Michael Mooney
www.michaelmooney.net
By Michael Mooney
March 9, 2012
A new mouse study said that vitamin E causes bone loss, contradicting what previous mice studies said.
The press ran with it, while providing no counterpoint, such as stating that this study contradicts several previous studies.
No, the press' first priority is to sell, sell, sell, so they value creating controversy, even when they have to blow the importance of a study like this far out of proportion.
Unfortunately, most readers don't know that they are being harmed by being misinformed.
The press could also have challenged the study, because it is but one study and it's a mouse study, which may not apply to humans.
What the previous mouse studies said was that vitamin E's anti-inflammatory effects can reduce the inflammatory activities that cause bone loss.
Here's what two studies said.
The first study showed that high dose vitamin E "enhanced bone quality as evident by improved material and structural bone properties" in old mice.
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Arjmandi B, et al. Vitamin E improves bone quality in the aged but not in young adult male mice. Journal of Nutritional Biochemistry. 2002 Sep;13(9):543.
Abstract
It is generally viewed that with advancing age, humans and other animals including mice experience a gradual decline in the rate of bone formation. This, in part, may be due to the rise in oxygen-derived free radical formation.
Vitamin E, a strong antioxidant, functions as a free radical scavenger that potentially can suppress bone resorption while stimulating bone formation.
Although the effects of vitamin E on immune functions are well documented, there is a paucity of information on its effect on skeletal health in vivo. The purpose of this study was to explore the influence of vitamin E supplementation on bone in young adult and old mice.
Six and twenty-four month-old male C57BL/6NIA mice each were divided into two groups and fed a diet containing either adequate (30 mg/kg diet) or high (500 mg/kg diet) levels of vitamin E.
Thirty days later, mice were killed and bones were removed for analyses including biomechanical testing using three-point bending and mRNA expressions of insulin-like growth factor-I (IGF-I), osteocalcin, and type 1alpha-collagen using Northern blot.
In old but not the young adult mice, high-dose vitamin E enhanced bone quality as evident by improved material and structural bone properties in comparison with adequate.
This improved quality was accompanied by increases in bone dry weight, protein, and mRNA transcripts for osteocalcin, type Ialpha-collagen, and IGF-I.
These data demonstrate that high-dose vitamin E has pronounced effects on bone quality as well as matrix protein in old mice by augmenting bone matrix protein without reducing bone mineralization as evidenced by unaltered bone density.
PMID: 12231425
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The second study said that when rats were challenged with bone loss, high-dose vitamin E protected against bone loss.
Smith BJ, et al. Vitamin E provides protection for bone in mature hind limb unloaded male rats. Calcified Tissue International. 2005 Apr;76(4):272-9. Epub 2004 Mar 8.
Abstract
The deleterious effects of skeletal unloading on bone mass and strength may, in part, result from increased production of oxygen-derived free radicals and proinflammatory cytokines.
This study was designed to evaluate the ability of vitamin E (alpha-tocopherol), a free-radical scavenger with antiinflammatory properties, to protect against bone loss caused by skeletal unloading in mature male Sprague-Dawley rats.
A 2 x 3 factorial design was used with either hindlimb unloading (HU) or normal loading (ambulatory; AMB), and low-dose (LD; 15 IU/kg diet), adequate-dose (AD; 75 IU/kg diet), or high-dose (HD; 500 IU/kg diet) vitamin E (DL-alpha-tocopherol acetate).
To optimize the effects of vitamin E on bone, dietary treatments were initiated 9 weeks prior to unloading and continued during the 4-week unloading period, at which time animals were euthanized and blood and tissue samples were collected.
Serum vitamin E was dose-dependently increased, confirming the vitamin E status of animals.
The high dose (HD) treatment improved oxidation parameters, as indicated by elevated serum ferric-reducing ability and a trend toward reducing tissue lipid peroxidation.
Histomorphometric analysis of the distal femur revealed significant reductions in trabecular thickness (TbTh), double-labeled surface (dLS/BS), and rate of bone formation to bone volume (BFR/BV) due by HU. AMB animals on the HD diet and HU animals on the LD diet had reduced bone surface normalized to tissue volume (BS/TV) and trabecular number (TbN); however, the HD vitamin E protected against these changes in the HU animals.
Our findings suggest that vitamin E supplementation provides modest bone protective effects during skeletal unloading.
PMID: 15742232
The next time you read an article that says that some vitamin that you thought was safe and was good for you isn't, please come back to the area on my website devoted to correcting misinformation in the press. http://www.michaelmooney.net/#Corrections
Be well,
Michael Mooney
www.michaelmooney.net