total body folate, such as acute alcohol ingestion (Eichner and Hillman, 1973).

In population surveys it is generally assumed that measuring serum folate alone does not differentiate between what may be a transitory reduction in folate intake or chronic folate deficiency accompanied by depleted folate stores and functional changes. Serum or plasma folate is, however, considered a sensitive indicator of dietary folate intake, as illustrated by the report of Jacques and colleagues (1993) in which plasma folate doubled across quartiles of folate intake assessed in a study of 140 people. In a controlled metabolic study, repeated measures over time in the same individual do reflect changes in status. Serum folate concentration may be a worthwhile diagnostic test if used and interpreted correctly in conjunction with other folate status indices (Lindenbaum et al., 1988).

Data from a metabolic study in which graded doses of folate were fed showed that urinary folate is not a sensitive indicator of folate status (Sauberlich et al., 1987). In that study, approximately 1 to 2 percent of dietary folate was excreted intact in the urine; excretion continued even in the face of advanced folate depletion. Other reports indicate that daily folate excretion on a normal diet ranges from 5 to 40 µg/day (Cooperman et al., 1970; Retief, 1969; Tamura and Stokstad, 1973).

The major route of whole-body folate turnover is by catabolism and cleavage of the C9-N10 bond producing pteridines and p-amino-benzoylglutamate (pABG) (Krumdieck et al. 1978; Saleh et al., 1982). Before excretion from the body, most pABG is N-acetylated to acetamidobenzoylglutamate (apABG). It is not known whether folate coenzymes are catabolized and excreted or whether they are recycled after metabolic utilization. In a study designed to estimate the folate requirements of pregnant and nonpregnant women, McPartlin and coworkers (1993) quantified the urinary excretion of pABG and apABG as a measure of daily folate utilization. This approach does not take into account endogenous fecal folate loss, which may be substantial (Krumdieck et al., 1978); thus, quantitation of urinary catabolites alone may result in an underestimation of the requirement.

The appearance of hypersegmented neutrophils, macrocytosis,