Little is known about Se intakes and status in very young New Zealand children. However, Se intakes below recommendations and lower Se status compared with international studies have been reported in New Zealand (particularly South Island) adults. The Baby-Led Introduction to SolidS (BLISS) randomised controlled trial compared a modified version of baby-led weaning (infants feed themselves rather than being spoon-fed), with traditional spoon-feeding (Control). Weighed 3-d diet records were collected and plasma Se concentration measured using inductively coupled plasma mass spectrometry (ICP-MS). In total, 101 (BLISS n 50, Control n 51) 12-month-old toddlers provided complete data. The OR of Se intakes below the estimated average requirement (EAR) was no different between BLISS and Control (OR: 0·89; 95 % CI 0·39, 2·03), and there was no difference in mean plasma Se concentration between groups (0·04 μmol/l; 95 % CI −0·03, 0·11). In an adjusted model, consuming breast milk was associated with lower plasma Se concentrations (–0·12 μmol/l; 95 % CI −0·19, −0·04). Of the food groups other than infant milk (breast milk or infant formula), ‘breads and cereals’ contributed the most to Se intakes (12 % of intake). In conclusion, Se intakes and plasma Se concentrations of 12-month-old New Zealand toddlers were no different between those who had followed a baby-led approach to complementary feeding and those who followed traditional spoon-feeding. However, more than half of toddlers had Se intakes below the EAR.

1. Sheep fed on a maintenance ration of wheaten-hay chaff or of wheaten-hay chaff–lucerne-hay chaff (1:1, w/w) became deficient or incipiently deficient in vitamin E.

2. Degenerative changes were observed in bone marrow and muscle, and liver function was impaired in some animals. These abnormalities were not influenced by the vitamin B12 status of the animals or by a shortage of cobalt in the rumen.

3. Plasma ascorbic acid levels may not have been optimum, and folic acid may not have been fully utilized by some sheep.

4. Liver function responded fairly rapidly to α-tocopheryl acetate, but skeletal muscle had not returned to normal after 28 weeks of treatment. A variable trend towards normal cellularity was found in bone marrow following supplementation with α-tocopheryl acetate.

5. A secondary deficiency or, alternatively, inefficient excretion or metabolism of a toxic material, may occur in vitamin E deficiency as a result of degenerative changes in the absorptive or excretory areas of the intestinal tract and be responsible for the bone marrow abnormality.

Excess calcium is well known to induce iron deficiency. Furthermore, excess calcium increases hepatic copper concentration and decreases renal copper concentration. We investigated the effect of iron supplementation on the tissue distribution of copper in rats given a high-calcium diet. Male rats (5 weeks old) were divided into four groups; a control group, and three groups given a diet containing 5-fold higher calcium than its requirement and an intraperitoneal iron supplementation of 0, 1 or 2 mg/week as iron dextran. The animals were fed their respective experimental diets with or without iron supplementation for 4 weeks. Although the high-calcium diet had no effect on calcium concentrations in the liver, kidney, testis, spleen and plasma, it reduced haematocrit and iron concentrations in the liver, kidney and testis and the rats had a moderate iron deficiency. The iron supplementation restored to normal these signs of iron deficiency. The high-calcium diet increased hepatic copper concentration but decreased plasma copper concentration and ceruloplasmin activity, which was restored by the iron supplementation. The copper concentration in bile was neither affected by the high-calcium diet nor the iron supplementation. The high-calcium diet decreased the copper concentration in the kidney, which was not restored by the iron supplementation. These results suggest that secondary iron deficiency stimulates hepatic accumulation of copper in rats given excess calcium by suppressing copper efflux into the circulation. The reduced renal copper concentration by excess calcium is independent of the iron deficiency.

Optimal maternal long-chain PUFA (LCPUFA) status is essential for the developing fetus. The fatty acid desaturase (FADS) genes are involved in the endogenous synthesis of LCPUFA. The minor allele of various FADS SNP have been associated with increased maternal concentrations of the precursors linoleic acid (LA) and α-linolenic acid (ALA), and lower concentrations of arachidonic acid (AA) and DHA. There is limited research on the influence of FADS genotype on cord PUFA status. The current study investigated the influence of maternal and child genetic variation in FADS genotype on cord blood PUFA status in a high fish-eating cohort. Cord blood samples (n 1088) collected from the Seychelles Child Development Study (SCDS) Nutrition Cohort 2 (NC2) were analysed for total serum PUFA. Of those with cord PUFA data available, maternal (n 1062) and child (n 916), FADS1 (rs174537 and rs174561), FADS2 (rs174575), and FADS1-FADS2 (rs3834458) were determined. Regression analysis determined that maternal minor allele homozygosity was associated with lower cord blood concentrations of DHA and the sum of EPA + DHA. Lower cord blood AA concentrations were observed in children who were minor allele homozygous for rs3834458 (β = 0·075; P = 0·037). Children who were minor allele carriers for rs174537, rs174561, rs174575 and rs3834458 had a lower cord blood AA:LA ratio (P < 0·05 for all). Both maternal and child FADS genotype were associated with cord LCPUFA concentrations, and therefore, the influence of FADS genotype was observed despite the high intake of preformed dietary LCPUFA from fish in this population.

Early life exposure to famine was associated with adulthood metabolic syndrome and nonalcoholic fatty liver disease (NAFLD), and NAFLD was also affected by cardiometabolic traits. However, the role of cardiometabolic traits in the associations from famine exposure to NAFLD was largely unknown. This study aimed to investigate whether the relationship between early life famine exposure and adulthood NAFLD risk was mediated by cardiometabolic traits. Overall, 7578 subjects aged 56·0 (sd 3·7) years in the Dongfeng–Tongji cohort were included and classified into late-exposed (1952–1954), middle-exposed (1954–1956), early-childhood-exposed (1956–1958), fetal-exposed (1959–1961) and non-exposed (1962–1966, reference) group according to the birth year. NAFLD was diagnosed by experienced physicians via abdominal B-type ultrasound inspection. Mediation analysis was used to evaluate the mediating effects of cardiometabolic traits. Compared with those non-exposed, after multivariable adjustment, participants in fetal-exposed group (OR: 1·37; 95 % CI 1·08, 1·73) had 37 % higher risk to develop NAFLD, and the overall childhood-exposed group had marginally significant association with NAFLD (OR: 1·39; 95 % CI 0·99, 1·94). Stratification analysis found the famine–NAFLD associations more evident in women and those born in areas severely affected by famine. Mediation analysis showed that cardiometabolic traits such as total cholesterol, TAG glucose index, γ-glutamyl transpeptidase, alkaline phosphatase and alanine aminotransferase mediated 6·7–22·2 % of the relation from famine exposure to higher NAFLD risk. Early life exposure to famine was related to increased adulthood NAFLD risk, and this relationship was partly mediated by cardiometabolic traits.

Low vitamin D level in HIV-positive persons has been associated with disease progression. We compared the levels of serum 25-hydroxyvitamin D (25(OH)D) in HIV-positive and HIV-negative persons, and investigated the role of nutritional supplementation and antiretroviral treatment (ART) on serum 25(OH)D levels. A randomised nutritional supplementation trial was conducted at Jimma University Specialized Hospital, Ethiopia. The trial compared 200 g/d of lipid-based nutrient supplement (LNS) with no supplementation during the first 3 months of ART. The supplement provided twice the recommended daily allowance of vitamin D (10 μg/200 g). The level of serum 25(OH)D before nutritional intervention and ART initiation was compared with serum 25(OH)D of HIV-negative individuals. A total of 348 HIV-positive and 100 HIV-negative persons were recruited. The median baseline serum 25(OH)D level was higher in HIV-positive than in HIV-negative persons (42·5 v. 35·3 nmol/l, P<0·001). In all, 282 HIV-positive persons with BMI>17 kg/m2 were randomised to either LNS supplementation (n 189) or no supplementation (n 93) during the first 3 months of ART. The supplemented group had a 4·1 (95 % CI 1·7, 6·4) nmol/l increase in serum 25(OH)D, whereas the non-supplemented group had a 10·8 (95 % CI 7·8, 13·9) nmol/l decrease in serum 25(OH)D level after 3 months of ART. Nutritional supplementation that contained vitamin D prevented a reduction in serum 25(OH)D levels in HIV-positive persons initiating ART. Vitamin D replenishment may be needed to prevent reduction in serum 25(OH)D levels during ART.

1. The plasma and blood volumes of twenty-eight Iraqi children were measured. Twenty-four of them were malnourished in varying degrees and four were normal children who acted as controls. None of the children was anaemic.

2. There was an increase in the plasma and blood volumes per unit body-weight correlating with the degree of malnourishment (P < 0·001).

3. There was little variation in the values for plasma and blood volumes when calculated per unit body length; the values were less constant when calculated per unit body surface.

4. The effect of age on the plasma and blood volumes per unit body-weight was less than the effect of the degree of malnutrition.

5. There was no correlation between the plasma volume of malnourished children and their corrected venous haematocrit, if children with severe anaemia were excluded.

The effect of hypoxic exposure on in vitro duodenal Fe uptake kinetics was studied in tissue fragments from rats that were fed or fasted overnight before study. Hypoxic exposure was for 3 d at 0·5 atm and fasting was for the last 18-24 h before Fe uptake determinations. The non-permeable Fe2+ chelator 3-(2-pyridyl)-5,6-bis-(4-phenyl-sulphonic acid)-l,2,4-triazine (ferrozine), and medium deoxygenation inhibited uptake in all experimental groups. Ferrozine sensitivity and mucosal Fe3+ reductase activity were greatest in hypoxic animals. Fe uptake was inhibited by membrane depolarization only after fasting or hypoxic exposure of the rats. The data demonstrated that Fe uptake by rat duodenal fragments involves at least two mechanisms: a membrane-potentialindependent mechanism which is not responsive to hypoxia and a second mechanism, induced by fasting or hypoxia, which is inhibited by membrane depolarization. Uptake is partially dependent on reduction of Fe3+ to Fe2+ and this is primarily associated with the second mechanism for uptake. These properties have been reported also in mouse and human Fe uptake, suggesting that the rat is a useful model for the study of basic mechanisms of Fe absorption

When readymade parenteral nutrition in multi-chamber bags is supplied without vitamins and minerals, these have to be added or given separately. Separate rapid infusion has logistical advantages but has been claimed to saturate tissue mechanisms, potentially increasing urine micronutrient losses. The present study compared urinary losses after fast (1 h) v. slow (10 h) trace elements infusion. The study enrolled thirty-nine consecutive patients who were starting parenteral nutrition postoperatively. One day’s dose of a complete intravenous micronutrient product was infused over 1 h and over 10 h, in random order, with a washout day after each infusion day. Urinary Zn, Mn, Se, Cr, Cu and Fe losses were measured by 24-h urine collection, recorded for each infusion day and subsequent washout day. For Zn, a dose of 100 μmol was given, and total urinary loss over the next 2 d was mean 40·6 (sd 23·8) μmol after the fast (1 h) infusion v. 33·4 (sd 25·4) μmol after the slow (10 h) infusion, that is, 7 % more of the 1-d dose was lost after fast infusion (P = 0·01). For Mn, after a dose of 1000 nmol, losses were 9·8 (sd 23·9) nmol after the fast infusion v. 22·1 (sd 47·2) nmol after the slow infusion, that is, 1 % more of the 1-d dose was lost after slow infusion (P = 0·04). There were no other significant differences: after 1 μmol Se, the losses were 1·5 (sd 0·6) μmol fast v. 1·3 (sd 0·5) μmol slow; after 200 nmol Cr, 257 (sd 92) μmol fast v. 246 (sd 107) nmol slow; after 8 μmol Cu, 1·6 (sd 1·4) μmol fast v. 1·5 (sd 1·3) μmol slow; and after 20 μmol Fe, 0·6 (sd 1·1) μmol fast v. 0·8 (sd 1·6) μmol slow (P > 0·05 for all). Overall, trace element retention appears to be minimally affected by infusion time.

Small for gestational age (SGA) is typically defined as birth weight < 10th percentile for age. Limited data are available regarding the growth of SGA preterm infants in relation to feeding type. We aimed to study SGA preterm infants fed fortified mother’s own milk (MOM) or preterm formula (PF) on growth patterns and catch-up growth at discharge and 2-year corrected age (CA). Our retrospective cohort study included data from medical records and follow-up questionnaires about SGA preterm infants born at < 37 weeks fed on MOM (n 40) and PF (n 40). Weight, length/height and head circumference (HC) were collected at birth, discharge and at 2-year CA, and Δ z-scores were calculated. The MOM group had significantly larger negative change in weight and length z-scores between birth and discharge, and smaller positive change in HC z-score (–0·47 (sd 0·41) v. −0·25 (sd 0·36), P = 0·01; −0·63 (sd 0·75) v. −0·27 (sd 0·75), P = 0·03; 0·13 (sd 0·67) v. 0·41 (sd 0·55), P = 0·04, respectively). Almost half of the MOM-fed infants experienced poor length growth by discharge compared with 22 % of PF-fed infants (P = 0·03). By 2-year CA, both groups had similar positive change in weight and HC z-scores, but MOM-fed infants had a slower increase in height z-score (0·64 (sd 1·30) v. 1·33 (sd 1·33), P = 0·02), and only 40 % had achieved catch-up height compared with 68 % of the PF group (P = 0·02). Our study indicates that fortified MOM-fed SGA preterm infants may need extra nutritional support in the first 2 years of life to achieve height growth potential.