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

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).

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.

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.