The composition of 500 foods has been stored in a computer in order to analyse a child's diet. The methodology of operations research is applied to a very simple problem: a diet with only two foods. The geometrical representation of the ‘feasible region’ and of the ‘objective function’ is illustrated. One of the analytical methods employable with many variables (foods) is considered. This method was used in trying to find diets allowing for the preferential use of selected foods while respecting recommended dietary allowances, the tastes of the child and other constraints. The theoretical difficulty of transferring this methodology to pediatric dietetics was examined. We solved a simple case utilizing this procedure.

Subjects aged 16–64 years (592; 258 men and 334 women), randomly selected from the population of Northern Ireland, kept a 7 d weighed record of all food and drink consumed. Social, personal and anthropometric data were also collected. From the weighed records food consumption was described in terms of forty-one food groups. Using principal components analysis, four distinct dietary patterns were generated which were identified as a traditional diet, a cosmopolitan diet, a convenience diet and a ‘meat and two veg’ diet. These dietary patterns were then correlated with sociocultural, lifestyle and anthropometric variables. It is clear that dietary behaviour is influenced by a number of inter-related sociocultural demographics and that identifiable population groups in Northern Ireland have different dietary behaviours.

Full blood counts, serum ferritin, vitamin B12 and folate, erythrocyte folate concentrations and nutrient intakes were estimated in twenty-three Indian vegetarian, twenty-two Caucasian omnivores and eighteen Caucasian vegetarian women aged 25–40 years. Energy and copper intakes were lower in the Indian women than in the Caucasians. Intakes of dietary fibre, vitamin C and folate were greater and the proportion of energy derived from fat was lower in the vegetarians than in the omnivores. Vitamin B12 and protein intakes were lower in both vegetarian groups than in the omnivores. Fe intake was similar in all the groups but haem Fe provided one-quarter of the Fe intake of the omnivores. Haemoglobin concentrations were generally inside the normal range in all groups, but were lower in the Indians as were mean corpuscular volume (MCV) and mean corpuscular haemoglobin (MCH). Higher MCV, MCH and lower erythrocyte (RBC) counts were observed in Caucasian vegetarians compared with the Caucasian omnivores. In both groups of vegetarians, concentrations of serum vitamin B12 and ferritin were markedly lower than in the omnivores. RBC folate concentrations were lower in the Indians than in either of the Caucasian groups when subjects taking supplements were excluded. It is concluded that vegetarians need to ensure they have adequate intakes of Fe and vitamin B12.

A study was conducted to investigate the effect of differential dose levels of methylxanthines on lactational performance, with respect to milk volume and composition and pup growth. The methylxanthines; caffeine, theophylline and theobromine, were administered via drinking water in the proportions occurring in tea, at a dose of 50, 1 and 2 mg/kg body-weight respectively to Wistar albino rats throughout pregnancy and for up to the 14th day of lactation. A fourth group received a mixture of all three methylxanthines. Maternal food and fluid intake and weight changes, as well as weight gain in the litter were monitored thrice weekly. Milk samples were collected from the dams on days 7 and 14 of lactation, while milk volume was measured on days 12–13 by a method using tritiated water. Results showed that caffeine and theobromine significantly enhanced litter weight (P < 0.01 and 0.05 respectively). In the caffeine group, enhanced litter growth was due to a significant increase (P < 0.05) in milk volume, consequent to increased maternal food intake (P < 0.05). In the theobromine group there was only a weak association between increased litter weight and milk volume. Theophylline had no effect on the volume or composition of milk, or litter weight. The combination of all three methylxanthines also failed to produce any of the positive effects observed with separate drug treatments.

About 450 pregnant women from a low-income group were recruited to study the effect of vitamin A supplementation on plasma vitamin A levels in the mother and cord and on the birth weights of the neonates. Results showed that supplementation with 1800 μg vitamin A/d for more than 12 weeks prevented the decline in plasma vitamin A that otherwise occurs during the last few weeks of pregnancy. This improvement in maternal values for vitamin A at a critical time of development favourably affected availability to the fetus, as reflected by the marked elevation in cord levels. Supplementation for a period of 12 weeks was found to be sufficient, since subsequent discontinuation did not alter the beneficial response. Apart from increasing maternal and cord vitamin A levels, vitamin A supplementation along with iron prevented, in this study, the significant decline in haemoglobin occurring at 26–28 weeks of gestation. The birth weights were not altered by vitamin A supplementation.

Wether sheep were fitted with rumen fistulas and polyethylene tubes to the abomasum and were given all nutrients by intragastric infusion. In Expt 1 volatile fatty acids (VFA) were given at 340, 450 and 630 kJ gross energy (GE)/kg metabolic weight (W0.75) and protein at 0, 150, 300, 600, 900 and 1500 mg nitrogen/kg W0.75. In Expt 2 VFA were infused at 450 kJ GE/kg W0.75 and protein at 0 and 300 mg N/kg W0.75. At all levels of energy intake in Expt 1 the N retention was significantly (P < 0.01) related to N intake. The basal N requirement was estimated to be 281 mg (SE 21.8) N/kg W0.75 at 340 kJ VFA/kg W0.75, 226 (SE 21.8) mg N/kg W0.75 at 450 kJ VFA/kg W0.75 and 207 (SE 19.4) mg N/kg W0.75 at 630 kJ VFA/kg W0.75. Plasma urea concentrations varied markedly in relation to protein intake and to energy supply. On the other hand plasma ammonia, glucose, insulin and creatinine concentrations, and also urinary excretion of purine derivatives and creatinine were not significantly affected by the treatments imposed. It was concluded that the urinary excretion of purine derivatives in ruminants was largely unaffected by moderate changes in energy intake and by large changes in protein intake.

The kinetics of urea metabolism were measured in children recovering from severe malnutrition. For a period of up to 10 d they received one of four diets which provided 711 kJ (170 kcal)/kg per d. Two groups received a diet with a high protein: energy (P:E) ratio of 10.6% (HP), enriched with either fat (HP/F) or maize starch and sucrose (HP/C). Two groups received a diet with a low P:E ratio of 8.8% (LP), enriched with either fat (LP/F) or maize starch and sucrose (LP/C). The rate of weight gain on the HP diets was significantly greater than on the LP diets. There was no difference in urea production between any of the four diets: HP/F 1.23 (SE 0.12), HP/C 1.37 (SE 0.14), LP/F 1.64 (SE 0.22), LP/C 1.15 (SE 0.15) mmol nitrogen/kg per h. On the HP diets urea excretion was 0.77 (SE 0.07) mmol N/kg per h. 61 % of production. There was significantly less urea excreted in the urine on diet LP/C than on LP/F (0.36 (SE 0.05) and 0.64 (SE 0.04) mmol N/kg per h respectively). A significantly greater percentage of the urea production was hydrolysed on the LP diets (61 %) compared with the HP diets (39 %), with the consequence that 50% of urea-N produced was available for synthetic activity on the LP diets compared with 30% on the HP diets. The increase in the urea hydrolysed on the LP diets was equivalent in magnitude to the decreased intake of N, so that overall intake plus hydrolysis did not differ between the LP and the HP diets. Crude N balance was similar on diets HP/F, HP/C and LP/C, but was significantly reduced on diet LP/F. These results show that there is an accommodation in urea kinetics during rapid catch-up weight gain, which becomes evident when the P:E ratio of the diet falls to 8.8%. It is proposed that, for a P:E ratio of 8.8%, protein is limiting for catch-up growth. When the intake has a P:E ratio of 8.8% the pattern of urea kinetics can be modified by the relative proportions of fat and carbohydrate in the diet. The measurement of urea kinetics provides a useful approach to the definition of the adequacy of the protein in the diet.

Dietary nitrate and nitrite may affect colonic pathophysiology. These anions influence fermentation, and nitrite has been shown to augment sodium absorption by the colon and participate in the formation of N-nitroso compounds. There is, however, no general agreement as to how much dietary nitrate and nitrite reaches the colon. To help resolve this question, balance studies were performed on six healthy ileostomy subjects who were given diets that varied in nitrate content from 0.83 to 5.20 mmol/d. Nitrate and nitrite excretion in ileal effluent and urine were measured by anion-exchange chromatography with conductivity detection. There was no significant nitrite in the diets, urine, or ideal effluent. Dietary nitrate was largely excreted in urine (1.31–4.25 mmol/d). The urinary excretion findings indicated net synthesis of nitrate at low dietary intakes and net catabolism of nitrate at high intakes. Nitrate losses in ileal effluent were very low (0.03–0.05 mmol/d, 0.03–0.06 mmol/kg) and unrelated to intake for all the diets. It is concluded that dietary nitrate and nitrite do not enter the colon from the small intestine in amounts that would affect fermentation and mucosal metabolism in man. The possibility of significant amounts of nitrate reaching the colon via blood in normal subjects has not been excluded.

The effect of feeding v. fasting, on tissue blood flow, oxygen uptake and proportional contributions of the portal drained viscera (PDV), liver (Expts 1 and 2) and hindquarters (HQ; Expt 2) to whole-body O2 uptake were studied in beef steers. The combined techniques of indirect calorimetry and net tissue flux, the latter being the product of arterio-venous concentration difference and blood flow, were used in the experiments. In response to fasting, whole-body O2 consumption decreased as did O2 uptake by all measured tissues except the liver (trend only in Expt 1). Blood flow to all measured tissues decreased during fasting and fractional uptake of O2 decreased in PDV and increased in liver and HQ (Expt 2). Proportional contribution of specific tissues to whole-body O2 uptake changed when animals were switched from the fed to the fasted state. The percentage consumed by PDV decreased from 25.4 to 19.9, by liver increased from 20.5 to 26.4 and by HQ was unchanged (9.6 and 10.5) in Expt 2. These significant responses in Expt 2 were observed as trends in Expt 1. The changes in proportional contribution of tissues to whole-animal O2 uptake reflect the changing metabolic role of specific tissues to lack of food supply. These findings emphasize the central role of the liver in metabolism and indicate that fasting (catabolic) measurements may not reflect the previous fed (anabolic) physiological state.

The impact of alcohol (ethanol) on resting energy expenditure of male non-obese volunteers was determined in two studies. In the first study the thermic effect of alcohol on resting metabolic rate (RMR) was assessed in ten male non-obese volunteers. In the second study the impact of alcohol on diet-induced thermogenesis (DIT) was determined in twelve male non-obese volunteers. Energy expenditure was measured with a ventilated-hood system. RMR was measured for 60 min with the subjects in a fasting state. In the first study subjects received in random order 20 g alcohol in concentrations of 75, 180 and 300 ml/I water respectively. After measurement of the RMR the thermic effect of alcohol was measured for 90 min. In the second study volunteers received in random order and in duplicate either a meal of food (2 MJ) plus an alcoholic aperitif (20 g alcohol in a 180 ml/1 solution) or an isoenergetic meal of food alone (2.55 MJ) plus a placebo aperitif containing no alcohol. DIT was measured for 240 min. Alcohol induced a significant thermic effect, which varied between 0.22 and 0.30 kJ/min. No systematic difference in DIT was observed among the different concentrations. DIT was not significantly affected by the ingestion of alcohol. Total DIT was 219 (SE 14) kJ for the alcohol treatment and 185 (SE 20) kJ for the control treatment. The results do not support the suggestion that alcohol is less efficiently used as an energy source in comparison with, for example, fats and carbohydrates.

The effect of underfeeding for 7 d (at 60 kJ/kg ideal body-weight) on the thermic and physiological responses to glucose and insulin infusions (hyperinsulinaemic euglycaemic clamp) was studied in six healthy women. Underfeeding had no significant effect on baseline metabolic rate, heart rate, forearm blood flow, diastolic blood pressure, blood intermediary metabolites, plasma insulin or catecholamines, but reduced both respiratory exchange ratio (RER; control (C) 0.86 (SE 0.02), underfed (U) 0.75 (SE 0.01) P < 0.01) and systolic blood pressure (by approximately 10 mmHg, P < 0.01). Baseline forearm glucose uptake and oxygen consumption were similar in both states. During the final 30 min of the glucose and insulin infusion, metabolic rate rose by 0.43 (SE 0.05) kJ/min in the C state, but no rise was seen in the U state (P < 0.01). Glucose disposal rate (C 47.9 (SE 1.8), U 47.3 (SE 4.1) μmol/kg per min) and storage rate (C 27.5 (SE 2.4), U 31.6 (SE 3.6) μmol/kg per min) were similar in both states, but glucose oxidation rate was reduced in the U state (C 20.5 (SE 1.7), U 15.4 (SE 0.7) μmol/kg per min; P < 0.05). RER rose to a higher value in the C state than in the U state (C 0.97 (SE 0.2), U 0.80 (SE 0.01); P < 0.01). During hyperinsulinaemia, the forearm glucose uptake and O2 consumption rose in both states. No significant differences were seen in the cardiovascular responses to hyperinsulinaemia in either state. Thus underfeeding abolishes the rise in thermogenesis and reduces glucose oxidation during glucose and insulin infusions in healthy women, but does not affect the glucose disposal or storage rates or the other measured responses.

Thirty-two crossbred wether lambs (initial live-weight 31 kg) were fed on a diet (metabolizable energy (ME) 12.8 MJ/kg) ad lib. (ADLIB) or restricted to maintain body-weight (MAINT) for a 21 d period. On days 0, 7, 14 and 21, four lambs per treatment were slaughtered, visceral organs weighed and tissues sampled. During the 21 d period, ME intake in ADLIB lambs increased quadratically with an average rate of live-weight gain of 425 g/d. In MAINT lambs, live weight (30 kg) was maintained, and daily ME intake (kJ/kg empty body-weight (EBW)0.75) declined (P < 0.01) quadratically with time. Weights of liver, stomach and small intestines as a percentage of EBW were increased in ADLIB lambs and decreased by 10–33 % in MAINT lambs (treatment × day, P < 0.01). In vitro liver oxygen consumption was not affected by level of feed intake. Estimates of whole-liver O2 consumption (mmol O2/d per kg EBW) increased in ADLIB lambs and were relatively constant in MAINT lambs. These findings suggest that level of feed intake changes the relative proportion of visceral organs to body mass. In addition, the effect of level of feed intake on changes in the relative contribution of visceral organs to whole-body metabolic rate appears to be primarily a result of differences in organ size rather than tissue-specific metabolic activity.

Maternal whole-body glucose entry rate and uterine and umbilical net uptakes of glucose and oxygen were measured in single-pregnant ewes which were either well-fed throughout, or fed at 0.3–0.4 predicted energy requirement for 7–21 d during late pregnancy. All ewes were studied while standing at rest and then while walking on a treadmill at 0.7 m/s on a 10° slope for 60 min. Underfed ewes suffered significant decreases in live weight and had lower fetal, but not placental, weights at 140–144 d gestation. Undernutrition also caused large decreases in maternal glycaemia and glucose entry rate, which were associated with equally large decreases in uterine and umbilical net uptakes and O2 quotients of glucose, and with a decrease in placental glucose transfer capacity. Exercise caused increases in maternal blood concentration, entry rate and uterine net uptake of glucose, the magnitudes of which were not significantly affected by plane of nutrition. Umbilical glucose uptake and placental glucose transfer capacity increased during exercise in underfed but not fed ewes. The fractional distribution of maternal glucose to the pregnant uterus, and of uterine glucose uptake to the fetus, were unaltered by undernutrition; during exercise, a disproportionately small fraction of the increased maternal glucose supply went to the uterus. The results confirm that the ovine conceptus responds to nutritional reduction in maternal glucose availability in a manner similar to non-uterine maternal tissues. Major reductions in glucose supply appear to override putative glucose-sparing mechanisms which may operate to favour the conceptus in better-nourished animals.

Fetal glucose kinetics were measured using a combination of isotope-dilution and Fick-principle methodology in single-pregnant ewes which were either well-fed throughout, or fed at 0.3–0.4 predicted energy requirement for 7–21 d during late pregnancy. All ewes were studied while standing at rest and then while walking on a treadmill at 0.7 m/s on a 10° slope for 60 min. Underfed ewes suffered major decreases in fetal total disposal rate, fetal-placental transfer and umbilical net uptake of glucose, each of which were significantly related to declines in maternal and fetal blood glucose concentrations respectively. In well-fed ewes, fetal endogenous glucose production was negligible, as indicated by the similarity between fetal utilization rate (total glucose disposal rate minus placental uptake of fetal glucose) and umbilical net uptake of glucose, and by nearly identical fetal and maternal arterial blood specific radioactivities of maternally infused D-[2-3H]glucose. By contrast, in underfed ewes, fetal utilization rate greatly exceeded umbilical net uptake of glucose, and the fetal:maternal [3H]glucose specific activity ratio declined significantly, suggesting induction of a substantial rate of fetal endogenous glucogenesis. Exercise caused increases in fetal total glucose disposal rate and glycaemia in fed and underfed ewes. In underfed ewes only, this was accompanied by increased placental uptake of fetal glucose and umbilical net glucose uptake, unchanged fetal glucose utilization and decreased fetal endogenous glucose production. It is concluded that fetal gluconeogenesis makes a major contribution to fetal glucose requirements in undernourished ewes. Increased maternal supply of fetal glucose during exercise substitutes for rather than adds to fetal endogenous glucogenesis.

The effect in rabbits of giving isonitrogenous purified diets containing casein, ovalbumin, fish protein, milk-whey protein and soya-bean protein were compared. The diets were balanced for cholesterol and for the amount and type of fat. When incorporated into low-cholesterol diets (0.8 g cholesterol/kg), casein, ovalbumin and soya-bean protein produced similar levels of serum cholesterol. With a high background of dietary cholesterol (1.5 g/kg), serum cholesterol concentrations increased with soya-bean protein, whey protein, casein and fish protein, in that order. Thus, the hypercholesterolaemic effect of casein in carefully balanced diets was only seen against a high-cholesterol background. The development of hypercholesterolaemia produced by giving fish protein was different from that produced by casein. First, less cholesterol accumulated in the very-low-density-lipoprotein fractions and more in the lipoproteins of higher density with fish protein than with casein. Second, fish protein, unlike casein, did not increase liver cholesterol. Third, transfer of rabbits from a diet containing soya-bean protein to one containing casein resulted in an immediate marked depression in neutral steroid and bile acid excretion in faeces. However, when rabbits were fed on the diet with fish protein after the diet with soya-bean protein, there was no significant depression in neutral steroid output and the depression in bile acid output was delayed. The present study suggests that different animal proteins cause hypercholesterolaemia by different mechanisms.

Mongrel dogs were fed, from weaning to 9 months of age, on one of two diets that differed only in the type of fat content (virgin olive oil or sunflower oil) to compare the composition of exocrine pancreatic secretion in the basal period and in response to food. In resting pancreatic flow, electrolytes and the specific activities of amylase, lipase and chymotrypsin were similar in both experimental groups. However, lipase and amylase outputs, and amylase and protein concentrations were significantly higher in the group fed on the diet rich in sunflower oil. Food intake was not followed by any change in flow-rate or electrolyte or protein content in the group given the diet rich in olive oil. Amylase activity and output were also lower in this group, as was lipase output, whereas activity and specific activity of chymotrypsin were lower in dogs fed on the diet containing sunflower oil. The differences traceable to the composition of the two types of dietary fat supplied may be related to the balance between factors that stimulate and inhibit pancreatic secretion.

Little is known about the ability of carnitine to modulate cell functions. As carnitine plays an important role in lipid metabolism we investigated the acute effect of L-carnitine, L-acetyl carnitine and L-propionyl carnitine (300 mg/kg per d; 4 d) on the basal and calcium-ionophore (A23187)-stimulated release of arachidonic acid metabolites from rat carrageenan-elicited peritoneal macrophages. A decrease in the number of peritoneal carrageenan-elicited macrophages was observed after feeding all three compounds. The basal release of prostaglandin E2, 6 keto-prostaglandin F1α and leukotriene B4 was stimulated by all treatments. In contrast, thromboxane B2 production was diminished by feeding carnitine and acetyl carnitine. A23187-stimulated synthesis of 6 keto-prostaglandin F1α and leukotriene B4 was further enhanced by all three compounds. Acetyl carnitine and propionyl carnitine also enhanced thromboxane B2 synthesis. However, no effects on prostaglandin E2 formation were detected. The 6 keto-prostaglandin F1α: thromboxane B2 ratio, calculated from the basal and A23187-stimulated values, was increased by carnitine treatment. In the presence of A23187 there was also an increase in the 6 keto-prostaglandin F1α: leukotriene B4 ratio. We conclude that carnitine, and possibly some of its derivatives, could modify the macrophage component of an inflammation in vivo.

The purpose of the 2 × 2 factorial study was to determine the effect of varying levels of dietary calcium (2.5 and 10 g/kg) and butterfat (50 and 200 g/kg) on lipid utilization and on development of colon tumours in animals initiated with 1,2-dimethylhydrazine dihydrochloride. Among rats fed on 200 g butterfat/kg, the fourfold increase in Ca intake induced more than a sevenfold increase in faecal excretion of total lipids and almost a fortyfold increase in faecal excretion of acid-extractable lipid. Among rats fed on 50 g butterfat/kg, the ingestion of supplemental Ca had a less dramatic effect and induced only a twofold increase in faecal excretion of total lipids and a threefold increase in acid-extractable lipid. The volume of intestinal adenocarcinomas was correlated with the excretion of acid-extractable lipid in faeces (R 0.369, P < 0.02). Caecal enzymic activity was not correlated with tumour incidence or size or faecal lipid excretion. Overall, the fourfold increase in Ca intakes decreased total lipid absorption significantly but by less than 6%.