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Treatment of mild hyperhomocysteinemia in vascular disease patients
D G Franken1, G H Boers, H J Blom
1Department of Medicine, University Hospital Nijmegen, The Netherlands.
Insights
Mild hyperhomocysteinemia, a risk factor for arteriosclerotic disease, can be effectively treated. Safe supplementation with vitamin B6, folic acid, and betaine normalizes homocysteine levels in most patients.
Area of Science:
- Cardiovascular Medicine
- Nutritional Biochemistry
- Metabolic Disorders
Background:
- Mild hyperhomocysteinemia is a known risk factor for premature arteriosclerotic disease.
- Previous attempts to normalize homocysteine levels have shown limited success.
- Effective treatment strategies for mild hyperhomocysteinemia are needed.
Purpose of the Study:
- To screen patients with premature occlusive arterial disease for mild hyperhomocysteinemia.
- To evaluate the efficacy of vitamin B6, folic acid, and betaine in normalizing homocysteine levels.
- To determine the prevalence of mild hyperhomocysteinemia in patients with premature arteriosclerotic disease.
Main Methods:
- Oral methionine loading tests were used to identify mild hyperhomocysteinemia in 421 patients.
- Patients received vitamin B6 (250 mg/day), followed by additional folic acid (5 mg/day) and/or betaine (6 g/day) if needed.
- Homocysteine levels were reassessed after 6 weeks of treatment.
Main Results:
- Mild hyperhomocysteinemia was identified in 33% of peripheral and 20% of cerebral arterial disease patients.
- Vitamin B6 alone normalized homocysteine in 56% of patients.
- Combined therapy with vitamin B6, folic acid, and betaine normalized levels in 95% of remaining cases.
Conclusions:
- Mild hyperhomocysteinemia is common in patients with premature arteriosclerotic disease.
- Treatment with vitamin B6, folic acid, and betaine is safe and highly effective.
- These supplements can normalize homocysteine levels, potentially reducing arteriosclerotic disease risk.
Abstract:
Mild hyperhomocysteinemia is recognized as a risk factor for premature arteriosclerotic disease. A few vitamins and other substances have been reported to reduce blood homocysteine levels, but normalization of elevated blood homocysteine concentrations with any of these substances has not been reported. Therefore, we screened 421 patients suffering from premature peripheral or cerebral occlusive arterial disease by oral methionine loading tests for the presence of mild hyperhomocysteinemia. Thirty-three percent of patients with peripheral and 20% of patients with cerebral occlusive arterial disease were identified with mild hyperhomocysteinemia (14% of the men, 34% of the premenopausal women, and 26% of the postmenopausal women). Mildly hyperhomocysteinemic patients were administered vitamin B6 250 mg daily. After 6 weeks methionine loading tests were again assessed to evaluate the effect of treatment. Patients with nonnormalized homocysteine concentrations were further treated with vitamin B6 250 mg daily and/or folic acid 5 mg daily and/or betaine 6 g daily, solely or in any combination. Vitamin B6 treatment normalized the afterload homocysteine concentration in 56% of the treated patients (71% of the men, 45% of the premenopausal women, and 88% of the postmenopausal women). Further treatment resulted in a normalization of homocysteine levels in 95% of the remaining cases. Thus, mild hyperhomocysteinemia, which is frequently encountered in patients with premature arteriosclerotic disease, can be reduced to normal in virtually all cases by safe and simple treatment with vitamin B6, folic acid, and betaine, each of which is involved in methionine metabolism.