Based on the premise that dietary nitrate is detrimental to human health, increasingly stringent regulations are being instituted to lower nitrate levels in food and water. Not only does this pose a financial challenge to water boards and a threat to vegetable production in Northern Europe, but also may be eliminating an important non-immune mechanism for host defence. Until recently nitrate was perceived as a purely harmful dietary component which causes infantile methaemoglobinaemia, carcinogenesis and possibly even teratogenesis. Epidemiological studies have failed to substantiate this. It has been shown that dietary nitrate undergoes enterosalivary circulation. It is recirculated in the blood, concentrated by the salivary glands, secreted in the saliva and reduced to nitrite by facultative Gram-positive anaerobes (Staphylococcus sciuri and S. intermedius) on the tongue. Salivary nitrite is swallowed into the acidic stomach where it is reduced to large quantities of NO and other oxides of N and, conceivably, also contributes to the formation of systemic S-nitrosothiols. NO and solutions of acidified nitrite, mimicking gastric conditions, have been shown to have antimicrobial activity against a wide range of organisms. In particular, acidified nitrite is bactericidal for a variety of gastrointestinal pathogens such as Yersinia and Salmonella. NO is known to have vasodilator properties and to modulate platelet function, as are S-nitrosothiols. Thus, nitrate in the diet, which determines reactive nitrogen oxide species production in the stomach (McKnight et al. 1997), is emerging as an effective host defence against gastrointestinal pathogens, as a modulator of platelet activity and possibly even of gastrointestinal motility and microcirculation. Therefore dietary nitrate may have an important therapeutic role to play, not least in the immunocompromised and in refugees who are at particular risk of contracting gastroenteritides.

Homo sapiens has developed during the course of over two million years. The social and physical conditions of life, the availability of milk and infant foods as well as the presence of diseases have all undergone radical transformations from the Stone Age, at first without and then with fire, to the hunter–gatherer, farmer–herder, agricultural and, now, developed societies. These changes in the human environment may have induced modifications in the length of pregnancy, the development of the neonate at birth, the duration of lactation, the composition of breast milk and use of weaning foods and milk substitutes. Darwinian selection for the nutrient, anti-infective and other components of breast milk may have been determined by the effects of nutrition, through genetic variations in milk composition, on the survival of infants and perhaps also on fecundity and disease resistance in later adult life. Today Darwinian selection may no longer be effective in maintaining or modifying human mammary function, because modern hygienic environments, together with the availability of nutritionally adequate breast-milk substitutes, permit infant survival even under conditions of total lactational failure. National and international promulgations strictly control the composition of infant formulas offered as breast-milk substitutes or as weaning foods. These recommendations are modified as beliefs suggest, and research indicates, the effects of nutrients and other factors on the health and well-being of the child. Preliminary observations on child health have often proved valuable in furthering research. Unquestioning acceptance of apparently desirable, but untested, epidemiological associations have led to unexpected but dangerous iatrogenic problems. Recommendations for change cannot safely be made without proper comparisons with present products and procedures under practical conditions. Such tests are time consuming and require protocols of appropriate statistical design and power while still meeting the required sociological and ethical constraints, but are essential to identify possible harmful effects of any proposed change. It is suggested that no novel ingredients should be added, or major changes permitted in any component, until appropriate trials have established the value and safety of the proposed modifications. Breast-feeding is vital to maximize infant survival in developing countries. There are major difficulties in assessing any differences in morbidity and mortality of breast-fed v. artificially reared infants in the developed world. Carefully controlled studies with comparisons of health and well-being, not only in infancy but throughout life, are desirable if the effects of infant nutrition on adult well-being, suggested by epidemiological studies, are to be validated and ultimately applied. There are considerable variations in the composition of breast milk. This variance suggests that it may ultimately be possible to design formulas better able to meet the needs of individual infants than the milk available from the mother's breast.

Six healthy lean male adults, given a mixed meal containing 3190 kJ (16% from protein, 44% from carbohydrate and 40% from fat) were studied for the next 370 min using arteriovenous cannulation techniques across superficial and deep forearm tissues. The meal produced no significant change in forearm blood flow or skin temperature. The major differences between superficial and deep forearm tissues were (a) creatinine release by deep tissues but not superficial tissues; (b) the release of non-esterified fatty acids (NEFA) by superficial tissues and uptake by deep tissues; and (c) the more prolonged large positive arteriovenous concentration difference for glucose across deep than superficial tissues. The similarities were (a) general pattern of individual amino acid exchanges and transient positive amino acid N balance after meal ingestion; (b) consistent uptake of glutamate and release of glutamine (the main carrier of N out of superficial and deep forearm tissues); (c) the magnitude of the arteriovenous concentration differences for glucose, NEFA and total amino acids were related to the changes in their circulating concentrations and to the oxidation of carbohydrate, fat, and protein in the whole body; and (d) increases in the arterio–deep venous and arterio–superficial venous differences for glucose did not result in increased release of lactate, alanine or pyruvate, implying no increase in the activity of glucose–lactate and glucose–alanine cycles between forearm tissues and the liver. This study suggests that in a number of ways superficial and deep tissues can be regarded, at least qualitatively, as behaving as a ‘single metabolic unit’.

Based on the premise that elevated blood pressure and low bone mass have both been associated with poor Ca nutriture and disturbances in Ca metabolism, a cross-sectional study was employed to determine if blood pressure and dietary Ca intake were significantly related to bone mass. Forty-seven men between 24–77 years of age with blood pressure values ranging from normal to mildly elevated comprised the study group. Blood pressure was measured with a random-zero sphygmomanometer. Bone mineral content (BMC) and density (BMD) of the hip, spine and total body were measured with dual-photon absorptiometry. Dietary intake and physical activity were also assessed. Multiple linear regression analysis was used for statistical analysis. After adjusting for known confounding variables (age, BMI, Ca intake, and others) diastolic blood pressure was negatively related to BMC (P ≤ 0·05) and BMD (P ≤ 0·01) of the total body, trochanteric region (P < 0·01) and Ward's triangle (P < 0·05), and to BMC of the femoral neck (P < 0·05) and lumbar spine, although the latter was just shy of statistical significance (P = 0·058). Systolic blood pressure was negatively related to trochanteric BMD (P = 0·04) and BMC (P = 0·06). Ca intake was positively related to total body BMD (P = 0·005), and BMC of the lumbar spine (P = 0·05). In this population of men, Ca intake was a positive predictor, and blood pressure was a negative predictor of regional measures of bone mass. These findings support the concept that independent of age, BMI and Ca intake, elevated blood pressure varies indirectly with bone mass and density, known predictors of osteoporotic fractures. Future studies are needed to determine whether elevated blood pressure is causally related to the development of low bone mass, and what role dietary Ca plays in that pathway.

Two experiments were carried out on cattle nourished entirely by intragastric infusion, to determine the extent to which glucose or a glucose precursor determines the response to protein infusion in energy-undernourished animals. In order to determine the requirement for glucose in 1-year-old fasting cattle, glucose was infused at increments to supply 0, 1·5, 2·5, 3·5, 4·5, 5·5 and 6·5 g/kg metabolic body weight (W0·75) and the effects on plasma β-hydroxybutyrate and N excretion were measured. At 5·5 g glucose/kg W0·75 plasma β-hydroxybutyrate was reduced to a basal level of 1·65 mmol/l and fasting N excretion reduced from 529 to 280 mg N/kg W0·75. No further reduction was observed with the higher level of 6·5 g glucose/kg W0·75. In the second trial, three steers were used in a 3 × 3 Latin square design and infused with a volatile fatty acid mixture of 65, 27 and 8 mol acetic, propionic and butyric acids respectively/100 mol, either at an estimated maintenance energy level of 450 kJ/kg W0·75 and supplying a calculated glucose equivalent level of 13·0 g/kg W0·75 (M1A), or at 1·5 × maintenance supplying a glucose equivalent of 20 g/kg W0·75 (M1·5A). Another mixture infused at the maintenance energy level contained 49, 43 and 8 mol acetic, propionic and butyric acids respectively/100 mol but with a glucose equivalent of 20 g/kg W0·75 (M1P). Casein was infused at each of these energy treatments to supply 0, 200, 400, 800, 1600 and 2500 mg N/kg W0·75 daily, and N balance and blood metabolites were measured. N retention increased linearly (r 0·98) with casein infusion. The coefficients for N retention were 0·55, 0·57 and 0·64 for M1A, M1·5A and M1P respectively. The mean efficiency of N utilization was 0·58. The results suggest that provided the glucose need is met there is no relationship between energy supply and efficiency and level of protein retention. However, the results also indicate that glucose requirement in cattle may be higher than that previously observed in sheep.

The effect of a maternal diet high in fat, similar to Western foods, and of diabetes on liver essential fatty acid composition of the mother and the newborn and sucking pups was investigated. Female Sprague-Dawley rats were fed on either a low-fat (42 g/kg) or a high-fat (329 g/kg) diet for 10 d before mating, throughout pregnancy and post-partum. On the first day of pregnancy, diabetes was induced by intravenous administration of streptozotocin in half the animals from the two diet groups. Half the pups were killed at birth, and the remaining pups and mothers at days 15 and 16 respectively. At birth, there was a significant reduction in the proportions of docosahexaenoic acid (DHA) in the liver phosphoglycerols and neutral lipids of the pups of both high-fat control and diabetic mothers compared with those of low-fat control and diabetic mothers. Diabetes decreased arachidonic (AA) and linoleic acid values in both the low- and high-fat groups at birth. The sucking pups of both the high-fat control and diabetic mothers exhibited a significant reduction in DHA and a concomitant compensatory increase in AA and a lowering in DHA–AA balance. In the mothers, the high-fat diet significantly increased the proportions of DHA in ethanolamine phosphoglycerols but had no observable effect in choline phosphoglycerols and neutral lipids. In the fetus the DHA level (g/100 g total fatty acids) was disproportionately reduced by the maternal high-fat diet. The adverse effect of the high-fat diet on the level of DHA (g/100 g total fatty acids) was greater in the neonate (and by implication the fetus) than in the sucking pups or mothers. It is concluded that a distortion of the biochemistry is induced in the offspring through a maternal high-fat diet, without genetic predisposition.

Experimental Mg deficiency leads to alterations in the immune response. Reduction of thymus weight and histological changes were previously observed in Mg-deficient rats after several weeks on a deficient diet, suggesting that functions of this immune organ may be affected by Mg deficiency. More recently, changes in the immune system during early Mg deficiency were shown. Thus, in the present study we examined modifications in the thymus during the early stages of Mg deficiency in weanling rats. From our results, it appears that Mg deficiency accelerates thymus involution. The assessment of apoptosis (enumeration of apoptotic cells on the basis of morphological criteria and intranucleosomal degradation of genomic DNA) showed greater values in thymuses from Mg-deficient rats as compared with controls. This was observed very early, since a significant difference was shown on the second day of deficiency, before reduced weight of thymus, which was recorded in the later period. These results indicate the relationship of accelerated thymus involution with an active process of cell death. Mg deficiency led to histological changes in the thymus. In the early stage of deficiency (second day) the presence of inflammatory cells was shown, suggesting that the inflammatory process was already occurring in the tissue studied. Later (eighth day) an increased proportion of epithelial reticular cells in the cortex was shown, indicating a remodelling process occurring in this period. Enhanced susceptibility to peroxidation also occurred very early during Mg deficiency. It may be hypothesized that disturbances in Mg status of short duration could have cellular effects with various deleterious consequences.