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RCT: Vitamin D supplementation may reduce arterial stiffness among individuals with high levels of oxidative stress

Posted on: December 27, 2014   by  Amber Tovey


A recent randomized controlled trial found that vitamin D supplementation reduced inflammation and oxidative stress in overweight, vitamin D deficient African Americans, but only decreased arterial stiffness in those with high levels of oxidative stress.

Arterial stiffness is the loss of elasticity in the arteries. It serves as a strong predictor for cardiovascular events, including stroke and heart attack, the two leading causes of death in the United States.

Vitamin D receptors are present in the arteries, which has led researchers to believe that vitamin D plays a role in arterial stiffness.

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2 Responses to RCT: Vitamin D supplementation may reduce arterial stiffness among individuals with high levels of oxidative stress

  1. [email protected]

    Our current state of knowledge that most soft tissue responses are from cell direct utilization of D3 as opposed to bone and gut calcium mechanism utilization of 25(OH)D should be specifically recognized as a limitation of study if bolus monthly dose is used and an end point is a soft tissue response. If D3 has a half life in the body of about 24 hours, that means that within 3 days there is almost none of the primary ingredient used by soft tissue after the initiation of the once monthly dose. Although 25(OH)D tightly bound to vitamin D binding protein level will remain raised if it has a half life in the body of about 3 weeks, it is tightly bound and not available to the soft tissues unless converted to 125 in the kidneys in very tiny amounts if it has only a half of about 2 hours. I appreciated that the authors cited a 2010 study by BW Hollis but the current state of knowledge presented by Hollis showing the autocrine system utilization by soft tissue cells of D3 directly converting to 125 for in-cell utilization and the heat microphotography demonstrating that activation should raise big red flags to limited effects of any bolus dose design for non-skeletal effect.
    Although we use 25(OH)D as the vitamin D status proxy, if maybe 85 percent of cell response is directly reliant on availability of D3, that D3 availability should be paramount in study design and analysis.

    • [email protected]

      Rep Seaton, so you are saying the “bolus” dose is of limited benefit. Why would a bolus dose be used in the first place? This would not simulate normal dosages of sunshine or food. Also what about other needs with vit D, such as vit A and magnesium? Seems that these should also be supplement or at least monitored. Would you know about this or any other caveats?

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