Serum Zinc, Copper, and Selenium Concentrations in Healthy Mothers During Pregnancy, Puerperium, and Lactation: A Longitudinal Study

Zinc deficiency is clearly teratogenic in animals (1). The catabolism of maternal tissues during pregnancy, however, seems to protect the fetus from the teratogenic effects of hypozincemia (2). In humans, most evidence suggesting the importance of zinc during pregnancy comes from patients with acrodermatitis enteropathica, an inherited severe zinc deficiency state. These patients have spontaneous abortions and malformed fetuses unless properly supplemented with zinc (3). Much less is known of the possible teratogenicity of copper deficiency (1). Deficiency of selenium, a third trace element, the availability of which in nutrition has been frequently questioned, has been connected with cardiomyopathy (4) and possibly with atherosclerosis (5) but not with teratogenicity. Serum zinc concentrations diminish during pregnancy (6,7). Moderate decrease is obviously physiological and explainable by hemodilution after the fourteenth week of gestation (8). At the beginning of pregnancy, however, the decrease must be related to other physiological factors (7). Low zinc concentrations in serum leukocytes and placental tissues have been reported in preeclamptic women (9,10), in mothers delivering prematurely (11), and in mothers delivering small-for-date babies (8). Copper levels increase during pregnancy and correlate with ceruloplasmin levels (8). In preeclamptic mothers, placental copper concentration was high (10) and serum copper lower than in controls (9). No data exist on serum selenium levels in pregnant and lactating women. Fasting serum zinc concentrations are slightly lower in Finns compared with inhabitants of many other countries (12). Serum copper values in Finns are in the range reported from other countries, but serum selenium tends to