Pseudotumor Cerebri als gevolg van het gebruik van aspartaam.
* June 2002 *
H. J. Roberts, M.D., FACP,
Townsend Letter for Doctors,
Pseudotumor cerebri is de verouderde benaming voor een ziektebeeld dat tegenwoordig Idiopathische Intracraniële Hypertensie wordt genoemd. Ook komt men wel de term "Benigne Intracraniële Hypertensie" tegen. De naam pseudotumor cerebri is te danken aan het feit dat men in het verleden eerst heeft gedacht dat de patiënt een hersentumor (gezwel in de hersenen) had, omdat deze zoals bij een hersentumor de verschijnselen vertoonde van verhoogde druk in het hoofd (of intracraniële hypertensie, zoals de vakterm luidt). Bij nader onderzoek bleek er toch geen hersentumor te zijn, vandaar de toevoeging "pseudo-" (wat betekent schijnbaar) bij tumor cerebri, en de toevoeging "benigne" (wat betekent goedaardig) bij intracraniële hypertensie. Omdat het beloop wat betreft de afwijkingen aan de oogzenuw toch niet altijd zo goedaardig is, is de term idiopathisch geïntroduceerd. Idiopathisch betekent niets anders dan dat de oorzaak onbekend is.
Deze informatie is gedeeltelijk afkomstig van de Nederlandse Vereniging van Neurochirurgen. Op deze website is ook meer informatie te vinden over diverse ziektebeelden.
Onderwerp: Pseudotumor Cerebri ten gevolge van de aspartaam ziekte
H. J. Roberts, M.D., FACP, Townsend Letter for Doctors, June 2002
Dizziness, unsteadiness, or both 376 (31%)
Confusion, memory loss, or both 376 (31%)
Severe drowsiness and sleepless 150 (13%)
Convulsions (grand mal epileptic attacks) 129 (11%)
Petit mal attacks and "absences" 96 ( 3%)
Severe slurring of speech 124 (10%)
Severe tremors 101 ( 8%)
Severe "hyperactivity" and "restless legs" 78 ( 6%)
Atypical facial pain 70 ( 6%) The foregoing complaints usually improved following aspartame avoidance and promptly recurred after resuming aspartame products, knowingly or inadvertently. Some examples:
* The aggravation or simulation of diabetic neuropathy by aspartame has been emphasized.
* More than 40 aspartame reactors were given the diagnosis of "probable multiple sclerosis" prior to an impressive remission after aspartame abstinence.
* A female aspartame reactor experienced Bell's palsy, paresthesias, blurred vision, dizziness, tinnitus, insomnia, depression and a dermatitis. She improved when diet colas were avoided, but then evidence recurrence of the Bell's palsy and other symptoms after resuming aspartame sodas. The suspected causative or aggravating role of aspartame in human brain cancer also warrants mention in this context. Mechanisms of Aspartame Neurotoxicity Each of the components of aspartame - phenylalanine (50%); aspartic acid (40%); and methyl ester (10%) that promptly becomes free methyl alcohol (methanol) after ingestion - and their multiple breakdown products after exposure to heat or during storage are potentially neurotoxic. The mechanisms may variously involve dopamine (derived from phenylalanine), cerebral cholecystokinin (CCK), serotonin, endorphins, other important neurotransmitters, neuroglucopenia, the unique permeability of the blood brain barrier to phenylalanine, and the "aging" effect of the steroisomer D-aspartic acid. Others include methanol-induced cerebral edema and fluid disturbances noted in humans and experimentally. The severe neurotoxic effects from chronic intake of free methanol are pertinent. Dr. Herbert S. Posner (National Institute of Environmental Health Sciences) wrote a review titled, "Biohazards of Methanol in Proposed New Uses," six years before FDA approval of aspartame. He emphasized failure to recognized the "delayed and irreversible effects on the nervous system of methanol...at widely varying levels of exposure and at rather low levels." The intake of methyl alcohol from natural sources is less than 10 mg. daily. Aspartame beverages average 55 mg. methanol per liter, but nearly twice as much in some sodas. Accordingly, individuals who drink five liters a day could ingest over 400 mg. methanol. Several aspects of chronic methanol intake are listed: * Methyl alcohol, the first component of aspartame released within the small intestine, is rapidly absorbed.
* Blood and methanol concentrations correlate with the amount of aspartame taken. The elevated blood methanol concentrations in normal subjects who ingest "abuse doses" may be detactable for eight or more hours.
* Humans are more vulnerable to methanol toxicity than animals.
* One-fourth of aspartame reactors experience eye problem, presumably in large measure due to methanol and its breakdown products.
* Methanol toxicity is enhanced by its slow rate of oxidation. Although the half life is about three hours in human volunteers who ingest small amounts (1-5 ml), complete oxidation to carbon dioxide usually requires several days.
* Methyl alcohol is detoxified through its oxidation to formaldehyde and within minutes to formate or formic acid. The latter contribute to nervous system and immune dysfunction. One mechanism involves the conjugation of formaldehyde with human serum albumin (F-HSA) to form a new antigenic determinant. Persons chronically exposed to formaldehyde develop anti F-HSA antibodies and elevated Tal cells (antigen memory cells), consistent with sustained antigenic stimulation of the immune system. Other studies clarify the chronic toxicity of aspartame-derived formaldehyde. The highly reactive formaldehyde molecules become bound to proteins and nucleic acids. The adducts formed are difficult to eliminate through usual metabolic pathways. Using adult male rats given oral aspartame C-labeled in the methanol carbon, Trocho et al convincingly demonstrated that formaldehyde derived from dietary aspartame binds to tissue components in vivo. Most of the radioactivity was bound to protein in plasma and liver, and had a long half life. It also was detected in brain, cornea,and retina. Furthermore, progressive accumulation of more label could be demonstrated when non-labeled aspartame was given over ten days, suggesting that aspartame-derived formaldehyde adducts are cumulative in tissue proteins and nucleic acids. These investigators commented, "The cumulative effects derived from the incorporation of label in the chronic administration model suggest that regular intake of aspartame may result in the progressive accumulation of formaldehyde adducts. It may be further speculated that the formation of adducts can help to explain the chronic effects of aspartame consumption on sensitive tissues such as brain." Addendum: Case histories of two additional women in their thirties with aspartame disease and pseudotumor cerebri have been received. Correspondence: H. J. Roberts, M.D., FACP 6708 Pamela Lane West Palm Beach, Florida 33405 USA Fax 561 - 547 - 8008 References 1. Roberts, H. J. Reactions Attributed to aspartame containing products 551 cases J App Nutr 1988:40:85-94. 2. Roberts, H. J. Aspartame (NutraSweet ) associated epilepsy Clin Res 1983,36:349A 3. Roberts, H. J. Aspartame (NutraSweet: Is It Safe? Philadelphia, The Charles Press 1989. 4. Roberts, H. J. Sweet'ner Dearest: bittersweet Vignettes About Aspartame (NutraSweet), West Palm Beach, Sunshine Sentinel Press, l992 5. Roberts, H. J. Defense Against Alzheimer's Disease: A Rational Blueprint for Prevention, West Palm Beach, Sunshine Sentinel Press, l996 6. Roberts, H. J. Aspartame and headache, Neurology l995; 45:1631-1633. 7. Roberts, H. J. Breast Implants or Aspartame (NutraSweet) Disease? West Palm Beach, Sunshine Sentinel Press l999. 8. Roberts, H. J. Difficult Diagnosis: A Guide to the Interpretation of Obscure Illness, Philadelphia, W. B. Saunders co, l958. 9. Wilson, DH Gardner, WJ Benign intracrnial hypertension with particular reference to its occurrences in fat young women Canad M A J l966;95;102-105. 10. Roberts, H. J. Complications associated with aspartame (NutraSweet) in diabetics, Clin res 1998;3;489A. 11. Roberts, H. J. Does aspartame cause human brain cancer? J Advnce M 1991;4 (Winter )23;1-24). 12. Menne FR aCute methyl alcohol poisoning, report of 22 incidences with postmortem examination Arch Path 1938;26;77 13. Bennett II Jr. Carey H Mitchell GL Jr. Cooper MN. Acute methyl alcohol poisoning; A review based on experiences in an outbreak of 32 cases. Medicine 1953;32;491. 14. Erlanson P, et al. Severe in ethanol intoxication; Acto Med Scand 1966;177;393. 15. Rao KR Aurora Al Mithalyan S Ramakrishnan S Biochemical changes in brain in methanol poisoning - an experimental study. Indian J M Res 1977;65-285-292. 16. Posner HS Biohazards of methanol in proposed new uses J Toxicol Environ Health l975; 1-153-171. 17 Monte, WC Aspartame: Methyl Alcohol and the Public Health J Appl Nutr 1984; 39;42-54. 18. Stegink HD Filer IJ Jr Aspartame Physiology and Biochemi8stry, New York Marcci Dekker Inc. l984. 19. Thrasher JF Broughton A, Micevich P Antibodies and immune profiles of individuals occupationally exposed to formaldehyde. Six case reports Am J Indust M 1988: 14;479-485 20. Trocho C. Pardo R. Rafecas T et al; Formaldehyde derived from dietary aspartame binds to tissue components in vivo Life Sci. 1998:63;337-349