Cobalamin is the general term used to describe a group of cobalt-containing compounds (corrinoids) that have a particular structure that contains the sugar ribose, phosphate, and a base (5, 6-dimethyl benzimidazole) attached to the corrin ring. Vitamin B₁₂ can be converted to either of the two cobalamin coenzymes that are active in human metabolism: methylcobalamin and 5-deoxyadenosylcobalamin. Although the preferred scientific use of the term vitamin B₁₂ is usually restricted to cyanocobalamin, in this report, B₁₂ will refer to all potentially biologically active cobalamins.

In the United States, cyanocobalamin is the only commercially available B₁₂ preparation used in supplements and pharmaceuticals. It is also the principal form used in Canada (B. A. Cooper, Department of Hematology, Stanford University, personal communication, 1997). Another form, hydroxocobalamin, has been used in some studies of B₁₂. Compared with hydroxocobalamin, cyanocobalamin binds to serum proteins less well and is excreted more rapidly (Tudhope et al., 1967).

B₁₂ is a cofactor for two enzymes: methionine synthase and L-methylmalonyl-CoA mutase. Methionine synthase requires methylcobalamin as a cofactor for the methyl transfer from methyltetrahydrofolate to homocysteine to form methionine and tetrahydrofolate. L-Methymalonyl-CoA mutase requires adenosylcobalamin to convert L-methymalonyl-CoA to succinyl-CoA in an isomerization reaction. In B₁₂ deficiency, folate may accumulate in the serum as a result of slowing of the B₁₂-dependent methyltransferase. An adequate supply of B₁₂ is essential for normal blood formation and neurological function.

Small amounts of B₁₂ are absorbed via an active process that requires an intact stomach, intrinsic factor (a glycoprotein that the parietal cells of the stomach secrete after being stimulated by food), pancreatic sufficiency, and a normally functioning terminal ileum. In the stomach, food-bound B₁₂ is dissociated from proteins in the presence of acid and pepsin. The released B₁₂ then binds to R proteins (haptocorrins) secreted by the salivary glands and the gastric mucosa. In the small intestine, pancreatic proteases partially de-

Front Matter (R1-R24)

Summary (1-16)

1 Introduction to Dietary Reference Intakes (17-26)

2 The B Vitamins and Choline: Overview and Methods (27-40)

3 A Model for the Development of Tolerable Upper Intake Levels (41-57)

4 Thiamin (58-86)

5 Riboflavin (87-122)

6 Niacin (123-149)

7 Vitamin B6 (150-195)

8 Folate (196-305)

9 Vitamin B12 (306-356)

10 Pantothenic Acid (357-373)

11 Biotin (374-389)

12 Choline (390-422)

13 Uses of Dietary Reference Intakes (423-436)

14 A Research Agenda (437-442)

A Origin and Framework of the Development of Dietary Reference Intakes (443-447)

B Acknowledgments (448-450)

C Système International d'Unités (451-452)

D Search Strategies (453-455)

E Methodological Problems Associated with Laboratory Values and Food Composition Data for B Vitamins (456-459)

F Dietary Intake Data from the Boston Nutritional Status Survey, 1981–1984 (460-465)

G Dietary Intake Data from the Continuing Survey of Food Intakes by Individuals (CSFII), 1994–1995 (466-477)

H Dietary Intake Data from the Third National Health and Nutrition Examination Survey (NHANES III), 1988–1994 (478-501)

I Daily Intakes of B Vitamins by Canadian Men and Women, 1990, 1993 (502-506)

J Options for Dealing with Uncertainties in Developing Tolerable Upper Intake Levels (507-511)

K Blood Concentrations of Folate and Vitamin B12 from the Third National Health and Nutrition Examination Survey (NHANES III), 1988–1994 (512-519)

L Methylenetetrahydrofolate Reductase (520-522)

M Evidence from Animal Studies on the Etiology of Neural Tube Defects (523-526)

N Estimation of the Period Covered by Vitamin B12 Stores (527-530)

O Biographical Sketches (531-536)

P Glossary and Abbreviations (537-540)

Index (541-567)