homocysteinemia may play a role in vascular injury by one or more of the following mechanisms: oxidative damage to the vascular endothelium, altering the thrombotic potential of the endothelium, increased coagulability, and decrease in the production of nitrous oxide.  A direct causal link has not yet been determined in human literature.
Plasma homocysteine levels are strongly influenced by diet as well as genetic factors.  The dietary components with the greatest effects are folic acid, vitamin B6, and vitamin B12.  Folic acid and other B vitamins help to breakdown homcysteine in the body.  Several human studies (including a recent multi-centered European trial) have found that higher blood levels of B vitamins are at least partly related to lower homocysteine concentrations.  Other studies have found that lower folic acid levels have been directly linked to a higher risk of stroke and fatal coronary disease.  There has been no strict controlled study that has shown vitamin B supplementation statistically reduces the risk of vascular disease and thromboembolic disease.
Cats are unique in homocysteine metabolism predisposing them to a greater alteration in blood homocysteine levels or levels of B vitamins.  Cats have a higher dietary need for methionine and vitamin B6 because they are obligatory carnivores.  Because of this, cats are predisposed to deficiencies in these nutrients due to inadequate intake, excessive losses, or altered metabolic state due to diseased conditions.
There have been two major reports dealing with these issues in cats, one from Tufts University and one from the Animal Medical Center.  The AMC report states that hyperhomocysteinemia was detected in cats with cardiomyopathy and cats with arterial thromboembolism.  The Tufts' report did not find significant elevations in homocysteine levels in cardiomyopathic cats with or without trombi. The Tufts' study, though, did find a correlation between low concentrations of B vitamins (especially B12)  and cardiomyopathy.  Both studies also report (as with the human literature) that we do not know if these low levels of B vitamins or these high homocysteine levels are a cause of thromboembolism or just a secondary effect.  The two things these studies do agree upon is that more research needs to be performed especially in terms of

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