| Abstract: | The origins of nutritional trace element deficiencies are summarized. Inadequate intake results in primary deficiency, whereas secondary or conditioned deficiencies can arise in several ways including trace element interactions. Evidence is presented and discussed for interactions of essential trace elements during prenatal and early postnatal development. Diets of widely different zinc and copper concentrations and ratios were fed to pregnant rats. Analysis of fetal outcome and copper and zinc concentrations of maternal and fetal livers showed that although there is an interaction between these metals it occurs only at levels of dietary copper deficiency. Iron and manganese interact so that high levels of one depress absorption of the other. Mice fed iron-supplemented diets had liver manganese concentrations lower than those of unsupplemented mice. Iron supplements at high but not low levels also depressed absorption of zinc. Conversely, zinc deficiency in pregnant rats caused higher than normal concentrations of iron in maternal and fetal liver. Trace element analyses of proprietary infant formulas indicate that in some, concentrations and ratios of these trace elements may be incorrect. The effects of essential trace element interactions during development should be further investigated. Caution is urged in considering levels of trace element supplements during pregnancy, lactation, or early childhood. |
