Investigations into the potential clinical applications of growth hormone (GH) has increased over the past 10 years, following the availability of human recombinant GH (hGH). Although GH replacement had proven to be effective and well-tolerated in GH-deficient children, its use was not widespread until the mid-1980s. Until then, supply had been limited because GH was obtained by extraction from pituitary glands of human cadavers. The purity of the extracted GH became an issue because of an association with outbreaks of Jacob-Creutzfeldt disease, a fatal neurodegenerative disorder. However, the manufacture of recombinant hGH in the 1980s prompted investigators to evaluate uses of GH beyond the treatment of GH-deficient children. As a result, investigators were encouraged to learn more about the basic mechanisms controlling the episodic nature of GH release and about the function of GH at the cellular level. In this introductory chapter, I first review the regulatory role of growth hormone releasing-hormone (GHRH), somatostatin (sst or SRIF), and the GH-secretagogue receptor (GHS-R), referring to relevant chapters in this volume. I then review the content of the remaining chapters. This will provide a brief summary of the current molecular understanding of the GH receptor and its potential role in the central nervous system (CNS) followed by an overview of the clinical aspects of GH deficiency, indications for its replacement, and associated benefits of direct and indirect GH replacement.
