ATHEROGENESIS AND THE HOMOCYSTEINE-FOLATE-COBALAMIN TRIAD - DO WE NEED STANDARDIZED ANALYSES

Background: Bioscientists, physicians and nutritionists are newly inte rested in the homocysteine-folate cobalamin triad, in part because hom ocysteine may be important both in atherogenesis and thrombogenesis. H omocysteine imbalance may be an early marker for cobalamin disorders b ecause cobalamin is a cofactor in remethylation of homocysteine to met hionine. Methods: In 139 men and 32 women of similar mean age of 65 ye ars, we measured markers which have been cited as risk for atheroscler osis: serum homocysteine, folate, total cobalamin, holotranscobalamin I and II, (TCI and TCII), total serum cholesterol (SCHOL), high densit y lipoprotein cholesterol (HDLC), triglycerides (STG) as well as red b lood cell (RBC) folate, food records and body composition by whole bod y counting of potassium-forty (K-40). Results: Statistical relationshi ps among the data showed healthy women had lower mean serum homocystei ne and their mean RBC folate and TCI and TCII were higher than men. Ei ghty-three subjects had TCII much lower than 60 pg/ml (subnormal), yet only 11 of these men and two women had total cobalamin <200 pg/ml (ab normal). Fifty-two subjects with serum homocysteine greater than 17.5 nmol/ml had TCII less than 60 pg/ml, suggesting serum homocysteine may be a marker for early cobalamin negative balance. None of the subject s in the study had serum folate below abnormal values, i.e., less than 1.6 mg/ml, All subjects had RBC folate within normal range. Serum hom ocysteine showed inverse relationship with RBC folate and serum total cobalamin, TCI and TCII. Conclusions: 1) importance of using serum hol otranscobalamin TCI and TCII as markers of cobalamin deficiency, 2) ne cessity to use documented quantitative components of dietary intake if strong comparisons are to be made among quantitative values of serum or plasma homocysteine, folate, cobalamin, and nutrients in food intak e.