Antioxidants Protect Against Bone Loss

The more we learn about genes the more obvious it becomes that nutrition is the key to health, including bone health.  A gene regulatory protein called Maf¹ has now been identified which is needed in order to change bone stem cells into the important bone-building carpenters called osteoblasts.  Too many free radicals, or the use of the diabetes drugs Avandia or Actos, causes Maf to turn off.  This causes the stem cells to turn into fat cells instead of osteoblasts, causing bone loss and risk for osteoporosis.

Over the past several years a large body of science has shown how inflammation, which invariably involves excess free radical production as a consequence, interferes with osteoblasts and causes excessive activity of the osteoclast demo crew.  This new study pinpoints the precise gene regulation that enables new osteoblasts to form.  It is simple math:  if you lack osteoblasts and have too many osteoclasts Type of bone cell that removes old, damaged bone by the process bone resorption. then you will lose bone density.

A primary mechanism that deactivates Maf is too many free radicals.  Excessive free radicals occur when you lack antioxidants and have various forms of stress that use up your antioxidants.  Almost any type of stress uses up antioxidants including a poor quality diet, pollution, alcohol, smoking, numerous medications, excessive exercise, no exercise, lack of sleep, pain, emotional stress, etc.  To remedy this problem you must offset stressors in your life and boost up antioxidants.

This study lends significant support to the fact that anti-inflammatory nutrients which typically have antioxidant activity are a primary tool to prevent bone loss.

On the other hand, the FDA has recently curtailed the use of the diabetes drug Avandia, but not its cousin Actos.  Both Avandia and Actos are known to causes a depletion of osteoblasts and an excess production of fat cells in bone.  Both drugs are linked to increased risk of breaking bones.  This new study explains the gene transcription mechanism on why these drugs are so adverse to bone health.