Hi Carey, Levodopa therapy is associated with high homocysteine levels. The COMT pathway is involved in the production of homocysteine from the conversion of levodopa. COMT inhibitors decrease this reaction. The increase in homocysteine levels does not occur with dopamine agonists.

(from my notes--do not have the reference)

Plasma total homocysteine depends on folic acid, B6 , B2 and B 12 which work together to support methylation from total homocysteine to methionine. However methylation of levodopa and dopamine by COMT interferes with this process by consuming methyl groups in the transmethylation reactions thereby increasing S-adenosylhomocyteine (SAH) concentrations in tissues which is rapidly converted to homocysteine, as well as significant decreases of SAMe.
Animal studies show levodopa induced hyperhomocysteinemia is consequence of significant O-methylation and that the COMT inhibitors can prevent such elevation of Hcy concentrations by reducing the O-methylation of levodopa.

Findings indicate levodopa induced hyperhomocysteinemia can be caused by competition at site of methylation, rather than by a defieiency of folate or other B vitamins
(I have read levodopa and B 6 should not be taken together, but that B6 is not contraindicated when taking levodopa. There is evidence one should not take too much B6 )