Lipids used in parenteral nutrition provide energy, building blocks and essential fatty acids. Traditionally, these lipids have been based on n-6 PUFA-rich vegetable oils particularly soyabean oil. This may not be optimal because soyabean oil may present an excessive supply of linoleic acid. Alternatives to use of soyabean oil include its partial replacement by medium-chain TAG, olive oil or fish oil, either alone or in combination. Lipid emulsions containing these alternatives are well tolerated without adverse effects in a wide range of hospitalised adult patients. Lipid emulsions that include fish oil have been used in parenteral nutrition in adult patients' post-surgery (mainly gastrointestinal). This has been associated with alterations in patterns of inflammatory mediators and in immune function and, in some studies, a reduction in length of intensive care unit and hospital stay. These benefits are emphasised through recent meta-analyses. Perioperative administration of fish oil may be superior to post-operative administration. Parenteral fish oil has been used in critically ill adults. Here, the influence on inflammatory processes, immune function and clinical endpoints is not clear, since there are too few studies and those that are available report contradictory findings. However, some studies found reduced inflammation, improved gas exchange and shorter length of hospital stay in critically ill patients if they receive fish oil. More and better trials are needed in patient groups in which parenteral nutrition is used and where fish oil may offer benefits.

Pharmaco-nutrients have beneficial effects on protective and immunological mechanisms in patients undergoing surgery, which are important for recovery after injury and in combating infectious agents. The aim of this review article was to outline the potential of the administration of nutritional substrates to surgical patients and the underlying mechanisms that make them particularly important in peri-operative care. Surgery causes a stress response, which has catabolic effects on the body's substrate stores. The amino acid glutamine is a stimulating agent for immune cells. It activates protective mechanisms through its role as a precursor for antioxidants and it improves the barrier function of the gut. Arginine also enhances the function of the immune system, since it is the substrate for T-lymphocytes. Furthermore, n-3 PUFA stabilise surgery-induced hyper-inflammation. Taurine is another substrate that may counteract the negative effects of surgical injury on acid–base balance and osmotic balance. These pharmaco-nutrients rapidly become deficient under the influence of surgical stress. Supplementation of these nutrients in surgical patients may restore their protective and immune-enhancing actions and improve clinical outcome. Moreover, pre-operative fasting is still common practice in the Western world, although fasting has a negative effect on the patient's condition and the recovery after surgery. This may be counteracted by a simple intervention such as administering a carbohydrate-rich supplement just before surgery. In conclusion, there are various nutritional substrates that may be of great value in improving the condition of the surgical patient, which may be beneficial for post-operative recovery.

The gastrointestinal microbiota is a complex ecosystem with each human individual hosting at least 160 different bacterial strains. Our understanding of its role is rapidly expanding as a result of the molecular microbiological techniques that can accurately characterise its composition and ‘omics’ technologies that measure its metabolic activity. Since 1995, extensive research has investigated the prebiotic concept, which describes how supplementation of some non-digestible oligosaccharides can stimulate the growth and/or activity of specific genera including bifidobacteria. However, the vast majority of studies are in healthy human subjects, with few undertaken in patients with disorders relevant to clinical nutrition. Marked alterations of the luminal microbiota have been demonstrated in patients with digestive disorders, highlighting mechanisms through which they might be involved in their pathogenesis, including higher clostridia in patients who develop diarrhoea during enteral nutrition and the influence of bifidobacteria on intestinal dendritic cell phenotype in Crohn's disease. The impact of prebiotics on the intestinal microbiota of healthy people has not been consistently replicated in patients with digestive disorders. For example, a number of studies show that inulin/oligofructose do not increase bifidobacteria in enteral nutrition and Crohn's disease. Indeed, in Crohn's disease and irritable bowel syndrome there is evidence that some prebiotics in high doses worsen functional symptoms. Unlike healthy human subjects, patients experience a number of issues that may alter their gastrointestinal microbiota (disease, antibiotics and inflammation) and the use of microbiota modifying therapies, such as prebiotics, do not always elicit the same effects in patients as they do in healthy people.

A well-functioning immune system is key to providing good defence against pathogenic organisms and to providing tolerance to non-threatening organisms, to food components and to self. The immune system works by providing an exclusion barrier, by identifying and eliminating pathogens and by identifying and tolerating non-threatening sources of antigens, and by maintaining a memory of immunological encounters. The immune system is complex involving many different cell types distributed throughout the body and many different chemical mediators some of which are involved directly in defence while others have a regulatory role. Babies are born with an immature immune system that fully develops in the first few years of life. Immune competence can decline with ageing. The sub-optimal immune competence that occurs early and late in life increases susceptibility to infection. Undernutrition decreases immune defences, making an individual more susceptible to infection. However, the immune response to an infection can itself impair nutritional status and alter body composition. Practically all forms of immunity are affected by protein–energy malnutrition, but non-specific defences and cell-mediated immunity are most severely affected. Micronutrient deficiencies impair immune function. Here, vitamins A, D and E, and Zn, Fe and Se are discussed. The gut-associated lymphoid tissue is especially important in health and well-being because of its close proximity to a large and diverse population of organisms in the gastrointestinal tract and its exposure to food constituents. Certain probiotic bacteria which modify the gut microbiota enhance immune function in laboratory animals and may do so in human subjects.

Diagnosis of metabolic syndrome includes a set of laboratory and physical findings, including central adiposity, elevated TAG, reduced HDL-cholesterol, hypertension and elevated fasting glucose or insulin resistance. While definitions have varied slightly, from a practical point of view, identifying dietary and lifestyle factors, including low levels of physical activity, are important in designing a diet and exercise programme that can help individuals with the metabolic syndrome to reduce the associated detrimental health consequences. Specific features of the metabolic syndrome require intervention, whether dietary or otherwise, to move towards normal ranges. It is important to remember that no one size or treatment fits all. While central obesity is perceived as the hallmark of the metabolic syndrome, other features need to be treated independently if they do not respond to lifestyle change. The future may hold treatments for the metabolic syndrome that involve modulation of inflammation.

The developmental origins of health and disease hypothesis postulates that exposure to a less than optimal maternal environment during fetal development programmes physiological function, and determines risk of disease in adult life. Much evidence of such programming comes from retrospective epidemiological cohorts, which demonstrate associations between birth anthropometry and non-communicable diseases of adulthood. The assertion that variation in maternal nutrition drives these associations is supported by studies using animal models, which demonstrate that maternal under- or over-nutrition during pregnancy can programme offspring development. Typically, the offspring of animals that are undernourished in pregnancy exhibit a relatively narrow range of physiological phenotypes that includes higher blood pressure, glucose intolerance, renal insufficiency and increased adiposity. The observation that common phenotypes arise from very diverse maternal nutritional insults has led to the proposal that programming is driven by a small number of mechanistic processes. The remodelling of tissues during development as a consequence of maternal nutritional status being signalled by endocrine imbalance or key nutrients limiting processes in the fetus may lead to organs having irreversibly altered structures that may limit their function with ageing. It has been proposed that the maternal diet may impact upon epigenetic marks that determine gene expression in fetal tissues, and this may be an important mechanism connecting maternal nutrient intakes to long-term programming of offspring phenotype. The objective for this review is to provide an overview of the mechanistic basis of fetal programming, demonstrating the critical role of animal models as tools for the investigation of programming phenomena.

Numerous effects of n-3 fatty acids EPA and DHA on functional responses of cells involved in inflammation and immunity have been described. Fatty acid-induced modifications in membrane order and in the availability of substrates for eicosanoid synthesis are long-standing mechanisms that are considered important in explaining the effects observed. More recently, effects on signal transduction pathways and on gene expression profiles have been identified. Over the last 10 years or so, significant advances in understanding the mechanisms of action of n-3 fatty acids have been made. These include the identification of new actions of lipid mediators that were already described and of novel interactions among those mediators and the description of an entirely new family of lipid mediators, resolvins and protectins that have anti-inflammatory actions and are critical to the resolution of inflammation. It is also recognised that EPA and DHA can inhibit activation of the prototypical inflammatory transcription factor NF-κB. Recent studies suggest three alternative mechanisms by which n-3 fatty acids might have this effect. Within T-cells, as well as other cells of relevance to immune and inflammatory responses, EPA and DHA act to disrupt very early events involving formation of the structures termed lipid rafts which bring together various proteins to form an effective signalling platform. In summary, recent research has identified a number of new mechanisms of action that help to explain previously identified effects of n-3 fatty acids on inflammation and immunity.

The aim of this review is to place a historical perspective on linking dyslipidaemia with atherosclerosis and emphasises previous knowledge about the impact on the lipoprotein profile and health in persons with mild dyslipidaemia and in those with defined genetic disorders. CVD is becoming the leading cause of death and disability in developed and developing countries and is strongly related to lifestyle factors that influence plasma lipoprotein concentrations. It is established that risk of complications from atherosclerosis increases with increasing LDL and decreasing HDL and that there is potentiation of risk when these and other risk factors co-exist. High-fat diets used for losing body mass may increase risk through dyslipidaemia. Pharmaceutical modulation of the lipoproteins has lowered risk powerfully but residual risk persists, possibly relating to existing disease as well as progression relating in many instances to dietary lipids. The impact of various dietary lipids is reviewed as they relate to the conventional lipoprotein profile in persons who do not have significant metabolic defects, as well as the impact on inherited metabolic disease such as familial hypercholesterolaemia, hypertriglyceridaemia and phytosterolaemia. For most persons with dyslipidaemias a significant benefit will be seen on the lipid profile by adopting a low saturated fat diet with less cholesterol intake.

The aims of this review paper are to provide an overview of the association of sodium intake with cardiovascular health, to identify sodium in our global food supply and to describe problems associated with assessment of dietary sodium intake. Excess sodium intake may contribute to the development of hypertension in some individuals, consequently increasing CVD risk. The average intake of sodium in populations around the world far exceeds the actual body's needs. Processed and restaurant foods contribute the most dietary sodium for Americans and other populations worldwide. There is a worldwide focus on reducing sodium content of food products in an effort to reduce health related issues associated with excessive salt and sodium intake in individuals. In several countries, regulations have been introduced to lower the sodium content of foods. Manufacturers are complying with these regulations by formulating new products to meet these standards. However, the variability in food sodium content poses challenges to researchers to accurately assess dietary sodium intakes of individuals. There are differences in sodium content of foods in databases compared with nutritional information provided by manufacturers for the same food products. Variations also exist in restaurant foods, where values differ from those available on restaurant websites. Sodium may be either underestimated or overestimated; it is not always on target. Awareness of the variability among food products is crucial but capturing sodium content of every food in the market is not feasible. Whenever possible, updating databases is critical. In conclusion, it is not feasible to capture the sodium content of every food in the marketplace but being aware of these differences is essential to assessing actual sodium consumption. Since biological determinations are burdensome and impractical, it is imperative for researchers and other health professionals to participate in the development and implementation of tools to accurately assess sodium intake in individuals.

In this paper, the nutrigenomics approach is discussed as a research tool to study the physiological effects of nutrition and consequently how nutrition affects health and disease (endpoints). Nutrigenomics is the study of the effects of foods and food constituents on gene expression; the analyses include analysis of mRNA, proteins and metabolites. Nutrigenomics may be useful in dealing with the challenges that nutrition research is facing; by integrating the description of numerous active genes and metabolic pathways stronger evidence and new biomarkers for subtle nutritional effects may be obtained. Also, a new definition of disease and health may be needed. The use of tests challenging homoeostasis is being proposed to help define health. Challenge tests may be able to demonstrate in a better way subtle beneficial effects of nutrition on health. The paper describes some basic concepts relevant to nutrition research as well as some of the possibilities that are offered by nutrigenomics technology. Some of its applications are described.

Although robust associations between dietary intake and population health are evident from conventional observational epidemiology, the outcomes of large-scale intervention studies testing the causality of those links have often proved inconclusive or have failed to demonstrate causality. This apparent conflict may be due to the well-recognised difficulty in measuring habitual food intake which may lead to confounding in observational epidemiology. Urine biomarkers indicative of exposure to specific foods offer information supplementary to the reliance on dietary intake self-assessment tools, such as FFQ, which are subject to individual bias. Biomarker discovery strategies using non-targeted metabolomics have been used recently to analyse urine from either short-term food intervention studies or from cohort studies in which participants consumed a freely-chosen diet. In the latter, the analysis of diet diary or FFQ information allowed classification of individuals in terms of the frequency of consumption of specific diet constituents. We review these approaches for biomarker discovery and illustrate both with particular reference to two studies carried out by the authors using approaches combining metabolite fingerprinting by MS with supervised multivariate data analysis. In both approaches, urine signals responsible for distinguishing between specific foods were identified and could be related to the chemical composition of the original foods. When using dietary data, both food distinctiveness and consumption frequency influenced whether differential dietary exposure could be discriminated adequately. We conclude that metabolomics methods for fingerprinting or profiling of overnight void urine, in particular, provide a robust strategy for dietary exposure biomarker-lead discovery.