BAN ASPARTAME - It Causes Rumsfeld Syndrome

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High levels of glycated and lipoxidated proteins and peptides in the body are repeatedly associated with chronic diseases. These molecules are strongly associated with activation of a specific receptor called RAGE and a long-lasting exaggerated level of inflammation in the body. RAGE, a member of the immunoglobulin superfamily of cell surface molecules and receptor for advanced glycation end products (AGE), known since 1992, functions as a master switch, induces sustained activation of nuclear factor kappaB (NFkappaB), suppresses a series of endogenous autoregulatory functions, and converts long-lasting proinflammatory signals into sustained cellular dysfunction and disease. Its activation is associated with high levels of dysfunctioning proteins in body fluids and tissues, and is strongly associated with a series of diseases from allergy and Alzheimer's to rheumatoid arthritis and urogenital disorders. (Stig B, Hajdù N, Endproducts and receptors of advanced glycation and lipoxidation (AGE, ALE, RAGE) and chronic diseases from the perspective of food and nutrition, Orv Hetil. 2008 Apr 27;149(17):771-8. Pubmed: University College, London Medical School Institute of Hepatology, London, United Kingdom). (see references below*).

Free amino groups of proteins react slowly with reducing sugars such as glucose by the glycation or Maillard reaction to form poorly characterized brown fluorescent compounds). This process is initiated by the condensation reaction of reducing sugars with free amino groups to form Schiff bases, which undergo rearrangement to form the relatively stable Amadori products). The Amadori products subsequently degrade into α-dicarbonyl compounds, deoxyglucosones). These compounds are more reactive than the parent sugars with respect to their ability to react with amino groups of proteins to form cross-links, stable end products called advanced Maillard products or advanced glycation end products (AGEs). AGEs are irreversibly formed and found to accumulate with aging, atherosclerosis, and diabetes mellitus, especially associated with long-lived proteins such as collagens, lens crystallines, and nerve proteins. It was suggested that the formation of AGEs not only modifies protein properties, but also induces biological damage in vivo). For example, AGEs deposited in the arterial wall could themselves generate free radicals capable of oxidizing vascular wall lipids and accelerate atherogenesis in hyperglycemic diabetic patients (ref: Expand+Hyung-Soon Yim et al, Free Radicals Generated during the Glycation Reaction of Amino Acids by Methylglyoxal, A MODEL STUDY OF PROTEIN-CROSS-LINKED FREE RADICALS, Journal of Biological Chemistry, 270, 28228-28233).

Glycation reactions between glucose and proteins in the bloodstream are produced under oxidative stress - ie in the presence of excess free radicals (Loske C, Neumann A, Cunningham AM, et al. Cytotoxicity of advanced glycation end products is mediated by oxidative stress. J Neural Transm., 1998; 105:1005-1015). Many if not most of the signs and symptoms of aging, as well as age-associated diseases, are identical to manifestations seen in hormone deficiencies and in premature aging, which is strongly associated with multiple hormone deficiencies. Most consequences of aging such as excessive free radical formation, imbalanced apoptosis system, tissue accumulation of waste products, and failure of repair systems, deficient immune system, poor gene polymorphisms, and premature telomere shortening are also associated, if not caused, by hormone deficiencies (Hertoghe T. The "multiple hormone deficiency" theory of aging: is human senescence caused mainly by multiple hormone deficiencies? Ann N Y Acad Sci. 2005; 1057:448-465). Up-regulation of putative pathologic pathways, accumulation of AGEs, activation of the renin-angiotensin system, oxidative stress, and increased expression of growth factors and cytokines are all associated with aging and some information is beginning to appear on the association and possible role of AGE in cysts syndromes (Diamanti-Kandarakis E, Piperi C, Kalofoutis A, Creatsas G. Increased levels of serum advanced glycation end-products in women with polycystic ovary syndrome. Clin Endocrinol. 2005; 62:37-43) especially in women with micro-parasite infection associated with vitamin B12 deficiencies.

An avoidance of foods rich in deranged proteins (or shock proteins produced by high heat cooking as in [microwaved foods and] mamak restaurants) and peptides, and the consumption of natural antioxidants, especially polyphenols, seem to counteract such a development (Journal of Parenteral and Enteral Nutrition 31:430-440, 2007) while a diet low in glycotoxins can markedly reduce advanced glycated end-products (AGE products) (Uribarri J, Peppa M, Cai W, et al. Restriction of dietary glycotoxins markedly reduces AGE toxins in renal failure patients. J Am Soc Nephrol. 2003; 14:728-731) that may lower health risks dramatically. It also points to the need to eliminate AGE products in patients with chronic disease to promote recovery or rejuvenation or achieve anti-aging results in aesthetics.

Nonenzymatic glycation, i.e. binding of monosaccharides to amino groups of proteins, gives rise to complex components called "advanced glycation end-products" (AGEs), which alter protein structure and functions, and participate in diabetic long-term complications. Glycation and oxidative stress are closely linked, and are often referred to as "glycoxidation" processes. Experimental data support these interactions.

Considering the key points as follows:

a) All glycation steps generate oxygen free radicals, some of these steps being common with those of lipid peroxidation.

b) AGEs bind to membrane receptors such as RAGE, and induce an oxidative stress and a pro-inflammatory status.

c) Glycated proteins modulate cellular oxidative functions: glycated collagens induce an inappropriate oxidative response in PMNs.

d) Products of lipid peroxidation (MDA) bind to proteins and amplify glycoxidation-induced damages.

Glycoxydation intensity increases in diabetes mellitus, ageing, renal failure and other pathological states with oxidative stress, (ref: Gillery P., Advanced glycation end products (AGEs), free radicals and diabetes, J Soc Biol. 2001;195(4):387-90 Pubmed:PMID: 11938555), all therapies aiming at limiting glycoxidation take into account its oxidative part but unfortunately drugs do not limit but rather increase free radicals that promote glycation reactions and can lead to the formation of more glycated proteins and AGE.

It has been almost 100 years since Malliard (Maillard LC. Action des acids amine sur des sucres: formation des melanoides per voie methodique. C R Acad Sci. 1912; 154: 66-68) described the nonenzymatic pathway for glycation of proteins and suggested that such chemically modified proteins could play a role in the pathogenesis of chronic diseases, particularly diabetes. However, it is only during the last 2 decades, and especially the last 5 years, that this concept has received wider attention among scientists. Still, most practicing physicians and nutrition experts are still unaware of the concept and its eventual implications on health (Bengmark Stig, Advanced Glycation and Lipoxidation End Products - Amplifiers of Inflammation: The Role of Food #105, 15 September 2007, RedOrbit}. Excess free radicals tend to rob electrons from molecules in the body and lead to establishment of inflammations at the cellular level that affect the integrity of cell membranes and affect optimal cell function and accordingly are one of the root causes for the development of chronic conditions. The progression of inflammations in cells and tissues leads to the development of a host of health problems: the other being toxins from bacteria, viruses and fungus and allergens from micro-parasites such as protozoa, and the production of abnormal proteins through altered biochemical pathways and chemicals that generate free radicals in the body.

The grand jury investigation was led by U.S. Attorney Samuel Skinner. In July 1, 1977, while the investigation was being conducted, Skinner left the Justice Department and took a job with Sidley & Austin - the law firm representing Searle. The statute of limitations eventually ran out and the grand jury disbanded without reaching any conclusions regarding Searle and its lab practices.
 
Donald Rumsfeld became president of G. D. Searle & Company in 1977 and was there until 1985.  In 1985 Monsanto purchased G.D. Searle, who held the patent to aspartame, the active ingredient in NutraSweet. Monsanto was apparently untroubled by aspartame's clouded past, including a 1980 FDA Board of Inquiry, comprised of three independent scientists, which confirmed that it "might induce brain tumors." 

The FDA refused to allow NutraSweet (aspartame) onto the market. It is a deadly neurotoxic drug masquerading as an additive. It interacts with all antidepressants, L-dopa, Coumadin, hormones, insulin, all cardiac medication, and many others leading to possible mental disorders. It also is a chemical hyper sensitization drug so that it interacts with vaccines, other toxins, other unsafe sweeteners like Splenda which has a chlorinated base like DDT and can cause auto immune disease. It has a synergistic and additive effect with MSG.

Both being excitotoxins, the aspartic acid in aspartame, and MSG, the glutamate people were found using aspartame as the placebo for MSG studies, even before it was approved. The FDA has known this for a quarter of a century and done nothing even though it is against the law. Searle went on to build a NutraSweet factory and had $9 million worth of inventory. As one Congress Report points out that the FDA has become cozy with the pharmaceutical industry.

Donald Rumsfeld was on President Reagan's transition team and on January 21, 1981, the day after Ronald Reagan's inauguration, Searle re-applied to the FDA for approval to use aspartame in food sweetener, and Reagan's new FDA commissioner, Arthur Hayes Hull, Jr., appointed a 5-person Scientific Commission to review the board of inquiry's decision.  The FDA set up a Board of Inquiry of the best scientists they had - who said aspartame is not safe and causes brain tumors, and the petition for approval was hereby revoked with a 3-2 decision. The FDA had actually banned aspartame based on this finding, only to have Searle Chairman Donald Rumsfeld (then the Secretary of Defense) vow to "call in his markers," to get it approved - ( http://www.soundandfury.tv/pages.Rumsfeld2.html  ).  The new FDA Commissioner, Arthur Hull Hayes, then installed a sixth member on the commission, and the vote became deadlocked. He then personally broke the tie in aspartame's favor. Hull later left the FDA under allegations of impropriety, served briefly as Provost at New York Medical College, and then took a position with Burson-Marsteller, the chief public relations firm for both Monsanto and GD Searle, rumored at $1000.00 a day, and has refused to talk to the press about this episode ever since.  

Among the many ironies of our modern world is that Gerald Ford awarded the Presidential Medal of Freedom - America's highest civilian honor - to Defense Secretary Donald Rumsfeld on January 19, 1977. Just a few weeks later on March 8, Rumsfeld became the CEO of G.D. Searle to take point on a mission to force the Food and Drug Administration to approve for human consumption a known carcinogen and neurotoxic poison. Mission accomplished: Today some 9,000 commonly consumed products are laced with this weapon of mass misery and millions of people live with chronic illnesses linked to the artificial sweetener aspartame.

At the highest dose level, 25 percent of the female rats developed lymphomas-leukemias compared with just 8.7 percent of the controls. These findings, which raised a firestorm of controversy and denial across the world, were published in the Environmental Health Perspectives in 2006 (Morando Soffritti, Fiorella Belpoggi, Davide Degli Esposti, Luca Lambertini, Eva Tibaldi, Anna Rigano, "First Experimental Demonstration of the Multipotential Carcinogenic Effects of Aspartame Administered in the Feed to Sprague-Dawley Rats," Environmental Health Perspectives March 2006;114(3):379-85) ought to properly raise a health alarm instead because the researchers determined that the threshold for a carcinogenic effect of aspartame was as low as 400 parts per million (ppm), concluding that:

"The results of this mega-experiment indicate that APM [aspartame] is a multipotential carcinogenic agent, even at a daily dose of 20 mg/kg body weight, much less than the current acceptable daily intake".

"It is the belief at The Idaho Observer that if some guy named Parkinson can have a disease named after him, then, Donald Rumsfeld ought to have his own disease, too. Hence, the term - Rumsfeld disease A., or The Rumsfeld Syndrome. I truly believe that we have the finest government oversight that money can buy....," but indeed "oversight" is a rather mild term - it is a health crime against HUMANITY supported by the health authorities that refuse to consider and act on the information provided by research on synthetic chemicals like aspartame.

And it adds to healthcare costs. A Danish study published in June, which included more than 59,000 Danish women, found that daily intake of artificially sweetened soft drinks may increase the risk of preterm delivery by as much as 78 percent (Halldorsson TI, Strøm M, Petersen SB, Olsen SF., "Intake of artificially sweetened soft drinks and risk of preterm delivery: a prospective cohort study of 59,334 Danish pregnant women", American Journal of Clinical Nutrition June 30, 2010 [Epub ahead of print]). According to a recent article in the British MailOnline, some British public health experts are now advising pregnant women to avoid aspartame-containing foods and beverages to protect their unborn child, as preterm delivery exposes the baby to a number of health risks - and staggering health care costs.

Besides, large doses of phenylalanine can lower important neurotransmitters like serotonin in the brain (H. L. Wang, V. H. Harwalkar and H. A. Waisman, "Effect of dietary phenylalanine and tryptophan on brain serotonin", Archives of Biochemistry and Biophysics April 1962; 97(1): 181-184), which induces numbness as it interferes with nerve protein formation and is also associated with a host of problems involving brain function, memory loss, depression, and development of tumors in the brain, including influences on satiety.

Decreased serotonin levels reduce feelings of satiety, which can then lead to over-eating or binge eating and has the potential towards obesity. Naturally, this finding supports a 2004 study at Purdue University, which found that rats fed artificially sweetened liquids ate more high-calorie food than rats fed high-caloric sweetened liquids (Davidson TL, Swithers SE., "A Pavlovian approach to the problem of obesity", Int J Obes Relat Metab Disord. July 2004;28(7):933-5) and that meant that more aspartame leads to more craving for high calorie foods and higher potential for weight gain (UT Health Center San Antonio Press Release, "New analysis suggests 'diet soda paradox' - less sugar, more weight", June 14, 2005 · Volume: XXXVIII · Issue: 24). Unfortunately, obese people tend to have relatively higher population of free radicals and that leads to a higher risk for the development of disease conditions in them. Large doses of aspartame can therefore trigger a vicious cycle leading to health problems and loss of productivity. Hence, excess aspartame consumption has a bearing on the national economy as well as on personal finances and insurance. But who cares? Doctors are recommending aspartame to diabetics!

If aspartame had been created and introduced by people in alternative medicine - same for the bogus test kits currently used by medical doctors to diagnose and treat HIV-AIDS, as the law does not allow for their use as such going by the disclaimers on these test kits and the fact that they test for a protein polymer fragment "whose significance is not known" - the health authorities would have come down on them with a slam hammer like a ton of bricks and played up the media against their consumption or use and might have branded them as a "bunch of jokers". Obviously that did not happen but on the contrary there is support for that kind of voodoo science.

"For the monitoring of diabetes mellitus, the concentration of serum glycated proteins is currently measured by a colorimetric reaction using the dye nitroblue tetrazolium. As this reduction may depend on superoxide ions (O2-), we checked whether glycated proteins were capable of generating O2- in vitro. We incubated ferricytochrome c with glucose, fructose, 1-deoxy-1-morpholino-D-fructose (an analog of the 1-desoxy-1-amino-fructose radical found in glycated proteins) and glycated proteins prepared from diabetic blood serum. We found that these substances, except free glucose, were all able to generate O2 (the oxygen free radical) - not only at alkaline pH, but even at pH 7.4 with a slower rate. The possibility of O2- formation from glycated proteins may explain some long term complications of diabetes mellitus" (Gillery P., Glycation of proteins as a source of superoxide, Diabete Metab. 1988 Jan-Feb;14(1):25-30).

Glycation of proteins produces 50-fold more of the toxic free radicals than nonglycated proteins. AGE induced free radicals activate the proinflammatory cytokine TNF-a (tumor necrosis factor alpha), known to be elevated in the elderly. TNF-a has been shown to be particularly high in inflammatory diseases of the joints (like rheumatoid arthritis), central nervous system (Alzheimer's disease, multiple sclerosis and ischemia) and it promotes neurodegeneration (Heininger K. A unifying hypothesis of Alzheimer's disease. IV. Causation and sequence of events. Rev Neurosci. 2000; 11 Spec No:213-328. Review). Abnormal proteins may be produced in nerves leading to numbness. Abnormal proteins in the arteries lead to their 'hardening' or stiffness and resultant hypertension, though there are other causes of hypertension as well. This whole process involving proinflammatory cytokine tends to deplete glutathione in cells. That appears to be a critical factor in decline of cell function and for establishment of the disease state. When the glutathione level in cells declines below the 80% level required for optimal function, the cell dies.

REFERENCES

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