The objective of the present review was to summarise the existing European published and ‘grey’ literature on the effectiveness of school-based interventions to promote a healthy diet in children (6–12 years old) and adolescents (13–18 years old). Eight electronic databases, websites and contents of key journals were systematically searched, reference lists were screened, and authors and experts in the field were contacted for studies evaluating school-based interventions promoting a healthy diet and aiming at primary prevention of obesity. The studies were included if they were published between 1 January 1990 and 31 December 2007 and reported effects on dietary behaviour or on anthropometrics. Finally, forty-two studies met the inclusion criteria: twenty-nine in children and thirteen in adolescents. In children, strong evidence of effect was found for multicomponent interventions on fruit and vegetable intakes. Limited evidence of effect was found for educational interventions on behaviour, and for environmental interventions on fruit and vegetable intakes. Interventions that specifically targeted children from lower socio-economic status groups showed limited evidence of effect on behaviour. In adolescents, moderate evidence of effect was found for educational interventions on behaviour and limited evidence of effect for multicomponent programmes on behaviour. In children and adolescents, effects on anthropometrics were often not measured, and therefore evidence was lacking or delivered inconclusive evidence. To conclude, evidence was found for the effectiveness of especially multicomponent interventions promoting a healthy diet in school-aged children in European Union countries on self-reported dietary behaviour. Evidence for effectiveness on anthropometrical obesity-related measures is lacking.

Since there is a reported interrelationship between vitamin A and Fe metabolism, and with immunological response, the objective was to evaluate the effect of a single dose of vitamin A administered to preschool children, on Fe and vitamin A nutritional status, anaemia and phagocytic function of neutrophils, 30 d after supplementation. A total of eighty children (sixty-eight supplemented and twelve controls) were supplemented orally with 200 000 IU (60 mg) vitamin A, and evaluated for nutritional, haematological and immunological responses at the beginning of the study and 30 d after supplementation. Parameters studied included Hb, serum ferritin, retinol and Fe concentrations, transferrin saturation, IL-4, interferon-γ and phagocityc capacity of neutrophils using non-fluorescent latex microbeads. After supplementation there was a significant increase in Hb concentration (P = 0·03), mean corpuscular Hb concentration (P = 0·001) and serum retinol (P = 0·0078). Prevalences of anaemia and vitamin A deficiency decreased significantly from 17·6 % to 13·2 % and from 25 % to 13·2 %, respectively. Regarding phagocytic function, there was a significant increase in the number of microbeads engulfed by neutrophils (P < 0·05) and no significant changes in cytokine concentrations at 1 month after treatment. A single dose of 200 000 IU (60 mg) vitamin A administered orally to a group of preschool children with a high prevalence of vitamin A deficiency enhanced serum retinol and Hb concentrations, decreased the prevalence of anaemia and vitamin A deficiency and improved the constitutive phagocytic capacity of neutrophils. Vitamin A supplementation could help to decrease vitamin A deficiency, anaemia prevalence and to improve the innate immunity response in preschool children. The effects were obtained without Fe supplementation.

Studies have shown that various antioxidants are decreased in different age-related degenerative diseases and thus, oxidative stress would have a central role in the pathogenesis of many disorders that involve neuronal degeneration, including Alzheimer's disease (AD). The present study aimed to assess the nutritional status of Se in AD patients and to compare with control subjects with normal cognitive function. The case–control study was carried out on a group of elderly with AD (n 28) and compared with a control group (n 29), both aged between 60 and 89 years. Se intake was evaluated by using a 3-d dietary food record. Se was evaluated in plasma, erythrocytes and nails by using the method of hydride generation atomic absorption spectroscopy. Deficient Se intake was largely observed in the AD group. AD patients showed significantly lower Se levels in plasma, erythrocytes and nails (32·59 μg/l, 43·74 μg/l and 0·302 μg/g) when compared with the control group (50·99 μg/l, 79·16 μg/l and 0·400 μg/g). The results allowed us to suggest that AD has an important relation with Se deficiency.

We have studied the effect of human serum, collected after red wine consumption (RWS), on TNF-α-dependent activation of transcription factors (NF-κB, activator protein-1 (AP-1) and cAMP response element-binding proteins) and on the expression of selected genes involved in cell adhesion or fibrinolysis processes in human primary endothelial cells (human umbilical vein endothelial cells (HUVEC)). Our data indicate that RWS containing RW metabolites, isolated after 40 min from an acute consume of wine (5 ml/kg body weight), induces nuclear translocation of NF-κB and AP-1 in the absence of any further stimulus. On the other hand, TNF-α treatment in the presence of RWS is associated with a delay in transcription factor activation and to a negative modulation on the expression of specific genes. Moreover, RWS stimulates c-jun binding to the tissue-type plasminogen activator cAMP responsive element consensus site modulating the expression of the specific gene downstream. These results confirm that RW metabolites affect the activity of different transcription factors playing an important preconditioning role in the modulation of the inflammatory pathway in endothelial cells. This is the first report on the effects of a complex food matrix, on the molecular mechanisms associated with inflammatory response in HUVEC cultured in condition that reproduces the physiological environment occurring in vivo.

Recently, broccoli, a vegetable of the Brassica family, has been found to protect the myocardium from ischaemic reperfusion injury through the redox signalling of sulphoraphane, which is being formed from glucosinolate present in this vegetable. Since cooked broccoli loses most of its glucosinolate, we assumed that fresh broccoli could be a superior cardioprotective agent compared to cooked broccoli. To test this, two groups of rats were fed with fresh (steamed) broccoli or cooked broccoli for 30 d, while a third group was given vehicle only for the same period of time. After 30 d, all the rats were sacrificed, and the isolated working hearts were subjected to 30 min ischaemia followed by 2 h of reperfusion. Both cooked and steamed broccolis displayed significantly improved post-ischaemic ventricular function and reduced myocardial infarction and cardiomyocyte apoptosis compared to control, but steamed broccoli showed superior cardioprotective abilities compared with the cooked broccoli. Corroborating with these results, both cooked and steamed broccolis demonstrated significantly enhanced induction of the survival signalling proteins including Bcl2, Akt, extracellular signal-regulated kinase 1/2, haemoxygenase-1, NFE2 related factor 2, superoxide dismutase (SOD1) and SOD2 and down-regulation of the proteins (e.g. Bax, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase) of the death signalling pathway, steamed broccoli displaying superior results over its cooked counterpart. The expressions of proteins of the thioredoxin (Trx) superfamily including Trx1 and its precursor sulphoraphane, Trx2 and Trx reductase, were enhanced only in the steamed broccoli group. The results of the present study documented superior cardioprotective properties of the steamed broccoli over cooked broccoli because of the ability of fresh broccoli to perform redox signalling of Trx.

Inflammatory bowel disease (IBD) is a major source of morbidity in children and adults. Its incidence is rising, particularly in young people. IBD carries a lifelong risk of cancer, which is proportional to disease duration. Drug and surgical treatments rarely offer cure and often carry a high side effect burden. Dietary therapy is highly effective in Crohn's disease. For these reasons, there is much interest in developing novel dietary treatments in IBD. Curcumin, a component of the spice turmeric, and an anti-inflammatory and anti-cancer agent, shows preclinical and clinical potential in IBD. Its mechanisms of action are unknown. Our aim was to assess the effect of curcumin on key disease mediators p38 mitogen-activated protein kinase (MAPK), IL-1β, IL-10 and matrix metalloproteinase-3 (MMP-3) in the gut of children and adults with IBD. Colonic mucosal biopsies and colonic myofibroblasts (CMF) from children and adults with active IBD were cultured ex vivo with curcumin. p38 MAPK, NF-κB and MMP-3 were measured by immunoblotting. IL-1β and IL-10 were measured by ELISA. We show reduced p38 MAPK activation in curcumin-treated mucosal biopsies, enhanced IL-10 and reduced IL-1β. We demonstrate dose-dependent suppression of MMP-3 in CMF with curcumin. We conclude that curcumin, a naturally occurring food substance with no known human toxicity, holds promise as a novel therapy in IBD.

Caffeine and caffeinated coffee (CC) elicit acute insulin insensitivity when ingested before a carbohydrate load. The effects of CC on glucose tolerance and insulin sensitivity when co-ingested with a high carbohydrate meal and on postprandial metabolism of a subsequent (second) carbohydrate load have not been studied. In a randomised, crossover design, ten healthy males ingested either CC (5 mg caffeine/kg body weight), decaffeinated coffee (DC) or water (W; equal volume) co-ingested with a high glycaemic index cereal followed 3 h later by a 75 g oral glucose tolerance test. After the initial meal, insulin area under the curve (AUC) and insulin sensitivity index did not differ between treatments, although glucose AUC for CC (107 (sem 18) mmol/l × 3 h) and DC (74 (sem 15) mmol/l × 3 h) was greater than W ( − 0·2 (sem 29) mmol/l × 3 h, P < 0·05). After the second carbohydrate load, insulin AUC for CC was 49 % and 57 % greater (P < 0·01) than for DC and W, respectively. Despite the greater insulin response, glucose AUC for CC (217 (sem 24) mmol/l × 2 h) was greater than both DC (126 (sem 11) mmol/l × 2 h, P = 0·01) and W (55 (sem 34) mmol/l × 2 h, P < 0·001). Insulin sensitivity index after the second meal was lower after CC (8·2 (sem 0·9)) compared with both DC (12·4 (sem 1·2), P < 0·01) and W (13·4 (sem 1·4), P < 0·001). Co-ingestion of CC with one meal resulted in insulin insensitivity during the postprandial phase of a second meal in the absence of further CC ingestion. Thus, CC may play a role in daily glycaemic management.

Numerous studies indicate that polyphenol-rich chocolate reduces fasting blood glucose, blood pressure (BP) and total cholesterol in healthy individuals and hypertensives with or without glucose intolerance. The aim of the present study was to investigate the effect of two doses of polyphenol-rich dark chocolate (DC) on fasting capillary whole blood glucose, total cholesterol and BP and to examine whether improvements in these parameters are associated with changes in adrenocorticoid excretion in overweight and obese individuals. The study used a randomised, single-blind, cross-over design where fourteen overweight and obese subjects were randomised to either take 20 g DC with 500 mg polyphenols then 20 g DC with 1000 mg polyphenols or vice-versa. Participants followed each diet for 2 weeks separated by a 1-week washout period. It was observed that the 500 mg polyphenol dose was equally effective in reducing fasting blood glucose levels, systolic BP (SBP) and diastolic BP (DBP) as the 1000 mg polyphenol dose suggesting that a saturation effect might occur with increasing dose of polyphenols. There was also a trend towards a reduction in urinary free cortisone levels with both groups although it did not reach statistical significance. No changes in anthropometrical measurements were seen. We suggest that more research is required to investigate the mechanism(s) by which polyphenol-rich foods influence health.

A study was conducted to assess the effect of substituting high levels of dietary fish oil (FO) and fishmeal (FM) for vegetable oil (VO) and plant protein (PP) on the intestinal arachidonic acid (AA) cascade in the carnivorous fish species Atlantic salmon. Four diets were fed to salmon over a period of 12 months, including a control FMFO diet, with varying replacements of plant-derived ingredients: 80 % PP and 35 % VO; 40 % PP and 70 % VO; 80 % PP and 70 %VO. Subsequently, fish were examined pre- (0 h) and post- (1 h) acute stress for blood parameters and intestinal bioactive lipidic mediators of inflammation (prostaglandins). Plasma cortisol responses were greatest in the FMFO group, while 80 % PP and 70 % VO fish exhibited increased plasma chloride concentrations. The n-3:n-6 PUFA ratio in intestinal glycerophospholipids from 70 % VO groups significantly decreased in both proximal and distal regions due to elevated levels of 18 : 2n-6 and the elongation/desaturation products 20 : 2n-6 and 20 : 3n-6. Increases in n-6 PUFA were not concomitant with increased AA, although the AA:EPA ratio did vary significantly. The 40 % PP and 70 % VO diet produced the highest intestinal AA:EPA ratio proximally, which coincided with a trend in elevated levels of PGF2α, PGE2 and 6-keto-PGF1α in response to stress. PGE2 predominated over PGF2α and 6-keto-PGF1α (stable metabolite of PGI2) with comparable concentrations in both intestinal regions. Cyclo-oxygenase-2 (COX-2) mRNA expression was an order of magnitude higher in distal intestine, compared with proximal, and was significantly up-regulated following stress. Furthermore, the 80 % PP and 70 % VO diet significantly amplified proximal COX-2 induction post-stress. Results demonstrate that high replacements with plant-derived dietary ingredients can enhance COX-2 induction and synthesis of pro-inflammatory eicosanoids in the intestine of salmon in response to acute physiological stress.

The objective of the present study was to investigate the effect of dietary phytate and microbial phytase on the lipase activity, lipid metabolism and mRNA expressions of fatty acid synthase (FASN) and leptin in broiler chickens. The study was conducted as a 2 × 3 factorial arrangement of treatments with phytate phosphorus at 0·20 and 0·40 % (added as the sodium phytate) and supplemental microbial phytase at 0, 500, or 1000 phytase units/kg. The results showed that phytase improved (P < 0·05) the growth performance and ileal digestibility of nutrients of broilers, but phytate had no effect (P>0·05) on these parameters, except the decrease (P < 0·01) in the digestibility of Ca. Phytate decreased (P < 0·05) the lipase activity, serum total cholesterol (T-CHO) and hepatic TAG, and elevated (P < 0·01) serum NEFA and HDL cholesterol. Phytase decreased (P < 0·05) serum NEFA, but increased (P < 0·01) serum T-CHO and hepatic TAG. Phytate and phytase also influenced (P < 0·01) the mRNA expressions of leptin in the liver. There were significant (P < 0·05) interactions of phytate and phytase on the concentrations of serum TAG and LDL cholesterol, hepatic NEFA and T-CHO, and the mRNA expressions of FASN. The results suggest that phytate and phytase can affect lipase activity and lipid metabolism of broiler chickens.

Conjugated linoleic acid (CLA) has been reported as having body fat lowering properties and the ability to modulate the inflammatory system in several models. In the present study, the effects of CLA added to saturated fat diets, from vegetable and animal origins, on the serum adipokine profile of obese Zucker rats were assessed. In addition, the fatty acid composition of epididymal and retroperitoneal adipose tissues was determined and a principal component analysis (PCA) was used to assess possible relationships between fatty acids and serum metabolites. Atherogenic diets (2 % cholesterol) were formulated with palm oil and ovine fat and supplemented or not with 1 % of a mixture (1:1) of cis-9, trans-11 and trans-10, cis-12-CLA isomers. CLA-fed animals exhibited lower daily feed intake, final body and liver weights, and hepatic lipids content. Total and LDL-cholesterol levels were increased in CLA-supplemented groups. CLA also promoted higher adiponectin and lower plasminogen activator inhibitor-1 (PAI-1) serum concentrations. In contrast to palm oil diets, ovine fat increased insulin resistance and serum levels of leptin, TNF-α and IL-1β. Epididymal and retroperitoneal adipose tissues had similar deposition of individual fatty acids. The PCA analysis showed that the trans-10, cis-12-CLA isomer was highly associated with adiponectin and PAI-1 levels. Summing up, CLA added to vegetable saturated enriched diets, relative to those from animal origin, seems to improve the serum profile of adipokines and inflammatory markers in obese Zucker rats due to a more favourable fatty acid composition.

The influence of fibre inclusion and transit time regulation on the performance, health status, microbial activity and population, physico-chemical characteristics of the hindgut digesta and intestinal morphology in early weaned pigs were examined. For these experiments, wheat bran (WB) was used as fibre source and loperamide as a drug (LOP) to increase the digesta transit time. In Expt 1, a total of 128 early weaned pigs were randomly distributed in a 2 × 2 factorial combination of WB inclusion (0 v. 40 g/kg) and LOP administration (0 v. 0·07 mg/kg body weight) during 13 d. For Expt 2, a total of twenty-four piglets were allotted to three dietary treatments for 15 d with the same basal diet (control diet) as Expt 1; a diet with 80 g/kg of WB and the combination of WB and LOP. In Expt 1, LOP improved the average daily feed intake and average daily gain of the animals (P = 0·001 and 0·007, respectively). The same result was obtained when WB was combined with LOP. The WB–LOP group also showed a higher concentration of SCFA (P = 0·013), acetic acid (P = 0·004) and propionic acid (P = 0·093). On the other hand, WB inclusion reduced the organic matter and crude protein digestibility (P = 0·001) and tended to decrease the enterobacteria population (P = 0·089). In Expt 2, WB increased the butyric acid concentration (P = 0·086). We concluded that the inclusion of WB to modify the intestinal microbiota activity combined with LOP may be beneficial to animal health and performance.

Plasma transforming growth factor (TGF)-β levels are high in the advanced stages of acute (wasting) pre-pubescent deficits of protein and energy. Consequently, this potently anti-inflammatory cytokine may help to sustain the depression of inflammatory immune competence in acute malnutrition. Our objective was to determine if plasma TGF-β levels rise during the early stages of acute malnutrition and, secondarily, to confirm the elevation reported previously in advanced weight loss. In two experiments, male and female C57BL/6J mice, initially 19 d old, consumed ad libitum a complete purified diet (group C), or in restricted daily quantities (group R) or had free access to an isoenergetic low-protein diet (group LP). TGF-β bioactivity in platelet-poor plasma was determined via inhibition of Mv1Lu mink lung cell proliferation after 3 d (Expt 1, early stage) or 14 d (Expt 2, advanced stage) of dietary intervention. At 3 d, mean plasma TGF-β bioactivities were 802 (C), 2952 (R) and 4678 (LP) pg/ml, and after 14 d mean bioactivities were 1786 (C), 5360 (R) and 5735 (LP) pg/ml. At both time points, the malnourished groups differed from age-matched controls (P ≤ 0·05). Thus, metabolically distinct weanling systems mimicking paediatric marasmus (group R) and kwashiorkor (group LP) exhibit an early rise in blood TGF-β concentration, and this cytokine joins corticosterone and IL-10 as a third anti-inflammatory hormone temporally positioned to contribute to the initiation (and maintenance) of malnutrition-associated immune depression. This investigation contributes new insight into the active anti-inflammatory form of immune competence that appears to prevail in acute pre-pubescent malnutrition.

Heat shock protein 70 (HSP70) is reported as the main factor responsible for the beneficial effects of glutamine (GLN) and as a negative regulator of high mobility group box protein-1 (HMGB-1) expression. Our aim was to determine whether GLN attenuates acute lung injury (ALI) by the inhibition of HMGB-1 expression during sepsis. Male Sprague–Dawley rats were subjected to caecal ligation and puncture (CLP) to induce sepsis. GLN or saline was administered through tail vein 1 h after CLP. Then, quercetin (Q), an inhibitor of HSP70, was utilised to assess the role of the enhanced HSP70. We observed the survival of the subjects. At 24 h post-CLP, we measured lung HSP70, phosphorylated heat shock factor-1 (HSF-1-p) and HMGB-1 expressions, NF-κB DNA-binding activity and ALI occurrence. We also measured serum HSP70, IL-6 and HMGB-1 concentrations. GLN improved survival during sepsis. In GLN-treated rats, lung HSP70 and HSF-1-p expressions were enhanced, lung HMGB-1 expression and NF-κB DNA-binding activity were suppressed, and ALI was attenuated. Furthermore, in GLN-administered rats, serum HSP70 concentration was higher, and serum IL-6 and HMGB-1 concentrations were lower than those in non-treated rats. Q inhibited the enhancement of HSP70 and HSF-1-p expressions and abrogated the GLN-mediated benefits. In conclusion, GLN attenuated ALI and improved survival by the inhibition of HMGB-1 expression during sepsis in rats. These benefits were associated with the enhancement of HSP70 expression by GLN.

Total parenteral nutrition (TPN) is still of great importance for haematopoietic stem cell transplantation (HSCT) patients because one of the major adverse effects of the high-dose therapy followed by HSCT is an inadequate oral nutrition intake. The aim of the study was analysis of TPN of young patients in the HSCT period. Twenty-two patients 1·8–20·8 year-old, median 5·4, treated with high-dose therapy and autologous HSCT because of malignancy were included into the study. Grafts contained 1·35–7·9 × 106, median 3·75 × 106 CD34+ cells/kg. Engraftment occurred as follows: granulocytes >0·5 × 109/l on +11 d (8–25); platelets >20 × 109/l on +23 d (12–67). Patients were given isoenergetic, isonitrogenous TPN until they consumed less than 50 % of their required diet orally. Proteins intake was 0·8–2·0 g/kg per d, fats intake 1·0–3·0 g/kg per d. Total non-proteins energies–nitrogen grams index was 140:1–200:1. Supplementation of electrolytes, microelements, trace elements and vitamins was dependent on individual patient requirement. TPN duration did not correlate with CD34+ cells number but correlated with platelets reconstitution. The assessment of nutritional condition demonstrated no differences in anthropometric parameters, but increase of serum albumin levels after TPN. Requirement for P3 −  was above the normal ranges and correlated positively with platelets reconstitution. Requirement for P3 −  and K+ was higher in patients with mucositis than in other patients. Any complications due to TPN were observed. Adequately composed isoenergetic and isonitrogenous TPN with replacement of electrolytes according to their requirement in the early post-transplantation period allows not only improvement in nutritional status of patients but also could contribute to reconstitution of haematopoiesis.

Frequent consumption of nuts lowers the risk of CHD. While lowering blood lipids is one of the mechanisms for cardioprotection, the present study sought to determine whether monounsaturated fat-rich almonds also influence other CHD risk factors such as inflammation and haemostasis. This was a randomised, controlled, crossover feeding study with twenty-five healthy adults (eleven men; fourteen women), age 22–53 years. Following a 2 week run-in phase (34 % energy from fat), subjects were assigned in random order to three diets for 4 weeks each: a heart-healthy control diet with no nuts ( < 30 % energy from fat), low-almond diet and high-almond diet (10 % or 20 % isoenergetic replacement of control diet with almonds, respectively). Serum E-selectin was significantly lower on the high-almond diet compared with the control diet. E-selectin decreased as the percentage of energy from almonds increased (P < 0·0001). C-reactive protein (CRP) was lower in both the almond diets compared with the control diet. A clear dose response was not observed for either E-selectin or CRP. There was no effect of diet on IL-6 or fibrinogen. Tissue plasminogen activator antigen was significantly lower on the control and high-almond diets compared with the low-almond diet, although the values were within normal range. In conclusion, consumption of almonds influenced a few but not all of the markers of inflammation and haemostasis. A clear dose response was not observed for any of the markers studied.

To determine the lipid content and fatty acid (FA) composition of breast milk from fifty-two lactating women between ninth and twelfth lactation weeks in rural North China. The mothers were questioned on their dietary habits. Total milk lipids extracts were transmethylated and analysed using GLC to determine FA contents. The mean lipid content was 40·21 (sd 1·43) g/l. SFA constituted 35·92 % of the total FA. Medium-chain and long-chain SFA presented levels of 10·91 and 25·01 %, respectively. MUFA and PUFA constituted 32·59 and 19·97 % of the total FA, respectively. Oleic, linoleic and α-linolenic acid (ALA) presented contents of 31·26, 17·73 and 1·03 %, respectively. Arachidonic acid had a content of 0·30 %, while DHA content was 0·19 %. Not any form of trans FA were found in human milk samples. A maternal diet transition is proceeding in China. Further investigation on the analysis of human milk FA composition is needed to upgrade the human milk database in China.

Resistant starch (RS), a non-viscous dietary fibre, may have postprandial effects on appetite regulation and metabolism, although the exact effects and mechanisms are unknown. An acute randomised, single-blind crossover study, aimed to determine the effects of consumption of 48 g RS on appetite compared to energy and available carbohydrate-matched placebo. Twenty young healthy adult males consumed either 48 g RS or the placebo divided equally between two mixed meals on two separate occasions. Effects on appetite were assessed, using an ad libitum test meal and 24-h diet diaries for energy intake, and using visual analogue scales for subjective measures. Changes to postprandial glucose, insulin and C-peptide were also assessed. There was a significantly lower energy intake following the RS supplement compared to the placebo supplement at both the ad libitum test meal (5241 (sem 313) v. 5606 (sem 345) kJ, P = 0·033) and over the 24 h (12 603 (sem 519) v. 13 949 (sem 755) kJ, P = 0·044). However, there was no associated effect on subjective appetite measures. Postprandial plasma glucose concentrations were not significantly different between supplements, but there was a significantly lower postprandial insulin response following the RS supplement (P = 0·029). The corresponding C-peptide concentrations were not significantly different, although the ratio of C-peptide to insulin was higher following the RS supplement compared to placebo (P = 0·059). These results suggest that consumption of 48 g RS, over a 24-h period, may be useful in the management of the metabolic syndrome and appetite. Further studies are required to determine the exact mechanisms.

There is controversy whether children should have a dietary supply of preformed long-chain polyunsaturated n-3 fatty acids EPA and DHA. The aims of the workshop were to review evidence for a possible benefit of a preformed EPA and/or DHA supply, of data required to set desirable intakes for children aged 2–12 years, and of research priorities. The authors concluded that EPA and DHA intakes per kg body weight may often be low in 2- to 12-year-old children, relative to intakes per kg body weight of breast-fed infants and adult intakes, but reliable data are scarce. Little information is available that increasing dietary intakes of EPA or DHA in children has benefits to physical or mental function or other health endpoints. Studies addressing EPA and DHA intakes and tissue status among groups of children with different dietary habits, and measures of relevant development and health endpoints, are needed for developing potential advice on desirable intakes of EPA and/or DHA in children. At this time it appears prudent to advise that dietary intakes in childhood are consistent with future eating patterns supporting adult health, such as prevention of metabolic disorders and CVD, supporting immune function, and reproductive health. In conclusion, the available information relating dietary EPA and DHA intakes in children aged 2–12 years to growth, development and health is insufficient to derive dietary intake recommendations for EPA and DHA. Adequately designed studies addressing dietary intakes, measures of status and relevant functional or health effects across this age group are needed.