The literature on predefined indexes of overall diet quality is reviewed. Their association with nutrient adequacy and health outcome is considered, but our primary interest is in the make-up of the scores. In total, twenty different indexes have been reviewed, four of which have gained most attention, and many others were based on those four. The various scores differ in many respects, such as the items included, the cut-off values used, and the exact method of scoring, indicating that many arbitrary choices have been made. Correlations in intake between dietary components may not be adequately addressed. In general, diet quality scores show an association with mortality or disease risk, but these relations are generally modest. Existing indexes do not predict morbidity or mortality significantly better than individual dietary factors. Although conclusions from the review may provide guidance in the construction of a diet quality score, it is questionable whether a dietary score can be obtained that is a much better predictor of health outcome.

Growth failure is a common yet complex problem of childhood chronic kidney disease caused by multiple factors encountered due to the primary disease or secondary to the renal impairment. This review seeks to describe the various patho-physiological mechanisms contributing to growth failure in the various stages of childhood with particular emphasis on nutritional problems and endocrine dysfunction encountered whilst managing these children. In addition, we shall examine the role of body composition in chronic kidney disease, their relationship with growth and nutrition and the potential effect of abnormalities in fat mass and lean mass on long-term morbidity and mortality.

Cu and Fe metabolism are known to be linked, but the interactions during pregnancy are less well studied. In the present study we used rats to examine the effect of Cu deficiency during pregnancy on Fe and Cu levels in maternal and fetal tissue and on the gene expression profile of proteins involved in Cu and Fe metabolism in the placenta. Rats were fed diets with different Cu contents before and during pregnancy. Samples were collected on day 21 of gestation. Cu levels, ceruloplasmin activity and serum Fe all decreased in maternal serum of Cu-deficient animals. Maternal liver Fe inversely correlated with liver Cu. Placental Cu levels decreased with no change in Fe. Fe and Cu levels both decreased in the fetal liver. The drop in maternal liver Cu was significantly correlated with a decrease in organ weight of fetal liver, lung and kidney. No changes were observed in mRNA expression of Cu transporter 1, Menkes P-type Cu-ATPase 7A, Wilson P-type Cu-ATPase 7B, cytochrome-c oxidase, and Cu chaperone Atox1 in the placenta of Cu-deficient dams. Transferrin receptor 1 and the Fe-responsive element (IRE)-regulated divalent metal transporter 1 (DMT1) were up regulated; while ferroportin and non-IRE1-regulated DMT1 levels did not change. These data show that Cu deficiency during pregnancy not only has a direct effect on Fe levels but also regulates the expression of Fe transporters. The pattern closely mirrors that seen in Fe deficiency, suggesting that the changes are a consequence of the decrease in serum Fe, implying that the developing fetus not only suffers from Cu, but also from Fe deficiency.

Human zinc deficiency is thought to be prevalent worldwide, particularly in populations with diets low in zinc and animal protein and high in inhibitors of zinc absorption, such as phytic acid. Confirmation of zinc deficiency is, however, difficult in the absence of a reliable and sensitive marker of zinc status. Under controlled conditions, T-lymphocyte metallothionein-2A (MT-2A) mRNA levels change in relation to zinc status and the objective of the present study was to investigate whether these transcript levels could be related to dietary zinc intake, plasma zinc or other biochemical parameters influenced by, or influencing, zinc metabolism in human subjects likely to be zinc deficient. Rural Koreans (n 110, age 50–80 years) with a range of zinc and phytic acid dietary intake were recruited for the study and blood samples were analysed for plasma zinc, HDL, LDL, α-tocopherol and thiobarbituric acid reactive substances, mononuclear cell (MNC) MT-2A mRNA, serum protein and albumin, and blood haematocrit, Hb and glucose. Multiple correlation and principal component analysis showed a significant negative correlation between plasma zinc and MNC MT-2A mRNA levels. Female subjects had higher MT-2A transcript levels than males and MT-2A mRNA levels tended to increase with age. There was no significant association between dietary zinc intake or any index of zinc intake relating to dietary inhibitors of zinc absorption. It is concluded that MNC MT-2A mRNA levels cannot be used to predict poor zinc nutrition.

To examine the associations of total plasma homocysteine (tHcy) with physical activity, cardiorespiratory fitness and fatness in children and adolescents, a cross-sectional study of 301 children (9–10 years old) and 379 adolescents (15–16 years old) was conducted. Physical activity was measured by accelerometry. Cardiorespiratory fitness was measured with a maximal ergometer bike test. Body fat was derived from the sum of five skinfold thicknesses. Genotyping for the methylenetetrahydrofolate reductase (MTHFR) 677C>T polymorphism was done by DNA sequencing. Fasting tHcy level was the outcome variable. Multiple regressions were used to determine the degree to which variance in tHcy was explained by physical activity, cardiorespiratory fitness and body fat, after controlling for potential confounders including MTHFR 677C>T genotype. tHcy levels were neither associated with any measure of level and pattern of physical activity nor with data on cardiorespiratory fitness, or body fat, in any age group after controlling for potential confounders including MTHFR 677C>T and even when subgroups 677TT and 677CC+CT were analysed separately. Mean values of tHcy were significantly higher in the TT subgroup compared with CC and CT subgroups in children (TT 7·4 μmol/l, CC 6·3 μmol/l, CT 6·6 μmol/l, P < 0·001 and P = 0·019, respectively) and adolescents (TT 16·9 μmol/l, CC 8·3 μmol/l, CT 9·0 μmol/l, both P < 0·001). The results suggest that physical activity, fitness and body fat are not associated with tHcy levels in children and adolescents, even after controlling for presence of the MTHFR 677C>T genotype, the main influence on tHcy levels in these subjects.

Liver fatty acid metabolism of male rats fed on a vitamin A-deficient diet for 3 months from 21 d of age was evaluated. Vitamin A restriction produced subclinical plasma and negligible liver retinol concentrations, compared with the control group receiving the same diet with 4000 IU vitamin A (8 mg retinol as retinyl palmitate)/kg diet. Vitamin A deficiency induced a hypolipidaemic effect by decreasing serum triacylglycerol, cholesterol and HDL-cholesterol levels. The decrease of liver total phospholipid was associated with low phosphatidylcholine synthesis observed by lower [14C]choline incorporation into phosphatidylcholine, compared with control. Also, liver fatty acid synthesis decreased, as was indicated by activity and mRNA expression of acetyl-CoA carboxylase (ACC), and incorporation of [14C]acetate into saponified lipids. A decrease of the PPARα mRNA expression was observed. Liver mitochondria of vitamin A-deficient rats showed a lower total phospholipid concentration coinciding with a decrease of the cardiolipin proportion, without changes in the other phospholipid fractions determined. The mitochondria fatty acid oxidation increased by 30 % of the control value and it was attributed to a high activity and mRNA expression of carnitine palmitoyltransferase-I (CPT-I). An increase in serum β-hydroxybutyrate levels was observed in vitamin A-deficient rats. Vitamin A deficiency alters the mitochondria lipid composition and also enhances fatty acid oxidation by modifiying the production of malonyl-CoA, the endogenous inhibitor of CPT-I, due to decreased activity of liver ACC. The incorporation of vitamin A into the diet of vitamin A-deficient rats reverted all the changes observed.

Conjugated linoleic acid (CLA) is a group of positional and geometric isomers of conjugated dienoic derivatives of linoleic acid. The present study was designed to determine whether 14-week CLA supplementation as triacylglycerols (3·76 g) with a 50 : 50 combination of the two main isomers (35 % cis-9, trans-11 and 35 % trans-10, cis-12) added to flavoured yoghurt-like products was able to alter body composition in healthy subjects and to alter the expression of several key adipose tissue genes (PPAR γ, lipoprotein lipase (LPL), hormone-sensitive lipase (HSL) and uncoupling protein 2 (UCP-2)). Forty-four healthy subjects were randomly assigned to consume daily either a CLA-supplemented yoghurt-like product or a placebo yoghurt for 98 d. There were no significant effects of CLA supplementation on body weight, fat mass or free fat mass. Basal energy expenditure expressed as kg free fat mass increased significantly in the CLA group (123·3 (sem 2·5) kJ/kg free fat mass per d on day 98 v. 118·7 (sem 2·3) kJ/kg free fat mass per d on day 0, P = 0·03). PPAR γ mRNA gene expression increased significantly with CLA supplementation (53 (sem 20) %, P < 0·01) and a significant reduction in mRNA levels of HSL was observed ( − 42 (sem 7) %, P = 0·01). The levels of UCP-2 and LPL mRNA were not affected. The present results suggest that a 98 d supplementation diet with a 50 : 50 mixture of the two CLA isomers cis-9, trans-11 and trans-10, cis-12 in a dairy product was unable to alter body composition, although a significant increase in the RMR has been induced. Moreover, changes in mRNA PPAR γ and HSL in adipose tissue were recorded.

Marine oil-derived n-3 fatty acids have been shown to stimulate intestinal Ca absorption in animal studies, but the effects of such fatty acids on Ca absorption in human subjects are relatively unknown. In particular, n-3 fatty acids may be of therapeutic value for some Crohn's disease patients who experience Ca malabsorption. Therefore, the aim of the present study was to investigate the effect of 20 : 5n-3 and 22 : 6n-3 on transepithelial Ca transport across monolayers of healthy Caco-2 cells as well as of TNF-α-treated Caco-2 cells (an in vitro model of Crohn's disease). Caco-2 cells were seeded onto permeable filter supports and allowed to differentiate into monolayers, which were treated with 80 μm-20 : 5n-3, 80 μm-22 : 6n-3, or 40 μm-20 : 5n-3+40 μm-22 : 6n-3 for 6 or 8 d, with or without co-treatment with TNF-α (10 ng/ml) (n 11–15 monolayers per treatment). On day 16, transepithelial and transcellular transport of 45Ca and fluorescein transport (a marker of paracellular diffusion) were measured. Treatment of healthy and inflamed Caco-2 cells with 20 : 5n-3, 22 : 6n-3 and both fatty acids combined for 8 d significantly (P < 0·005–0·01) increased total transepithelial Ca transport compared with that in control, effects which were mediated by an enhanced rate of transcellular Ca transport. The effects of n-3 fatty acids on Ca absorption after 6 d were less clear-cut. In conclusion, the present in vitro findings highlight the need to investigate the effect of marine oil-based n-3 fatty acids on Ca absorption in vivo in studies of healthy human subjects as well as of Crohn's disease patients.

The effects of graded levels (0 %, 0·5 %, 0·75 and 1 %) of dietary conjugated linoleic acid (CLA) were assessed on 97 g rainbow trout. Fish were fed to satiation twice a day for 12 weeks. At the end of the experiment, all groups of fish weighed more than 250 g and no significant differences were detected in growth performance, feed conversion, nutrient or energy utilisation or body composition between treatments. A decrease in liver lipid content resulted from including CLA and was accompanied by a reduction in malic enzyme activity. The muscle saturated acid and PUFA content did not vary between dietary treatments, despite the increasing concentration of stearic acid and CLA. In the liver, however, both fractions increased significantly with dietary CLA. Moreover, the MUFA decreased significantly in both muscle and liver. CLA was incorporated into tissue lipids, with levels in flesh (2·1–4·2 %) being 2-fold higher than in liver (0·8–1·9 %). In muscle, the percentage of cis-9, trans-11 isomer ranged from 39·5 % to 41·8 % and that of trans-10, cis-12 isomer from 31·4 % to 33·4 % of total CLA. The incorporation of CLA isomers in the liver varied with dietary treatment, and the cis-9, trans-11 isomer seemed to be more efficiently incorporated than trans-10, cis-12. Sensory data indicated slight-to-moderate differences between the trout fed with and without CLA. The present results suggest that 250 g rainbow trout can incorporate CLA in both muscle and liver, contributing to the production of a functional food.

Forty-eight, 21-d-old pigs were used to examine the effects of different types of cooked white rice on starch digestion, digesta and fermentation characteristics, shedding of β-haemolytic Escherichia coli and performance after weaning. Pigs received one of three rice-based diets: (i) medium-grain Amaroo (AM), (ii) long-grain Doongara (DOON), and (iii) waxy (WAXY). The remainder of the diet consisted predominantly of animal proteins. A fourth diet contained mainly wheat, barley and lupins (WBL). On days 1, 3, 7 and 9 after weaning, a faecal swab was taken for assessment of β-haemolytic E. coli and faecal consistency. Apparent digestibility of starch measured in the ileum 14 d after weaning was highest (P = 0·004) in AM and WAXY and lowest, but the same (P>0·05), in DOON and WBL. Starch digestibility in the rectum was highest in all rice diets (P < 0·001). Digesta viscosity was highest in pigs fed WBL in both the ileum (P < 0·001) and caecum (P = 0·027). Pigs fed rice generally had lighter (P < 0·05) gastrointestinal organs than pigs fed WBL. Performance of pigs was similar for all treatments; however, pigs fed rice-based diets had a higher (P < 0·001) carcass percentage than pigs fed WBL. Pigs fed WBL produced more acid (P < 0·05) but had lower molar proportions of acetate (P < 0·05), isobutyrate (P < 0·01) and isovalerate (P < 0·001) and a higher molar proportion of butyrate (P < 0·01) in the large intestine than pigs fed rice. Shedding of E. coli was low; however, pigs fed AM and WBL shed less E. coli than pigs fed other diets.

Protein–energy malnutrition is a syndrome in which anaemia together with multivitamin and mineral deficiency may be present. The pathophysiological mechanisms involved have not, however, yet been completely elucidated. The aim of the present study was to evaluate the pathophysiological processes that occur in this anaemia in animals that were submitted to protein–energy malnutrition, in particular with respect to Fe concentration and the proliferative activity of haemopoietic cells. For this, histological, histochemical, cell culture and immunophenotyping techniques were used. Two-month-old male Swiss mice were submitted to protein–energy malnutrition with a low-protein diet (20 g/kg) compared with control diet (400 g/kg). When the experimental group had attained a 20 % loss of their original body weight, the animals from both groups received, intravenously, 20 IU erythropoietin every other day for 14 d. Malnourished animals showed a decrease in red blood cells, Hb concentration and reticulocytopenia, as well as severe bone marrow and splenic atrophy. The results for serum Fe, total Fe-binding capacity, transferrin and erythropoietin in malnourished animals were no different from those of the control animals. Fe reserves in the spleen, liver and bone marrow were found to be greater in the malnourished animals. The mixed colony-forming unit assays revealed a smaller production of granulocyte–macrophage colony-forming units, erythroid burst-forming units, erythroid colony-forming units and CD45, CD117, CD119 and CD71 expression in the bone marrow and spleen cells of malnourished animals. These findings suggest that, in this protein–energy malnutrition model, anaemia is not caused by Fe deficiency or erythropoietin deficiency, but is a result of ineffective erythropoiesis.

Excessive I in the diet of pregnant sheep can reduce the concentration of antibodies in the blood plasma of the lambs after they have consumed colostrum. Our aim was to determine the dose of dietary I that would avoid this effect, and to relate this to changes in the concentrations of hormones and metabolites in the lambs. Four groups of pregnant ewes received concentrate containing 5·5, 9·9, 14·8, and 21·0 mg I/kg DM, respectively. Hay and molasses (containing 0·16 and 0·29 mg I/kg DM, respectively) were available ad libitum. The lambs were prevented from suckling for the first 24 h of life and were fed a fixed quantity of artificial colostrum in four feeds. At 24 h, the average plasma concentrations of immunoglobulin G in the lambs were 6·08, 5·06, 3·18 and 3·10 g/l for the 5·5, 9·9, 14·8 and 21·0 mg/kg groups, respectively. Supplementation with I was associated with higher levels of tri-iodothyronine and thyroxine in the lambs at birth. There was no effect of treatment on the plasma concentrations of insulin, cortisol, glucose or NEFA in the lambs. The concentration of dietary I that had an effect on the immunoglobulin concentration in the lambs is marginally above the levels added to commercial concentrate feeds; we tentatively identify 9·9 mg I/kg DM (approximately 9 mg I/ewe per day) as the upper safe limit of I supplementation according to the criterion of the concentration of immunoglobulin G in the plasma of lambs at 24 h after birth.

Experimental evidence suggests that most herbs and spices possess a wide range of biological and pharmacological activities that may protect tissues against O2-induced damage. The objectives of the present study were: first, to determine the effects of plant extracts on the viability, membrane integrity, antioxidant status and DNA integrity of Caco-2 cells and second, to investigate the cytoprotective and genoprotective effects of these plant extracts against oxidative stress in Caco-2 cells. The plant extracts examined were rosemary (Rosmarinus officinalis L.), oregano (Origanum vulgare L.), sage (Salvia officinalis L.) and echinacea (Echinacea purpurea L.). Cell membrane integrity was assessed by the lactate dehydrogenase release assay. Viability was determined by the neutral red uptake assay (NRUA) and the concentration of compound that resulted in 50 % cell death (IC50) was calculated. Antioxidant status of the cells was assessed by measuring GSH content, catalase activity and superoxide dismutase activity. To examine their cytoprotective and genoprotective effects, Caco-2 cells were pre-treated with each plant extract for 24 h followed by exposure to H2O2. DNA damage was assessed by the comet assay and cell injury was determined by the NRUA. Rosemary was the most toxic (IC50 123 μg/ml) and echinacea the least toxic (IC50 1421 μg/ml). Sage was the only plant extract to affect the antioxidant status of the cells by increasing GSH content. Sage, oregano and rosemary protected against H2O2-induced DNA damage (olive tail moment and percentage tail DNA), whereas protection against H2O2-induced cytotoxicity was afforded by sage only.

Xanthophylls, such as lutein and zeaxanthin, have received increasing interest in recent years because of positive correlations between their consumption and the prevention of eye diseases. Numerous human intervention studies have been conducted with lutein to estimate the bioavailability from different formulations. The present study was designed to obtain basic data on the absorbance efficiency of the monohydroxylated counterparts of lutein and zeaxanthin: α- and β-cryptoxanthin. A corn-oil-based diet comprising ß-cryptoxanthin from papaya purée and α-cryptoxanthin from green carrot leaves was fed to five female Wistar rats for 8 consecutive days at a rate of 17·3 nmol/d and 9·2 nmol/d, respectively. The identity of the xanthophylls in the supplement was ascertained by LC-(APCI)MS analyses, and xanthophylls present in liver and plasma samples were determined by HPLC/diode array detector (DAD). The β-cryptoxanthin concentrations of rat livers in the treatment group were statistically distinguishable (P < 0·01) from those present in the livers of the control group that were fed a basic diet. α-Cryptoxanthin, the second xanthophyll present in the supplement, was not found in rat livers in the treatment group. Plasma samples were free of xanthophylls. This is the first report proving that β-cryptoxanthin has a higher absorption efficiency than α-cryptoxanthin in rats, at least from a minimally processed oil-based xanthophyll supplement.

Previous clinical vitamin A trials have found no consistent effect on diarrhoeal disease and respiratory tract infection. These inconsistent results may be due to the distinct effects vitamin A supplementation has among children stratified by factors related to socio-economic status, nutritional status and season. We evaluated the effect of supplementation on the overall incidence of diarrhoeal disease and respiratory tract infections and on the incidence among children stratified by these factors. A total of 188 children, aged 6–15 months, from periurban, marginalized communities of Mexico City were assigned to receive vitamin A ( < 12 months of age, 20 000 IU retinol; ≥ 12 months, 45 000 IU retinol) or a placebo every 2 months, and were followed for up to 15 months. Project personnel visited households twice a week to determine the onset and duration of diarrhoeal disease and respiratory tract infections. Vitamin A supplementation had no significant effect on risk of overall diarrhoeal disease but reduced mild watery diarrhoea (incidence rate ratio (RR) 0·69; 95 % CI 0·50, 0·93) and cough with fever (RR 0·69; 95 % CI 0·48, 0·98). Vitamin A supplementation decreased diarrhoeal disease during the summer (RR 0·74; 95 % CI 0·57, 0·94), among non-stunted children (RR 0·69; 95 % CI 0·52, 0·93) and among children from households with better socio-economic measures. Heterogeneity in the response to vitamin A supplementation may reflect heterogeneity in the aetiology and epidemiology of diarrhoeal disease and respiratory tract infections and the impact that supplementation has on the immune response.

Elevated breast milk (BM) Na concentration is regarded as responsible for elevated Na intake. To verify the clinical significance of milk Na concentration, we studied the relationship between BM Na+ concentration and infants' daily Na+ intake, infants' daily BM intake (DBMI) and percentage weight loss (%WL) in healthy newborn infants. All mothers who gave birth to a single healthy infant, between February and March 2004 at the Obstetric Clinic of University of Messina (Italy), were invited to participate if they were willing to attempt to breastfeed exclusively. BM Na+ concentration, DBMI, Na+ intake and %WL were determined on the third day after delivery. Statistical analysis was performed by Spearman's correlation test, classification and regression trees and the generalised linear model. Of the 270 eligible mothers, 208 participated in the study. The results showed that on the third day postpartum BM Na+ concentration was 23·05 (sd 1·10) mmol/l, mean DBMI was 202 (sd 68·9) g/d, and mean Na+ intake was 4·36 (sd 0·22) mmol/d and 1·36 (sd 0·07) mmol/kg per d. BM Na+ concentration was inversely related to infant DBMI, and Na+ intake was directly related to infant DBMI and not to BM Na+ concentration. %WL was significantly correlated only to DBMI. In conclusion, the present data demonstrate, for the first time, that when lactogenesis is suboptimal, BM Na+ concentration is higher, but infants' Na+ intake is lower. Finally, the present data probably suggest that for the clinical assessment of breast-feeding, evaluation of milk intake remains the best method.

Interest in functional foods is increasing. The aim of the present study was to investigate breads supplemented with functional components. One was bread supplemented with inulin, linseed and soya fibre (prebiotic bread). The other was a prebiotic antioxidant bread (pre-aox-bread), which additionally contained green tea powder, herbs and tomato paste. The effects of these two breads on immunological and antioxidative parameters were compared with control bread (placebo). Twenty smokers and eighteen non-smokers were enrolled in the randomised parallel study, which consisted of a control period and an intervention period, each lasting for 5 weeks. Daily intake of bread and nutrients did not differ between the intervention and the control period. Most of the twenty-three investigated immunological parameters measured in peripheral blood were unaffected. However, the percentage of CD19 increased after intervention with prebiotic bread, whereas intercellular adhesion molecule-1 (ICAM-1) and CD3+NK+ (P < 0·05) decreased in both intervention arms. The ferric reducing ability of plasma (FRAP) was increased after consumption of the pre-aox-bread for non-smokers (1256 v. 1147 μmol/l; P = 0·019) and remained unchanged for smokers consuming the pre-aox-bread. All analysed carotenoids (P ≤ 0·001) in plasma were increased after the consumption of pre-aox-bread. The concentrations of uric acid and α-tocopherol rose after intervention with both breads. ICAM-1 as a marker of stress decreased after consuming the prebiotic bread. In conclusion, increased plasma concentrations of carotenoids and the responses observed with the FRAP assay after intervention with the pre-aox-bread indicate a unique response in terms of antioxidative potentials for this type of functional food.

Serum Se concentrations and dietary Se intakes have been determined in relation to age, sex, ethnicity, region and index of deprivation in a nationally representative sample of New Zealand children aged 5–14 years from the 2002 National Children's Nutrition Survey. Dietary intake was assessed from computer-assisted, multiple-pass 24 h diet recall interviews (n 3275). Serum Se concentrations were obtained from a subset of urban-based children (n 1547). Mean (95 % CI) serum Se concentration in children was 0·96 (0·93, 1·00) μmol/l. Males (1·00 μmol/l) had higher serum Se levels than females (0·93 μmol/l; P = 0·027). Mäori children had lower serum Se than Pacific Islands children (P = 0·038) and New Zealand European and Other children (P = 0·005). Children in the Upper North Island (1·06 μmol/l) had higher mean serum Se values than those in the Lower North Island (0·98 μmol/l, P < 0·0005) and South Island (0·79 μmol/l, P < 0·0005), and serum Se in the Lower North Island was higher than that in the South Island (P < 0·0005). Mean dietary Se intake was 36 (34, 37) μg/d. The intakes of children aged 5–6 years (31 μg/d) were lower than those of children aged 7–10 and 11–14 years (35 and 38 μg/d, respectively; P < 0·00 005) and the intakes of 7–10-year-olds were lower than those of 11–14-year-olds (P = 0·002). Serum Se was associated with dietary Se after adjusting for all variables, including region (P = 0·006). The Se status of our children falls in the middle of the international range of serum Se concentrations, but that for children in the South Island is among the lowest values reported and may be a cause for concern.

Deficiency of oestrogen at menopause decreases intestinal Ca absorption, contributing to a negative Ca balance and bone loss. Mg deficiency has also been associated with bone loss. The purpose of the present investigation was to test the hypothesis that treatment with a spray-dried mixture of chicory oligofructose and long-chain inulin (Synergy1; SYN1) would increase the absorption of both Ca and Mg and alter markers of bone turnover. Fifteen postmenopausal women (72·2 (sd 6·4) years) were treated with SYN1 or placebo for 6 weeks using a double-blind, placebo-controlled, cross-over design. Fractional Ca and Mg absorption were measured using dual-tracer stable isotopes before and after treatment. Bone turnover markers were measured at baseline, 3 and 6 weeks. Fractional absorption of Ca and Mg increased following SYN1 compared with placebo (P < 0·05). Bone resorption (by urinary deoxypyridinoline cross-links) was greater than baseline at 6 weeks of active treatment (P < 0·05). Bone formation (by serum osteocalcin) showed an upward trend at 3 weeks and an increase following 6 weeks of SYN1 (P < 0·05). Closer examination revealed a variation in response, with two-thirds of the subjects showing increased absorption with SYN1. Post hoc analyses demonstrated that positive responders had significantly lower lumbar spine bone mineral density than non-responders (dual X-ray absorptiometry 0·887 ± 0·102 v. 1·104 ± 0·121 g/cm2; P < 0·01), and changes in bone turnover markers occurred only in responders. These results suggest that 6 weeks of SYN1 can improve mineral absorption and impact markers of bone turnover in postmenopausal women. Further research is needed to determine why a greater response was found in women with lower initial spine bone mineral density.