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Hospital Form To Make Sure You Aren't Given Aspartame As A Patient - Print This Out, Please

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Case IX-K-5 (FDA Project #3898; Courtesy, Dr. Linda Tollefson)

A 76-year-old woman with longstanding cirrhosis died in progressive "liver coma." In his correspondence to a consumer advocate, her husband indicated that she had been "in pretty good health" until October 1983 when an elevated blood glucose concentration was found. Tolbutamide and diet were prescribed. In an attempt to avoid sugar, she used four packets of an ATS daily in coffee, cereal and desserts.

The patient evidenced dramatic deterioration within two weeks. It was manifest by indifference to her surroundings, forgetfulness, slurred speech, dizziness, impaired vision, loss of interest concerning food and her favorite television programs, and a change in gait. She made irrelevant statements as if hallucinating. Her condition deteriorated to the point of becoming incontinent and bedridden. A diagnosis of "hepatic encephalopathy" was made.

Related Biochemical Aspects

Deterioration of brain function in patients with severe liver disease has been attributed to the retention of phenylalanine and other amino acids (Fischer 1971). Striking changes in amino acid metabolism are known to occur in liver disease - particularly the hydroxylation rates of phenylalanine, tyrosine and tryptophan. The elevated phenylalanine concentrations in patients with cirrhosis rise significantly after protein consumption (Fernstrom 1979). Methanol poisoning (Chapter XXI) creates another serious problem in patients with liver disease. The enzymes alcohol dehydrogenase and aldehyde dehydrogenase are involved in methanol metabolism. The considerable alcohol dehydrogenase activity of the liver decreases when it is diseased.

One mechanism may be the production of tumor necrosis factor (TNF)-a. It is an early event in many types of liver injury that triggers the release of other cytokines, and then the destruction of liver cells.

A vicious cycle involving aggravated hypoglycemia also can occur. Contributory causes include the tendency to "hepatic hypoglycemia" among persons with severe liver disease (owing difficulty in storing and metabolizing glycogen), aspartame-induced hypoglycemia (Chapter XIV), the use of glucose-lowering drugs for control of diabetes, and the failure of diabetics receiving such drugs or insulin to take interval feedings. For example, the physician who prescribed tolbutamide for Case IX-K-4 "said nothing about diet."

Hemochromatosis (iron storage disease; hepatic iron overload; bronze diabetes) might be aggravated in its pre-cirrhotic stage by aspartame consumption (see Case XIII-1), especially through insulin stimulation (Chapter XIV). Related features of insulin resistance - in addition to hyperinsulinemia - are increased body mass, elevated lipids, and abnormal glucose tolerance.

The separate entity of primary hepatic iron overloads differs from genetic hemochromatosis because transferring saturation is normal, as is the frequency of the HLA A3 genotype (Ferrannini 2000). It has been suggested that insulin's primary action in stimulating glucose transport is coupled with a redistribution of transferring receptors to the cell surface where they mediate extracellular iron uptake.

Martini: This is the end of the chapter. Please also see the Aspartame Resource Guide: http://www.mpwhi.com/aspartame_resource_guide.pdf

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photo: Picture of Dr. M. Soffritti (Director General of the Ramazzini Foundation) and Dr. Betty Martini at the Mt. Sinai Medical School, where he received the prestigious Irving J. Selikoff Award. New study with low doses released again showing (more...)
 

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