TheTruthAboutStuff.com

Review 1 - Published November 2007

Monte WC. 2007, Is your Diet Sweetener killing you? Fitness Life Nov. 33: 31-33

 

Abby Cormack is a young lady from Wellington who recently made headlines because of serious adverse reactions her physician attributed to her use of the artificial sweetener aspartame. She sent me an email to ask for help. I was happy to assist since I have seen hundreds of similar complaints (1). Aspartame contains methanol(14,48,5). Methanol is a dangerous poison that, over time, is known to remove the insulation from nerve axons(18,53), producing symptoms identical to Multiple Sclerosis (MS)(2). In fact, in the German scientific literature, Swiss physician, Dr Hugo Henzi, argued eloquently, that naturally occurring methanol was the cause of Multiple Sclerosis(5,6,8,9,10).

My name is Dr. Woodrow Monte. My 26 year career as Professor at Arizona State University was devoted to research and teaching of the composition and safety of foods. For 25 years I have had serious concerns about the consequences of the consumption of Aspartame. In 1983, I filed the first petition to the US Food and Drug Administration seeking Aspartame’s removal from foods(39). My 287 page petition, containing copious documentation of published research, was denied without explanation. In 1984, I wrote the first scientific article warning of the methanol produced when Aspartame is consumed(1).

This issue of aspartame safety is embedded in a quagmire of politics(39). Aspartame’s approval by the American Food and Drug Administration (FDA) was championed, by the former US Secretary of Defense Donald Rumsfeld. At the time of Aspartame’s FDA approval, he was president of the company that invented it and which stood to make considerable financial gain from its manufacture and sales(39,56).

NZFAS Public Relations for the Beverage Industry The New Zealand Food Safety Authority (NZFSA) has endorsed Aspartame safety in all of their handouts, for the most part paraphrasing the claims of the sweetener industry(39,56). The New Zealand government currently is considering a measure which endorses diet sweeteners as replacement for sugar sweetened beverages in schools. Inexpensively produced aspartame from China is the product most likely to be selected to replace sugar. Fizzy drink beverage manufacturers stand to reap a substantial profit from the money saved substituting aspartame for sugar. But at what cost to the public health? Despite vigorous protest, the NZFSA has maintained a pro-aspartame stance. They have chosen not to allocate resources for study of the many hundreds of scientific works that comprise just the methanol toxicity literature. I have studied this scientific literature and, in the remainder of this article, will present to you what I have learned, and why I believe, it is so important to reject this proposed measure.

The Science: Aspartame tastes sweet because, attached to it, is a molecule of methanol (wood alcohol). The methanol is very loosely bound and will fly off with the slightest heating or when consumed(20,51). Because methanol’s toxicity is well known, millions of dollars were invested by Aspartame’s inventors in an attempt to attach some other “safer” substance, but this attempt was not successful. With the approval of Aspartame, a new source of methanol was added to what is a very short list of methanol containing foods.

Methanol - Trojan Horse: Why is methanol dangerous? Inside cells, methanol is converted to formaldehyde(30), an undetectable toxin and recognized cancer causing agent of the highest order (Group I)(11). Even when formaldehyde is injected directly into a living human, it turns into formal hydrate(4,27), a very aggressive molecule that instantly attaches to any protein molecule which it makes contact. The formaldehyde molecule then completely disappears within the cover of the much larger protein(31,32). No diagnostic procedures, can detect a protein molecule so changed, yet the damaged molecule, loses function.

Damaged protein molecules are not tolerated by the immune system. Specific detection sites for “formaldehyde modified protein” are found on white blood cells called macrophages(23,24). Macrophages seek out and destroy these proteins at a rate 100 times faster than proteins not treated with formaldehyde(25). Upon autopsy, macrophages are found in the damaged areas of the brains of those who have died with MS(42,44).

Pharmaceutical companies use formaldehyde treatment of viral proteins to greatly enhance antibody production during the manufacture of vaccines(26). However, the effect of formaldehyde (resulting from methanol poisoning) on human proteins, has not been examined as a cause of autoimmunity.

A Question Never Answered: In response to these concerns, spokespersons for the soft drink beverage industry and for NZFSA claim that there is a large amount of methanol consumed in the normal diet and that a “little” more from aspartame will do no harm. This is their only justification for allowing more of this toxin to be introduced into foods. No estimate has been publicly presented by these spokespersons regarding the amount of methanol consumed per person, per day in the average diet. Consistent with the data in my published research(1), I believe that the amount of methanol in the typical diet without artificial sweeteners would be less than 8 milligrams per day. One can of aspartame sweetened diet cola yields 16 milligrams of methanol(47), more than twice the amount of methanol from other sources in a typical diet.

Fresh fruits and vegetables contain small traces of methanol(28,29) but their consumption is not problematic, in that, during fermentation in the gut, they produce a natural substance that stops the conversion of methanol to formaldehyde(35,36). In fact, before Aspartame, methanol in the normal human diet came primarily from heat processed plant foods such as canned fruit and vegetables and their juices(33). While there are unusually high levels of methanol in black currant and tomato juices(1,19,33), these foods are included only occasionally in most diets and, thus, would have little impact on an average person’s methanol intake(1).

Methanol is only found in natural foods that contain pectin(33), the glue that holds certain plants together. Fortunately, the bond that holds the methanol to pectin is so strong that it rarely breaks(36), or breaks only under certain conditions. These conditions include fermentation(35) or the high temperatures of the food canning process(1,28,29,34). Even under these conditions only a small percentage of pectin’s methanol is released(35,36). (It is interesting to note that MS was first documented as a disease(45) at about the time that canning began to flourish in Europe(46). Further, humans have no enzymes for pectin digestion (36), thus making pectin consumption rather unlikely to yield much methanol. In contrast, aspartame consumption yields methanol always and readily(20,48).

The Second Attempt to put Methanol into Foods A hundred years ago the scientific community believed methanol was benign and swore to its safety with disastrous consequences(21). At the turn of the century, industry scientist wanted to use the newly developed, inexpensive and odorless form of wood alcohol,… methanol, to extract vanilla and other flavorings(17,21). Over the previous 50 years, many toxicity studies performed in reputable laboratories showed that more methanol than ethanol is required to kill a test animal(15,30). Testing of this sort was repeated with monkeys, dogs, rabbits and laboratory rats(17,30). Each time with the same result.

This data was presumed to support the safety of methanol consumption. Accordingly, food and drug industries proceeded to use methanol in patent medicines and to produce flavorings. Soon after the first bottles of methanol laden extracts appeared on the market, many fell seriously ill(17). The stories that linked suffering, blindness and death were discounted by the scientific community as “anecdotal” and unrelated to the methanol which “had gone through so much testing”(17). When incidence of death(16) and vision loss(37) continued to mount, professionals surmised that some “impurity” had found its way into individual products. They maintained that nothing was wrong with methanol per se(17,30). Thousands died before the scientific community determined that animals and humans do not metabolize methanol in the same manner(52). Eventually, scientists learned that a liver enzyme that metabolizes methanol, present in animals but absent in humans accounts for methanol’s toxicity for humans(52). While animals consume methanol safely, as little as 2 teaspoons can be lethal for a human(16). Since that time methanol has been forbidden in foods and must always be packaged with a label showing a skull and crossbones, the universal symbol for poison(49).

Why I question the Safety of the worlds most tested food additive: The inventors of aspartame would have the advantage of hindsight when designing studies for determining the safety of their methanol containing product. Inexplicably, all of their toxicological testing was conducted on the same selection of animals that falsely supported methanol’s safety more than 60 years earlier(48).

Despite this bias in sample selection, long term toxicity studies of Aspartame has shown an increased likelihood of cancer in test animals(50), an outcome not examined in earlier methanol studies. As a consequence, Aspartame became the first additive in the history of the US FDA denied approval for use in foods by the scientists of a Public Board of Inquiry (39,57). Ultimate approval did occur, however, and it resulted not from additional research but rather from political intervention(39). What was remarkable was the method used to bend science to the will of an aggressive drug company. When it was clear that chances of approval were waning, representatives of the company sought out the few laboratories in the United states that were performing methanol research. These laboratories were, in effect, hired to help prove aspartame is safe(39). Participating labs were tasked to find an animal that would respond as a human does to methanol(39), then to find a way to prove that formaldehyde was not producing the symptoms of methanol poisoning in that animal(39).

If formaldehyde was proved the cause of the symptoms and death from methanol poisoning, (the opinion held by the scientific community at that time(21,30), formaldehyde’s inability to be detected would put a quick end to any hope for the approval of Aspartame. Millions of dollars bought many scientific papers, few indicating the research therein was “contracted” by the manufacturers of the product(39). This “research” is now forever embedded in the scientific literature. Scientists who were on the corporate dole are now considered “experts” in the field of methanol safety.

It should be noted that research not funded by the manufacturer of Aspartame has led to different conclusions. For example, 10 years ago an independent Spanish laboratory found that Aspartame most definitely turns into formaldehyde(7,40).

Because of differences across species in the production of enzymes that metabolize methanol, the results of animal research with Aspartame cannot safely be generalized to humans. Humans have become the test subjects in a 27-year long experiment on Aspartame safety. Unfortunately, the damage that methanol can cause is being revealed in populations of Aspartame consumers such as Abby Cormack. The issue is complex but the choice is simple. Fortunately there are several other readily available, artificial sweeteners that do not contain dangerous toxins. Therefore, it just makes good sense to keep Aspartame out of our schools.

 

Woodrow Monte Ph.D.
Professor of Food Science (retired)
Arizona USA

 

* please go to TheTruthAboutStuff.com to see my 1984 article for a full discussion of this issue and references for this article.

 

 

Reference List

 

1. Monte WC. 1994. Aspartame; Methanol and the Public Health. Journal of Applied Nutrition. 36(1):42

2. Monte WC, Glanzman D. and Johnston CS. 1990. Methanol as a Model Etiologic Agent in Multiple Sclerosis. FASEB 74th annual meeting Feb 26;4(3):Abstract

3. Personal Communication,2006. Bill Richardson, 1/1/2006

4. Kallen RG, Jencks WP. 1966. Equilibria for the Reaction of Amines with Formaldehyde and Protons in Aqueous Solution. J Biol Chem 241 (24): 5864

5. Henzi, H. 1980. The Methanol Hypothesis A New Concept of Multiple Sclerosis: (M Sr N), Juris Druck, Zurich (1980)

6. Schwyzer, RU. Henzi, H. 1983. Multiple Sclerosis: Plaques Caused by 2-Step Demyelination? Medical Hypothesis. 12:129

7. Trocho C., Pardo R, Fafecas I, Virgili J, Remesar X, Fernandez-Lopez, J A. Formaldehyde derived from dietary aspartame binds to tissue components in vivo. Life Sci 1988: 63: 337

8. Henzi, H. 1984. Chronic Methanol Poisoning with the Clinical and Pathologic-Anatomical Features of Multiple Sclerosis Medical Hypothesis. 13:63

9. Schwyzer, RU. Henzi, H. 1988. Reflections on the Pathogenesis of Optic (Retrobulbar) Neuritis in Multiple Sclerosis. Medical Hypothesis. 27:167

10. Schwyzer, RU. Henzi, H. 1992. Multiple Sclerosis: Prevention of Serious Illness – Vision of a Desired Future for Newly Ascertained Patients. Medical Hypothesis. 37:115

11. Rousseau M-C, Straif K. Siemiatycki J. 2005, IARC Carcinogen Update. Environmental Health Perspectives 113, (9) A580

12. Apol AG. 1981. Health Hazard Evaluation Report. PB82-19464 8. NIOSH U. S .Dept. of Health and Human Services HETA 81-177, 178,988 University of Washington Seattle, Washington

13. Center for Disease Control 1976. Occupational Exposure to Methyl Alcohol. U.S. Department of Health, Education, and Welfare HEW.NIOSH Pub No .(76-148)

14. Anonymous1984. Aspartame for use as a Sweetener in Carbonated Beverages. Searle Research and Development. Petition submitted to the United States Food and Drug Administration - FAP 2A3661

15. Eisenberg AA. 1917. Visceral Changes in Wood Alcohol Poisoning by Inhalation. American Journal of Public Health. 7:765

16. Bennett IL, Cary FH, Michell GL. and Cooper MN. 1953. Acute Methyl Alcohol Poisoning; A Review Based on Experience in an Outbreak of 323 Cases. Medicine 32:431

17. Wimer WW, Russell JA, and Kaplan HL. 1983. Alcohols Toxicology. Alcohols Toxicology, Noyes Data Corporation. 8

18. Gaul HP, Wallace CJ, Auer RN, et al. 1995. MR findings in methanol intoxication. AJNR Am J Neuroradiol 1995;16:1783

19. Francot P and Geoffroy P. 1956. Le Methanol dans les jus de fruits, les boissons, fermentees, les alcools et spiritueux. Revue Des Fermentations Et Des Industries Alimentaires. 11:279

20. Davoli F. Cappellini L. Airoldi L. Fanelli R. 1986. Serum methanol concentrations in rats and in men after a single dose of aspartame. Food Chem Toxicol. 24(3):187

21. Schneck SA. 1979. Methyl alcohol. Handbook of Clinical Neurophysiology. 36:351

22. Personal Communication

23. Horiuchi S, Takata K, and Morino Y. 1985. Scavenger Receptor for Aldehyde-modified Proteins. The Journal of Biological Chemistry. 261(11):4962

24. Horiuchi S, Takata K, and Morino Y. 1985. Purification of a Receptor for Formaldehyde-treated Serum Albumin from Rat Liver. The Journal of Biological Chemistry. 260(1):482

25. Horiuchi S, Takata K, and Morino Y. 1985. Characterization of a Membrane-associated Receptor from Rat Sinusoidal Liver Cells That Binds Formaldehyde-treated Serum Albumin. The Journal of Biological Chemistry. 260(1):475

26. Metz, B., W. Jiskoot, W.E. Hennink, D.J.A. Crommelin, and G.F.A. Kersten, Physicochemical and immunochemical techniques predict the quality of diphtheria toxoid vaccines. Vaccine, 2003. 22: 156-167

27. Streitwieser A and Heathcock CH. 1985. Introduction to Organic Chemistry. Macmillan Publishing Co. 3rd Ed.:357

28. Kirchner JG and Miller JM. 1967. Volatile Water-Soluble and Oil Constituents of Valencia Orange Juice. Agricultural and Food Chemistry. 5(4):283

29. Lund ED, Kirkland CL, and Shaw PE. 1981. Methanol, Ethanol, and Acetaldehyde Contents of Citrus Products. Agricultural and Food Chemistry. 29:361

30. Koivusalo M. 1956. Studies on the Metabolism of Methanol and Formaldehyde in the Animal Organism. Acta Physiologica Scandinavica. 39.:1

31. Buys CHCM, De Jong ASH, Bouma JMW, and Gruber M. 1975. Rapid Uptake by Liver Sinusoidal Cells of Serum Albumin Modified with Retention of its Compact Conformation. Biochimica et Biophysica Acta. 392:95

32. Buys CHCM, Elferink GL, Bouma JMW, Gruber M, and Nieuwenhuis P. 1973. Proteolysis of Formaldehyde-treated Albumin in Kupffer Cells and Its Inhibition by Suramin. Journal of the Reticuloendothelial Society. 14:209

33. Gruner O and Bilzer N. 1983. Methanol content of fruit-juices. Its significance in congener analysis. Blutalkohol. 20:241

34. Casey JC, Self R, and Swain T. 1963. Origin of Methanol and Dimethyl Sulphide from Cooked Foods. Nature. 200:885

35. Braverman JBS and Lifshitz A. 1957. Pectin Hydrolysis in Certain Fruits during Alcoholic Fermentation. Food Technology. July:356

36. Campbell LA and Palmer GH. 1994. Pectin in Topics in Dietary Fiber Research. Pectin in Topics in Dietary Fiber Research, Spiller GA and Amen RJ (eds.).Plenum Press, New York, 105

37. Fink WH. 1994. The ocular pathology of methyl-alcohol poisoning. Amer J Ophthal. 26:694,802

38. Millman RB. 1982. Alcohol; The Friendly Foe. In Science Year, The World Book Science Annual. 112

39. Gordon G. 1987. UPI Investigative Report NutraSweet Questions Swirl (How Sweet It Isn't). Seattle Times Oct.:

40. Tephly TR: 1999. Comments on the purported generation of formaldehyde from the sweetener aspartame. Life Sci 65: 157-160. [ letter, not peer-reviewed]

41. Lutton JD. Winston R. Rodman TC. 2004. Multiple Sclerosis: Etiological Mechanisms and Future Directions. Experimental Biology and Medicine 229:12-20

42. Eisenberg AA. 1917. Visceral Changes in Wood Alcohol Poisoning by Inhalation. American Journal of Public Health. 7:765

43. Alexander L, Berkeley AW, and Alexander AM. 1961. Multiple Sclerosis Prognosis and Treatment. Multiple Sclerosis Prognosis and Treatment. Charles C Thomas Publisher USA

44. Hallpike JF, Adams CWM, and Tourtellotte WW. 1983. Multiple Sclerosis. Pathology, diagnosis and management, Williams & Wilkins, Baltimore

45. History of MS, 2007 Multiple Sclerosis Trust, http://www.mstrust.org.uk/information/a2z/history.jsp

46. The History of Food Canning. http://www.westlerfoods.com/pdf/canning_process.pdf

47. Scientific Abuse in Methanol / Formaldehyde Research related to Aspartame http://www.holisticmed.com/aspartame/abuse/methanol.html

48. Anonymous1994. Aspartame for use as a Sweetener in Carbonated Beverages. Searle Research and Development. Petition submitted to the United States Food and Drug Administration - FAP 2A3661

49. Methanol Danger Sign, T&B Westline

50. Soffritti M. Belpoggi F. Esposti DD. Lambertini L. Tibaldi E. and Rigano A. 2006,Results of Long-Term Carcinogenicity Bioassay on Sprague-Dawley Rats Exposed to Aspartame Administered in Feed. Ann. N.Y. Acad. Sci. 1076: 559

51. Soffritti M. Belpoggi F. Cevolani D. Guarino M. Padovani M. and Maltoni C. 2002,Results of Long-Term Results of Long-Term Experimental Studies on the Carcinogenicity of Methyl Alcohol and Ethyl Alcohol in Rats N.Y. Acad. Sci. 982: 46

52. Roe O. 1982. Species Differences in Methanol Poisoning. I. Minimal Lethal Doses, Symptoms, and Toxic Sequelae of Methanol Poisoning in Humans and Experimental Apter 18,376,390. CRC Critical Reviews in Toxicology. 275

53. Rao KR, Aurora AL, Muthaiyan S, and Ramakrishnan S. 1977. Methanol toxicity - an experimental study. Bull. Jawaharlal Inst. Post-Grad.Med.Educ.Res. 2:1

54. Walton, R.G., R. Hudak, and R.J. Green-Waite. 1993. Adverse Reactions to Aspartame: Double-Blind Challenge in Patients from a Vulnerable Population. Biological Psychiatry 34:13

55. Smith EN and Taylor RT. 1982. Acute Toxicity of Methanol in the Folate-Deficient Acatalasemic Mouse. Toxicology 25:271

56. Thomas P. 2005 Aspartame: The Shocking Story of the World’s Bestselling Sweetener. The Ecologist Sept. 36

57. Department of Health and Human Services U.S. FDA. 1979 Decision of the Public Board of Inquiry (Docket No. 75F-0355). 44 Fed. Reg. 31716

58. Center for Disease Control 1984. Evaluation of Consumer Complaints Related to Aspartame Use. Morbidity and Mortality Weekly Report. 33:605

59. Center for Disease Control 1976. Occupational Exposure to Methyl Alcohol. U.S. Department of Health, Education, and Welfare HEW.NIOSH Pub No .(76-148)

60. Office of Hon Pete Hodgson, NZ Minister of Health. 2007, Personal Communication