The practice of giving estrogen to normal girls destined to become taller than they wish goes back to the 1940s. The train of thought leading up to the first trials includes two basic observations. First, it was noted that children in whom persistent precocity syndromes develop early in life become short adults and have premature epiphyseal closure. Second, and conversely, in the absence of the gonadal steroids, the epiphyses remain open indefinitely and growth continues beyond the usual age of cessation. While the majority of these cases are complicated by the presence of pituitary disease and the fact that because of their lack of growth hormone the patients are small, the early clinicians bolstered their faith in the converse by their admiration of the enormous size reputed to be attained by the harem eunuchs.
These observations prompted two conclusions. First, gonadal steroids were not only responsible for closing the epiphyses but also for "turning off" secretion of growth hormone. Thus, in the early 1930s, it was reasoned that while children would be well endowed, adults must lack any circulating pituitary growth hormone, save in the rare instance of acromegaly. These were the concepts that led to the treatment of that disorder first with gonadal extracts,1,2 then, when pure steroids became available, with androgens and estrogens.3 The effect of testosterone was disappointing; the beneficial influence of estrogen, however, was so impressive as to be taken as proof of the earlier drawn conclusion that it is the gonadal steroids that normally turn off growth hormone secretion at adolescence.
Pre-VersusPostmenopausal Age, Estradiol, and Peptide-Secretagogue Type Determine Pulsatile Growth Hormone Secretion in Healthy Women: Studies Using Submaximal Agonist Drive and an Estrogen Clamp
