The ability of nuts to improve the blood lipid profile and reduce the risk of CHD is now well established. The interest that health effects of nuts have gained recently has brought the possible benefits of consuming nuts, such as improvement in the conditions of the metabolic syndrome, and their potential to prevent and control diabetes into focus. Results from cohort studies have associated nut consumption with a reduced risk of developing diabetes and CVD. However, few randomised controlled trials have assessed the effect of nuts on diabetes control, and those that have been undertaken have shown improvements in blood lipids but not in the glycaemic control. Diabetes agencies are increasingly recognising the importance of controlling postprandial glycaemia fluctuations. Acute feeding studies indicate that nuts have minimal effects on rising postprandial blood glucose levels when eaten alone, and diminish the postprandial glycaemic response when consumed with high-glycaemic index carbohydrate foods in both normoglycaemic and type 2 diabetic individuals. Nuts have a healthy nutritional profile, high in MUFA and PUFA, are a good source of vegetable protein and are rich in fibre, vitamins and minerals. Incorporation of nuts in the diet may therefore improve the overall nutritional quality of the diet. While more research is required to establish the ability of nuts to improve glycaemic control in the long run, early data indicate that the inclusion of nuts in the diets of individuals with diabetes and the metabolic syndrome is warranted, in view of their potential to reduce CHD risk.

Primary school children in the UK have the choice of a school meal provided by the school or a packed lunch provided from home. Currently, more than half of primary school children have a packed lunch. New food-based standards for school meals were introduced in English primary schools in 2006, followed by nutrient-based standards in 2008. No formal comparisons of primary school lunches by lunch type have been undertaken to date. The present review identified seven studies from 1990 to 2007 measuring lunchtime nutrient intake in children aged 5–11 years having a school meal and children having a packed lunch. Pooled estimates for each nutrient were as follows: energy intake was 543 (95 % CI 233, 854) kJ higher in packed lunches; total sugar intake was 14·0 (95 % CI 10·3, 17·7) g higher in packed lunches; non-milk extrinsic sugar intake was 11·7 (95 % CI 7·3, 16·2) g higher in packed lunches; saturated fat intake was 4·7 (95 % CI 2·4, 7·1) g higher in packed lunches and Na intake was 357 (95 % CI 174, 539) mg higher in packed lunches. Differences between school meals and packed lunches were larger for all nutrients after the introduction of food-based standards compared with the period of no standards. However, differences between before and after standards did not reach statistical significance. The nutritional quality of packed lunches is poor compared with school meals. The introduction of food-based standards for school meals in 2006 has moderately improved the nutrient content of school meals, slightly widening the nutritional gap between school meals and packed lunches.

The purpose of the present study was to identify the association of the Pro12Ala polymorphism in the PPAR-γ2 gene with diabetes, insulinaemia and insulin resistance. A meta-analysis study was carried out based on studies conducted in the last 10 years, using the databases PubMed, ISI Web of Knowledge, High Wire Press and Scielo, and the reference lists of the obtained articles. We included original studies that showed the relationship between the Pro12Ala polymorphism in the PPAR-γ2 gene and type 2 diabetes mellitus (T2DM), insulinaemia and insulin resistance. Statistical analyses were conducted using the program RevMAn 5.0. The Mantel–Haenszel test was used to estimate the OR and the 95 % CI of the dichotomous variable, while the standardised effect size was used to estimate the average standardised mean difference and 95 % CI of continuous variables. The studies were subgrouped by ethnicity and overweight status. Forty-one studies were analysed, including a global sample of 30 612 subjects. We found a significant association of the Ala allele with the lowest risk of T2DM in Caucasians (OR 0·80; 95 % CI 0·65, 0·98), lower serum insulin (standardised effect size: − 0·05; 95 % CI − 0·09, − 0·00; P = 0·04), and greater sensitivity to insulin in overweight individuals (homeostasis model assessment of insulin resistance standardised effect size: − 0·07; 95 % CI − 0·13, − 0·01; P = 0·02). Considering that the Pro12Ala polymorphism in the PPAR-γ2 gene is one of the factors related to insulin sensitivity, the present study demonstrated a significant effect of the Ala allele on lower development of T2DM in Caucasians and greater sensitivity to insulin in overweight subjects.

During pregnancy, growth of the foetus depends on an adequate glycine supply because it is needed for synthesis of fetal DNA, collagen and serine. Since pregnant adolescent girls give birth to lower birth weight babies, it is possible that they do not produce sufficient glycine to meet overall demands as their adult counterparts, especially after an overnight fast. The objective of the study was to measure and compare the flux of glycine among adolescents and adult women in the first and third trimesters of pregnancy. Glycine flux was measured by continuous intravenous infusion of 2H2-glycine in eight overnight fasted adolescents and in eight adult women in the first and third trimesters of pregnancy. There was a significant interaction between subject's age and time of pregnancy (P = 0·02), as weight-specific glycine flux decreased by 39 % from trimesters 1 to 3 in the adolescents but increased by approximately 5 % in the adults. Whole body glycine flux also decreased significantly in the adolescent group (P < 0·05) from trimesters 1 to 3, and this was associated with a significant reduction in plasma glycine concentration. In trimester 3, there was a positive correlation between glycine flux and the subject's age indicating that younger subjects had slower fluxes. These findings suggest that after a brief period of food deprivation, the pregnant adolescent cannot maintain glycine production as her adult counterpart in late pregnancy. It is possible that this inability to maintain endogenous glycine production makes her foetus more vulnerable to impaired growth if food deprivation becomes more frequent or is prolonged.

Previous studies have reported the anti-inflammatory properties of pomegranate extracts, suggesting that ellagitannins (ET) and ellagic acid (EA) are the main anti-inflammatory compounds. However, both ET and EA are metabolised in vivo by the gut microbiota to yield urolithins (Uro) which can be found in the gut and in systemic bloodstream. The present study was carried out to evaluate the individual effect of EA and their microbiota-derived metabolites Uro on colon fibroblasts upon IL-1β treatment as an in vitro inflammation model. Uro-A and Uro-B (10 μm) inhibited PGE2 production (85 and 40 %, respectively) after IL-1β stimulation, whereas EA did not show any effect. Uro-A, but not Uro-B, down-regulated cyclo-oxygenase-2 (COX-2) and microsomal PGE synthase-1 (mPGES-1) mRNA expression and protein levels. Both Uro inhibited NF-κB translocation to nucleus. Slight but significant effects were found in the activation of mitogen-activated protein kinase (MAPK) pathways. Uro-A lowered c-Jun N-terminal kinase phosphorylation state, and both Uro inhibited p38 activation. No metabolites derived from Uro or EA were found in the cell media upon incubation of EA or Uro with the cells, and only traces of the compounds were found inside the cells. The present results suggest that Uro, mainly Uro-A, are the main compounds that are responsible for the pomegranate anti-inflammatory properties. The mechanism of action implicated seems to be via the inhibition of activation of NF-κB and MAPK, down-regulation of COX-2 and mPGES-1 expressions, and consequently,via the reduction of PGE2 production. Taking into account that Uro did not enter the cells, a competitive binding for IL-1β membrane receptor cannot be discarded.

Mucositis resulting from cancer chemotherapy is a serious disorder of the alimentary tract. Emu oil has demonstrated anti-inflammatory properties in animal models of arthritis and wound healing; however, its effects on the intestine remain unknown. We investigated emu oil for its potential to decrease the severity of mucositis in a rat model. Female Dark Agouti rats (110–150 g) were orogastrically gavaged with emu oil (0·5 or 1 ml) or water (1 ml) for 5 d before intraperitoneal injection of 5-fluorouracil (5-FU, 150 mg/kg) or saline (control), and this was continued up to the day of sacrifice (48, 72 and 96 h post 5-FU administration). Histological (villus height, crypt depth (CD) and disease severity score) and biochemical (myeloperoxidase (MPO) activity) parameters were determined in intestinal tissues collected at sacrifice. Sucrase activity in vivo was quantified by the sucrose breath test. Activated neutrophil activity (MPO) in the ileum was significantly decreased by emu oil (0·5 ml, 451 (sem 168) U/g and 1 ml, 503 (sem 213) U/g) compared with 5-FU-treated controls (1724 (sem 431) U/g) 96 h post 5-FU administration. There were also significant increases in CD (152 (sem 8) μm) in the ileum of rats that receivied 1 ml emu oil at 96 h compared with 5-FU-treated controls (CD (106 (sem 12) μm)). Emu oil did not affect sucrase activity. Emu oil decreased acute ileal inflammation, and improved mucosal architecture in the intestine during recovery from chemotherapy in rats. Further studies investigating the potential benefits of emu oil as a nutritional supplement for the treatment of intestinal disorders are indicated.

Inconsistent results exist from human and animal studies for Se and methionine (Met) regarding their influence on homocysteine (HCys) and cholesterol (Chol) metabolism. To elucidate these contradictions, sixty-four weanling albino rats were divided into eight groups of 8, and were fed diets containing four different Se levels (15, 50, 150 and 450 μg/kg) either in combination with the recommended Met level of 3 g/kg (C15, C50, C150 and C450) or with an increased Met concentration of 15 g/kg (M15, M50, M150 and M450) for 8 weeks. Plasma HCys was twofold higher in the Se-supplemented C groups than in group C15. Met addition also doubled plasma HCys compared with the respective C groups. In contrast, the expression of the key enzymes of glutathione biosynthesis in the liver was significantly lowered by Se and in particular by Met. Liver Chol concentration was significantly higher in all the Se-supplemented C and M groups than in groups C15 and M15. Plasma Chol was, however, lowered. The uninfluenced expression of sterol-regulatory element-binding protein 2 and of hydroxymethyl-glutaryl-CoA reductase, the increased LDL receptor expression and the reduced expression of the hepatobiliary Chol exporter ATP-binding-cassette-transporter 8 (ABCG8) by Se and/or Met explain these findings. We conclude that the elevation of plasma HCys in rats by Se and Met results from a higher export into plasma. The fact that Se in particular combined with Met increases liver Chol but reduces plasma Chol should be addressed in future investigations focussing on the regulation of ABCG8, which is also selectively involved in the reverse transport of phytosterols in the small intestine.

Linseed oil, being rich in 18 : 3n-3, represents an alternative source of n-3 PUFA in the maternal diet. However, little is known about the effect of this oil on the long chain n-3 PUFA composition of offspring, which are required for normal growth and maturation of numerous organs. The main objective of the experiment was therefore to investigate fatty acid composition of tissues from sows at the end of gestation and from piglets during the first week of postnatal life in response to maternal dietary linseed oil intake. Sows received either a lard (LAR)-based diet or a linseed oil (LSO)-based diet during gestation and lactation. Fatty acid composition was evaluated in sow plasma, placenta and milk, and in different tissues of piglets on days 0, 3, 7, 21 and 32. The LSO diet increased the proportions of n-3 PUFA and especially 22 : 6n-3 in the placenta. The carcass of LSO piglets at birth contained greater proportions of 20 : 5n-3, 22 : 5n-3 and 22 : 6n-3. The LSO sow milk exhibited greater proportions of 18 : 3n-3 compared with the LAR sow milk. The piglets suckling LSO sows had greater proportions of 18 : 3n-3, 20 : 5n-3 and 22 : 5n-3 in plasma and carcass. The proportions of 22 : 5n-3 and 22 : 6n-3 were greater in the brain of LSO piglets than in that of LAR piglets during the suckling period. In conclusion, LSO in the maternal diet during gestation and lactation increases 22 : 6n-3 concentrations in the placenta and in the foetus carcass, and it maintains 22 : 6n-3 concentrations in the brain during the first week of postnatal life.

Malnutrition during foetal life can induce modifications in the phenotype of an individual. The present study aimed to observe effects of low foetal life protein provision on modifications of the phenotype and changes in the progeny of 1-year-old female mink (F1 generation) offspring of mothers fed a low-protein diet. Traits studied included reproductive performance, energy and protein metabolism, and key hepatic enzymes associated with glucose homeostasis and metabolic hormones. The F0 generation offspring were fed either a low-protein (14 % of metabolisable energy (ME) from protein – FLP1) or an adequate-protein (29 % of ME from protein – FAP1) diet for the last 17·9 (sd 3·6) d of gestation. The F1 dams were studied at birth and at 1 year of age, during their first reproductive cycle, after maintenance on an adequate diet from birth and thereafter. Metabolic traits during gestation and lactation were largely unaffected by foetal life protein provision, but birth weight in the F2 generation was higher (P = 0·003) among FLP2 kits than among FAP2 kits. Furthermore, the relative abundance of pyruvate kinase mRNA was significantly (P = 0·007) lower, and fructose-1,6-bisphosphatase mRNA tended (P = 0·08) to be lower in FLP2 foetuses than in FAP2 foetuses, showing some similar difference in the F2 generation and F1 generation foetuses, suggesting an effect on some hepatic enzymes affecting glucose homeostasis being transmitted from the F1 to the F2 generation. These findings indicate that even though energy and nitrogen metabolism displayed no effect of protein provision during early life, programming effects still appeared at the molecular level in the following generation.

The H2 breath test is ideal for orocaecal transit time (OCTT) measurement, as it is non-invasive and inexpensive. Indigestible substrates added to a test meal are metabolised by the colonic bacteria, resulting in the production of H2 which is detected in end-exhalation breath. However, the substrates themselves can alter the transit times in the gastrointestinal tract. The aim of the present study is to compare OCTT and gastric emptying (GE) when lactulose in liquid (L-L), solid lactulose (L-S) and solid inulin (IN-S) are added to a test meal, and subsequently, to examine if inulin alters GE. Firstly, ten male volunteers were tested on three occasions. Volunteers ate a pancake breakfast containing 100 mg of 13C-octanoic acid and either 12 g of L-L, 12 g of L-S or 12 g of IN-S in a randomised order. Secondly, seven male volunteers were tested twice with meals containing either 12 g of IN-S or no substrate (NO-S). L-L induced the shortest OCTT (85·3 (sd 42·8) min) compared with L-S (162·4 (sd 62·6) min) and inulin (292·4 (sd 66·7) min; P = 0·007). GE half-time and lag phase (L-L: 61 (sd 9); L-S: 57 (sd 10); IN-S: 52 (sd 10) min; P = 0·005) were also affected, with L-L being the slowest. Thirdly, inulin reduced GE lag and latency phases (P < 0·05) compared with NO-S. Lactulose accelerates OCTT but delays GE compared with inulin. Inulin accelerates the onset of stomach emptying, but it has no effect on GE half-time. For these reasons, inulin is the preferred substrate for the H2 breath test.

The aim of the present study is to evaluate the possible influence of virgin olive oil (VOO) on the effect of acetylsalicylic acid (ASA) in platelet aggregation, prostanoid and NO production and retinal vascular pattern in rats with experimental type 1-like diabetes. We used 100 male Wistar rats that were distributed into five groups: (1) non-diabetic rats (NDR); (2) untreated diabetic rats (DR); (3) DR treated with ASA (2 mg/kg per d per os (p.o.)); (4) DR treated with VOO (0·5 ml/kg per d p.o.); (5) DR treated with ASA plus VOO. The duration of diabetes was 3 months, and each treatment was administered from the first day of diabetes. Variables that were quantified were platelet aggregation (Imax), thromboxane B2 (TxB2), aortic prostacyclin (6-keto-PGF1α) and NO, and the percentage of retina with horseradish peroxidase-permeable vessels (HRP-PV). Diabetic rats showed a higher Imax (35 %) and TxB2 (63 %) than NDR, and a lower 6-keto-PGF1α, NO and HRP-PV than NDR ( − 74·6 %). ASA and VOO administration reduced these differences and prevented the percentage of HRP-PV ( − 59·7 % with ASA and − 46·7 % with VOO). The administration of ASA plus VOO showed a strong platelet inhibition (80·2 v. 23·4 % for VOO and 50·6 % for ASA+VOO, P < 0·0001), and reduced HRP-PV differences to − 31·6 % (P < 0·001 with respect to DR and P < 0·0001 with respect to DR treated with ASA). In conclusion, the administration of VOO to rats with type 1-like diabetes mellitus improves the pharmacodynamic profile of ASA, and increases its retinal anti-ischaemic effect.

Long-chain PUFA (LCPUFA) supplementation of formula can have beneficial effects on neurodevelopmental outcome in early infancy, but uncertainty exists regarding effects after 6 months. The present study is the first to investigate whether consumption by term infants of formula containing LCPUFA for the first 2 months after birth improves neurological condition of these children at 9 years of age. A prospective, double-blind, randomised control study was performed in two groups of healthy term infants: a control group with standard formula (n 169) and a LCPUFA-supplemented group (LF; n 146). A breast-fed group (BF; n 159) served as a reference. At age 9 years, children were neurologically assessed according to Touwen, resulting in a Neurological Optimality Score and information on severity and type of minor neurological dysfunction (MND). Information on potential confounders was collected at enrolment and follow-up. Multivariate analyses were carried out to evaluate the effect of nutrition while adjusting for confounders. Attrition (28 %) was selective: drop-outs in the LF group were more often boys and had a significantly lower mental developmental index at 18 months. Neurological optimality and severity and type of MND at 9 years did not differ between the two formula groups. Children in the BF group showed significantly less often fine manipulative dysfunction than formula-fed children. In conclusion, LCPUFA supplementation of formula during the first 2 postnatal months in healthy term infants does not alter neurological function at school age. The study confirmed that breast-fed infants have a slightly better neurodevelopmental outcome than formula-fed infants.

Factors controlling the concentration of resistant starch (RS) in foods are of considerable interest on account of the potential for this type of fibre to deliver health benefits to consumers. The present study was aimed at establishing changes in starch granule morphology as a result of human small-intestinal digestion. Volunteers with ileostomy consumed six selected foods: breakfast cereal (muesli), white bread, oven-baked French fries, canned mixed beans and a custard containing either a low-amylose maize starch (LAMS) or a high-amylose maize starch (HAMS). Analysis showed that digesta total RS (as a fraction of ingested starch) was: muesli, 8·9 %; bread, 4·8 %; fries, 4·2 %; bean mix, 35·9 %; LAMS custard, 4·0 %; HAMS custard, 29·1 %. Chromatographic analysis showed that undigested food contained three major starch fractions. These had average molecular weights (MW) of 43 500 kDa, 420 kDa and 8·5 kDa and were rich in amylopectin, higher-MW amylose and low-MW amylose, respectively. The low-MW amylose fraction became enriched preferentially in the stomal effluent while the medium-MW starch fraction showed the greatest loss. Fourier transform IR spectroscopy showed that absorbance at 1022 per cm decreased after digestion while the absorbance band at 1047 per cm became greater. Such changes have been suggested to indicate shifts from less ordered to more ordered granule structures. Further analysis of amylose composition by scanning iodine spectra indicated that the MW of amylose in ileal digesta was lower than that of undigested amylose. It appears that high-MW amylose is preferentially digested and that MW, rather than amylose content alone, is associated with resistance of starch to digestion in the upper gut of humans.

Large-scale aetiological studies of obesity and its pathological consequences require accurate measurements of adipose mass, distribution and subtype. Here, we compared the validity of three abdominal obesity assessment methods (dual-energy X-ray absorptiometry (DXA), ultrasound and anthropometry) against the gold-standard method of computed tomography (CT) in twenty-nine non-diseased middle-aged men (BMI 26·5 (sd 3·1) kg/m2) and women (BMI 25·5 (sd 3·2) kg/m2). Assessments of adipose mass (kg) and distribution (total subcutaneous (TSAT), superficial subcutaneous (SSAT), deep subcutaneous (DSAT) and visceral (VAT)) were obtained. Spearman's correlations were performed adjusted for age and sex. VAT area that was assessed using ultrasound (r 0·79; P < 0·0001) and waist circumference (r 0·85; P < 0·0001) correlated highly with VAT from CT, as did BMI (r 0·67; P < 0·0001) and DXA (r 0·70; P < 0·0001). DXA (r 0·72; P = 0·0004), BMI (r 0·71; P = 0·0003), waist circumference (r 0·86; P < 0·0001) and ultrasound (r 0·52; P = 0·015) were less strongly correlated with CT TSAT. None of the comparison measures of DSAT was strongly correlated with CT DSAT (all r approximately 0·50; P < 0·02). BMI (r 0·76; P < 0·0001), waist circumference (r 0·65; P = 0·002) and DXA (r 0·75; P < 0·0001) were all fairly strongly correlated with the CT measure of SSAT, whereas ultrasound yielded a weaker yet statistically significant correlation (r 0·48; P = 0·03). Compared with CT, visceral and subcutaneous adiposity can be assessed with reasonable validity using waist circumference and BMI, respectively. Ultrasound or DXA does not generally provide substantially better measures of these traits. Highly valid assessments of DSAT do not appear to be possible with surrogate measures. These findings may help guide the selection of measures for epidemiological studies of obesity.

In Norway, children and adolescents consume only about half of the national five-a-day recommendation. There are also rather large social inequalities in health, and in eating behaviours. In order to increase fruit and vegetable (FV) intake, a subscription programme was initiated in 1996 and made nationwide in 2003, and a free programme (without parental payment) has been implemented nationwide from 2007. The objective of the present study is to evaluate the effect of these efforts. Pupils in the sixth and seventh grades (age 10–12 years) at twenty-seven schools responded to a questionnaire in 2001 (n 1488, 85 %) and in 2008 (n 1339, 78 %). FV intake was measured by a 24-h recall. In 2001, none of the schools had any organised school fruit programme. In 2008, five schools participated in the free school fruit programme, ten schools participated in the subscription programme and twelve schools did not participate in any official programme. The increases in fruit intake at school were 0·49, 0·29 and 0·18 portions/school day, respectively, for the Free Fruit 08, Subscription 08 and No Programme 08 schools (time × group P < 0·001), and 0·74, 0·39 and 0·16 portions/d for fruit intake all day (time × group P = 0·04). No group effect was observed for vegetable intake. There has been an increase in pupils' fruit intake from 2001 to 2008 in Norway, and the school fruit programmes seem to have been effective. A great challenge remains in increasing vegetable intake.

Serotonergic hypofunction is associated with a depressive mood state, an increased drive to eat and preference for sweet (SW) foods. High-trait anxiety individuals are characterised by a functional shortage of serotonin during stress, which in turn increases their susceptibility to experience a negative mood and an increased drive for SW foods. The present study examined whether an acute dietary manipulation, intended to increase circulating serotonin levels, alleviated the detrimental effects of a stress-inducing task on subjective appetite and mood sensations, and preference for SW foods in high-trait anxiety individuals. Thirteen high- (eleven females and two males; anxiety scores 45·5 (sd 5·9); BMI 22·9 (sd 3·0)kg/m2) and twelve low- (ten females and two males; anxiety scores 30·4 (sd 4·8); BMI 23·4 (sd 2·5) kg/m2) trait anxiety individuals participated in a placebo-controlled, two-way crossover design. Participants were provided with 40 g α-lactalbumin (LAC; l-tryptophan (Trp):large neutral amino acids (LNAA) ratio of 7·6) and 40 g casein (placebo) (Trp:LNAA ratio of 4·0) in the form of a snack and lunch on two test days. On both the test days, participants completed a stress-inducing task 2 h after the lunch. Mood and appetite were assessed using visual analogue scales. Changes in food hedonics for different taste and nutrient combinations were assessed using a computer task. The results demonstrated that the LAC manipulation did not exert any immediate effects on mood or appetite. However, LAC did have an effect on food hedonics in individuals with high-trait anxiety after acute stress. These individuals expressed a lower liking (P = 0·012) and SW food preference (P = 0·014) after the stressful task when supplemented with LAC.

The UK Food Standards Agency (FSA) convened an international group of scientific experts to review three Agency-funded projects commissioned to provide evidence for the relative contributions of two sources, dietary vitamin D intake and skin exposure to UVB rays from sunlight, to vitamin D status. This review and other emerging evidence are intended to inform any future risk assessment undertaken by the Scientific Advisory Committee on Nutrition. Evidence was presented from randomised controlled trials to quantify the amount of vitamin D required to maintain a serum 25-hydroxy vitamin D (25OHD) concentration >25 nmol/l, a threshold that is regarded internationally as defining the risk of rickets and osteomalacia. Longitudinal evidence was also provided on summer sunlight exposure required to maintain 25OHD levels above this threshold in people living in the British Isles (latitude 51°–57°N). Data obtained from multi-level modelling of these longitudinal datasets showed that UVB exposure (i.e. season) was the major contributor to changes in 25OHD levels; this was a consistent finding in two Caucasian groups in the north and south of the UK, but was less apparent in the one group of British women of South Asian origin living in the south of the UK. The FSA-funded research suggested that the typical daily intake of vitamin D from food contributed less than UVB exposure to average year-round 25OHD levels in both Caucasian and Asian women. The low vitamin D status of Asian women has been acknowledged for some time, but the limited seasonal variation in Asian women is a novel finding. The Workshop also considered the dilemma of balancing the risks of vitamin D deficiency (from lack of skin exposure to sunlight in summer) and skin cancer (from excessive exposure to sunlight with concomitant sunburn and erythema). Cancer Research UK advises that individuals should stay below their personal sunburn threshold to minimise their skin cancer risk. The evidence suggests that vitamin D can be produced in summer at the latitude of the UK, with minimal risk of erythema and cell damage, by exposing the skin to sunlight for a short period at midday, when the intensity of UVB is at its daily peak. The implications of the new data were discussed in the context of dietary reference values for vitamin D for the general population aged 4–64 years. Future research suggestions included further analysis of the three FSA-funded studies as well as new research.

The consensus workshop, organised on behalf of the Food Standards Agency, was convened to recommend the most appropriate and secure method for measuring vitamin D status in the UK. Workshop participants (the Expert Panel) were invited on the basis of expertise in current 25-hydroxyvitamin D (25OHD) assays, or expertise in vitamin D nutrition and metabolism or detailed knowledge and experience in the National Diet and Nutrition Survey (NDNS). A decision support matrix, which set out the particular criteria by which the different options were scored and evaluated, was used to structure the discussion. The Expert Panel agreed that five methods for measuring 25OHD should be evaluated according to eleven criteria, selected on the basis of their relevance to the NDNS. All three of the evaluating subgroups of the Expert Panel produced similar total scores over the eleven criteria for the different methods; they scored LC–MS/MS and HPLC-UV similarly highly, while the scores for the immunoassay methods were lower. The Expert Panel recommended that an LC–MS/MS method should be the preferred method for the NDNS. A detailed specification for the method will be required to ensure comparability between NDNS and the National Health and Nutrition Examination Survey in the US facilitating future comparisons. The Expert Panel also recommended that the method should be carried out in a laboratory with appropriate expertise, competency and history of records of good performance. The method should be standardised against the National Institute of Standards and Technology SRM 972. If the recommended LC–MS/MS is adopted, the Expert Panel indicated that the method should be able to discriminate the C-3 epimer of 25OHD3, especially if used to measure 25OHD in young infants in the forthcoming Diet and Nutrition Survey of Infants and Young Children, who are known to have high circulating concentrations of the C-3 epimer.