Highly bioavailable vitamin B1
- A highly bioavailable source of vitamin B1
- Supports nerve and eye function in diabetics
- Helps prevent sugar-related kidney damage
- Provides a high capsule count for flexible dosing options
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Benfotiamine is a natural form of thiamin (vitamin B1) that has been proven to be 5 times more absorbable than regular thiamin and has better penetration through cellular membranes. The benefit of benfotiamine centers around its ability to block a harmful process in the body called protein glycation, which creates Advanced Glycation End-products (AGEs), a role that is not shared by thiamin.
AGEs are formed when cells are exposed to consistently high levels of blood sugar. They can lead to significant tissue and DNA damage, speed up the aging process, and ultimately lead to diabetic-related nerve damage in the hands and feet and damage to blood vessels in the eyes and kidneys. Benfotiamine has the unique ability to block the formation of AGEs and supplementation can help reduce nerve pain and improve nerve function. Many randomized, double-blind, placebo-controlled human trials have proven that benfotiamine powerfully supports nerve function in diabetic neuropathy.
AOR’s Benfotiamine is one of the few products to contain this active form of B1 in an evidence-based dose. With our modern high-sugar diet, millions are experiencing the many negative effects that excessive sugar has on the body. Those looking for protection against these negative effects such as accelerated cellular aging and nerve damage should consider AOR’s Benfotiamine.
Benfotiamine is a natural and bioavailable source of vitamin B1 and may be helpful in reducing the symptoms and complications of having poor blood sugar control. AOR’s Benfotiamine is one of the few products to contain this active form of B1 in an evidence-based dose.
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. This allows for the use of benfotiamine to elicit all of the benefits of vitamin B1, such as the metabolism of carbohydrates, protein, and fat, in a highly efficient manner.
AOR™ guarantees that all ingredients have been declared on the label. Contains no wheat, gluten, corn, nuts, peanuts, sesame seeds, sulphites, mustard, soy, dairy, eggs, fish, shellfish or any animal by product.
Take one capsule daily with food, or as directed by a qualified health care practitioner.
Do not use if you are pregnant or breastfeeding. Persons with thiamin hypersensitivity should not take this product.
- Healthy aging
- Nerve function
- Thiamin deficiency
The information and product descriptions appearing on this website are for information purposes only, and are not intended to provide or replace medical advice to individuals from a qualified health care professional. Consult with your physician if you have any health concerns, and before initiating any new diet, exercise, supplement, or other lifestyle changes.
Non-medicinal Ingredients: microcrystalline cellulose and sodium stearyl fumarate. Capsule: hypromellose.
The “Caramelization of the Flesh”
Advanced Glycation End-products, or “AGEs” as they’re appropriately called, are the end result of the complex chemical process through which the structure of proteins is warped by exposure to sugars or by other, much more reactive molecules. AGE chemistry is the cause of the “browning” you see when you roast a chicken or make toast, but the same “browning” chemistry is at work in your body every day of your life. In your arteries. In your kidneys. In your heart, your eyes, your skin, your nerves. In every cell, the sugar that your body uses for fuel is busily at work at this very moment, caramelizing your body through exactly the same chemical processes that caramelize onions or peanut brittle.
Glycation math is simple: more sugar equals more AGEd proteins. As a result, people with poor blood sugar control begin to feel the effects of glycation at much younger ages than do people with more normal blood sugar levels. Watching people with unstable blood sugar levels age is like watching “normal” aging played on fast-forward. Slowly, imperceptibly, AGE reactions create chemical handcuffs, which gum up your proteins, deactivate your enzymes, trigger unhealthy biochemical signaling in your cells, and damage your DNA. Aging you.
Make that: AGEing you.
Two Ways to AGE
There are two major ways that AGEs can form inside the body. One way is through a simple series of chemical reactions known as the “Maillard Pathway,” known from food chemistry for a century. But more recently, scientists have come to understand another pathway of AGE formation – a distinctly biological pathway, which only occurs within your cells because of the body’s metabolism of carbohydrates.
When blood sugar levels rise, some key kinds of cells – including nerve cells (neurons) and the cells that make up the fine blood vessels of the retina of the eye and the filtering units (glomeruli) of the kidney – are also flooded with glucose. The resulting high sugar levels within these cells cause a logjam in the normal cellular metabolism of glucose. This backlog results in a buildup within the cell of super-reactive glucose-metabolic intermediates known as triosephosphates. And once that happens, the excess triosephosphates attack the surrounding proteins, lipids, and DNA, causing AGE damage from within the heart of the cell. These cells are thus the most vulnerable to the complications of blood sugar instability.
Drugs do exist which can inhibit the formation of AGE, but none are available on the market as yet, and one of the most promising candidates (aminoguanidine) has shown signs of toxicity in human trials and appears to have been abandoned by its developers. On the other hand, some companies are selling supplements that are marketed as “AGE-inhibitors.” But while many of the herbs and other nutrients may be valuable, and many even inhibit AGEing in a test tube, there’s no evidence that most of these “AGE-blocking” ingredients have any effect on AGEing in your body at the dosages used. Examples include thyme extract, inositol, acetyl-L-carnitine, taurine, and a whole host of antioxidants (including n-acetyl-cysteine (NAC) and flavonoids, such as quercetin and resveratrol).
TPP: Our Hero … in Chains!
There is a nutrient that could, in theory, pack a potent wallop against the AGE onslaught: Thiamin Pyrophosphate (TPP), the active coenzyme form of the B-complex vitamin thiamin. In 1996, researchers showed that TPP could step in to stop AGE formation at the most important point in the process: the late, irreversible conversion of Amadori products into full-blown AGEs. What’s more, TPP can exert a two-pronged AGE-inhibiting effect in the body, because boosting TPP in cells stressed by high glucose concentrations opens up an important biochemical “safety valve” in the normal metabolism of blood sugar through an enzyme known as transketolase. Activating transketolase allows the body to shunt excess triosephosphates into a safe alternative metabolic pathway, preventing the logjam that leads to the buildup of triosephosphates and the formation of AGE.
Unfortunately, this does not mean that loading up on regular thiamin (vitamin B1) will free you from glycation’s sticky shackles. The problem is that your body’s ability to absorb and metabolize conventional thiamin supplements is very limited. In fact, no matter how much thiamin you take, you don’t materially increase plasma levels beyond what you get from the first 12 milligrams of the dose. And then getting thiamin into the cells to do its job is just as tricky.
You might think that you can get around this problem by taking supplements containing TPP itself, instead of plain old thiamin. Unfortunately, as part of the normal cellular absorption process, specific enzymes actually strip TPP of its phosphate groups. As a result, you get no additional AGE-battling benefit from taking preformed thiamin pyrophosphate instead of standard thiamin. In fact, when you take supplements based on TPP itself, studies show that thiamin levels and biological activity are actually lower than if you take the same amount of regular thiamin!
Benfotiamine: the TPP Solution
Fortunately, an effective way to boost thiamin pyrophosphate in your cells does exist: Benfotiamine (S-benzoylthiamine-O-monophosphate). Benfotiamine is a derivative of thiamine. Although benfotiamine is not lipid soluble, it has been shown to have very good bioavailability. This is because benfotiamine is converted into another compound, called S-benzoylthiamin, by the enzymes present in the cells of the intestinal mucosa. S-benzoylthiamine has better fat solubility, and therefore passes easily through cell membranes. S-benzoylthiamine is then transported to the liver where it is converted to thiamine and released into the bloodstream.
As a result, your body absorbs Benfotiamine better than thiamin itself, and levels of thiamin and also TPP remain higher for longer. Thiamin absorption from Benfotiamine has been shown to be about five times as great as from conventional thiamin supplements.
Studies have shown that Benfotiamine is even more bioavailable than the other thiamine-related compounds called allithiamines, including thiamin tetrahydrofurfuryl disulfide/TTFD. By effectively increasing levels of thiamin itself, Benfotiamine dramatically boosts AGE-fighting thiamin pyrophosphate and cell-shielding transketolase activity in your body.
Shielding Nerve Structure
While most “anti-AGE” supplements rely on test-tube “browning” experiments as the “evidence” of efficacy, Benfotiamine has been proven in multiple real-world human and animal studies to reduce AGE formation and support tissue structure and function in those with unstable blood sugar levels.
Most impressively, many randomized, double-blind, placebo-controlled human trials have proven that Benfotiamine powerfully supports healthy nerve function. In one trial, 24 people suffering with unstable blood sugar levels took either Benfotiamine (plus doses of common B6 and B12 similar to those used in mutivitamins) or a look-alike dummy pill, spread out into three pills over the course of the day, for twelve weeks. The participants started with 320 milligrams of Benfotiamine per day for the first two weeks, followed by 120 milligrams for the rest of the trial. Before and after the trial, the function of patients’s nerve cells were tested using nerve conduction velocity (NCV) and vibratory perception threshold (which tests the nerves’s sensitivity by determining the lowest level at which vibrations applied at key nerve sites are first felt).
At the end of the trial, the vibration perception threshold had “clearly” improved by 30% in those who had taken the Benfotiamine supplements, while it had worsened in the placebo group by 5% at one site and by 32% at another. At the same time, people taking Benfotiamine experienced statistically significant improvements in nerve conduction velocity from the feet, even as this aspect of nerve function deteriorated in those taking the look-alike pills!
The power of Benfotiamine to improve vibratory perception threshold and nerve conduction velocity have been confirmed in other trials. Clinical trials have also shown that Benfotiamine supports nerve function in those with blood sugar instability as measured by many other methods. For instance, Benfotiamine users experience a 50% reduction in diabetic nerve pain, along with an increased ability of the nerves to detect an electrical current, respond to electrical stimulation, and regulate the heartbeat. Similarly, Benfotiamine prevents this loss of control from happening in the first place in dogs with neuropathy. In another human clinical trial, a B-vitamin combination using Benfotiamine as its thiamin source was put head-to-head with a B-complex supplement that included a megadose of conventional thiamin. Benfotiamine proved its effectiveness on several of these key parameters, while the standard thiamin pill failed.
These benefits are not due to changes in blood sugar levels (either fasting, or after a meal, or averaged over several months (as measured by HbA1c), or improvements in metabolic benchmarks. They are the direct results of Benfotiamine’s AGE-fighting, metabolic-balancing powers.
Benfotiamine in Other Vulnerable Tissues
More recently, new studies have begun to document Benfotiamine’s ability to shield other tissues from AGE damage. One just-published study tested the ability of thiamin and Benfotiamine to protect rodents’ retinas from the ravages of AGE.
The researchers then gave one group of rodents with unstable blood sugar Benfotiamine supplements, and left another group with unstable blood sugar levels unsupplemented, keeping a third group of healthy animals as a control group. Nine months later, they examined the animals’ eyes, testing the level of AGE in their retinas, examining metabolic abnormalities of the cells, and looking for acellular capillaries (the dead husks left behind when the cells of the tiny blood vessels of the eye die).
Benfotiamine supplements normalized AGE levels in the retinas of those rats with unstable blood sugar levels, as well as several key metabolic parameters within the unhealthy animals’ cells – without influencing body weight or blood sugar (as measured by HbA1c). More importantly, Benfotiamine prevented the AGE-associated retinal damage. After nine months of unstable blood sugar levels, unhealthy animals had suffered three times as many acellular capillaries as were found in healthy animals. But with the protection afforded by Benfotiamine, the number of acellular capillaries in the supplemented animals who had poor blood sugar control was indistinguishable from that of their normal, healthy cousins!
And there’s another AGE-related disease that researchers believe Benfotiamine may fight: the loss of kidney function which accompanies “normal” aging, and which is accelerated by high blood sugars. Dr. Paul Thornalley of the University of Essex has just completed a study designed to see if Benfotiamine will protect diabetic rodents against kidney damage. While the results have not yet been published, Dr. Thornalley has indicated that both megadose thiamin and Benfotiamine caused clear-cut reductions in the leakage of protein – with Benfotiamine showing itself to be the superior intervention. A second study is now underway to see if Benfotiamine will actually improve kidney function in unhealthy animals with pre-existing kidney damage, as it has already been shown to do in the nerves of animals and humans with unstable blood sugar levels.
The End of an AGE
These are not test-tube studies. The results experienced when taking Benfotiamine occur not merely in labs, but in lives: in the bodies – and in the health – of living things, from experimental animals to human beings. In Benfotiamine, we finally have a proven way to protect tissues from the AGE assault.
With the rise of blood sugar problems and health complications that come with it, many are searching for antioxidant protection against the ravaging effects of advanced glycation end products in the body. Some of the most common supplements used for this purpose include the B vitamins, antioxidants and herbs that help to lower blood sugar levels and or protect the body.
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. “Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy.” Nat Med. 2003 Mar; 9(3): 294-9.
Koltai MZ. “Prevention of cardiac autonomic neuropathy in dogs with Benfotiamine.” In Gries FA, Federlin K. “Benfotiamine in the Therapy of Polyneuropathy.” New York: Georg Thieme Verlag, 1998; 45-9.
Lin J, Alt A, Liersch J, Bretzel RG, Brownlee MA, Hammes HP. “Benfotiamine inhibits intracellular formation of advanced glycation endproducts in vivo.” Diabetes. 2000 May; 49(Suppl1): A143 (P583).
Loew D. “Pharmacokinetics of thiamine derivatives especially of Benfotiamine.” Int J Clin Pharmacol Ther. 1996 Feb; 34(2): 47-50.
Stracke H, Lindemann A, Federlin K. “A Benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy.” Exp Clin Endocrinol Diabetes 1996; 104(4): 311-6.
Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. “Effectiveness of different Benfotiamine dosage regimens in the treatment of painful diabetic neuropathy.” Arzneimittelforschung. 1999 Mar; 49(3): 220-4.
The multifaceted therapeutic potential of benfotiamine.
Pharmacological Research. 2010; 61:482–488
Pitchai Balakumar, Ankur Rohilla, Pawan Krishan, Ponnu Solairaj, Arunachalam Thangathirupathi.
Thiamine, known as vitamin B1, plays an essential role in energy metabolism. Benfotiamine (Sbenzoylthiamine O-monophoshate) is a synthetic S-acyl derivative of thiamine. Once absorbed, benfotiamine is dephosphorylated by ecto-alkaline phosphatase to lipid-soluble S-benzoylthiamine. Transketolase is an enzyme that directs the precursors of advanced glycation end products (AGEs) to pentose phosphate pathway. Benfotiamine administration increases the levels of intracellular thiamine diphosphate, a cofactor necessary for the activation transketolase, resulting in the reduction of tissue level of AGEs….. Chronic hyperglycemia accelerates the reaction between glucose and proteins leading to the formation of AGEs, which form irreversible cross-links with many macromolecules such as collagen….. Experimental studies have elucidated that binding of AGEs to their specific receptors (RAGE) activates mainly monocytes and endothelial cells and consequently induces various inflammatory events. Moreover, AGEs exaggerate the status of oxidative stress in diabetes thatmayadditionally contribute to functional changes in vascular tone control observed….. The anti-AGE property of benfotiamine certainly makes it effective for the treatment of diabetic neuropathy, nephropathy and retinopathy. Interestingly, few recent studies demonstrated additional non-AGE-dependent pharmacological actions of benfotiamine. The present review critically analyzed the multifaceted therapeutic potential of benfotiamine.
Benfotiamine reduces genomic damage in peripheral lymphocytes of hemodialysis patients.
Naunyn Schmiedebergs Arch Pharmacol. 2008 Sep;378(3):283-91.
Schupp N, Dette EM, Schmid U, Bahner U, Winkler M, Heidland A, Stopper H.
Hemodialysis patients have an elevated genomic damage in peripheral blood lymphocytes (PBLs) and an increased cancer incidence, possibly due to accumulation of uremic toxins like advanced glycation end products (AGEs). Because the vitamin B1 prodrug benfotiamine reduces AGE levels….. and dialysis patients often suffer from vitamin B1 deficiency, we conducted two consecutive studies supplementing hemodialysis patients with benfotiamine. In both studies, genomic damage was measured as micronucleus frequency of PBLs before and at three time-points after initiation of benfotiamine supplementation. AGE-associated fluorescence in plasma, and in the second study additionally, the antioxidative capacity of plasma was analyzed. Benfotiamine significantly lowered the genomic damage of PBLs in hemodialysis patients of both studies independent of changes in plasma AGE levels. The second study gave a hint to the mechanism, as the antioxidative capacity of the plasma of the treated patients clearly increased, which might ameliorate the DNA damage.
Benfotiamine in diabetic polyneuropathy (BENDIP): results of a randomised, double blind, placebo-controlled clinical study.
Exp Clin Endocrinol Diabetes. 2008 Nov;116(10):600-5.
Stracke H, Gaus W, Achenbach U, Federlin K, Bretzel RG.
AIM: Efficacy and safety of benfotiamine in treatment of diabetic polyneuropathy.
METHODS: Double blind, placebo-controlled, phase-III-study. 181 patients were screened. 165 patients with symmetrical, distal diabetic polyneuropathy were randomised to one of three treatment groups entering the wash-out phase and 133/124 patients were analysed in the ITT/PP analysis: Benfotiamine 600 mg per day (n=47/43), benfotiamine 300 mg per day (n=45/42) or placebo (n=41/39).
RESULTS: After 6 weeks of treatment, the primary outcome parameter NSS (Neuropathy Symptom Score) differed significantly between the treatment groups (p=0.033) in the PP (per protocol) population. In the ITT (intention to treat) population, the improvement of NSS was slightly above significance (p=0.055). The TSS (Total Symptom Score) showed no significant differences after 6 weeks of treatment. The improvement was more pronounced at the higher benfotiamine dose and increased with treatment duration. In the TSS, best results were obtained for the symptom “pain”. Treatment was well tolerated in all groups.
CONCLUSION: Benfotiamine may extend the treatment option for patients with diabetic polyneuropathy based on causal influence on impaired glucose metabolism. Further studies should confirm the positive experiences.
High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfontiamine.
Eur J Clin Pharmacol. 2000 Jun;56(3):251-7.
Frank T, Bitsch R, Maiwald J, Stein G.
OBJECTIVE: The influence of either orally administered S-benzoylthiamine-O-monophosphate (benfotiamine) or thiamine nitrate on the thiamine status was tested in a randomised, two-group comparison study in 20 end-stage renal disease (ESRD) patients. Main outcome measures were the pharmacokinetics of thiamine diphosphate (TDP) in blood, the in vitro erythrocyte transketolase activity, its activation coefficient (alpha-ETK) and the TDP concentration in erythrocytes.
METHODS: After ingestion of a single dose of either 100 mg thiamine nitrate (corresponding to 305 micromol thiamine) or 100 mg benfotiamine (corresponding to 214 micromol thiamine), the blood levels of thiamine phosphate esters were analysed by means of high-performance liquid chromatography for a 24-h period. The TDP concentration in erythrocytes was calculated using the haematocrit and TDP concentration in blood. Erythrocyte transketolase activity and alpha-ETK were measured before and 10 h after administration. The pharmacokinetics of TDP in blood were compared with healthy subjects of other studies retrieved from database query.
RESULTS: Regarding the blood concentrations of TDP, the patients with ESRD had a 4.3 times higher area under the concentration time curve after benfotiamine administration than after thiamine nitrate. After benfotiamine administration, the peak plasma concentration of TDP exceeded that in healthy subjects by 51%. In the ESRD patients, after 24 h, the mean TDP concentration in erythrocytes increased from 158.7 /-30.9 ng/ml initially to 325.8 /-50.9 ng/ml after administration of benfotiamine and from 166.2 /-51.9 ng/ml to 200.5 /-50.0 ng/ml after thiamine nitrate administration. The ratio between the maximum erythrocyte TDP concentration and basal concentration was 2.66 /-0.6 in the benfotiamine group and 1.44 /-0.2 in the group receiving thiamine nitrate (P < 0.001). After 24 h, it was 2.11 /-0.4 and 1.23 /-0.2, respectively. The transketolase activity increased from 3.54 /-0.7 microkat/l initially to 3.84 /-0.6 microkat/l after benfotiamine intake (P = 0.02) and from 3.71 /-0.8 microkat/l to 4.02 /-0.7 microkat/l after thiamine nitrate intake (P = 0.08). Likewise, alpha-ETK decreased from initially 1.10 /-0.07 to 1.04 /-0.04 (P = 0.04) and from 1.12 /-0.05 to 1.08 /-0.06 (P = 0.09). After 24 h, the phosphorylation ratio in whole blood decreased from 12.9 /-6.9 initially to 5.6 /-3.2 after benfotiamine administration (P = 0.02) and from 13.5 /-7.3 to 9.0 /-4.8 (P = 0.03) after administration of thiamine nitrate. No correlation between erythrocyte TDP concentration and transketolase activity and/or alpha-ETK was observed in ESRD patients, either before or 10 h after administration.
CONCLUSION: Compared with thiamine nitrate, the oral administration of benfotiamine leads to higher TDP concentrations in erythrocytes accompanied with a significant improvement of the erythrocyte transketolase activity in ESRD patients.
Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy.
Arzneimittelforschung. 1999 Mar;49(3):220-4.
Winkler G, Pál B, Nagybéganyi 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) on the 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.
A Benfotiamine – vitamin B combination in treatment of diabetic polyneuropathy.
Exp Clin Endocrinol Diabetes. 1996 104: 311-316.
H. Stracke, A. Lindemann, K. Federlin.
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.
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