Dietary reference values (DRV) are estimates of the daily amounts of nutrients or food energy that meet the needs of healthy people. In the UK, three terms are used to express these estimates, assuming a normal distribution of requirements in a population. These are the estimated average requirement, the lower reference nutrient intake and the reference nutrient intake. DRV are for use in a variety of settings, including the assessment of adequacy and safety of nutrient or energy intake in a population group, in the design of meal provision in care settings, in food labelling and in considering food fortification strategies. DRV, and other expressions of nutrient requirements, assume a relationship between the intake of a nutrient and some criterion of adequacy, the outcome. Estimates of requirements are based on a diverse range of measures of adequacy, according to available evidence. The Scientific Advisory Committee on Nutrition (SACN) is the body responsible for reviewing and setting DRV for the UK population. The work of SACN is guided by a framework of evidence that relates food and nutrients to health. There have been calls for the harmonisation of approaches used in the setting of nutrient requirements, globally, and an increased transparency in the decision-making process. Some progress has been made in this regard, but there is a great deal of work to be done.

Vitamin D is a unique nutrient. First, it acts as a pro-hormone and secondly, the requirement for vitamin D can be met by both endogenous synthesis from sunlight and by dietary sources. This complicates the determination of dietary requirements for vitamin D, which along with the definition of optimal vitamin D status, have been highly controversial and much debated over recent years. Adolescents are a population group at high risk of low vitamin D status, which is concerning given the important role of vitamin D, and calcium, in promoting normal bone mineralisation and attainment of peak bone mass during this rapid growth phase. Dietary vitamin D recommendations are important from a public health perspective in helping to avoid deficiency and optimise vitamin D status for health. However limited experimental data from winter-based dose–response randomised trials in adolescents has hindered the development of evidence-based dietary requirements for vitamin D in this population group. This review will highlight how specifically designed randomised trials and the approach adopted for estimating such requirements can lead to improved recommendations. Such data indicate that vitamin D intakes of between 10 and about 30 µg/d may be required to avoid deficiency and ensure adequacy in adolescents, considerably greater than the current recommendations of 10–15 µg/d. Finally this review will consider the implications of this on public health policy, in terms of future refinements of vitamin D requirement recommendations and prioritisation of public health strategies to help prevent vitamin D deficiency.

The present study was carried out to evaluate dietary Mn requirements of broilers from 22 to 42 d of age using molecular biomarkers. Chickens were fed a conventional basal maize–soyabean meal diet supplemented with Mn as Mn sulphate in graded concentrations of 20 mg Mn/kg from 0 to 140 mg Mn/kg of diet for 21 d (from 22 to 42 d of age). The Mn response curves were fitted for ten parameters including heart Mn-containing superoxide dismutase (MnSOD) mRNA and its protein expression levels and the DNA-binding activities of specificity protein 1 (Sp1) and activating protein-2 (AP-2). Heart MnSOD mRNA and protein expression levels showed significant quadratic responses (P<0·01), and heart MnSOD activity showed a broken-line response (P<0·01), whereas Mn content and DNA-binding activities of Sp1 and AP-2 in the heart displayed linear responses (P<0·01) to dietary Mn concentrations, respectively. The estimates of dietary Mn requirements were 101, 104 and 94 mg/kg for full expressions of MnSOD mRNA level, MnSOD protein level and MnSOD activity in the heart, respectively. Our findings indicate that heart MnSOD mRNA expression level is a more reliable indicator than heart MnSOD protein expression level and its activity for the evaluation of Mn requirement of broilers, and about 100 mg Mn/kg of diet is required for the full expression of heart MnSOD in broilers fed the conventional basal maize–soyabean meal diet from 22 to 42 d of age.

Previous research shows that older men tend to have lower nutritional intakes and higher risk of under-nutrition compared with younger men. The objectives of this study were to describe energy and nutrient intakes, assess nutritional risk and investigate factors associated with poor intake of energy and key nutrients in community-dwelling men aged ≥75 years participating in the Concord Health and Ageing in Men Project – a longitudinal cohort study on older men in Sydney, Australia. A total of 794 men (mean age 81·4 years) had a detailed diet history interview, which was carried out by a dietitian. Dietary adequacy was assessed by comparing median intakes with nutrient reference values (NRV): estimated average requirement, adequate intake or upper level of intake. Attainment of NRV of total energy and key nutrients in older age (protein, Fe, Zn, riboflavin, Ca and vitamin D) was incorporated into a ‘key nutrients’ variable dichotomised as ‘good’ (≥5) or ‘poor’ (≤4). Using logistic regression modelling, we examined associations between key nutrients with factors known to affect food intake. Median energy intake was 8728 kJ (P5=5762 kJ, P95=12 303 kJ), and mean BMI was 27·7 (sd 4·0) kg/m2. Men met their NRV for most nutrients. However, only 1 % of men met their NRV for vitamin D, only 19 % for Ca, only 30 % for K and only 33 % for dietary fibre. Multivariate logistic regression analysis showed that only country of birth was significantly associated with poor nutritional intake. Dietary intakes were adequate for most nutrients; however, only half of the participants met the NRV of ≥5 key nutrients.

The present study was carried out to investigate whether the dietary histidine requirement to reduce cataract development is higher than that for growth in Atlantic salmon smolts (Salmo salar L.) after seawater transfer and whether dietary vegetable oils contribute to cataractogenesis. Duplicate groups of salmon smolts were fed ten experimental diets with either fish oil (FO) or a vegetable oil (VO) mix replacing 70 % FO and histidine at five target levels (10, 12, 14, 16 and 18 g His/kg diet) for 13 weeks after seawater transfer. The VO diet-fed fish exhibited somewhat inferior growth and feed intakes compared with the FO diet-fed fish, irrespective of the dietary histidine concentration. Both cataract prevalence and severity were negatively correlated with the dietary histidine concentration, while lens N-acetyl-histidine (NAH) concentrations were positively correlated with it. The fatty acid profiles of muscle, heart and lens reflected that of the dietary oils to a descending degree and did not affect the observed cataract development. Muscle, heart and brain histidine concentrations reflected dietary histidine concentrations, while the corresponding tissue imidazole (anserine, carnosine and NAH) concentrations appeared to saturate differently with time. The expression level of liver histidase was not affected by the dietary histidine concentration, while the liver antioxidant response was affected in the VO diet-fed fish on a transcriptional level. The lowest severity of cataracts could be achieved by feeding 13·4 g His/kg feed, independently of the dietary lipid source. However, the present study also suggests that the dietary histidine requirement to minimise the risk of cataract development is 14·4 g His/kg feed.

The concept of a healthy and environmentally sustainable diet is not new, but with increasing concern about future global food security and climate change there is a renewed interest in this topic. Dietary intakes in UK accounts for approximately 20–30% of total annual greenhouse gas emissions (GHGE), with the greatest contributions coming from high intakes of meat and dairy products. Dietary proposals to help mitigate climate change (i.e. reduce GHGE) have focused on reducing consumption of meat and dairy products, but this must be considered in the context of the whole diet, alongside any possible nutritional consequences for health. Bringing together health and environmental impact of the diet raises the question of whether a healthy diet can also be an environmentally sustainable diet. While recent research showed that it is possible to achieve a realistic diet that meets dietary requirement for health and has lower GHGE, it cannot be assumed that a healthy diet will always have lower GHGE. With different combinations of food it is possible to consume a diet that meets dietary requirements for health, but has high GHGE. It is important to understand what constitutes a sustainable diet, but this then needs to be communicated effectively to try and change well-established dietary intakes of the population. Studies show that understanding of sustainable diets is poor and there are many misconceptions (e.g. the overestimation of the protein requirements for a healthy diet), which could contribute to the barriers towards changing dietary intakes.

Dietary Reference Intake (DRI) values exist for vitamins and minerals, and provide a guideline on the optimal dose range to avoid deficiency and prevent toxicity. Polyphenols are widely distributed in plant foods, and have been linked to improved human health through reduced risk of chronic diseases, especially cardiovascular. Although they do not cause classical deficiencies, recently they have been discussed as ‘lifespan essentials because they are needed to achieve a full lifespan by reducing the risk of a range of chronic diseases. A recent meta analysis shows promising actions of polyphenols from cocoa, soya and tea on flow mediated dilation, blood pressure and LDL cholesterol. Many epidemiological studies support the action of polyphenols or polyphenol-rich foods on health, but there are still many gaps in our knowledge. More adequately powered, randomised, placebo controlled human studies are needed on polyphenols. There is a large number of structurally different polyphenols which are relevant for health, and obtaining enough information to set a DRI for each of these will not be feasible in the foreseeable future. A new approach is needed, and a new way of thinking, which would apply not only to polyphenols but also to other phytochemicals. Today, a target intake value of polyphenols as ‘lifespan essentials’ needs to be based on the amount of polyphenols in ‘5-a-day’. We are heading in the right direction towards a DRI, but bioavailability and dose-effects, including toxic levels, need to be established before DRIs can be considered.

Human selenium (Se) requirements are currently based on biochemical markers of Se status. In rats, tissue glutathione peroxidase-1 (Gpx1) mRNA levels can be used effectively to determine Se requirements; blood Gpx1 mRNA levels decrease in Se-deficient rats, so molecular biology-based markers have potential for human nutrition assessment. To study the efficacy of molecular biology markers for assessing Se status in humans, we conducted a longitudinal study on 39 subjects (age 45 ± 11) in Reading, UK. Diet diaries (5 day) and blood were obtained from each subject at 2, 8, 17 and 23 weeks, and plasma Se, glutathione peroxidase (Gpx3) enzyme activity, and selenoprotein mRNA levels were determined. There were no significant longitudinal effects on Se biomarkers. Se intake averaged 48 ± 14 μg/d. Plasma Se concentrations averaged 1·13 ± 0·16 μmol/l. Plasma Se v. energy-corrected Se intake (ng Se/kJ/d) was significantly correlated, but neither Gpx3 activity v. Se intake (ng Se/kJ/d) nor Gpx3 activity v. plasma Se was significantly correlated. Collectively, this indicates that subjects were on the plateaus of the response curves. Selenoprotein mRNAs were quantitated in total RNA isolated from whole blood, but mRNA levels for Gpx1, selenoprotein H, and selenoprotein W (all highly regulated by Se in rodents), as well selenoprotein P, Gpx3, and phospholipid hydroperoxide glutathione peroxidase were also not significantly correlated with plasma Se. Thus selenoprotein molecular biomarkers, as well as traditional biochemical markers, are unable to further distinguish differences in Se status in these Se replete subjects. The efficacy of molecular biomarkers to detect Se deficiency needs to be tested in Se-deficient populations.