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ne 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 nerveconduction 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 diabetics 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 diabetic dogs. 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 thestandard 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 diabetic rodents’ retinas from the ravages of AGE. The researchers then gave one group of diabetic rodents Benfotiamine 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 whenthe cells of the tiny blood vessels of the eye die). Benfotiamine 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, Benfotiamine 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 Benfotiamine, 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 Benfotiamine 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 Benfotiamine will protect diabetic rodentsagainst 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 diabetic animals with pre-existing kidney damage, as it has already been shown to do in the nerves of diabetic animals and humans. 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. References 1. Loew D. “.” Int J Clin Pharmacol Ther. 1996 Feb; 34(2): 47-50. 2 . Stracke H, Lindemann A, Federlin K. “.” Exp Clin Endocrinol Diabetes 1996; 104(4): 311-6. 3 . Lin J, AltA, Liersch J, Bretzel RG, Brownlee MA, Hammes HP. “.” Diabetes. 2000 May; 49(Suppl1): A143 (P583). 4 . 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. “.” Nat Med. 2003 Mar; 9(3): 294-9. 5 . Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P. “.” Arzneimittelforschung. 1999 Mar; 49(3): 220-4. 6 . 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.
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