An abundant, balanced dietary intake of long-chain polyunsaturated fatty acids is an absolute requirement for sustaining the very rapid expansion of the hominid cerebral cortex during the last one to two million years. The brain contains 600 g lipid/kg, with a long-chain polyunsaturated fatty acid profile containing approximately equal proportions of arachidonic acid and docosahexaenoic acid. Long-chain polyunsaturated fatty acid deficiency at any stage of fetal and/or infant development can result in irreversible failure to accomplish specific components of brain growth. For the past fifteen million years, the East African Rift Valley has been a unique geological environment which contains many enormous freshwater lakes. Paleoanthropological evidence clearly indicates that hominids evolved in East Africa, and that early Homo inhabited the Rift Valley lake shores. Although earlier hominid species migrated to Eurasia, modem Homo sapiens is believed to have originated in Africa between 100 and 200 thousand years ago, and subsequently migrated throughout the world. A shift in the hominid resource base towards more high-quality foods occurred approximately two million years ago; this was accompanied by an increase in relative brain size and a shift towards modem patterns of fetal and infant development. There is evidence for both meat and fish scavenging, although sophisticated tool industries and organized hunting had not yet developed. The earliest occurrences of modem H. sapiens and sophisticated tool technology are associated with aquatic resource bases. Tropical freshwater fish and shellfish have long-chain polyunsaturated lipid ratios more similar to that of the human brain than any other food source known. Consistent consumption of lacustrine foods could have provided a means of initiating and sustaining cerebral cortex growth without an attendant increase in body mass. A modest intake of fish and shellfish (6–12% total dietary energy intake) can provide more arachidonic acid and especially more docosahexaenoic acid than most diets contain today. Hence, ‘brain-specific’ nutrition had and still has significant potential to affect hominid brain evolution.

The effects on mood of reducing dietary fat while keeping the energy constant were examined in ten male and ten female healthy volunteers aged between 20 and 37 years. Each volunteer consumed a diet containing 41% energy as fat for 1 month. For the second month half of the subjects changed to a low-fat diet (25% energy from fat) and the remainder continued to eat the diet containing 41% energy from fat. Changes in mood and blood lipid concentrations were assessed before, during and at the end of the study. Profile of mood states (POMS) ratings of anger–hostility significantly increased in the intervention group after 1 month on the low-fat diet, while during the same period there was a slight decline in anger–hostility in the control subjects (group F 6.72; df 1,14; P = 0.021). Tension–anxiety ratings declined in the control group consuming the higher fat diet but did not change in the group consuming the low-fat diet (group F 6.34; df 1,14; P = 0.025). There was a decline in fasting concentrations of HDL-cholesterol after the low-fat diet and a small increase in subjects consuming the medium-fat diet (group F 4.96; df 1,12; P = 0.046), but no significant changes in concentrations of total serum cholesterol, LDL-cholesterol or triacylglycerol were observed. The results suggest that a change in dietary fat content from 41 to 25% energy may have adverse effects on mood. The alterations in mood appear to be unrelated to changes in fasting plasma cholesterol concentrations.

Fe absorption was estimated in adults and infants from the erythrocyte incorporation of Fe isotopes added to infant formula. Fe absorption was measured in adults using radioisotopes, and in infants with a stable-isotope technique. In adults, the geometric mean Fe absorption from a ready-to-feed soya formula with its native phytic acid content was 2·4%. This increased to 6·0% (P < 0·05) after almost complete dephytinization. In infants, mean Fe absorption values were 3·9 and 8·7% respectively from the same products (P <0·05). In adults, mean Fe absorption from a spray-dried soya formula containing 110mg ascorbic acid/I was 4·1%, increasing to 5·3% (P < 0·05) when ascorbic acid was doubled to 220 mg/l. In infants, mean Fe absorption values were 5·7 and 9·5% (P < 0·05) from the same products. Mean Fe absorption from a milk-based formula was 6·5% in adults compared with 6·7% in infants. All meals in the adult and infant studies were fed using an identical meal size of 217g. Increasing the meal size threefold in adults did not change fractional Fe absorption. Mean Fe absorption values for each meal were lower in adults than in infants, but the relative inhibitory effect of phytic acid and the enhancing effect of ascorbic acid were similar. We conclude that Fe absorption studies in adults can be used to assess the influence of enhancers and inhibitors of Fe absorption in infant formulas fed to infants. Further studies, however, are required to extend these findings to weaning foods and complete meals.

Tea is a beverage consumed widely throughout the world. The existence in tea of chemopreventing compounds possessing antimutagenic, anticarcinogenic and antioxidative properties has been reported. High intakes of tea and foods containing flavonoids have recently been shown to be negatively correlated to the occurrence of CHD. However, tea may contain other compounds with similar activities. Using a new gas chromatographic–mass spectrometric method we measured lignans and isoflavonoids in samples of twenty commercial teas (black, green and red varieties) and, for comparison, six coffees. Both unbrewed and brewed tea were investigated. The analysis of the teas yielded relatively high levels of the lignans secoisolariciresinol (5.6–28.9 mg/kg; 15.9–81.9 μmol/kg) and matairesinol (0.56–4.13 mg/kg; 1.6–11.5 μmol/kg) but only low levels of isoflavonoids. Because the plant lignans, as well as their mammalian metabolites enterolactone and enterodiol, have antioxidative properties and these mammalian lignans occur in high concentrations in plasma, we hypothesize that lignan polyphenols may contribute to the protective effect of tea on CHD.

The role of cholecystokinin (CCK) in modulating feed intake depression in parasite-infected lambs was investigated using CCK receptor antagonists (L364–718 and loxiglumide). Four experiments were carried out using ewe lambs infected with 4000 Trichostrongylus colubriformis larvae/d or non-infected controls (n 8, live weight 25 kg). Animals were fed daily on a nutritionally complete pelleted diet and had free access to water. In the first experiment, infected and non-infected animals were injected subcutaneously with CCK antagonist (100 μg L364–718) or carrier alone as a single dose. In the second experiment, CCK antagonist (loxiglumide: 0, 5, 10 or 20mg/kg live weight) was injected into a jugular vein immediately before feeding. In the third experiment, animals were infused continuously with the CCK antagonist (loxiglumide; 10mg/kg per h) for 10 min before feeding and for the first 2 h of feeding. In the final experiment, lambs were fitted with an indwelling cerebral ventricular cannula and infused with a CCK antagonist (loxiglumide, 162μg/min), CCK agonist (CCK-8, 2.5 pmol/min), loxiglumide plus CCK-8 or sterile saline solution alone via the cannula for 30 min before feeding and for the first 60 min of feeding. In all the experiments short-term feed intake was recorded at 10 and 15 min intervals for the first and second hours of feeding respectively, then at hourly intervals for the remainder of the 8 h recording period. Peripheral injection with L364–718 or loxiglumide did not elevate feed intake in either the infected or non-infected animals. However, feed intake was increased (P < 0.05) in the short term by central infusion of loxiglumide, this effect being greater in the infected animals and apparently due to an elevation in intake during the second hour of feeding. CCK-8 depressed short term feed intake only in the infected animals (P < 0.05). Total daily feed consumption was not influenced by any of the pharmacological agents. The results indicate an involvement of central CCK receptors in regulation of feed intake depression following gastrointestinal parasitism of sheep and the possibility of a similar role in non-infected sheep. They do not support the singular importance of a peripheral action of CCK in determining satiety.

Cholecystokinin: Loxiglumide: Feed intake: Gastrointestinal parasites

Within the overall objective of whether ruminants are able to form conditioned aversions (CFA) toward a food flavour associated with the administration of an aversive stimulus which occurs naturally in food plants (oxalic acid, OA), two specific objectives were tested: (1) whether the rate and degree of formation of CFA are dependent on the dose rate of OA administered and (2) whether the persistence of formed CFA depends on the previous dose rate of OA. Sheep were conditioned to associate the specific flavour of one of two novel foods with either the oral administration of OA or equivalent placebos. Four dose rates of OA were tested (0.06, 0.12, 0.18 and 0.24 g/kg sheep live weight per d), with twelve sheep per dose. Each conditioning period lasted for 8 d and was repeated four times. At the end of each conditioning period the preference for the two flavours was measured in short-term, 20min preference tests. The persistence of the CFA was measured at 0, 7, 21 and 49 d after the completion of the conditioning phase with long-term, 3 h preference tests. The results of the experiment indicated that: (1) the rate and degree of formation of CFA were dependent on the rate of administration of OA; (2) sheep required repeated exposures to the lower dose rates of OA in order to develop CFA and these CFA did not persist in the absence of continual reinforcement; (3) CFA to the higher dose rates of OA were developed after as little as one exposure and persisted over a period of at least 7 weeks. These findings are consistent with the expectation that ruminants should be able to select a diet which minimizes the risk of consumption of potentially harmful foods, whilst at the same time maintaining a degree of flexibility in their feeding behaviour.

Alternative models for analyses of liver and mammary transorgan data were formulated and fitted to liver and mammary data sets respectively. The models considered metabolite inputs to and effluxes from an extracellular pool. In general, fits were greatly improved over previous efforts using other models (Miller et al. 1991a; Hanigan et al. 1992; Wray-Cahen et al. 1997). Errors of prediction were generally less than 15% for liver and less than 20% for mammary glands. With the possible exception of glutamine for the udder, all metabolites exhibited linear responses to extracellular concentrations within the observed ranges of inputs. However, prediction biases were evident for β-hydroxybutyrate, acetate, and propionate by liver and for arginine, histidine, citrulline and glycerol by mammary tissue. These biases were hypothesized to be caused by the existence of additional regulatory complexity. With the exception of histidine, parameter estimates for essential amino acid removal by liver were 2–3-fold lower than for mammary gland. Infusion of an amino acid mixture into the mesenteric vein did not alter parameter estimates for removal of amino acids by the liver. Treatment of cows with bovine somatotropin resulted in changes in mammary parameter estimates for aspartate, glutamate, leucine, phenylalanine, glucose, and glycerol.

The effect of intake on urea production, entry into the digestive tract and return of N to the ornithine cycle was studied in four sheep. Each sheep received 0–6, 1–2 and 1.8 × estimated maintenance energy intake quantities of grass pellets for 9 d. After 4 d of adjustment, N balance measurements were conducted between days 5 and 8. From day 7 to day 9 animals were continuously infused, via the jugular vein, with [15N15N]urea and three urine samples were collected at approximately 2h intervals 48–54h after the start of infusion. Total urea and enrichments of [15N15N]- and [14N15N]urea in the urine samples were determined. Urea production was calculated from the isotopic dilution of [15N15N]urea and entry into the gastrointestinal tract (GIT) obtained from the difference between this and urinary urea elimination. Urea which enters the GIT undergoes hydrolysis to liberate NH3 which may be reabsorbed and enter the ornithine cycle, in which case the product is [14N15N]urea, based on the probabilities of labelled and unlabelled N providing ureagenic precursors. The quantity of urea-N which returns to the ornithine cycle from the GIT can thus be calculated. Existing models based on this approach yield overestimates of the fate of individual urea molecules due to a failure to allow for multiple recycling of [14N15N]urea species through the GIT. Refinements introduced to cover this resulted in a 33–48 % reduction in calculated return of label for the current study. The present model also predicted that 95 % of the label movements across the GIT could be accommodated by three or fewer entries and returns of urea-N and 99 % by recycling for a maximum of six occasions. Urea-N production increased with intake (P < 0.001) and exceeded digestible N values at all intakes. Urea which entered the digestive tract, both in absolute terms (P < 0.001) and as a proportion of production (0.62, 0.69, 0.73; P = 0.027), increased with intake. The proportion of entry into the digestive tract which was returned to the ornithine cycle remained reasonably constant (0.37–0.41) across all intakes but the absolute amount increased (5.6, 9.2 and 15.0gN/d; P < 0.001) with intake. If allowance is included for losses of 15N in faeces then the approach offers a relatively simple means of estimating anabolic reuse of urea by digestive tract micro-organisms and can complement data obtained from the technically more demanding arterio-venous and multiple-isotope techniques used hitherto.

Urea: Gastrointestinal tract: [15N]kinetics: Sheep

Indian River male broiler chickens growing from 7 to 28 d of age were fed on diets containing either 120 or 210 g crude protein and 0 or 1 mg triiodothyronine (T3)/kg diet to study in vitro lipogenesis (IVL). In addition, a carry-over period (180 g crude protein/kg diet from 28 to 40 d of age) was used to test the persistence of prior treatment effects. The higher protein level increased, but T3 decreased (P < 0.01) growth and feed consumption at 28 d of age. The lower protein level increased (P < 0.05) and T3 decreased IVL in 28-d-old chickens. These effects were only sustained for 6 d following the switch to a common diet at 28 d. IVL at 40 d of age was not affected by either crude protein or T3 fed during the 7–28 d period. The higher protein level increased plasma insulin-like growth factor-1 during the period from 7 to 28 d; however, this effect lasted for only 6 d following the switch to a common diet. Plasma growth hormone (GH) at 28 d of age was inversely related to dietary protein level. Changing to a common level of crude protein did not change plasma GH values at 12 d, indicating that the nutritional state of the young chicken may affect GH at a later period of life. Metabolic changes noted in this study were rapid and maintained for a short period of time following the feeding of a common diet.

Lipogenesis: Dietary protein: Triiodothyronine

The effects of freeze-dried soya milk (SM) and Bifidobacterium-fermented soya milk (FSM) on plasma and liver lipids, and faecal steroid excretion were estimated in hamsters fed on a cholesterol-free or cholesterol-enriched diet. Hamsters fed on the cholesterol-free diet containing 300 g FSM/kg had lower levels of plasma VLDL + LDL cholesterol than the animals fed on the control diet. SM in the diet produced a similar pattern without significant differences. In the cholesterol-enriched diet group, SM and FSM decreased the levels of plasma total cholesterol and VLDL + LDL-cholesterol. SM and FSM decreased the plasma triacylglycerol level in both the cholesterol-free and -enriched diet groups. The liver total cholesterol contents in the SM and FSM groups were lower than that in the control group, for hamsters fed on the cholesterol-free diet. The liver triacylglycerol content was not modified by SM or FSM in hamsters fed on either the cholesterol-free or -enriched diet. SM and FSM increased the total bile acid excretion and the proportion of cholesterol entering the cholic acid biosynthesis pathway in both the cholesterol-free and -enriched diet groups. SM and FSM did not affect neutral steroid excretion in the cholesterol-free or -enriched diet group. There was an inverse relationship between VLDL + LDL-cholesterol and faecal bile acid excretion in hamsters fed on the cholesterol-free (r −0.670, P < 0.01) and cholesterol-enriched (r −0.761, P < 0.001) diets respectively. These results indicated that SM had an anti-atherogenic effect, and that this effect was not diminished by prior fermentation.