Information from the Boston Nutritional Status Survey on use of B6 supplements by a free-living elderly population is given in Appendix F. For those reporting use of supplements, the fiftieth percentile of supplemental B6 intake was 2.2 mg for both men and women. Approximately 26 percent of all adults reported taking a B6-containing supplement in 1986 (Moss et al., 1989).
No adverse effects have been associated with high intake of vitamin B6 from food sources. This review focuses on pyridoxine, the form of B6 that was consumed in the reports cited below. Large oral supplemental doses of pyridoxine used to treat many conditions, including carpal tunnel syndrome and premenstrual syndrome, have been associated with the development of sensory neuropathy and dermatological lesions (Cohen and Bendich, 1986; Schaumburg and Berger, 1988). The causal association between high-dose pyridoxine and neuropathy has been well documented in animals since 1940 (Unna and Antopol, 1940) and in humans since 1983 (Schaumburg et al., 1983).
Sensory Neuropathy. The first clinical report of pyridoxine-induced neurotoxicity in humans (Schaumburg et al., 1983) describes seven patients (five women and two men) with severe sensory neuropathy of the extremities after 2,000 to 6,000 mg/day of pyridoxine for 2 to 40 months. Four individuals were unable to walk. Neurological signs and symptoms were diagnosed through objective neurological assessment and improved in all patients after withdrawal of medication. Other reports of peripheral sensory neuropathy associated with high-dose pyridoxine therapy (1 to 4 g/day) appeared in the 1980s (Baer, 1984; Bredesen and Parry, 1984; De Zegher et al., 1985; Friedman et al., 1986). The pathogenesis of pyridoxine-induced peripheral sensory neuropathy and dose-response relationships have been well-described in animal models (Phillips et al., 1978; Schaeppi and Krinke, 1985). Review of the limited data involving lower pyridoxine doses (Bernstein and Lobitz, 1988; Del Tredici et al., 1985)