Best Benfotiamine 150mg vitamins and Herbs.

Best Benfotiamine 150mg

Best Benfotiamine
120 Veggie Caps

Each capsule 
contains:

Benfotiamine..........80mg

Excipients: modified 
cellulose (veggie cap),
cellulose, silicon dioxide

Suggested 
Adult Use: Take two capsules daily.

120 Veggie Caps

Each 
capsule contains:

Benfotiamine..........150mg

Excipients: 
modified cellulose (veggie cap),
cellulose, silicon 
dioxide



Benefits

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), 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.6 

 

Benfotiamine
stimulates transketolase, a cellular enzyme essential for maintenance of normal
glucose metabolic pathways.*



Transketolase
diverts the excess fructose-6-phosphate and glyceraldehyde-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,
compromising 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

 

Safety

Suggested Adult Use: One capsule daily, with
or without food.

 

Benfotiamine has an
excellent tolerability profile and can be taken for long periods without
adverse effects.3,12

 

Scientific References

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 species and experimental diabetic neuropathy (Abstract) Diabetologia
2001; 44(Suppl1):A39.

 


     
		  

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The Best Benfotiamine 150mg Sale Price: $17.09 - Vitamins or Herbs Should be taken as directed on the bottle.