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B-12 Extreme

The Most Potent Vitamin B-12 Supplement Available

B-12 ExtremeVitamin B-12 Deficiencies Are Common and Effects Widespread

Even minor deficiencies of Vitamin B-12 can effect nearly every system in the body including:

  •  Energy. Deficiencies of vitamin B-12 can cause anemia, fatigue, shortness of breath and weakness.

  • The Nervous System.  B-12 deficiency causes neurological changes including numbness and tingling in the hands and feet,  balance problems, depression, confusion, poor memory and Alzheimer's-like symptoms. Long-term deficiencies of B-12 can result in permanent impairment of the nervous system.

  • The Gastro-Intestinal System. B-12 deficiency can cause decreased appetite, constipation, diarrhea or alternating constipation / diarrhea, weight loss and abdominal pain.

  • The Immune System. Vitamin B-12 is necessary for normal functioning of white blood cells. Studies show that B-12 helps regulate Natural-Killer T-cells and prevents chromosome damage.

  • The Cardiovascular System. Vitamin B-12 participates in the conversion of homocysteine to methionine. Elevated homocysteine levels are a known independent risk factor for heart attack, stroke and thrombosis. Without adequate B-12 levels, homocysteine levels typically rise.

  • Special Senses: degenerative changes in the central nervous system caused by B-12 deficiency can also affect the optic nerve, resulting in blue-yellow color blindness.

  • In Infants and Children, signs of vitamin B-12 deficiency include failure to thrive, movement disorders, delayed development, and megaloblastic anemia.

Vitamin B-12 deficiency can be present before blood tests reveal the deficiency.

Four Forms of B-12 --- Which One is Best?

Cobalamin is a collective term for four closely related forms of B-12 --- cyanocobalamin, methylcobalamin, hydroxycobalamin, and adenosylcobalamin (dibencozide).

Cyanocobalamin, the most common form of B-12 found in nutritional supplements, has the lowest biological activity and must be converted in the liver to methylcobalamin or adenosylcobalamin before it can be utilized.

Because it can be converted to other forms of B-12, cyanocobalamin can be considered the “mother form” of B-12. However, this conversion is inefficient and some people may not benefit cyanocobalamin due to lack of assimilation or conversion.

Methylcobalamin is considered by many researchers to be the most active form of vitamin B-12. It protects the nervous system by regulating glutamate- induced neuronal damage (common in aging)  and promoting nerve cell regeneration.

Methylcobalamin is the only form of vitamin B-12 that participates in regulating circadian rhythms (sleep/wake cycles). It has been shown to improve sleep quality and refreshment from sleep, as well as increasing feelings of well-being, concentration and alertness.

Adenosylcobalamin (dibencozide), the second highly active form of vitamin B-12, is essential for energy metabolism. It is required for normal myelin sheath formation and nucleoprotein synthesis. Deficiencies are associated with nerve and spinal cord degeneration.

Hydroxocobalamin is a unique form of B-12 that participates in detoxification, especially cyanide detoxification. Cyanide levels are often elevated in smokers, people who eat cyanide-containing food (like cassava) and those with certain metabolic defects.

Excess cyanide in the tissues blocks conversion of cyanocobalamin to methylcobalamin or adenosylcobalamin. In such instances, hydroxocobalamin may be the vitamin B-12 of choice. Hydroxycobalamin is FDA- approved as a treatment for cyanide poisoning.

Given the subtle yet important differences between these forms of B-12, an ideal formula might be one which contains all four forms.

Oral Vs. Injectable: Which Delivery System is Preferred?

Although many people including some physicians still believe that injectable vitamin B-12 is the preferred route of administration, it is well-known and widely accepted that oral vitamin B-12 is equally as effective as injection in treating pernicious anemia and other B-12 deficient states.

B-12 Extreme: All 4 Forms of Vitamin B-12, Highest Potency Available

Supplement Facts

Serving Size: 1 tablet

Servings Per Container: 30

Amount Per Serving

%DV

Vitamin B-12

35,000 mcg (35 mg)

583,333%

Methylcobalamin

12,500 mcg

208,333%

Dibencozide

12,500 mcg

208,333%

Cyanocobalamin

7,500 mcg

12,500%

Hydroxocobalamin

2,500 mcg

41,667%

* Percent Daily Values are based on a 2000 calorie diet

Product & Usage Information:

  • Daily Use: Take one tablet, once or twice daily as a dietary supplement, or as recommended by your health care provider. Allow tablet to fully dissolve under tongue.
  • Inactive Ingredients: Sorbitol, Natural Strawberry Flavor, Natural Color, Magnesium Stearate, Silicon Dioxide

B-12 Extreme: 35 mg (35,000 mcg), 30 sublingual tablets. $44.97

Enter Quantity Desired and Click "Add To Cart" Button

References:

 1.) Herbert V. Vitamin B-12 in Present Knowledge in  Nutrition. 17th ed. Washington, D.C.: International Life  Sciences Institute Press,1996.
 2.) Combs G. Vitamin B-12 in The Vitamins. New York: Academic  Press, Inc, 1992.
 3.) Healton EB, Savage DG, Brust JC, Garrett TF, Lindenbaum J. Neurological aspects of cobalamin deficiency. Medicine 1991;70:229-244.
 4.) Herbert V and Das K. Vitamin B-12 in Modern Nutrition in  health and disease. 8th ed. Baltimore: Williams & Wilkins, 1994.
 5.) Zittoun J and Zittoun R. Modern clinical testing strategies in cobalamin and folate deficiency. Sem Hematol  1999;36:35-46.
 6.) Bottiglieri T. Folate, vitamin B-12, and  neuropsychiatric disorders. Nutr Rev 1996;54:382-90.
 7.) Roze E, Gervais D, Demeret S, Ogier de Baulny H, Zittoun J, Benoist JF, Said G, Pierrot-Deseilligny C, Bolgert F.Neuropsychiatric disturbances in presumed late-onset cobalamin C disease.Arch Neurol. 2003 Oct;60(10):1457-62.
 8.) Robertson JS, Hsia YE, Scully KJ.Defective leukocyte metabolism in human cobalamin defieciency: impaired propionate oxidation and serine biosynthesis reversible by cyanocobalamin therapy.J Lab Clin Med. 1976 Jan;87(1):89-97.
 9.) Tamura J, Kubota K, Murakami H, Sawamura M, Matsushima T, Tamura T, Saitoh T, Kurabayshi H, Naruse T. Immunomodulation by vitamin B-12: augmentation of CD8+ T lymphocytes and natural killer (NK) cell activity in vitamin B-12-deficient patients by methyl-B-12 treatment. Clin Exp Immunol. 1999 Apr;116(1):28-32.
 10) Fenech MF, Dreosti IE, Rinaldi JR.Folate, vitamin B-12, homocysteine status and chromosome damage rate in lymphocytes of older men. Carcinogenesis. 1997 Jul;18(7):1329-36.
 11.) Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment  of High Blood Cholesterol in Adults (Adult Treatment Panel III). NationalCholesterol Education Program, NationalHeart,  Lung, and Blood Institute, National Institues of Health,  September 2002. NIHPublication No. 02-5215.
 12.) Selhub J, Jacques PF, Bostom AG, D'Agostino RB, Wilson  PW,Belanger AJ, O'Leary DH, Wolf PA, Scaefer EJ, Rosenberg  IH. Association between plasma homocysteine concentrations  and extracranial carotid-artery stenosis. N Engl J Med 1995;332:286-91.
 13.) Rimm EB, Willett WC, Hu FB, Sampson L, Colditz G A,  Manson J E, Hennekens C, Stampfer M J. Folate and vitamin B6  from diet and supplements in relation to risk of coronary  heart disease among women. J Am Med Assoc 1998;279:359-64. 
 14.) 23) Refsum H, Ueland PM, Nygard O, Vollset SE. Homocysteine  and cardiovascular disease. Annu Rev Med 1998;49:31-62.
 15.) Boers GH. Hyperhomocysteinemia: A newly recognized risk factor for vascular disease. Neth J Med 1994;45:34-41.  
 16.) Selhub J, Jacques PF, Wilson PF, Rush D, Rosenberg IH.  Vitamin status and intake as primary determinants of  homocysteinemia in an elderly population. J Am Med Assoc  1993;270:2693-8.
 17.) Malinow MR. Plasma homocyst(e)ine and arterial occlusive diseases: A mini-review. Clin Chem 1995;41:173-6. 
 18.) Flynn MA, Herbert V, Nolph GB, Krause G. Atherogenesis  and the homocysteine-folate-cobalamin triad: do we need standardized analyses? J Am Coll Nutr 1997;16:258-67. 
 19.) Fortin LJ, Genest J, Jr. Measurement of homocyst(e)ine in the prediction of arteriosclerosis. Clin Biochem  1995;28:155-62.
 20.) Siri PW, Verhoef P, Kok FJ. Vitamins B6, B-12, and folate: Association with plasma total homocysteine and risk of coronary atherosclerosis. J Am Coll Nutr 1998;17:435-41.  
 21.) Remacha AF, Souto JC, Rámila E, Perea G, Sarda MP, Fontcuberta J.Enhanced risk of thrombotic disease in patients with acquired vitamin B-12 and/or folate deficiency: role of hyperhomocysteinemia.Ann Hematol. 2002 Nov;81(11):616-21. Epub 2002 Nov 9.
 22.) Beers, M.H., Berkow, R. et al. The Merck Manual of Diagnosis and Therapy, Seventeenth Edition, 1999 Merck and  Co., Chapter 127 page 867.
 23.) Monsen ALB and Ueland PM. Homocysteine and  methylmalonic acid in diagnosis and risk assessment from  infancy to adolescent. American Journal of Clinical  Nutrition 2003; 78:7-21.
 24.) Carmel R. Megaloblastic anemias. Curr Opin  Hematol 1994;1:107-12.
 25.) Oh R, Brown DL. Vitamin B-12 deficiency. Am Fam  Physician. 2003 Mar 1;67(5):979-86.
 26.) Pennypacker LC, Allen RH, Kelly JP, Matthews LM, Grigsby J, Kaye K, Lindenbaum J, Stabler SP.High prevalence of cobalamin deficiency in elderly outpatients.J Am Geriatr Soc. 1992 Dec;40(12):1197-204.
 27.)  Rajan S, Wallace JI, Brodkin KI, Beresford SA, Allen RH, Stabler SP.Response of elevated methylmalonic acid to three dose levels of oral cobalamin in older adults.J Am Geriatr Soc. 2002 Nov;50(11):1789-95.
 28.)  Akaike A, Tamura Y, Sato Y, Yokota T. Protective effects of a vitamin B-12 analog, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons. Eur J Pharmacol. 1993 Sep 7;241(1):1-6.
 29.) Kikuchi M, Kashii S, Honda Y, Tamura Y, Kaneda K, Akaike A.Protective effects of methylcobalamin, a vitamin B-12 analog, against glutamate-induced neurotoxicity in retinal cell culture. Invest Ophthalmol Vis Sci. 1997 Apr;38(5):848-54.
 30.) Watanabe T, et al. 1994. Ultra-high dose methylcobalamin promotes nerve regeneration in experimental acrylamide neuropathy. J Neurol Sci 122:140-43.
 31.) Mayer G.,Kroger M., Meier-Ewert K.Effects of vitamin B-12 on performance and circadian rhythm in normal subjects. Neuropsychopharmacology,1996, vol. 15, no5, pp. 456-464.
 32.) Olle Selinus, B. J. Alloway. Essentials of Medical Geology. Academic Press, 2005,p.519.ISBN 0126363412.
 33.) The Pharmacological Basis of Therapeutics, Goodman and Gillman, Tenth Edititon, Page-1503-1513.
 34.) R.S.Satoskar & S.D. Bhanderkar. Pharmacology and Therapeutics, Revised 12th, Page No.424-425.
 35.) Linnell JC, Matthews DM. Cobalamin metabolism and its clinical aspects. Clin Sci (Lond). 1984 Feb;66(2):113-21.
 36.) Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B-12, Pantothenic Acid, Biotin, and Choline. Washington, DC: National Academy Press; 2000.
 37.) Lederle FA. Oral cobalamin for pernicious anemia: back from the verge of extinction. J Am Geriatr Soc 1998;46:1125-7.
 38.) Kuzminski AM, Del Giacco EJ, Allen RH, Stabler SP, Lindenbaum J. Effective treatment of cobalamin deficiency with oral cobalamin. Blood 1998;92: 1191-8.
 39.) Lederle FA. Oral cobalamin for pernicious anemia. Medicine's best kept secret? JAMA 1991;265:94-5.
 40.) Bolaman Z, Kadikoylu G, Yukselen V, Yavasoglu I, Barutca S, Senturk T.Oral versus intramuscular cobalamin treatment in megaloblastic anemia: a single-center, prospective, randomized, open-label study.Clin Ther. 2003 Dec;25(12):3124-34.
 41.) Swain R. An update of vitamin B-12 metabolism and deficiency states.J Fam Pract. 1995 Dec;41(6):595-600.
 42.) Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Thiamin, riboflavin, niacin, vitamin B6, folate, vitamin B-12, pantothenic acid, biotin, and choline. National Academy Press. Washington, DC, 1998. 
 43.) van Goor L, Woiski MD, Lagaay AM, Meinders AE, Tak PP.Review: cobalamin deficiency and mental impairment in elderly people. Age Ageing. 1995 Nov;24(6):536-42.
 44.) Martin DC, Francis J, Protetch J, Huff FJ. Time dependency of cognitive recovery with cobalamin replacement: report of a pilot study. J Am Geriatr Soc. 1992 Feb;40(2):168-72.
 45.) National Institutes of Health Fact Sheet on vitamin B-12 http://ods.od.nih.gov/factsheets/vitaminB-12.asp
 46.) Louwman MW, van Dusseldorp M, van de Vijver FJ, Thomas CM, Schneede J, Ueland PM, Refsum H, van Staveren WA. Signs of impaired cognitive function in adolescents with marginal cobalamin status. Am J Clin Nutr. 2000 Sep;72(3):762-9.
 47.) Nilsson-Ehle H. Age-related changes in cobalamin (vitamin B-12) handling. Implications for therapy. Drugs Aging. 1998 Apr;12(4):277-92.
 48.) Garcia A, Paris-Pombo A, Evans L, Day A, Freedman M.Is low-dose oral cobalamin enough to normalize cobalamin function in older people?J Am Geriatr Soc. 2002 Aug;50(8):1401-4.
 49.) Kwok T, Tang C, Woo J, Lai WK, Law LK, Pang CP.Randomized trial of the effect of supplementation on the cognitive function of older people with subnormal cobalamin levels.Int J Geriatr Psychiatry. 1998 Sep;13(9):611-6.

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