Description

Discussion
The water-soluble B vitamins have to be absorbed in the small intestine and then go to the liver where they are
biotransformed into their active coenzyme forms. Active B contains vitamins B1 (thiamine), B2 (riboflavin), B6
(pyridoxine), and B12 (methylcobalamin) in their physiologically-active form making them easier to absorb and
“ready-for-use.” For example, in patients receiving pyridoxine HCl, only 33 percent responded with an increase
in plasma pyridoxal-5’-phosphate (P5P); however, the level increased in all of the patients receiving P5P.*[1]
Folate is provided as 5-methyltetrahydrofolate (5-MTHF), which bypasses metabolic steps to folate bioactivity.
Despite research showing that folic acid and 5-MTHF have equivalent bioavailability and that supplementation
with large doses of folic acid can “force” its conversion to the more active form, 5-MTHF may be the preferred
form to replenish folate. This may be especially applicable to those with digestive challenges or genetic variations
in folate metabolism.[2-4] In this formula, 5-MTHF is provided as Quatrefolic—the glucosamine salt of 5-MTHF.
In vitro and in vivo studies have proven that Quatrefolic has greater stability, solubility, and bioavailability over
calcium salt forms of 5-MTHF. Folate is stored in small amounts in red blood cells (RBC), and RBC folate has
been shown to be higher after supplementation with 5-MTHF compared to folic acid and placebo. Likewise,
patients given 5 mg of 5-MTHF experienced plasma levels of 5-MTHF 700% greater than patients given folic
acid.*[5]
Another unique ingredient in this formula is benfotiamine (S-benzoylthiamine O-monophosphate), a safe, fatsoluble
analog of thiamine. One study showed that it not only raised blood and tissue levels of thiamine at least
five times higher than the water-soluble salt, but it also remained bioavailable after oral administration up to 3.6
times longer than thiamine salt.[6] Benfotiamine is the most potent of a class of thiamine-derived compounds
present in small quantities in members of the Allium genus. The superiority of its biological activity compared
to thiamine rests in its structure—a thiazole ring opens to allow easy diffusion through a membrane and then
closes to become structurally active.*
Benfotiamine increases transketolase activity, thereby diverting from three natural, yet destructive metabolic
pathways: 1) it decreases the glucose metabolites that lead to the buildup of certain types of detrimental
advanced glycation end products (AGEs); 2) it normalizes protein kinase C activity; 3) it protects the retina
by preventing the activation of NF-kappaB therein.[7] Research suggests it may also protect the kidneys and
endothelial cells.[8] Benfotiamine is useful for replenishing thiamine, this may be especially true in individuals
that use the vitamin at a higher rate or in those with lifestyle habits that deplete it.*[9-11]

Medicinal Ingredients (per vegetarian capsule)
Vitamin B1 (Thiamine hydrochloride) ……………………………………………………………………………. 20 mg
Vitamin B2 (Riboflavin 5’-phosphate sodium) ………………………………………………………………… 20 mg
Niacinamide …………………………………………………………………………………………………………….. 130 mg
Folate (Quatrefolic® (6S)-5-methyltetrahydrofolic acid, glucosamine salt) ………………………. 400 mcg
Vitamin B6 (Pyridoxal 5-Phosphate) ……………………………………………………………………………. 20 mg
Vitamin B12 (Methylcobalamin) ……………………………………………………………………………….. 400 mcg
Biotin ……………………………………………………………………………………………………………………. 400 mcg
Vitamin B5 (Calcium D-pantothenate) …………………………………………………………………………. 150 mg
Benfotiamine …………………………………………………………………………………………………………………… 20 mg
Choline (Choline dihydrogen citrate) …………………………………………………………………………….. 30 mg
Niacin ………………………………………………………………………………………………………………………. 10 mg
Non-Medicinal Ingredients
Hypromellose, stearic acid, magnesium stearate, silica.
Recommended Dose
Adults: Take 1 capsule daily with food, or as directed by a healthcare practitioner.
Consult a healthcare practitioner for use beyond 12 weeks. Do not use if pregnant or breastfeeding. Persons with thiamine
hypersensitivity should not take product.
People sensitive to nicotinic acid may experience flushing of the skin that is generally mild and transient.

References
1. Labadarios D, Rossouw JE, McConnell JB, et al. Vitamin B6 deficiency in chronic liver disease – evidence for increased degradation of pyridoxal-5-phosphate. Gut. 1977;18:23-27.
[PMID: 838399]
2. Yakut M, Ustün Y, Kabaçam G, et al. Serum vitamin B(12) and folate status in patients with inflammatory bowel diseases. Eur J Intern Med. 2010 Aug;21(4):320-23. [PMID: 20603044]
3. Halsted CH, Villanueva JA, Devlin AM. Folate deficiency, methionine metabolism, and alcoholic liver disease. Alcohol. 2002 Jul;27(3):169-72. [PMID: 12163145]
4. Kluijtmans LA, Van den Heuvel LP, Boers GH, et al. Molecular genetic analysis in mild hyperhomocysteinemia: a common mutation in the methylenetetrahydrofolate reductase gene is a
genetic risk factor for cardiovascular disease. Am J Hum Genet. 1996 Jan;58(1):35-41. [PMID:8554066]
5. Willems FF, Boers GH, Blom HJ, et al. Pharmacokinetic study on the utilisation of 5-methyltetrahydrofolate and folic acid in patients with coronary artery disease. Br J Pharmacol. 2004
Mar;41(5):825-30. [PMID: 14769778]
6. Loew D. Pharmacokinetics of thiamine derivatives especially of benfotiamine. Int J Clin Pharmacol Ther. 1996 Feb;34(2): 47-50. [PMID: 8929745]
7. Thornalley PJ. The potential role of thiamine (vitamin B1) in diabetic complications. Curr Diabetes Rev. 2005 Aug;1(3):287-98. [PMID: 18220605]
8. Stirban A, Negrean M, Stratmann B, et al. Benfotiamine prevents macro- and microvascular endothelial dysfunction and oxidative stress following a meal rich in advanced glycation end
products in individuals with type 2 diabetes. Diabetes Care. 2006 Sep;29(9):2064-71. [PMID: 16936154]
9. Woelk H, Lehrl S, Bitsch R, et al. Benfotiamine in treatment of alcoholic polyneuropathy: an 8-week randomized controlled study (BAP I Study). Alcohol. 1998 Nov-Dec;33(6):631-38.
[PMID: 9872352]
10. Ayazpoor U. Chronic alcohol abuse. Benfotiamine in alcohol damage is a must [in German]. MMW Fortschr Med. 2001 Apr 19;143(16):53. [PMID: 11367995]
11. Schupp N, Schmid U, Heidland A, et al. New approaches for the treatment of genomic damage in end-stage renal disease. J Ren Nutr. 2008 Jan;18(1):127-33. [PMID: 18089459]