Q: How can I lower my homocysteine levels?

A:  Homocysteine is a derivative of the amino acid methionine and elevated plasma homocysteine is associated with an increased risk of heart disease and mental decline. Though we know it is possible to bring down homocysteine, the question is whether supplementing to bring the numbers down is worth it. At this point the research is not clear to whether there are any practical, clinical benefits; studies actually show there are non.

As far as side-effects, the water soluble B vitamins (6,9,12) are pretty safe in general. Nevertheless, Some research suggests that taking folic acid in doses of 800-1200 mcg might increase the risk of heart attack in heart patients. There is also a hint of cancer risk, specifically lung or prostate cancer. I didn’t find any long-term studies on the harm of high dose B12 and B6. There is also supplementation with betaine and choline.
My conclusion is that taking as low as two times the RDA for the B vitamins along with low doses of betaine or choline, such as 50 mg, is a safe long-term approach. I would recommend trying that first and rechecking after two months, and then playing with the dosage from there.
I’ve also included and made comments on a few interesting abstracts below.

Homocysteine, vitamin B-12, folic acid and the cognitive decline in the elderly.

Department of Biochemistry, Faculty of Medicine of Sousse, 4002 Sousse, Tunisie.

Hyperhomocysteinemia is a risk factor for neurological diseases, but the underlying pathophysiology has not been adequately explained. Mild hyperhomocysteinemia, which is sometimes associated with a low plasma level of vitamin B9, B12 and folic acid, is responsible in the toxicity in neural cell by activating NMDA receptor. Indeed, even if vitamin supplementation has clearly proven its efficiency on lowering plasma levels of homocysteine, recent studies do not show any positive effect of vitamin therapy on cognitive function. The hypothesis that this therapy is inefficient has been recently reinforced by two randomized trials on the effects of vitamin supplementation. Several hypotheses still need to be explored: Mechanisms of homocysteine toxicity and that of total uselessness of vitamin supplementation; the possible need to complete the actual data with further, more powerful studies in order to prove the role of homocysteine in the development of neurodegenerative diseases and a clinical effect of vitamin therapy.

There is one other supplement that may also be an option, however. See this study on betaine below:

Low dose betaine supplementation leads to immediate and long term lowering of plasma homocysteine in healthy men and women.
Olthof MR. J Nutr. 2003.

High plasma homocysteine is a risk for cardiovascular disease and can be lowered through supplementation with 6 g/d of betaine. However, dietary intake of betaine is approximately 0.5-2 g/d. Therefore, we investigated whether betaine supplementation in the range of dietary intake lowers plasma homocysteine concentrations in healthy adults. Four groups of 19 healthy subjects ingested three doses of betaine or placebo daily for 6 wk. A methionine loading test was performed during run in, on d 1 of betaine supplementation, and after 2 and 6 wk of betaine supplementation. Fasting plasma homocysteine after 6-wk daily intakes of 1.5, 3 and 6 g of betaine was 12% less than in the placebo group, respectively. Furthermore, the increase in plasma homocysteine after methionine loading on the 1st d of betaine supplementation was 16% less than in the placebo group, respectively, and after 6 wk of supplementation was 23% less, respectively. Thus, doses of betaine in the range of dietary intake reduce fasting and postmethionine loading plasma homocysteine concentrations. A betaine-rich diet might therefore lower cardiovascular disease risk.

But there is the consideration of betaine’s the lipid raising effect:

Effects of betaine intake on plasma homocysteine concentrations and consequences for health.
Curr Drug Metab. 2005.
High plasma concentrations of homocysteine may increase risk of cardiovascular disease. Folic acid lowers plasma homocysteine by 25% maximally, because 5-methyltetrahydrofolate is a methyl donor in the remethylation of homocysteine to methionine. Betaine (trimethylglycine) is also a methyl donor in homocysteine remethylation, but effects on homocysteine have been less thoroughly investigated. Betaine in high doses (6 g/d and higher) is used as homocysteine-lowering therapy for people with hyperhomocysteinemia due to inborn errors in the homocysteine metabolism. Betaine intake from foods is estimated at 0.5-2 g/d. Betaine can also be synthesized endogenously from its precursor choline. Studies in healthy volunteers with plasma homocysteine concentrations in the normal range show that betaine supplementation lowers plasma fasting homocysteine dose-dependently to up to 20% for a dose of 6 g/d of betaine. Moreover, betaine acutely reduces the increase in homocysteine after methionine loading by up to 50%, whereas folic acid has no effect. Betaine doses in the range of dietary intake also lower homocysteine. This implies that betaine can be an important food component that attenuates homocysteine rises after meals. If homocysteine plays a causal role in the development of cardiovascular disease, a diet rich in betaine or choline might benefit cardiovascular health through its homocysteine-lowering effects. However betaine and choline may adversely affect serum lipid concentrations, which can of course increase risk of cardiovascular disease. However, whether the potential beneficial health effects of betaine and choline outweigh the possible adverse effects on serum lipids is as yet unclear.