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Vitamin Therapy Can Still Reduce Stroke, Researchers Contend

Jan. 12, 2012 — A commentary by University of Western Ontario's David Spence and Harvard School of Public Health's Dr. Meir Stampfer in this week's Journal of the American Medical Association argues vitamin therapy still has a role to play in reducing stroke.


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Vitamin B therapy was once widely used to lower homocysteine levels and too much of this amino acid in the bloodstream was linked to increased risk of stroke and heart attack. But several randomized trials found lowering homocysteine levels with B vitamins did not result in a cardiovascular benefit.

A study by Spence, a scientist with the Robarts Research Institute at Western's Schulich School of Medicine & Dentistry, found Vitamin B therapy actually increased cardiovascular risk in patients with diabetic nephropathy.

He says this commentary provides insights that overturn the widespread belief that homocysteine is dead. He says two key issues have been overlooked in the interpretation of several clinical trials: the key role of vitamin B12, and the newly recognized role of renal failure.

"It is now clear that the large trials showing no benefit of vitamin therapy obscured the benefit of vitamin therapy because they lumped together patients with renal failure and those with good renal function, says Spence, the author of How to Prevent Your Stroke. "The vitamins are harmful in renal failure, and beneficial in patients with good renal function, and they cancel each other out."

The commentary also contends most of the trials did not use a high enough dose of vitamin B12.

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The above story is reprinted from materials provided by University of Western Ontario.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. J. D. Spence, M. J. Stampfer. Understanding the Complexity of Homocysteine Lowering With Vitamins: The Potential Role of Subgroup Analyses. JAMA: The Journal of the American Medical Association, 2011; 306 (23): 2610 DOI: 10.1001/jama.2011.1834
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