Interleukin-6 and Tumor Necrosis Factor-alpha, Which May Boost Homocysteine by Decreasing Hepatic S-Adenosylmethionine, May Mediate the Cardiovascular Risk Associated with Moderately Elevated Homocysteine

Although moderate elevations of the metabolite homocysteine (hcy) correlate with increased risk for heart attack and stroke, the failure of vitamin therapies which lower hcy to reduce vascular risk reveals that moderately elevated hcy per se does not cause heart disease. Why then do hcy levels correlate with risk? It is proposed that hcy levels are often elevated because of the actions of the hormone-like compounds interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) on the liver – and that these hormones do indeed promote vascular disease, in part by inducing the liver to make the pro-inflammatory factor serum amyloid A. Hence, lowering the level or the activity of IL-6 and TNF-alpha may be expected to alleviate the excess cardiovascular risk associated with elevated hcy.

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