The coordinated regulation of metabolic fuel selection is crucial to energy homeostasis. Philip Randle and his colleagues developed the fundamental concept of interplay between carbohydrate and lipid fuels in relation to the requirement for energy utilisation and storage. Their insight has fashioned current understanding of the regulation of metabolism in health and disease, as well as providing a springboard for research into the roles of lipid derivatives in insulin resistance and, at the transcriptional level, lipid-regulated nuclear hormone receptors.

In 1995, Anderson et al. published a meta-analysis, derived from most of the clinical studies on soya proteins given to individuals with varying levels of cholesterolaemia that had been reported up to that time. The meta-analysis clearly indicated that cholesterolaemias were generally reduced by diets with soya given as a partial or total substitution of animal proteins, with final mean total and LDL-cholesterol reductions of 23·2 mg/dl and 21·7 mg/dl, respectively. These findings were recently strongly criticised, based on the evaluation of later studies, frequently involving individuals with normal or moderately elevated cholesterolaemias. In the present paper, these more recent studies were re-evaluated using a ‘nomogram’ prepared on the basis of the quartiles of initial cholesterol concentrations in the Anderson meta-analysis and their corresponding CI for net cholesterol change. The five studies belonging to the first quartile and thirteen out of the fourteen belonging to the second quartile gave results perfectly in line with the nomogram. Out of the fourteen studies belonging to the third quartile, ten agreed with the nomogram and two gave lower cholesterol reductions, whereas two gave higher reductions. Unfortunately, none of the recent studies belonged to the fourth quartile as treatment with statins or other lipid-lowering drugs is now mandatory in the presence of very high cholesterol levels. The re-evaluation thus shows that the thirty-three studies published in the past 10 years are in agreement with the Anderson meta-analysis and confirm its validity.

Use of n-3 fatty acids (FA) has been reported to be beneficial for cancer patients. We performed a systematic review of the literature in order to issue recommendations on the clinical use of n-3 FA in the cancer setting. A systematic search was performed in MEDLINE, EMBASE, Cochrane and Healthstar databases. We selected clinical trials or prospective observational studies including patients with cancer and life expectancy >2 months, in which enteral supplements with n-3 FA were administered. Parameters evaluated individually were clinical (nutritional status, tolerance, survival and hospital stays), biochemical (inflammatory mediators), and functional (functional status, appetite and quality of life (QoL)). Seventeen studies met the inclusion criteria; eight were of high quality. The panel of experts established the following evidence: (1) oral supplements with n-3 FA benefit patients with advanced cancer and weight loss, and are indicated in tumours of the upper digestive tract and pancreas; (2) the advantages observed were: increased weight and appetite, improved QoL, and reduced post-surgical morbidity; (3) there is no defined pattern for combining different n-3 FA, and it is recommended to administer >1·5 g/day; and (4) better tolerance is obtained administering low-fat formulas for a period of at least 8 weeks. All the evidences were grade B but for ‘length of treatment’ and ‘advantage of survival’ it was grade C. Our findings suggest that administration of n-3 FA (EPA and DHA) in doses of at least 1·5 g/day for a prolonged period of time to patients with advanced cancer is associated with an improvement in clinical, biological and QoL parameters.

There is increasing concern that high intakes of added sugars might compromise intakes of micronutrients. The objectives of this systematic review were (1) to determine whether dietary added sugar intake was associated with micronutrient intakes, and if so, whether there was evidence of micronutrient dilution as a result of higher dietary added sugar intake and (2) if micronutrient dilution was present, to determine whether there was sufficiently robust evidence to support a threshold effect above which there was a significant decline in micronutrient intake or status relative to the recommended intakes. A systematic computerised literature search was undertaken, limited to studies written in English published from 1980 onwards and further studies identified through hand searching papers. Fifteen studies that assessed associations between intakes of added sugars or non-milk extrinsic sugars and micronutrients were included. Overall, there are insufficient data and inconsistency between studies in relationships between added sugars and micronutrient intakes, with no clear evidence of micronutrient dilution or a threshold for a quantitative amount of added sugar intake for any of the micronutrients investigated. The current evidence base is considerably constrained by methodological issues. Further research is required to determine which food products high in added sugars might adversely affect micronutrient intakes by displacing other food items from the diet. Analyses should take into account the magnitude of any observed associations to determine their true biological significance.

Plasma total homocysteine concentrations (tHcy) are a putative risk factor for CVD. Tea is a rich dietary source of polyphenols and caffeine, both of which may raise tHcy. However, it is possible that much of any effect is transitory and may be influenced by the consumption of food. Our objective was to investigate the acute effect of tea, at a dose representative of ordinary population intakes, on tHcy and to determine whether consumption of a meal influences the magnitude of any effect. Measurements of tHcy were performed in twenty participants at baseline and 3.5 h after drinking three cups of black tea or hot water (consumed at time 0, 1.5 and 3 h) with and without a meal: a total of four treatments administered in random order. Drinking tea resulted in an acute increase in tHcy (0·30 (95 % CI 0·04, 0·56) μmol/l, P = 0·022). The meal resulted in an acute decrease in tHcy ( − 0·42 (95 % CI − 0·68, − 0·16) μmol/l, P = 0·002). There was no interaction between tea and meal on tHcy (P = 0·40); that is, the effect of tea on tHcy was not different in the fasting and non-fasting state. Our results suggest that drinking black tea can cause a small acute increase in tHcy and that this effect is not enhanced in the non-fasting state. Given that results of population studies have generally shown a negative association between tea intake and tHcy, the significance of these findings to CVD risk remains uncertain.

The PPARγ Pro12Ala polymorphism has been associated in several studies with a decreased risk of obesity, type 2 diabetes and insulin resistance. Weak hints are available about the influence of PPARγ Pro12Ala on postprandial metabolism. In 708 men, aged 45 to 65 years the PPARγ2 Pro12Ala genotypes were determined and postprandial TAG, insulin, glucose and NEFA after a standardized mixed fat meal and insulin and glucose after a glucose load (oral glucose tolerance test; OGTT) were assessed. Using the total sample, we did not find a significant impact of the genotype on the postprandial metabolism. In the subgroup with BMI < 30 kg/m2, fasting and postprandial TAG and insulin levels as well as homeostasis model assessment of insulin resistance (HOMA) were significantly lower in the Ala12Ala group than in the Pro12Pro group after the mixed meal. In contrast, the groups did not differ in insulin levels and HOMA after the OGTT. To investigate if differences between a fat-containing meal and OGTT are caused by adiponectin, we examined a BMI- and age-matched subgroup. No differences were found between the genotypic groups. The effects of the PPARγ2 polymorphism on insulin sensitivity are mediated by affluent dietary fat. We did not find evidence that adiponectin as a fatty-acid-dependent adipocyte factor is a causative factor for this phenomenon.

Little is known about the biological effect of folate in the protection against mitochondrial (mt) oxidative decay. The objective of the present study was to examine the consequence of folate deprivation on mt oxidative degeneration, and the mechanistic link underlying the relationship. Male Wistar rats were fed with an amino acid-defined diet containing either 8 (control) or 0 (folate-deficient, FD) mg folic acid/kg diet. After a 4-week FD feeding period, significant elevation in oxidative stress was observed inside the liver mitochondria with a 77 % decrease in mt folate level (P < 0·001), a 28 % reduction in glutathione peroxidase activity (P = 0·0333), a 1·2-fold increase of mt protein carbonyls (P = 0·0278) and an accumulated 4834 bp large-scale deletion in mtDNA. The elicited oxidative injuries in FD liver mitochondria were associated with 30 % reduction of cytochrome c oxidase (CcOX) activity (P = 0·0264). The defective CcOX activity in FD hepatocytes coincided with mt membrane potential dissipation and intracellular superoxide elevation. Exposure of FD hepatocytes to pro-oxidant challenge (32 μm-copper sulphate for 48 h) led to a further loss in CcOX activity and mt membrane potential with a simultaneous increase in superoxide production. Preincubation of pro-oxidant-treated FD hepatocytes with supplemental folic acid (10–1000 μm) reversed the mt oxidative defects described earlier and diminished superoxide overproduction. Increased supplemented levels of folic acid strongly correlated with decreased lipid peroxidation (γ − 0·824, P = 0·0001) and protein oxidative injuries (γ − 0·865, P = 0·0001) in pro-oxidant-challenged FD liver mitochondria. Taken together, the results demonstrated that folate deprivation induces oxidative stress in liver mitochondria, which is associated with CcOX dysfunction, membrane depolarization and superoxide overproduction. The antioxidant activity of supplemental folic acid may partially, if not fully, contribute to the amelioration of pro-oxidant-elicited mt oxidative decay.

ApoE is secreted by macrophages at the lesion site of the atherosclerotic plaque, where it is thought to play a protective role against atherosclerosis independently of its effects on lipid metabolism. Of the three common isoforms for apoE, apoE4 is associated with higher risk of cardiovascular disease (CVD). In vitro studies have shown that recombinant apoE may act as an antioxidant in an isoform-dependent manner (E2>E3>E4). The oxidative status of the macrophages plays a key role in the process of atherosclerosis. In the present study the possible differential actions of apoE3 and apoE4 on several parameters of oxidative status were determined in stably transfected murine macrophages (RAW 264·7-apoE3 and -apoE4). No differences between genotypes were observed after peroxide challenge in either protection against cytotoxicity or in cell membrane oxidation, and modest differences were observed in the non-enzymatic antioxidants (glutathione and α-tocopherol) in apoE3 v. apoE4 macrophages. Importantly, cells secreting apoE4 showed increased membrane oxidation under basal conditions, and produced more NO and superoxide anion radicals than the apoE3 macrophages after stimulation. The present data suggest that apoE genotype influences the oxidative status of macrophages, and this could partly contribute to the higher CVD risk observed in apoE4 carriers.

Recent studies have shown that dietary oxidised fats influence the lipid metabolism in rats by activation of PPARα. In this study, we investigated whether a mildly oxidised fat causes activation of PPARα in pigs which are non-proliferators like man. Eighteen pigs were assigned to two groups and received either a diet containing 90 g/kg of a fresh fat or the same diet with 90 g/kg of an oxidised fat prepared by heating for 24 h at 180°C in a deep fryer. Pigs fed the oxidised fat had a higher peroxisome count, a higher activity of catalase and a higher mRNA concentration of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase in the liver and a higher concentration of 3-hydroxybutyrate in plasma than pigs fed the fresh fat (P < 0·05). Hepatic mRNA concentrations of acyl-CoA oxidase and carnitine palmitoyltransferase-1 tended to be increased in pigs fed the oxidised fat compared to pigs fed the fresh fat (P < 0·10). Pigs fed the oxidised fat, moreover, had higher mRNA concentrations of sterol regulatory element-binding protein (SREBP)-1 and its target genes acetyl-CoA carboxylase and stearoyl-CoA desaturase in the liver and higher mRNA concentrations of SREBP-2 and its target genes 3-hydroxy-3-methylglutary-CoA reductase and LDL receptor in liver and small intestine. In conclusion, this study shows that even a mildly oxidised fat causes activation of PPARα in the liver of pigs. Up-regulation of SREBP and its target genes in liver and small intestine suggests that the oxidised fat could stimulate synthesis of cholesterol and TAG in these tissues.

β-Cryptoxanthin (β-CX), a provitaminic carotenoid of potential interest for health, is found principally in Citrus fruit in both free and esterified forms. Little is known about the intestinal absorption of β-CX especially with regard to the esterified forms. The aim of this study was to evaluate the absorption of free and esterified β-CX using simulated digestion coupled with the Caco-2 model. Bioaccessibility was investigated by measuring the transfer of carotenoids from different citrus juices into micelles using an in vitro digestion system. Then, carotenoid uptake was evaluated by adding carotenoid-rich micelles (from the in vitro digestion) or synthetic micelles (made from synthetic lipids and carotenoids purified from citrus juice) to human intestinal cells (Caco-2 TC7 clone). Our results showed that β-cryptoxanthin esters (β-CXE) were partially hydrolysed during the in vitro digestion. The bioaccessibility of free β-CX measured was significantly higher (40 (sd 1·05) %) than that of β-carotene (30 (sd 1·9) %) and β-CXE (16 (sd 1·5) %). In the same way, the incorporation of free β-CX (27 (sd 1·01) %) into synthetic micelles exceeded (P < 0·05) that of β-carotene (10 (sd 0·7) %) and β-CXE (8·8 (sd 0·4) %). In the case of micelles from in vitro digestion, the uptake of β-carotene, free β-CX and β-CXE forms by Caco-2 cells was 14·3 (sd 1·8), 3·9 (sd 1·3), and 0·7 (sd 0·08) % respectively. These results showed a preferential uptake by Caco-2 cells of β-carotene and free β-CX compared with the two esters of β-CX.

A [13CO2] breath test was applied as a non-invasive method to study the catabolism of ingested amino acids shortly after a meal. This test requires the ingestion of a [1-13C]-labelled amino acid and the analysis of expired air for [13C] enrichment and CO2. The recovery of label as [13CO2] reflects the catabolism of the [1-13C]-labelled substrate. Such a non-steady state approach provides information that is complementary to the information obtained by steady-state methods using a primed continuous infusion of tracer amino acids during the fed state. In a model study with twenty adult male rats, two groups of animals were fed twice a day with one of two semi-synthetic iso-energetic diets. One diet contained egg white protein (EW) as the sole amino acid source. The second diet contained a mixture of free amino acids with a pattern similar to that of the EW diet. On day 5 of the dietary treatment, l-[1-13C]leucine, either bound in EW protein or in free form, was ingested as part of the morning meal. The expired air was sampled at 30 min intervals for 5 h. The rate of recovery ranged from 0 % to 6 % of the dose/h. Up to 120 min after the onset of the meal, the recovery values for the free amino acid diet were higher than those for the EW diet. Differences in recovery reflect differences in postprandial utilisation. The differences in label recovery were mainly determined by the [13C] enrichment of the expired air. As a consequence, CO2 measurements are not mandatory when CO2 production is comparable.

We examined the physiological importance of bovine dietary proteins in rats fed diets prepared from bovine Achilles' tendons and arteries. Rats were fed for 4 weeks, with a 20 % casein diet (CON), in comparison with two diets containing 15 % casein and 5 % of either bovine Achilles' tendon (AC) or artery (AR) protein preparations. The serum total cholesterol concentration and non-HDL-cholesterol level in the AR-fed group were significantly lower (P < 0·05) than those in the CON-fed group at the end of the 4-week feeding period. The hepatic mRNA were measured, and the hydroxyl methyl glutaryl-CoA reductase mRNA level was significantly lower (P < 0·05) in the AR-fed group compared with the CON-fed group. Total hepatic cholesterol concentration in AC-fed rats was significantly (P < 0·05) higher than in the CON-fed group. The serum TAG concentration and fatty acid synthase mRNA level in AC- and AR-fed groups were significantly lower (P < 0·05) compared with the CON-fed group throughout the feeding period. Faecal neutral sterol excretion was significantly (P < 0·05) higher in the AC- and AR-fed groups compared with the CON-fed group. The results of the present study demonstrate that some bovine dietary proteins have similar functions as dietary fibres, lowering serum lipid concentration by enhancing faecal neutral sterol excretion or suppressing lipid synthesis in the liver. Moreover, favourable amino acid compositions in the AR and AC preparations may also have a lowering effect on plasma lipid concentration in bovine protein diet-fed groups.

Several studies have described reduced plasma concentrations of arginine, the substrate for nitric oxide synthase (NOS) in infants with necrotizing enterocolitis (NEC). No information on the plasma concentrations of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) in patients with NEC is currently available. We investigated whether plasma concentrations of arginine, ADMA, and their ratio differ between premature infants with and without NEC, and between survivors and non-survivors within the NEC group. In a prospective case–control study, arginine and ADMA concentrations were measured in ten premature infants with NEC (median gestational age 193 d, birth weight 968 g), and ten matched control infants (median gestational age 201 d, birth weight 1102 g), who were admitted to the Neonatal Intensive Care Unit. In the premature infants with NEC, median arginine and ADMA concentrations (μmol/l), and the arginine:ADMA ratio were lower compared to the infants without NEC: 21·4 v. 55·9, P = 0·001; 0·59 v. 0·85, P = 0·009 and 36·6 v. 72·3, P = 0·023 respectively. In the NEC group, median arginine (μmol/l) and the arginine:ADMA ratio were lower in non-surviving infants than in surviving infants: 14·7 v. 33·8, P = 0·01 and 32·0 v. 47·5, P = 0·038 respectively. In premature infants with NEC not only the NOS substrate arginine, but also the endogenous NOS inhibitor ADMA and the arginine:ADMA ratio were lower than in infants without NEC. In addition, low arginine and arginine:ADMA were associated with mortality in infants with NEC. Overall, these data suggest that a diminished nitric oxide production may be involved in the pathophysiology of NEC, but this needs further investigation.

The available evidence suggests that metabolic control mechanisms are programmed early in life. Previous studies of pregnant rats fed low-protein diets have suggested that the vegetable oils used in the experimental diets influence the outcome. The present study investigated the offspring of female rats fed semi-synthetic diets containing either 180 or 90 g casein/kg with 70 g/kg (w/w) of either corn oil or soya oil during gestation. During lactation, the dams received stock diet, and the offspring were subsequently weaned onto the stock diet. The offspring of dams fed the low-protein diets were smaller at birth. At 25 weeks of age, the offspring were subjected to an oral glucose tolerance test. In the offspring of dams fed the diet containing soya oil, the area under the insulin curve was affected by the protein content of the maternal diet. There was no effect of protein on the area under the insulin curve in the offspring of dams fed the diet prepared with corn oil. There were no differences in plasma glucose concentrations. The levels of mRNA for acetyl-CoA carboxylase-1 in the livers of female offspring were affected by the protein and oil content of the maternal diet. The level of carnitine palmitoyl transferase mRNA was affected by the protein content of the maternal diet. The present study suggests that PUFA in the maternal diet can interact with protein metabolism to influence the development of the offspring. This may involve the higher content of α-linolenic acid in soya oil compared with corn oil.

In a single-dosing crossover study, we investigated the ability of apple fruit consumption to protect human lymphocytes against peroxide-induced damage to DNA. Six healthy, non-smoking male volunteers were placed for 2 d on an antioxidant-poor (AP) diet. After 48 h of AP diet, the volunteers were required to consume a homogenate obtained from 600 g of red delicious unpeeled apples or water (500 ml); blood samples were collected 0, 3, 6 and 24 h post-consumption. To evaluate whether the apple intake was sufficient to restore resistance of DNA to oxidative damage, for each subject at any time point the plasma total antioxidant activity, reactive oxygen species (ROS) formation and induction of micronuclei (MN) in isolated lymphocytes following hydrogen peroxide (H2O2) treatment were measured. Results indicated a significant inhibition (58 %, P < 0·05) of H2O2-induced MN frequency in the plasma samples collected at 3 h after apple consumption, as compared with plasma samples collected at 0 h (4·17 (sd 1·83) v. 9·85 (sd 1·87) MN/1000 binucleated (BN) cells, respectively). A gradual return towards the value observed at 0 h was recorded starting from 6 to 24 h. MN frequency induced by H2O2 was significantly influenced by plasma total antioxidant activity (r = –0·95, P < 0·05) and by the increase of intracellular ROS formation (r = 0·88, P < 0·05). These findings suggest that the consumption of whole apple provides a useful dietary source of active scavengers to protect cells and tissue from oxidative stress and related DNA injury.

Inulin-type fructans are fermented by gut bacteria to yield SCFA, including butyrate which is trophic for colonocytes and induces glutathione S-transferases (GST) that detoxify carcinogens. Since little is known on similar effects by complex fermentation samples, we studied related products in non-transformed human colonocytes. Inulin enriched with oligofructose (1 : 1, Synergy1) was fermented with human gut flora. SCFA were quantified and a SCFA mixture was prepared accordingly. Colonocytes were incubated (4–12 h) with the Synergy1 fermentation supernatant (SFS), faeces control, a mixture of the three major SCFA (each 0–15 %, v/v) or butyrate (0–50 mm). Metabolic activity was determined to assess trophic effects and cytotoxicity. Expression of ninety-six genes related to biotransformation was studied using cDNA macroarrays. Results on modulated GST were reassessed with real-time PCR and GST activity was measured. Fermentation of inulin resulted in 2–3-fold increases of SCFA. The samples were non-cytotoxic. SFS increased metabolic activity, pointing to trophic effects. The samples modulated gene expression with different response patterns. Key results were that GSTM2 (2·0-fold) and GSTM5 (2·2-fold) were enhanced by SFS, whereas the SCFA mixture reduced expression. The faeces control enhanced GSTA4 (2·0-fold), but reduced GSTM2 (0·2-fold) and GSTM5 (0·2-fold). Real-time qPCR confirmed the induction of GSTM2 and GSTM5 by SFS and of GSTA4 and GSTT2 by butyrate. Activity of GST was not modulated. High concentrations of fermentation products were well tolerated by primary colonocytes, pointing to trophic effects. The induction of GST by the SFS may protect the cells from carcinogenic compounds.

The effects of the absence of protozoa in the rumen of lambs on animal growth, rumen fermentation, microbial diversity and fatty acid profiles in abomasal fluid and intramuscular fat were measured in ten control and ten protozoa-free (PF) lambs. PF lambs were prepared by isolating them from ewes within the first 24 h after birth. The PF and control lambs were kept for 4 months in two different fields and received a daily supplement of 250 g concentrate. The bacterial populations visualised by denaturing gradient gel electrophoresis differed between the two groups of animals and showed a higher bacterial diversity in control lambs than in PF lambs. Abomasal contents from control lambs contained higher concentrations of 22 : 5n-3 and 22 : 6n-3 and lower concentrations of vaccenic acid (trans-11–18 : 1) and 20 : 3n-6 than PF lambs. The rest of the fatty acids, including the conjugated linoleic acid (CLA) isomers, were present at the same concentrations in abomasal contents from both experimental groups. Fatty acid composition in intramuscular fat showed differences between the groups. PF lambs had higher proportions of 18 : 0, 18 : 3, trans-10, cis-12-CLA and total SFA than control lambs. Control lambs had higher proportions of cis-9–18 : 1, cis-9, cis-12–18 : 2, 20 : 3n-6, 22 : 6n-3 (DHA) and MUFA. In conclusion, rumen defaunation led to higher tissue levels of the trans-10, cis-12-CLA isomer and SFA and lower PUFA:SFA ratio and n-3 PUFA in lamb muscle.

The evidence for an association between poor nutrition in early life and subsequent obesity is inconclusive. In the present study, we investigated the associations between stunting, wasting and underweight at 2 and 4 years of age, and body composition in adolescence in male subjects studied since birth. The 1982 Pelotas Birth Cohort Study included all children born in maternity hospitals and living in the urban area of the city of Pelotas, Southern Brazil. All males born in 1982 were legally required to enlist in the army between January and April 2000. We were thus able to track 2250 subjects in 2000 (78·9 % of the original cohort). Anthropometric measurements were collected in 1984 and 1986, and body composition was assessed in 2000. In the present analysis, we used as predictors the nutritional indices height-for-age, weight-for-height and weight-for-age presented in six categories. Outcomes included fat, lean and body mass indices and fat:lean mass ratio, derived from anthropometric and bioimpedance measurements. ANOVA and linear regression were used in the analyses to adjust for confounding. All predictors were positively associated with fat and body mass indices. Height-for-age Z score at age 2 or 4 years was not associated with lean mass index, but all other predictors were associated. Fat:lean mass ratio was associated only with weight-for-height Z score. Our results suggest that undernutrition is not a risk factor for overweight and obesity in our population and may partially protect against fatness in adolescence.

Previous data from Vietnam show that anaemia is highly prevalent among schoolchildren, who are considered not to be iron deficient. Trichuris infection doubled the risk of anaemia. The present study aimed to evaluate the hypothesis that de-worming is more effective than iron fortification in an anaemic, infection-prone population. In a trial with a 2 × 2 factorial design, 425 anaemic children aged 6–8 years were randomly assigned to receive either iron-fortified noodles or placebo, and mebendazole or placebo. Outcomes considered were change in haematological indicators of iron status (Hb, serum ferritin (SF), serum transferrin receptor (TfR) and haemoglobinopathies analysis); inflammations (C-reactive protein (CRP)); parasite infection status (hookworm, Trichuris and Ascaris infection); and IgE. ANOVA and logistic regression were used to assess the effects of iron fortification and de-worming on Hb, SF, TfR, body iron and anaemia. Hb improved in all groups after 6 months of intervention. Iron fortification significantly improved Hb, SF and body iron (2·6 g/l, 16·3 μg/l and 1 mg/kg, respectively). Prevalence of elevated IgE was very high at baseline (99 %) and significantly reduced to about 75 % in all groups after intervention. De-worming unexpectedly showed no effect on Hb, iron status and IgE level. It is concluded that iron fortification slightly improved anaemia and iron status in anaemic schoolchildren in rural Vietnam that were not considered iron deficient. Chronic infection or other unidentified factors may play an important role in the seasonal reduction of anaemia seen in all treatment groups.