The problem is that it containes some methyl achohol which has a very loose bond that can be easily be broken by heat. It can lead to cataract development.
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!
Symptoms of Aspartame Toxicity:
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.
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 transitory leaving to an increase 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 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. Why is it being shipped in trucks were the inside temperature is well above the point of the severe weakling of the bond. One of causes for cataracts may be the toxic accumulation of methyl alcohol.
Aspartame is classed as an ‘excitotoxin’ the same as MSG. When they act in conjunction, they are synergistic!
To go on, 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 switched. It might be switched once again. Often the person may accumulate several of these and overdose themselves! However, so long as they seem normal the Doctor does not have any clue.
Over eating leads to another problem. 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 is:
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.
Re: http://www.uklupus.co.uk/aspart/html
Re: http://www.mercola.com/article/aspartame/fraud.htm
Re: http://www.wnho.net/the_ecologist_aspartame_report.htm
Re http://www.angelfire.com/az/sthurston/aspartame.html
Re: http://www.medical-library.net.sites/_aspartame_disease.html
Re: http://www.snopes.com/medical/toxins/aspertame.asp
Re: http:www.lightparty.com/Health/DietCokeAspartame.hmtl
Re: http://www.aspartame.ca/indexa.html
pdf:
http://archive.gao.gov/d4t4/130780.pdf
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.
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:
BENFOTIAMINE
(S-benzyolthiamine-O-monophosphate)
This document found on http://drbvitamins.com/nutritionalproducts_details.asp?id=8
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
Ingredients:
SUPPLEMENT FACTS
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
dioxide.
Suggested Adult Use: One capsule daily with or without food.
CONTAINS NOTHING OTHER THAN LISTED INGREDIENTS
Benefits
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
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 cycle (citric acid cycle). The Krebs cycle is the primary
source of cellular metabolic energy.
Safety:
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
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.
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.
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.