The hCG Group: the Key Molecules in Human Evolution, Human Life, and Human Death

Abstract

The term hCG refers to a group of molecules with common amino acid sequence, different glycosylation, and multimeric structure. These molecules include the pregnancy hormone hCG, made by placental syncytiotrophoblast cells, and the pregnancy autocrine hyperglycosylated hCG, made by placental cytotrophoblast cells, which drives placental growth during pregnancy and implantation of the placenta. Most human cancers make hyperglycosylated hCG free β-subunit. This drives cancer malignancy by following the invasive implantation pathway. Whereas hCG functions by acting on an hCG/LH joint receptor, hyperglycosylated hCG and hyperglycosylated hCG free β-subunit function by antagonizing a TGFβ receptor. CG and hyperglycosylated hCG first evolved with early simian primates. The early simian CG and hyperglycosylated CG were nonacidic rapidly clearing molecules. With their evolution evolved a primitive form of hemochorial placentation, primitive in that it was only minimally promoted by CG and hyperglycosylated CG. With the evolution of advanced simian primates came acidic variant of hCG and hyperglycosylated CG. The more acidic CG was longer circulating and more effectively promoted the establishment and growth of hemochorial placentation. With the evolution of humans came a very acidic variant of CG and hyperglycosylated CG. This was very much longer circulating and was an effective stimulant of hemochorial placentation. Early prosimian primates had a brain of 0.07 % of body mass, early simian primates had a brain mass of 0.17 %, advanced simian primates of 0.74 %, and humans of 2.4 %. Research indicates that brain mass grew with improving CG and hyperglycosylated CG activity and improving hemochorial placentation activity. The super CG variant produced by humans plays a key role in human pregnancy implantation and in failures of pregnancy, hypertense pregnancy, and invasion by gestational trophoblastic diseases. Research today shows that hyperglycosylated CG and hyperglycosylated CG free β-subunit drive most human trophoblastic and nontrophoblastic malignancies.