An overview for health professionals
Additive Survivors’ Network (UK)
Additives Survivors’ Network (UK)
was at the time the author wrote this affiliated to the Green Network and the Green Network Charitable Trust, Charity registration No. 1028693. ASN is now a stand alone pressure group. ASPARTAME CONCERNS
Why is aspartame in our food?
Aspartame is not related to sugar. but has an intensely sweet taste. For these reasons it is widely used by diabetics, weight-watchers and by many people being careful about their dental or general health. At one-third of the cost of sugar, it is also cheap 3. Why are we concerned?
Members of the Additive Survivors’ Network have watch with alarm as aspartame has encroached upon our supermarket shelves. Alarm, because we have experienced, or
observed at first hand, severely debilitating side effects linked to this substance. We have
spent months, or years, struggling to identify what was causing our symptoms with little
assistance from the medical profession This experience has made us acutely aware of how
difficult it is to trace the source of reactions which may emerge days, or even weeks, after
the first exposure to the damaging substance, and which mimic or exacerbate a multitude
of other diseases.
Aspartame’s potential to cause metabolic disturbances
During digestion, aspartame releases methanol and two amino acids, aspartic acid and phenylalanine, into the body. These are biologically active chemicals which are known to disturb many metabolic processes, both directly and indirectly: Methanol The body deals with methanol by converting it to formate, which is then excreted. It can also give rise to formaldehyde, diketopiperazine (a carcinogen) and a number of other highly toxic derivatives. All of these can arise within aspartame containing products if storage conditions are not ideal 12. Methanol toxicity is considered to be due to accumulation of formate rather than methanol itself 43, but recent research has demonstrated that formaldehyde adducts accumulate in the tissues, in both proteins and nucleic acids, after aspartame ingestion 46. Besides its role in amino acid metabolism and protein structures in all tissues, aspartic acid can be a precursor to glutamate asparagine and glutamine 43. Like glutamate, which is the principal excitatory neurotransmitter in the brain, aspartic acid is a neuronal excitor 24. It is commonly repeated that blood aspartic acid levels do not increase after ingestion of aspartame. One of the biggest studies commissioned by its manufacturers tells us that “in most cases aspartate concentrations were not significantly affected by aspartame ingestion” 42, 43: but read another way, this means that in some cases aspartic acid was, indeed, raised. Even transient increases in a powerful neural stimulator are enough to induce neuroendocrine disturbances 30. When taken together, aspartic acid and the common food additive monosodium glutamate have a synergistic toxic effect on neurones in the brain 24, 29. Conditions presenting with hypergluteinaemia (e.g. gout, viral infection) may, similarly, carry an increased risk of damage from aspartame 29. Phenylalanine Besides its role in amino acid metabolism and protein structures in all tissues, phenylalanine is a precursor for tyrosine, serotonin 14, noradrenalin, dopamine, phenylethylamine 52 and phenylacetate (this interferes with brain development and fatty acid metabolism) 25. Phenylalanine has a major function in neurotransmitter regulation 4. Dietary sources of phenylalanine in the blood have been extensively studied because of the recognised danger they pose to youngsters suffering from phenylketonuria (PKU). Most ingested phenylalanine is converted to tyrosine in the liver 4, but increases in blood levels of both phenylalanine and tyrosine after aspartame administration to humans are well documented 10, 11. What the above brief summary tells us is that aspartame may start off as a single, apparently simple, dietary substance but that it becomes a cocktail of chemicals which can
disturb a wide range of processes in the body, including amino acid metabolism, protein
structure and metabolism, nucleic acid integrity, neuronal function and endocrine
balances, besides producing more than one known toxin.
What problems could aspartame cause?
Because amino acids interact with each other, ingesting any one as a single chemical instead of as a small percentage of a natural proteinaceous food risks unbalancing all tissue amino acid profiles 4, 50. It has been repeatedly stressed that such imbalances will result in a derangement of amino-acid metabolism in the brain 6, 10, 14, 31, 50, leading, for example, to cognitive disorders 40. seizures 27,33,48, mania 48 and affective disorders 48, 49, The tissue permeability alterations associated with, for example, diabetes 14, 35, 37, obesity 4, 48, malnutrition 14, 34 and brain circulatory abnormalities 48 will make people with these conditions more susceptible to such adverse effects. One concerned scientist lists 22 chronic neurodegenerative diseases which could be exacerbated by this sweetener 24. Amino acid flux between tissues is largely hormone-dependent, suggesting an increased risk of adverse effects from aspartame during pregnancy 35, 37, 48, lactation 35 and when taking oral contraceptives 37 or some prescribed drugs such as L-dopa, methyldopa or monamine oxidase inhibitors 18, 26, 35. Liver disease causes complex and severe changes in amino acid metabolism 4, 14, 35, 47 which will increase susceptibility to adverse effects from aspartame and implies a risk to anyone with a history of substance abuse 35. Besides the recognised danger to PKU children 13, 29 which has led to a ruling that all products containing this sweetener must carry a warning label, the PKU heterozygotes in the population (about 2%) 28, 41 are also at increased risk from aspartame 8, 9, 20, 35, 50; since most such people are unidentified, they will be unaware of this. Other vulnerable groups include the elderly 48, 35 and any one whose health is already compromised 35. At particular risk are children, whose smaller body size results in proportionately greater exposure to the sweetener and whose developing tissues are uniquely susceptible to damage 29, 30, 31, 35. Recently, aspartame has been added to the growing list of additives which act in concert to promote attention deficiency and hyperactivity15. In an American study of 78,000 middle-aged women, the rate of weight gain in aspartame users was paradoxically significantly greater than in any other group2. It has been suggested that the use of aspartame can result in disordered eating patterns due, for example, to an uncoupling of the taste and energy content of food 1, 2 catecholamine disturbance, inappropriate cholecystokinin release or inappropriate generation of the enzymes and hormones of the cephalic phase response 2. What complaints have been made about aspartame?

Since aspartame entered the food chain in the early 1980s 32 the American Food and Drug
Administration (FDA) have received thousands of notifications of adverse effects 36.
These are summarised below as published in 1987 45, beside our own information
collected in Britain during the month of January, 2000.

1987 (USA)
2000 (UK)
The 1987 FDA records also show which products were associated with the complaints received about aspartame: Product Reporting rates are not, of course, occurrence rates45.
Why has aspartame been approved for food use?

Aspartame has been one of the most extensively examined substances ever. In preparing
this review, I have traced over 450 citations, of which I have read 67 (all I could get hold
of). There is very little consistency in the experimental results nor agreement between expert scientists: for every problem indicated by one experiment, there is another study reporting opposite findings (for example, check out references 7, 22, 38, 39 & 44). Consider for a moment the difficulties in carrying out feeding experiments, especially on human beings: the sample sizes are necessarily small; the age, nutritional and emotional status of each subject, besides genetic and medical predispositions, will all contribute to their reactions; a host of technical limitations, such as the form in which aspartame has actually been administered and the possibility of desensitisation, will interfere. Review also the complexity of aspartame and its physiological effects outlined earlier. Perhaps it is not surprising that recorded reactions are not uniform. But this variability has conveniently allowed experimental observations which raised awkward questions to be rejected. The same rationale was used to approve thalidomide. The range of reported adverse effects is enormous (the American Food and Drug Administration alone had a list of 92 in 1995) but perhaps not unexpected when you examine the huge potential for metabolic disturbance already described. This lack of any consistent pattern of symptoms has, however, been used as the reason to pronounce aspartame safe. The experience of members of the Additives Survivors Network is that it can take several weeks of regular aspartame consumption before the symptoms of toxicity become severe, yet, very few long-term experiments have been attempted and cumulative toxic effects have hardly been explored at all. Anti-aspartame campaigners in America have produced reviews in which they claim that every study funded by the manufacturers of aspartame found no problem, while
the vast majority of work undertaken by independent scientists revealed concerns 12 I
haven’t been able to confirm this, but was disturbed to read in one of biggest trials funded
by aspartames manufacturers 21 that, when one subject dropped out of the test due to the
severity of his reactions, he was repeatedly re-challenged with the sweetener until no
reaction was found and that this was used to conclude that aspartame was not involved in
his problems. The complexity of the toxin and inherent variability of the individual leave
such conclusions open to question.
We need your help.

Hundreds of case studies have now been collected implicating aspartame as a cause of
severe debilitation 35, 36 especially from migraine 16, 17, 9, 23, 28 headache 17, 21 & 44 seizures51
and panic attacks 5 & 48; recently, addictive properties of the sweetener have also been
described36. The people in these reports were taking aspartame routinely in their food
believing it to be in the interests of their health. These cases have, of course, only been
picked up by health professionals actively seeking them. Health carers have not been
alerted to the potential problem because the authorities (formerly the MAFF, now the
FSA, and the Department of Health in the UK, and the FDA in the USA) have not taken
individual complaints seriously.
The Additive Survivors’ Network is dedicated to supporting individuals suffering from symptoms which may be linked to aspartame, and to raising awareness among the medical professionals who are most likely to encounter them. We urge you to report any cases you identify to: We also suggest that people who suspect they are suffering problems with aspartame consider trying the ‘60-day no aspartame trial’. This involves avoiding ALL aspartame for 60 days by reading the labels of all food, drink, sweets and vitamins very carefully. If their symptoms are caused by the sweetener they should reduce during this time. To assist the public in reporting suspected side-effects from aspartame to the authorities, the Additives Survivors’ Network has prepared a simple Report Form. This can be obtained from the ASN co-ordinators (see front of report) by sending a 4” x 8” S.A.E. The A S N Co-ordinators would, of course, be pleased to hear the comments of findings of any health professionals concerned about the effects of aspartame or other additives. REFERENCES 1. Blundell J E. and Hill A.J. Letter to the Editor, Lancet. 1986. 1092-3 Blundell J.E. and Hill A.J. and Rogers P.J., Effects of Aspartame on Appetite and Food Intake, in ‘Dietary Phenylalanine and Brian Function’, Ed. R. J. Wurtman and E. Ritter-Walker, 1988, Birkhauser. Brown, Catherine, Sweet talking guise, Glasgow Herald Magazine, 22nd May 1999 Cabellero B. and Wurtman R.J., Control of Plasma Phenylalanine Levels, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter- Drake M.E., Letter to the Editor, Lancet, 1986’, 631 During M.J., Acworth IN. and Wurtman R.J., An In Vivo Study of Dopamine Release in Striatum: The Effects of Phenylalanine, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E.Ritter-Walker, 1988, Birkhauser Elsas L.J., Letter to the Editor, NEJM, 1988, 318 (18), 1201 Elsas J.J. and Trotter J.F., Changes in Physiological Concentrations of Blood Phenylalanine Produce Changes in Sensitive Parameters of Human Brain Function, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser. Eriksson T. and Carlsson A., Adrenergic Influence on Plasma and Brain Concentrations of Phenylalanine and Other Large Neutral Amino Acids in Rats, in ‘Dietary Phenylalanine and Brain Function’, Ed R J Wurtman and E. Ritter-Walker, 1 988 Birkhäuser Boston Effects of Aspartame Ingestion on Large Neutral Amino Acids and Monoamine neurotransmitters in the Central Nervous System, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, 11. Filer L.J. and Stegink L.D., Effect of Aspartame on Plasma Phenylalanine Concentration in humans, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser 12. Gold, Mark, Aspartame Toxicity Information Centre (12 East Side Drive, 2-18 Concord, NH 03301, USA) Epidemiology and Natural History of Phenylketonuria and Other hyperpheylalaninemias, in Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser 14. Hawkins R.A., Mans A M and Biebuyck JF., Regional Transport and Other Neutral Amino Acids Across the Blood-Brain Barrier, in ‘Dietary Phenylalanine and Brain Function’, Ed. R J. Wurtman and E. Ritter-Walker, 1988. Birkhauser 15. Hyperactive Children’s Support Group (71 Whyke Lane, Chichester, West Sussex, 16. Johns DR., Letter to the Editor, NEJM, 1986, 315, 456 17. Johns DR., Aspartame and Headache, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser 18. Kim K.C., Tasch M.K. and Kim S.H., The Effect of Aspartame on 50% Convulsion Doses of Lidocaine, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhauser The Effect of Aspartame Consumption on Migraine Headache: Preliminary Results, in ‘Dietary Phenylalanine and Brain Function Ed R.J. Wurtman and E. Ritter-Walker, 1 988, Birkhauser 20. Krause W., Halminski M., Naglak M., McDonald L., Salvo R., Freides D., Epstein C., Cembure P., Averbook A. and Elsas L.J., Effect of High Plasma Phenylalanine Concentration in Older Early-Treated PKU Patients: Performance, neurotransmitter Synthesis, and EEG mean Power Frequency, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser 21. Leon AS., Hunninghake D.B., Bell C. Rassin D.K. and Tephly T.R. Safety of Long- term large doses of Aspartame, Arch Intern Med, 1989, 149, 2318-24 22. Lipton S.A., Newman L.C. and Solomon S., Letter to the Editor, NEJM, 1988, 318 23. Lipton S.A., Newman L.C., Cohen J.S. and Solomon S., Aspartame as a dietary trigger of headache, Headache 1989, 29(2), 90-2 24. Lipton S.A. and Rosenburg PA., Excitatory Amino Acids as a Final Common Pathway for Neurological Disorders, NEJM, 1994, 330, 613-20 25 Loo Y.H Wisnickwski K E Hyde K R. Fulton T R. Lin Y. Y. and Wisniewski H.M., The Neurotoxic Metabolite of Phenylalanine in Phenylketonuria, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser 26. Maher T.J. and Kiritsy P.J., Aspartame Administration Decreases the Entry of a- Methyldopa into the Brain of Rats, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988. Birkhäuser 27. Maher T.J. and Wurtman R.J., Possible neurologic effects of aspartame, a widely used food additive, Environ. Health Perspect., 1987 75 53-7 28. Matalon R., Michals K., Sullivan D. Wideroff L. and Levy P Aspartame Consumption in Normal Individuals and Carriers for Phenylketonuria, in ‘Dietary Phenylalanine and Brain Function’, Ed. R J Wurtman and E. Ritter’-Walker, 1988, Birkhauser 29. Olney J W Letter to the Editor, NEJM, 1975, 292(23) 30. Olney J W Excitotoxic food additives relevance of animal studies to human safety, Neurobehav. Toxicol. Teratol., 1984, 6(6), 455-62 Phenylalanine Transport at the Human blood-Brain Barrier, in’ Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser The Regulatory Process and Aspartame: Why the Controversy?, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser 33. Pinto J.M.B. and Maher T.J., Aspartame, Phenylalanine, and Seizures in Experimental Animals, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhauser Patterns of Phenylalanine Metabolites, Vitamin B6 Status, and Learning Disabilities in Phenylketonuria Children: Modeling for Diet Criteria, in ‘Dietary Phenylalanine and Brain Function’, Ed R J Wurtman and E. Ritter-Walker, Neurological, Psychiatric, and Behavioral Reactions to Aspartame in 505 Aspartame Reactors, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser 36. Roberts H.J., communication in the ‘Townsend Letter for Doctors and Patients’, (11 Tyler Street, Port Townsend, WA 98368, USA), January, 2000 Sardesai B.M Holliday J F., Kumar G.K. and Dunbar J C Effect of Aspartame in in ‘Dietary Phenylalanine and Brain Function, Ed. R.J Wurtman 38. Schiffman 8.8 Buckley C.E. Sampson H.A. Massey E.W., Baraniuk J.N. Follett J V. and Warwick Z.S. Aspartame and susceptibility to headache, NEJM, 1987, 317 (19), 81-5 39. Schiffman S S. Buckley C.E Sampson H.A., Massey E.W., Baraniuk J.N. Follett J.V. and Warwick Z.S. Letter to the Editor, NEJM, 1988, 318(18), 1201-2 40. Spiers P., Schomer K., Saboujian L., Lieberman H., Wurtman R., Duguid F., McCarten R. and Lyden M., Aspartame and Human Behaviour: Cognitive and Behavioural Observations, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser 41. Stegink L.D., Filer L.J., Baker CL. and McDonnell J.E., Effect of Aspartame Loading upon Plasma and Erythrocyte Amino Acid Levels in Phenylketonuric Heterozygotes and Normal Adult Subjects, J. Nutr., 1979, 109, 708-15 42. Stegink L.D., Filer L.J., and Baker CL., Repeated Ingestion of Aspartame- Sweetened Beverage: Effect on Plasma Amino Acid Concentrations in Normal Adults, Metabolism, 1988, 37(3), 246-51 43. Stegink L.D., Filer L.J., Bell E.F., Ziegler E.E. and Tephly T.R., Effect of Repeated Ingestion of Aspartame-Sweetened Beverage on Plasma Amino Acid, Blood Methanol, and Blood Formate Concentrations, Metabolism, 1989, 38(4), 357-63 44. Steinmetzer R.V. and Kunkel R.S., Letter to the Editor, NEJM, 1988, 318(18), 1201 45. Tollefson L., Barnard R.J. and Glinsmann W H Monitoring of Adverse Reactions to Aspartame Reported to the U.S. Food and Drug Administration, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker, 1988, Birkhäuser 46. Trocho C., Pardo R., Rafecas I. Virgili J., Remesar X. Fernandez-Lopez J.A. and Alemany M., Formaldehyde derived from dietary aspartame binds to tissue components in vivo, Life Sci, 1998, 63 337-49 47. Uribe M, Letter to the Editor, NEJM, 1982, 306, 173 48. Walton The Possible Role of Aspartame in Seizure Induction, in ‘Dietary Phenylalanine and Brain Function’, Ed. R.J. Wurtman and E. Ritter-Walker. 1988, Birkhauser 49. Walton R.G., Hudak P. and Green-Waite R.J. Adverse reactions to aspartame: double-blind challenge in patients from a vulnerable population, Biol. Psychiatry. 1993. 34. 13-7 50. Wurtman R J Letter to the Editor, NEJM. 1983. 309. 429-30 Wurtman R J Letter to the Editor, Lancet, 1985, 1060 Facts and Myths Related to the Regulation of Phenylalanine and Other Amino ‘Dietary Phenylalanine and Brain Function’, Wurtman and E. Ritter-Walker. 1988. Birkhäuser Use and Acids, in Ed. R.J. However, ASN (UK) would appreciate acknowledgement While every care has been taken to present this material accurately, members of the Additive Survivors’ Network cannot accept responsibility


Microsoft word - acutely hazardous waste.doc

California Code of Regulations Title 22, Division 4.5, Chapter 11, Article 4, §66261.33 List of Acutely Hazardous Wastes Substance Acetamide, N-(aminothioxomethyl) Acetamide, 2-fluoro Acetic acid, fluoro-, sodium salt 1-Acetyl-2-thiourea Acrolein Aldicarb Aldicarb sulfone Aldrin Allyl alcohol Aluminum phosphide (RT) 5-(Aminomethyl)-3-isoxazolol 4-Aminopyridine Ammonium picrate (R) Ammoniu

Edward Ray, MD PRE-OPERATIVE INSTRUCTIONS FOR PATIENTS HAVING MONITORED OR GENERAL ANESTHESIA Name of Patient: _____________________________________________________________ DO NOT take aspirin or ibuprofen (ex. Aleve, Advil, Motrin) for one week prior to surgery. See attached list of other medications/supplements/herbals to avoid. DO NOT smoke* or drink any alcoholic beverages on th

© 2010-2017 Pdf Pills Composition