“…A reflection of this role is the increased circulating level of the peptide at these times Stevenson, Hillyard, MacIntyre, Cooper & Whitehead, 1979). Conversely, there is evidence that failure of ovarian function at the menopause (whether natural or artificial) is followed by a fall in circulating calcitonin levels accompanied by evidence of increased osteoclastic activity (Stevenson, MacIntyre & Whitehead, 1982;Taggert, Chesnut, Ivey, Baylink, Sisom, Huber & Roos, 1982). Certainly, the reversal of the fall in circulating calcitonin levels (Morimoto, Tsuji, Okada, Onishi & Kumahara, 1980;Stevenson, Abeyasekera, Hillyard, Phang, MacIntyre, Campbell, Lane, Townsend, Young & Whitehead, 1983) by oestrogen administration and the evidence that calcitonin can inhibit postmenopausal bone loss suggests that the hormone has a normal physiological role in maintaining skeletal integrity.…”