We propose that the high serum TSH levels in men with Gleason 8 prostate cancer is a result of the elaboration of TSH by cancer cells. Bone mineral density in the face of normal levels of thyroid hormone depends on an intact response to TSH, which ordinarily suppresses both osteoblast and osteoclast differentiation, thereby exerting control over bone remodelling. However, with abnormally high TSH levels this process may become deranged, promoting the development of bone metastases. If TSH production by prostate cancer cells could be suppressed, the incidence of bone metastases might be reduced.