Zinc supplementation increases growth and circulating insulin-like growth factor I (IGF-I) in growth-retarded Vietnamese children

Abstract

To determine whether zinc deficiency might be involved in the failure to thrive observed in undernourished Vietnamese children, we assessed growth, incidence of infections, and circulating insulin-like growth factor I (IGF-I) concentrations in a double-blind study of zinc supplementation. Growth-retarded children (n=146) aged 4-36 mo were paired according to age, sex, commune, Z scores for weight (WAZ) and for height (HAZ), and number of siblings, and were randomly assigned to receive either 153 micromol (10 mg) Zn/d or a placebo for 5 mo. Weight, height, and episodes of infection were recorded each month and plasma IGF-I was measured 1 and 5 mo after the start of zinc supplementation. Multiple-linear-regression analysis for paired data showed that zinc supplementation increased weight (+0.5 +/- 0.1 kg; P<0.001) and height (+1.5+/-0.2 cm; P<0.001) after 5 mo compared with placebo treatment. The relative risk of infectious episodes in the zinc-treated subjects was reduced 3-fold for diarrhea (P=0.012) and 2.5-fold for respiratory infections (p=0.057). The probability of having at least two episodes of diarrhea or respiratory infection was 2.9- and 3.2-fold lower, respectively, in zinc-treated subjects between 1 and 5 mo (P=0.018), whereas they did not change in placebo-treated subjects (P-0.584). After 1 mo, IGF-I concentration (-x+/-SD) in zinc-treated subjects was 2.8+/-0.3 nmol/L compared with 1.9+/-0.2 nmol/L in placebo-treated subjects (P=0.021). After 5 mo, the values were 3.4+/-0.5 nmol/L (zinc-treated) and 2.0+/-0.3 nmol/L (placebo-treated; P=0.044). Our study suggests that zinc deficiency may limit growth in nutritionally deprived children. Because the increase in growth velocity resulting from zinc supplementation was associated with increased plasma IGF-I concentrations, we suggest that the growth-stimulating effect of zinc might be mediated through changes in circulating IGF-I.