Chronic pelvic pain (CPP) can be identified as a chronic nociceptive, inflammatory and neuropathic pain characterised by spontaneous pain and an exaggerated response to painful and/or innocuous stimuli. This pain condition is extremely debilitating and usually difficult to treat. Currently, the main approaches to treatment include counselling supported by reassuring ultrasound scanning or psychotherapy, attempting to provide reassurance using laparoscopy to exclude serious pelvic pathology, hormonal therapy and neuroablative treatment to interrupt nerve pathways. Dietary supplementation has been suggested as a means to treat chronic medical illnesses that are poorly responsive to prescription drugs or in which therapeutic options are limited, costly or carry a high side-effect profile. A comprehensive search of the PubMed database was performed using the search terms ‘chronic pelvic pain’, ‘oxidative stress’, ‘antioxidants’ and ‘dietary therapy’. The systematic review focuses on both randomised and non-randomised controlled trials from 2005 onwards, in which CPP was the end point. Given the complexity and not well-understood aetiology of CPP, its treatment is often unsatisfactory and limited to partial symptom relief. Dietary therapy with antioxidants improves function of the immune system and in fighting free radical damage. Agents with antioxidant activity are able to improve CPP without undesired effects and any important metabolic changes associated with hormonal suppression therapy. In conclusion, dietary therapy with antioxidants could be considered as a new effective strategy in the long term for CPP, and may be better accepted by patients. Further randomised trials with larger series and long-term follow-up to confirm these observations are needed.

Critically ill patients frequently suffer from gastrointestinal dysfunction as the intestine is a vulnerable organ. In critically ill patients who require nutritional support, the current guidelines recommend the use of enteral nutrition within 24–48 h and advancing towards optimal nutritional goals over the next 48–72 h; however, this may be contraindicated in patients with acute gastrointestinal injury because overuse of the gut in the acute phase of critical illness may have an adverse effect on the prognosis. We propose that trophic feeding after 72 h, as a partial gut rest strategy, should be provided to critically ill patients during the acute phase of illness as an organ-protective strategy, especially for those with acute gastrointestinal injury.

Neutering or spaying is a commonly recommended veterinary procedure. However, veterinarians are often confronted with conflicting findings and differences in concepts regarding practice and proper nutritional management after the procedure. The objective of the present review was to bring to light the most recent literature, summarise it and discuss the findings focusing on the risks and benefits of neutering in dogs and cats, and to determine the appropriate nutritional management for these animals.

Cognitive outcomes are frequently implemented as endpoints in nutrition research. To reduce the number of statistical comparisons it is commonplace for nutrition researchers to combine cognitive test results into a smaller number of broad cognitive abilities. However, there is a clear lack of understanding and consensus as to how best execute this practice. The present paper reviews contemporary models of human cognition and proposes a standardised, evidence-based method for grouping cognitive test data into broader cognitive abilities. Both Carroll's model of human cognitive ability and the Cattell–Horn–Carroll (CHC) model of intelligence provide empirically based taxonomies of human cognition. These models provide a cognitive ‘map’ that can be used to guide the handling and analysis of cognitive outcomes in nutrition research. Making use of a valid cognitive nomenclature can provide the field of clinical nutrition with a common cognitive language enabling efficient comparisons of cognitive outcomes across studies. This will make it easier for researchers, policymakers and readers to interpret and compare cognitive outcomes for different interventions. Using an empirically derived cognitive nomenclature to guide the creation of cognitive composite scores will ensure that cognitive endpoints are theoretically valid and meaningful. This will increase the generalisability of trial results to the general population. The present review also discusses how the CHC model of cognition can also guide the synthesis of cognitive outcomes in systematic reviews and meta-analysis.

Associated with the obesity epidemic, non-alcoholic fatty liver disease (NAFLD) has become the leading liver disease in North America. Approximately 30 % of patients with NAFLD may develop non-alcoholic steatohepatitis (NASH) that can lead to cirrhosis and hepatocellular carcinoma (HCC). Frequently animal models are used to help identify underlying factors contributing to NAFLD including insulin resistance, dysregulated lipid metabolism and mitochondrial stress. However, studying the inflammatory, progressive nature of NASH in the context of obesity has proven to be a challenge in mice. Although the development of effective treatment strategies for NAFLD and NASH is gaining momentum, the field is hindered by a lack of a concise animal model that reflects the development of liver disease during obesity and the metabolic syndrome. Therefore, selecting an animal model to study NAFLD or NASH must be done carefully to ensure the optimal application. The most widely used animal models have been reviewed highlighting their advantages and disadvantages to studying NAFLD and NASH specifically in the context of obesity.

Animal experiments and cross-sectional or prospective longitudinal research in human subjects suggest a role for nutrition in cognitive ageing. However, data from randomised controlled trials (RCT) that seek causal evidence for the impact of nutrients on cognitive ageing in humans often produce null results. Given that RCT test hypotheses in a rigorous fashion, one conclusion could be that the positive effects of nutrition on the aged brain observed in other study designs are spurious. On the other hand, it may be that the design of many clinical trials conducted thus far has been less than optimal. In the present review, we offer a blueprint for a more targeted approach to the design of RCT in nutrition, cognition and brain health in ageing that focuses on three key areas. First, the role of nutrition is more suited for the maintenance of health rather than the treatment of disease. Second, given that cognitive functions and brain regions vary in their susceptibility to ageing, those that especially deteriorate in senescence should be focal points in evaluating the efficacy of an intervention. Third, the outcome measures that assess change due to nutrition, especially in the cognitive domain, should not necessarily be the same neuropsychological tests used to assess gross brain damage or major pathological conditions. By addressing these three areas, we expect that clinical trials of nutrition, cognition and brain health in ageing will align more closely with other research in this field, and aid in revealing the true nature of nutrition’s impact on the aged brain.

The objectives were firstly to assess the evidence that homocysteine is a significant and independent risk factor for vascular disease with special reference to cardiovascular disease, and secondly to evaluate the evidence that a food staple fortified with folic acid will reduce this problem on a population basis.

The structure of plasma homocysteine (tHcy) is described. Homocysteine, a highly reactive compound, is synthesized from the amino acid, methionine, and is metabolized by two pathways, the catabolic transsulphuration route via cystathionine β-synthase (EC 4.2.1.22) and the remethylation path using 5-methyltetrahy-drofolate polyglutamate, the product of 5,10-methylenetetrahydrofolate reductase (MTHFR; EC 1.1.1.171), via the cobalamin dependent enzyme, methionine synthase (MS; EC 2.1.1.13).

The mechanisms whereby hyper-tHcy is produced include both increased rates of synthesis and decreased metabolism. The latter may occur owing to nutritional deficiency of the vitamin cofactors which are necessary for the normal function of the metabolic enzymes. In particular, folate is required for methylene reductase, pyridoxal phosphate for cystathionine synthase and cobalamin for methionine synthase. When these vitamins are deficient hyper-tHcy is induced and this occurs especially in the elderly. Alternatively, a variant form of methylene reductase has recently been described which occurs in nearly 10% of the normal population. This variant is associated with hyper-tHcy, especially in situations associated with a low folate nutritional status.

Meta-analysis of both retrospective case-control studies, nested prospective case-control surveys and a secondary trial of mortality in postmyocardial infarct patients have shown that the association of hyper-tHcy with vascular disease is beyond doubt. This has been further supported by direct assessments of the degree of vascular disease in the carotid brachial and aortic arteries in relation to tHcy levels. Furthermore, treatment with a cocktail of the vitamin cofactors has produced lowering of tHcy levels and regression of the vascular disease in the carotid arteries of affected individuals.

Suggested pathogenic mechanisms in vascular disease induced by hyper-tHcy include vascular endothelial cell dysfunction, smooth muscle proliferation and derangements of normal intravascular regulation mechanisms. A variety of clinical conditions are known to be associated with a high incidence of thromboembolic complications. Some of these are associated with hyper-tHcy.

Low physiological doses of folic acid, as well as pharmocological doses, lower tHcy. However, because of the poor bioavailability of food folate (50%) and the considerable chemical instability of the naturally occurring reduced forms of folate, in most people it would require unacceptably high consumption of green vegetables to accomplish the necessary increase in intracellular folate and reduction in tHcy. Accordingly, folic acid, the nonreduced synthetic form of the vitamin, which is 100% bioavailable and chemically extremely stable, should be added to a food staple such as flour to ensure maximum protection for most of the population.

Amino acid bioavailability is critical for muscle protein synthesis (MPS) and preservation of skeletal muscle mass (SMM). Ageing is associated with reduced responsiveness of MPS to essential amino acids (EAA). Further, the older adult population experiences anabolic resistance, leading to increased frailty, functional decline and depleted muscle mass preservation, which facilitates the need for increased protein intake to increase their SMM. This review focuses on the role of proteins in muscle mass preservation and examines the contribution of EAA and protein intake patterns to MPS. Leucine is the most widely studied amino acid for its role as a potent stimulator of MPS, though due to inadequate data little is yet known about the role of other EAA. Reaching a conclusion on the best pattern of protein intake has proven difficult due to conflicting studies. A mixture of animal and plant proteins can contribute to increased MPS and potentially attenuate muscle wasting conditions; however, there is limited research on the biological impact of protein blends in older adults. While there is some evidence to suggest that liquid protein foods with higher than the RDA of protein may be the best strategy for achieving high MPS rates in older adults, clinical trials are warranted to confirm an association between food form and SMM preservation. Further research is warranted before adequate recommendations and strategies for optimising SMM in the elderly population can be proposed.

Cereals and cereal products have a long history of use by humans. Recently, there have been some discussions regarding level of processing as a descriptor to define food products, including cereal-based foods. This has led to a somewhat emotional debate on food processing. Given the widespread inclusion of cereals in the diet, this review highlights the history of cereal processing as well as their consumption by humans. It provides an evidence-based discussion on their production, contribution to human nutrition, benefits and disadvantages. The present review illustrates the impact of processing on nutrients, as well as non-nutrients specifically in bread and ready-to-eat breakfast cereals (RTEC), two cereal-based foods which are widely consumed and integral parts of food-based dietary guidelines globally. As a category, most cereals must be processed in some way to enable consumption by humans as we are not equipped to survive exclusively on raw grains. Even thousands of years ago, the processing of cereals was a common practice by humans, turning raw grains into palatable, safe and nutritious foods. Modern processes for cereal-based products are efficient in providing safe and good-quality products to satisfy population needs, as well as helping to meet consumer expectations by providing a range of foods that allows for a varied and balanced diet. Today, RTEC and bread make significant contributions to dietary energy and nutrient requirements and underpin food-based dietary guidance globally. They have been positively linked with intake of dietary fibre, vitamins and minerals, especially when consumed as whole grain.

The mammary gland, a unique exocrine organ, is responsible for milk synthesis in mammals. Neonatal growth and health are predominantly determined by quality and quantity of milk production. Amino acids are crucial maternal nutrients that are the building blocks for milk protein and are potential energy sources for neonates. Recent advances made regarding the mammary gland further demonstrate that some functional amino acids also regulate milk protein and fat synthesis through distinct intracellular and extracellular pathways. In the present study, we discuss recent advances in the role of amino acids (especially branched-chain amino acids, methionine, arginine and lysine) in the regulation of milk synthesis. The present review also addresses the crucial questions of how amino acids are transported, sensed and transduced in the mammary gland.

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.

Adequate protein intake is essential for the maintenance of whole-body protein mass. Different methodological approaches are used to substantiate the evidence for the current protein recommendations, and it is continuously debated whether older adults require more protein to counteract the age-dependent loss of muscle mass, sarcopenia. Thus, the purpose of this critical narrative review is to outline and discuss differences in the approaches and methodologies assessing the protein requirements and, hence, resulting in controversies in current protein recommendations for healthy older adults. Through a literature search, this narrative review first summarises the historical development of the Food and Agriculture Organization/World Health Organization/United Nations University setting of protein requirements and recommendations for healthy older adults. Hereafter, we describe the various types of studies (epidemiological studies and protein turnover kinetic measurements) and applied methodological approaches founding the basis and the different recommendations with focus on healthy older adults. Finally, we discuss important factors to be considered in future studies to obtain evidence for international agreement on protein requirements and recommendations for healthy older adults. We conclude by proposing future directions to determine ‘true’ protein requirements and recommendations for healthy older adults.

The weaning transition is characterised by morphological, histological and microbial changes, often leading to weaning-associated disorders. These intestinal changes can partly be ascribed to the lack of luminal nutrition arising from the reduced feed intake common in pigs after weaning. It is increasingly becoming clear that changes in the supply with enteral nutrients may have major impacts on intestinal gene expression. Furthermore, the major dietary constituents, i.e. carbohydrates, fatty acids and amino acids, participate in the regulation of intestinal gene expression. However, nutrients may also escape digestion by mammalian enzymes in the upper gastrointestinal tract. These nutrients can be used by the microflora, resulting in the production of bacterial metabolites, for example, SCFA, which may affect intestinal gene expression indirectly. The present review provides an insight on possible effects of reduced feed intake on intestinal gene expression, as it may occur post-weaning. Detailed knowledge on effects of reduced feed intake on intestinal gene expression may help to understand weaning-associated intestinal dysfunctions and diseases. Examples are given of intestinal genes which may be altered in their expression due to supply with specific nutrients. In that way, gene expression could be modulated by dietary means, thereby acting as a potential therapeutic tool. This could be achieved, for example, by influencing genes coding for digestive or absorptive proteins, thus optimising digestive function and metabolism, but also with regard to immune response, or by influencing proliferative processes, thereby enhancing mucosal repair. This would be of special interest when designing a diet to overcome weaning-associated problems.

Controlling energy homeostasis involves modulating the desire to eat and regulating energy expenditure. The controlling machinery includes a complex interplay of hormones secreted at various peripheral endocrine endpoints, such as the gastrointestinal tract, the adipose tissue, thyroid gland and thyroid hormone-exporting organs, the ovary and the pancreas, and, last but not least, the brain itself. The peripheral hormones that are the focus of the present review (ghrelin, leptin, thyroid hormones, oestrogen and insulin) play integrated regulatory roles in and provide feedback information on the nutritional and energetic status of the body. As peripheral signals, these hormones modulate central pathways in the brain, including the hypothalamus, to influence food intake, energy expenditure and to maintain energy homeostasis. Since the growth of the literature on the role of various hormones in the regulation of energy homeostasis shows a remarkable and dynamic expansion, it is now becoming increasingly difficult to understand the individual and interactive roles of hormonal mechanisms in their true complexity. Therefore, our goal is to review, in the context of general physiology, the roles of the five best-known peripheral trophic hormones (ghrelin, leptin, thyroid hormones, oestrogen and insulin, respectively) and discuss their interactions in the hypothalamic regulation of food intake.

The ultimate goal in the design of infant formula is to achieve the outcome seen in breast fed infants. This review of lipids in infant formulas for term infants begins by referring to the lipid composition of human milk, and relates that to differences in lipid digestion and metabolism which exist between breast fed and formula fed infants and which may significantly influence fatty acid bioavailability.

Recommendations are made for the lipid content and fatty acid composition of term infant formulas (especially for lauric, linoleic, α-linolenic, long chain 20 and 22C n-3 and n-6 polyunsaturated fatty acids and the trans fatty acids).

Further research is required to define more clearly the long term nutritional, growth and developmental effects of structured lipids in formulas for term infants. More information is required on the differential handling of LCPUFA and other fatty acids at the organ and cellular level. There is a need for large (multi-centre) randomized studies to determine the short and long term functional effects of LCPUFA supplementation. Further research and development is required to determine a commercial source of LCPUFA which is safe, effective and economic. Further information is required on the short and long term effects of cholesterol intake during infancy, and in particular its relationship to LCPUFA metabolism. Long term studies should be initiated to determine the relationship of infant diet (especially saturated fatty acid and cholesterol intake) to the development of cardiovascular disease.