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BENFO-AOR-12b |
Benfotiamine 80 mg x 120 capsules per bottle x 12 bottles (AOR) |
12 bottles |
300.00 |
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peter@vitaspace.comSYNONYMS: Benfotiamin = Benfotiamine = Benfothiamine = S-benzoylthiamine-O-monophosphate
CAS# = 22457-89-2
Benfotiamine is a powerful "late-phase" inhibitor of Advanced Glycation Endproduct (AGE) formation.
120 Vegi-Caps
100% Vegetarian
Each
Capsule Contains
Thiamin (as Benfotiamine 80 mg) ......... 55 mg
Other ingredients: microcrystalline cellulose. Capsule: vegetarian
Suggested
Use
Take two to four vegi-caps daily, preferably with meals, or as directed by a qualified health consultant.
Main
Applications
As reported by literature:
•Aging
•AGE
Inhibitor
•Brain Support
•Thiamin Deficiency
Source
Pharmaceutical Synthesis
Pregnancy
/ Nursing
No studies have been conducted. Best to avoid.
Cautions
None.
ABSTRACTS:
Pharmacokinetics
of thiamine derivatives especially of benfotiamine.
Int
J Clin Pharmacol Ther 1996 Feb; 34(2): 47-50.
Loew
D.
Pharmacokinetic
data of orally administered lipid-soluble thiamine analogues like benfotiamine
are reviewed and assessed. It is quite clear that benfotiamine is absorbed much
more better than water-soluble thiamine salts: maximum plasma levels of thiamine
are about 5 times higher after benfotiamine, the bioavailability is at maximum
about 3.6 times as high as that of thiamine hydrochloride and better than other
lipophilic thiamine derivates. The physiological activity (alphaETK) increased
only after benfotiamine was given. Due to its excellent pharmacokinetic profile
benfotiamine should be preferred in treatment of relevant indications.
A
benfotiamine-vitamin B combination in treatment of diabetic polyneuropathy.
Exp
Clin Endocrinol Diabetes 1996; 104(4): 311-6.
Stracke
H, Lindemann A, Federlin K.
In
a double-blind, randomized, controlled study, the effectiveness of treatment
with a combination of Benfotiamine (an Allithiamine, a lipid-soluble derivative
of vitamin B1 with high bioavailability) plus vitamin B6/B12 on objective
parameters of neuropathy was studied over a period of 12 weeks on 24 diabetic
patients with diabetic polyneuropathy. The results showed a significant
improvement (p = 0.006) of nerve conduction velocity in the peroneal nerve and a
statistical trend toward improvement of the vibration perception threshold.
Long-term observation of 9 patients with verum over a period of 9 months support
the results. Therapy-specific adverse effects were not seen. The results of this
double-blind investigation, of the long-term observation and of the reports in
the literature support the contention that the neurotropic benfotiamine-vitamin
B combination represents a starting point in the treatment of diabetic
polyneuropathy.
Benfotiamin
inhibits intracellular formation of advanced Glycation endproducts in vivo.
Diabetes. 2000 May; 49(Suppl1): A143(P583).
Lin J, Alt A, Liersch J, Bretzel RG, Brownlee MA, Hammes HP.
We have demonstrated previously that intracellular formation of the advanced
glycation end product (AGE) N-[Epsilon]-(carboxymethyl)lysine (CML) inversely
correlates with diabetic vascular complications independently from glycemia (Diabetologia
42, 603, 1999). Here, we studied the effect of benfotiamine, a
lipid-soluble thiamine derivative with known AGE-inhibiting properties in-vitro
on the intracellular formation of (CML) and methylglyoxal-derived AGE in red
blood cells. Blood was collected from 6 Type 1 diabetic patients (2m, 4f, age
31.8 ± 5.5 years; diabetes duration 15.3 ± 7.0 years) before and after
treatment with 600 mg/day benfotiamine for 28 days. In addition to HbA1c (HPLC),
CML and methylglyoxal were measured using specific antibodies and a quantitative
blot technique. While treatment with benfotiamine did not affect HbA1c levels
(at entry: 7.18 ± 0.86%; at conclusion 6.88 ± 0.88%; p not significant),
levels of CML decreased by 40% (737 ± 51 arbitrary units/mg protein (AU) vs 470
± 86 AU; p<0.01). The levels of intracellular methylglyoxal were reduced by
almost 70% (1628 ± AU vs 500 ± 343 AU; p<0.01). The data indicate that
thiamine derivatives are effective inhibitors of both intracellular
glycoxidation and AGE formation.
Benfotiamine
blocks three major pathways of hyperglycemic damage and prevents experimental
diabetic retinopathy.
Nat
Med 2003 Mar; 9(3): 294-9.
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.
Three
of the major biochemical pathways implicated in the pathogenesis of
hyperglycemia induced vascular damage (the hexosamine pathway, the advanced
glycation end product (AGE) formation pathway and the diacylglycerol (DAG)-protein
kinase C (PKC) pathway) are activated by increased availability of the
glycolytic metabolites glyceraldehyde-3-phosphate and fructose-6-phosphate. We
have discovered that the lipid-soluble thiamine derivative benfotiamine can
inhibit these three pathways, as well as hyperglycemia-associated NF-kappaB
activation, by activating the pentose phosphate pathway enzyme transketolase,
which converts glyceraldehyde-3-phosphate and fructose-6-phosphate into
pentose-5-phosphates and other sugars. In retinas of diabetic animals,
benfotiamine treatment inhibited these three pathways and NF-kappaB activation
by activating transketolase, and also prevented experimental diabetic
retinopathy. The ability of benfotiamine to inhibit three major pathways
simultaneously might be clinically useful in preventing the development and
progression of diabetic complications.
Effectiveness
of different benfotiamine dosage regimens in the treatment of painful diabetic
neuropathy.
Arzneimittelforschung
1999 Mar; 49(3): 220-4.
Winkler
G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P.
The
therapeutic effectiveness of a benfotiamine (CAS 22457-89-2)-vitamin B
combination (Milgamma-N), administered in high (4 x 2 capsules/day, = 320 mg
benfotiamine/day) and medium doses (3 x 1 capsules/day), was compared to a
monotherapy with benfotiamine (Benfogamma) (3 x 1 tablets/day, = 150 mg
benfotiamine/day) in diabetic patients suffering from painful peripheral
diabetic neuropathy. In a 6-week open clinical trial, 36 patients (aged 40
to 70 yrs) having acceptable metabolic control (HbA1c < 8.0%) were randomly
assigned to three groups, each of them comprising 12 participants. Neuropathy
was assessed by five parameters: the pain sensation (evaluated by a modified
analogue visual scale), the vibration sensation (measured with a tuning fork
using the Riedel-Seyfert method) and the current perception threshold (CPT)
onthe peroneal nerve at 3 frequencies: 5, 250 and 2000 Hz). Parameters were
registered at the beginning of the study and at the end of the 3rd and 6th week
of therapy. An overall bneneficial therapeutic effect on the neuropathy status
was observed in all three groups during the study, and a significant improvement
in most of the parameters studied appeared already at the 3rd week of therapy (p
< 0.01). The greatest change occurred in the group of patients receiving the
high dose of benfotiamine (p < 0.01 and 0.05, resp., compared to the othr
groups). Metabolic control did not change over the study. It is concluded that
benfotiamine is most effective in large doses, although even in smaller daily
dosages, either in combination or in monotherapy, it is effective.
Prevention
of cardiac autonomic neuropathy in dogs with Benfotiamin.
Koltai MZ.
In Gries FA, Federlin K. Benfotiamin in the Therapy of Polyneuropathy.
New York: Georg Thieme Verlag, 1998; 45-9.
Experimentally-induced diabetes of the dog leads to
disturbances in the autonomous neurological function of the heart after
approximately 3 months of continuously- observed diabetes. As signs of autonomic
cardiac neuropathy, the heart rate variability and Valsalva ratio clearly fell
in the untreated diabetic animals. Oral benfotiamin, administered from the sixth
day after diabetes-induction, prevented or at least delayed these changes.
According to the results, treatment with fat-soluble benfotiamin can play an
important role in the therapy and prevention of cardiac autonomic neuropathy,
apart from any effect on diabetic metabolic disturbances.
PRODUCT SUMMARY FROM THE SUPPLIER (AOR):
Benfotiamine and the "Caramelization of the Flesh"
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.
Glycation
math is simple: more sugar equals more AGEd 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.
Make
that: AGEing you.
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 that are thus
the most vulnerable to the complications of diabetes.
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 and appears to have been abandoned
by its developers. On the other hand, some companies are selling supplements
marketed as “AGE-inhibitors.” But while many of these herbs and other
nutrients may be valuable, and may even inhibit AGEing in a test tube,
there’s no evidence that most of these
“AGE-blocking” ingredients have any effect on AGEing in your body
at the dosages used. Examples include thyme
extract, inositol, acetyl-L-carnitine,
and a whole host of antioxidants (including
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!
Benfotiamine:
the TPP Solution
Fortunately,
an effective way to boost thiamin
pyrophosphate in your cells does exist: Benfotiamine
(S-benzoylthiamine-O-monophosphate).
Benfotiamine is the most potent of the allithiamines,
a 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).
Benfotiamine’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 Benfotiamine
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 Benfotiamine
is even more bioavailable than the other allithiamines,
including thiamin tetrahydrofurfuryl
disulfide/TTFD. Yet Benfotiamine
is actually less toxic than
conventional thiamin supplements!
By
effectively increasing levels of thiamin itself, Benfotiamine
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, Benfotiamine
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 Benfotiamine
powerfully supports nerve function in diabetic neuropathy. In one trial, 24
people suffering with diabetic neuropathy took either Benfotiamine
(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 Benfotiamine
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
(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 Benfotiamine 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 nerve
conduction 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 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 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 when the 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 rodents against 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.
LINKS TO ADDITIONAL BENFOTIAMIN ARTICLES:
Click on the links to read the abstracts or full articles.
http://www.aecom.yu.edu/home/news/benfotiamine.htm
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9791922&dopt=Abstract
http://www.easd.org/37th/Abs01/148.html