The WHO recommends exclusive breast-feeding for the first 6 months of life. At present, <2 % of mothers who breast-feed in the UK do so exclusively for 6 months. We propose the testable hypothesis that this is because many mothers do not provide sufficient breast milk to feed a 6-month-old baby adequately. We review recent evidence on energy requirements during infancy, and energy transfer from mother to baby, and consider the adequacy of exclusive breast-feeding to age 6 months for mothers and babies in the developed world. Evidence from our recent systematic review suggests that mean metabolisable energy intake in exclusively breast-fed infants at 6 months is 2·2–2·4 MJ/d (525–574 kcal/d), and mean energy requirement approximately 2·6–2·7 MJ/d (632–649 kcal/d), leading to a gap between the energy provided by milk and energy needs by 6 months for many babies. Our hypothesis is consistent with other evidence, and with evolutionary considerations, and we briefly review this other evidence. The hypothesis would be testable in a longitudinal study of infant energy balance using stable-isotope techniques, which are both practical and valid.

Particular intestinal bacteria are capable of metabolizing the soya isoflavone daidzein to equol and/or O-desmethylangolensin (O-DMA), and the presence of these metabolites in urine after soya consumption are markers of particular intestinal bacteria profiles. Prevalences of equol producers and O-DMA producers are approximately 30–50 % and 80–90 %, respectively, and limited observations have suggested that these daidzein-metabolizing phenotypes are stable within individuals over time. Characterizing stability of these phenotypes is important to understand their potential as markers of long-term exposure to particular intestinal bacteria and their associations with disease risk. We evaluated concordance within an individual for the equol-producer and O-DMA-producer phenotypes measured at two time points (T1, T2), 1–3 years apart. Phenotypes were ascertained by analysing equol and O-DMA using GC-MS in a spot urine sample collected after 3 d soya (source of daidzein) supplementation. In ninety-two individuals without recent (within 3 months before phenotyping) or current antibiotics use, 41 % were equol producers at T1 and 45 % were equol producers at T2, and 90 % were O-DMA producers at T1 and 95 % were O-DMA producers at T2. The percentage agreement for the equol-producer phenotype was 82 and for the O-DMA-producer phenotype was 89. These results indicate that these phenotypes are stable in most individuals over time, suggesting that they provide a useful biomarker for evaluating disease risk associated with harbouring particular intestinal bacteria responsible for, or associated with, the metabolism of the soya isoflavone daidzein.

The effect of the nature and form of supply of dietary lipids on larval development was investigated in European sea bass larvae, by considering the expression of several genes involved in morphogenesis. Fish were fed from 7 to 37 d post-hatch with five isoproteic and isolipidic compound diets incorporating different levels of EPA and DHA provided by phospholipid or neutral lipid. Phospholipid fraction containing 1·1 % (PL1 diet) to 2·3 % (PL3 diet) of EPA and DHA sustained good larval growth and survival, with low vertebral and cephalic deformities. Similar levels of EPA and DHA provided by the neutral lipid fraction were teratogenic and lethal. Nevertheless, dietary phospholipids containing high levels of DHA and EPA (PL5 diet) induced cephalic (8·5 %) and vertebral column deformities (35·3 %) adversely affecting fish growth and survival; moreover, a down-regulation of retinoid X receptor α (RXRα), retinoic acid receptor α, retinoic acid receptor γ and bone morphogenetic protein-4 genes was also noted in PL5 dietary group at day 16. High levels of dietary PUFA in neutral lipid (NL3 diet) first up-regulated the expression of RXRα at day 16 and then down-regulated most of the studied genes at day 23, leading to skeletal abnormalities and death of the larvae. A moderate level of PUFA in neutral lipids up-regulated genes only at day 16, inducing a lesser negative effect on growth, survival and malformation rate than the NL3 group. These results showed that retinoid pathways can be influenced by dietary lipids leading to skeletal malformation during sea bass larvae development.

Lactation alters maternal metabolism and increases food intake in rats to support milk production. Pancreatic lipase (PL) is primarily responsible for fat digestion in adults and is regulated by dietary fat. The present research determined the regulation of PL by lactation and dietary fat. In Expt 1, eighteen Sprague–Dawley dams and twelve age-matched virgins (controls) were fed a low-fat diet (LF; 11 % energy as safflower oil) for 7–63 d. At postpartum (day 0), peak lactation (day 15) and post-lactation (day 56) and after 7 d in virgins, the pancreas was removed for mRNA and enzyme analyses. In Expt 2, thirty-six Sprague–Dawley dams were fed LF until day 9 postpartum when dams were divided into three groups of twelve; one continued to be fed LF, one was fed a moderate-fat diet (MF; 40 % energy as safflower oil); and one was fed a high-fat diet (HF; 67 % energy as safflower oil) diet. At peak lactation (day 15) and post-lactation (day 56), the pancreas was removed for mRNA and enzyme analyses. Expt 1 revealed that lactation and post-lactation significantly (P<0·001) decreased PL mRNA (67 % and 76 %, respectively), but only post-lactation decreased PL activity. Increased dietary fat in Expt 2 significantly increased PL mRNA (LF<MF<HF, P<0·001) and PL activity (LF<MF=HF, P<0·02) in both lactation and post-lactation. In summary, lactation and post-lactation decreased PL mRNA significantly even though dietary fat still regulated PL activity and mRNA in lactation and post-lactation.

Cellular retinol-binding protein type II (CRBPII) is involved in the transport of vitamin A and its metabolism in the small intestine. In the present study, we demonstrated diet-related variations in CRBPII expression in rat jejunum. The CRBPII protein and mRNA levels increased in parallel after the start of feeding period regardless of whether the feeding period was restricted to the hours of darkness or of light. In addition, this variation was observed in the rats fed high-fat diet or low-fat diets, but not in those fed a fat-free diet or in fasted rats. A similar diet-induced variation was seen in the mRNA of liver-type fatty acid-binding protein in rat jejunum. In the transient transfection experiment, unsaturated fatty acid increased rat CRBPII gene promoter activity via the PPARα/retinoid X receptor-α heterodimer. Taken together, these results suggest that the diet-related variation in CRBPII expression in rat jejunum may be brought about by the transcriptional induction of CRBPII gene expression mainly triggered by dietary fatty acids.

The relative benefit of replacing saturated fatty acid with linoleic acids is still being debated because a linoleic acid-enriched diet increases oxidative and inflammatory stresses, although it is associated with a reduction in serum cholesterol levels. The present study was conducted to evaluate the effect of dietary supplementation of linoleic acid-rich (HL) fat, compared with a saturated fatty acid-rich (SF) fat on atherosclerotic lesion areas, serum and liver cholesterol levels, oxidative stress (urinary isoprostanes and serum malondialdehayde) and inflammatory stress (expression of aortic monocyte chemoattractant protein-1; MCP-1) in apo E-deficient mice. Male and female apo E-deficient mice (8 weeks old; seven to eight per group) were fed an AIN-76-based diet containing SF fat (50 g palm oil and 50 g lard/kg) or HL fat (100 g high-linoleic safflower-seed oil/kg) for 9 weeks. Compared with the SF diet, the HL diet lowered atherosclerosis (P<0·05). It reduced serum total cholesterol levels (P<0·05), increased HDL-cholesterol levels (P<0·05) and lowered liver esterified cholesterol levels (P<0·01). The HL diet-fed mice showed increased expression of MCP-1 mRNA (P<0·05), serum levels of malondialdehayde (P<0·05) and urinary excretion of 2,3-dinor-5,6-dihydro-8-iso-prostaglandin F2α; P<0·05). These results suggest that having biomarkers in vivo for oxidative stress and inflammatory status of endothelial cells does not necessarily indicate predisposition to an increased lesion area in the aortic root in apo E-deficient mice fed an HL or SF diet.

We examined the effects of adzuki bean resistant starch on serum cholesterol and hepatic mRNA in rats fed a cholesterol diet. The mRNA coded for key regulatory proteins of cholesterol metabolism. The control rats were fed 15 % cornstarch (basal diet, BD). The experimental rats were fed BD plus a 0·5 % cholesterol diet (CD), or a 15 % adzuki resistant starch plus 0·5 % cholesterol diet (ACD) for 4 weeks. The serum total cholesterol and VLDL + intermediate density lipoprotein + LDL-cholesterol levels in the ACD group were significantly lower than those in the CD group throughout the feeding period. The total hepatic cholesterol concentrations in the CD and ACD groups were not significantly different. The faecal total bile acid concentration in the ACD group was significantly higher than that in the BD and CD groups. Total SCFA and acetic acid concentrations in the ACD group were significantly higher than those in the CD group but there were no significant differences in the concentrations between the ACD and BD groups. The hepatic LDL-receptor mRNA and cholesterol 7α-hydroxylase mRNA levels in the ACD group were significantly higher than those in the CD group and the hepatic 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase mRNA level in the ACD group was significantly lower than in the CD group. The results suggest that adzuki resistant starch has a serum cholesterol-lowering function via enhancement of the hepatic LDL-receptor mRNA and cholesterol 7α-hydroxylase mRNA levels and faecal bile acid excretion, and a decrease in the hepatic HMG-CoA reductase mRNA level, when it is added to a cholesterol diet.

Intravenous lipid emulsions (ILE) have demonstrated advantages including prevention of essential fatty acid (EFA) deficiency; however, too much EFA can down regulate fatty acid elongation leading to an imbalance of nutritional compounds in plasma and cell membranes. An olive oil-based ILE containing long-chain triacylglycerols (LCT) with a low content (20 %) of PUFA was administered for home parenteral nutrition (HPN) and compared with a conventional soyabean oil-based ILE (PUFA content, 60 %). Thirteen patients (26–92 years) with stable intestinal failure were randomised after a 1-month run-in period with a medium-chain triacylglycerols–LCT-based ILE, to receive 3 months of HPN with either olive oil- (n 6) or soyabean oil-based (n 7) ILE. The nutritional impact and safety of HPN, oral intakes and absorption rates, phospholipid fatty acids in plasma and lymphocyte cell membrane were assessed. The only clinical event reported was one case of pneumonia (soya group). In both groups, 20 : 3n-9:20:4n-6 ratios remained within normal ranges (0·03–0·07). There was a significant increase of γ-linolenic acid (γ-LA) in plasma and lymphocyte cell membrane (P=0·02) and of oleic acid in plasma (P<0·01) in the olive compared with the soya group. A significant correlation was found between γ-LA (day 90 – day 0) in plasma and PUFA parenteral intakes (P=0·02), but neither with fat intakes nor with fat absorption rates. In conclusion, plasma and lymphocyte EFA pattern remained in normal ranges without EFA deficiency with both lipid emulsions, despite a lower content of n-3 and n-6 series with the olive oil-based ILE.

The glycaemic response to eight potato varieties commercially available in Great Britain was compared against a glucose standard in a non-blind, randomised, repeated measure, crossover design trial. Seventeen healthy subjects (three males, fouteen females), mean age 32 (sd 13) years and mean BMI 22·3 (sd 3·6) kg/m2, were recruited to the study. Subjects were served portions of eight potato varieties and a standard food (glucose), on separate occasions, each containing 50 g carbohydrate. Capillary blood glucose was measured from finger-prick samples in fasted subjects (0 min) and at 15, 30, 45, 60, 90 and 120 min after the consumption of each test food. For each potato variety, the glycaemic index (GI) value was calculated geometrically by expressing the incremental area under the blood glucose curve (IAUC) as a percentage of each subject's average IAUC for the standard food. The eight potato varieties exhibited a wide range in GI values from 56 to 94. A trend was seen whereby potatoes with waxy textures produced medium GI values, whilst floury potatoes had high GI values. Considering the widespread consumption of potatoes in Great Britain (933–1086 g per person per week), this information could be used to help lower the overall GI and glycaemic load of the diets of the British population.

The objective of this paper is to provide glycaemic index (GI) and glycaemic load (GL) values for a variety of foods that are commercially available in the UK and to compare these with previously published values. Fasted subjects were given isoglucidic (50 or 25 g carbohydrate) servings of a glucose reference at least two to three times, and test foods once, on separate occasions. For each test food, tests were repeated in at least eight subjects. Capillary blood glucose was measured via finger-prick samples in fasting subjects (0 min) and at 15, 30, 45, 60, 90 and 120 min after the consumption of each test food. The GI of each test food was calculated geometrically by expressing the incremental area under the blood glucose response curve (IAUC) of each test food as a percentage of each subject's average IAUC for the reference food. GL was calculated as the product of the test food's GI and the amount of available carbohydrate in a reference serving size. The majority of GI values of foods tested in the current study compare well with previously published values. More importantly, our data set provides GI values of several foods previously untested and presents values for foods produced commercially in the UK.

Insulin use is common in type 2 diabetes and is frequently accompanied by weight gain, the composition of which is poorly understood. The present study evaluates insulin-induced body composition changes. Body weight and composition of thirty-two type 2 diabetic patients undergoing their first 12 months of insulin therapy were compared with those observed in thirty-two type 2 diabetic patients previously treated on insulin (minimum 1 year). Body composition was determined by simultaneous body water spaces (bioelectrical impedance analysis) and body density measurements. After 6 months, glycosylated Hb (HbA1c) significantly improved in the newly treated group (P<0·0001), but remained stable in those treated previously. HbA1c did not differ between 6 and 12 months in the two groups. Body weight significantly (P=0·04) changed over 12 months in those newly treated only (+2·8 kg), essentially comprising fat-free mass (P=0·044). Fat mass remained unchanged (P=0·85) as did total body water, while extracellular: total body water ratio tended to increase in those newly treated (P=0·059). Weight changes correlated with HbA1c changes (R2 0·134, P=0·002) in the initial 6 months only. Insulin therapy leads to weight gain (2·8 kg), predominantly fat-free mass, over 12 months. After 6 months, newly treated patients continued gaining weight despite an unchanged HbA1c, suggesting the potential anabolic role of insulin in subsequent gains. Therefore, in the initial 6 months, weight gain can be attributed to a ‘glucose control-related effect’ and further gain appears to be due to a ‘non-glucose control-related’ effect of insulin treatment.

The prenatal diet can program an individual's cardiovascular system towards later higher resting blood pressure and kidney dysfunction, but the extent to which these programmed responses are directly determined by the timing of maternal nutritional manipulation is unknown. In the present study we examined whether maternal nutrient restriction targeted over the period of maximal placental growth, i.e. days 28–80 of gestation, resulted in altered blood pressure or kidney development in the juvenile offspring. This was undertaken in 6-month-old sheep born to mothers fed control (100–150 % of the recommended metabolisable energy (ME) intake for that stage of gestation) or nutrient-restricted (NR; 50 % ME; n 6) diets between days 28 and 80 of gestation. Controls were additionally grouped according to normal (>3, n 7) or low body condition score (LBCS; <2, n 6), thereby enabling us to examine the effect of maternal body composition on later cardiovascular function. From day 80 to term (approximately 147 d) all sheep were fed to 100 % ME. Offspring were weaned at 12 weeks and pasture-reared until 6 months of age when cardiovascular function was determined. Both LBCS and NR sheep tended to have lower resting systolic (control, 85 (SE 2); LBCS, 77 (SE 3); NR, 77 (SE 3) mmHg) and diastolic blood pressure relative to controls. Total nephron count was markedly lower in both LBCS and NR relative to controls (LBCS, 59 (SE 6); NR, 56 (SE 12) %). Our data suggest that maternal body composition around conception is as important as the level of nutrient intake during early pregnancy in programming later cardiovascular health.

The objective of the present study was to investigate the postprandial metabolism of two starches with contrasting rates of hydrolysis in vitro. Characterized using the Englyst method of in vitro starch classification, C*Set 06 598 contained predominantly rapidly digestible starch and C*Gel 04 201 contained predominantly slowly digestible starch. Each test starch, naturally enriched with 13C, was fed to ten healthy female volunteers as part of a moderate fat test meal (containing 75 g test starch and 21 g fat), in a double-blind randomized crossover design. The metabolic response to each starch was measured after an overnight fast, in an acute 6 h study, before and after 14 d of daily consumption of 75 g test starch. During each acute study, blood samples were taken at 15 min intervals for the first 2 h and at 30 min intervals for the remaining 4 h. Breath 13CO2 enrichment was measured at the same time points and indirect calorimetry was performed for 20 min every 40 min immediately before and throughout the study. Significantly more rapid, greater changes in postprandial plasma glucose, NEFA and serum insulin concentrations were observed after consumption of the rapidly digestible starch. Breath 13CO2 output over the first 3–4 h rose rapidly then began to decline following consumption of the rapidly digestible starch, but plateaued for the slowly digestible starch. The 14 d adaptation period did not affect any of the glycaemic or lipaemic variables but there was a reduction in postprandial plasminogen activator inhibitor-1 concentrations. These data confirm that starches characterized as predominantly rapidly digestible versus slowly digestible by the Englyst procedure provoke distinctly different patterns of metabolism postprandially.

The vitamin K concentration in the circulation and the availability of vitamin K to bone may be affected by factors influencing lipoprotein metabolism, such as apoE genotype. The relationships between markers of vitamin K status, bone mineral content and apoE genotype were studied in healthy older men and women aged 60–83 years, 177 from Shenyang, China, and 132 from Cambridge, UK. Fasting plasma was analysed for vitamin K1, triacylglycerol, total osteocalcin, undercarboxylated osteocalcin (ucOC) and apoE genotype. Hip bone mineral content was measured using dual-energy X-ray absorptiometry. Subjects were grouped according to apoE genotype as E2/3, E3/3 and [E3/4+E4/4]. The mean plasma vitamin K1 concentration of the three genotype groups was significantly higher and the percentage ucOC was lower in the Chinese than in the British subjects (P<0·01). A higher vitamin K1 concentration was found in subjects with [E3/4+E4/4] than those with either E2/3 or E3/3 in Cambridge (32·2 (SE 14·6) %, P=0·03; 24·6 (SE 10·7) %, P=0·02). Similar trends were observed although were not statistically significant in Shenyang (26·5 (18·9) %, P=0·16; 23·1 (13·0) %, P=0·08). Subjects with [E3/4+E4/4] had a lower percentage ucOC (total osteocalcin adjusted) than did those with either E2/3 or E3/3 in Shenyang (65·1 (27·2) %, P=0·02; 49·6 (19·9) %, P=0·01 respectively) but not in Cambridge. This study demonstrates that a superior vitamin K status is associated with the apoE4 genotype in healthy older individuals from China and the UK.

The effects of Se on thyroid metabolism in a New Zealand population are investigated, including (a) the relationship between Se and thyroid status, and (b) the effect of Se supplementation on thyroid status. The data used come from two cross-sectional studies of Se, I, thyroid hormones and thyroid volume (studies 1 and 4), and three Se intervention studies in which thyroid hormones, Se and glutathione peroxidase (GPx) activities were measured (studies 2, 3 and 5). There were no significant correlations between Se status and measures of thyroid status after controlling for sex at baseline or after supplementation in any of the studies. When data from study 4 were divided into two groups according to plasma Se, plasma thyroxine (T4) was lower in males with higher plasma Se levels (P=0·009). Se supplementation increased plasma Se and GPx activity, but produced only small changes in plasma T4 and triiodothyronine (T3):T4 ratio. In study 2, there was a significant reduction in plasma T4 (P=0·0045). In studies 3 and 5 there were small decreases in plasma T4 and a small increase in the T3:T4 ratio, which were not significantly different from placebo groups. Lack of significant associations between plasma Se and thyroid status, and only small changes in T4 suggest that Se status in New Zealand is close to adequate for the optimal function of deiodinases. Adequate plasma Se may be approximately 0·82–0·90 μmol/l, compared with 1·00–1·14 μmol/l for maximal GPx activities.

We evaluated the adverse effect of asymptomatic Helicobacter pylori infection in children on the response to Fe supplementation. One hundred and sixty-nine children aged 1–10 years from the urban poor community underwent a [13C]urea breath test for H. pylori and haematological tests at admission and after 8 weeks. Both H. pylori-positive and -negative children were randomly assigned to receive ferrous fumarate syrup (20 mg elemental Fe twice daily) or placebo for 8 weeks and a single dose of vitamin A (33,000μg). Admission findings were compared between H. pylori-positive and -negative children. Response to Fe was compared between Fe-supplemented H. pylori-positive and -negative children. Seventy-nine per cent of the children were aged 1–5 years and half of them were boys. In eighty-five H. pylori-positive and eighty-four H. pylori-negative children, the differences in mean Hb (112 (sd 12·6) v. 113 (sd 12·0) g/l), haematocrit (34 (sd 3·5) v. 35 (sd 3·2) %) and ferritin (23·8 v. 21·0 μg/l) were similar. After 8 weeks of Fe supplementation, mean Hb was 5·3 g/l more (95 % CI 1·59, 9·0) and haematocrit was 1·4 % more (95 % CI 0·2, 2·6) in H. pylori-negative (n 44) compared with H. pylori-positive (n 42) children. Mean ferritin was similar at admission and improved in both H. pylori-positive and -negative children. Asymptomatic H. pylori infection was not associated with higher rates of anaemia or Fe deficiency in children, but had a significant adverse effect on response to Fe therapy. However, this result is based on exploratory analysis and needs confirmation.

The present study measuring resting energy expenditure (REE; kJ/d) longitudinally using indirect calorimetry in six elderly women aged ≥70 years following surgery for hip fracture, describes changes over time (days 10, 42 and 84 post-injury) and compares measured values to those calculated from routinely applied predictive equations. REE was compared to REE predicted using the Harris Benedict and Schofield equations, with and without accounting for the theoretical increase in energy expenditure of 35 % secondary to physiological stress of injury and surgery. Mean (95 % CI) measured REE (kJ/d) was 4704 (4354, 5054), 4090 (3719, 4461) and 4145 (3908, 4382) for days 10, 42 and 84, respectively. A time effect was observed for measured REE, P=0·003. Without adjusting for stress the mean difference and 95 % limits of agreement for measured and predicted REE (kJ/kg per d) for the Harris Benedict equation were 1 (−9, 12), 10 (2, 18) and 9 (1, 17) for days 10, 42 and 84, respectively. The mean difference and 95 % limits of agreement for measured and predicted REE (kJ/kg per d) for the Schofield equation without adjusting for stress were 8 (−3, 19), 16 (6, 26) and 16 (10, 22) for days 10, 42 and 84, respectively. After adjusting for stress, REE predicted from the Harris Benedict or Schofield equations overestimated measured REE by between 38 and 69 %. Energy expenditure following fracture is poorly understood. Our data suggest REE was relatively elevated early in recovery but declined during the first 6 weeks. Using the Harris Benedict or Schofield equations adjusted for stress may lead to overestimation of REE in the clinical setting. Further work is required to evaluate total energy expenditure before recommendations can be made to alter current practice for calculating theoretical total energy requirements of hip fracture patients.

Endogenous vitamin D deficiency (low serum 25(OH)D3) is a necessary but insufficient requirement for the genesis of vitamin D-deficiency rickets and osteomalacia. The magnitude of the independent contributions of dietary factors to rachitic and osteomalacic risk remains uncertain. We reanalysed two weighed dietary surveys of sixty-two cases of rickets and osteomalacia and 113 normal women and children. The independent associations of four dietary variables (vitamin D, Ca, fibre and meat intakes) and daylight outdoor exposure with rachitic and osteomalacic relative risk were estimated by multivariate logistic regression. Meat and fibre intakes showed significant negative and positive associations respectively with rachitic and osteomalacic relative risk (RR; zero meat intake: RR 29·8 (95 % CI 4·96, 181), P<0·001; fibre intake: RR 1·53 (95 % CI 1·01, 2·32), P+0·043). The negative association of meat intakes with rachitic and osteomalacic relative risk was curvilinear; relative risk did not fall further at meat intakes above 60 g daily. Daylight outdoor exposure showed a significant negative association with combined relative risk (RR 0·33 (95 % CI 0·17, 0·66), P<0·001). Operation of the meat and fibre risk factors was related to sex, age and dietary pattern (omnivore/lactovegetarian), mainly determined by religious affiliation. The mechanism by which meat reduces rachitic and osteomalacic risk is uncertain and appears independent of revised estimates of meat vitamin D content. The meat content of the omnivore Western diet may explain its high degree of protection against nutritional rickets and osteomalacia from infancy to old age in the presence of endogenous vitamin D deficiency.

The aim of this study was to describe dietary glycaemic index (GI) and glycaemic load (GL) values in the diets of Danish children, and to examine the associations between dietary GI, GL and body fatness. Data were collected during 1997–8 as part of the European Youth Heart Study. The study population comprised 485 children aged 10 years and 364 children aged 16 years from Odense County, Denmark. Dietary GI and GL were estimated using international food tables, and the associations between energy-adjusted dietary GI, GL and body fatness were analysed by multiple linear regression. The mean daily dietary GI value was 85 (SD 6·9) with a range of 62–111. No significant differences were found between age groups and gender. The daily dietary GL was higher among boys aged 16, with a GL of 330 (sd 95) (P<0·05), compared with girls or younger boys. Dietary GL was higher among 10-year-old boys than girls (250 (sd 81) v. 230 (sd 66) P<0·05), whereas dietary GL among 16-year-old girls was 230 (sd 56). Neither dietary GI nor GL was associated with the sum of four skinfolds (ΣSF) among girls or among 10-year-old boys. Among 16-year-old boys, significant associations were observed between dietary GI and ΣSF (β+0·60, SE+0·21, P=0·006), and between dietary GL and ΣSF (β+0·15, SE+0.06, P=0·009). In conclusion, dietary GI and GL were positively associated with body fatness among Danish boys aged 16 years, whereas no associations were found among girls or younger boys.