This was first introduced after sacchine was banned in Canada and then in the United States. The subitute was 'a so-called vegetable based sweetner. This was a powdered 'sweetner with different flavors.  But this didn't catch on very well until the manufactures found a method of adding an ingedient that allowed it to be carbonated. The first trial marketing was done in Phoenix, Arizona where the temperatures were excedingly hot. Then it was promoted via firms with a lot of employees and prodessional staff.

        Then this targeted the Amerind tribes such as the Navaho, the Zuni, the Publo and the others that lived in the "Four Points" area.  The name given to this sweetner was very misleading. The soft drink industry promoted it as the 'so-called-sweetner was much less expensive than suger so all the manufactures of 'diet drinks endosed it as for persons with diabetes this seemed very safe!

        (The the essential scan that is rerely done is to use gas chromatography, to locate traces of formaldehyde in the patients blood. If it is alowed to increase it may lead to seizures (often sunlight may trigger them), or even a sudden stress can act as a trigger! SO, STOP DRINKING DIET DRINKS! Recovery is difficult as it is very addictive!)

        Because only about 30 to 35% of people are affected by Aspartame, it is not considered a health risk. Even the Heart and Stroke Foundation Endorses it. However web-sites dealing with PKU were professionaly blocked or hacked. The feeling was that only the manufactures of "Diet-Drinks" had the motivation and rge funding to accomplish this. Then an English web-site began to publish things relating to PKU, as they were very difficult to block - after this, Canadian web-sites followed on.

        In 2002 a friend at MIT, who was part of the survey at MIT, sent me an e-mail warning me about the bad side efects.  He  stated that  the problem is that Aspartame containes some methyl achohol which has a very loose bond that can be easily be broken by heat. It can lead to cataract development. As I had developed cataracts I stopped drinking diet drinks. The recovery was pure hell.  I began to visit MacDonalds every morning and eating two "Breakfast burrito's" with a large coffee with milk and sugar." I am not diabetic nor does it run in my family." Stopping it was pure hell, I had to walk two laps around the Shopping Plaza attempting to ignore the severe pain.

   Symptoms of Aspartame Toxicity:

        It begins gradually with a feeling of nervousness and/or mild headaches. Often it seems to add a craving for carbohydrates as these increase the serotonin level and calm the person. The Aspirin seems to work as the first ‘cure’. A gradual increase in weight takes place because of eating more ‘comfort foods’. However, the increase in level of serotonin is only transitory, leaving to an increased hunger for carbohydrates. The consequence is a sequence of eating more, and inevitable gain in weight. Once more Aspirin seems the obvious solution and hemorrhoids can follow, as well as an increase in the permeability of the intestine. E-pylori infection might follow making the possibility of food born bacteria causing sickness and/or vomiting. A case of gastric reflux seems inevitable.

        What is cause of Aspartame toxicity? The molecular bond in the methyl molecule is very weak. When it is heated, the amount of methyl alcohol that is released is staggering. I have to ask, why is it being shipped in trucks? There, the inside temperature is well above the point of the severe weakning of the bond.

        One of causes for cataracts may be the ineviable toxic accumulation of methyl alcohol. But because some people drink enough grain alcohol, this may dilute the side effects of the methyl alcohol!

        Remember that Aspartame is classed as an ‘excitotoxin’ the same as MSG. When they act in conjunction, the effects are synergistic!

        To continue, because the increase in serotonin ceases, Prozac or some other an anti-depressant is given. But, the relief does not last and the scrip for the medication is increased. To get another 'scrip' another doctor may get involed; then it might be switched once again. Often the person may accumulate several of these and overdose themselves! However, so long as they seem normal some Doctors do not have any clue. that the patient is overdosing themselves.

        Now the over eating leads to another problem as it leads to an addiction.Then the excess behavor increases, leading to buying sprees. These might be hoarding of food, clothes, knick-knacks, costume jewelry or shoes. Because of the weight gain, several sizes will accumulate. If extra space is available such as a spare bedroom, all the extra accumulation of stuff will be ‘stashed’ out of sight.

        The person might contact what normally be a mild case of food poisoning, but the throat damage from the acid reflux might be so severe that swallowing might be impossible. Whatever anti-depressants that were part of the subjects daily life cannot be swallowed. De-hydration follows with kidney failure and jaundice. The yellow tinge of the skin is the consequence. The sudden withdrawal of the anti-depressants is so severe that heart failure can happen.

        The Symptoms of Aspartame Toxicity, are encountered so rarely that a Doctors mis-diagnosis is common.

         Aspartame affects the hypothalamus; in this case, the blood-brain barrier is circumvented. Unfortunately the hypothalamus is so important in controlling the endocrine system that it has to do with thyroid function, adrenal gland function, reproductive function, growth, so that it is a critical factor in health. The consequences can be serious. Aspartic acid in NeutraSweet can alter the function of these chemicals in the hypothalamus and it affects the heart muscle and may lead to sudden cardiac death or, at least, seizures. It may decrease the level of glucose in the brain and bring on chronic fatigue syndrome.

         What follows seems inevitable. The person may be judged on the basis of the symptoms they present rather than the persons character.

A simple visual test might be:

   1) Obesity.
   2) Carrying a bottle of a diet drink or the constant need to have a diet drink on hand.

    Non visual, is addiction to snacks with MSG.

Warning: Avoid Aspartame as the Mayo Clinic cautions patients that it might increase the SED rate and may cause some people to exhibit the symptoms of Myasthenia Gravis, MS or Lupus.


    The latter paper is very important as it is a perfect example of how money can cause total disregard of the aberrant side effects that excitetoxins can have on people!

    Both MSG and Aspartame are classed as excitetoxins and may cross the blood brain
barrier, in times of stress.

    The final intent is to not only normalize the T-cells, reduce the SLE cell count, normalize the Sed Rate and stabilize the homocystene level as much as possible. Hyper-homocystene may be linked to Alzheimer's.

Treating PKU:

    By neurosurgeon Russel Blaylock M. D. (c) 2003

        The most important starting point of any detoxification program is to avoid any exposure to toxin or toxins. This means avoiding even small amounts, especially since once sensitized to the toxin even minute amounts can produce full-blown toxicity. This is especially so with accumulative toxins, such as aspartame. It shown conclusively that the metabolic products of methanol breakdown, formaldehyde in particular accumate on the DNA and cellular proteins. Once you have cleansed your diet of the toxin and it's metabolic products from your system will begin.

        Central to this process is the body's detoxification system, which exists in all the cells of the body with the bulk of detoxification taking place in the liver. The detoxification process is divided into two components called Phase I and Phase II, which work in tandem. Toxins pass through Phase I and then into Phase II where they are further detoxified and made water-soluble for eventual disposal. It is now known that you can significantly enhance the body's ability to detoxify these substances though judicial use of specific supplements. Of the two systems phase II is most important and most often impaired.

The following is a list of nutrients that enhance detoxification:

In addition to detoxification, other nutrients play a more direct role in protecting cells and in promoting their recovery from toxicity. These include: W-W Suggests adding three 200mg extracts of wild blueberry daily. In addition use cinnamon (acts as a catalyst for the production and regulation of insulin in the body. The addition Ginger to food preparation exerts a calming effect against stress. There are many gluten reduced foods available as well as lowered sodium level foods. Avoid soft drinks that are high in sugar and caffine - in the morning have coffee high in calcium. At night a small abount of dark chocolate is OK.



                    This document found on

            Benfotiamine (S-benzyolthiamine-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).2 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.3


            Serving Size  1 capsule
            Servings per container 120 servings
            Amount per serving % Daily Value not established
            Benfotiamine  150 mg
            Other ingredients: modified cellulose, (vegetarian capsule), cellulose, silicon
            Suggested Adult Use: One capsule daily with or without food.


            Benfotiamine raises the blood level of thiamine pyrophosphate (TPP), the
            biologically active co-enzyme of Thiamine.4 Thiamine and its
            Co-enzyme,TPPThiamine (vitamin B1) plays an essential part in the
            metabolism of glucose, through actions of its 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

            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 cycle (citric acid cycle). The Krebs cycle is the primary
            source of cellular metabolic energy.


            Suggested Adult Use: Take two capsules daily.

            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.

       Scientific References:

            1. Bitsch R, Wolf M, M?ller 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

            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

            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.

        Some possible side effects of PKU may be linked to blood flow 'stasis' in rhe small vesseles caused by the presence of  formaldehyde. As this is cumulative, a steady deterioration can take place over several years od exposure. Gradually, a steady partial paralyses will occour. The fine blood vessels in the fingers of dominant hand will be involved. Unfortunately this process can take place over several years; so most doctors won't be able to diagnose the cause until the damage is irrevocable.

        Another much more serious side effect is the creation of irritated areas on the scalp caused by the release of formaldehyde. That is the reason many hair treatments have been been banned because of the toxic side effects. Formaldehyde can damage nerves in the fingers. Often it's mistaken for severe cases of carpal tunnel syndrome.  But this is a very seious case of mis-diagnosis. Other essentoals such as the pitutary gland may be involved. Again common side effects seem to be mis-classified.

        Another side effect is stress related, it affects the vagus nerve, (fight or flight), and often mimics asthma. It can result in severe difficulty in respoding to prolongation of excess stress.

        I have seen other people with PKU mis- classified as PKU is now the name applied only to infants.  This might be intentional as the best way to cover somthing up is to rename it.

        It seems ironic that the thousands trailers that were ordered by FEMA to provide temperary housing for the New Orleans Flood victims couldn't be used because they had high levels of formaldehyde in the drywall.

        Some were eventually sold. However the children and some of the parents complaied about eye irritation and conjunctivitis, and other illnesses. Now, FEMA is attempting to buy them back at the full list price (as compensation for the 'strange maladies' suffered by the people who lived in them).

        Rumsfield sold the patents on aspartaime to Monsanto and made millions of dollars. He is blaming the effects on 'depleated uranium' that was used by both sides in the Gulf War.

Background of author During the last thirty-five years, William M. D. Wright has done extensive company-funded and/or classified research in several fields. These included perception, parallel-thought, hyperbaric diving (including saturation diving), hypoxia, hypothermia, isolation, visual and hearing problems, stereo perception, enzyme reactions under high pressure, and other associated fields.




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