Environmental factors are important in the aetiology of glucose intolerance, type II diabetes and IHD. The lack of vitamin D, which is necessary for adequate insulin secretion, relates demographically to increased risk of myocardial infarction. These disorders are connected, degenerative vascular disease increasing with glucose intolerance and diabetes and, with its risk factors, comprising syndrome ‘X’. Evidence is presented suggesting that vitamin D deficiency may be an avoidable risk factor for syndrome ‘X’, adding another preventative measure to current recommendations which are aimed at reducing the worldwide epidemic of these disorders. Experimentally, vitamin D deficiency progressively reduces insulin secretion; glucose intolerance follows and becomes irreversible. Relationships between vitamin D status, glucose tolerance and 30 min insulin secretion during oral glucose tolerance tests are reported in British Asians; insulin secretion, but not glycaemia, improving with short-term supplementation. Studies showing reduction in blood pressure and in risk of heart attack and diabetes with exercise (usually outdoor), rarely consider the role of vitamin D status. Glycaemia and insulin secretion in elderly European men, however, relate to vitamin D status, independent of season or physical activity. Prolonged supplementation can improve glycaemia. Hypertension improves with vitamin D treatment with or without initial deficiency. Vitamin D status and climate are reviewed as risk factors for myocardial infarction; the risk reducing with altitude despite increasing cold. Glycaemia and fibrinogenaemia improve and insulin secretion increases in summer. Variation in vitamin D requirements could arise from genetic differences in vitamin D processing since bone density can vary with vitamin D-receptor genotype. Vitamin D receptors are present in islet β cells and we report insulin secretion in healthy Asians differing profoundly with the Apa I genotype, being independent of vitamin D status. Those at risk of vitamin D deficiency include the elderly, those living indoors or having a covered-up style of dress, especially dark-skinned immigrants, and pregnant women, and these are groups recognized as being at increased risk of diabetes.

Phyto-oestrogens have emerged from their esoteric role in animal husbandry following the hypothesis that the human Western diet is relatively deficient in these substances compared with societies where large amounts of plant foods and legumes are eaten. Evidence is beginning to accrue that they may begin to offer protection against a wide range of human conditions, including breast, bowel, prostate and other cancers, cardiovascular disease, brain function, alcohol abuse, osteoporosis and menopausal symptoms. Of the two main classes of these weak oestrogens, the isoflavones are under intensive investigation due to their high levels in soyabean. Like the ‘anti-oestrogen’ Tamoxifen, these seem to have oestrogenic effects in human subjects in the cardiovascular system and bone. Although previously only available from food, isoflavones are now being marketed in health-food supplements or drinks, and tablets may soon be available over the counter as ‘natural’ hormone-replacement therapy. In cancer, anti-oestrogenic effects are thought to be important, although genistein especially has been shown to induce wide-ranging anti-cancer effects in cell lines independent of any hormone-related influence. There are few indications of harmful effects at present, although possible proliferative effects have been reported. In infants, the effects of high levels in soya milk formulas are uncertain. The second group, lignans, have been less investigated despite their known anti-oestrogenic effects and more widespread occurrence in foods. Investigation of the possible benefits of phyto-oestrogens is hampered by lack of analytical standards and, hence, inadequate methods for the measurement of low levels in most foods. This problem may prove to be a major dilemma for regulatory authorities, clinicians and others wishing to advise the general public on whether these compounds really do have the health benefits attributed to them.

During endurance exercise, skeletal muscle relies mainly on both carbohydrate (CHO) and fat oxidation to cover energy needs. Numerous scientific studies have shown that increasing the exercise intensity leads to a progressive utilization of CHO. The latter will induce a state of glycogen depletion which is generally recognized as being a limiting factor for the continuation of strenuous exercise. Different dietary interventions have been proposed to overcome this limitation. A high-CHO diet during periods of intense training and competition, as well as CHO intake during exercise, are known to maintain a high rate of CHO oxidation and to delay fatigue. However, it has been recognized also that enhancing fatty acid (FA) oxidation during exercise induces a reduced rate of glycogen degradation, resulting in an improved endurance capacity. This is most strikingly observed as a result of frequent endurance exercise which improves a number of factors known to govern the FA flux and the oxidative capacity of skeletal muscle. Such factors are: (1) blood flow and capillarization; (2) lipolysis of triacylglycerol (TAG) in adipose tissue and circulating TAG and transport of FA from blood plasma to the sarcoplasm; (3) availability and rate of hydrolysis of intramuscular TAG; (4) activation of the FA and transport across the mitochondrial membrane; (5) the activity of enzymes in the oxidative pathway; (6) hormonal adaptations, i.e. sensitivity to catecholamines and insulin. The observation that the plasma FA concentration is an important factor in determining the rate of FA oxidation, and that some dietary factors may influence the rate of FA supply to muscle as well as to the mitochondria, has led to a number of dietary interventions with the ultimate goal to enhance FA oxidation and endurance performance. It appears that experimental data are not equivocal that dietary interventions, such as a high-fat diet, medium-chain TAG-fat emulsions and caffeine intake during exercise, as well as L-carnitine supplementation, do significantly enhance FA oxidation during exercise. So far, only regular endurance exercise can be classified as successful in achieving adaptations which enhance FA mobilization and oxidation.

Fe deficiency is considered to be the commonest of nutritional deficiencies worldwide. Adverse effects are stated to include lower growth rate and impaired cognitive scores in children and poor pregnancy outcome and lower working capacity in adults. In the present review, Fe intake, stores of the element, the magnitude of deficiencies and the benefits from interventions, as reflected in the results of clinical trials, are discussed. Because of inadequacies of knowledge in numerous respects, more information is needed regarding the extent to which clinical trials relate to public health realities, before introducing regional or national supplementation programmes. While Fe supplements are needed in certain groups, and in particular regions, increased dietary intakes could be supplied by food fortification, as well as by individual improvements in intake.

Ammonium tetrathiomolybdate (TTM) is the treatment of choice for chronic Cu poisoning in sheep and is recommended in Wilson's disease. However, the long-term effects have not been fully evaluated and some evidence questions the long-term safety of the drug. The aim of the present study was to investigate the systemic distribution and retention of Cu and Mo in TTM-treated sheep of different breeds and Cu status. Low-Cu Cambridge sheep were divided into a TTM trial group (3·4 mg/kg, subcutaneously, on three alternate days per month, for 5 months) and a control group, and were killed at the end of the course or 7 months later. High-Cu sheep consisting of a Cu-supplemented (150 mg/kg) Cambridge group and a North Ronaldsay group were administered TTM as before and compared with untreated controls. Brain, liver, kidney, heart, skeletal muscle, pituitary, adrenals, testes and ovaries were retained for metal analysis. Mo accumulated in all organs including brain and pituitary (P < 0·02) in all TTM trial groups and was retained after cessation of treatment, except in liver, kidney and skeletal muscle. Cu was increased (P < 0·02) and retained in the cerebellum and medulla oblongata in the TTM-treated high-Cu Cambridge groups. Brain Cu v. Mo concentrations showed a strongly positive correlation (r 0·7) in the high-Cu Ronaldsay group 7 months after TTM treatment. It is concluded that TTM is not all excreted but (Mo) is widely distributed and retained in many organs including brain and pituitary. In addition TTM may redistribute some displaced excess liver Cu (Cu-TTM) to the brain. The consequences of these disturbances await clarification.

The role of maternal diet in the development of the fetal brain has not been adequately explored. Marine n-3 fatty acids have, however, been proposed to be important for brain development. The present case–control study aimed to investigate the relationship between dietary intake during pregnancy and the occurrence of cerebral palsy (CP) in the offspring. Children with CP (n 109), born between 1984 and 1988 to mothers residing in the Greater Athens area, were identified at any time in 1991 or 1992 through institutions delivering care and rehabilitation. Successful nutritional interviews were conducted with ninety-one of these children. Controls were chosen among the neighbours of the CP cases or were healthy siblings of children with neurological diseases other than CP, seen by the same neurologists as the children with CP. A total of 278 control children were chosen, and 246 of them were included in the nutritional study. Guardians of all children were interviewed in person on the basis of a questionnaire covering obstetric, perinatal socioeconomic and environmental variables. A validated semiquantitative food-frequency questionnaire of 111 food items was used to estimate maternal dietary intake during pregnancy. Statistical analysis was done by modelling the data through logistic regression. Food groups controlling for energy intake were alternatively and simultaneously introduced in a core model containing non-nutritional confounding variables. Consumption of cereals (mostly bread) and fish intake were inversely associated with CP (P < 0·05 and P < 0·09 respectively) whereas consumption of meat was associated with increased risk (P < 0·02). A protective effect of fish consumption and a detrimental effect of meat intake have been suggested on the basis of earlier work and appear to be biologically plausible. If corroborated by other studies, these results could contribute to our understanding of the nutritional influences on fetal brain development.

A lower BMR of Indians, when compared with Westerners matched for age, sex, and either surface area or body weight, has often been reported in the literature and has been interpreted to reflect an ethnic influence on BMR. To determine the contribution of body composition to these observed differences in BMR, we analysed the data on ninety-six Indians and eighty-one Caucasian Australians of both sexes, aged 18–30 years, studied in Bangalore, India and Melbourne, Australia. Absolute BMR and BMR adjusted for body weight were significantly lower in Indians when compared with Australians of the corresponding sex. However, BMR adjusted for fat-free mass (FFM) in men, and BMR adjusted for FFM and fat mass (FM) in women, were not significantly different between the two groups. Stepwise regression of FFM, FM, sex (0 = women; 1 = men) and ethnicity (0 = Indian; 1 = Australian) on BMR, resulted in the following relationship for the combined data on all subjects: BMR=88.7 × FFM (kg) + 1713 (n 177; r 0.92; r2 0.85; see 425 kJ). The Indian equations of Hayter & Henry (1994), based on body weight, resulted in a significant bias (measured – predicted BMR) of 318 (SE 54) kJ/d in Indian men and -409 (SE 70) kJ/d in Indian women. The equation of Cunningham (1991), based on FFM, accurately predicted the BMR of Indian men, Indian women and Australian men. The small but significant bias of 185 (SE 61)kJ/d in Australian women, may be explained by the significant contribution of FM to BMR in this group. The present study does not provide any evidence for an ethnic influence on basal metabolism. The results strongly support the use of FFM, rather than body weight, for the prediction of BMR in population groups of varying body size and composition. This would allow an accurate estimation of BMR and hence energy requirements in population groups worldwide.

The aim of the present study was to evaluate changes in participation in physical activity and in fat and alcohol intake associated with ageing. This issue was examined in adults (n 207) who were tested between 1978 and 1982 and re-tested 12 years later. These adults were 42.3 (sd 4.9) years of age at baseline. Their children (n 122) were tested over the same follow-up period. They were, on average, 12.5 (sd 1.9) years at entry into the study. A decrease in the proportion of daily energy intake as fat and an increase in participation in vigorous physical activities were observed over the 12-year period in both groups. The proportion of dietary energy as alcohol remained stable in adults whereas it increased markedly in children. Correlation analyses between baseline and follow-up levels were significant for dietary fat and alcohol intake in adults. In children, the levels of these variables in the growing years did not predict the levels attained 12 years later. Even though the adults displayed changes in fat balance generally following current public health recommendations, a substantial increase in skinfold thicknesses was observed in these subjects during follow-up. This observation suggests that there is a strong effect of age-related factors on fat balance.

The present study examined the endogenous urinary excretion of purine derivatives (PD; allantoin, uric acid and xanthine plus hypoxanthine) in fed animals. Four Rasa Aragonesa ewes fitted with simple cannulas in the rumen and proximal duodenum were used. Animals were given a lucerne (Medicago sativa) hay diet, as sole feed (A) or supplemented, respectively, with 220 (B), 400 (C), and 550 (D) g rolled barley grain/d following a 4 × 4 random factorial design. Duodenal flow of purine bases (PB) was determined by the dual-phase marker system. 15N was infused continuously into the rumen to label exogenous or microbial PB. Duodenal PB flow and urinary excretion of PD increased with digestible organic matter intake showing a constant recovery of duodenal PB. The isotope dilution of PD in urine samples confirmed the presence of an endogenous fraction, originating from tissues, that increased from 115.2 (SE 5.84) μmol/kg W0.75 for the basal diet to 304.2 (SE 7.6) μmol/kg W0.75 at the highest level of duodenal PB.

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.

Preterm and term transitional milks of human subjects and mature milks of human subjects, non-human primates and non-primates were analysed for free amino acids (AA) using precolumn phenylisothiocyanate derivatization and liquid chromatography. Differences in free AA between three types of human milk were small. Milks of pinnipeds (seals and sea lions) contained the highest levels of total free AA (8634–20 862 μmol/1), while the milks of cows and sheep had the lowest levels of total free AA (1061–1357 μmol/1). The milks of human subjects, chimpanzees (Pan troglodytes), gorillas (Gorilla gorilla), elephants (Elephas maximus), horses and pigs had intermediate levels of total free AA (3069–7381 μmol/1). Glutamic acid was the most abundant free AA in milks of human subjects (1339–2157 μmol/1), non-human primates (423–2528 μmol/1), elephants (1332 μmol/1), horses (1119 μmol/1), and cows (349 μmol/1). Taurine was the most abundant free AA in milks of pinnipeds (5776–13 643 μmol/1), pigs (1238 μmol/1), goats (1150 μmol/1) and sheep (341 μmol/1). Taurine was the second most abundant free AA in milks of human subjects and non-human primates, while histidine was the second most abundant free AA in milks of pinnipeds. Milks of each species had a distinctive free AA pattern which may reflect the relative importance of the free AA during early postnatal development.

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.

Epidemiological evidence shows that a diet high in monounsaturated fatty acids (MUFA) but low in saturated fatty acids (SFA) is associated with reduced risk of CHD. The hypocholesterolaemic effect of MUFA is known but there has been little research on the effect of test meal MUFA and SFA composition on postprandial lipid metabolism. The present study investigated the effect of meals containing different proportions of MUFA and SFA on postprandial triacylglycerol and non-esterified fatty acid (NEFA) metabolism. Thirty healthy male volunteers consumed three meals containing equal amounts of fat (40g), but different proportions of MUFA (12, 17 and 24% energy) in random order. Postprandial plasma triacylglycerol, apolipoprotein B-48, cholesterol, HDL-cholesterol, glucose and insulin concentrations and lipoprotein lipase (EC 3.1.1.34) activity were not significantly different following the three meals which varied in their levels of SFA and MUFA. There was a significant difference in the postprandial NEFA response between meals. The incremental area under the curve of postprandial plasma NEFA concentrations was significantly (P = 0·03) lower following the high-MUFA meal. Regression analysis showed that the non-significant difference in fasting NEFA concentrations was the most important factor determining difference between meals, and that the test meal MUFA content had only a minor effect. In conclusion, varying the levels of MUFA and SFA in test meals has little or no effect on postprandial lipid metabolism.