helps maintain healthy cells in the presence of blood glucose, controls formation of Advanced Glycation Endproducts (AGEs) and normalizes cellular processes fueled by glucose metabolites.
Benfotiamine (S-benzoylthiamine-O-monophosphate) is a synthetic derivative of thiamin, belonging to the family of compounds known as "allithiamines."
Benfotiamine is fat-soluble and thus more bioavailable and physiologically active than thiamin.* Characteristic of the allithiamines is an open thiazole ring within the chemical structure of these thiamine-related compounds, making them fat (lipid) soluble. In contrast, thiamine, which is water soluble, has a closed thiazole ring. The lipid solubility of benfotiamine, conferred by this open ring, increases its bioavailablity.
Benfotiamine is readily absorbed at higher doses, in contrast to absorption of water-soluble thiamin salts, which decreases at higher doses, due to saturation of absorption sites in the intestines.1 In a double-blind, cross-over trial, comparing bioavailability of benfotiamine to that of thiamine in 12 subjects, benfotiamine caused an average 5-fold greater increase in blood thiamine levels than thiamin mononitrate, with a concomitant greater thiamine concentration in erythrocytes (red blood cells). Benfotiamine readily passes through intestinal mucosal cells, where it is converted into physiologically active thiamine. Benfotiamine inceases blood levels of thiamine pyrophosphate (TPP), the primary thiamin co-enzyme.
Benfotiamine and Glucose Metabolism
Benfotiamine normalizes cellular processes fueled by glucose metabolites.
As long as glucose remains at normal levels, excess glucose metabolites do not accumulate within the cell. The bulk of the cellís glucose supply is converted to pyruvic acid, which serves as substrate for production of acetyl CoA, the primary fuel for the Krebs cycle. Of the total amount of metabolic energy (in the form of ATP) released from food, the Krebs cycle generates about 90 percent.5 In the presence of elevated glucose levels, the electron transport chain, the final ATP-generating system in the mitochondrion, produces larger than normal amounts of the oxygen free radical "superoxide." This excess superoxide inhibits glyceraldehyde phosphate dehydrogenase (GAPDH), a key enzyme in the conversion of glucose to pyruvic acid, resulting in an excess of intermediate metabolites known as "triosephosphates." Increase triosephophate levels trigger several cellular mechanisms that result in potential damage to vascular tissue. Cells particularly vulnerable to this biochemical dysfunction are found in the retina, kidneys and nerves.
Benfotiamine has been shown to block three of these mechanisms: the hexosamine pathway, the diaglycerol-protein kinase C pathway and the formation of Advanced Glycation End-poducts. As discussed below, benfotiamine does this by activating transketolase, a key thiamin-dependent enzyme.
One capsule daily, with or without food.