The evolution of regular chorionic gonadotropin (CG) and hyperglycosylated CG are linked with the evolution of hemochorial placentation in primates. Recent research with humans shows that regular CG promotes spiral artery angiogenesis and hyperglycosylated CG controls invasion by implanting trophoblast cells. It is inferred that the evolution of regular CG and hyperglycosylated CG in early simian primates, the first species to produce these CG forms, established hemochorial placentation in this species. The circulating half-lives, and thus the circulating concentrations, of regular CG and hyperglycosylated CG increased in advanced simian primates and increased further in humans, seemingly causing greater myometrial invasion and superior angiogenesis in hemochorial placentation in advanced primates and humans. Advanced hemochorial placentation is associated with relatively high proportions of pregnancy failures in humans. This can be explained by considering human implantation inadequate in terms of invasion requirements. The demanding implantation required by the human embryo is seemingly dependent on adequate production of hyperglycosylated CG. Failures in hemochorial placentation invasion lead to anoxia and cause preeclampsia and eclampsia uniquely in humans, which can also be attributed to inadequate hyperglycosylated CG signaling. We propose here that inadequate regular CG and hyperglycosylated CG molecules are the evolutionary causes of these obstetric complications in humans.