The presence of folic acid in enriched cereal grain products and the higher bioavailability of folic acid than food folate led to the expression of the 1998 folate RDA, 400 microg/d, as dietary folate equivalents (DFE). DFE are defined as: mug natural food folate + 1.7 x microg synthetic folic acid. The 1.7 multiplier was based on assumptions that added folic acid was 85% available and food folate was 50% available. The 85/50 ratio also inferred that the bioavailability of food folate was approximately 60% relative to added folic acid. The objective of this long-term controlled feeding study was to assess the dietary folate equivalency of folic acid. After a 2-wk period of folate restriction, women (n = 42, 18-45 y old) consumed either 400 or 800 microg DFE/d derived from various combinations of food folate and folic acid for 12 wk. Folic acid was converted to DFE using the 1.7 multiplier from the DFE calculation and was consumed with a meal throughout the treatment period. Folate status response to the various treatments was assessed during wk 12-14. Serum folate, RBC folate, and plasma total homocysteine did not differ among the 400 microg DFE/d groups or among the 800 microg DFE/d groups. In contrast, consumption of 800 microg DFE/d led to higher (P = 0.05) serum and RBC folate than consumption of 400 microg DFE/d. These data support the validity of the 1.7 multiplier in the DFE equation and suggest that food folate bioavailability is approximately 60% that of added folic acid when consumed as part of a mixed diet.
Glycine N-methyltransferase (GNMT) is a key regulatory protein in folate metabolism, methionine availability, and transmethylation reactions. Perturbations in GNMT may lead to aberrations in homocysteine metabolism, a marker of numerous pathologies. The primary objective of this study was to examine the influence of the GNMT 1289 C-->T alone, and in combination with the methylenetetrahydrofolate reductase (MTHFR) 677 C-->T variant, on plasma total homocysteine concentrations in healthy young women (n = 114). Plasma total homocysteine was measured at baseline (wk 0) and after 2 wk of controlled folate restriction (135 microg/d as dietary folate equivalents). Plasma homocysteine concentrations did not differ among the GNMT C1289T genotypes at baseline. However, after folate restriction, women with the GNMT 1289 TT genotype (n = 16) had higher (P = 0.019) homocysteine concentrations than women with the CT (n = 51) or CC (n = 47) genotype. The influence of the GNMT 1289 C-->T variant on homocysteine was dependent on the MTHFR C677T genotype. In subjects with the MTHFR 677 CC genotype, homocysteine was greater (P < or = 0.05) for GNMT 1289 TT subjects relative to 1289 CT or CC subjects. However, in subjects with the MTHFR 677 TT genotype, plasma homocysteine concentrations did not differ among the GNMT C1289T genotypes. Overall, these data suggest that the GNMT 1289 C-->T polymorphism influences plasma homocysteine and is responsive to folate intake.
The phosphatidylcholine data suggest that the lower folate status observed in African American women may also be associated with lower choline status. In turn, diseases linked to folate may also be linked to choline.
Our previous work has demonstrated that choline and folate are interrelated and that ethnicity is a determinant of folate status. Specifically, African American women have lower folate nutriture relative to Caucasian and Mexican American women under conditions of controlled folate intake. This study sought to examine the influence of ethnicity and controlled folate intake on choline status. Forty‐two women of Mexican American (n=14), African American (n=14), and Caucasian (n=14) descent consumed a folate restricted diet (135 mcg DFE/d) for 7 weeks, followed by 7 weeks of folate treatment with either 400 or 800 mcg DFE/d. Total choline intake remained unchanged throughout the study at approximately 350 mg/d. Plasma choline and its derivatives were measured by LC‐MS/MS at weeks 0, 7, and 14. Plasma betaine was modified by ethnicity and level of folate treatment (week x ethnicity x folate interaction; P=0.0392), and tended to decline for all subjects during folate restriction (week effect; P=0.0783). Also, plasma betaine tended to increase less in African Americans receiving treatment with 800 mcg DFE/d relative to other ethnic groups (ethnicity x folate interaction; P=0.052). Phosphatidylcholine declined during folate restriction (week effect; P<0.001) and tended to increase in Mexican American and Caucasian women and decline in African American women during folate treatment (week x ethnicity interaction; P=0.056). These data suggest that the lower folate status observed in African American women relative to Caucasian and Mexican American women is also associated with lower choline status. In turn, diseases that are linked to folate nutriture may also be linked to choline status.
Supported by the NIH grant S06GM53933 and funds from the California Agricultural Research Initiative.
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