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Its not just any need ones which fight... Advanced Glycation Endproducts, 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. Its this chemistry which changes nerve tissue and facilitates the change in senses in aging.

Glycation math is simple: more sugar equals more AGE'd proteins. As a result, people with diabetes begin to feel the effects of glycation at much younger ages than do people with more normal blood sugar levels. Watching people with diabetes 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. This is also partially why low carbohydrate diets work well for some people and those with neurological problems such as autism, Alzheimer's, and even heavy metal toxicity.

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 cell - including nerve cells (neurons) and the cells that make up the fine blood cells 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. It's these cells are thus the most vulnerable to the complications of diabetes and other functional disorders.

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 candidate (aminoguanidine) has shown signs of toxicity in human trials so therefore appears to have been abandoned by its developers.

On the other hand, some companies are selling supplements 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" antioxidants have any effect on prevention against AGEing in your body at the dosages used.
Just more myths and aging....possibly.

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!

Benfotiamin: the TPP Solution

Fortunately, an effective way to boost thiamin pyrophosphate in your cells does exist: Benfotiamin (S-benzoylthiamine-O-monophosphate). Benfotiamin is the most potent of the allithiamines, an unique class of thiamin-derived compounds present in trace quantities in roasted crushed garlic and other vegetables from the Allium genus (such as onions, shallots, and leeks).

Benfotiamin's unique open-ringed structure makes it able to pass directly through cell membranes, readily crossing the intestinal wall and being taken straight into the cell.

As a result, your body absorbs Benfotiamin better than thiamin itself, and levels of thiamin and TPP remain higher for longer. Thiamin absorption from Benfotiamine is about five times as great as from conventional thiamin supplements. And the effect is even more impressive at the tissue level: brain and muscle, for instance, take in five- to twentyfive-fold as much thiamin in the form of allithiamines as they do of an equal amount of regular thiamin.

And Benfotiamin is even more bioavailable than the other allithiamines, including thiamin tetrahydrofurfuryl disulfide/TTFD. Yet Benfotiamin is actually less toxic than conventional thiamin supplements!

By effectively increasing levels of thiamin itself, Benfotiamin 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, Benfotiamin has been proven in multiple real-world human and animal studies to reduce AGE formation and support tissue structure and function in diabetics.

Most impressively, many randomized, double-blind, placebo-controlled human trials have proven that Benfotiamin powerfully supports nerve function in diabetic neuropathy. In one trial, 24 people suffering with diabetic neuropathy took either Benfotiamin (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 Benfotiamin 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 (VPT) (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 Benfotiamin 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 Benfotiamin 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 Benfotiamin to improve vibratory perception threshold and nerve conduction velocity have been confirmed in other trials. Clinical trials have also shown that Benfotiamin supports nerve function in diabetics as measured by many other methods. For instance, Benfotiamin 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, Benfotiamin prevents this loss of control from happening in the first place in diabetic dogs. In another human clinical trial, a B-vitamin combination using Benfotiamin as its thiamin source was put head-to-head with a B-complex supplement that included a megadose of conventional thiamin. Benfotiamin 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 Benfotiamin's AGE-fighting, metabolic-balancing powers.


More recently, new studies have begun to document Benfotiamin's ability to shield other tissues from AGE damage. One just-published study tested the ability of thiamin and Benfotiamin to protect diabetic rodents' retinas from the ravages of AGE.

The researchers then gave one group of diabetic rodents Benfotiamin supplements, and left another group unsupplemented, keeping a third group of nondiabetic 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).

Benfotiamin supplements normalized AGE levels in the diabetics' retina, as well as several key metabolic parameters within the diabetic animals' cells - without influencing body weight or blood sugar (as measured by HbA1c). More importantly, Benfotiamin prevented the AGE-associated retinal damage.

After nine months of diabetes, diabetic animals had suffered three times as many acellular capillaries as were found in healthy animals. But with the protection afforded by Benfotiamin, the number of acellular capillaries in the supplemented diabetics was indistinguishable from that of their normal, healthy cousins!

And there's another AGE-related disease that researchers believe Benfotiamin may fight: the loss of kidney function which accompanies "normal" aging, and which is accelerated by diabetes.

Dr. Paul Thornalley of the University of Essex has just completed a study designed to see if Benfotiamin will protect diabetic rodents against kidney damage. While the results have not yet been published, Dr. Thornalley has indicated that both megadose thiamin and Benfotiamin caused clear-cut reductions in the leakage of protein - with Benfotiamin showing itself to be the superior intervention.

A second study is now underway to see if Benfotiamin will actually improve kidney function in diabetic animals with pre-existing kidney damage, as it has already been shown to do in the nerves of diabetic animals and humans.

Benfotiamin and Heavy Metal Toxicity

Very recent studies have suggested that vitamin B1 had increased the effectiveness of chelators such as DMSA to reduce liver and kidney lead and other heavy metal loads. In particular the most effective form was benfotiamin.

Dentally, thiamin has been shown to help health conditions such as Bell's Palsy, Tic Douloureux, decreases dental caries, fractures (that would include any of the body), herpes simplex and herpes zoster (shingles), hypersensitive teeth, postoperative pain, dry socket, TMJ pain, etc. Ongoing research is looking at its role in Alzheimer's Disease, autism, neurtransmitter balancing, brain disorders, multiple sclerosis.

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 Benfotiamin, we finally have a proven way to protect tissues from the AGE assault.

BENFOTIAMIN is available Here

Selected References

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 Benfotiamin-vitamin B combination in treatment of diabetic polyneuropathy. Exp Clin Endocrinol Diabetes. 1996;104(4):311-6.

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

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 Feb 18 [epub ahead of print]; doi:10.1038/nm834.

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

Koltai MZ. Prevention of cardiac autonomic neuropathy in dogs with Benfotiamin. In Gries FA

Langlais PJ, McRee RC, Nalwalk JA, Hough LB Depletion of brain histamine produces regionally selective protection against thiamine deficiency-induced lesions in the rat. Metab Brain Dis 2002 Sep;17(3):199-210

Dhawan M, Kachru DN, Tandon SK. Influence of thiamine and ascorbic acid supplementation on the antidotal efficacy of thiol chelators in experimental lead intoxication, Arch Toxicol 1988;62(4):301-4

Ito Y, Niiya Y, Otani M, Shima S. Effect of thiamine on the excretion of subcutaneously injected lead in rats. Toxicol Lett 1987 Aug;37(3):221-8

Tandon SK, Prasad S, Effect of thiamine on the cadmium-chelating capacity of thiol compounds, Hum Exp Toxicol 2000 Sep;19(9):523-8

L. Pantoni, L. Poggesi, A. Repice and D. Inzitari. "Disappearance of motor tics after Wernicke's encephalopathy in a patient with Tourette's syndrome." Neurology, 48:381-383 (1997).

A. Brenner. "The effects of megadoses of selected B complex vitamins on children with hyperkinesis: controlled studies with long-term follow-up." Journal of Learning Disabilities, 15(5):258-264 (1982).

L. Reinken, H. Stolley and W. Droese. "Biochemical assessment of thiamine nutrition in childhood." European Journal of Pediatrics, 131:229-235 (1979)

A.B. Mukherjee, S. Svoronos, A. Ghazanfari, P.R. Martin, A. Fisher, B. Roecklein, D. Rodbard, R. Staton, D. Behar, C.J. Berg and R. Manjunath. "Transketolase abnormality in clutured fibrobnlasts from familial chronic alcoholic men and their male offspring." The Journal of Clinical Investigation, 79:1039-1043 (1987)

J.P. Blass and G.E. Gibson. "Abnormality of a thiamine-requiring enzyme in patients with Wernicke-Korsakoff syndrome". The New England Journal of Medicine, 297:1367-1370 (1977).

R.L. Hoffman. "The natural approach to attention deficit disorder: drug-free ways to treat the roots of this childhood epidemic." Good Health Guide published by Keats Publishing, Inc., New Canaan, Connecticut, 1997