Effect of consumption of food cooked in iron pots on iron status and growth of young children: a randomised trial.

BACKGROUND: In less-developed countries, novel strategies are needed to control iron-deficiency anaemia, the most common form of malnutrition. METHODS: We undertook a community-based randomised controlled trial to assess the effects of iron or aluminium cooking pots in young Ethiopian children. Analysis was by intention-to-treat. The primary outcomes were change in children's haemoglobin concentration, weight, or length over the study period. We also did a laboratory study of total and available iron in traditional Ethiopian foods cooked in iron, aluminium, and clay pots. FINDINGS: 407 children, one per household, entered the study. The change in haemoglobin concentration was greater in the iron-pot group than in the aluminium-pot group (mean change to 12 months 1.7 [SD 1.5] vs 0.4 [1.0] g/dL; mean difference between groups 1.3 g/dL [95% Cl 1.1-1.6]). The mean differences between the groups in weight and length gain to 12 months (adjusted for baseline weight or length) were 0.6 cm (95% CI 0.1-1.0) and 0.1 kg (-0.1 to 0.3). The laboratory study showed that total and available iron was greatest in foods cooked in iron pots, except for available iron in legumes for which there was no difference between types of pot. INTERPRETATION: Ethiopian children fed food from iron pots had lower rates of anaemia and better growth than children whose food was cooked in aluminium pots. Provision of iron cooking pots for households in less-developed countries may be a useful method to prevent iron-deficiency anaemia.

Failure of IGF-I infusion to promote growth in Zn deficient hypophysectomized rats.

The retarded growth of zinc-deficient rats is associated with low plasma insulin-like growth factor-I (IGF-I). To determine whether the low circulating IGF-I concentrations are responsible for the stunted growth, the growth response of zinc-deficient hypophysectomized rats to supplementation with recombinant human IGF-I (hIGF-I) was investigated. There were three dietary groups: zinc-deficient (0.9 mg zinc/kg diet), controls (66 mg zinc/kg diet) and zinc-adequate pair-fed (66 mg zinc/kg diet). All rats in each group received hIGF-I (150 micrograms/day) by subcutaneous infusion for 12 days, except for half of the animals in the control group which were sham-treated and which received vehicle infusion for the same period of time. The magnitude of the change was small, nevertheless infusion of hIGF-I significantly increased (p < 0.05) the body weight, tail length, liver weight and tibial epiphyseal width of control animals. This growth effect of hIGF-I was inhibited by lack of zinc in the diet, as evidenced by continuous weight loss, no increase in tail length and lowered tibial epiphyseal width in zinc-deficient animals. We conclude that systemic supplementation of hIGF-I can promote growth in hypophysectomized rats. The absence of weight gain and bone growth in zinc-deficient animals during the infusion period suggests that the growth promoting effect of circulating IGF-I is impaired by zinc deficiency.

Zinc deficiency inhibits the direct growth effect of growth hormone on the tibia of hypophysectomized rats.

The effect of zinc deficiency on the direct-growth effect of growth hormone (GH) on tibia growth in hypophysectomized rats was studied. There were three dietary groups. Zinc deficient (ZD) group (0.9 mg/kg diet), control (C) group (66 mg/kg diet) and zinc adequate pair fed (PF) group (66 mg zinc/kg diet). All rats in each group received local infusion of recombinant human-growth hormone (hGH) (1 microgram/d), except for half of the animals in the control group, which were sham-treated, receiving vehicle infusion only. The substances were infused continuously for 13 d by osmotic minipumps through a catheter implanted into the right femoral artery. Food intake was lower and body weight loss was greater in ZD, and PF animals compared with C animals (p < 0.001). Tissue-zinc concentration and plasma alkaline-phosphatase activity were decreased (p < 0.05) by dietary-zinc deficiency. GH infusion increased the tibial-epiphyseal width of the treated right limb, but not of the noninfused left limb in C and PF animals. However, in ZD rats, no difference was found between the infused and the noninfused limbs. These results demonstrate that zinc deficiency inhibits the direct-growth effect of GH on long-bone growth.

Selected nutrient intakes and blood serum mineral concentrations of elderly humans fed regular and sweet acidophilus milks.

Calorie, protein, fat, calcium, phosphorus and manganese intakes were retrospectively calculated from the self-recorded intakes of 12 elderly humans, who were fed regular and sweet acidophilus milks in addition to their normal free choice diets. Blood serum of the subjects was analyzed for total calcium, ionized calcium, phosphorus and manganese at the beginning of the study, at cross-overtime of milk treatments and at the end of the study. Total serum calcium, serum ionized calcium and phosphorus levels of the subjects were significantly higher at the end of the eight week study compared to pre-study levels (p < 0.05). The kind of milk had no effect on serum levels of total calcium, ionized calcium, phosphorus and manganese. High dietary levels of calcium and phosphorus had no significant effect on serum manganese concentrations.

The effects of sugar-beet fibre supplementation for five weeks on zinc, iron and copper status in human subjects.

The present study was conducted to evaluate the effects of fibre supplementation on zinc, iron and copper status in human subjects. Ten males (53 +/- 8 years of age) participated in this study which consisted of three phases: baseline-1 period (2 weeks) in which subjects were on their normal, habitual dietary intake, followed by a period of fibre supplementation (5 weeks) in which subjects were supplemented with 26 g dietary fibre/d, and baseline-2 period (4 weeks) in which fibre supplement was withdrawn. Parametric measurements of zinc, iron and copper status were conducted on weeks 1,2 (zero-time), 7 and 11. Results showed that fibre supplementation for 5 weeks did not cause any significant change in the status of zinc (measured by concentration of zinc in plasma and urine and alkaline phosphatase activity), iron (measured by packed cell volume (PCV%), HB, transferrin saturation % and ferritin), or copper (measured by plasma copper concentration and erythrocyte superoxide dismutase activity). We conclude that consumption of sugar-beet fibre added to the daily diet does not constitute any risk with respect to zinc, iron and copper nutriture.

Fibre in enteral formulae: effects of sugar-beet versus soy fibre on zinc and folic acid absorption in human subjects.

The present study was conducted to compare the effect of soypolysaccharide (Fibrem) and sugar-beet (Fibrex) on zinc and folic acid absorption when incorporated into enteral formulae. Following an overnight fast, 15 adults were challenged with an oral dose of zinc (60 mg) and folic acid (600 mug) given with enteral formula without fibre, or with 15g of dietary fibre from Fibrem or Fibrex. Serum concentrations of zinc and folic acid were measured at zero-time and at hourly intervals for up to 5h. Results showed that Fibrem caused a significant decrease in the concentrations of zinc and folic acid. However, Fibrex caused a slight increase in serum zinc concentration and a less pronounced decrease in serum folic acid concentration as compared to Fibrem. We conclude that for patients who are at risk of zinc or folic acid deficiency, the fibre source in enteral formulae should be selected carefully.

Protein and fat utilization by humans as affected by calcium phosphate, calcium carbonate, and manganese gluconate supplements.

The object of this study was to determine the effect of calcium carbonate or calcium phosphate supplements on dietary protein and fat utilization from low and high manganese diets. During the 63-day study, the 14 human adult subjects ate a constant laboratory controlled diet. In separate periods, subjects consumed the basal diet alone or with supplements of calcium carbonate, calcium carbonate plus manganese gluconate, calcium phosphate, or calcium phosphate plus manganese gluconate. Contrast analyses of data indicated that manganese gluconate supplementation of diets, when combined with either calcium phosphate or calcium carbonate, increased fecal losses of fat. When used as single supplements, both calcium phosphate and calcium carbonate depressed fecal fat loss in comparison with values when no supplements were used. Manganese gluconate supplements depressed fecal nitrogen losses calculated as a percentage of dry fecal weight.