Abstract
Observations on osteoporosis from the sixth century onwards have shown that stress is the main causative factor. This has been confirmed by animal experiments, using rabbits, with stress simulated by the administration of cortisone. For normal health, the hormonal anticatabolic/catabolic ratio should remain on the anticatabolic side. Stress, emotional or otherwise, can tip the balance over to the catabolic side. In the presence of progestational compounds (in the pill or hormone replacement therapy), much lower levels of stress are needed. The main types of osteoporosis are disuse, with a lower blood flow through bone, steroid-induced and thrombus-induced osteoporosis. When the anticatabolic/catabolic ratio tips to the catabolic side, cell membranes become more rigid. Osteogenic precursor cells coalesce to form osteoclasts, which remove bone. Memory cells are affected, and also those responsible for the absorption of food from the gut. Increased catabolic levels also lead to the production of abnormal megakaryocytes. These produce sticky platelets that immediately coalesce to form thrombi. Many can block blood vessels in cortical bone, killing the osteocytes. Later the dead bone is removed by phagocytic cells. Other thrombi are deposited elsewhere in the body, including the coronary arteries. In these ways, hormone replacement therapy may cause osteoporosis, thrombi, heart attacks and senility, rather than preventing them.