The regulation of lipogenesis mechanisms related to consumption of n-3 PUFA is poorly understood. The aim of the present study was to find out whether α-linolenic acid (ALA) or DHA uptake can have an effect on activities and gene expressions of enzymes involved in lipid metabolism in the liver, subcutaneous adipose tissue and longissimus dorsi (LD) muscle of growing–finishing pigs. Six groups of ten pigs received one of six experimental diets supplemented with rapeseed oil in the control diet, extruded linseed, microalgae or a mixture of both to implement different levels of ALA and DHA with the same content in total n-3. Results were analysed for linear and quadratic effects of DHA intake. The results showed that activities of malic enzyme (ME) and fatty acid synthase (FAS) decreased linearly in the liver with dietary DHA. Although the expression of the genes of these enzymes and their activities were poorly correlated, ME and FAS expressions also decreased linearly with DHA intake. The intake of DHA down-regulates the expressions of other genes involved in fatty acid (FA) metabolism in some tissues of pigs, such as fatty acid desaturase 2 and sterol-regulatory element binding transcription factor 1 in the liver and 2,4-dienoyl CoA reductase 2 in the LD muscle. FA oxidation in the LD muscle and FA synthesis decreased in the liver with increasing amount of dietary DHA, whereas a retroconversion of DHA into EPA seems to be set up in this last tissue.

The long-term effects on growth performance, body composition, plasma metabolites, liver and intestine glucose and lipid metabolism were assessed in gilthead sea bream juveniles fed diets without carbohydrates (CH–) or carbohydrate-enriched (20 % gelatinised starch, CH+) combined with two lipid sources (fish oil; or vegetable oil (VO)). No differences in growth performance among treatments were observed. Carbohydrate intake was associated with increased hepatic transcripts of glucokinase but not of 6-phosphofructokinase. Expression of phosphoenolpyruvate carboxykinase was down-regulated by carbohydrate intake, whereas, unexpectedly, glucose 6-phosphatase was up-regulated. Lipogenic enzyme activities (glucose-6-phosphate dehydrogenase, malic enzyme, fatty acid synthase) and ∆6 fatty acyl desaturase (FADS2) transcripts were increased in liver of fish fed CH+ diets, supporting an enhanced potential for lipogenesis and long-chain PUFA (LC-PUFA) biosynthesis. Despite the lower hepatic cholesterol content in CH+ groups, no influence on the expression of genes related to cholesterol efflux (ATP-binding cassette G5) and biosynthesis (lanosterol 14 α-demethylase, cytochrome P450 51 cytochrome P450 51 (CYP51A1); 7-dehydrocholesterol reductase) was recorded at the hepatic level. At the intestinal level, however, induction of CYP51A1 transcripts by carbohydrate intake was recorded. Dietary VO led to decreased plasma phospholipid and cholesterol concentrations but not on the transcripts of proteins involved in phospholipid biosynthesis (glycerol-3-phosphate acyltransferase) and cholesterol metabolism at intestinal and hepatic levels. Hepatic and muscular fatty acid profiles reflected that of diets, despite the up-regulation of FADS2 transcripts. Overall, this study demonstrated that dietary carbohydrates mainly affected carbohydrate metabolism, lipogenesis and LC-PUFA biosynthesis, whereas effects of dietary lipid source were mostly related with tissue fatty acid composition, plasma phospholipid and cholesterol concentrations, and LC-PUFA biosynthesis regulation. Interactions between dietary macronutrients induced modifications in tissue lipid and glycogen content.

High-producing dairy cows enter a period of negative energy balance during the first weeks of lactation. Energy intake is usually sufficient to cover the increase in energy requirements for fetal growth during the period before calving, but meeting the demand for energy is often difficult during the early stages of lactation. A catabolic state predominates during the transition period, leading to the mobilisation of energy reserves (NEFA and amino acids) that are utilised mainly by the liver and muscle. Increased uptake of mobilised NEFA by the liver, combined with the limited capacity of hepatocytes to either oxidise fatty acids for energy or to incorporate esterified fatty acids into VLDL results in fatty liver syndrome and ketosis. This metabolic disturbance can affect the general health, and it causes economic losses. Different nutritional strategies have been used to restrict negative effects associated with the energy challenge in transition cows. The provision of choline in the form of rumen-protected choline (RPC) can potentially improve liver function by increasing VLDL exportation from the liver. RPC increases gene expression of microsomal TAG transfer protein and APOB100 that are required for VLDL synthesis and secretion. Studies with RPC have looked at gene expression, metabolic hormones, metabolite profiles, milk production and postpartum reproduction. A reduction in liver fat and enhanced milk production has been observed with RPC supplementation. However, the effects of RPC on health and reproduction are equivocal, which could reflect the lack of sufficient dose–response studies.

We aimed to examine the contribution of blood lipids to the association between BMI and blood pressure (BP) in children with overweight and obesity. Data were collected in elementary and high schools of Chaoyang District, Beijing, China in 2012. Participants’ weight, height, BP and fasting plasma lipid profile were measured by standard protocols. Mediation analysis was used to examine the mediation role of blood lipids on the relation between BMI and BP, with age included as a covariate. We found that in boys 8·29 % (mediation effect=0·106, P=0·012) of the association between BMI and systolic BP was mediated through TAG. TAG mediated 12·53 % (mediation effect=0·093, P=0·018) and LDL-cholesterol mediated 7·75 % (mediation effect=0·57, P=0·046) of the association between BMI and diastolic BP was mediated by TAG and LDL-cholesterol, respectively. However, blood lipids did not show the mediation effect in girls. Our findings suggested that there was a sex difference in the contribution of blood lipids to the association between BMI and BP. Controlling TAG or LDL-cholesterol may be beneficial for reducing the risk of the BMI-related high BP in overweight boys; however, this outcome is not the case when controlling TAG or LDL-cholesterol in girls. This study may provide clues to explore the underlying mechanism of the association between obesity and hypertension.

We assessed the effect of vitamin D supplementation on related biochemistry, infection and dentition of the infant. In a double-blind, placebo-controlled trial conducted in Lucknow, India (latitude 26°N), 230 mother –newborn pairs were randomised to receive, for 9 months, 3000µg/month oral vitamin D3 by the mother (group A) or 10µg/d by the infant (group B) or double placebo (group C). All babies received 15 min of sun exposure (unclothed) during massage. Infants’ median 25-hydroxyvitamin D (25(OH)D) was lower in group C (median 45·3; interquartile range (IQR) 22–59·5 nmol/l) than in groups A (median 60·8; IQR 41·3–80·5 nmol/l (P<0·01)) and B (median 61·3; IQR 41·3–75·3 nmol/l (P<0·05)) at 3·5 months. Infant 25(OH)D correlated negatively with infant parathyroid hormone (r −0·46, P<0·01). Elevated alkaline phosphatase (>7.5µkat/l) was significantly more frequent in group C babies (16 %) than in group A (4 %) or group B (0 %) babies. The number of days with respiratory or diarrhoeal infection by 9 months of age was higher in group C (median 46·5; IQR 14·8–73·3 d) than in group A (median 18·5; IQR 8·8–31·0 d (P<0·01)) or group B (median 13·0; IQR 7·0–28·5 (P<0·05)). We conclude that monthly maternal or daily infant supplementation with vitamin D along with sun exposure is superior to sun exposure alone in maintaining normal infant 25(OH)D at 3·5 months, and provide protection from elevated alkaline phosphatase and infectious morbidity.

The aim of the present study was to determine whether the type of protein ingested influences the efficiency of catch-up (CU) growth and bone quality in fast-growing male rats. Young male Sprague–Dawley rats were either fed ad libitum (controls) or subjected to 36 d of 40 % food restriction followed by 24 or 40 d of re-feeding with either standard rat chow or iso-energetic, iso-protein diets containing milk proteins – casein or whey. In terms of body weight, CU growth was incomplete in all study groups. Despite their similar food consumption, casein-re-fed rats had a significantly higher body weight and longer humerus than whey-re-fed rats in the long term. The height of the epiphyseal growth plate (EGP) in both casein and whey groups was greater than that of rats re-fed normal chow. Microcomputed tomography yielded significant differences in bone microstructure between the casein and whey groups, with the casein-re-fed animals having greater cortical thickness in both the short and long term in addition to a higher trabecular bone fraction in the short term, although this difference disappeared in the long term. Mechanical testing confirmed the greater bone strength in rats re-fed casein. Bone quality during CU growth significantly depends on the type of protein ingested. The higher EGP in the casein- and whey-re-fed rats suggests a better growth potential with milk-based diets. These results suggest that whey may lead to slower bone growth with reduced weight gain and, as such, may serve to circumvent long-term complications of CU growth.

The objective of this study was to determine the protective effect of glutamate (Glu) in Cu-induced oxidative injury in fish intestine in vivo and enterocytes in vitro. The results indicated that exposure to 6 mg/l Cu for 72 h induced the production of reactive oxygen species, thereby increasing protein oxidation and lipid peroxidation in enterocytes of grass carp in vitro. Cells exposed to Cu alone resulted in a significant increase in lactate dehydrogenase release, which is accompanied by depletions of antioxidants, including total superoxide dismutase (T-SOD), glutathione S-transferase (GST), glutathione reductase (GR), anti-superoxide anion (ASA), anti-hydroxy radical (AHR) activities and GSH content. Pre-treatment with Glu remarkably prevented the toxic effects of Cu on the T-SOD, GST, GR, AHR, and ASA activities and GSH content in enterocytes. However, Cu induced an adaptive increase in the activities of catalase and glutathione peroxidase (GPx). Glu supplementation further increased GPx activity in enterocytes. Interestingly, the experiment in vivo showed that Glu pre-supplementation significantly elevated SOD, GPx, GST, GR, ASA and AHR activities, as well as GSH content. Further results showed that pre-treatment with Glu could alleviate Cu-induced oxidative injury by elevating antioxidant enzyme activities through regulating the expression of NF-E2-related nuclear factor 2 (Nrf2) mRNA. Together, these results indicated that Glu could attenuate Cu-induced cellular oxidative damage in fish intestine, likely mediated through Nrf2 signalling pathways regulating mRNA expressions of antioxidant enzyme genes and synthesis of GSH.

The gut microbiota exerts a role in type 2 diabetes (T2D), and deviations from a mutualistic ecosystem layout are considered a key environmental factor contributing to the disease. Thus, the possibility of improving metabolic control in T2D by correcting gut microbiome dysbioses through diet has been evaluated. Here, we explore the potential of two different energy-restricted dietary approaches – the fibre-rich macrobiotic Ma-Pi 2 diet or a control diet recommended by Italian professional societies for T2D treatment – to correct gut microbiota dysbioses in T2D patients. In a previous 21-d open-label MADIAB trial, fifty-six overweight T2D patients were randomised to the Ma-Pi 2 or the control diet. For the present study, stools were collected before and after intervention from a subset of forty MADIAB participants, allowing us to characterise the gut microbiota by 16S rRNA sequencing and imputed metagenomics. To highlight microbiota dysbioses in T2D, the gut microbiota of thirteen normal-weight healthy controls were characterised. According to our findings, both diets were effective in modulating gut microbiome dysbioses in T2D, resulting in an increase of the ecosystem diversity and supporting the recovery of a balanced community of health-promoting SCFA producers, such as Faecalibacterium, Roseburia, Lachnospira, Bacteroides and Akkermansia. The Ma-Pi 2 diet, but not the control diet, was also effective in counteracting the increase of possible pro-inflammatory groups, such as Collinsella and Streptococcus, in the gut ecosystem, showing the potential to reverse pro-inflammatory dysbioses in T2D, and possibly explaining the greater efficacy in improving the metabolic control.

Broad-spectrum antibiotic use can disrupt the gastrointestinal microbiota resulting in diarrhoea. Probiotics may be beneficial in managing this type of diarrhoea. The aim of this 10-week randomised, double-blind, placebo-controlled, parallel study was to investigate the effect of Lactobacillus helveticus R0052 and Lactobacillus rhamnosus R0011 supplementation on antibiotic-associated diarrhoea in healthy adults. Subjects were randomised to receive 1 week of amoxicillin–clavulanic acid (875 mg/125 mg) once per day, plus a daily dose of 8×109 colony-forming units of a multi-strain probiotic (n 80) or placebo (n 80). The probiotic or placebo intervention was maintained for 1 week after completion of the antibiotic. Primary study outcomes of consistency and frequency of bowel movements were not significantly different between the probiotic and placebo groups. The secondary outcomes of diarrhoea-like defecations, Gastrointestinal Symptoms Rating Scale scores, safety parameters and adverse events were not significantly different between the probiotic intervention and the placebo. A post hoc analysis on the duration of diarrhoea-like defecations showed that probiotic intervention reduced the length of these events by 1 full day (probiotic, 2·70 (sem 0·36) d; placebo, 3·71 (sem 0·36) d; P=0·037; effect size=0·52). In conclusion, this study provides novel evidence that L. helveticus R0052 and L. rhamnosus R0011 supplementation significantly reduced the duration of diarrhoea-like defecations in healthy adults receiving antibiotics.

Whether supplemental Ca has similar effects to dietary Ca on vascular and bone markers is unknown. The present trial investigated the feasibility of applying dietary and supplemental interventions in a randomised-controlled trial (RCT) aiming to estimate the effect of supplemental Ca as compared with dietary Ca on vascular and bone markers in postmenopausal women. In total, thirteen participants were randomised to a Ca supplement group (CaSuppl) (750 mg Ca from CaCO3+450 mg Ca from food+20 µg vitamin D supplement) or a Ca diet group (CaDiet) (1200 mg Ca from food+10 µg vitamin D supplement). Participants were instructed on Ca consumption targets at baseline. Monthly telephone follow-ups were conducted to assess adherence to interventions (±20 % of target total Ca) using the multiple-pass 24-h recall method and reported pill count. Measurements of arterial stiffness, peripheral blood pressure and body composition were performed at baseline and after 6 and 12 months in all participants who completed the trial (n 9). Blood and serum biomarkers were measured at baseline and at 12 months. Both groups were compliant to trial interventions (±20 % of target total Ca intake; pill count ≥80 %). CaSuppl participants maintained a significantly lower average dietary Ca intake compared with CaDiet participants throughout the trial (453 (sd 187) mg/d v. 1241 (sd 319) mg/d; P<0·001). There were no significant differences in selected vascular outcomes between intervention groups over time. Our pilot trial demonstrated the feasibility of conducting a large-scale RCT to estimate the differential effects of supplemental and dietary Ca on vascular and bone health markers in healthy postmenopausal women.

Exclusive breast-feeding (EBF) for 6 months supports optimal infant growth, health and development. This paper examined whether maternal HIV status was associated with EBF and other infant feeding practices. Pregnant women were enrolled after HIV counselling, and their babies were followed up for up to 1 year. Data on household socio-economics and demographics, maternal characteristics and infants’ daily diet were available for 482 infants and their mothers (150 HIV-positive (HIV-P), 170 HIV-negative (HIV-N) and 162 HIV-unknown (HIV-U)). Survival analyses estimated median EBF duration and time to introduction of liquids and foods; hazards ratios (HR) used data from 1–365 and 1–183 d, adjusting for covariates. Logistic regression estimated the probability of EBF for 6 months. Being HIV-P was associated with a shorter EBF duration (139 d) compared with HIV-N (163 d) and HIV-U (165 d) (P=0·004). Compared with HIV-N, being HIV-P was associated with about a 40 % higher risk of stopping EBF at any time point (HR 1·39; 95 % CI 1·06, 1·84; P=0·018) and less than half as likely to complete 6 months of EBF (adjusted OR 0·42; 95 % CI 0·22, 0·81; P=0·01). Being HIV-P tended to be or was associated with a higher risk of introducing non-milk liquids (HR 1·34; 95 % CI 0·98, 1·83; P=0·068), animal milks (HR 2·37; 95 % CI 1·32, 4·24; P=0·004) and solids (HR 1·56; 95 % CI 1·10, 2·22; P=0·011) during the first 6 months. Weight-for-age Z-score was associated with EBF and introducing formula. Different factors (ethnicity, food insecurity, HIV testing strategy) were associated with the various feeding behaviours, suggesting that diverse interventions are needed to promote optimal infant feeding.

α-Tocopherol is the principal source of vitamin E, an essential nutrient that plays a crucial role in maintaining healthy brain function. Infant formula is routinely supplemented with synthetic α-tocopherol, a racaemic mixture of eight stereoisomers with less bioactivity than the natural stereoisomer RRR-α-tocopherol. α-Tocopherol stereoisomer profiles have not been previously reported in the human brain. In the present study, we analysed total α-tocopherol and α-tocopherol stereoisomers in the frontal cortex (FC), hippocampus (HPC) and visual cortex (VC) of infants (n 36) who died of sudden infant death syndrome or other conditions. RRR-α-tocopherol was the predominant stereoisomer in all brain regions (P<0·0001) and samples, despite a large intra-decedent range in total α-tocopherol (5–17 μg/g). Mean RRR-α-tocopherol concentrations in FC, HPC and VC were 10·5, 6·8 and 5·5 μg/g, respectively. In contrast, mean levels of the synthetic stereoisomers were RRS, 1–1·5; RSR, 0·8–1·0; RSS, 0·7–0·9; and Σ2S 0·2–0·3 μg/g. Samples from all but two decedents contained measurable levels of the synthetic stereoisomers, but the intra-decedent variation was large. The ratio of RRR:the sum of the synthetic 2R stereoisomers (RRS+RSR+RSS) averaged 2·5, 2·3 and 2·4 in FC, HPC and VC, respectively, and ranged from 1 to at least 4·7, indicating that infant brain discriminates against synthetic 2R stereoisomers in favour of RRR. These findings reveal that RRR-α-tocopherol is the predominant stereoisomer in infant brain. These data also indicate that the infant brain discriminates against the synthetic 2R stereoisomers, but is unable to do so completely. On the basis of these findings, investigation into the impact of α-tocopherol stereoisomers on neurodevelopment is warranted.

We conducted a systematic review and meta-analysis to compare the effect of breast-feeding and formula-feeding on body composition of preterm infants. We searched the literature using PubMed, Cochrane Central Library Issue, Ovid (Medline), Embase and other resources such as Google Scholar, electronic databases and bibliographies of relevant articles; two reviewers collected and extracted data independently. All the authors assessed risk of bias independently using the Newcastle–Ottawa Scale (NOS). A fixed-effects meta-analysis was undertaken with RevMan 5 software (The Cochrane Collaboration) using the inverse variance method (P≥0·05; χ2 test). In contrast, a random-effects meta-analysis was carried out. Altogether, 630 articles were identified using search strategy, and the references within retrieved articles were also assessed. A total of six studies were included in this systematic review. In formula-fed infants, fat mass was higher at term (mean difference 0·24 (95 % CI 0·17, 0·31) kg), fat-free mass was higher at 36 weeks of gestational (mean difference 0·12 (95 % CI 0·04, 0·21) kg) and the percentage of fat mass was higher at 36 weeks of gestation (mean difference 3·70 (95 % CI 1·81, 5·59) kg) compared with breast-fed infants. Compared with breast-feeding, formula-feeding is associated with altered body composition from birth to term in preterm infants. The effects of formula-feeding on preterm infant body composition from term to 12-month corrected age are inconclusive in our study. Well-designed studies are required in the future to explore the effects of formula-feeding compared with breast-feeding.

Dietary patterns analysis is an emerging area of research. Identifying distinct patterns within a large dietary survey can give a more accurate representation of what people are eating. Furthermore, it allows researchers to analyse relationships between non-communicable diseases (NCD) and complete diets rather than individual food items or nutrients. However, few such studies have been conducted in developing countries including India, where the population has a high burden of diabetes and CVD. We undertook a systematic review of published and grey literature exploring dietary patterns and relationships with diet-related NCD in India. We identified eight studies, including eleven separate models of dietary patterns. Most dietary patterns were vegetarian with a predominance of fruit, vegetables and pulses, as well as cereals; dietary patterns based on high-fat, high-sugar foods and more meat were also identified. There was large variability between regions in dietary patterns, and there was some evidence of change in diets over time, although no evidence of different diets by sex or age was found. Consumers of high-fat dietary patterns were more likely to have greater BMI, and a dietary pattern high in sweets and snacks was associated with greater risk of diabetes compared with a traditional diet high in rice and pulses, but other relationships with NCD risk factors were less clear. This review shows that dietary pattern analyses can be highly valuable in assessing variability in national diets and diet–disease relationships. However, to date, most studies in India are limited by data and methodological shortcomings.

The aims of the present study were to provide nationally representative data on fruit and vegetable consumption in Vietnam, and to assess the accuracy of the reported numbers of ‘standard servings’ consumed. Data analysed were from a multi-stage stratified cluster survey of 14 706 participants (46·5 % males, response proportion 64·1 %) aged 25−64 years in Vietnam. Measurements were made in accordance with the WHO STEPwise approach to surveillance of non-communicable diseases (STEPS) protocols. Approximately 80 % of Vietnamese people reported having less than five servings of fruit and vegetables daily in a typical week. Fruit and vegetable intake reported in ‘standard serving’ sizes was positively correlated with levels of education completed and household income (P<0·001 for trend). The correlations between summary values for each province reflect some known demographic, geographical and climatic characteristics of the country. For example, provinces at higher latitude had higher mean servings of vegetables (r 0·90), and provinces with higher proportions of urban population had higher mean servings of fruit (r 0·40). In conclusion, about eight in ten Vietnamese people aged 25–64 years did not meet WHO recommendations for daily consumption of at least five servings of fruit and vegetables. On the basis of the consistency of the data collected with other estimates and with physical and demographic characteristics of the country, the WHO STEPS instrument has construct validity for measuring fruit and vegetable intake, but with two issues identified. The issues were seasonal variation in reporting and a limitation on the usefulness of the information for associative analyses.

Findings from observational studies have suggested a possible relation between Ca and breast cancer risk. However, the results of these studies are inconclusive, and the dose–response relationship between Ca intake and risk of breast cancer remains to be determined. A meta-analysis of prospective studies was conducted to address these issues. PubMed and Embase databases were searched for relevant studies concerning the association between Ca intake and breast cancer up to March 2016. The summary relative risks (RR) with 95 % CI were calculated with a random-effects model. The final analysis included eleven prospective cohort studies involving 26 606 cases and 872 895 participants. The overall RR of breast cancer for high v. low intake of Ca was 0·92 (95 % CI 0·85, 0·99), with moderate heterogeneity (P=0·026, I2=44·2 %). In the subgroup analysis, the inverse association appeared stronger for premenopausal breast cancer (RR 0·75; 95 % CI 0·59, 0·96) than for postmenopausal breast cancer (RR 0·94; 95 % CI 0·87, 1·01). Dose–response analysis revealed that each 300 mg/d increase in Ca intake was associated with 2 % (RR 0·98; 95 % CI 0·96, 0·99), 8 % (RR 0·92; 95 % CI 0·87, 0·98) and 2 % (RR 0·98; 95 % CI 0·97, 0·99) reduction in the risk of total, premenopausal and postmenopausal breast cancer, respectively. Our findings suggest an inverse dose–response association between Ca intake and risk of breast cancer.

Several studies have investigated the potential benefits of marine n-3 PUFA in CVD, generally suggesting a lower risk of CHD. However, recent trials have questioned these results. This study investigated the association of fish consumption with dietary intake of marine n-3 PUFA with incident myocardial infarction (MI). In a Danish cohort study, 57 053 subjects between 50 and 64 years of age were enrolled from 1993 to 1997. From national registries, we identified all cases of incident MI. Dietary fish consumption was assessed using a semi-quantitative food questionnaire, including twenty-six questions regarding fish intake. In addition, we calculated the intake of total and individual marine n-3 PUFA. During a median follow-up of 17·0 years, we identified 3089 cases of incident MI. For both men and women, a high intake of fatty fish was inversely related to incident MI. Thus, when comparing the highest and the lowest quintile of fatty fish intake, we found a 12 % lower relative risk of MI in men (hazard ratio (HR) 0·88; 95 % CI 0·77, 1·00) and a 22 % lower relative risk in women (HR 0·78; 95 % CI 0·63, 0·96) after adjustments. For women, similar associations were observed for individual and total marine n-3 PUFA. In contrast, intake of lean fish was not associated with MI. In conclusion, incident MI was inversely related to a high intake of fatty fish, but not lean fish. However, test for trends across quintiles was not statistically significant. In general, this study supports the view that consumption of fatty fish may protect against MI.

This study aimed to examine the dietary glycaemic index (GI) and glycaemic load (GL) of Australian children and adolescents, as well as the major food groups contributing to GL, in the recent 2011–2012 Australian Health Survey. Plausible food intake data from 1876 children and adolescents (51 % boys), collected using a multiple-pass 24-h recall, were analysed. The GI of foods was assigned based on a step-wise published method using values from common GI databases. Descriptive statistics were calculated for dietary GI, GL and contribution to GL by food groups, stratified by age group and sex. Linear regression was used to test for trends across age groups for BMI, dietary GI and GL, and intakes of energy, nutrients and food groups. Pearson’s χ2 test was used to test for differences between age groups for categorical subject characteristic variables. Mean dietary GI and GL of participants were 55·5 (sd 5·3) and 137·4 (sd 50·8), respectively. The main contributors to dietary GL were starchy foods: breads, cereal-based dishes, breakfast cereals, flours, grains and potatoes accounted for 41 % of total GL. Sweetened beverages, fruit and vegetable juices/drinks, cake-type desserts and sweet biscuits contributed 15 %. No significant difference (at P<0·001) was observed between sexes. In conclusion, Australian children and adolescents appear to consume diets with a lower GI than European children. Exchanging high-GI foods for low-GI alternatives within core and non-core foods may improve diet quality of Australian children and adolescents.