This review summarises evidence for an association between vitamin D status and CVD and the mechanisms involved. Vitamin D 3 is predominantly provided by the action of UVB from sunlight on skin. Average UK diets supply 2-3 μg/d vitamin D but diets containing at least one portion of oily fish per week supply about 7 μg/d. Pharmacological doses of vitamin D 2 (bolus injection of 7500 μg or intakes >50 μg/d) result in a smaller increase in plasma 25 (OH)D than those of D 3 but physiological doses 5-25 μg/d seem equivalent. Plasma 25 (OH)D concentrations are also influenced by clothing, obesity and skin pigmentation. Up to 40 % of the population have plasma 25(OH)D concentrations <25 nmol/l in the winter compared with <10 % in the summer. The relative risk of CVD death is 1·41 (95 % CI 1·18, 1·68) greater in the lowest quintile of plasma 25(OH)D according to meta-analysis of prospective cohort studies. Acute deficiency may inhibit insulin secretion and promote inflammation thus increasing the risk of plaque rupture and arterial thrombosis. Chronic insufficiency may increase arterial stiffness. There is no evidence to support claims of reduced CVD from existing trials with bone-related health outcomes where vitamin D was usually co-administered with calcium. Although several trials with cardiovascular endpoints are in progress, these are using pharmacological doses. In view of the potential toxicity of pharmacological doses, there remains a need for long-term trials of physiological doses of D 2 and D 3 with CVD incidence as the primary outcome. Ergocalciferol: Cholecalciferol: Cardiovascular riskVitamin D deficiency causes rickets in children and osteomalacia in adults and may contribute to the causation of CVD. Cholecalciferol (vitamin D 3 ) is made by the action of UVB light on the skin but is also provided in the diet from foods of animal origin (eggs, oily fish and meat). Ergocalciferol (vitamin D 2 ) is present in fungi that have been exposed to UVB irradiation. Both forms of vitamin D undergo 25-hydroxylation in the liver to form 25(OH) metabolites, most of which circulate in plasma bound to the vitamin D binding protein (VDBP). In the kidney, 25 hydroxyvitamin D (25(OH)D) is converted to the biologically active metabolite 1,25 dihydroxyvitamin D (1,25 (OH) 2 D) by the action of 1α-hydroxylase (Fig. 1). This then binds to the vitamin D receptor, which is a highaffinity nuclear hormone receptor that regulates gene expression (1) . Measurement of serum 25(OH)D to assess vitamin D status has predominantly used immunoassays, which show lower sensitivity (about 30 %) to D 2 metabolites than gold-standard methods such as HPLC/tandem MS. Formerly, a lack of standardisation of methods and appropriate quality control made comparisons between studies difficult (2) . The situation has been remedied by the availability (3) of standard reference serum (SRM 972, National Institute of Standards and Technology) and a quality control programme in the UK organised by the Vitamin D External Quality Assessment Scheme (4) . It has...

Children with or at risk of faltering growth require nutritional support and are often prescribed oral nutritional supplements (ONS). This randomised controlled trial investigated the effects of energy-dense paediatric ONS (2.4 kcal/ml, 125 ml: cONS) versus 1.5 kcal/ml, 200 ml ONS (sONS) in community-based paediatric patients requiring oral nutritional support. Fifty-one patients (mean age 5.8 years (SD 3)) with faltering growth and/or requiring ONS to meet their nutritional requirements were randomised to cONS (n = 27) or sONS (n = 24) for 28 days. Nutrient intake, growth, ONS compliance and acceptability, appetite and gastro-intestinal tolerance were assessed. Use of the cONS resulted in significantly greater mean total daily energy (+ 531 kcal/day), protein (+ 10.1 g/day) and key micronutrient Preliminary findings of this study have previously been presented at 4th International Conference on Nutrition and Growth, Amsterdam 2017 as Sorensen et al. Improved compliance, nutritional intakes and growth with a high energy density, low volume paediatric oral nutritional supplement (http://2017.nutrition-growth.kenes.com/abstract-submission/2016abstract-book#.WMq_FtJ95hF) Communicated by Mario Bianchetti

No abstract