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The Homocysteine and Cardiovascular Disease connection: Further Information.

 

Further Information on the Homocysteine and Cardiovascular Disease connection.

A recent study in the journal, Circulation, has cast some doubt on the exactl nature of the link between homocysteine and heart disease. An editorial in that publication implied that we may in fact be somewhat premature in how we have viewed the role of homocysteine.

While it may be true that we do not yet have all of the facts, we need to be careful to keep everything in proper perspective. We do know that there is a connection, and we do know that increasing the B vitamins folate, B6 and B12, with a lowering of homocysteine, seems to be protective. It is certain worth trying for those who are at risk. What is the downside of increasing our supplement and or dietary intake of these inexpensive and beneficial nutrients?

Steve Austin, N.D., wrote an insightful commentary in the Quarterly Review of Natural Medicine 12-31-98 p. 305-307

His article was titled Clouds Appear in the Relationship Between Homocysteine and Cardiovascular Disease.

 

Readers of this column know that numerous trials report a positive link between serum homocysteine and coronary heart disease (CHD). Likewise, there is clear evidence that folic acid and to a lesser extent vitamins B6 and B12 lower homocysteine levels. As homocysteine induces vascular damage both in vitro and in animal models, it has been widely assumed that homocysteine is not simply a marker, but rather probably a contributory agent.

Recently, a large (232 coronary heart disease cases) nested (prospective) casecontrol study by Folsom, et al. in Circulation was unable to solidly confirm an independent correlation between elevated homocysteine and cardiovascular disease (average follow up of 3.3 years).(1) In that report, higher B6 status (measured as pyridoxal 5'-phosphate) correlated strongly with protection, but dietary B6 did not, nor did other B vitamins. If the relationship between PLP and cardiovascular protection had anything to do with homocysteine, folic acid status should have also been linked to protection because folate status is a much stronger determinant of homocysteine levels than is B6 status.

A skeptical editorial appeared in the same issue of Circulation.(2) In that editorial, the follow points were made, with literature support:

?Myocardial infarction increases homocysteine, providing a different perspective on what might be chicken and what might be egg.

?In vitro experiments purporting to show that homocysteine is atherogenic are conducted at concentrations far in excess of what really occurs in vivo.

?There is at least some animal evidence that B-vitamin supplementation-induced decreases in homocysteine are not accompanied by improvement in endothelial function.

?Several lines of research have not linked genetic defects in enzyme activation that cause homocysteine elevations to vascular disease, suggesting that the strong link between homocysteine and CHD may not be cause and effect.

An hypothesis is put forward in the editorial that possibly the inflammatory component of atherosclerosis increases demand for folic acid, and the drop in folate status causes homocysteine to rise, but only as a marker -- not as a significant player.

On the other hand, the editorial acknowledges that B-vitamin deficiency might be directly linked to heart disease and treating with supplements might be protective, though the consequent fall in homocysteine might merely be the decline of an uninvolved marker.

There remains little question that B-vitamin supplementation lowers homocysteine(3) -- the recent public

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