B-12 Supreme
The Most Potent Vitamin B-12 Supplement Available
Vitamin B-12 Deficiencies Are Common and Effects Widespread
Even minor deficiencies of Vitamin B-12 can effect nearly every system in the
body including:
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 Supreme: All 4 Forms of Vitamin B-12, Highest Potency
Available
|
Supplement Facts |
| Serving Size: 1 sublingual tablet |
| Servings Per Container: 30 |
 |
| Amount Per
Serving |
%DV |
|
|
| Vitamin B-12 |
35 mg |
583,333%* |
|
|
(as
Methylcobalamin 12.5mg,
Dibencozide(adenosylcobalamine) 12.5mg,
Cyanocobalamin 7.5mg,
Hydroxocobalamin 2.5mg) |
|
|
| * Daily Value not established |
|
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 Supreme: 35 mg, 30 sublingual tablets.
$39.95
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.
|
