Search Term: " Benfotiamine "
Support Healthy Circulation and Arterial Function with Benfotiamine!
Benfotiamine is a derivative nutrient of thiamine (vitamin B1). Usually, many people suffering from peripheral neuropathy lack this crucial nutrient. Thiamine, Vitamin B1, is highly required for the nervous system to keep functioning properly. Maintaining adequate levels of Thiamine through diet alone is hard. Benfotiamine works to nourish the nerves and reverse the effects of peripheral neuropathy. It helps to support blood circulation, enhance arterial function and healthy blood vessels.
Increases blood circulation and vessel health
Benfotiamine helps to increase the rate of blood flow, especially for those patients suffering from low blood circulation. It is also required for the health of the nervous system and is required for the biosynthesis of a number of cell constituents, including certain neurotransmitters. Just like Vitamin B1, Benfotiamine demonstrated itself as a miracle worker when somebody suffering severely from beriberi got on his feet within hours after being injected with the nutrient. Since then, it has been performing the same "miracle" without fail.Benfotiamine also assists mental health, particularly warding off depression while facilitating memory functions and learning. It's deficiency will no doubt bring back the dreaded beriberi, while minor deficiencies will be manifested in the human body as extreme fatigue, irritability, constipation, edema and an enlarged liver. Forgetfulness, gastrointestinal disturbances, heart changes, irritability, and breathing difficulties are also common symptoms.
Promotes arterial functionBenfotiamine has been proven to improve the structural integrity of the veins and the entire circulatory system. Usually, people with varicose veins have an increased tendency to develop fibrin deposits in the tissue surrounding the affected veins. This causes the skin to become hard and lumpy. There is a decreased ability to break down fibrin, a compound involved in clot formation, thus an increased risk of the formation of a thrombus which may potentially cause life-threatening complications. Benfotiamine nutrient helps to promote fibrin breakdown hence promote the functioning of the arteries while enhancing the flood of blood.
Benfotiamine A Natural Solution Or Miracle Substance To Control Blood Sugar?
February 19, 2008 04:25 PM
The term "miracle" has been in use for hundreds of years when it comes to products that are claimed to aid health. Does this mean that it's always false? Not necessarily. Occasionally a seemingly "new" product will enter the spotlight and draw the attention of the public. Often, after a series of tests and trials, these products fade into oblivion because they didn't actually perform in the ways purported. There are exceptions to this rule; as with the supplement Benfotiamine.
Benfotiamine is a natural solution to many problems in the human body. This product is one of nature's best sources of thiamine; or B-1. The FDA has approved this additive as a dietary supplement. Vitamin B-1 is a necessary substance in the body because it maximizes the results of your carbohydrate intake. It also helps with stress, improves your mental health and strengthens your general nervous system.
Benfotiamine is commonly found in trace amounts within such substances as roasted garlic, onions, leeks and shallots. Many years ago, a Japanese pharmaceutical company attempted to bring attention to this substance. Unfortunately, their efforts gained little traction. Recently, a physician produced a published article detailing the benefits of Benfotiamine and since then the product has rapidly gained popularity.
This product has been tested for individuals with conditions pertaining to diabetes, but the full scope of clinical testing does not end there. Benfotiamine has been tested for decades for its effects and capabilities in helping all types of conditions.
For those with diabetes, this substance has been reported to alleviate sciatica as well as improve general cellular and circulation health. Neuropathy is a painful condition encountered by individuals with diabetes. There are several other related conditions that have all responded well to this supplement.
This supplement has helped many with diabetes, but also helps those without it. This supplement has also been reported to have benefits for: nerve health, improved blood pressure, fibromyalgia and has been used in the treatment of Alzheimer's disease. It has been suggested that Benfotiamine contains many anti-aging properties that help the body.
Vitamin B-1 is reported to combat motion sickness. It helps in the treatment of the painful condition known as "shingles," helps lessen post-operative dental pain and even repels biting insects. B-1 is found naturally in many products including whole wheat foods, dairy products, peanuts, oatmeal and rice husks.
Benfotiamine has no known interactions with prescription medications and, in turn, helps replenish the body with thiamine. There are some prescription drugs that will cause a B-1 deficiency if no supplements are taken.
Benfotiamine is lipid-soluble (or fat-soluble) and this quality means the idea of "overdosing" is nearly impossible. It metabolizes quickly and does not build up in the human body. There are certain individuals who require a higher dose to be most effective. Those who love caffeine, who are pregnant, who smoke or drink alcohol may have a B-1 deficiency.
There are many forms of this product, but capsules seem to be the most common outside of the food groups. The effects are noted to take anywhere from two to three weeks to fully develop. If you are interested in starting a regimen of Benfotiamine, or any supplement, consult your physician first.
Benfotiamine raises the blood level of thiamine pyrophosphate (TPP)
August 02, 2005 03:52 PM
Benfotiamine raises the blood level of thiamine pyrophosphate (TPP), the biologically active co-enzyme of thiamine.4
Thiamine and its Co-enzyme, TPP
Thiamine (vitamin B1) plays an essential part in the metabolism of glucose, through actions of it co-enzyme TPP (thiamine pyrophosphate). TPP is formed by the enzymatically-catalyzed addition of two phosphate groups donated by ATP to thiamine. TPP also goes by the name "thiamine diphosphate." In the cytoplasm of the cell, glucose, a 6-carbon sugar, is metabolized to pyruvic acid, which is converted into acetyl-CoA, otherwise known as "active acetate." Acetyl CoA enters the mitochondrion, where it serves as the starting substrate in the Kreb’s cycle (citric acid cycle). The Krebs cycle is the primary source of cellular metabolic energy. TPP, along with other co-enzymes, is essential for the removal of CO2 from pyruvic acid, which in turn is a key step in the conversion of pyruvic acid to acetyl CoA. CO2 removal from pyruvic acid is called "oxidative decarboxylation," and for this reason, TPP was originally referred to as "cocarboxylase." TPP is thus vital to the cell’s energy supply. Benfotiamine helps maintain healthy cells in the presence of blood glucose. Acting as a biochemical "super-thiamin," it does this through several different cellular mechanisms, as discussed below.
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 cell’s 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), as 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 kinease C pathway and the formation of Advanced Glycation End-poducts. As discussed below, Benfotiamine does this by activating transketolase, a key thiamin-dependent enzyme.6 Benfotiamine stimulates tranketolase, a cellular enzyme essential for maintenance of normal glucose metabolic pathways.* Transketolase diverts the excess fructose-6-phosphate and glyceraldehydes-3-phosphate, (formed by the inhibition of GAPDH, as mentioned above), into production of pentose-5-phosphates and erythrose-4-phosphate and away from the damaging pathways. Benfotiamine activates transketolase activity in bovine aortic endothelial cells incubated in glucose.6 To test Benfotiamine’s ability to counteract these metabolic abnormalities caused by elevated blood glucose, studies have been done in diabetic rats. Benfotiamine increases transketolase activity in the retinas of diabetic rats, while concomitantly decreasing hexosamine pathway activity, protein kinase C activity and AGE formation.6
Benfotiamine and Protein glycation Benfotiamine controls formation of Advanced Glycation End-products (AGEs).
AGEs have an affinity for proteins such as collagen, the major structural protein in connective tissue. AGEs are formed through abnormal linkages between proteins and glucose. This occurs via a non-enzymatic glycosylation reaction similar to the "browning reaction" that takes place in stored food.7 At high glucose concentrations, glucose attaches to lysine, forming a Schiff base, which in turn forms "early glycosylation products." Once blood glucose levels return to normal levels, the amount of these early glycosylation products decreases, and they are not particularly harmful to most tissue proteins. On long-lived proteins such as collagen, however, early glycosylation products are chemically rearranged into the damaging Advanced Glycation End-products. AGE formation on the collagen in coronary arteries causes increased vascular permeability. This vessel "leakiness" allows for abnormal cross-linking between plasma proteins and other proteins in the vessel wall, comprising vascular function and potentially occluding the vessel lumen. A number of other potentially harmful events may also occur, including production of cytokines that further increase vascular permeability. Endothelin-1, a strong vasoconstrictor, is over produced, increasing the possibility of thrombosis and generation of oxygen free radicals is stimulated.8 It is vitally important to support normal glucose metabolic pathways so that formation of AGEs is minimized. Benfotiamine, in the test tube (in vitro) prevents AGE formation in endothelial cells cultured in high glucose by decreasing the glucose metabolites that produce AGEs.9 Endothelial cells make up the membranes that line the inner walls of organs and blood vessels. In a rat study comparing the effects of Benfotiamine with water-soluble thiamin, Benfotiamine inhibited AGE formation in diabetic rats while completely preventing formation of "glycooxidation products," which are toxic by products of chronic elevated blood glucose. AGE levels were not significantly altered by thiamin.10 Benfotiamine also normalized nerve function in the animals. After three months of administration, "nerve conduction velocity (NCV)," a measure of nerve function, was increased by both Benfotiamine and thiamin; at six months, NCV was normalized by Benfotiamine, whereas thiamin produced no further increases in this parameter.
Dysfunctional glucose metabolic pathways leading to AGE formation occurs in endothelial cells of the kidneys. In a recent animal study, Benfotiamine was administered to rats with elevated glucose levels. Benfotiamine increased transketolase activity in the kidney filtration system of these rats, while at the same time shifting triosephophates into the pentose pathway and preventing protein leakage.11
Benfotiamine has an excellent tolerability profile and can be taken for long periods without adverse effects.3,12 The statements in this fact sheet have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
1. Bitsch R, Wolf M, Möller J. Bioavailability assessment of the lipophilic Benfotiamine as compared to a water-soluble thiamin derivative. Ann Nutr Metab 1991;35(2):292-6.
2. Schreeb KH, Freudenthaler S, Vormfelde SV, et al. Comparative bioavailability of two vitamin B1 preparations: Benfotiamine and thiamine mononitrate. Eur J Clin Pharmacol 1997; 52(4):319-20.
3. Loew D. Pharmacokinetics of thiamine derivatives especially of Benfotiamine. Int J Clin Pharmacol Ther 1996;34(2):47-50.
4. Frank T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfontiamine. Eur J Clin Pharmacol. 2000;56(3):251-7.
5. Pike RL, Brown ML. Nutrition, An Integrated Approach, 3rd Ed. New York:MacMillan; 1986:467.
6. Hammes H-P, Du X, Edlestein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic neuropathy. Nat Med 2003;9(3):294-99.
7. Monnier VM, Kohn RR, Cerami A. Accelerated age-related browning of human collagen in diabetes mellitus. Proc Natl Acad Sci 1984;81(2):583-7.
8. Brownlee M. The pathological implications of protein glycation. Clin Invest Med 1995;18(4):275-81.
9. Pomero F, Molinar Min A, La Selva M, et al. Benfotiamine is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol 2001;38(3):135-8.
10. Stracke H, Hammes HP, Werkman D, et al. Efficacy of Benfotiamine versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes 2001;109(6):300-6.
11. Babaei-Jadidi R, Karachalias N, Ahmed N, et al. Prevention of incipient diabetic nephropathy by high-dose thiamine and Benfotiamine. Diabetes 2003;52(8):2110-20.
12. Bergfeld R, MatsumaraT, Du X, Brownlee M. Benfotiamin prevents the consequences of hyperglycemia induced mitochondrial overproduction of reactive oxygen specifies and experimental diabetic neuropathy (Abstract) Diabetologia 2001; 44(Suppl1):A39.