The epidemiological data that directly examine whole grain v. refined grain intake in relation to weight gain are sparse. However, recently reported studies offer insight into the potential role that whole grains may play in body-weight regulation due to the effects that the components of whole grains have on hormonal factors, satiety and satiation. In both clinical trials and observational studies the intake of whole-grain foods was inversely associated with plasma biomarkers of obesity, including insulin, C-peptide and leptin concentrations. Whole-grain foods tend to have low glycaemic index values, resulting in lower postprandial glucose responses and insulin demand. High insulin levels may promote obesity by altering adipose tissue physiology and by enhancing appetite. The fibre content of whole grains may also affect the secretion of gut hormones, independent of glycaemic response, that may act as satiety factors. Future studies may examine whether whole grain intake is directly related to body weight, and whether the associations are primarily driven by components of the grain, including dietary fibre, bran or germ.

The constraints to high levels of milk production imposed by a high-quality-pasture diet, and development of feeding strategies to overcome these limitations, were examined by modelling the nutritional status of New Zealand Friesian and North American Holstein–Friesian dairy cows grazing high-quality pasture. The Cornell Net Carbohydrate and Protein System (CNCPS) was used to predict sensitivity of milk production to a 10 % change in the composition of pasture nutrients. The rate at which fibre and protein were degraded in the rumen and the value given to effective fibre and lignin content significantly affected the supply of metabolisable energy and protein, and the profile of amino acid supply. The first limiting factor in milk production when only high-quality pasture was fed was metabolisable energy supply, while specific amino acids, particularly methionine and lysine, limited milk production when > 20 g/kg diet consisted of a grain supplement. Compared with cows fed a total mixed ration in confinement, North American Holstein–Friesians grazing all pasture produced less milk (29.6 v. 44.1 kg/d). Of the difference in milk production 61 % could be attributed to a lower DM intake (19 kg/d v. 23.4 kg/d). Predictions using the CNCPS indicated that supply of metabolisable energy was the first-limiting factor for milk production from high-quality pasture (251 g crude protein (N× 6.25)/kg, 432 g neutraldetergent fibre/kg, 77 % in vitro DM digestibility), rather than metabolisable protein or amino acids. In addition, these nutritional limitations imposed by pasture diets will be greater for dairy cow genotypes that have not been selected for high performance within a pasture system.

Cystic fibrosis (CF) is a genetically-inherited disorder that results in energy imbalance. Undernutrition is common in children with CF and associated with poor health outcomes. To ensure optimal growth and nutrition, children with CF are recommended to consume 120–150% of the recommended daily allowance (RDA) for energy, but most studies show they typically are only able to achieve 100% of the RDA. While biological factors clearly contribute to poor dietary adherence, recent studies have documented behavioural and environmental barriers to adherence that includes parent-child interaction at mealtimes. While not ‘abnormal’, parent behaviours such as paying increased attention to the child in the form of coaxing, commanding and feeding when the child is engaged in behaviours incompatible with eating (food refusal, talking, leaving the meal) may serve to reinforce these child non-eating behaviours. Thus, dietary counselling alone, albeit necessary, is typically insufficient because of failure to specifically address these behavioural and environmental barriers to dietary treatment. Behavioural intervention that targets both nutrition education and behavioural management has been found to be effective in achieving an average increased energy intake of 4200 kJ (1000)kcal/d and weight gain of 1·48 kg over 9 weeks in children with CF. This intervention utilizes self-monitoring, goal setting and shaping to structure the delivery of treatment. It also teaches parents to utilize child behaviour-management techniques to motivate children to increase their energy intake. These behavioural strategies include differential attention (praising and ignoring), contingency management and behavioural contracting. The potential application of these techniques to dietary counselling is suggested.

Epidemiological evidence suggests that diets rich in fruit and vegetables decrease the risk of premature mortality from major clinical conditions, including cancer and heart disease. However, it is not yet clear which components or combination of components in fruit and vegetables are protective and what is their mechanism of action. Such scientific uncertainty does not seem to inhibit the marketing of a huge range of plant-based concoctions, promoted as ‘magic bullets’ for optimum health. For example, the purported health-giving properties of plant polyphenols represent a case in which enthusiastic marketing claims may far exceed the current scientific evidence. Even when good experimental evidence exists, results need to be interpreted with caution in relation to human health benefits, as polyphenols may have limited bioavailability and may also be extensively metabolised. In addition, some polyphenols can be toxic and mutagenic in some cell culture systems. Until more is known about the activity and metabolic fate of polyphenols in the body, it would be better for the consumer to increase fruit and vegetable intake, and also to be wary of claims that these compounds are a panacea for good health.

Feed formulation to meet nutritional requirements of livestock is becoming increasingly challenging. Regulations have banned the use of traditional high-quality protein supplements such as meat-and-bone meal, pollution from animal excreta of N and P is an issue and antibiotics are no longer available as insurance against the impact of enteric infection and feed anti-nutritional factors. The improved genetic potential of livestock is increasing daily requirement for energy and protein (essential amino acids). To benefit from the enhanced growth potential of livestock diets with high nutrient density are needed that can be formulated from crops without increased cost. Genetic modification of commodity crops used to manufacture animal feed in order to improve the density and quality of available nutrients is a potential solution to some of these problems. Furthermore, crops may be used as biofactories to produce molecules and products used in animal feed with considerable reductions in manufacturing fixed costs. Nevertheless, there are considerable not insurmountable challenges, such as the creation of sufficient economic value to deliver benefit to all members in the feed production chain, which is an essential element of identity preserving and delivering the technology to livestock producers. Individual output traits in the major commodity crops may not provide sufficient value to adequately compensate all the members of the feed production chain. Successful adoption of output traits may rely on inserting combinations of agronomic input traits with specific quality traits or increasing the value proposition by inserting combinations of output traits.

Growth failure and poor nutritional status are features of children with chronic disease. Oral protein–energy supplements are one of a number of interventions provided with the aim of improving nutritional status in these children. The present paper describes a Cochrane systematic review assessing the efficacy of these products in children with chronic disease. The objective was to examine the evidence that in children with chronic disease oral protein–energy supplements alter nutrient intake, nutritional indices, survival and quality of life. All randomised controlled trials of the use of oral protein–energy supplements in children with chronic disease were identified through searching electronic databases and hand searching the abstract books of nutrition conferences. Studies identified were independently assessed for eligibility and methodological quality, and data on outcomes of interest were combined in a meta-analysis where possible. Two trials were eligible for inclusion in the review, both of which were undertaken with children with cystic fibrosis. No statistical differences could be found between treatment and control groups when data from both studies were combined. Oral protein–energy supplements are widely used to improve the nutritional status of children with chronic disease. No conclusions can be drawn on the efficacy of these products based on the limited data available. Further randomised controlled trials are required to investigate the use of these products in children with chronic disease. Until further data are available, these products should be used with caution.

Cancer is the major cause of death in the UK, and the Government has set a target to reduce death rate from cancer in individuals 75 years by ≥20% by 2010. Whilst earlier diagnosis and more effective treatments will contribute to meeting this target, there are considerable opportunities to prevent cancer by improving diet and other aspects of lifestyle. There is now a good understanding of the biological basis of carcinogenesis, which is providing the basis for mechanistic investigation of the chemo-preventive properties of certain foods and food components. It is becoming increasingly clear that there are important interactions between an individual's genotype (characterised by single nucleotide polymorphisms in particular genes) and habitual diet that modulate the risk of developing cancer. The technology to support this post-genomic revolution in nutrition research is now widely available, but brings with it considerable challenges in terms of study design and ethics. However, in the absence of a robust body of evidence on which dietary strategies will benefit which individuals, soundly based genetically-targeted nutrition advice to the public on cancer prevention is a little way in the future.

Diverticulosis is a condition that is associated with ageing. The older the individual the more likely they are to have diverticulosis, but this process is not necessarily inevitable. Diverticula are a herniation through the wall of the sigmoid colon and are likely to be a consequence of a weakness in the colonic wall or prolonged exposure to increased intracolonic pressure consequent on a low dietary fibre intake. The tensile strength of the colon declines with age and becomes least in the distal colon. Adult Africans living in Africa eat a high-fibre diet and are free from diverticulosis. Their colons are stronger, wider and thinner than those Scottish adults of the same age. The strength of the colon is in part dependent on collagen fibres and their diameter. The collagen fibrils on the left side of the colon are smaller and more tightly packed than those of the right side of the colon. Ageing and the presence of colonic diverticulosis are associated with smaller more-tightly-packed collagen fibrils. An animal model was established to investigate the effect of a lifelong high- and low-fibre diet on the development of colonic diverticulosis. The findings show that a high-fibre diet from birth, and preferably a maternal high-fibre diet, lessen the risk of diverticulosis with age.

Malnutrition has long been recognised as a risk factor for post-operative morbidity and mortality. Traditional metabolic and nutritional care of patients undergoing major elective surgery has emphasised pre-operative fasting and re-introduction of oral nutrition 3–5 d after surgery. Attempts to attenuate the consequent nutritional deficit and to influence post-operative morbidity and mortality have included parenteral, enteral and oral sip feeding. Recent studies have emphasised that an enhanced rate of recovery can be achieved by a multi-modal approach focused on modulating the metabolic status of the patient before (e.g. carbohydrate and fluid loading), during (e.g. epidural anaesthesia) and after (e.g. early oral feeding) surgery. Using such an approach preliminary results on patients undergoing elective colo-rectal surgery indicate a significant reduction in hospital stay (traditional care, n 48, median stay 10 d v. enhanced recovery programme, n 33, median stay 7d; P<0·01) can be achieved. Such findings emphasise the potential role of multi-modal care programmes in the promotion of early recovery from major surgical trauma.

Establishing a definition for dietary fibre has historically been a balance between nutrition knowledge and analytical method capabilities. While the most widely accepted physiologically-based definitions have generally been accurate in defining the dietary fibre in foods, scientists and regulators have tended, in practice, to rely on analytical procedures as the definitional basis in fact. As a result, incongruities between theory and practice have resulted in confusion regarding the components that make up dietary fibre. In November 1998 the president of the American Association of Cereal Chemists (AACC) appointed an expert scientific review committee and charged it with the task of reviewing and, if necessary, updating the definition of dietary fibre. The committee was further charged with assessing the state of analytical methodology and making recommendations relevant to the updated definition. After due deliberation, an updated definition of dietary fibre was delivered to the AACC Board of Directors for consideration and adoption (Anon, 2000; Jones 2000/7). The updated definition includes the same food components as the historical working definition used for approximately 30 years (a very important point, considering that the majority of the research of the past 30 years delineating the positive health effects of dietary fibre is based on that working definition). However, the updated definition more clearly delineates the make-up of dietary fibre and its physiological functionality. As a result, relatively few changes will be necessary in analytical methodology. Current methodologies, in particular AACC-approved method of analysis 32–05 (Grami, 2000), Association of Official Analytical Chemists' official method of analysis 985.29 (Horwitz, 2000a) or AACC 32–07 (Grami, 2000) Association of Official Analytical Chemists 991.43 (Horwitz, 2000a) will continue to be sufficient and used for most foods. A small number of additional methods will be necessary to quantify the dietary fibre levels in foods containing fibres such as fructans (polymers and oligomers of fructose, inulin), modified dextrins, and/or synthetic dietary fibre analogues.

Interventions for prevention and treatment of childhood obesity typically target increases in physical activity and, more recently, reductions in physical inactivity (sedentary behaviour such as television viewing). However, the evidence base for such strategies is extremely limited. The main aim of the present review was to update the systematic review and critical appraisal of evidence in the light of the recent rapid expansion of research in this area. Randomised controlled trials (RCT) that targeted activity or inactivity, that followed up children or adolescents for at least 1 year and that included an objective weight-related outcome measure were included. Trials were appraised using previously published criteria (Harbour & Miller, 2001), and literature search strategies described previously (Reilly et al. 2002) were updated to May 2002. A total of four new RCT, two new systematic reviews and one meta-analysis were identified. The evidence base has increased markedly since the completion of earlier reviews, although high-quality evidence is still lacking. The evidence on childhood obesity prevention is not encouraging, although promising targets for prevention are now clear, notably reduction in sedentary behaviour. There is stronger evidence that targeting activity and/or inactivity might be effective in paediatric obesity treatment, but doubts as to the generalisability of existing interventions, and the clinical relevance of the interventions is unclear. Further research in settings outside the USA is urgently needed, and two ongoing RCT in Scotland are summarised.

The urgency generated by drug-resistant strains of malaria has accelerated anti-malarial drug research over the last two decades. While synthetic pharmaceutical agents continue to dominate research, attention increasingly has been directed to natural products. The present paper explores the larger context in which plant use occurs and considers how the selection of medicinal plants has evolved over millennia as part of the larger human effort to mediate illness. First attention is directed to indigenous medicinal plants whose anti-malarial activity is based on an oxidant mode of action, by which intracellular constituents lose electrons (become more electropositive). Next, parallels are drawn between these plant substances and a suite of malaria-protective genetic traits: glucose-6-phosphate dehydrogenase deficiency; haemoglobins S, C and E; α- and β-thalassemias. These erythrocyte anomalies are classic examples of Darwinian evolution, occurring in high frequency in populations who have experienced considerable selective pressure from malaria. Characterized by discrete loci and pathophysiologies, they are united through the phenomenon of increased erythrocyte oxidation. In this model, then, oxidant anti-malarial plants are culturally constructed analogues, and molecular mimics, of these genetic adaptations. To further reinforce the scheme, it is noted that the anti-malarial action of pharmaceutical agents such as chloroquine and mefloquine duplicates both the genetic anomalies and the folk therapeutic models based in oxidant plants. This discussion coheres around a theoretical foundation that relates plant secondary metabolites (oxidants) to plasmodial biochemistry and human biological and cultural adaptations to malaria. Co-evolution provides a theoretical link that illuminates how medical cultures manage the relationships among humans, plants, herbivores and their respective pathogens.

Conjugated linoleic acids (CLA) have been shown to have anti-carcinogenic, anti-obesity, anti-atherogenic and immunomodulatory functions. The basis for these effects has not been fully explained, but probably involves effects of CLA on eicosanoid metabolism, cytokine production and\or gene expression. The predominant isomer (85–90%) in the natural sources of CLA has the cis-9, trans-11 configuration. As interest in CLA grew and synthetic forms became available, the number of studies examining the effects of dietary CLA in rodents, human subjects and livestock has increased greatly. In the late 1990 s the observation that CLA had anti-obesity effects was reported. Subsequently, it was determined that this effect in mice could be attributed to the trans-10, cw-12 isomer that, along with the cis-9,trans-11 isomer, predominates in the synthetic forms of CLA. The santi-obesity response varies in magnitude depending on species, and has not been consistent in non-rodents. In general, the response is greatest in mice and less or absent in other species. The basis for this lack of consistency is not clear and is unlikely to be accounted for by differences in the source of CLA. In the pig variation in body fat of animals may account for differences in responsiveness. There is no direct evidence of an anti-carcinogenic effect of CLA in human subjects or livestock. Indirect evidence from in vitro studies with cell lines, as well as epidemiological studies, suggest that CLA may be relevant as a natural anti-carcinogen. The immunomodulatory effects of CLA may have application in livestock production as an alternative to the use of feed antibiotics, or as a means of improving the response to vaccination and conferring disease resistance. The recent literature on the effects of CLA, with emphasis on its anti-obesity effects, is reviewed.

Vitamin D is produced endogenously when the skin is exposed to sunlight and can be obtained exogenously from a few natural food sources, from food fortification and from supplements. Generally, vitamin D intake is low ≤2–3 μg/d in Europe. Casual exposure to sunlight is thought to provide most of the vitamin D requirement of the human population. However, skin synthesis of vitamin D may not compensate for the low nutritional intake in Europe, even in countries with high supplies from food fortification and supplements. For assessment of vitamin D nutritional status the concentration of 25-hydroxyvitamin D (25(OH)D) in serum is considered to be an accurate integrative measure reflecting an individual's dietary intake and cutaneous production. A substantial percentage of the elderly and adolescents in Europe have a low concentration of 25(OH)D; in the elderly this percentage ranges from approximately 10 in the Nordic countries to approximately 40 in France. Low vitamin D status seems to be aggravated by disease and immobility, and by a low frequency of supplement use.

The relationship between frequency of consumption of whole-grain foods and cancer risk has been analysed using data from an updated series of case-control studies conducted in Northern Italy between 1983 and 1997. The overall dataset included the following incident histologically-confirmed neoplasms: oral cavity and pharynx 524, oesophagus 410, stomach 745, colon 955, rectum 625, liver 435, gallbladder 65, pancreas 402, larynx 388, soft tissue sarcomas 217, breast 3412, endometrium 750, ovary 971, prostate 127, bladder 431, kidney 190, thyroid 428, Hodgkin's disease 201, non-Hodgkin's lymphomas 529, multiple myelomas 185. Controls were 10 058 patients admitted to hospital for acute non-neoplastic conditions unrelated to long-term modifications in diet, tobacco or alcohol use. The multivariate odds ratios for the highest category of whole-grain cereal consumption were 0.3–0.5 for upper digestive tract and respiratory neoplasms and colon, 0.6 for rectum and liver, 0.4 for gallbladder, 0.8 for pancreas, 0.2 for soft tissue sarcomas, 0.9 for breast and endometrium, 0.7 for ovary, 0.7 for prostate, 0.4 for bladder and kidney, 1.1 for thyroid and about 0.5 for lymphomas and 0.6 for myelomas. In this population whole-grain food consumption is an indicator of reduced risk of several neoplasms.

The direct effects of physical activity interventions on energy expenditure are relatively small when placed in the context of total daily energy demands. Hence, the suggestion has been made that exercise produces energetic benefits in other components of the daily energy budget, thus generating a net effect on energy balance much greater than the direct energy cost of the exercise alone. Resting metabolic rate (RMR) is the largest component of the daily energy budget in most human societies and, therefore, any increases in RMR in response to exercise interventions are potentially of great importance. Animal studies have generally shown that single exercise events and longer-term training produce increases in RMR. This effect is observed in longer-term interventions despite parallel decreases in body mass and fat mass. Flight is an exception, as both single flights and long-term flight training induce reductions in RMR. Studies in animals that measure the effect of voluntary exercise regimens on RMR are less commonly performed and do not show the same response as that to forced exercise. In particular, they indicate that exercise does not induce elevations in RMR. Many studies of human subjects indicate a short-term elevation in RMR in response to single exercise events (generally termed the excess post-exercise O2 consumption; EPOC). This EPOC appears to have two phases, one lasting 2 h and a smaller much more prolonged effect lasting up to 48 h. Many studies have shown that long-term training increases RMR, but many other studies have failed to find such effects. Data concerning long-term effects of training are potentially confounded by some studies not leaving sufficient time after the last exercise bout for the termination of the long-term EPOC. Long-term effects of training include increases in RMR due to increases in lean muscle mass. Extreme interventions, however, may induce reductions in RMR, in spite of the increased lean tissue mass, similar to the changes observed in animals in response to flight.

Physical activity influences energy metabolism in human subjects by increasing activity-induced energy expenditure and resting metabolic rate for several hours after exercise. On the other hand, physical activity increases mechanical energy efficiency, suggesting that trained subjects would need less energy for daily activities. The underlying mechanism by which physical activity influences energy metabolism is largely unknown. The skeletal muscle-specific homologue of uncoupling protein (UCP) 1, UCP3, could possibly play a major role in energy expenditure. UCP3 is, like UCP1, able to uncouple respiration from ATP production. A strong link or association between the UCP3 gene and energy metabolism was found. Furthermore, UCP3 mRNA expression is related to sleeping metabolic rate, and thyroid hormone, a powerful stimulator of energy expenditure, up regulates UCP3. Finally, mice overexpressing UCP3 are hyperphagic but lean. These findings indicated that UCP3 is related to energy metabolism and that UCP3 could have a role in the effect of physical activity on energy expenditure. Thus, acute exercise up regulates UCP3, whereas endurance training results in the down-regulation of UCP3 protein content. Only a minimal amount of physical activity is needed for down-regulation of UCP3. Moreover, there is very strong evidence that UCP3 is negatively related to mechanical energy efficiency, suggesting that the down-regulation of UCP3 with training increases mechanical energy efficiency. Taken together, although the exact function of UCP3 is still unknown, exercise and training studies clearly show that under certain circumstances UCP3 is strongly related to human energy metabolism, possibly as a secondary effect of its (yet) unknown primary function.

Prolonged vitamin D deficiency resulting in rickets is seen mainly during rapid growth. A distinct age distribution has been observed in the Copenhagen area where all registered hospital cases of rickets were either infants and toddlers or adolescents from immigrant families. Growth retardation was only present in the infant and toddler group. A state of deficiency occurs months before rickets is obvious on physical examination. Growth failure, lethargy and irritability may be early signs of vitamin D deficiency. Mothers with low vitamin D status give birth to children with low vitamin D status and increased risk of rickets. Reports showing increasing rates of rickets due to insufficient sunlight exposure and inadequate vitamin D intake are cause for serious concern. Many countries (including the USA from 2003) recommend vitamin D supplementation during infancy to avoid rickets resulting from the low vitamin D content of human milk. Without fortification only certain foods such as fatty fish contain more than low amounts of vitamin D, and many children will depend entirely on sun exposure to obtain sufficient vitamin D. The skin has a high capacity to synthesize vitamin D, but if sun exposure is low vitamin D production is insufficient, especially in dark-skinned infants. The use of serum 25-hydroxyvitamin D to evaluate vitamin D status before development of rickets would be helpful; however, there is no agreement on cut-off levels for deficiency and insufficiency. Furthermore, it is not known how marginal vitamin D insufficiency affects children's bones in the long term.

Loss of function of the adenomatous polyposis coli (APC) tumour suppressor gene through truncating mutations or other means is an early event in most colo-rectal cancer (CRC). The AFC gene encodes a large multifunctional protein that plays key roles in several cellular processes, including the wnt signalling pathway where an intact APC protein is essential for down regulation of β-catenin. The APC protein also plays a role in regulation of cell proliferation, differentiation, apoptosis, cell-cell adhesion, cell migration and chromosomal stability during mitosis. Acquisition of a non-functional APC gene can occur by inheritance (in the disease familial adenomatous polyposis (FAP)) or by a sporadic event in a somatic cell. Whilst there is strong epidemiological evidence that variation in diet is a major determinant of variation in CRC incidence, conventional adenoma recurrence trials in sporadic cases of the disease have been relatively unsuccessful in identifying potentially protective food components. Since the genetic basis of CRC in FAP and in sporadic CRC is similar, intervention trials in FAP gene carriers provide an attractive strategy for investigation of potential chemo-preventive agents, since smaller numbers of subjects and shorter time frames are needed. The Concerted Action Polyp Prevention (CAPP) 1 Study is using a 2×2 factorial design to test the efficacy of resistant starch (30 g raw potato starch-Hylon VII (1:1, w/w)/d) and aspirin (600 mg/d) in suppressing colo-rectal adenoma formation in young subjects with FAP. Biopsies of macroscopically-normal rectal mucosa are also being collected for assay of putative biomarkers of CRC risk.