The objective of the present paper is to review the methods of measuring micronutrient intake adequacy for individuals and for populations in order to ascertain best practice. A systematic review was conducted to locate studies on the methodological aspects of measuring nutrient adequacy. The results showed that for individuals, qualitative methods (to find probability of adequacy) and quantitative methods (to find confidence of adequacy) have been proposed for micronutrients where there is enough data to set an average nutrient requirement (ANR). If micronutrients do not have ANR, an adequate intake (AI) is often defined and can be used to assess adequacy, provided the distribution of daily intake over a number of days is known. The probability of an individual's intake being excessive can also be compared with the upper level of safe intake and the confidence of this estimate determined in a similar way. At the population level, adequacy can be judged from the ANR using the probability approach or its short cut – the estimated average requirement cut-point method. If the micronutrient does not have an ANR, adequacy cannot be determined from the average intake and must be expressed differently. The upper level of safe intake can be used for populations in a similar way to that of individuals. All of the methodological studies reviewed were from the American continent and all used the methodology described in the Institute of Medicine publications. The present methodology should now be adapted for use in Europe.

Magnesium deficiency may be induced by a diet impoverished in magnesium. This nutritional deficit promotes chronic inflammatory and oxidative stresses, hyperexcitability and, in mice, susceptibility to audiogenic seizures. Potentiation by low-magnesium concentrations of the opening of N-methyl-d-aspartate (NMDA) receptor/calcium channel in in vitro and ex vivo studies, and responsiveness to magnesium of in vivo brain injury states are now well established. By contrast, little or no specific attention has been, however, paid to the in vivo NMDA receptor function/excitability in magnesium deficiency. The present work reports for the first time that, in mice undergoing chronic nutritional deprivation in magnesium (35 v. 930 parts per million for 27 d in OF1 mice), NMDA-induced seizure threshold is significantly decreased (38 % of normal values). The attenuation in the drop of NMDA seizure threshold (percentage of reversal) was 58 and 20 % upon acute intraperitoneal administrations of magnesium chloride hexahydrate (28 mg magnesium/kg) and the antioxidant ebselen (20 mg/kg), respectively. In nutritionally magnesium-deprived animals, audiogenic seizures are completely prevented by these compound doses. Taken as a whole, our data emphasise that chronic magnesium deprivation in mice is a nutritional in vivo model for a lowered NMDA receptor activation threshold. This nutritional model responds remarkably to acute magnesium supply and moderately to acute antioxidant administration.

The objective of the present study was to determine marginal vitamin A deficiency (VAD) by testing the hydrolysis of retinoyl glucuronide (RAG) to retinoic acid (RA) in children. Previous studies in rats showed that hydrolysis occurred when rats were vitamin A deficient. Children (n 61) aged 3–18 years, were divided into two groups, I and II. Blood was collected from the children in Group I (n 19) who were not dosed with RAG. Children in Group II (n 42) were administered all-trans retinoyl glucuronide (RAG) orally, and blood was collected 4 h after the dose. All serum samples were analysed for retinoids and carotenoids. RA was detected in serum only when serum retinol was < 0·85 μmol/l. Thus, hydrolysis of RAG to RA occurred in children with VAD or marginal VAD. Serum retinol was < 0·35 μmol/l in twenty-one children, 0·35–0·7 μmol/l in twenty-three children, 0·7–0·9 μmol/l in eleven children and >1 μmol/l in six children. Mean serum retinol in sixty-one children was 0·522 (sd 0·315) μmol/l. Mean β-carotene (0·016 (sd 0·015) μmol/l) was far below normal compared to the level of lutein (0·176 (sd 0·10) μmol/l) in sixty-one children. A low β-carotene level might be due to a low intake of carotene but high demand for vitamin A. The RAG hydrolysis test may prove to be a useful approach for the determination of marginal VAD with no clinical or subclinical signs of VAD. High prevalence of VAD amongst certain communities in Assam cannot be ruled out.

The present study gives further evidence for the recently found association between variants of the fatty acid desaturase 1 fatty acid desaturase 2 (FADS1 FADS2) gene cluster and PUFA in blood phospholipids and explores this association for cellular fatty acids in erythrocyte membranes. In a subgroup of adults participating in the Bavarian Nutrition Survey II, a cross-sectional population-based study conducted in Bavaria, Germany, allelic variation in three selected loci of the FADS1 FADS2 gene cluster was analysed and used for haplotype construction. Associations with plasma phospholipid PUFA (n 163) and PUFA in erythrocyte membranes (n 535) were investigated by regression analysis. All haplotypes of the original five-loci haplotypes of our previous study could be replicated. In addition, associations with serum phospholipid PUFA were confirmed in the present data set. Although less pronounced, associations between FADS1 FADS2 haplotypes and PUFA in erythrocyte membranes, particularly arachidonic and dihomo-γ-linolenic acid, could be established. We provide the first replication of the association of the FADS1 FADS2 gene cluster with PUFA in blood phospholipids. For the first time, such associations were also shown for PUFA in cell membranes.

The present analysis investigated the effect of soya foods on serum levels of six inflammatory markers, leptin, adiponectin, monocyte attractant protein 1 (MCP-1), macrophage inflammatory protein-1b (MIP-1b), IL-6 and C-reactive protein (CRP), and their relationship with BMI and lifetime soya intake. We randomised twenty-four men to a high- (two daily servings with 30–35 mg isoflavones per serving) or a low-soya diet for 3 months. After a 1-month washout period, the men crossed over to the other treatment. We used a multiplex bead immunoassay to measure leptin, adiponectin, MCP-1 and MIP-1b and ELISA assays for IL-6 and CRP. The statistical analysis applied mixed models that incorporated the four repeated measurements. The men had a mean age of 58·7 (sd 7·2) years and a mean BMI of 28·4 (sd 4·9) kg/m2. We observed no significant intervention effect of the soya treatment on any of the six markers. After adjustment for age and ethnicity, highly significant associations of BMI and body weight with leptin and MCP-1 emerged. Men with high soya intake early in life also had higher levels of leptin and MCP-1, whereas no association was seen for soya intake during adulthood. MIP-1b, adiponectin, IL-6 and CRP were not related to BMI, body weight or soya intake at any time in life. No intervention effect of soya foods on markers of inflammation was observed in this small study, but adiposity and early-life soya intake were related to higher leptin and MCP-1 levels.

Coffee and tea may influence glycaemic responses but it is not clear whether they affect the glycaemic index (GI) value of foods. Therefore, to see if coffee and tea affected the mean and sem of GI values, the GI of fruit leather (FL) and cheese puffs (CP) were determined twice in ten subjects using the FAO/WHO protocol with white bread as the reference food. In one series subjects chose to drink 250 ml of either coffee or tea with all test meals, while in the other series they drank 250 ml water. The tests for both series were conducted as a single experiment with the order of all tests being randomised. Coffee and tea increased the overall mean peak blood glucose increment compared with water by 0·25 (sem 0·09) mmol/l (P = 0·02), but did not significantly affect the incremental area under the glucose response curve. Mean GI values were not affected by coffee or tea but the sem was reduced by about 30 % (FL: 31 (sem 4) v. 35 (sem 7) and CP: 76 (sem 6) v. 75 (sem 8) for coffee or tea v. water, respectively). The error mean square term from the ANOVA of the GI values was significantly smaller for coffee or tea v. water (F(18, 18) = 2·31; P = 0·04). We conclude that drinking coffee or tea with test meals does not affect the mean GI value obtained, but may reduce variability and, hence, improve precision.

Elevated C-reactive protein (CRP), IL-6 and retinol-binding protein 4 (RBP4) levels are associated with insulin resistance and diabetes mellitus. Phytoestrogens (including lignans and isoflavones) may enhance the management of diabetes and are hypothesized to act through inflammation pathways. The present study explored the effects of flaxseed-derived lignan on inflammatory factors and RBP4 concentrations in type 2 diabetics, who have higher levels of these biomarkers. Seventy community-dwelling diabetic patients (twenty-six men and forty-four post-menopausal women) with mild hypercholesterolaemia completed a randomized, double-blind, placebo-controlled, cross-over trial of supplementation with flaxseed-derived lignan capsules (360 mg/d) or placebo for 12 weeks, separated by an 8-week wash-out period. The participants maintained their habitual diets and levels of physical activity. Baseline to follow-up concentrations of CRP increased significantly within the placebo group (1·42 (sem 0·19) v. 1·96 (sem 0·22) mg/l, P < 0·001), but were comparatively unchanged in the lignan-supplemented group (1·67 (sem 0·19) v. 1·90 (sem 0·26) mg/l, P = 0·94); a significant difference was observed between treatments ( − 0·45 (95 % CI − 0·76, − 0·08) mg/l, P = 0·021). This effect was confined to women (P = 0·016), but not observed in men (P = 0·49). No between-treatment differences were found with regard to IL-6 or RBP4; though IL-6 concentrations increased significantly from baseline to follow-up in both groups (P = 0·004 and P < 0·001 following lignan and placebo treatments, respectively). The study suggests that lignan might modulate CRP levels in type 2 diabetics. These results need to be confirmed by further large clinical trials of longer duration.

Insulin-induced gene 2 (insig-2) protein is known to play important roles in cholesterol and TAG metabolism both in vivo and in vitro. One particularly interesting single nucleotide polymorphism (SNP), rs7566605, located 10 kb upstream of INSIG2 was reported to have the strongest association with obesity among 86 604 SNP, while the relationship with dyslipidaemia is uncertain. Eight hundred and eighty-five Japanese Americans (347 men and 538 women) and 378 Japanese (182 men and 196 women) were enrolled, and the rs7566605 SNP, which is consistent with either G or C, was determined. We investigated the association between the rs7566605 SNP and the prevalence of hypercholesterolaemia or hypertriacylglycerolaemia, or obesity parameters, as assessed by BMI, waist girth and percentage body fat. There were no significant differences in BMI, waist girth and percentage body fat according to the genotype in each of the four groups, which was divided by population and sex. The prevalence of hypercholesterolaemia was significantly different between the genotypes in Japanese American female subjects (GG, 62·2 %; GC, 57·1 %; CC, 42·1 %; P = 0·021), but not in the other subjects. In Japanese American women, the subjects with the CC genotype had a 0·43-fold decreased risk (95 % CI 0·24, 0·80) for hypercholesterolaemia compared with the GG genotype after adjustment for age, percentage body fat, smoking status and hormone replacement therapy. The CC genotype of the rs7566605 SNP is suggested to be a protective genetic factor against the progression of hypercholesterolaemia on a high-fat diet, especially in Japanese female subjects.

The aim of this study was to determine the effect of dietary quercetin supplementation on blood lipids and TNF-α levels according to the apoE genotype in apoE3 and apoE4 targeted gene replacement mice. In a two-factorial design female apoE3 and apoE4 mice were fed semi-synthetic diets without (controls) and with quercetin (2 mg/g diet) for 6 weeks. Feeding the quercetin-supplemented diets significantly increased plasma levels of quercetin and isorhamnetin both in apoE3 and apoE4 mice. There was no significant effect of apoE genotype on plasma quercetin levels. ApoE3 and apoE4 transgenic mice exhibited similar plasma levels of apoE and cholesterol which were not significantly affected by dietary quercetin supplementation. In mice receiving the basal diet without quercetin supplementation, levels of TNF-α in whole blood stimulated ex vivo with lipopolysaccharide were higher in apoE3 as compared to apoE4 transgenic mice. Dietary quercetin significantly lowered levels of TNF-α by 44 % in apoE3 mice relative to apoE3 mice receiving the unsupplemented diets. In apoE4 mice a moderate (20 %) but not significant decrease in TNF-α levels in response to the quercetin supplementation was evident. Following quercetin supplementation TNF-α levels were similar between apoE3 and apoE4 transgenic mice. Current findings indicate that apoE3 mice are more responsive to the TNF-α lowering properties of dietary quercetin supplementation as compared to apoE4 animals.

Breast-feeding is the predominant postnatal transmission route for HIV-1 infection in children. However, a majority of breast-fed infants do not become HIV-infected despite continuous exposure to the virus through their mothers' milk over many months. What protects some breast-fed infants from HIV-1 infection? HIV-1 entry across the infant's mucosal barrier is partially mediated through binding of the HIV-1 surface glycoprotein gp120 to dendritic cell-specific ICAM3-grabbing non-integrin (DC-SIGN) on human dendritic cells. Lewis antigen glycans, present in human milk, bind to DC-SIGN and inhibit HIV-1 transfer to CD4+T lymphocytes. Human milk contains a high amount of unbound, complex oligosaccharides (5–10 g/l) that carry one or more Lewis antigen glycans, and we hypothesized that they compete with gp120 for DC-SIGN binding. Here, we show in two independent assays that physiological concentrations of human milk oligosaccharides significantly reduce gp120 binding to DC-SIGN by more than 80 %. These results may provide an additional explanation for the inhibitory effects of human milk on HIV-1 mother-to-child-transmission. Identifying the specific milk oligosaccharides that interact with DC-SIGN may guide the development of glycan-based drugs that prevent transmission of HIV-1 and other pathogens that use DC-SIGN as an entry point. However, blocking DC-SIGN may be a two-edged sword.

Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have antioxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Multidrug resistance gene-deficient (mdr1a− / − ) mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet–gene interactions and potential effects of foods on remission or development of IBD. The present study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a− / −  mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets (control (AIN-76A), control +0·2 % curcumin or control +0·1 % rutin) and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a− / −  mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways, probably mediated by pregnane X receptor (Pxr) and peroxisome proliferator-activated receptor α (Ppara) activation of retinoid X receptor (Rxr). These results indicate the potential of global gene expression and pathway analyses to study and better understand the effect of foods in modulating colonic inflammation.

This randomized, double-blind, placebo-controlled study was conducted to compare the effect of a 15-week weight-reducing programme ( − 2900 kJ/d) coupled with a calcium plus vitamin D (calcium+D) supplementation (600 mg elemental calcium and 5 μg vitamin D, consumed twice a day) or with a placebo, on body fat and on spontaneous energy/macronutrient intake. Sixty-three overweight or obese women (mean age 43 years, mean BMI 32 kg/m2) reporting a daily calcium intake < 800 mg participated in present study. Anthropometric variables, resting energy expenditure and spontaneous energy intake were measured before and after the 15-week programme. The calcium+D supplementation induced no statistically significant increase in fat mass loss in response to the programme. However, when analyses were limited to very low-calcium consumers only (initial calcium intake ≤ 600 mg/d, n 7 for calcium+D, n 6 for placebo), a significant decrease in body weight and fat mass (P < 0·01) and in spontaneous dietary lipid intake (P < 0·05) was observed in the calcium+D but not in the placebo group. In very low-calcium consumers, change in fat mass was positively correlated with change in lipid intake. During the weight-reducing programme, a calcium+D supplementation was necessary in female overweight/obese very low-calcium consumers to reach significant fat mass loss that seemed to be partly explained by a decrease in lipid intake. We propose that this change in lipid intake could be influenced by a calcium-specific appetite control.

Observational epidemiological studies have shown that low carotenoid intake and/or low carotenoid blood levels increase the risk of degenerative diseases like age-related macular degeneration. Functional foods enriched with plant sterol or stanol esters may lower serum concentrations of fat-soluble carotenoids. Theoretically, as a result the macular pigment optical density (MPOD), a marker for eye health, may change. We carried out a double-blind placebo-controlled human intervention trial with a duration of 18 months to evaluate the possible effects of plant stanol and sterol esters on serum lutein/zeaxanthin concentration in relation to the MPOD. Forty-seven subjects were randomly assigned to one of the three treatment groups: margarine without added plant sterols or stanols, plant sterol-enriched margarine, or plant stanol-enriched margarine. Serum cholesterol and lutein/zeaxanthine concentrations and the MPOD were evaluated at baseline and at study end. Changes in lipid-adjusted serum lutein/zeaxanthine concentrations between baseline and study end differed significantly between the three groups (P = 0·001). We found no differences in the MPOD between the three treatment groups, despite the differences in both absolute and cholesterol-standardized serum lutein/zeaxanthine concentrations. This shows that the observed reduction in serum carotenoid concentrations during 18 months consumption of these functional foods does not affect MPOD.

The purpose of the present study was to conduct a systematic review of the literature on the value of the methods used to assess dietary patterns for measuring nutrient intake adequacy in the population. Systematic review on Pubmed database up to April 2008. The search included specific key words and MeSH terms. No language limit was set. Only studies that compared food patterns with nutrient intake adequacy or nutrient biomarkers were included in the analysis. The search resulted in 1504 articles. The inclusion and exclusion criteria limited the selection to thirty articles. Nineteen studies evaluated the usefulness of the dietary patterns, either a priori defined (thirteen studies), or defined by factor analysis (four studies) or by cluster analysis (two studies), but only nine of them tested their validity (four a priori defined and four a posteriori defined). Diet indices showed moderate to good validity results for measuring the adequacy of intakes for α-carotene, β-carotene, vitamin C, vitamin B6, Ca, folic acid, Fe and Mg. The factor analysis approach showed moderate to good validity correlations with the adequacy of intake of α-carotene, β-carotene, lutein, lycopene, vitamin C, vitamin B6 and folic acid. Vitamin B12 and vitamin E are the micronutrients with less probability of being adequately assessed with dietary patterns a priori or a posteriori defined. Diet indices are tools with fair to moderate validity to assess micronutrient intake adequacy.

A study was conducted in healthy elderly living independently in senior housing to assess the impact of a probiotic yoghurt supplement on small intestinal bacterial overgrowth. Twenty-three participants with positive and thirteen participants with negative hydrogen breath test were studied before and after a period of 4 weeks of probiotic yoghurt administration. Intestinal permeability, plasma endotoxin levels, phagocytic activity of leucocytes, cytokine production by monocytes and free radical response of neutrophils were determined. Intestinal permeability was similar for the two groups and was unaffected by probiotic treatment. Both plasma endotoxin levels and the basal phagocytic activity of leucocytes decreased after yoghurt intake in the two groups. Exposure of monocytes and neutrophils ex vivo led to an increased cytokine response and free radical response, respectively. The normalisation of the various cytokine responses was more apparent in the group with positive breath test. In addition, the plasma levels of lipoplysaccharide binding protein and soluble CD14, lipoplysaccharide pattern recognition receptors and surrogate markers of lipoplysaccharide permeability were diminished by the end of the study. In conclusion, probiotic administration in the elderly normalises the response to endotoxin, and modulates activation markers in blood phagocytes, and therefore may help reduce low-grade chronic inflammation.

The objective of the study was to assess whether the timing of increased dietary protein throughout the day influences the feelings of fullness during energy balance (EB) and restriction (ER). Nine men (age 48 (sem 6) years; BMI 32·7 (sem 0·7) kg/m2) randomly completed five controlled feeding trials, each consisting of 3 d of EB, followed by 3 d of ER of a 3138 kJ/d (750 kcal/d) reduction). The diet was composed of a normal amount of protein (NP) (0·8 g protein/kg per d), or an additional amount of protein (HP) (+0·6 g protein/kg per d) given at breakfast (HP-B), lunch (HP-L), dinner (HP-D) or equally divided among all meals (HP-E). Meal-related (3 h postprandial) and overall (15 h composite) feelings of fullness were assessed from thirteen-point, numbered, linear category scale questionnaires (reported as arbitrary units (au)). When comparing HP treatments, the data are presented as difference from NP. No differences in meal-related or overall fullness were observed among HP treatments during EB. During ER, the HP-B led to greater meal-related fullness (+137 (sem 44) au × 180 min) compared to HP-D ( − 1 (sem 37) au × 180 min; P = 0·003), but not for HP-L (+62 (sem 53) au × 180 min; P = 0·188) or HP-E-B (+92 (sem 85) au × 180 min; P = 0·587). HP-B also led to greater overall (15 h) fullness (+404 (sem 162) au × 900 min) v. HP-L (+33 (sem 162) au × 900 min; P = 0·009) and HP-D ( − 60 (sem 132) au × 900 min; P = 0·05), but not HP-E (+274 (sem 165) au × 900 min; P = 0·188). The initial and sustained feelings of fullness following protein consumption at breakfast suggests that the timing of protein intake differentially influences satiety during ER.

Selenium is an important trace element with anti-cancer properties. In the present study, the apoptosis-inducing effects of organic selenium derivatives, namely methyl-l-selenocysteine and selenomethionine, were evaluated in vitro on human tumour-derived cell lines from breast, liver, colon, brain, skin and a non-tumorigenic line of epithelial origin. Apoptosis was assessed by cell-death detection immunoassay on cytoplasmic cell lysates. Breast carcinoma cells were highly sensitive to the organic selenium compounds, manifesting apoptosis at concentrations as low as 0·113 μm (0·0205 μg/ml) selenium. By contrast, non-tumorigenic mammary epithelial cells displayed poor sensitivity to selenium, requiring a substantially high concentration of the trace element of 87·9 μm (16·0 μg/ml). The cell lines derived from hepatoma and neuroblastoma showed intermediate sensitivity, with colon carcinoma cells manifesting the lowest sensitivity to the trace element. These results indicate intrinsic differences in the sensitivity of human tumour derivatives to selenium-mediated apoptosis, providing experimental support for the development of organic selenium compounds as anti-neoplastic agents against solid tumours displaying selective apoptotic sensitivity to these compounds.

Oranges are rich sources of flavonoids that are bioactive and may protect against age-related diseases. The absorption of orange flavanones may be affected by factors such as processing and subject anthropometric variables, and the bioactivity of the absorbed phytochemicals depends on how they are metabolised during absorption. In a randomised cross-over study, twenty subjects consumed a single portion of orange fruit (150 g) or juice (300 g) that contained the flavanones narirutin and hesperidin, and an additional 109 subjects across a broad age range (18–80 years) consumed the juice. Flavanone metabolites were measured in regularly collected samples of plasma and urine. After consumption of fruit or juice, flavanone conjugates, but not the aglycones, were detected in plasma and urine. The flavanone conjugates were shown to include the 7- and 4′-O-monoglucuronides of naringenin, the 7- and 3′-O-monoglucuronides of hesperetin, two hesperetin diglucuronides and a hesperetin sulfo-glucuronide, but no aglycones or rutinosides. Analysis of the plasma pharmacokinetic and urinary excretion data on a dose-adjusted basis indicated no difference in absorption or excretion of either flavanone between the fruit and juice matrices. In the extended urinary excretion dataset the individual variation was very large (range 0–59 % urinary yield). There was a small but significant (P < 0·05) decrease in the excretion of hesperetin (but not naringenin) with increasing age (P < 0·05), but the effects of sex, BMI and contraceptive pill use were shown not to be associated with the variation in flavanone excretion.

In Middle-Eastern countries, more particularly in Lebanon, the incidence of vitamin D deficiency has been found to be surprisingly high in schoolchildren and young individuals. However, the prevalence and risk factors for vitamin D inadequacy amongst Lebanese osteoporotic women seeking medical health care has never been studied. We analysed vitamin D-inadequacy risk factors among the 251 Lebanese postmenopausal osteoporotic women (from both Muslim and Christian communities) who participated in a vitamin D international epidemiological study. Vitamin D inadequacy prevalence (25-hydroxyvitamin D (25(OH)D) < 30 ng/ml) was 84·9 %. 25(OH)D was negatively correlated with BMI (r − 0·41; P < 0·001) and positively correlated with educational level (r 0·37; P < 0·001) and self-reported general health (r 0·17; P < 0·01). No significant correlation was found with age and no seasonal variation was observed. There was no significant correlation between 25(OH)D and sun exposure index or vitamin D-rich food consumption. However, 25(OH)D strongly correlated with vitamin D supplement intake (r 0·48; P < 0·0001). Muslim community participants had lower 25(OH)D levels compared with their Christian counterparts (P < 0·001). They also had higher BMI, lower educational level and vitamin D supplement consumption and followed more frequently a dress code covering the arms (P < 0·0001 for all variables). In a multivariate model, in Muslims, inadequate vitamin D supplements and a dress code covering the arms are the independent predictors of 25(OH)D inadequacy (P < 0·001 for both variables). However, in Christians, the predictors are inadequate vitamin D supplements, high BMI and low educational level (P < 0·001; P = 0·002 and P = 0·02 respectively). There is an urgent need to increase vitamin D supplement use in Middle-Eastern osteoporotic women, more particularly in those from the Muslim community.

The interindividual variation in ApoE plasma concentration is considerable, mainly determined by apoE genotype and sex. However, a large amount of variability remains unexplained by these factors. We have evaluated whether the quantity and quality of dietary fat interacts with the apoE genotype and sex modifying ApoE plasma levels in young healthy subjects. Eighty-four volunteers (sixty-six apoE3/3, eight apoE4/3 and ten apoE3/2) were subjected to three dietary periods, each lasting 4 weeks. The first was a SFA-enriched diet (38 % fat and 20 % SFA), which was followed by a carbohydrate (CHO)-rich diet (30 % fat, < 10 % SFA and 55 % carbohydrate) or a MUFA-rich diet (38 % fat and 22 % MUFA) following a randomised crossover design. apoE2 carriers have the highest ApoE levels, whereas apoE4 individuals show the lowest concentration after the SFA, CHO and MUFA diets. Women had significantly higher ApoE concentration than men only after the consumption of the SFA diet. The SFA diet increased the ApoE plasma concentration when compared with the CHO- and MUFA-rich diets in women, but not in men. In women, but not in men, the shift from the SFA- to CHO- or MUFA-rich diets significantly decreased the ApoE concentration in apoE3/2 and apoE3/3 subjects, whereas no differences were observed in women with the apoE4/3 genotype. Sex and apoE genotype determine ApoE plasma levels; however, this effect is dependent on dietary fat.