in a substantial underestimation of body stores. Coburn and colleagues (1988a) estimated the B6 content of muscle biopsies and, by assuming that muscle represented 80 percent of the body B6 store, calculated a total body store of about 1,000 µmol (167 mg). Extrapolation of data from studies with experimental animals to assess the B6 requirement for maintenance and growth (Coburn et al., 1987, 1988b) indicates that 1 mg of PN would be an adequate intake for the adult. Modeling of human B6 pools has also led to an assessment of a minimum requirement of about 0.4 mg/day of PN (Coburn, 1990).
The classical clinical symptoms of B6 deficiency are a seborrheic dermatitis (Mueller and Vilter, 1950), microcytic anemia (Snyderman et al., 1953), epileptiform convulsions (Bessey et al., 1957; Coursin, 1954), and depression and confusion (Hawkins and Barsky, 1948). Microcytic anemia reflects decreased hemoglobin synthesis. The first enzyme and committed step in heme biosynthesis, aminolevulinate synthase, uses PLP as a coenzyme. Because PLP is also a coenzyme of decarboxylases that are involved in neurotransmitter synthesis, defects in some of these enzymes could explain the onset of convulsions in B6 deficiency. Many studies have demonstrated that the levels of neurotransmitters such as dopamine, serotonin, and γ-aminobutyrate are reduced in B6-depleted experimental animals, especially in extreme B6 depletion (Dakshinamurti and Stephens, 1969; Dakshinamurti et al., 1991, 1993; Sharma and Dakshinamurti, 1992; Sharma et al., 1994; Stephens et al., 1971). Some of these studies were reviewed in a conference report (Dakshinamurti, 1990). However, it has not been definitely shown whether the convulsions are due to the reduced level of one of these neurotransmitters in particular. Guilarte (1993) proposed that the convulsions are caused by abnormal tryptophan metabolites that accumulate in the brain in B6 deficiency.
Electroencephalogram (EEG) abnormalities have also been reported in controlled studies of B6 depletion. In one depletion-repletion study (Kretsch et al., 1991) 2 of 11 young women placed on a diet containing less than 0.05 mg of B6 exhibited abnormal EEG patterns within 12 days. The abnormal patterns were promptly corrected by 0.5 mg/day of PN. Similar abnormalities were reported in young men placed on a diet containing less than 0.06 mg/day of B6 for 21 days (Canham et al., 1964). However, no EEG changes were detected when young men were placed on a diet containing