Diets high in monounsaturated fatty acids (MUFA) are increasingly being recommended as a highly-effective cholesterol-lowering strategy in populations at risk of CHD. However, the need for a re-appraisal of the benefits of diets rich in MUFA became apparent as a result of recent studies showing that meals high in olive oil cause greater postprandial activation of blood coagulation factor VII than meals rich in saturated fatty acids. The present review evaluates the evidence for the effects of MUFA-rich diets on fasting and postprandial measurements of haemostasis, and describes data from a recently-completed long-term controlled dietary intervention study. The data show that a background diet high in MUFA has no adverse effect on fasting haemostatic variables and decreases the postprandial activation of factor VII in response to a standard fat-containing meal. Since the same study also showed a significant reduction in the ex vivo activation of platelets in subjects on the high-MUFA diet, the overall findings suggest that there is no reason for concern regarding adverse haemostatic consequences of high-MUFA diets.

Approximately 5–7 % of all infants are born prematurely, and birth before 37 weeks is the most common cause of neonatal mortality, morbidity and long-term disability. Premature infants are poorly equipped for life outside the womb, and oxidant stress has been implicated in the aetiology of visual impairment in these infants, who are often exposed to increased O2 concentrations and high light intensity in neonatal units. The carotenoids lutein and zeaxanthin, which give the macular area of the eye its yellow colour, are located in the retinal pigment epithelium of the eye, and are believed to play a role in protecting it against oxidative and light damage. The macular pigments are of dietary origin, and green leafy vegetables are the primary source of lutein and zeaxanthin. Lutein is one of the five most common carotenoids found in the diet. There is current interest in the macular pigment in relation to age-related macular degeneration, but these pigments may also have a protective role in the retinal pigment epithelium of the newborn infant. Little information is available on blood lutein and zeaxanthin levels in neonates. Levels of lutein in human milk are two to three times higher than those of β-carotene, whereas their concentrations in the mothers’ blood are approximately the same. Human milk is the main dietary source of lutein and zeaxanthin for infants until weaning occurs. The biochemical mechanisms which mediate the transport of the macular carotenoids into the eye are not known, but tubulin has been identified as the major carotenoid-binding protein, and may play a role in the physiology of the macula.

Many patients with dementia lose the ability to feed themselves in the advanced stages of the disease. Tube feeding is sometimes initiated to overcome feeding difficulties. Recent studies have questioned the appropriateness of tube feeding in these patients. There is limited research to support the benefits of enteral nutrition in patients with advanced dementia. Deciding whether to tube feed or to withhold tube feeding from a patient with dementia poses a difficult challenge, and many carers may make decisions without adequate information and with an overly hopeful view of the future clinical course. Numerous studies have examined opinions about life-sustaining treatments; many individuals do not want to be tube fed if they were to develop dementia. Results from studies examining the opinions of physicians and other health professionals regarding the use of tube feeding in these patients are conflicting. A number of factors, such as race and cultural background may affect decisions. Healthcare professionals, relatives and patients must be aware of the realistic expectations of tube feeding in patients with dementia, as it can be difficult to withdraw once it has been initiated.

Leptin is a 16 kDa hormone which has been shown to have a major physiological role in the control of energy balance. Leptin is produced primarily in white adipose tissue, although there is evidence for its production in brown adipose tissue (BAT) and the placenta. BAT is critically important for the initiation of non-shivering thermogenesis in the newborn through the BAT-specific uncoupling protein (UCP), UCP1. This factor is particularly important in lambs in which levels of UCP1 peak at birth, concomitant with a rapid decline in plasma leptin levels. Our studies have examined the effect of acute and chronic administration of leptin to neonatal lambs, investigating effects on colonic temperature, UCP1 and thermogenic potential of BAT. Administration of leptin in sequential physiological doses of 10, 100 and 100 µg to neonatal lambs caused a modest increase in colonic temperature which was not observed in weight-matched vehicle-treated controls. This increase in colonic temperature was not mediated by an increase in either abundance or thermogenic potential of UCP1, as previously shown in adult rodents. UCP1 mRNA levels were 30 % lower in leptin-treated lambs, which is also contradictory to findings in adult rodents. Leptin treatment resulted in a dose-dependent rise in plasma leptin, with levels at the end of the study being almost twenty times greater in leptin-treated animals. To determine whether these findings in neonatal lambs were transient due to the complex milieu of hormones present after birth, we examined the effect of chronic leptin treatment over 6 d. Pairs of lambs were treated daily, from the second to seventh day of life with 100 µg leptin or vehicle. Colonic temperatures of leptin- and vehicle-treated animals remained similar throughout the study. UCP1 abundance was significantly lower in the leptin-treated animals, suggesting that the drop in UCP1 mRNA seen in the previous study had been translated to protein levels. In conclusion, the decline in plasma leptin levels at birth may be a signal to initiate enteral feeding. In lambs, the rapid loss of UCP1 mRNA, which occurs within the first few days of life, appears to be accelerated by leptin administration, possibly stimulating the development of white adipose tissue and generation of body heat through mechanisms other than non-shivering thermogenesis by UCP1 in BAT.

World population will reach an estimated nine billion by 2050. Given this factor and continued economic development in today's low-income countries, the total global demand for food will increase approximately threefold over the coming half-century. Meanwhile, against this background, newly-occurring global environmental changes such as climate change are anticipated to affect food production. Other incipient large-scale environmental changes likely to affect food production include stratospheric O3 depletion, the accelerating loss of biodiversity (with knock-on effects on crop and livestock pest species) and the perturbation of several of the great elemental cycles of N and S. The ways in which these various environmental influences affect the production of food (crops and livestock on land, and wild and cultivated fisheries) are complex and interactive. Uncertainties therefore persist about how global climate change is likely to affect world and regional food production. On balance, recent modelling-based estimates indicate that, in the medium to longer term, if not over the next several decades, climate change is likely to affect crop yields adversely, especially in food-insecure regions. The prospect of increased climatic variability further increases the risks to future food production. Given these possible though uncertain adverse impacts of climatic and other environmental changes on world food production, there is a need to apply the Precautionary Principle. There are finite, and increasingly evident, limits to agro-ecosystems and to wild fisheries. Our capacity to maintain food supplies for an increasingly large and increasingly expectant world population will depend on maximising the efficiency and sustainability of production methods, incorporating socially-beneficial genetic biotechnologies, and taking pre-emptive action to minimise detrimental ecologically-damaging global environmental changes.

Before about 1750 there was no substantial secular fall in protein–energy malnutrition (PEM) over large areas, nor reason to expect it. We have since learned that sufficient economic advance (poverty reduction) plus scientific advance (in medicine and food production) are achievable to eliminate mass PEM. The two advances are linked via increased demand for labour, and hence wages and employment, for those formerly too poor to afford adequate food. The extra employment income arises first from smallholder and employee food production, and later, as labour is released, from a wide range of specialised, increasingly non-farm, production, with employment income traded for food. This process eliminated mass hunger in Europe in 1750–1960. Only by 1975 had PEM in the developing world retreated to (very high) 1936–8 levels, but it fell sharply in Asia and Latin America in 1975–1990, due to unprecedented growth in staples yields, smallholder and farm employment income, and hence the poor's purchasing power over food. However, since 1990, poverty reduction has slowed (before reaching most of Africa), alongside much slower-staples yield growth, increasing water shortages, and big shifts of grain and land from man to farm animals. These trends prefigure declining progress against PEM in coming decades, unless there is renewed, employment-intensive food-staples-yield growth. That process requires reorienting crop biotechnology and water science towards the needs of small tropical farmers and their staple food crops, and shifting land towards them. Mass PEM is indeed largely due to inadequate ‘food entitlements’ by the hungry, but will not be remedied without growth in their employment, based on further advances in food-staples yields per unit land and water. Recent evidence suggests that early PEM may increase lifelong risks of infection and/or degenerative disease. This factor would increase the ‘squeeze’ on health resources in low-income countries, between the diseases of poverty and those of old age. That situation increases the need to readdress PEM by renewed progress in food production and land distribution.

The millennium promises a dramatic politicisation of the food question. In addition to the prominent issues of food security, hunger and nutrition, bioengineering, food safety and quality, there are related issues of environmental sustainability, power, sovereignty and rights. All these issues are deeply implicated in the current corporate form of globalisation, which is transforming historic global arrangements by subordinating public institutions and the question of food security to private solutions. The present paper questions the self-evident association between globalisation and nutritional improvement.

The perception of healthiness and/or safety, tenderness, juiciness and aroma or flavour are important quality criteria that influence the decision of a consumer to purchase beef. Beef production systems represent the combined and interacting effects of genotype, gender, age at slaughter and nutrition before slaughter. The present paper highlights recent information on how beef production systems can be modified to enhance the tenderness, flavour and healthiness of beef. Carcass management post-slaughter has a larger effect on meat tenderness than gender, genotype or feeding systems. Optimum ‘pasture to plate’ management systems are being established to ensure beef tenderness. The chemistry underlying beef flavour is complex, with in excess of 140 components identified in cooked beef volatiles. Flavour of beef is influenced by cattle diet, but assessment of flavour by a taste panel is subject to the previous experiences and preferences of the panellists. Modern lean beef can have an intramuscular fat concentration of 25–50 g/kg and can be considered a low-fat food. As the quantity of grass in the diet of cattle is increased, there is a decrease in saturated fatty acid concentration, and an increase in the n-3 polyunsaturated fatty acid and conjugated linoleic acid concentrations. It is concluded that there is opportunity to exploit the diet of cattle to produce tender flavoursome beef that has an increased conjugated linoleic acid concentration, a lower fat concentration and a fatty acid profile more compatible with current human dietary recommendations.

Protected denomination of origin (PDO) cheeses have distinctive sensorial characteristics. They can be made only from raw milk possessing specific features, which is processed through the ‘art’ of the cheesemaker. In general, the distinctive sensorial traits of PDO cheese cannot be achieved under different environmental–production conditions for two main reasons: (1) some milk features are linked to specific animal production systems; (2) cheese ripening is affected by the interaction between milk (specific) and the traditional technology applied to the transformation process (non-specific). Also, the environment for a good ripening stage can be quite specific and not reproducible. With reference to milk, factors of typicality are species and/or breed, pedo–climatic conditions, animal management system and feeding. Other factors that influence cheese quality are milk treatments, milk processing and the ripening procedures. The technology applied to most cheeses currently known as PDO utilizes only raw milk, rennet and natural lactic acid bacteria, so that milk must be, at its origin, suitable for processing. The specific milk characteristics that ensure a high success rate for PDO cheeses are high protein content and good renneting properties, appropriate fat content with appropriate fatty acid composition and the presence of chemical flavours originating from local feeds. Moreover, an appropriate microflora is also of major importance. The factors that contribute to achieving milk suitable for transformation into PDO cheese are genetics, age, lactation stage, season and climate, general management and health conditions, milking and particularly feeding, which affect nutrient availability, endocrine response and health status, and also the presence of microbes and chemical substances which enrich or reduce the milk–cheese quality. Many of these factors are regulated by the Producer Associations. However, the secret of the success of PDO cheeses is the combination of modern technology and tradition, with the objective of adapting the product to market demand, without losing specificity, originality and authenticity.

The high mortality rate associated with human infections caused by Escherichia coli strains of the serotype O157:H7 has brought to public attention the importance of ruminants as reservoirs of food-borne pathogens. In addition to established examples such as salmonella, campylobacter and listeria, recent evidence is emerging of the role of food in the transmission of Helicobacter pylori and Mycobacterium paratuberculosis. Food-borne pathogens harboured by ruminants are spread through shedding in the faeces and subsequent faecal contamination of raw food. Ruminant shedding appears to be affected by diet and, of particular concern, may be increased during fasting regimens imposed during transport to the slaughterhouse. The survival of food-borne pathogens in the ruminant gut is affected by many factors including microbe–microbe interactions, interactions involving plant metabolites and the presence of inhibitory end-product metabolites such as short-chain fatty acids. The potential importance of digesta flow and bacterial detachment in shedding of food-borne pathogens is discussed. Experimental procedures with dangerous pathogens have constraints, particularly in animal experimentation. This situation may be overcome by the use of rumen-simulating fermentors. One such system which, like the natural rumen, has a different turnover rate for solid and liquid digesta, was found to maintain rumen-like variables over an 11 d period. This system may prove useful for the study of dietary effects on food-borne pathogens.

Nutritional advice from doctors and other health workers is held in high regard by the general public. It is important, therefore, to ensure that the advice given is sound and safe. Historically, the training in nutrition for the health professions has been piecemeal and selective. As a first step in the development of national standards, a core curriculum on nutrition for health professionals was developed as part of the National Nutrition Task Force. Designed for undergraduates, the curriculum sought to provide a standard for training which would ensure safe practice. The curriculum, which has been accepted by all undergraduate medical schools, identifies eighteen bullet points covering: the principles of nutritional science; public health nutrition; clinical nutrition and nutritional support. Postgraduate training for doctors is the responsibility of the Royal Colleges, who have formed an Intercollegiate Group on nutrition. This group has developed an intercollegiate foundation course in nutrition which lasts for 1 week and is offered at different centres around the country. Using the Intercollegiate Course as a base, individual Colleges are exploring how they might best develop the next level of training by identifying the educational needs for nutrition in different sub-specialities. There is some discussion as to whether it is timely to develop a defined clinical speciality in human nutrition. Within these developments, nutritionists and dietitians are identified as a resource to be called upon by other health professionals, and therefore it is important that in their own training they are suitably equipped to take on this challenge.

Predisposition to poor skeletal health resulting in osteoporotic fracture is a major public health problem, the future economical impact of which is likely to be phenomenal. Two mechanisms principally determine adult bone health: (1) maximum attainment of peak bone mass (PBM); (2) the rate of bone loss with advancing age. Both aspects are regulated by a combination of endogenous and exogenous factors, and although genetic influences are believed to account for up to 75 % of the variation in bone mass, there is still room for modifiable factors to play a vital role. Weight-bearing physical activity is beneficial to the skeleton, but clarification of the exact type, intensity and duration required for optimum bone mass is needed. Excessive levels of exercise, which result in amenorrhoea, are detrimental to skeletal health. The importance of Ca to bone remains controversial. There is evidence that Ca is effective in reducing late post-menopausal bone loss, but more research is required on the long-term benefit of increased Ca intake on PBM attainment. Vitamin D ‘insufficiency’ appears to be widespread amongst population groups and is an area of considerable public health concern. The role of other micronutrients on bone metabolism remains to be fully quantified, but data from a combination of experimental, clinical and observational studies suggest a positive link between alkaline-forming foods and indices of bone health. The influence of nutrient–gene interactions on the skeleton requires further elucidation, but it may be useful in the future to target nutrition advice at those individuals who are genetically susceptible to osteoporosis.

Currently ‘accepted’ treatments for bone disease utilise drugs that inhibit osteoclastic bone resorption; these lead to a reduction in subsequent bone loss and thence, indirectly, to an increase in bone mass and fewer fractures. Three classes of compounds currently form the mainstay of therapy for osteoporosis: oestrogens (hormone-replacement therapy), ‘selective oestrogen receptor modulators’ and the bisphosphonates. Problems of patient compliance, real or theoretical long-term toxicological risks and the lack of bone anabolic agents of clinical utility suggest that there is a need for the development of further novel osteoclast resorption inhibitors. Recent biological and genetic findings in the area of bone cell function have led to the identification of new drug targets. These drugs include agents that (directly or indirectly): inhibit osteoclast adhesion to bone matrix; modify osteoclast differentiation; act on the proton pump and hence affect extracellullar acidification; antagonise extracellular enzymes that are involved in bone matrix protein degradation. Particular emphasis is placed in the present review on the evaluation of antagonists of αvβ3 integrin-mediated cell adhesion for use in bone disease. The wealth of new agents being developed suggests that resorption inhibition will be the best treatment for osteoporosis in the short to medium term, with the long-term aim still being toward developing anabolic drugs or cell therapeutics.

Ca nutritional requirements and bone Ca turnover can be assessed using numerous techniques. Among these techniques are bone mass measurements, tracer kinetic studies, bone histomorphometry and biochemical studies. Stable-isotope-based kinetic studies offer unique advantages in their ability to assess both Ca absorption and turnover. This approach is safe and readily applicable to subjects of all ages. Ca is essential for growth and maintenance of bone mineral throughout life. During pregnancy, increased intestinal absorption of Ca by the mother provides much of the Ca supplied to the fetus. During infancy, Ca supplied in human milk is primarily derived from maternal bone stores, which are quickly replenished during and after weaning. Early childhood is a time of relatively slow bone growth, with a rapid increase occurring during puberty. Recent kinetic studies demonstrate an increase in both Ca absorption and bone Ca deposition associated with early puberty. Bone Ca deposition reaches a maximum in females shortly before menarche. At that time the bone Ca deposition rate is approximately five times that of adulthood. The decline in bone Ca deposition rate is gradual after menarche. Ca absorption from the diet shows a gradual decline in adulthood as well. Ca supplementation, in the presence of adequate vitamin D, is effective in enhancing bone mineral content in childhood and in helping to maintain bone mineral content in adults. Maintaining adequate Ca nutriture throughout life may be necessary to minimize the risk of bone-loss disorders.