodization of salt, goitre was endemic due to low soil I. A total of 189 subjects (102 males, eighty-seven females) were recruited from the Dunedin Blood Transfusion Centre, and 144 (sixty-seven males, seventyseven females) from the Waikato Blood Transfusion Centre between November 1993 and June 1994. Blood was taken for thyroid hormone assays, and subjects collected a fasting overnight urine specimen, a double-voided fasting urine sample, and a complete 24 h specimen for iodide and creatinine analyses. Positive correlations (P < 0.0001) between daily iodide excretion and iodide concentrations in fasting and double-voided fasting urines, identical median values for iodide concentrations in the three samples, and similar numbers of subjects classified as at risk from I deficiency disorders according to the International Committee for the Control of Iodine Deficiency Disorders/World Health Organization categories (World Health Organization, 1994) confirmed indications from earlier studies that fasting urine samples were suitable for population studies. However 24 h urinary iodide excretion remains the recommended measure for individual I status. Waikato residents excreted more iodide in urine and all measures were significantly greater than for Otago residents. However median urinary iodide excretions for both areas (60 and 76 μg/d for Otago and Waikato respectively) were considerably lower than those reported previously for New Zealand. Thyroid hormone concentrations were within normal ranges. Our findings suggest that I status of New Zealanders may no longer be considered adequate and may once again be approaching levels of intake associated with clinical I deficiency.

The hepatic responses of late gestation, dry dairy cows to acute (6 h) infusions of an amino acid (AA) mixture (Synthamin; 0.0, 1.1, 2.2, 4.4, 8.8 and 17.6 mmol/min) into the mesenteric vein were determined. Neither blood flow nor O2 consumption across the portal-drained viscera (PDV) and liver was significantly altered by infusion. Similarly, there were no effects on net absorption, or hepatic removal, of acetate, propionate, butyrate or NH3. Glucose PDV appearance was unchanged but hepatic glucose production increased (P = 0.032) by 0.2 mmol/min per mmol/min of AA infused. Additional extraction of alanine, glycine (both infused) and glutamine (not infused) by the liver was sufficient to account for most of the extra C required for glucose synthesis. The N that would be liberated from these glucogenic AA would also account for a large proportion of the increase in urea-N produced in response to the AA infusion. This supports the concept of a correlation between gluconeogenesis and ureagenesis. Furthermore, the amide-N liberated from the extracted glutamine would contribute up to 0.17 of hepatic NH3 flux and assist in balancing N inputs into the carbamoyl phosphate and arginosuccinate entry points of the ornithine cycle. Rates of fractional extraction of the various AA by the liver were best fitted by linear equations, indicating that even at the highest rates of administration (approximately twice maximal physiological absorption) the transport systems were not saturated. Hepatic fractional extractions of infused essential AA were highest for methionine (0.83) and phenylalanine (0.87) with the lowest proportion removed observed for valine (0.25), leucine (0.30), lysine (0.31) and isoleucine (0.49). For the non-essential AA, the highest apparent fractional extractions were for glycine (0–73), arginine (0.79) and tyrosine (0.63) followed by alanine (0.54), proline (0.47) and serine (0–37). Hepatic removal of AA-N exceeded the increase in urea-N formation such that, at the highest rate of infusion, approximately 10 mmol/min of the extracted AA was apparently available for hepatic anabolism, more than is required to account for assumed increases in liver mass and export protein synthesis. Similarly, the amount of AA available for peripheral tissue protein gain, when assessed against phenylalanine supply as the limitation, would be the equivalent of a maximum of 0.5 g protein retained/min (6 mmol AA-N/min). This would provide sufficient AA for replenishment of peripheral (muscle) protein stores plus support of the placenta and fetus.

The effect of exogenous glucose supply by either intrajugular (IJG) or intraduodenal (IDG) infusion at 2.0 mg glucose/kg body weight per min was investigated in four wether sheep (average weight 44 (sd 4) kg) chronically catheterized in the carotid artery and portal veins. Sheep were fed on a dried grass pellet diet hourly using continuous belt feeders. Whole-body glucose irreversible loss (IL) rate, measured with [6-3H[glucose, was increased by 0.5 and 0.8 of exogenous supply for IJG and IDG infusions respectively. Portal glucose utilization, measured by isotope dilution across the portal-drained viscera, was unaffected by additional glucose regardless of the route of glucose supply (P = 0.76 for control ν. glucose infusions) and was a constant proportion of glucose IL (0.28) for all treatments. Portal plasma flow was higher during IDG infusions compared with IJG infusions (1.65 ν. 1.44 litres/min, P=0.055). Circulating total free amino acid concentrations fell during glucose infusions (2146, 1808 and 1683 μmol/l for control, IJG and IDG treatments respectively, P=0.067 for treatment effect) but net portal absorption was not affected by increased glucose supply. Recovery in the portal vein of [1-13C[leucine infused into the duodenum averaged 0.65 and was not affected by increasing glucose supply to the gut tissues. The results show that glucose utilization by gut tissues is responsive to changes in both vascular and luminal glucose supply. The effects of changing gut tissue use of glucose and increased whole body glucose IL on metabolism of nutrients is discussed.

Rapeseed and rapeseed press cake were tested in four long-term experiments with a total of ninety-eight pigs. Rapeseed contained 20 and rapeseed press cake 19 mmol glucosinolates/kg DM. The proportion of the tested rapeseed products in feed amounted to 0 (control), 50, 100 and 150 g/kg diet. Moist-heat-treated rapeseed and rapeseed press cake with an extremely low glucosinolate content were also given at 150 g/kg diet. Each dietary rapeseed product level was given with 125 or 250 μg supplementary I/kg diet. Reduced feed intake and growth retardation were found in groups receiving 150 g rapeseed products/kg diet; in the case of rapeseed the impairments were significant. Rapeseed products ≥ 100 g/kg diet increased the thyroid weight and decreased the serum thyroxine (T4) concentration. Higher I dosage brought the serum T4 concentration to the level of the control group and retarded thyroid enlargement. Intake of rapeseed products lowered the I content of the thyroid; however, there was no significant difference between groups given 0·9 mmol glucosinolates/ kg diet and those receiving three times as much. Degrading glucosinolates by moisture and heat prevented feed intake depression and growth retardation. In the case of treated rapeseed the decreased serum T4 concentration and increased thyroid weight persisted, indicating formation of some antithyroid compounds due to myrosinase (EC 3.2.3.1) activation. A maximal glucosinolate content of 2 mmol/kg diet and additional I application are a prerequisite for using rapeseed products in pig feeding.

The possible involvement of thyroid hormones in avian diet-induced thermogenesis (DIT) was investigated in two lines of cockerels divergently selected for high (R-) or low (R+) food efficiency. For a given body weight, R+ cockerels exhibited a higher food intake than R- cockerels (+49 to +76%) and increased DIT (+25%). Plasma thyroxine (T4) levels did not differ between lines whatever the feeding status of the birds. Plasma 3,5,3'-triiodothyronine (T3) level was lower in fasted R+ than in fasted R- cockerels while the opposite was observed after a meal. Iopanic acid injections reduced both plasma T3 concentrations and heat production to the same levels in both lines. Hepatic 5'-deiodinase activity measured with an exogenous sulfhydryl group (dithiothreitol) did not differ between lines, but when the sulfhydryl group was omitted, the activity was higher in R+ than in R- birds (90 ν. 42 pmol T3/min per liver). T3-binding capacity of isolated hepatic nuclei was higher (+76%) in R+ than in R- birds. Long-term or acute pair-feeding of R+ cockerels to the level of R- controls did not alter these results. The present results suggest that T3, mainly originating from peripheral conversion of T4 to T3, is involved in DIT in the R+ line. Availability of endogenous sulfhydryl groups appears to play an important part in the modulation of hepatic deiodinase activity. The higher concentration of nuclear T3 receptors may further increase the effects of the hormone, suggesting a major role of thyroid hormones associated with catecholamines in the stimulation of avian DIT. The underlying thermogenic mechanisms remain to be elucidated.

A model of Mg metabolism in sheep is proposed. It is based on standard Michaelis-Menten enzyme kinetics to describe the transport of Mg across the rumen wall and passive diffusion to describe the absorption of Mg in the hindgut. Factors known to have an effect on Mg metabolism in farm animals, namely the concentrations of K and Mg in the diet, and the physico-chemical conditions within the rumen as determined by the type of diet, are incorporated into the model. Consideration of the rumen as the only site of Mg absorption provided an inadequate mechanistic description of Mg metabolism in sheep. To ensure compatibility between predicted Mg absorption and recent independent data sets for Mg balances, it was necessary to include in the model aspects of Mg absorption that operate in the hindgut. The results from this model suggest that there is a need for a series of experiments to determine the important aspects of Mg transport in the hindgut of sheep. Mechanisms of homeostasis are discussed.

The Japanese quail has been used as a model of human atherosclerosis to investigate the mechanisms underlying the development of vascular lesions, i.e. hyperlipoproteinaemia and impaired endogenous antioxidant status. In the present study, Japanese quail were fed on semi-purified diets containing butter, beef tallow or soyabean-oil blends, with either 0.5 or 5 g cholesterol/kg for 9 weeks to examine the effects of dietary fat blends varying in fatty acid composition and cholesterol intake on plasma lipids and aortic atherosclerotic plaque and sterol composition. These findings were related to possible diet-induced changes in antioxidant status of selected tissues. Hypercholesterolaemia was confirmed (P < 0.001) in birds fed on high-cholesterol (HC) diets. Plasma total cholesterol concentration and cholesterol content of lipoprotein fractions in hypercholesterolaemic birds were lower (P < 0.05) in quail fed on the soyabean-oil blend. Plasma triacylglycerol content was increased (P < 0.001) in HC-fed birds. Dietary fat blends did not influence plasma triacylglycerol levels. Tissue antioxidant status (catalase (EC 1.11.1.6), glutathione peroxidase (EC 1.11.1.9), glutathione reductase (EC 1.6.4.1) and superoxide dismutase (EC 1.15.1.1) activities and glutathione content) was generally not greatly affected by dietary fat blend or cholesterol treatment. Birds fed on HC diets exhibited severe (P < 0.001) atherosclerotic plaque in aortas which was not influenced by the source of dietary fat blend. Scanning electron microscopy confirmed results of visual aortic plaque scoring using dissecting light microscopy. Several cholesterol oxides were identified and quantified in aortic plaque from HC-fed birds (5,6α-epoxy-5α-cholesterol, 7β-hydroxycholesterol and 7-ketocholesterol) regardless of dietary fat blend. The results indicate that dietary fat blends varying in polyunsaturated: saturated fatty acid ratios only marginally influence the degree of hypercholesterolaemia in atherosclerosis-susceptible quail fed on atherogenic diets only, and are not a factor, compared with sterol feeding, in modulating the degree of atherosclerosis or the aortic oxysterol content in these same birds. Moreover, diet-induced hyperlipoproteinaemia had only a small effect on antioxidant status of selected tissues examined.

This study was designed to quantify starch digestion within the small and large bowels separately when raw potato starch (RPS) was included at 0-240 g/kg in diets fed to growing male Wistar rats. RPS was incorporated in the diets at the expense of maize starch which was expected to be almost completely digested in the small bowel. The digestibility of the maize starch was 0.99 but only 0.28 of the RPS was digested before the terminal ileum so that with increasing intakes of RPS there was a progressive increase in starch supply to the large bowel (LB). Of this starch 0.77, 0.72 and 0.73 was fermented in the large bowel when RPS constituted 80, 160 and 240 g/kg diet respectively. With increasing RPS intake, there was a curvilinear response in molar proportion of butyrate in caecal contents with a maximum value at about 80 g RPS/kg diet. The molar proportion of acetate increased linearly, that of propionate was unchanged, whilst proportions of the minor short-chain fatty acids all declined markedly with increasing RPS intake. The novel marker Bacillus stearothermophilus spores (BSS) was compared with CrEDTA in estimation of whole-gut mean transit time (MTT) when given together in a single test meal. Whilst estimates of MTT for the two markers were strongly correlated within individual rats (r2 0.72), BSS produced estimates that were 13 h longer than those based on CrEDTA. Neither marker detected a change in MTT with increasing RPS intake but, with both, the rate constant (k1) for the ‘largest mixing pool’ declined significantly (P < 0.001) as dietary RPS concentration was changed from 0-240g/kg.