Though bad odour has always been associated with animal production, it did not attract much research attention until in many countries the odour production and emission from intensified animal production caused serious nuisance and was implicated in the health problems of individuals living near animal farms. Odour from pig production facilities is generated by the microbial conversion of feed in the large intestine of pigs and by the microbial conversion of pig excreta under anaerobic conditions and in manure stores. Assuming that primary odour-causing compounds arise from an excess of degradable protein and a lack of specific fermentable carbohydrates during microbial fermentation, the main dietary components that can be altered to reduce odour are protein and fermentable carbohydrates. In the present paper we aim to give an up-to-date review of studies on the relationship between diet composition and odour production, with the emphasis on protein and fermentable carbohydrates. We hypothesise how odour might be changed and/or reduced by altering the diet of pigs. Research so far has mainly focused on the single effects of different levels of crude protein and fermentable carbohydrates on odour production. However, also important for odour formation are the sources of protein and fermentable carbohydrates. In addition, it is not only the amount and source of these compounds that is important, but also the balance between them. On the basis of our review of the literature, we hypothesise that odour nuisance from pig production facilities might be reduced significantly if there is an optimum balance between protein and fermentable carbohydrates in the diet of pigs.

Evidence from different directions, including observational and experimental studies, points to a role of vitamin D status in low-intensity chronic inflammation and insulin resistance in type 2 diabetes mellitus (T2DM). It has been recognised that insulin resistance and low-intensity chronic inflammation are risk factors for T2DM. Thus, vitamin D status can be implicated in the aetiology of TD2M. It is suggested that the relationship between vitamin D and low-intensity chronic inflammation and insulin resistance in T2DM can be mediated in part by the immune-modulating properties of the active form of vitamin D (1-α,25-dihydroxyvitamin D3; 1,25(OH)2D3), which is able to down regulate the production of pro-inflammatory cytokines – particularly TNF-α, and IL-6. However, an association between vitamin D status and these features, which is independent of BMI, has been also reported. Non-calcaemic effects of vitamin D can be associated with health outcomes other than those traditionally attributed to the vitamin.

The present review summarises the potential nutritional and physiological functions of betaine as a feed additive in relation to performance criteria in livestock production. Betaine, the trimethyl derivative of the amino acid glycine, is a metabolite of plant and animal tissues. In plants, betaine is particularly synthesised and accumulated as an osmoprotectant against salt and temperature stress. In animals, betaine is the product of choline oxidation or it originates from nutritional sources. Over the past decades, numerous studies have been carried out to investigate the potential effects of betaine supplementation on animal performance. Due to its chemical structure, betaine shows the characteristics of a dipolar zwitterion resulting in osmoprotective properties. Promoting effects on the intestinal tract against osmotic stress occurring during diarrhoea or coccidiosis have been reported following betaine supplementation in pigs and poultry. There is also some evidence that dietary betaine may improve the digestibility of specific nutrients. As a product of choline oxidation, betaine is involved in transmethylation reactions of the organism. Betaine as a methyl donor provides its labile methyl groups for the synthesis of several metabolically active substances such as creatine and carnitine. Supplementation with betaine may decrease the requirement for other methyl donors such as methionine and choline. There is also some evidence for enhanced methionine availability after dietary supplementation of betaine resulting in improved animal performance. Alterations in the distribution pattern of protein and fat in the body have been reported following betaine supplementation. A more efficient use of dietary protein may result from a methionine-sparing effect of betaine, but also direct interactions of betaine with metabolism-regulating factors have to be considered. Though the mode of action of betaine as a carcass modifier remains open, there is, however, growing evidence that betaine could have a positive impact both on animal performance and carcass quality.

Following the high-profile studies on hormone replacement therapy which provided little evidence in support of the drug therapy improving future health, there remains a growing demand for dietary solutions for maintaining health and preventing disease as women age. Although interest in the relative importance of phyto-oestrogens to human health has increased dramatically over the last decade, the effective dose for health benefits and hypothetical issues on safety remain to be resolved. Plausible mechanisms and epidemiological data are available to support the concept that phyto-oestrogen-rich diets exert physiological effects, but optimal doses and sources of these compounds have still not been elucidated for specific health benefits. In addition, much of the current mechanistic data are difficult to interpret as the experiments have incorporated levels of phyto-oestrogens that may not be achievable in vivo and have to date only used aglycones and glycosides of the pure compounds rather than examining the biological effects of gut and liver metabolites. The present review will concentrate on the isoflavone subclass of phyto-oestrogens, as, to date, these compounds have received most attention from both a commercial and research perspective.

Southeast Asian women have a lower incidence of breast cancer than their counterparts in the West. Epidemiological studies have indicated that soya consumption may be a contributing factor. Carcinogenesis is a process involving multiple stages. The present review attempts to fit the cellular mechanisms attributed to soya isoflavones into these different stages. Many cell-culture studies have reported the growth-inhibitory effect of soya isoflavones; however, with the non-physiological concentrations employed in these studies it would be difficult to explain the protection mechanisms observed in epidemiological studies. Our laboratory has previously found that genistein inhibits cytochrome P450 (CYP)1A1 and CYP1B1. The inhibition implies that soya consumption may have the potential to prevent chemical carcinogenesis. The preferential inhibition of CYP1B1 may also block the oestrogen-initiated carcinogenesis. The antagonism of oestrogen receptor (ER) binding can affect the cell-proliferative phase, which is likely to be important in the promotion stage of breast cancer. Since our laboratory and others have indicated that genistein at physiological concentrations has no effect on the downstream activities of ER binding, the antagonism of ER is not likely to be a contributing factor in the disease prevention. Moreover, soya isoflavones cannot inhibit aromatase (CYP19), which is the enzyme responsible for oestrogen synthesis. In the present review various cellular activities altered by soya isoflavones are discussed

Maintaining a correct balance of N is essential for life. In mammals, the major sources of N in the diet are amino acids and peptides derived from ingested proteins. The immediate endproduct of mammalian protein catabolism is ammonia, which is toxic to cells if allowed to accumulate. Therefore, amino acids are broken down in the liver as part of the ornithine–urea cycle, which results in the formation of urea – a highly soluble, biochemically benign molecule. Mammals cannot break down urea, which is traditionally viewed as a simple waste product passed out in the urine. However, urea from the bloodstream can pass into the gastrointestinal tract, where bacteria expressing urease cleave urea into ammonia and carbon dioxide. The bacteria utilise the ammonia as an N source, producing amino acids and peptides necessary for growth. Interestingly, these microbial products can be reabsorbed back into the host mammalian circulation and used for synthetic processes. This entire process is known as ‘urea nitrogen salvaging’ (UNS). In this review we present evidence supporting a role for this process in mammals – including ruminants, non-ruminants and man. We also explore the possible mechanisms involved in UNS, including the role of specialised urea transporters.

The possible role played by artificial sweeteners in the long-term maintenance of body weight is considered. Although artificial sweeteners can play a role in a short-term energy-controlled diet, the evidence that they are helpful over a longer period is limited. In those in the recommended weight range there is evidence of compensation; that is, the consumption of low-energy foods is followed by an increased energy intake to make up the lost energy. Energy compensation is more likely in those not displaying dietary restraint. The desire to remove sugar from the diet reflects an assumption that its intake is associated with obesity. However, the consumption of energy-dense food, that almost entirely reflects a high fat and low water content, is the best predictor of obesity. Diets offering a high proportion of energy in the form of carbohydrate tend to contain low levels of fat. There are several reports that the use of artificial sweeteners leads to an increased consumption of fat. The weak ability of fat to satisfy hunger makes it easy to overeat fatty foods; in contrast, carbohydrates promote a feeling of ‘fullness’. Various short-term studies have found that carbohydrate consumed as a liquid, rather than a solid, is more likely to result in weight gain.

Non-alcoholic steatohepatitis (NASH) may be associated with a number of clinical conditions, but it occurs most commonly in patients with insulin resistance. There is as yet no established disease-modifying treatment, and a safe and broadly available agent that targets hepatic steatosis, insulin resistance, inflammation and fibrosis is necessary. The polyphenolic compound curcumin exhibits antioxidant and anti-inflammatory properties, inhibits NF-κB and activates PPAR-γ. In rodents, curcumin prevents dietary-induced hepatic steatosis, hepatic stellate cell activation and production of fibrotic proteins, and ameliorates steatohepatitis induced by the intake of alcohol or a methionine–choline-deficient diet. Indirect evidence suggests that curcumin may improve insulin sensitivity in diabetes and inflammatory states. The present paper reviews the numerous cellular and animal studies indicating that curcumin attenuates many of the pathophysiological processes involved in the development and progression of NASH. It is suggested that basic and clinical studies on curcumin in the development and progression of NASH are indicated.

The effect of psychological stress on health is becoming a serious concern, with figures from the World Health Organization showing that stress-related disorders affect nearly 450 million individuals worldwide. Heightened physiological stress responses and psychosocial factors have been linked to disease pathways such as hypertension and CVD. This has prompted significant interest within the scientific community, public health bodies and industry to employ interventions to control and reduce the impact of stress on health. There is now strong potential for functional foods to offer stress management benefits. Various physiological pathways have been targeted by specific dietary supplements for stress reduction, including the hypothalamic–pituitary–adrenal axis and sympathetic nervous system. Presently there are a number of ingredients, which include vitamin C, milk proteins, a number of herbal extracts (ginkgo biloba, ginseng, kava, valerian and lemon balm), and n-3 fatty acids, that have demonstrated potential stress reactivity-lowering and mood-enhancing effects, although further work is required to substantiate the efficacy in human subjects. Dietary supplements that can alleviate excessive stress responses may play an increasingly important role for the maintenance of health in a stressful environment. However, future research should employ a greater range of measures that will provide stronger evidence to substantiate functional food claims for stress relief.

Insulin resistance underlies type 2 diabetes, CVD and the metabolic syndrome, driven by changes in diet, lifestyle, energy over–consumption and obesity. Nutritional recommendations for insulin resistance remain an area of controversy, particularly the quantity and types of dietary carbohydrate. The present review gives an overview of insulin resistance, its relationship to impaired insulin secretion and the metabolic syndrome, research methodologies used to measure insulin action and the epidemiological and intervention studies on the relationship between dietary carbohydrate and insulin resistance. Epidemiological studies provide little evidence to suggest that total dietary carbohydrate predicts risk of type 2 diabetes, and high–carbohydrate, high–fibre diets with low–glycaemic index (GI) may even contribute to diabetes prevention. Despite inherent limitations associated with techniques used to measure insulin resistance and dietary assessment, most intervention studies reveal an increase in glucose tolerance or insulin sensitivity with high–carbohydrate, low–fat diets in non–diabetic and diabetic individuals. When energy is restricted the source or reduced content of carbohydrate does not appear to be as important as fat for body weight. Thus, low energy intake is key to weight loss and augmentation of insulin sensitivity. Given this, widespread adoption of popular low–carbohydrate high–fat diets highlights the necessity to evaluate dietary interventions regarding safety and metabolic effects. While current evidence supports FAO/WHO recommendations to maintain a high–carbohydrate diet with low–GI foods, the relationships between carbohydrate and insulin sensitivity remains an important research area. Emerging technologies should further enhance understanding of gene–diet interactions in insulin resistance, providing useful information for future nutrition policy decisions.

Kidney diseases are the ninth leading cause of death in the USA. In these patients cardiovascular mortality is greater than in the general population. This observation, not completely explained by the so-called ‘traditional’ cardiovascular risk factors, lead the authors to postulate other ‘emerging’ ones found in chronic renal failure patients. Among these new findings, nutritional status, considered as the balance existing between nutrient requirements and intakes, plays an important role for the development of cardiovascular diseases. In fact several nutritional parameters are widely known as pathophysiological determinants of cardiovascular disturbances, which are based on accelerated atherosclerosis, due especially to enhanced oxidative stress and endothelial dysfunction. Chronic renal failure is a clinical condition that from many points of view seems to be a chronic inflammatory state, and many studies confirm this observation. This influences nutritional status especially in dialysis patients. Malnutrition is related in turn to accelerated atherosclerosis thus leading to a postulated ‘malnutrition, inflammation, atherosclerosis’ (MIA) syndrome in which malnutrition, inflammation and atherosclerosis contribute to an elevated cardiovascular mortality rate. The present review explores this issue, first by describing epidemiological aspects of malnutrition in chronic renal failure patients and then by analysing the specific biochemical and metabolic features of these patients.

The role of diet in promoting health and preventing disease is difficult to elucidate due to its complex network of foods and nutrients. Besides total energy intake, dietary composition is probably the most important discriminator within and between populations. Dietary composition is reflected in dietary patterns, which have recently gained popularity. The present paper reviews the most commonly applied methods to identify dietary patterns, data-driven methods such as factor and cluster analysis, investigator-driven methods such as indices and score, and methods combining the two, namely reduced rank regression. We describe the techniques and their application, discuss strengths and limitations, and discuss the usefulness of dietary pattern analyses.

The Mediterranean diet is rich in vegetables, cereals, fruit, fish, milk, wine and olive oil and has salutary biological functions. Epidemiological studies have shown a lower incidence of atherosclerosis, cardiovascular diseases and certain kinds of cancer in the Mediterranean area. Olive oil is the main source of fat, and the Mediterranean diet's healthy effects can in particular be attributed not only to the high relationship between unsaturated and saturated fatty acids in olive oil but also to the antioxidant property of its phenolic compounds. The main phenolic compounds, hydroxytyrosol and oleuropein, which give extra-virgin olive oil its bitter, pungent taste, have powerful antioxidant activity both in vivo and in vitro. The present review focuses on recent works analysing the relationship between the structure of olive oil polyphenolic compounds and their antioxidant activity. These compounds' possible beneficial effects are due to their antioxidant activity, which is related to the development of atherosclerosis and cancer, and to anti-inflammatory and antimicrobial activity.

Hormesis defines an effect where exposure to a low dose of a toxic agent results in a beneficial response. It has been described in organisms exposed to low-dose radiation, heat stress, and chemicals. The effect is characterised by a J-shaped dose–response as opposed to a linear dose–response. Confirmation of the general phenomena of hormesis has proved difficult due to the lack of appropriate methodology and the absence of well-defined mechanisms to support the experimental observations. In the nutritional field there are few reports of its existence. The clearest illustration of the effect is seen in animals that are energy restricted when there is a clear benefit in the reduction of age-related disease, and an extension of maximum lifespan. DNA microarray experiments have shown that there is a down regulation of the stress-response genes that are up regulated through the ageing process. Electrophilic phytochemicals, that have been shown to have beneficial health effects at low doses, up regulate the antioxidant–electrophile response element. This probably occurs through an alteration in the redox state of the target cells which causes activation of protein kinases, the activation of the Nrf2 transcription factor and the up regulation of the phase II enzymes, similar to responses that occur under mild chemical stress. This situation might enable organisms to adapt to stress such that the effects of a subsequent exposure to a harmful challenge are reduced. There may be a permanent alteration in cellular homeostasis, or redox state, if the low level exposure is maintained. It remains to be proven if such a situation occurs in response to chronic low-dose exposure to dietary phytochemicals such that the target cells are better able to respond to a subsequent stress challenge.

A wide variety of nutritional exposures have been proposed as possible risk factors for Parkinson's disease (PD) with plausible biological hypotheses. Many studies have explored these hypotheses, but as yet no comprehensive systematic review of the literature has been available. MEDLINE, EMBASE, and WEB OF SCIENCE databases were searched for existing systematic reviews or meta-analyses of nutrition and PD, and one meta-analysis of coffee drinking and one meta-analysis of antioxidants were identified. The databases were searched for primary research articles, and articles without robust methodology were excluded by specified criteria. Seven cohort studies and thirty-three case–control (CC) studies are included in the present systematic review. The majority of studies did not find significant associations between nutritional factors and PD. Coffee drinking and alcohol intake were the only exposures with a relatively large number of studies, and meta-analyses of each supported inverse associations with PD. Factors that were reported by at least one CC study to have significantly increased consumption among cases compared with controls were: vegetables, lutein, xanthophylls, xanthins, carbohydrates, monosaccharides, junk food, refined sugar, lactose, animal fat, total fat, nuts and seeds, tea, Fe, and total energy. Factors consumed significantly less often among cases were: fish, egg, potatoes, bread, alcohol, coffee, tea, niacin, pantothenic acid, folate and pyridoxine. In three cohort studies, two reported borderline decreased relative risks and one a significant increased risk with vitamin C intake. One cohort reported an inverse association between caffeine intake and PD. Three cohorts reported significant positive association in men between dairy products and PD.

A considerable literature has been published on the health benefits of fish, oil-rich fish and fish oils and their constituent long-chain (LC) n-3 PUFA. Evidence from epidemiological studies highlights the cardioprotective attributes of diets rich in fish, especially oil-rich fish. Data from intervention trials are consistent in suggesting that LC n-3 PUFA lower the risk of CVD, probably by the multiple mechanisms of lowering serum triacylglycerols, improving the LDL:HDL ratio, anti-arrhythmic effects on heart muscle, improved plaque stability, anti-thrombotic effects and reduced endothelial activation. Research indicates LC n-3 PUFA provision has an impact during development, and there is preliminary evidence that docosahexaenoic acid supplementation during pregnancy could optimise brain and retina development in the infant. LC n-3 PUFA are also postulated to ameliorate behavioural and mental health disturbances such as depression, schizophrenia, dementia and attention deficit hyperactivity disorder. However, despite some positive evidence in each of these areas, use of LC n-3 PUFA in these conditions remains at the experimental stage. In the case of immune function, there is little doubt that LC n-3 PUFA have a positive effect. Although intervention trials in rheumatoid arthritis show strong evidence of benefit, evidence for efficacy in other inflammatory conditions, including Crohn's disease, ulcerative colitis, psoriasis, lupus, multiple sclerosis, cystic fibrosis and asthma, is inconsistent or inadequate. More promising evidence in some conditions may come from studies which attempt to modify the fetal environment using LC n-3 PUFA supplementation during pregnancy.

Dietary isoflavones are thought to be cardioprotective due to their structural similarity to oestrogen. Oestrogen is believed to have beneficial effects on endothelial function and may be one of the mechanisms by which premenopausal women are protected against CVD. Decreased NO production and endothelial NO synthase activity, and increased endothelin-1 concentrations, impaired lipoprotein metabolism and increased circulating inflammatory factors result from oestrogen deficiency. Oestrogen acts by binding to oestrogen receptors α and β. Isoflavones have been shown to bind with greater affinity to the latter. Oestrogen replacement therapy is no longer thought to be a safe treatment for prevention of CVD; isoflavones are a possible alternative. Limited evidence from human intervention studies suggests that isoflavones may improve endothelial function, but the available data are not conclusive. Animal studies provide stronger support for a role of isoflavones in the vasculature, with increased vasodilation and endothelial NO synthase activity demonstrated. Cellular mechanisms underlying the effects of isoflavones on endothelial cell function are not yet clear. Possible oestrogen receptor-mediated pathways include modulation of gene transcription, and also non-genomic oestrogen receptor-mediated signalling pathways. Putative non-oestrogenic pathways include inhibition of reactive oxygen species production and up regulation of the protein kinase A pathway (increasing NO bioavailability). Further research is needed to unravel effects of isoflavones on intracellular regulation of the endothelial function. Moreover, there is an urgent need for adequately powered, robustly designed human intervention studies in order to clarify the present equivocal findings.

The glycaemic index (GI) concept was originally introduced to classify different sources of carbohydrate (CHO)-rich foods, usually having an energy content of >80 % from CHO, to their effect on post-meal glycaemia. It was assumed to apply to foods that primarily deliver available CHO, causing hyperglycaemia. Low-GI foods were classified as being digested and absorbed slowly and high-GI foods as being rapidly digested and absorbed, resulting in different glycaemic responses. Low-GI foods were found to induce benefits on certain risk factors for CVD and diabetes. Accordingly it has been proposed that GI classification of foods and drinks could be useful to help consumers make ‘healthy food choices’ within specific food groups. Classification of foods according to their impact on blood glucose responses requires a standardised way of measuring such responses. The present review discusses the most relevant methodological considerations and highlights specific recommendations regarding number of subjects, sex, subject status, inclusion and exclusion criteria, pre-test conditions, CHO test dose, blood sampling procedures, sampling times, test randomisation and calculation of glycaemic response area under the curve. All together, these technical recommendations will help to implement or reinforce measurement of GI in laboratories and help to ensure quality of results. Since there is current international interest in alternative ways of expressing glycaemic responses to foods, some of these methods are discussed.