Results of basal plasma homocyst(e)ine concentrations in patients reported in the literature are reviewed, with emphasis on the series of subjects analyzed by the author. Findings support the hypothesis that plasma homocyst(e)ine is a risk factor for coronary, cerebral and peripheral arterial occlusive diseases, as well as for carotid thickening. Results of four studies show that heritability influences plasma homocyst(e)ine. Moreover, data suggest that a graded risk for atherothrombotic disease is distributed across the entire distribution of plasma homocyst(e)ine levels. Elevated levels of homocyst(e)ine can be decreased effectively by supplementary folate, occasionally requiring the addition of vitamin B-12, vitamin B-6, choline or betaine. Consequently, it is important that placebo-controlled clinical trials be conducted to determine whether the clinical evolution of arterial occlusive diseases is influenced by those supplements.