Everyday FREE SHIPPINGFedEx Ground — Continental USwith a purchase of $75 or more
Build your own list of favorite items for easy reordering
In U.S. Call: 888-803-5333 International: 001.212.665.8070
Security Seals
  

BCN Office Hours: 9am to 5pm Monday Through Thursday

BCN Online Store Hours: 24/7 - That's every day, all day

My Account: Sign In

Be as specific as possibe for best search results


» BCN Formulas

» A.C. Grace UNIQUE E

AOR

» Adrenal Support

» Antioxidants

» Blood Sugar Balance

» Bone & Joint Health

» Brain/Neurological Health

» Cardiovascular System

» Detoxification

» Digestion

» Energy & Fatigue

» Eye Health

» Immune System

» Inflammation

» Kidney & Urinary Health

» Sleep

» Thyroid Support

» Vitamins

» Weight Management

» Boiron Homeopathics

» FoodScience of Vermont

» Freeda Vitamins

» Herbalist & Alchemist

» Hyalogic - True HA

» Jarrow Formulas

» MushroomScience

» Labrix Services

» Longevity Science

» Pure Body Institute

» Pharmax

» RX Vitamins

» Sonne's

» Your Energy Systems

» FEATURED PRODUCTS

» SHOP BY CATEGORY

» FAMILY Nutrition

» • Women's Nutrition

» • Children's Nutrition

» • Men's Nutrition

» • Senior Vitamins

» Anti-Aging

» Bone and Joint

» Calcium Formulas

» CoQ10 / QH - Ubiquinol

» Cleansing

» Detox Nutrition & Herbs

» Digestive Health

» Energy

» Heart & Cardiovascular

» Herbal Products

» Immune Support

» KOSHER PRODUCTS

» Magnesium

» Mind, Memory & Mood

» Natural Hormones

» Omega 3 Fish Oils

» Phytosterols

» Probiotics

» Skin Care

» Urinary Tract Support

» Vision & Eye Health

» Vitamin D3

» Weight Management

» SPECIALS

» Your Personal Best

» Iron Supplements

» Pop-Up Specials

» Hold

» Kidney Support

» Internet Only Specials

Safe, Secure,
Online Ordering with:

Safe, Secure Ordering, By QuickSSL, 128-bit SSL certificate

Contact
Beachwood Canyon,
Naturally, Ltd.

Security Seals
Certified Seal
Privacy Seals
Business Seals


Benfotiamine 120 vegi-caps
Benfotiamine 120 vegi-caps Quantity in Basket: None
Code: AOR-BENFO


Price: $21.09

Quantity:  

Benfotiamine from AOR™ Advanced Orthomolecular Research
Bio-active Vitamin B1*
Dosage: n/a
Size: 120 vegi-caps
Category: AOR
Product Number: 08051
Product Code: AOR-BENFO

Benfotiamine is a naturally-occurring form of thiamin (vitamin B1). Benfotiamine's superior ability to penetrate cell membranes increases its bioavailability over conventional thiamin supplements. Benfotiamine is a powerful "late-phase" inhibitor of Advanced Glycation Endproduct (AGE) formation. Benfotiamine relieves the symptoms of diabetic neuropathy and may reduce the risk of diabetic complications.

Main Applications
As reported by literature:
• Aging
• AGE Inhibitor
• Brain Support
• Thiamin Deficiency

AOR™ guarantees that no ingredients not listed on the label have been added to the product. Contains no wheat, gluten, corn, nuts, dairy, soy, eggs, fish, shellfish or any other animal byproduct.

Source: Pharmaceutical Synthesis.

Suggested Use: Commence with two capsules twice daily for the first month; you may then continue at this dose or reduce to two capsules daily, or as directed by a qualified health care practitioner.

CAUTIONS: Persons with thiamine hypersensitivity should not take this product.
Pregnancy/Nursing: No studies have been conducted. Best to avoid.
Other Label Information: Keep out of the reach of children.

SUPPLEMENT FACTS:
Serving Size: 2 capsules
Servings Per Container: 60
Amount %DV
Benfotiamine 160 mg **

Other ingredients: microcrystalline cellulose. Capsule: hypromellose, water.
** Daily value not established.

Research:

Diabetic neuropathy: new strategies for treatment. Diabetes Obes Metab. 2007 Jun 26; Várkonyi T, Kempler P.

Current therapeutic possibilities can be divided into two groups: the pathogenetically oriented and the symptomatic therapy. One of the most important component of etiology-based treatment is the stabilization of glycemic control. Based on efficacy and safety data benfotiamine and alpha-lipoic acid should be considered as first choices among pathogenetically oriented treatments of diabetic neuropathy. Promising data were published about the aldose reductase inhibitor ranirestat. The symptomatic effect of antiepileptic drugs in diabetic painful neuropathy (DPN) is originated from several possible pharmacological properties. Pregabalin and gabapentin have the highest efficacy and the lowest frequency of adverse events among these drugs. Antidepressants also extensively used for symptomatic treatment in DPN. In the last years several studies were published about the benefial effect of duloxetine. Most likely combination therapy will be frequently applied in the future for the treatment of DPN, the optimal choice could be to combine pathogenetically oriented and symptomatic treatment.

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.Heart and Diabetes Center NRW, Georgstrasse 11, 32545 Bad Oeynhausen, Germany. Stirban A, Negrean M, Stratmann B, Gawlowski T, Horstmann T, Gotting C, Kleesiek K, Mueller-Roesel M, Koschinsky T, Uribarri J, Vlassara H, Tschoepe D.

OBJECTIVE: Diabetes is characterized by marked postprandial endothelial dysfunction induced by hyperglycemia, hypertriglyceridemia, advanced glycation end products (AGEs), and dicarbonyls (e.g., methylglyoxal [MG]). In vitro hyperglycemia-induced MG formation and endothelial dysfunction could be blocked by benfotiamine, but in vivo effects of benfotiamine on postprandial endothelial dysfunction and MG synthesis have not been investigated in humans until now.
RESEARCH DESIGN AND METHODS: Thirteen people with type 2 diabetes were given a heat-processed test meal with a high AGE content (HAGE; 15.100 AGE kU, 580 kcal, 54 g protein, 17 g lipids, and 48 g carbohydrates) before and after a 3-day therapy with benfotiamine (1,050 mg/day). Macrovascular flow-mediated dilatation (FMD) and microvascular reactive hyperemia, along with serum markers of endothelial disfunction (E-selectin, vascular cell adhesion molecule-1, and intracellular adhesion molecule-1), oxidative stress, AGE, and MG were measured during both test meal days after an overnight fast and then at 2, 4, and 6 h postprandially.
RESULTS: The HAGE induced a maximum reactive hyperemia decrease of -60.0% after 2 h and a maximum FMD impairment of -35.1% after 4 h, without affecting endothelium-independent vasodilatation. The effects of HAGE on both FMD and reactive hyperemia were completely prevented by benfotiamine. Serum markers of endothelial dysfunction and oxidative stress, as well as AGE, increased after HAGE. These effects were significantly reduced by benfotiamine.
CONCLUSIONS: Our study confirms micro- and macrovascular endothelial dysfunction accompanied by increased oxidative stress following a real-life, heat-processed, AGE-rich meal in individuals with type 2 diabetes and suggests benfotiamine as a potential treatment.

Pharmacokinetics of thiamine derivatives especially of benfotiamine. Int J Clin Pharmacol Ther 1996 Feb; 34(2): 47-50. Loew D.

Pharmacokinetic data of orally administered lipid-soluble thiamine analogues like benfotiamine are reviewed and assessed. It is quite clear that benfotiamine is absorbed much more better than water-soluble thiamine salts: maximum plasma levels of thiamine are about 5 times higher after benfotiamine, the bioavailability is at maximum about 3.6 times as high as that of thiamine hydrochloride and better than other lipophilic thiamine derivates. The physiological activity (alphaETK) increased only after benfotiamine was given. Due to its excellent pharmacokinetic profile benfotiamine should be preferred in treatment of relevant indications.

A benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes 1996; 104(4): 311-6. Stracke H, Lindemann A, Federlin K.

In a double-blind, randomized, controlled study, the effectiveness of treatment with a combination of Benfotiamine (an Allithiamine, a lipid-soluble derivative of vitamin B1 with high bioavailability) plus vitamin B6/B12 on objective parameters of neuropathy was studied over a period of 12 weeks on 24 diabetic patients with diabetic polyneuropathy. The results showed a significant improvement (p = 0.006) of nerve conduction velocity in the peroneal nerve and a statistical trend toward improvement of the vibration perception threshold. Long-term observation of 9 patients with verum over a period of 9 months support the results. Therapy-specific adverse effects were not seen. The results of this double-blind investigation, of the long-term observation and of the reports in the literature support the contention that the neurotropic benfotiamine-vitamin B combination represents a starting point in the treatment of diabetic polyneuropathy.

Benfotiamin inhibits intracellular formation of advanced Glycation endproducts in vivo. Diabetes. 2000 May; 49(Suppl1): A143(P583). Lin J, Alt A, Liersch J, Bretzel RG, Brownlee MA, Hammes HP.

We have demonstrated previously that intracellular formation of the advanced glycation end product (AGE) N-[Epsilon]-(carboxymethyl)lysine (CML) inversely correlates with diabetic vascular complications independently from glycemia (Diabetologia 42, 603, 1999). Here, we studied the effect of benfotiamine, a lipid-soluble thiamine derivative with known AGE-inhibiting properties in-vitro on the intracellular formation of (CML) and methylglyoxal-derived AGE in red blood cells. Blood was collected from 6 Type 1 diabetic patients (2m, 4f, age 31.8 ± 5.5 years; diabetes duration 15.3 ± 7.0 years) before and after treatment with 600 mg/day benfotiamine for 28 days. In addition to HbA1c (HPLC), CML and methylglyoxal were measured using specific antibodies and a quantitative blot technique. While treatment with benfotiamine did not affect HbA1c levels (at entry: 7.18 ± 0.86%; at conclusion 6.88 ± 0.88%; p not significant), levels of CML decreased by 40% (737 ± 51 arbitrary units/mg protein (AU) vs 470 ± 86 AU; p < 0.01). The levels of intracellular methylglyoxal were reduced by almost 70% (1628 ± AU vs 500 ± 343 AU; p < 0.01). The data indicate that thiamine derivatives are effective inhibitors of both intracellular glycoxidation and AGE formation.

Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med 2003 Mar; 9(3): 294-9. Hammes HP, Du X, Edelstein D, Taguchi T, Matsumura T, Ju Q, Lin J, Bierhaus A, Nawroth P, Hannak D, Neumaier M, Bergfeld R, Giardino I, Brownlee M.

Three of the major biochemical pathways implicated in the pathogenesis of hyperglycemia induced vascular damage (the hexosamine pathway, the advanced glycation end product (AGE) formation pathway and the diacylglycerol (DAG)-protein kinase C (PKC) pathway) are activated by increased availability of the glycolytic metabolites glyceraldehyde-3-phosphate and fructose-6-phosphate. We have discovered that the lipid-soluble thiamine derivative benfotiamine can inhibit these three pathways, as well as hyperglycemia-associated NF-kappaB activation, by activating the pentose phosphate pathway enzyme transketolase, which converts glyceraldehyde-3-phosphate and fructose-6-phosphate into pentose-5-phosphates and other sugars. In retinas of diabetic animals, benfotiamine treatment inhibited these three pathways and NF-kappaB activation by activating transketolase, and also prevented experimental diabetic retinopathy. The ability of benfotiamine to inhibit three major pathways simultaneously might be clinically useful in preventing the development and progression of diabetic complications.

Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung 1999 Mar; 49(3): 220-4. Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P.

The therapeutic effectiveness of a benfotiamine (CAS 22457-89-2)-vitamin B combination (Milgamma-N), administered in high (4 x 2 capsules/day, = 320 mg benfotiamine/day) and medium doses (3 x 1 capsules/day), was compared to a monotherapy with benfotiamine (Benfogamma) (3 x 1 tablets/day, = 150 mg benfotiamine/day) in diabetic patients suffering from painful peripheral diabetic neuropathy (DNP). In a 6-week open clinical trial, 36 patients (aged 40 to 70 yrs) having acceptable metabolic control (HbA1c < 8.0%) were randomly assigned to three groups, each of them comprising 12 participants. Neuropathy was assessed by five parameters: the pain sensation (evaluated by a modified analogue visual scale), the vibration sensation (measured with a tuning fork using the Riedel-Seyfert method) and the current perception threshold (CPT) onthe peroneal nerve at 3 frequencies: 5, 250 and 2000 Hz). Parameters were registered at the beginning of the study and at the end of the 3rd and 6th week of therapy. An overall bneneficial therapeutic effect on the neuropathy status was observed in all three groups during the study, and a significant improvement in most of the parameters studied appeared already at the 3rd week of therapy (p < 0.01). The greatest change occurred in the group of patients receiving the high dose of benfotiamine (p < 0.01 and 0.05, resp., compared to the othr groups). Metabolic control did not change over the study. It is concluded that benfotiamine is most effective in large doses, although even in smaller daily dosages, either in combination or in monotherapy, it is effective.

The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide medical advice to individuals. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes. Any reproduction in whole or part and in print or electronic form without express permission is strictly forbidden. Permission to reproduce selected material may be granted by contacting AOR Inc.

Copyright © 2005, Advanced Orthomolecular Research

*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.