According to prevailing unitary model of involutional osteoporosis, female postmenopausal bone loss can be divided into two separate phases: the accelerated, transient phase, which is most distinct over the subsequent decade after the menopause and accounts for 20-30% of the cancellous bone loss and 5-10% of the cortical bone loss (type I osteoporosis), and the following gradual, continuous bone loss (type II osteoporosis). Estrogen deficiency is currently quite unanimously accepted as the primary cause of type I osteoporosis, as well as also a major determinant of type II osteoporosis, and quite plausibly, the quest to uncover the origin of type I (and II) osteoporosis has focused on the estrogen withdrawal-related skeletal changes at and around the menopause. However, given that the cyclical secretion of estrogen begins normally in early adolescence and continues over the entire fertile period (excluding the potential periods of pregnancy) until the eventual cessation of female reproductive capability, one could argue that this menopause-oriented approach is limited in scope. In this review, some classic findings of the pubertal effects of estrogen on female bones are presented, findings that were paramount to Fuller Albright when he first described the disease called postmenopausal osteoporosis in 1940, but studies/findings that have failed to attract the attention they deserve. When these findings are incorporated with the primary function of the axial skeleton and long bones, the locomotion, an alternative, novel explanation for the function of estrogen and accordingly, the origin of the accelerated phase of postmenopausal bone loss, is proposed: estrogen packs mechanically excess bone/mineral into the female skeleton at puberty, a bone stock that later serves as the origin of the type I postmenopausal osteoporosis.