Osteoporosis drugs are widely used to promote bone growth. And, in fact, they do their job well. Use of osteoporosis drugs does result in increased bone density, but does not significantly reduce fracture risk over a patient’s lifetime.
But there’s more to it than that. Before prescribing a medication, a doctor should understand how that medication works in the body.
Yet few doctors understand what most medications, including osteoporosis drugs, do to the body. If they did, these drugs would not be prescribed so much.
Bone building is a complex process that requires the two major types of bone cells — osteoblasts and osteoclasts — to work together to remove old, injured tissue and replace it with new bone. Osteoporosis drugs poison an enzyme in the osteoclasts, causing them to die.
The osteoclasts are responsible for removing old and injured bone tissue so that the osteoblasts can build new, stronger bone. When the osteoclasts are poisoned, the normal metabolic pathways for bone growth are disrupted. This may result in thicker bones, but those are not stronger bones.
In fact, research is beginning to show that women who take osteoporosis medications for long periods of time can suffer atypical bone fractures — the bones spontaneously breaking without a major force applied to them.
It doesn’t take an expert to predict that the long-term use of osteoporosis medications will result in poor bone health. A simple look at the biochemistry of bone metabolism, and how the osteoporosis drugs affect it, shows that these drugs are not leading to better bone health.
So if osteoporosis drugs are not effective, how should this condition be treated? Basic bone biochemistry can point us in the right direction. Osteoblasts and osteoclasts need to be supported with nutrients in order to function optimally. The best nutrients for the bones include:
• Vitamin D
• Vitamin K2
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