The relationship between calcium intake and the appearance of edema-, proteinuria-, and hypertension-gestosis (EPH-gestosis) in pregnancy is examined in the present paper. Epidemiological data indicating that in populations with low calcium intake the incidence of eclampsia is higher, are reviewed. This association cannot be explained by socioeconomic factors alone, since populations with low socioeconomic levels whose traditional diets contain foods rich in calcium, such as those of Guatemala and Ethiopia, demonstrate low incidences of eclampsia. Studies of food supplementation of pregnant women are also reviewed, and it is noted that the intake of supplements containing calcium is associated with decreased incidence of toxemia. The basic physiopathological mechanism of EPH-gestosis increases peripheral vasoconstriction, explains most of the symptomatology of this disorder. It has been noted that individuals with high calcium intake have lower blood pressure and that rats with restricted calcium intake develop hypertension that is reversible by calcium administration. Furthermore, the eclampsia syndrome is quite similar to that of tetany caused by hypocalcemia. During pregnancy certain alterations in the consumption and metabolism of calcium develop. On the one hand, the high fetal consumption of calcium dramatically increases the requirements, and on the other, an operational decrease in the renal and osseus compensating mechanisms for hypocalcemia occurs. Both lead to an obvious state of deficiency not seen at any other physiological stage of a woman's life. Further study and research are needed to evaluate or reject the hypothesis raised by these observations. If the hypothesis of a causal role of calcium deficiency in the occurrence of EPH-gestosis were to be confirmed, it would be of considerable public health importance, since early calcium supplementation to pregnant women might reduce the incidence of this disease.