|LE Magazine July 2004|
The Multiple Benefits of this Complex Supplement
Vitamin B12 (cobalamin), nature’s most chemically complex vitamin, also has been called its most beautiful, owing to the rich, dark red color of its crystals. But praise for the last B vitamin to be identified is hardly limited to its physical properties: B12’s vital role in the treatment of pernicious anemia has won it a dedicated following among physicians for decades. Vitamin B12 also has been shown to guard against stroke and heart disease, and contribute to relieving asthma, bursitis, depression, low blood pressure, multiple sclerosis, and even certain mental disorders. More recently, recognition of the essential role of one form of the compound—methylcobalamin—in supporting a variety of basic neurological functions has added to vitamin B12’s growing reputation as an indispensable supplement in the maintenance of a healthy mind and body.
Methylcobalamin helps moderate glutamate in the brain and support normal brain cell activity. Methylcobalamin also has been shown to encourage healthy cognitive, memory, and emotional function.1
The Different Forms of B12
Animal products are the principal food sources of B12, but paradoxically, plants and animals cannot produce the compound. Only bacteria are believed to manufacture the vitamin. Cobalamin actually is the collective term for four cobalt-containing compounds known as corrinoids. The term vitamin B12 typically is used to refer to cyanocobalamin, the main form of the vitamin typically used in nutritional supplements. Of the other three forms, methylcobalamin, one of the two coenzyme forms of cobalamin, is active in the central nervous system and is a vital cofactor in the conversion of homocysteine to methionine.
Central to Protein Synthesis
Cobalamin deficiency leads to a reduced synthesis of methionine synthase, the key enzyme responsible for the conversion of homocysteine to methionine. The result is a high level of serum homocysteine and a decreased level of methionine.4
Benefits Beyond Anemia Treatment
Moreover, it is now understood that a significant number of cognitive and emotional aptitudes depend on an optimal level of vitamin B12. In cognitive tests of elderly people, those who had the poorest scores had the lowest blood levels of vitamin B12. People diagnosed with depression have low plasma levels of cobalt, the mineral that forms the center of the vitamin B12 molecule.
B12 Absorption Declines with Age
Another possible contributing factor is pernicious anemia, which severely reduces gastric secretion of intrinsic factor. In view of its association with a variety of antibodies, including at least two types of intrinsic factor antibodies, pernicious anemia is an autoimmune process. Intrinsic factor blocking antibody, which prevents the binding of vitamin B12 to the intrinsic factor molecule, is present in more than 50% of patients with pernicious anemia and only rarely is encountered in other conditions.7
Deciding Between Shots and Pills
The problem with typical oral cobalamin supplementation is that the cobalamin may not be converted into adequate amounts of methylcobalamin required by the body to correct neural damage or decline.8
The easiest way around this problem is to bypass the liver entirely. Taking methylcobalamin sublingually (that is, dissolving it in tablet form under the tongue) allows the supplement to enter the bloodstream directly and has been shown to enhance absorption as much as fivefold.
Determining an Optimal Dose
Vitamin B12 has been shown to be extremely safe and nontoxic, even in high doses. Everyday supplementation (300 to 1000 mcg) is a good starting point. Deficiency-related conditions require supplementing with at least 1 mg (1000 mcg) daily as part of a comprehensive nutrient program. According to recent data, supplementing with 2000 mcg per day addresses the symptoms of B12 deficiency, including elevated homocysteine and neurological problems.9,1
1. Akaike A, Tamura Y, Sato Y, Yokota T. Protective effects of a vitamin B12 analog, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons. Eur J Pharmacol. 1993 Sep 7;241(1):1-6.
2. Verhoef P, Kok FJ, Kruyssen DA, et al. Plasma total homocysteine, B vitamins, and risk of coronary atherosclerosis. Arterioscler Thromb Vasc Biol. 1997 May;17(5):989-95.
3. Eikelboom JW, Lonn E, Genest J Jr, Hankey G, Yusuf S. Homocyst(e)ine and cardiovascular disease: a critical review of the epidemiologic evidence. Ann Intern Med. 1999 Sep 7;131(5):363-75.
4. Beyer K, Lao JI, Latorre P, et al. Methionine synthase polymorphism is a risk factor for Alzheimer’s disease. Neuroreport. 2003 Jul 18;14(10):1391-4.
5. Metz J. Cobalamin deficiency and the pathogenesis of nervous system disease. Annu Rev Nutr. 1992;12:59-79.
6. Harty RF, Leibach JR. Immune disorders of the gastrointestinal tract and liver. Med Clin North Am. 1985 Jul;69(4):675-704.
7. Irvine WJ. Immunoassay of gastric intrin- sic factor and the titration of antibody to intrinsic factor. Clin Exp Immunol. 1966 Jan;1(1):99-118.
8. Ide H, Fujiya S, Asanuma Y, Tsuji M, Sakai H, Agish Y. Clinical usefulness of intrathecal injection of methylcobalamin in patients with diabetic neuropathy. Clin Ther. 1987;9(2):183-92.
9. Schnyder G, Roffi M, Flammer Y, Pin R, Hess OM. Effect of homocysteine-lower- ing therapy with folic acid, vitamin B12, and vitamin B6 on clinical outcome after percutaneous coronary intervention: the Swiss Heart study: a randomized con- trolled trial. JAMA. 2002 Aug 28;288(8):973-9.
10. Shojania AM. How do you diagnose and manage vitamin B12 deficiency? Prairie Med J. 1994;64:141-2.