The Spanish deer population had a major problem back in 2005; they suffered antler breakage at an alarming rate. Researchers determined that harsh winter conditions had resulted in a dietary manganese deficiency that was causing the problem. And this has now led researchers to propose a new human theory for osteoporosis based on manganese deficiency. I find this story rather interesting and think the hypothesis has merit.

Ever since basketball star Bill Walton’s recurring fractures (in a young, healthy male) were traced to diet-induced manganese deficiency, the role of manganese in bone health has been acknowledged. Manganese is needed to help calcium form the proper structural matrix of bone, as well as assisting calcium absorption.

Deers are interesting because they are constantly sending calcium from other bones to their antler bones. The lack of manganese inhibited the antler bones from forming properly. This led researchers to ponder on the priority of how manganese is used in the human body and whether or not manganese deficiency could actually cause bone loss in humans.

They reasoned that our bodies have many needs for manganese, especially in glial cells of the brain. Bones are in a constant state of turnover, taking down old bone and building new bone in its place. As old bone is being taken down, magnesium is released and then used again to help make new bones. However, what if there was a need for manganese some other place which had a higher priority. Possibly the manganese would be diverted away from bones to help out.

The researchers focused on the glial cells in the brain, which have a high need for manganese to run antioxidant enzyme systems. They analyzed 113 patients who were operated on for osteoporosis and osteoarthritis. 40% of those operated on for osteoporosis showed some form of cerebral dysfunction whereas this was not the case in any of the 68 patients operated on for osteoarthritis.

Manganese is also crucial for the function of the antioxidant enzyme within cells known as manganese superoxide dismutase (Mn-SOD) that impacts cellular function and thyroid metabolism. Thyroid hormone governs the rate of oxygen use inside cells as a natural part of the metabolic activity that determines metabolic rate. During this process oxygen is converted to the free radical O2 (superoxide anion), which must be cleared by Mn-SOD activity so as to protect the mitochondria from elevated free radical damage.

I have used manganese for years, along with selenium, to help individuals improve their thyroid function and cellular metabolism. This basic understanding of manganese need in virtually every cell of our body, combined with increasing free radical distress during aging, certainly lends to the notion that manganese being temporarily released from bone could be drawn to other areas in need and then not be available to support new born formation. Certainly, poor thyroid function has been linked to poor bone status.

While manganese is not the only reason for bone loss, this emerging picture indicates that if it is lacking bone health is compromised. This is more likely to be the case if there is also an issue with cognitive function and/or sluggish thyroid.



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