Diabeticine, Diabecon, and Benfotiamine :: was: article on vitamin C...

[Guest guest]

Diabeticine is for diabetics. Helps control blood glucose levels w/o

alopathic drugs. Helps re-vitalize the pancreas. See here:

http://www.techmedica.com/diabeticine.html

 

Diabecon is similar. I am not sure which is better, so I take both

these days. See list of research papers here:

http://www.himalayahealthcare.com/researchpaper/diabecon.htm

 

 

Benfotiamine is a lipid soluble form of Thiamin (vitamin B1).

Regular thiamin can cause problems if taken in large quantity.

Benfotiamine gets into cells better & can be taken in much larger

doses.

 

Good to help prevent diabetic retinapathy. See here:

http://www.diabetesireland.ie/view.asp?ID=1000

 

Below is the full text of a great website on Benfotiamine. URL at

end. For hotlinks, use the website URL.

 

Alobar

 

 

Courtesy of Advanced Orthomolecular Research

Advanced Glycation End Products

 

 

Advanced Glycation End products, 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 AGE'd 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. This is also partially why low

carbohydrate diets work well for some people and those with

neurological problems such as autism, Alzheimer's, and even heavy

metal toxicity.

 

Two Ways to AGE Back To Top

 

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 are thus the most

vulnerable to the complications of diabetes and other functional

disorders.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

so therefore appears to have been abandoned by its developers. On the

other hand, some companies are selling supplements are marketed as

" AGE-inhibitors. " But while many of the herbs and other nutrients may

be valuable, and many 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, taurine, and a whole host of

antioxidants (including n-acetyl-cysteine (NAC) and flavonoids, such

as quercetin and resveratrol).

 

TPP: Our Hero … in Chains! Back To Top

 

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 Back To Top

 

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, an 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 Back To Top

 

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 (VPT)

(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 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 Back To Top

 

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.

 

Benfotiamine and Heavy Metal Toxicity Back To Top

 

Very recent studies have suggested that vitamin B1 had increased the

effectiveness of chelators such as DMSA to reduce liver and kidney

lead and other heavy metal loads. In particular the most effective

form was benfotiamine.

 

Dentally, thiamin has been shown to help health conditions such as

Bell's Palsy, Tic Douloureux, decreases dental caries, fractures (that

would include any of the body), herpes simplex and herpes zoster

(shingles), hypersensitive teeth, postoperative pain, dry socket, TMJ

pain, etc. Ongoing research is looking at its role in Alzheimer's

Disease, autism, neurtransmitter balancing, brain disorders, multiple

sclerosis.

 

In a paper written by Frances Jurmak, professor of biochemistry, she

shows the relationship between low B1/Magnesium and ADHD, nausea and

Tourette's syndrome..all of which her son suffered from until she

started supplementing him. Within 30 hours his mood greatly improved,

the nausea and all tics vanished.

 

The End of an AGE Back To Top

 

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.

 

 

Click on the link below to view other clinical research studies

concerning Benfotiamine at PubMed. PubMed was developed by the

National Center for Biotechnology Information (NCBI) at the National

Library of Medicine (NLM) and is located at the National Institutes of

Health (NIH).

 

 

PubMed

 

ABC News.com

 

 

Selected References Back To Top

 

Loew D. Pharmacokinetics of thiamine derivatives especially of

benfotiamine. Int J Clin Pharmacol Ther. 1996 Feb;34(2):47-50.

 

Stracke H, Lindemann A, Federlin K. A Benfotiamine-vitamin B

combination in treatment of diabetic polyneuropathy. Exp Clin

Endocrinol Diabetes. 1996;104(4):311-6

 

Lin J, Alt A, Liersch J, Bretzel RG, Brownlee MA, Hammes HP.

Benfotiamine inhibits intracellular formation of advanced glycation

endproducts in vivo. Diabetes. 2000 May;49(Suppl1):A143(P583).

 

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. Benfotiamine blocks three major pathways of hyperglycemic

damage and prevents experimental diabetic retinopathy. Nat Med. 2003

Feb 18 [epub ahead of print]; doi:10.1038/nm834.

 

Winkler G, Pal B, Nagybeganyi E, Ory I, Porochnavec M, Kempler P.

Effectiveness of different Benfotiamine dosage regimens in the

treatment of painful diabetic neuropathy. Arzneimittelforschung. 1999

Mar; 49(3): 220-4.

 

Koltai MZ. Prevention of cardiac autonomic neuropathy in dogs with

Benfotiamine. In Gries FA

 

Langlais PJ, McRee RC, Nalwalk JA, Hough LB Depletion of brain

histamine produces regionally selective protection against thiamine

deficiency-induced lesions in the rat. Metab Brain Dis 2002

Sep;17(3):199-210

 

Dhawan M, Kachru DN, Tandon SK. Influence of thiamine and ascorbic

acid supplementation on the antidotal efficacy of thiol chelators in

experimental lead intoxication, Arch Toxicol 1988;62(4):301-4

 

Ito Y, Niiya Y, Otani M, Shima S. Effect of thiamine on the excretion

of subcutaneously injected lead in rats. Toxicol Lett 1987

Aug;37(3):221-8

 

Tandon SK, Prasad S, Effect of thiamine on the cadmium-chelating

capacity of thiol compounds, Hum Exp Toxicol 2000 Sep;19(9):523-8

 

L. Pantoni, L. Poggesi, A. Repice and D. Inzitari. " Disappearance of

motor tics after Wernicke's encephalopathy in a patient with

Tourette's syndrome. " Neurology, 48:381-383 (1997).A. Brenner. " The

effects of megadoses of selected B complex vitamins on children with

hyperkinesis: controlled studies with long-term follow-up. " Journal of

Learning Disabilities, 15(5):258-264 (1982).

 

L. Reinken, H. Stolley and W. Droese. " Biochemical assessment of

thiamine nutrition in childhood. " European Journal of Pediatrics,

131:229-235 (1979) A.B. Mukherjee, S. Svoronos, A. Ghazanfari, P.R.

Martin, A. Fisher, B. Roecklein, D. Rodbard, R. Staton, D. Behar, C.J.

Berg and R. Manjunath. " Transketolase abnormality in clutured

fibrobnlasts from familial chronic alcoholic men and their male

offspring. " The Journal of Clinical Investigation, 79:1039-1043 (1987)

 

J.P. Blass and G.E. Gibson. " Abnormality of a thiamine-requiring

enzyme in patients with Wernicke-Korsakoff syndrome " . The New England

Journal of Medicine, 297:1367-1370 (1977).

 

R.L. Hoffman. " The natural approach to attention deficit disorder:

drug-free ways to treat the roots of this childhood epidemic. " Good

Health Guide published by Keats Publishing, Inc., New Canaan,

Connecticut, 1997

 

 

http://www.emuhealthproducts.com/advancedglycation.html

 

On 9/21/05, Dave R Hermanson <tumblweed4 wrote:

>

> Could you please tell me(us) what diabeticine and benfotiamine are??

> I'd like to know...

>