Fe deficiency is relatively common in pregnancy and has both short- and long-term consequences. However, little is known about the effect on the metabolism of other micronutrients. A total of fifty-four female rats were fed control (50 mg Fe/kg) or Fe-deficient diets (7·5 mg/kg) before and during pregnancy. Maternal liver, placenta and fetal liver were collected at day 21 of pregnancy for Cu and Zn analysis and to measure expression of the major genes of Cu and Zn metabolism. Cu levels increased in the maternal liver (P=0·002) and placenta (P=0·018) of Fe-deficient rats. Zn increased (P<0·0001) and Cu decreased (P=0·006) in the fetal liver. Hepatic expression of the Cu chaperones antioxidant 1 Cu chaperone (P=0·042) and cytochrome c oxidase Cu chaperone (COX17, P=0·020) decreased in the Fe-deficient dams, while the expression of the genes of Zn metabolism was unaltered. In the placenta, Fe deficiency reduced the expression of the chaperone for superoxide dismutase 1, Cu chaperone for superoxide dismutase (P=0·030), ceruloplasmin (P=0·042) and Zn transport genes, ZRT/IRT-like protein 4 (ZIP4, P=0·047) and Zn transporter 1 (ZnT1, P=0·012). In fetal liver, Fe deficiency increased COX17 (P=0·020), ZRT/IRT-like protein 14 (P=0·036) and ZnT1 (P=0·0003) and decreased ZIP4 (P=0·004). The results demonstrate that Fe deficiency during pregnancy has opposite effects on Cu and Zn levels in the fetal liver. This may, in turn, alter metabolism of these nutrients, with consequences for development in the fetus and the neonate.

Non-communicable diseases are projected to become the most common causes of death in Africa by 2030. The impact on health of epidemiological and nutritional transitions in sub-Saharan Africa remains unclear. To assess the trends of dietary fatty acids over time in Uganda, we examined fatty acids in serum collected from individuals in rural south-west Uganda, at three time points over two decades. Independent cross-sectional samples of 915 adults and children were selected from the general population cohort in 1990 (n 281), 2000 (n 283) and 2008 (n 351). Serum phospholipid fatty acids were measured by GC. Multivariate regression analyses were performed to compare the geometric means of fatty acids by time period. Serum fatty acid profiling showed high proportions of SFA, cis-MUFA and industrial trans-fatty acids (iTFA), likely to be biomarkers of high consumption of palm oil and hydrogenated fats. In contrast, proportions of n-6 and n-3 PUFA from vegetable oils and fish were low. From 1990 to 2008, serum phospholipids showed increases in absolute amounts of SFA (17·3 % increase in adults and 26·4 % in children), MUFA (16·7 % increase in adults and 16·8 % in children) and n-6:n-3 PUFA (40·1 % increase in adults and 39·8 % in children). The amount of elaidic acid, iTFA from hydrogenated fats, increased in children (60·1 % increase). In this rural Ugandan population, we show evidence of unfavourable trends over time of dietary fatty acids.

Conversion of α-linolenic acid (ALA) into the longer chain n-3 PUFA has been suggested to be affected by the dietary intake of linoleic acid (LA), but the mechanism is not well known. Therefore, the purpose of this study was to evaluate the effect of a low-LA diet with and without oestrogen on the fatty acid conversion enzymes and transcription factors. Rats were fed a modified American Institute of Nutrition-93G diet with 0% n-3 PUFA or ALA, containing low or high amounts of LA for 12 weeks. At 8 weeks, the rats were injected with maize oil with or without 17β-oestradiol-3-benzoate (E) at constant intervals for the remaining 3 weeks. Both the low-LA diet and E significantly increased the hepatic expressions of PPAR-α, fatty acid desaturase (FADS) 2, elongase of very long chain fatty acids 2 (ELOVL2) and ELOVL5 but decreased sterol regulatory element binding protein 1. The low-LA diet, but not E, increased the hepatic expression of FADS1, and E increased the hepatic expression of oestrogen receptor-α and β. The low-LA diet and E had synergic effects on serum and liver levels of DHA and on the hepatic expression of PPAR-α. In conclusion, the low-LA diet and oestrogen increased the conversion of ALA into DHA by upregulating the elongases and desaturases of fatty acids through regulating the expression of transcription factors. The low-LA diet and E had a synergic effect on serum and liver levels of DHA through increasing the expression of PPAR-α.

We have recently reported that soluble dietary fibre, glucomannan, increased colonic alkaline phosphatase (ALP) activity and the gene expression without affecting the small-intestinal activity and that colonic ALP was correlated with gut mucins (index of intestinal barrier function). We speculated that dietary fermentable carbohydrates including oligosaccharides commonly elevate colonic ALP and gene expression as well as increase mucin secretion and microbial fermentation. To test this hypothesis, male Sprague–Dawley rats were fed a diet containing 30 % lard with or without 4 % fructo-oligosaccharides (FOS), galacto-oligosaccharides (GOS), raffinose (RAF) and lactulose (LAC), which are non-digestible oligosaccharides or isomalto-oligosaccharides (IMOS; some digestible oligosaccharides) for 2 weeks. Colon ALP activity, the gene expression and gut luminal variables including mucins, organic acids and microbiota were measured. Colonic ALP was significantly elevated in the FOS, RAF and LAC groups, and a similar trend was observed in the GOS group. Colonic expression of intestinal alkaline phosphatase (IAP-I), an ALP gene, was significantly elevated in the FOS, GOS and RAF groups and tended to be increased in the LAC group. Dietary FOS, GOS, RAF and LAC significantly elevated faecal mucins, caecal n-butyrate and faecal ratio of Bifidobacterium spp. Dietary IMOS had no effect on colonic ALP, mucins, organic acids and microbiota. Colon ALP was correlated with mucins, caecal n-butyrate and faecal Bifidobacterium spp. This study demonstrated that non-digestible and fermentable oligosaccharides commonly elevate colonic ALP activity and the expression of IAP-I, with increasing mucins and microbial fermentation, which might be important for protection of gut epithelial homoeostasis.

Results of intervention studies on the effects of α-linolenic acid (ALA; C18 : 3n-3) on blood pressure (BP) are conflicting. Discrepancies between studies may be due to differences in study population, as subjects with increased baseline BP levels may be more responsive. Therefore, we examined specifically the effects of ALA on 24-h ambulatory blood pressure (ABP) in (pre-)hypertensive subjects. In a double-blind, randomised, placebo-controlled parallel study, fifty-nine overweight and obese adults (forty males and nineteen females) with (pre-)hypertension (mean age of 60 (sd 8) years) received daily 10 g refined cold-pressed flaxseed oil, providing 4·7 g (approximately 2 % of energy) ALA (n 29) or 10 g of high-oleic sunflower oil as control (n 30) for 12 weeks. Compliance was excellent as indicated by vial count and plasma phospholipid fatty-acid composition. Compared with control, the changes of –1·4 mmHg in mean arterial pressure (MAP; 24 h ABP) after flaxseed oil intake (95 % CI –4·8, 2·0 mmHg, P=0·40) of –1·5 mmHg in systolic BP (95 % CI –6·0, 3·0 mmHg, P=0·51) and of –1·4 mmHg in diastolic BP (95 % CI –4·2, 1·4 mmHg, P=0·31) were not statistically significant. Also, no effects were found for office BP and for MAP, systolic BP, and diastolic BP when daytime and night-time BP were analysed separately and for night-time dipping. In conclusion, high intake of ALA, about 3–5 times recommended daily intakes, for 12 weeks does not significantly affect BP in subjects with (pre-)hypertension.

High Na intake and chronically elevated cortisol levels are independently associated with the development of chronic diseases. In adults, high Na intake is associated with high levels of urinary cortisol. We aimed to determine the association between urinary Na and K and urinary cortisol in a cross-sectional sample of Australian schoolchildren and their mothers. Participants were a sample of Australian children (n 120) and their mothers (n 100) recruited through primary schools. We assessed Na, K, free cortisol and cortisol metabolites in one 24 h urine collection. Associations between 24 h urinary electrolytes and 24 h urinary cortisol were assessed using multilevel mixed-effects linear regression models. In children, urinary Na was positively associated with urinary free cortisol (β=0·31, 95 % CI 0·19, 0·44) and urinary cortisol metabolites (β=0·006, 95 % CI 0·002, 0·010). Positive associations were also observed between urinary K and urinary free cortisol (β=0·65, 95 % CI 0·23, 1·07) and urinary cortisol metabolites (β=0·02, 95 % CI 0·03, 0·031). In mothers, urinary Na was positively associated with urinary free cortisol (β=0·23, 95 % CI 0·01, 0·50) and urinary cortisol metabolites (β=0·008, 95 % CI 0·0007, 0·016). Our findings show that daily Na and K intake were positively associated with cortisol production in children and their mothers. Investigation of the mechanisms involved and the potential impact of Na reduction on cortisol levels in these populations is warranted.

Health professionals consider the evaluation of eating habits to be challenging, given the potential biases of dietary questionnaires based on self-reported data. Circulating carotenoid concentrations are reliable biomarkers of dietary carotenoid intake and could be useful in the validation of dietary assessment tools. However, there is a sex difference in circulating carotenoids, with women displaying higher concentrations compared with men independent of intake. The aim of the present study was to identify the correlates of plasma carotenoid concentrations among men (n 155) and women (n 110) enrolled in six fully controlled dietary interventions with varying dietary carotenoid intakes. We looked at the associations of post-intervention fasting plasma carotenoid concentrations (α-carotene, β-carotene, β-cryptoxanthin, lutein, lycopene and zeaxanthin) with physical and metabolic characteristics. We found that increased body weight (r –0·47, P<0·0001) and waist circumference (r –0·46, P<0·0001) were associated with lower plasma total carotenoid concentrations, while elevated plasma LDL-cholesterol (r 0·49, P<0·0001) and HDL-cholesterol (r 0·50, P<0·0001) concentrations were correlated with higher total carotenoids in plasma. Women had significantly higher plasma total carotenoid concentrations compared with men, despite significantly lower dietary carotenoid intake. Adjustment of circulating carotenoid concentrations for plasma HDL-cholesterol eliminated sex difference in plasma carotenoid concentrations. Our results suggest that physical characteristics as well as plasma lipids are associated with circulating carotenoid concentrations and that these variables should be taken into account when using plasma carotenoids as biomarkers for food intake in men and women.

Supplementation with n-3 fatty acids can influence inflammation and markers of arterial stiffness that are increased in patients with rheumatoid arthritis (RA). However, it is unknown whether specific patterns of dietary fatty acid intake are similarly associated. In a longitudinal study, eighty-six RA patients reported their dietary intake and had arterial stiffness measured using the augmentation index (AIx) at baseline and 8 months. Latent profile analysis (LPA) was performed to characterise patterns of fatty acid intake using sixteen major fatty acids. Models for two to six profiles were compared using the Akaike and Bayesian information criteria. Associations between AIx and the profiles were adjusted for age, sex, disease activity, fish oil supplementation, medications, physical activity and socio-economic status. LPA identified five distinct profiles. Profile 1 subjects (n 7) reported significantly higher intake of palmitoleic acid (16 : 1), arachidonic acid (20 : 4n-6), EPA (20 : 5n-3), DHA (22 : 6n-3) and docosapentaenoic acid (22 : 5n-3) (P<0·001 for each) than profiles 2 (n 14), 3 (n 19), 4 (n 23) and 5 (n 23) and significantly higher grilled and tinned fish consumption. The AIx varied significantly across the five profiles (P=0·023); subjects in profile 1 had a significantly lower AIx than those in profile 3 (β=–7·2 %; 95 % CI –11·5, –2·9; P=0·001) who had the lowest reported intake of n-3 fatty acids. Fish oil supplementation was also independently associated with lower AIx (β=–4·15 %; 95 % CI –6·73, –1·56; P=0·002). A diet characterised by a higher reported intake of n-3 fatty acids, palmitoleic acid (16 : 1) and arachidonic acid (20 : 4n-6) is associated with a lower AIx in RA patients.

Pancreatic-insufficient children with cystic fibrosis (CF) receive age-group-specific vitamin D supplementation according to international CF nutritional guidelines. The potential advantageous immunomodulatory effect of serum 25-hydroxy vitamin D (25(OH)D) on pulmonary function (PF) is yet to be established and is complicated by CF-related vitamin D malabsorption. We aimed to assess whether current recommendations are optimal for preventing deficiencies and whether higher serum 25(OH)D levels have long-term beneficial effects on PF. We examined the longitudinal relationship between vitamin D intake, serum 25(OH)D and PF in 190 CF children during a 4-year follow-up period. We found a significant relationship between total vitamin D intake and serum 25(OH)D (β = 0·02; 95 % CI 0·01, 0·03; P = 0·000). However, serum 25(OH)D decreased with increasing body weight (β = –0·79; 95 % CI –1·28, –0·29; P = 0·002). Furthermore, we observed a significant relationship between serum 25(OH)D and forced expiratory volume in 1 s (β = 0·056; 95 % CI 0·01, 0·102; P = 0·018) and forced vital capacity (β = 0·045; 95 % CI 0·008, 0·082; P = 0·017). In the present large study sample, vitamin D intake is associated with serum 25(OH)D levels, and adequate serum 25(OH)D levels may contribute to the preservation of PF in children with CF. Furthermore, to maintain adequate levels of serum 25(OH)D, vitamin D supplementation should increase with increasing body weight. Adjustments of the international CF nutritional guidelines, in which vitamin D supplementation increases with increasing weight, should be considered.

Determining the predictors of serum retinol at mid-pregnancy is relevant for planning interventions aimed at improving vitamin A status of pregnant women and their offspring. This prospective study assessed predictors of serum retinol at the beginning of the third trimester of pregnancy. We enrolled 442 pregnant women living in the urban area of Cruzeiro do Sul, Western Brazilian Amazon. Demographic, socio-economic, environmental and clinical characteristics as well as obstetric history, anthropometric, dietary and biochemical data, including serum retinol, were gathered between 16 and 20 gestational weeks. Serum retinol also measured at the beginning of the third trimester of pregnancy (approximately 28 gestational weeks) was the outcome of interest. Multiple linear regression models were used to evaluate associations with the outcome. Overall, the following variables explained serum retinol at the beginning of the third trimester of pregnancy in the adjusted model (R2 = 11·1 %): seasonality (winter season – November to April; β=0·134; 95 % CI 0·063, 0·206), weekly consumption of Amazonian fruits (β=0·087; 95 % CI 0·012, 0·162) and retinol concentrations between 16 and 20 gestational weeks (β=0·045; 95 % CI 0·016, 0·074) were positively associated, whereas having a smoker in the house was negatively associated (β=–0·087; 95 % CI: –0·166, –0·009). Consumption of pro-vitamin A-rich fruits by pregnant women should be encouraged. Passive smoking may play a role in decreasing vitamin A status as a proxy of smoking exposure during pregnancy.

This study investigates how dietary patterns and scores are associated with subsequent BMI and waist:height ratio (WHtR), and how BMI and WHtR are associated with subsequent dietary patterns or scores, from 2–3 to 10–11 and 4–5 to 14–15 years of age. In the Longitudinal Study of Australian Children, height, weight and waist circumference were measured biennially in children, yielding BMI z-score and WHtR. Parents, latterly children, reported frequency of child consumption of 12–16 food/drink items during the previous 24 h. At each wave, we empirically derived dietary patterns using factor analyses, and dietary scores based on the 2013 Australian Dietary Guidelines. We used structural-equation modelling to investigate cross-lagged associations (n 1972–2882) between diet and body composition measures in univariable and multivariable analyses. Dietary scores/patterns did not consistently predict WHtR and BMI z-score in the next wave, nor did BMI z-score and WHtR consistently predict diet in the next wave. The few associations seen were weak and often in the opposite direction to that hypothesised. The largest effect, associated with each standard deviation increase in BMI in wave 5 of the K cohort (age 12–13 years), was a 0·06 standard deviation estimated mean increase in dietary score (higher quality diet) in the subsequent wave (95 % CI 0·02, 0·11, P=0·003). Associations between dietary patterns/scores and body composition were not strongly evident in either direction. Better quantitative childhood dietary tools feasible for large-scale administration are needed to quantify how dietary patterns, energy intake and anthropometry co-develop.

The present study examined the association between high-quality diet (using the Mediterranean diet (MD) as an example) and well-being cross-sectionally and prospectively in Spanish children and adolescents. Participants included 533 children and 987 adolescents at baseline and 527 children and 798 adolescents at 2-year follow-up, included in the UP&DOWN study (follow-up in schoolchildren and adolescents with and without Down’s syndrome). The present study excluded participants with Down’s syndrome. Adherence to an MD was assessed using the KIDMED index. Well-being was measured using the Positive and Negative Affect Schedule and the KIDSCREEN-10 questionnaire. Associations between MD adherence and well-being were assessed using multi-level, mixed-effects linear regression. At baseline, MD adherence was positively related to health-related quality of life in secondary school girls and boys (β=0·41, se 0·10, P<0·001; β=0·46, se 0·10, P<0·001, respectively) and to positive affect in secondary school girls and boys (β=0·16, se 0·05, P=0·006; β=0·20, se 0·05, P<0·001, respectively) and in primary school boys (β=0·20, se 0·08, P=0·019). At 2-year follow-up, MD adherence was negatively related to negative affect in secondary school adolescent girls and boys (β=–0·15, se 0·07, P=0·047; β=–0·16, se 0·06, P=0·019, respectively), and MD adherence was associated with higher positive affect scores in secondary school girls (β=0·30, se 0·06, P<0·001) and in primary school boys (β=0·20, se 0·09, P=0·023). However, MD adherence at baseline did not predict well-being indicators at 2-year follow-up. In conclusion, higher MD adherence was found to behave as a protective factor for positive well-being in cross-sectional analysis.

Changes in added sugar intake have been associated with corresponding changes in body weight. Potential mechanisms, particularly the impact of added sugar intake on appetite, warrant exploration. A systematic literature review of randomised controlled trials investigated the association between added sugar consumption and appetite in overweight and obese adults. A systematic search of Medline, Cochrane CENTRAL, Web of Science and CINAHL included studies that examined the relationship between added sugar intake and appetite markers, in comparison with a group with lower added sugar intake. A total of twenty-one articles describing nineteen studies were included in the review. The effect of added sugar on appetite was explored separately by reported comparisons of added sugar type and their effect to three study outcomes: energy consumption (n 20 comparisons); satiety (n 18); and appetite hormones, leptin (n 4) or ghrelin (n 7). Increased added sugar consumption did not impact subsequent energy intake (n 9), nor did it influence satiety (n 12) or ghrelin levels (n 4). Differences in the total daily energy intake were comparable with the differences in energy values of tested products (n 3). Added sugar intake was reported to increase leptin levels (n 3). This review did not find a consistent relationship between added sugar intake and appetite measures, which may be partially explained by variations in study methodologies. There is a need for randomised controlled trials examining a range of added sugar sources and doses on appetite in overweight and obese adults to better understand implications for weight gain.