With world attention now focusing on the Olympics, the question as to the extent to which nutrient intakes can affect athletic performance is highly topical; in this context, the article

We are all familiar with the dietary guideline exhorting us to eat so many portions of oily fish per week in order to boost our intakes of n-3 long-chain PUFA, but it is perhaps not so widely realised that the fish must themselves be provided with dietary n-3 long-chain PUFA or, possibly, their precursors (though, as in humans, the ability of carnivorous fish to elongate and desaturate n-3 PUFA appears to be limited).

The present review examines renewable sources of oils with n-3 long-chain ( ≥ C20) PUFA (n-3 LC-PUFA) as alternatives to oil from wild-caught fish in aquafeeds. Due to the increased demand for and price of wild-caught marine sources of n-3 LC-PUFA-rich oil, their effective and sustainable replacement in aquafeeds is an industry priority, especially because dietary n-3 LC-PUFA from eating fish are known to have health benefits in human beings. The benefits and challenges involved in changing dietary oil in aquaculture are highlighted and four major potential sources of n-3 LC-PUFA for aquafeeds, other than fish oil, are compared. These sources of oil, which contain n-3 LC-PUFA, specifically EPA (20 : 5n-3) and DHA (22 : 6n-3) or precursors to these key essential fatty acids, are: (1) other marine sources of oil; (2) vegetable oils that contain biosynthetic precursors, such as stearidonic acid, which may be used by fish to produce n-3 LC-PUFA; (3) single-cell oil sources of n-3 LC-PUFA; (4) vegetable oils derived from oil-seed crops that have undergone genetic modification to contain n-3 LC-PUFA. The review focuses on Atlantic salmon (Salmo salar L.), because it is the main intensively cultured finfish species and it both uses and stores large amounts of oil, in particular n-3 LC-PUFA, in the flesh.

Physical training is known to induce a biochemical adaptive response which might require an increase in the ingestion and/or the absorption of micronutrients. A question that is still being raised is whether acute or chronic exercise modifies antioxidant requirements. First, the present review brings to light the most crucial studies on the topic. Second, it interprets the established relationships between antioxidant micronutrient intakes and the adaptive response of antioxidant systems. Finally, it exposes the major questions connected with antioxidant micronutrient requirements for athletes. To this effect, the training-load interaction with nutrition is taken into account. As oxidative stress cannot be avoided, the imbalance between oxidants and antioxidants can be alleviated to minimise oxidative damage and outcomes. There is growing evidence that one specific antioxidant cannot by itself prevent oxidative stress-induced damage, as direct adverse effects of supplementation are attributed to undesirable synergic effects. Other effects can be supposed that limit the endogenous adaptive effect of training. High doses of antioxidant supplements can minimise the effects of radical oxygen species themselves or generate pro-oxidant effects. Effects are only exhibited when nutritional status is deficient. There are no convincing effects of supplementation in well-trained athletes. Risk/benefit analysis emerges on evidence for an unknown risk of supranutritional intakes, a supposed impairment of adaptive effects and a still unknown long-term risk. Appropriate status can be achieved by a diversified and balanced diet, adapted to specific needs, by awareness of high-density food intakes (avoiding products containing a low density of micronutrients).

The evolutionary origin of the mammary gland has been difficult to establish because little knowledge can be gained on the origin of soft tissue organs from fossil evidence. One approach to resolve the origin of lactation has compared the anatomy of existing primitive mammals to skin glands, whilst another has examined the metabolic and molecular synergy between mammary gland development and the innate immune system. We have reviewed the physiology of lactation in five mammalian species with special reference to these theories. In all species, milk fulfils dual functions of providing protection and nutrition to the young and, furthermore, within species the quality and quantity of milk are highly conserved despite maternal malnutrition or illness. There are vast differences in birth weight, milk production, feeding frequency, macronutrient concentration, growth rate and length of lactation between rabbits, quokkas (Setonix brachyurus), pigs, cattle and humans. The components that protect the neonate against infection do so without causing inflammation. Many protective components are not unique to the mammary gland and are shared with the innate immune system. In contrast, many of the macronutrients in milk are unique to the mammary gland, have evolved from components of the innate immune system, and have either retained or developed multiple functions including the provision of nourishment and protection of the hatchling/neonate. Thus, there is a strong argument to suggest that the mammary gland evolved from the inflammatory response; however, the extensive protection that has developed in milk to actively avoid triggering inflammation seems to be a contradiction.

Selected biochemical evidence suggests a potential role for n-3 long-chain PUFA (n-3PUFA) in the regulation of mood and behaviour. The present paper reviews the relevant evidence, to date, from epidemiological studies, clinical studies and intervention trials. Most evidence is available investigating a role for n-3PUFA in depression, depressive illness and suicidal behaviour, but work is also available on anxiety and anxiety-related disorders, fatigue and fatigue-related disorders, aggression, hostility and anti-social behaviour, inattention, impulsivity and attention deficit hyperactivity disorder and schizophrenic disorders. For all these aspects of mood and behaviour, the evidence available is currently limited and highly inconsistent, both in terms of study methodology and study findings. There is a clear need for further work in this area.

The pyridine nucleotide NAD+ is derived from dietary niacin and serves as the substrate for the synthesis of cyclic ADP-ribose (cADPR), an intracellular Ca signalling molecule that plays an important role in synaptic plasticity in the hippocampus, a region of the brain involved in spatial learning. cADPR is formed in part via the activity of the ADP-ribosyl cyclase enzyme CD38, which is widespread throughout the brain. In the present review, current evidence of the relationship between dietary niacin and behaviour is presented following investigations of the effect of niacin deficiency, pharmacological nicotinamide supplementation and CD38 gene deletion on brain nucleotides and spatial learning ability in mice and rats. In young male rats, both niacin deficiency and nicotinamide supplementation significantly altered brain NAD+ and cADPR, both of which were inversely correlated with spatial learning ability. These results were consistent across three different models of niacin deficiency (pair feeding, partially restricted feeding and niacin recovery). Similar changes in spatial learning ability were observed in Cd38− / −  mice, which also showed decreases in brain cADPR. These findings suggest an inverse relationship between spatial learning ability, dietary niacin intake and cADPR, although a direct link between cADPR and spatial learning ability is still missing. Dietary niacin may therefore play a role in the molecular events regulating learning performance, and further investigations of niacin intake, CD38 and cADPR may help identify potential molecular targets for clinical intervention to enhance learning and prevent or reverse cognitive decline.

Following the discovery of TNF-α and leptin as secretory products of adipocytes in the early 1990s, subsequent obesity research focused on the new functional role of adipose tissue, as an active endocrine organ. Many more inflammatory peptides have been linked to adiposity, which ultimately characterised obesity as a state of low-grade systemic inflammation, or ‘metaflammation’ which may link obesity to its co-morbidities. The aim of the present review is to examine the effects of weight loss on inflammation in overweight and obese, but otherwise healthy, populations. Studies were broadly classified into four types (diet, physical activity, diet and physical activity combined, and surgical interventions) and discussed according to the method used to induce weight loss. All studies measured at least one obesity-related inflammatory marker (ORIM). The overall finding from the present review is that weight loss does improve inflammation in terms of both the inflammatory (C-reactive protein, TNF-α, IL-6 and leptin) and anti-inflammatory (adiponectin) ORIM. Within this, the greatest improvements in ORIM are observed in studies achieving a weight loss of at least 10 %. However, a number of methodological issues have been identified as potential limitations within the literature including the sex and age of subjects, sample size, study duration and the assessment of body composition. In conclusion, although a period of weight loss per se is capable of reversing the unfavourable inflammatory profile evident in the obese state, further studies are required to determine the time needed, in which a reduced weight is maintained, in order to benefit from improved inflammatory status long term.

Sugar-sweetened soft drinks (SSD) are a special target of many obesity-prevention strategies, yet critical reviews tend to be more cautious regarding the aetiological role of SSD in promoting excess body weight. Since ongoing evaluation of this issue is important, the present systematic review re-examined the evidence from epidemiological studies and interventions, up to July 2008. Database searches of Medline, Cochrane reviews, Google scholar and a hand search of cross-references identified forty-four original studies (twenty-three cross-sectional, seventeen prospective and four intervention) in adults and children, as well as six reviews. These were critically examined for methodology, results and interpretation. Approximately half the cross-sectional and prospective studies found a statistically significant association between SSD consumption and BMI, weight, adiposity or weight gain in at least one subgroup. The totality of evidence is dominated by American studies where SSD consumption tends to be higher and formulations different. Most studies suggest that the effect of SSD is small except in susceptible individuals or at high levels of intake. Methodological weaknesses mean that many studies cannot detect whether soft drinks or other aspects of diet and lifestyle have contributed to excess body weight. Progress in reaching a definitive conclusion on the role of SSD in obesity is hampered by the paucity of good-quality interventions which reliably monitor diet and lifestyle and adequately report effect sizes. Of the three long-term (>6 months) interventions, one reported a decrease in obesity prevalence but no change in mean BMI and two found a significant impact only among children already overweight at baseline. Of the six reviews, two concluded that the evidence was strong, one that an association was probable, while three described it as inconclusive, equivocal or near zero. Reasons for some discrepancies are presented.

Prospective cohort studies suggest that higher intakes of dairy products, in particular milk, are associated with a decreased risk of colorectal cancer (CRC). In Western populations, dairy products are major contributors to dietary Ca, which may have chemopreventive effects in the colon. The pooling of data from prospective studies suggests a significant protective effect of Ca on CRC risk. Randomised controlled trials with Ca supplements have been conducted with both colorectal adenoma and CRC as endpoints. Results suggest that Ca supplementation at a level of 1000–2000 mg/d reduces adenoma recurrence in individuals with a previous adenoma but has no effect on CRC incidence. There is evidence that the risk reduction from dairy foods may not be solely due to their high Ca content. Dairy products contain other potential chemopreventive components such as vitamin D, butyric acid, conjugated linoleic acid, sphingolipids, and probiotic bacteria in fermented products such as yoghurt. The present review will focus on the epidemiological evidence (and in particular prospective cohort studies) investigating the relationship between dairy product consumption and risk of CRC. An outline of the proposed mechanisms responsible for the protective effect of both Ca and other potential chemopreventive components in dairy products will also be presented.

Ruman degradation is crucial in the supply of dietary nutrients to meet the nutrient demands of the anaerobic microbes and body tissues of ruminant animals. Therefore, it is essential to study the dynamics of rumen degradation of various feeds before their potential use to formulate nutritious diets for ruminant animals. Amongst many methods that have been used in the past, the in sacco method has been the most effective method to study rumen degradation. However, this method is undesirable due to its implications for animal welfare and costs. While many in vitro methods have been tested as possible alternatives to the in sacco method to study rumen degradation of feeds, they were unable to remove the need to use fistulated animals to obtain rumen fluid. Although solubility, enzyme- and faeces-based in vitro methods do not require rumen fluid, they still need data from either the in sacco method or the rumen fluid-based in vitro methods for comparison and validation. Therefore, there is a need to develop in vitro methods that do not require the need to surgically modify ruminants to obtain rumen fluid to study rumen degradation. We review the potentials and problems associated with the existing methods to study rumen degradation and their implications for the animal industry in different situations.

The metabolic syndrome is an important risk factor for type 2 diabetes mellitus and CVD. Epidemiological studies have now suggested protective effects of dairy product consumption on the development of this syndrome. Here we review the physiological effects and possible mechanisms involved of three main dairy constituents (Ca, protein, fat) on important components of the metabolic syndrome. Ca supplements improve the serum lipoprotein profile, particularly by decreasing serum total and LDL-cholesterol concentrations. They also lower systolic and diastolic blood pressure. Insufficient evidence exists for a significant role of Ca supplements or dairy in body-weight management. Effects of Ca may be related to intestinal binding to fatty acids or bile acids, or to changes in intracellular Ca metabolism by suppressing calciotropic hormones. Dietary proteins may increase satiety in both the short and longer term, which may result in a reduced energy intake. They have also been reported to improve the serum lipoprotein profile as compared with carbohydrates. Dairy proteins are precursors of angiotensin-I-converting enzyme-inhibitory peptides, which may lower blood pressure. Such effects, however, have inconsistently been reported in human studies. Finally, conjugated linoleic acid, which effectively lowers body weight in animals, has no such effect in humans in the quantities provided by dairy products. To reduce the intake of SFA, the consumption of low-fat instead of high-fat dairy products is recommended. In conclusion, more research is warranted to better understand the physiological effects and the mechanisms involved of dairy products in the prevention and treatment of the metabolic syndrome.

Many in vivo trials have evaluated the effects of grape products on different CVD risk factors. Most published studies have dealt with some specific aspects of mechanisms of grape flavonoid action or have focused only on one product, such as wine. The aim of the present paper is to review trials dealing with grape products and CVD published during the last 13 years (seventy-five trials). Polyphenols, alcohol and dietary fibre are the main constituents of the tested products. In animal and human studies, grape products have been shown to produce hypotensive, hypolipidaemic and anti-atherosclerotic effects, and also to improve antioxidant status as measured in terms of plasma antioxidant capacity, oxidation biomarkers, antioxidant compounds or antioxidant enzymes. Differences in the design of the studies and in the composition of the tested products (not always provided) could explain the different results of these studies.

The present review comes from the authors of the recent Scientific Advisory Committee on Nutrition (SACN) review Update on Trans Fatty Acids and Health, and focuses on assessing the strength of the evidence for a link between trans-fatty acid (trans-FA) intake and cancer. It evaluates a range of human ecological, case–control and prospective studies with trans-FA exposure assessed using either dietary assessment methods or trans-FA levels in tissues. Relevant animal studies are also presented in order to elucidate potential mechanisms. It concludes that there is weak and inconsistent evidence for a relationship between trans-FA and breast or colorectal cancer. Evidence for an association between trans-FA and prostate cancer is limited, but a recent large case–control study has shown a strong interaction between risk and trans-FA intake for the RNASEL QQ/RQ genotype that is present in about 35 % of the population. This potential association requires further investigation. The single study on non-Hodgkin's lymphoma reported a strong positive association, but only used a single assessment of dietary trans-FA made at the start of the study in 1980, and the significant changes in trans-FA intakes between then and the end of follow-up in 1994 limit the reliability of this observation. There is insufficient evidence to allow any differentiation between the effects of trans-FA from animal or vegetable origin on cancer risk.

Diet, nutritional status and lifestyle practices are significant determinants of the risk of certain cancers. In 1997 The World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) developed a series of evidence-based recommendations to help reduce the population and individual risk of cancer. However, guidance for evaluating concordance or compliance with these recommendations is limited. To illustrate the challenges in evaluation, four publications were reviewed that explored the task of creating operative criteria from which to assess concordance with the tenets of the WCRF/AICR recommendations. Three documents dealt with secondary analysis, whereas one was a prospective inquiry, with procedures and instruments designed to obtain responses to WCRF/AICR cancer-prevention specification. One considered only population-goal criteria, and two dealt implicitly or explicitly with criteria at both population and individual levels. The assessment approaches used by the authors were compared with alternative semantic and conceptual interpretations of the WCRF/AICR population goals and individual guidelines. Attempts to develop operative criteria for assessment of concordance (reflecting either a more superficial or more in-depth parsing of recommendations) have been inconsistent. The results indicate that the language of the WCRF/AICR leaves a certain degree of semantic ambiguity for evaluation purposes. Future design of prospective studies for analyses of behaviours and relevant exposures (including those reported in the 2007 WCRF/AICR report) should carefully consider evaluation criteria and fully document detailed methodology.

The central nervous system undertakes the homeostatic role of sensing nutrient intake and body reserves, integrating the information, and regulating energy intake and/or energy expenditure. Few tasks regulated by the brain hold greater survival value, particularly important in farmed ruminant species, where the demands of pregnancy, lactation and/or growth are not easily met by often bulky plant-based and sometimes nutrient-sparse diets. Information regarding metabolic state can be transmitted to the appetite control centres of the brain by a diverse array of signals, such as stimulation of the vagus nerve, or metabolic ‘feedback’ factors derived from the pituitary gland, adipose tissue, stomach/abomasum, intestine, pancreas and/or muscle. These signals act directly on the neurons located in the arcuate nucleus of the medio-basal hypothalamus, a key integration, and hunger (orexigenic) and satiety (anorexigenic) control centre of the brain. Interest in human obesity and associated disorders has fuelled considerable research effort in this area, resulting in increased understanding of chronic and acute factors influencing feed intake. In recent years, research has demonstrated that these results have relevance to animal production, with genetic selection for production found to affect orexigenic hormones, feeding found to reduce the concentration of acute controllers of orexigenic signals, and exogenous administration of orexigenic hormones (i.e. growth hormone or ghrelin) reportedly increasing DM intake in ruminant animals as well as single-stomached species. The current state of knowledge on factors influencing the hypothalamic orexigenic and anorexigenic control centres is reviewed, particularly as it relates to domesticated ruminant animals, and potential avenues for future research are identified.