A Century of Growth Hormone from Pierre Marie (1886) to Creutzfeldt-Jakob Disease (1985)

The century from1886 to 1985 was auspicious for those with an interest in growth. A clinically recognized overgrowth syndrome was named acromegaly. It explained some earlier described patients and even distant historical figures. Quickly this clinical syndrome was tied to a pituitary tumor and therapy from a group of innovative neurosurgeons. Contemporaneously, failure of the pituitary was recognized and noted to be a cause of severe growth failure and infantilism. Experimentally, new techniques were developed to hypophysectomize animals from tadpoles to rats as well as to learn to extract, purify and replace the missing pituitary hormones with increasingly pure and potent extracts from bovine pituitaries.

These developments led to the concept of species specificity for growth hormone (GH), that is, only primate GH was biologically effective in primates, as well as the active core hypothesis which postulated that all species had GH molecules with active centers for their pleotropic effects and that unmasking them might make portions of the animal GH molecules active in man. In the end that has not proven correct, but became moot given the explosion of the molecular biology era with its virtually unlimited supply of recombinant hGH.

Human (primate) GH is species specific and to date the active core hypothesis which might have provided biologically effective peptides, derived from animal or human GHs, and likely to be synthesized with the techniques available at that time (mid-1960s) were never required given that rhGH was approved for clinical use in those with hypopituitarism.