Zinc is present in and indispensable to all forms of life. Zinc is essential for the normal growth of human beings, and zinc proteins have been shown to be involved in the transcription and translation of the genetic material. Zinc deficiency has been incriminated in infertility, abortions, malformations, fetal intrauterine growth retardation, premature and postmature births, perinatal death, and abnormal deliveries with dystocia and placental ablation. Risk groups for developing zinc deficiency, which in turn might modify the expression of the underlying disease, are found among those with insufficient food intake, especially in protein malnutrition; abnormal mucosal uptake, as in celiac disease; abnormal intestinal losses, as in steatorrhea and inflammatory bowel disease; abnormal renal excretion, as in diabetes with insufficient metabolic control; alcoholism; and treatment with diuretic drugs. Zinc deficiency could be identified by means of fasting serum or plasma samples or the more laborious estimation of zinc in leucocytes or monocytes if sampling and handling is carefully performed and if stressful situations and acute-phase reactions as fever, delivery, or abortion are avoided. Zinc therapy in identified low-zinc groups has given favorable results and has reduced the frequencies of premature birth, placental ablation, perinatal death, and postmaturity. It is suggested, as we did in 1980, that these data are compatible with the presence of a zinc-deficiency syndrome in pregnancy, which includes increased maternal morbidity, abnormal taste sensations, abnormally short or prolonged gestations, inefficient labor, atonic bleeding, and increased risks to the fetus such as malformations, growth retardation, prematurity, postmaturity, and perinatal death.