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Folate deficiency has been associated with vascular disease resulting in heart attack, peripheral vascular disease and stroke. One of the most exciting papers to be published recently, Decreased Rate of Coronary Restenosis After Lowering of Plasma Homocysteine Levels in The New England Journal of Medicine, studied the effect of lowering plasma homocystein levels on restenosis (reblockage) after coronary angioplasty. It revealed that a combination of folate (1 mg), vitamin B12 (400 mcg) and B6 (10 mg) significantly reduces homocystein levels and decreases the rate of restenosis after coronary angioplasty. B6, while it does not lower homocysteine, may have other beneficial effects and has been shown to alter platelet function. No significant side effects were reported. The mechanism whereby elevated homocysteine mediates these effects is not currently known. It has been shown that traditional methods of measuring folate may be insufficient to detect deficiencies resulting in elevated homocysteine that may be amenable to therapy. Folate has been recommended as therapy for patients with rheumatoid arthritis on methotrexate and for depressed patients who fail to respond to antidepressant therapy. In patients with non-insulin dependant diabetes on metformin, elevations of homocysteine amenable to therapy by folate have been demonstrated. Also in diabetics elevated homocysteine levels were associated with elevated mean arterial blood pressure. Low serum folate and high homocysteine levels have been associated with an increased risk of colon cancer. Elevated homocysteine and low serum foate levels have been noted in patients with both untreated and treated hypothyroidism. During pregnancy low concentrations of folate are associated with increased risk of preterm delivery, infant low birth weight and fetal growth retardation, and folate supplementation has been shown to decrease incidence of certain birth defects. References Schnyder S et al. Decreased rate of coronary restenosis after lowering of plasma homocysteine levels. NEJM 2001 Nov29;345(22):1593-1600. Hultberg B et al. Marginal folate deficiency as a possible cause of hyperhomocystinaemia in stroke patients. Eur J Clin Chem Biochem 1997 Jan;35(11):25-8. Fava M et al. Folate, vitamin B12, and homocysteine in major depressive disorder. Am J Psychiatry 1997 Mar;154(3);426-8. Myocardial infarction in young women in relation to plasma total homocysteine, folate, and a common variant in the methyl;enetetrahydrofolate reductase gene. Circulation 1997 Jul 15;96(2):412-7. Fenech MF et al. Folate. Vitamin B12, homocysteine status and chromosome damage rate in lymphocytes of older men. 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Plasma total homocysteine response to oral doses of folic acid and pyridoxine hydrochloride (vitamin B6) in healthy individuals. Oral doses of Vitamin B6 reduces concentrations of serum folate. Scand J Clin Lab Invest 1999 Apr;59(2):139-46. Brouwer IA et al. Low-dose folic acid supplementation decreases plasma homocysteine concentrations: a randomized trial. Am J Clin nutr 1999 Jan;69(1):99-104. Moustapha A et al. Homocysteine: an emerging age-related cardiovascular risk factor. Geriatrics 1999 Apr;54(4):41, 44-6, 49-51. Kato I et al. Serum folate, homocysteine and colorectal cancer risk in women: a nested case-control study. Br J Cancer 1999 Apr;79(11-12):1917-22. De Jong SC et al. Determinants of fasting and post-methionine homocysteine levels in families predisposed to hyperhomocysteinemia and premature vascular disease, Arterioscler Thromb Vasc Biol 1999 May;19(5):1316-24. Tokgozoglu SL et al. 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