Date: Wed, 7 Nov 2001 16:08:12 -0800 (PST) From: bowendrjim@yahoo.com (Dr. Bowen) Subject: 11 To: bettym19@mindspring.com (Mrs. Betty Martini) ---------------------- THE BITTER TRUTH ABOUT ARTIFICIAL SWEETENERS Aspartame sugar substitutes cause worrying symptoms from memory loss to brain tumours. But despite US FDA approval as a 'safe' food additive, aspartame is one of the most dangerous substances ever to be foisted upon an unsuspecting public. ««««««««««««««««««««««««««««««««««««««««»»»»»»»»»»»»»»»»»»»»»»»»»»»»»» © 1995 by Mark D. Gold, 35 Inman St, Cambridge, MA 02139, USA Phone: (617) 497 7843, E-mail: mgold@tiac.net www.holisticmed.com ««««««««««««««««««««««««««««««««««««««««»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»» Aspartame is the technical name for the brand names, NutraSweet, Equal, Spoonful, and Equal-Measure. Aspartame was discovered by accident in 1965, when James Schlatter, a chemist of G.D. Searle Company was testing an anti-ulcer drug. Aspartame was approved for dry goods in 1981 and for carbonated beverages in 1983. It was originally approved for dry goods on July 26, 1974, but objections filed by neuroscience researcher Dr John W. Olney and Consumer attorney James Turner in August 1974 as well as investigations of G.D. Searle's research practices caused the US Food and Drug Administration (FDA) to put approval of aspartame on hold (December 5, 1974). In 1985, Monsanto purchased G.D. Searle and made Searle Pharmaceuticals and The NutraSweet Company separate subsidiaries. Aspartame is, by far, the most dangerous substance on the market that is added to foods. Aspartame accounts for over 75 percent of the adverse reactions to food additives reported to the US Food and Drug Administration (FDA). Many of these reactions are very serious including seizures and death as recently disclosed in a February 1994 Department of Health and Human Services report.(1) A few of the 90 different documented symptoms listed in the report as being caused by aspartame include: Headaches/migraines, dizziness, seizures, nausea, numbness, muscle spasms, weight gain, rashes, depression, fatigue, irritability, tachycardia, insomnia, vision problems, hearing loss, heart palpitations, breathing difficulties, anxiety attacks, slurred speech, loss of taste, tinnitus, vertigo, memory loss, and joint pain. According to researchers and physicians studying the adverse effects of aspartame, the following chronic illnesses can be triggered or worsened by ingesting of aspartame:(2) Brain tumors, multiple sclerosis, epilepsy, chronic fatigue syndrome, parkinson's disease, alzheimer's, mental retardation, lymphoma, birth defects, fibromyalgia, and diabetes. Aspartame is made up of three chemicals: Aspartic acid, phenylalanine, and methanol. The book, Prescription for Nutritional Healing, by James and Phyllis Balch, lists aspartame under the category of "chemical poison." As you shall see, that is exactly what it is. ASPARTIC ACID (40% OF ASPARTAME) Dr Russell L. Blaylock, a professor of Neurosurgery at the Medical University of Mississippi, recently published a book thoroughly detailing the damage that is caused by the ingestion of excessive aspartic acid from aspartame. [Ninety nine percent of monosodium glutamate 9MSG) is glutamic acid. The damage it causes is also documented in Blaylock's book.] Blaylock makes use of almost 500 scientific references to show how excess free excitatory amino acids such as aspartic acid and glutamic acid in our food supply are causing serious chronic neurological disorders and a myriad of other acute symptoms.(3) SUMMARY OF HOW ASPARTATE (AND GLUTAMATE) CAUSE DAMAGE Aspartate and glutamate act as neurotransmitters in the brain by facilitating the transmittion of information from neuron to neuron. Too much aspartate or glutamate in the brain kills certain neurons by allowing the influx of too much calcium into the cells. This influx triggers excessive amounts of free radicals which kill the cells. The neural cell damage that can be caused by excessive aspartate and glutamate is why they are referred to as "excitotoxins." They "excite" or stimulate the neural cells to death. Aspartic acid is an amino acid. Taken in its free form (unbound to proteins) it significantly raises the blood plasma level of aspartate and glutamate. The excess aspartate and glutamate in the blood plasma shortly after ingesting aspartame or products with free glutamic acid (glutamate precursor) leads to a high level of those neurotransmitters in certain areas of the brain. The blood brain barrier (BBB) which normally protects the brain from excess glutamate and aspartate as well as toxins 1) is not fully developed during childhood, 2) does not fully protect all areas of the brain, 3) is damaged by numerous chronic and acute conditions, and 4) allows seepage of excess glutamate and aspartate into the brain even when intact. The excess glutamate and aspartate slowly begin to destroy neurons. The large majority (75%+) of neural cells in a particular area of the brain are killed before any clinical symptoms of a chronic illness are noticed. A few of the many chronic illnesses that have been shown to be contributed to by long-term exposure excitatory amino acid damage include: Multiple sclerosis (MS), ALS, memory loss, hormonal problems, hearing loss, epilepsy, Alzheimer's disease, Parkinson's disease, hypoglycemia, AIDS dementia, brain lessions, and neuroendocrine disorders. The risk to infants, children, pregnant women, the elderly, and persons with certain chronic health problems from excitotoxins are great. Even the Federation of American Societies For Experimental Biology (FASEB), which usually understates problems and mimmicks the FDA party-line, recently stated in a review that "it is prudent to avoid the use of dietary supplements of L-glutamic acid by pregnant women, infants, and children. The Existence of evidence of potential endocrine responses, i.e., elevated cortisol and prolactin, and differential responses between males and females, would also suggest a neuroendocrine link and that supplemental L-glutamic acid should be avoided by women of childbearing age and individuals with affective disorders."(4) Aspartic acid from aspartame has the same deleterious effects on the body as glutamic acid. The exact mechanism of acute reactions to excess free glutamate and aspartate is currently being debated. As reported to the FDA, those reactions include:(5) Headaches/migraines, nausea, abdominal pains, fatigue (blocks sufficient glucose entry into brain), sleep problems, vision problems, anxiety attacks, depression, and asthma/chest tightness. One common complaint of persons suffering from the effect of aspartame is memory loss. Ironically, in 1987, G.D. Searle, the manufacturer of aspartame, undertook a search for a drug to combat memory loss caused by excititory amino acid damage. Blaylock is one of many scientists and physicians who are concerned about excititory amino acid damage caused by ingestion of aspartame and MSG. A few of the many experts who have spoken out against the damage being caused by aspartate and glutamate include Adrienne Samuels, Ph.D., an experimental psychologist specializing in research design. Another is Olney, a professor in the department of psychiatry, School of Medicine, Washington University, a neuroscientist and researcher, and one of the world's foremost authorities on excitotoxins. (He informed Searle in 1971 that aspartic acid caused holes in the brain of mice.) Also included is Francis J. Waickman, M.D., a recipient of the Rinkel and Forman Awards, and Board certified in Pediatrics, Allergy, and Immunology. Other concerned scientists include: John R. Hain, M.D., Board Certified Forensic Pathologist, and H.J. Roberts, M.D., FACP, FCCP, Diabetic Specialist, and selected by a national medical publication as "The Best Doctor in the US" John Samuels is concerned, also. He compiled a list of scientific research sufficient to show the dangers of ingesting excess free glutamic and aspartic acid. And there are many more who can be added to this long list. PHENYLALANINE (50% OF ASPARTAME) Phenylalanine is an amino acid normally found in the brain. Persons with the genetic disorder, phenylketonuria (PKU) cannot metabolize phenylalanine. This leads to dangerously high levels of phenylalanine in the brain (sometimes lethal). It has been shown that ingesting aspartame, especially along with carbohydrates can lead to excess levels of phenylalanine in the brain even in persons who do not have PKU. This is not just a theory, as many people who have eaten large amounts of aspartame over a long period of time and do not have PKU have been shown to have excessive levels of phenylalanine in the blood. Excessive levels of phenylalanine in the brain can cause the levels of seratonin in the brain to decrease, leading to emotional disorders such as depression. It was shown in human testing that phenylalanine levels of the blood were increased significantly in human subjects who chronically used aspartame.(6) Even a single use of aspartame raised the blood phenylalanine levels. In his testimony before the US Congress, Dr Louis J. Elsas showed that high blood phenylalanine can be concentrated in parts of the brain, and is especially dangerous for infants and fetuses. He also showed that phenylalanine is metabolised much more effeciently by rodents than by humans.(7) One account of a case of extremely high phenylalanine levels caused by aspartame was recently published the the "Wednesday Journal" in an article entitled "An Aspartame Nightmare." John Cook began drinking 6 to 8 diet drinks every day. His symptoms started out as memory loss and frequent headaches. He began to crave more aspartame-sweetened drinks. His condition deteriorated so much that he experienced wide mood swings and violent rages. Even though he did not suffer from PKU, a blood test revealed a phenylalanine level of 80 mg/dl. He also showed abnormal brain function and brain damage. After he kicked his aspartame habit, his symptoms improved dramatically.(8) As Blaylock points out in his book, early studies measuring phenylalanine buildup in the brain were flawed. Investigators who measured specific brain regions and not the average throughout the brain notice significant rises in phenylalanine levels. Specifically the hypothalamus, medulla oblongata, and corpus striatum areas of the brain had the largest increases in phenylalanine. Blaylock goes on to point out that excessive buildup of phenylalanine in the brain can cause schizophrenia or make one more susceptible to seizures. Therefore, long-term, excessive use of aspartame may provided a boost to sales of seratonin reuptake inhibitors such as Prozac and drugs to control schizophrenia and seizures. METHANOL (AKA WOOD ALCOHOL/POISON) (10% OF ASPARTAME) Methanol/wood alcohol is a deadly poison. Some people may remember methanol as the poison that has caused some "skid row" alcoholics to end up blind or dead. Methanol is gradually released in the small intestine when the methyl group of aspartame encounter the enzyme chymotrypsin. The absorption of methanol into the body is sped up considerably when free methanol is ingested. Free methanol is created from aspartame when it is heated to above 86 Fahrenheit (30 Centigrade). This would occur when aspartame-containing product is improperly stored or when it is heated (e.g., as part of a "food" product such as Jello). Methanol breaks down into formic acid and formaldehyde in the body. Formaldehyde is a deadly neurotoxin. An EPA assessment of methanol states that methanol "is considered a cumulative poison due to the low rate of excretion once it is absorbed. In the body, methanol is oxidized to formaldehyde and formic acid; both of these metabolites are toxic." The recommend a limit of consumption of 7.8 mg/day. A one-liter (approx. 1 quart) aspartame-sweetened beverage contains about 56 mg of methanol. Heavy users of aspartame-containing products consume as much as 250 mg of methanol daily or 32 times the EPA limit.(9) Symptoms from methanol poisoning include headaches, ear buzzing, dizziness, nausea, gastrointestinal disturbances, weakness, vertigo, chills, memory lapses, numbness and shooting pains in the extremities, behavioral disturbances, and neuritis. The most well knowm problems from methanol poisoning are vision problems including misty vision, progressive contraction of visual fields, blurring of vision, obscuration of vision, retinal damage, and blindness. Formaldehye is a known carcinogen, causes retinal damage, interferes with DNA replication, causes birth defects.(10) Due to the lack of a couple of key enzymes, humans are many times more sensitive to the toxic effects of methanol than animals. Therefore, tests of aspartame or methanol on animals do not accurately reflect the danger for humans. As pointed out by Dr Woodrow C. Monte, Director of the Food Science and Nutrition Laboratory at Arizona State University, "There are no human or mammalian studies to evaluate the possible mutagenic, teratogenic, or carcinogenic effects of chronic administration of methyl alcohol."(11) He was so concerned about the unresolved safety issues that he filed suit with the FDA requesting a hearing to address these issues. He asked the FDA to "slow down on this soft drink issue long enough to answer some of the important questions. It's not fair that you are leaving the full burden of proof on the few of us who are concerned and have such limited resources. You must remember that you are the American public's last defense. Once you allow usage (of aspartame) there is literally nothing I or my colleagues can do to reverse the course. Aspartame will then join saccharin, the sulfiting agents, and God knows how many other questionable compounds enjoined to insult the human constitution with governmental approval."(10) Shortly thereafter, the Commissioner of the FDA, Arthur Hull Hayes, Jr., approved the use of aspartame in carbonated beverages, he then left for a position with G.D. Searle's Public Relations firm.(11) It has been pointed out that some fruit juices and alcoholic beverages contain small amounts of methanol. It is important to remember, however, that methanol never appears alone. In every case, ethanol is present, usually in much higher amounts. Ethanol is an antidote for methanol toxicity in humans.(9) The troops of Desert Storm were "treated" to large amounts of aspartame-sweetened beverages which had been heated to over 86o F. in the Saudi Arabian sun. Many of them returned home with numerous disorders similar to what has been seen in persons who have been chemically poisoned by formaldehyde. The free methanol in the beverages may have been a contributing factor in these illnesses. Other breakdown products of aspartame such as DKP (discussed below) may also have been a factor. In a 1993 act that can only be described as "unconscionable," the FDA approved aspartame as an ingredient in numerous food items that would always be heated to above 86F (30C). DIKETOPIPERAZINE (DKP) DKP is a by-product of aspartame metabolism. DKP has been implicated in the occurance of brain tumors. Olney noticed that DKP, when nitrosated in the gut, produced a compound which was similar to N-nitrosourea, a powerful brain tumor causing chemical. Some authors have said that DKP is produced after aspartame ingestion. I am not sure if that is correct. It is definately true that DKP is formed in liquid aspartame-containing products during prolonged storage. G.D. Searle conducted animal experiments on the safety of DKP. The FDA found numerous experimental errors occured, including "clerical errors, mixed-up animals, animals not getting drugs they were supposed to get, pathological specimens lost because of improper handling," and many other errors.(12) These sloppy laboratory procedures may explain why both the test and control animals had sixteen times more brain tumors than would be expected in experiments of this length. In an ironic twist, shortly after these experimental errors were discovered, the FDA used guidelines recommened by G.D. Searle to devlop the Industry-wide FDA standards for Good Laboratory Practies.(11) DKP has also been implicated as a cause of uterine polyps and changes in blood cholesterol by FDA Toxicologist Dr Jacqueline Verrett in her testimony before the US Senate.(13) AILMENTS RESULTING FROM ASPARTAME The components of aspartame can lead to a wide variety of ailments. Some of these problems occur gradually, others are immediate, acute reactions. There is an enormous population of people who are suffering from symtpoms contributed to by aspartame, yet they have no idea why herbs or drugs are not helping relieve their problems. There are other users of aspartame who appear not to be suffering immediate reactions to aspartame. But even these individuals are susceptible to the long-term damage caused by excitatory amino acids, phenylalanine, methanol, and DKP. A few of the many disorders that are of particular concern to me include the following. Birth Defects. Dr Diana Dow Edwards, a researcher was funded by Monsanto to study possible birth defects caused by the ingestion of aspartame. After preliminary data showed damaging information about aspartame, funding for the study was cut off. A Gentetic Pediatrician at Emory University has testified that aspartame is causing birth defects.7360-367. In the book, While Waiting: A Prenatal Guidebook by George R. Verrilli, M.D. and Anne Marie Mueser, it is stated that aspartame is suspected of causing brain damage in sensitive individuals. A fetus may be at risk for these effects. Some researchers have suggested that high doses of aspartame may be associated with problems ranging from dizziness and subtle brain changes to mental retardation. Cancer (Brain Cancer). In 1981, Satya Dubey, an FDA statistician, stated that the brain tumor data on aspartame was so "worrisome" that he could not recommend approval of NutraSweet.(14) In a two-year study conducted by the manufacturer of aspartame, twelve of the 320 rats fed a normal diet and aspartame developed brain tumors while none of the control rats had tumors. Five of the twelve tumors were in rats given a low dose of aspartame.(15) The approval of aspartame was a violation of the Delaney Amendment which was supposed to prevent cancer-causing substances such as methanol (formaldehye) and DKP from entering our food supply. The late Dr Adrian Gross, an FDA toxicologist, testified before the US Congress that aspartame was capable of producing brain tumors. This made it illegal for the FDA to set an allowable daily intake at any level. He stated in his testimony that Searle's studies were "to a large extent unreliable" and that "at least one of those studies has established beyond any reasonable doubt that aspartame is capable of inducing brain tumors in experimental animals...." He concluded his testimony by asking, "What is the reason for the apparent refusal by the FDA to invoke for this food additive the so-called Delaney Amendment to the Food, Drug and Cosmetic Act? .... And if the FDA itself elects to violate the law, who is left to protect the health of the public?"(16) In the mid-1970s it was discovered that the manufacturer of aspartame falsified studies in several ways. One of the techniques used was to cut tumors out of test animals and put them back in the study. Another technique used to falsify the studies was to list animals that had actually died as surviving the study. Thus, the data on brain tumors was likely worse than discussed above. In addition, a former employee of the manufacturer of aspartame, Raymond Schroeder told the FDA on July 13, 1977 that the particles of DKP were so large that the rats could dicriminate between the DKP and their normal diet.(12) It is interesting to note that the incidence of brain tumors in persons over 65 years of age has increase 67% between the years 1973 and 1990. Brain tumors in all age groups has jumped 10%. The greatest increase has come during the years 1985-1987.(17) In his book, Aspartame (NutraSweet). Is it Safe?, Roberts gives evidence that aspartame can cause a particularly dangerous form of cancer - primary lymphoma of the brain. Diabetes. The American Diabetes Association (ADA) is actually recommending this chemical poison to persons with diabetes. According to research conducted by H.J. Roberts, a diabetes specialist, a member of the ADA, and an authority on artificial sweetners, aspartame: 1) Leads to the precipitation of clinical diabetes. 2) Causes poorer diabetic control in diebetics on insulin or oral drugs. 3) Leads to the aggravation of diabetic complications such as retinopathy, cataracts, neuropathy and gastroparesis. 4) Causes convulsions. In a statement concerning the use of products containing aspartain by persons with diabetes and hypoglycemia, Roberts says: "Unfortunately, many patients in my practice, and others seen in consultation, developed serious metabolic, neurologic and other complications that could be specifically attributed to using aspartame products. This was evidenced by: "The loss of diabetic control, the intensification of hypoglycemia, the occurrence of presumed 'insulin reactions' (including convulsions) that proved to be aspartame reactions, and the precipitation, aggravation or simulation of diabetic complications (especially impaired vision and neuropathy) while using these products. "Dramatic improvement of such features after avoiding aspartame, and the prompt predictable recurrence of these problems when the patient resumed aspartame products, knowingly or inadvertently." Roberts goes on to say: "I regret the failure of other physicians and the American Diabetes Association (ADA) to sound appropriate warnings to patients and consumers based on these repeated findings which have been described in my corporate-neutral studies and publications." Blaylock stated that excitotoxins such as that found in aspartame can precipitate diabetes in persons who are genetically susceptible to the disease.(5) Emotional Disorders. A double blind study of the effects of aspartame on persons with mood disorders was recently conducted by Dr Ralph G. Walton. Since the study wasn't funded/controlled by the makers of aspartame, The NutraSweet Company refused to sell him the aspartame. Walton was forced to obtain and certify it from an outside source. The study showed a large increase in serious symptoms for persons taking aspartame. Since some of the symptoms were so serious, the Institutional Review Board had to stop the study. Three of the participants had said that they had been "poisoned" by aspartame. Walton concludes that "individuals with mood disorders are particularly sensitive to this artificial sweetener; its use in this population should be discouraged."(18) Aware that the experiment could not be repeated because of the danger to the test subjects, Walton was recently quoted as saying, "I know it causes seizures. I'm convinced also that it definitely causes behavioral changes. I'm very angry that this substance is on the market. I personally question the reliability and validity of any studies funded by the NutraSweet Company."(19) There are numerous reported cases of low brain serotonin levels, depression and other emotional disorders that have been linked to aspartame and often are relieved by stopping the intake of aspartame. Researchers have pointed out that increasing in phenylalanine levels in the brain, which can and does occur in persons without PKU, leads to a decreased level of the neurotransmitter, serotonin, which leads to a variety of emotional disorders. Dr William M. Pardridge of UCLA testified before the US Senate that a youth drinking four 16-ounce bottles of diet soda per day leads to an enormous increase in the phenylalanine level. Epilepsy/Seizures. With the large and growing number of seizures caused by aspartame, it is sad to see that the Epilepsy Foundation is promoting the "safety" of aspartame. At Massachusetts Institute of Technology, 80 people who had suffered seizures after ingesting aspartame were surveyed. Community Nutrition Institute concluded the following about the survey: "These 80 cases meet the FDA's own definition of an imminent hazard to the public health, which requires the FDA to expeditiously remove a product from the market." Both the Air Force's magazine Flying Safety and the Navy's magazine, Navy Physiology published articles warning about the many dangers of aspartame including the cumlative deliterious effects of methanol and the greater likelihood of birth defects. The articles note that the ingestion of aspartame can make pilots more susceptible to seizures and vertigo. Twenty articles sounding warnings about ingesting aspartame while flying have also appeared in the National Business Aircraft Association Digest (NBAA Digest 1993), Aviation Medical Bulletin (1988), The Aviation Consumer (1988), Canadian General Aviation News (1990), Pacific Flyer (1988), General Aviation News (1989), Aviation Safety Digest (1989), and Plane & Pilot (1990) and a paper warning about aspartame was presented at the 57th Annual Meeting of the Aerospace Medical Association (Gaffney 1986). Recently, a hotline was set up for pilots suffering from acute reactions to aspartame ingestion. Over 600 pilots have reported symptoms including some who have reported suffering grand mal seizures in the cockpit due to aspartame.(21) One of the original studies on aspartame was performed in 1969 by an independent scientist, Dr Harry Waisman. He studied the effects of aspartame on infant primates. Out of the seven infant monkeys, one died after 300 days and five others had grand mal seizures. Of course, these negative findings were not submitted to the FDA during the approval process.(22) Why don't we hear about these things? The reason many people do not hear about serious reactions to aspartame is twofold: 1) Lack of awareness by the general population. Aspartame-caused diseases are not reported in the newspapers like plane crashes. This is because these incidents occur one at a time in thousands of different locations across the US. 2) Most people do not associate their symptoms with the long-term use of aspartame. For the people who have killed a significant percentage of the brain cells and thereby caused a chronic illness, there is no way that they would normally associate such an illness with aspartame consumption. How aspartame was approved is a lesson in how chemical and pharmaceutical companies can manipulate government agencies such as the FDA, "bribe" organizations such as the American Dietetic Association, and flood the scientific community with flawed and fraudulent industry- sponsored studies funded by the makers of aspartame. Erik Millstone, a researcher at the Science Policy Research Unit of Sussex University has compiled thousands of pages of evidence, some of which have been obtained using the freedom of information act 23, showing: 1. Laboratory tests were faked and dangers were concealed. 2. Tumors were removed from animals and animals that had died were "restored to life" in laboratory records. 3. False and misleading statements were made to the FDA. 4. The two US Attorneys given the task of bringing fraud charges against the aspartame manufacturer took positions with the manufacturer's law firm, letting the statute of limitations run out. 5. The Commissioner of the FDA overruled the objections of the FDA's own scientific board of inquiry. Shortly after that decision, he took a position with Burson-Marsteller, the firm in charge of public relations for G.D. Searle. A Public Board of Inquiry (PBOI) was conducted in 1980. There were three scientists who reviewed the objections of Olney and Turner to the approval of aspartame. They voted unanimously against aspartame's approval. The FDA Commissioner, Dr Arthur Hull Hayes, Jr. then created a 5-person Scientific Commission to review the PBOI findings. After it became clear that the Commission would uphold the PBOI's decision by a vote of 3 to 2, another person was added to the Commission, creating a deadlocked vote. This allowed the FDA Commissioner to break the deadlock and approve aspartame for dry goods in 1981. Dr Jacqueline Verrett, the Senior Scientist in an FDA Bureau of Foods review team created in August 1977 to review the Bressler Report (a report that detailed G.D. Searle's abuses during the pre-approval testing) said: "It was pretty obvious that somewhere along the line, the bureau officials were working up to a whitewash." In 1987, Verrett testified before the US Senate stating that the experiments conducted by Searle were a "disaster." She stated that her team was instructed not to comment on or be concerned with the overall validity of the studies. She stated that questions about birth defects have not been answered. She continued her testimony by discussing the fact that DKP has been shown to increase uterine polyps and change blood cholesterol and that increasing the temperature of the product leads to an increase in production of DKP.(13) Revolving doors The FDA and the manufacturers of aspartame have had a rovolving door of employment for many years. In addition to the FDA Commissioner and two US Attorneys leaving to take positions with companies connected with G.D. Searle, four other FDA officials connected with the approval of aspartame took positions connected with the NutraSweet industry between 1979 and 1982 including the Deputy FDA Commissioner, the Special Assistant to the FDA Commissioner, the Associate Director of the Bureau of Foods and Toxicology and the Attorney involved with the Public Board of Inquiry.(24) It is important to realize that this type of revolving-door activity has been going on for decades. The Townsend Letter for Doctors (11/92) reported on a study revealing that 37 of 49 top FDA officials who left the FDA took positions with companies they had regulated. They also reported that over 150 FDA officials owned stock in drug companies they were assigned to manage. Many organizations and universities receive large sums of money from companies connected to the NutraSweet Association, a group of companies promoting the use of aspartame. In January 1993, the American Dietetic Association received a US$75,000 grant from the NutraSweet Company. The American Dietetic Association has stated that the NutraSweet Company writes their "Facts" sheets.(25) Many other "independent" organizations and researchers receive large sums of money from the manufacturers of aspartame. The American Diabetes Association has received a large amount of money from Nutrasweet, including money to run a cooking school in Chicago (presumably to teach diabetes how to use Nutrasweet in their cooking). A researcher in New England who has pointed out the dangers of aspartame in the past is now a Monsanto consultant. Another researcher in the Southeastern US had testified about the dangers of aspartame on fetuses. An investigative reporter has discovered that he was told to keep his mouth shut to avoid causing the loss of a large grant from a diet cola manufacturer in the NutraSweet Association. What is the FDA doing to protect the consumer from the dangers of aspartame? Less than nothing. In 1992, the FDA approved aspartame for use in malt beverages, breakfast cereals, and refrigerated puddings and fillings. In 1993 the FDA approved aspartame for use in hard and soft candies, non-alcoholic favored beverages, tea beverages, fruit juices and concentrates, baked goods and baking mixes, and frostings, toppings and fillings for baked goods. In 1991, the FDA banned the importation of stevia. The powder of the leaf has been used for hundreds of years as an alternative sweetner. It is used widely in Japan with no adverse effects. Scientists involved in reviewing stevia have declared it to be safe for human consumption - something which has been well known in many parts of the world where it is not banned. Everyone that I have spoken with in regards to this issue believes that stevia was banned to keep the product from taking hold in the US and cutting into sales of aspartame.(26) What is the US Congress doing to protect the consumer from the dangers of aspartame? Nothing. What is the US Administration (President) doing to protect the consumer from the dangers of aspartame? Nothing. Aspartame consumption is not only a problem in the US. It is being sold in over 70 countries throughout the world. ASPARTAME CAN BE FOUND IN: - instant breakfasts - breath mints - cereals - sugar-free chewing gum - cocoa mixes - coffee beverages - frozen desserts - gelatin desserts - juice beverages - laxatives - multivitamins - milk drinks - pharmaceuticals and supplements - shake mixes - soft drinks - tabletop sweeteners - tea beverages - instant teas and coffees - topping mixes - wine coolers - yogurt I have been told that aspartame has been found in products where it is not listed on the label. One must be particular careful of pharmaceuticals and supplements. I have been informed that even some supplements made by well-known supplement manufacturers such as Twinlabs contain aspartame. The information I have related above is just the tip of the iceberg as far as damaging information about aspartame. In order for the reader to find out more, I have included some resources below. BOOKS » Blaylock, Russell L., Excitotoxins: The Taste That Kills (Health Press, Santa Fe, New Mexico, c1994). One of the best books available on excitotoxins. Well worth reading! » H. J. Roberts, M.D., Aspartame (NutraSweet), Is it Safe? Available from the Aspartame Consumer Safety Network. » Sweet'ner Dearest, Available from the Aspartame Consumer Safety Network » Mary Nash Stoddard, The Deadly Deception, Available from the Aspartame Consumer Safety Network. » Barbara Mullarkey, Editor, Bittersweet Aspartame - A Diet Delusion, » Available from the Aspartame Consumer Safety Network. » The Aspartame Consumer Safety Network, The Aspartame Consumer Safety Network Synopsis. » Dennis Remington, M.D. and Barbara Higa, R.D., The Bitter Truth About Artificial Sweetners, Available from the Aspartame Consumer Safety Network ««««««««««««««««««««««««««««««««««««««««»»»»»»»»»»»»»»»»»»»»»»»»»»»»»»» REFERENCES (1) Department of Health and Human Services, Report on All Adverse Reactions in the Adverse Reaction Monitoring System, (February 25 and 28, 1994). (2) Compiled by researchers, physicians, and artificial sweetner experts for Mission Possible, a group dedicated to warning consumers about aspartame. (3) Excitotoxins: The Taste That Kills, by Russell L. Blaylock, M.D. (4) Safety of Amino Acids, Life Sciences Research Office, FASEB, FDA Contract No. 223-88-2124, Task Order No. 8. (5) FDA Adverse Reaction Monitoring System. (6) Wurtman and Walker, "Dietary Phenylalanine and Brain Function," Proceedings of the First International Meeting on Dietary Phenylalanine and Brain Function., Washington, D.C., May 8, 1987. (7) Hearing Before the Committee On Labor and Human Resources United States Senate, First Session on Examing the Health and Safety Concerns of Nutrasweet (Aspartame). (8) Account of John Cook as published in Informed Consent Magazine. "How Safe Is Your Artificial Sweetner" by Barbara Mullarkey, September/October 1994. (9) Woodrow C. Monte, Ph.D., R.D., "Aspartame: Methanol and the Public Health," Journal of Applied Nutrition, 36 (1): 42-53. (10) US Court of Appeals for the District of Columbia Circuit, No. 84- 1153 Community Nutrition Institute and Dr Woodrow Monte v. Dr Mark Novitch, Acting Commissioner, US FDA (9/24/85). (11) Aspartame Time Line by Barbara Mullarkey as published in Informed Consent Magazine, May/June 1994. (12) FDA Searle Investigation Task Force. "Final Report of Investigation of G.D. Searle Company." (March 24, 1976) (13) Testimony of Dr Jacqueline Verrett, FDA Toxicologist before the US Senate Committee on Labor and Human Resources, (November 3, 1987). (14) Internal FDA memorandum. (15) Analysis prepared by Dr John Olney as a statement before the Aspartame Board of Inquire of the FDA. Also Excitotoxins by Russell Blaylock, M.D. (16) Congressional Record SID835: 131 (August 1, 1985) (17) National Cancer Institute SEER Program Data. (18) Walton, Ralph G., Robert Hudak, Ruth Green-Waite "Adverse Reactions to Aspartame: Double-Blind Challenge in Patients from a Vulnerable Population," Biological Psychiatry, 1993:34:13-17. (19) Barbara Mullarkey, "How Safe Is Your Artificial Sweetner," September/October 1994 issue of Informed Consent Magazine. (20) US Air Force. "Aspartame Alert." Flying Safety, 48 (5): 20-21 (May 1992). (21) Reported by the Aspartame Consumer Safety Network. (22) Barbara Mullarkey, Bittersweet Aspartame, A Diet Delusion. (23) Millstone, Eric "Sweet and Sour." The Ecologist, 25 (March/April 1994). (24) Mary Nash Stoddard, Editor, "The Deadly Deception," Aspartame Consumer Safety Network. (25) ADA Courier, January 1993, Volume 32, Number 1. (26) "FDA Rejects AHPA Stevia Petition" by Mark Blumenthal, Whole Foods, April 1994. temperature of 110oF could reach temperatures of 38oC (101oF) to 39oC (103oF) (0.92-0.94 x 110oF). "Overall, the study, considered together with representative historical temperature data show that soft drinks will frequently be exposed to temperatures of 32oC (90oF) to 49oC (120oF). In some cases product temperatures as high as 66oC (151oF) (especially in the southwestern United States) can be reached. "The effects of these high product temperatures on [aspartame] degradation and the formation of degradation products, and the effects of temperature variation (for example, soft drinks displayed at a service station may reach temperatures of 49oC (120oF) for most of the afternoon, drop in temperature overnight, and heat up again during the following day) cannot be determined from the data submitted by Searle to the FDA." When aspartame in liquid is subjected to high temperatures, the breakdown of aspartame and the formation of large amounts of DKP happens very quickly as shown by Prudel (1986). In addition, Boehm and Bada showed that high tempatures can cause racemization of the free amino acids leading to significant amounts of unnatural D-type amino acids-- much more than is produced through cooking normal, healthy foods (Boehm 1984). Gaines (1987) also showed that racemization can occur in the breakdown products of aspartame. The health affects of large amounts of these D-type amino acids are not well known. In a statement submitted to the U.S. Senate hearings on aspartame, Dr. Jeffrey Bada had this to say about aspartame decomposition (Bada 1987): "Aspartame, a dipeptide containing the amino acids phenylalanine and aspartic acid, is prone to a number of decomposition/alteration reactions. Dominant are cyclization to the cyclic dipeptide or diketopiperazine [DKP] and stereochemical (racemization) inversion producing the unnatural D-stereoisomers of the amino acids. .. In some instances, however, these reactions are very significant, and the reaction products which are produced are not well-studied as far as their nutritional/toxicological properties are concerned. Some examples where these reactions could be significant are in soft drinks exposed to warm temperatures for prolonged periods and in consumer misuse of aspartame such as in cooking or baking." In an article for the Wednesday Journal, Jeffrey Bada, Ph.D. discusses some of his concerns relating to the chemical rearrangement of aspartame (Mullarkey 1992, page 10): "The chemistry of aspartame is changed when Boiled," says Bada. "There is internal rearrangement of its structure. The L-isomers of phenylalanine and aspartic acid change to unnatural D-isomers which are metabolized differently. How it is metabolized is anybody's guess. "Searle people," Bada Continues, "tend to dismiss stereo chemical inversion as unimportant. Chris Tschanz, director of aspartame clinical research, and Louis D. Stegnik, M.D. of the University of Iowa College of Medicine, visited me and admitted that nobody thought of looking at aspartame the way we did." In 1993, the FDA approved aspartame for use in tea beverages, baked goods and mixes, frostings and toppings (Mullarkey 1994a, page 51). There are many products on the market which contain aspartame and are heated to high temperatures. Therefore, Dr. Bada's comment of aspartame's "misuse" in cooking or baking no longer applies--it is now a condoned use of aspartame. Beta-aspartame is another breakdown product which has been found in aspartame-containing products which may contribute to health problems in some individuals (Lawrence 1987, Stamp 1989b). The fact that it occurs in small amounts does not necessarily mean that it is harmless. It has been shown that aspartame can react with other food additives to form chemicals of unknown health consequences. Hussein showed that aspartame reacts with aldehydes which are commonly found flavor compounds in sodas and chewing gum (Hussein 1984). Cha has shown that aspartame can react with vanillin used in foods (Cha 1988). These reactions are very important considerations. As an example of how additive reactions can cause the formation of toxic substances, researchers tested three different food additives individually on mice. None of the mice reacted negatively. When the three food additives were tested in pairs, the mice became ill. When all three food additives were tested at once, the mice died (Ershoff 1976). Aspartame In Solid Food Products Graves showed that in a dried and acidified state, aspartame that is heated to 230oF breaks down into its components as described above (Graves 1987). It was also shown that other, previously unknown degredation products are formed when the dried product is heated to high temperatures. This type of aspartame breakdown would occur in baking goods that contain aspartame. Conclusion Aspartame-containing products which are ingested in the real-world are chemically very different than 98-100% aspartame which is given in laboratory experiments. The large amount of breakdown products such as DKP, free phenylalanine, methanol, and others may play an important role in aspartame's negative health affects. Aspartame's strong tendancy to react with other food ingredients to form unique chemical compounds and the tendancy of the free amino acids to racemize at high temperatures are also very important considerations regarding its toxicity. Please keep this in mind while you read the rest of this review. What people are ingesting in the real world IS NOT the same aspartame as it was originally put into the food, but a very different and possibly much more dangerous toxic chemical soup. 2. Average Daily Intake of Aspartame The article states: "The replacement of all sweeteners with aspartame has been estimated to yield an intake of 867 mg of aspartame/day, which translates to only 87 mg of methanol." Before we can discuss aspartame toxicity, it is crucial to set the record straight regarding aspartame intake. The statement in the article has three problems: a. The increasing use of aspartame has not lead to a decreased use in caloric sweeteners. According to the U.S. Department of Agriculture, the per capita consumption of aspartame quadrupled between the years 1983 and 1988 (USDA 1988). Since that time, the use of aspartame has continued to increase. Dr. H.J. Roberts reported on Wall Street Journal articles which stated that "the diet beverage market was increasing at a rate of 20-25% annually" and that "consumers began drinking up to six times as many diet drinks as those using sugared sodas." (WSJ 1988, WSJ 1989) Gregory Gordon wrote in a UPI Investigation that "Roy Burry, an analyst with Kidder-Peabody, Inc., said the exploding diet market now accounts for 24 percent of soft drink sales, compared with 10 percent in the late 1970s, and is growing at 20 to 25 percent a year (Gordon 1987, page 484 of US Senate 1987). From 1982 to 1988, the per capita consumption of caloric sweeteners jumped from 123.2 pounds to 133.5 pounds per year. Therefore the increased use of aspartame has not decreased the use of caloric sweetener products in the United States (USDA 1988). b. Studies have shown that when their diet is not closely monitored, many people use artificial sweeteners in addition to sugar products and not instead of sugar products (Chen 1991, Stellman 1986). Therefore, an increased use of aspartame will not necessarily alter the sugar-craving feeding behavior of the majority of persons. If they consume a non- sugar, aspartame-containing beverage at one point in the day, they will simply make up for the lack of sugar at some other point in the day. Some studies have shown an increased consumption of sugar due to aspartame (Blundell 1986). In fact, Stellman showed that outside the confines of the highly structured, supervised environment, the subjects he surveyed who choose to use artificial sweeteners actually gained weight. Roberts (1988) showed in his survey of people outside of the laboratory that 5% of the people reported adverse reactions had extreme weight loss when using aspartame and tended towards anorexia. He also noted that 6% of the respondants had a unexplained weight gain which averaged 19 pounds! c. Since diet products with aspartame have few calories and since many people have been conned into believing that they are safe, a significant percentage of people would likely "throw caution to the wind," by drinking large quantities of diet soft drinks and eating large quantities of other products with aspartame. This is something that they would not be as likely to do with high-calorie, sugar-containing products. The NutraSweet Company has been trying to convince people that persons who ingesting aspartame regularly ingest only 1-3 mg/kg (of body weight)/day of aspartame (Butchko 1991, Abrams 1992). This is based on surveys and diaries of consumers. What these surveys do not mention is that aspartame-containing products are often ingested as part of snacks and that people often forget what snacks they've eaten. This was aptly described by Dr. Richard Wurtman of MIT in a meeting with FDA officials on April 21, 1986 (Lisa 1994, page 201): "[NutraSweet's estimates of current use] show, among other things, that people consume less aspartame in the summer than in other months, a finding which violates good sense and reason. (This probably reflects the fact -- affirmed in our laboratories at MIT -- that people have much more difficulty accurately remembering snack than meal intakes . . . and most of the aspartame in the American diet comes via cold beverages and other snack foods.)" Another set of similar surveys shows that persons living in Canada (7- day survey) have more than 2.5 times the daily intake of aspartame than persons living in the U.S. (at the 90th percentile level of consumption). This is ridiculous because aspartame ingestion (the bulk of which comes from cold diet beverages) in warm climates would almost certainly be much larger than in cold climates. In addition, it appears that it is mathematically impossible for Canada to have an equal per capita aspartame consumption let alone a much greater per capita consumption. Aspartame net sales outside the U.S. amounts to only 10% of all net sales (Monsanto 1994) Canada's population is 10.8% of the U.S. population (CIA 1994). Therefore, Canada's per capita intake of aspartame cannot possibly be even equal to that in the U.S., even in the extremely unlikely scenerio where all aspartame sold outside the U.S. is sold only to Canada. (According to figures provided by the NutraSweet Company, the percentage of regular aspartame users in the United States and Canada are approximately the same (Farber 1989, page 56, Butchko 1991). Another preposturous claim can be seen in a paper by Butchko (1991). In this paper aspartame consumption for 6-12 year old children was shown to decrease significantly from 1984 (the year after aspartame was approved for use in carbonated beverages) to 1989 despite nearly tripling the sales of aspartame from the middle of 1984 to 1989. (USDA 1988, Monsanto 1990). By the time this survey began the percentage of regular aspartame eaters in this age category was approximately 25% (Abrams 1991) according to NutraSweet Company figures. The NutraSweet Company admits that the use of aspartame had not risen to over 50% of the U.S. population at that time (Farber 1989, page 56). Therefore, an increase in the percentage of regular aspartame users could not have possibly accounted for the bulk of the increase in sales. Who are they kidding!? It shows that these surveys cannot be trusted to show anything close to accurate figures. Perhaps another reason the average daily intake of aspartame from these surveys is so low is due to the way that the amount of aspartame ingested is calculated. For example, Abrams (1991) points out that what is recorded on these surveys is not the amount of aspartame ingested, but only "the number of times an APM [aspartame] containing item of food was eaten on that day by that person." This value is then multiplied by the "average number of grams per eating occasion of that food for a person of that age and sex group" to give the total number of milligrams of aspartame ingested. However, the "average number of grams per eating occasion of that food for a person of that age and sex group" is drawn from a 1977-1978 USDA National Food Consumption Survey. Therefore, the calculations for the total milligrams of aspartame ingested is based on an old survey which is probably equally inaccurate as far as snack food ingestion goes and is most likely out of date. For example, these calculations assume that the average person would ingest the exact same amount of soft drink or diet food per item 1977 as they would in 1994. With the skyrocketing popularity of one- and two-liter bottles of soft drinks and the marketing push for diet foods, this is a ridiculous assumption. By making this assumption, NutraSweet are skewing the per capita intake figures and are using this "information" to justify studies on very small amounts of aspartame. What the NutraSweet tries to show with flawed studies and surveys is often contradicted by other studies which they fund or by statements made by their representatives. In 1976, Frey showed that children who are 7 to 12 years old can have an aspartame intake anywhere from 35 mg/kg to 76 mg/kg per day when aspartame-containing snack food is notrestricted (Frey 1976) (Note: No aspartame capsules were administered to the 7-12 year-old children. Only the 13-21 year-old children received capsules.). Three studies on obese individuals showed that their aspartame intake averaged 20 mg/kg per day (ranging from 8 to 36 mg/kg per day) (Porikos 1984). The Frey study and the three studies by Porikos monitored aspartame intake much more closely than the surveys often quoted by NutraSweet researchers. Those surveys relied on the ability of people to remember their snacks. In an article from Science Times, Jane E. Brody states the following (Brody 1985): "The drug agency has set an allowable daily intake of 50 milligrams of aspartame per kilogram of body weight, and the agency predicted that actual average use would run around eight to ten milligrams. According to Dr. Gaull of Searle, levels of use found in a national survey last spring showed that the average was then already twice that--19 milligrams--and the maximum level consumed by 'aspartame abusers' was 28 milligrams. A United States attorney representing the F.D.A. said in court last month that average consumption is now 30 milligrams and that many consumers are above the 50 milligrams maxiumum suggested." Farber gave an example of what a typical aspartame consumption may be for a child (Farber 1989, page 146): "An 8-year-old of 20 kg, might eat the following: Cereal 250.0 mg Soda 200.0 mg Milkshake 350.0 mg Ice Pop 250.0 mg Total 1,050.0 mg of aspartame "This would equal 52.5 mg/kg of aspartame consumption....' [Note that even for a 60 kg adult, the above-listed example would amount to over 17 mg/kg per day.] On a hot Summer day, the child may ingest the aspartame listed above and several more carbonated beverages. There may be many children who are ingesting a full 2-liter bottle of pop during an active Summer day (1100 mgs. of aspartame). On top of that ingestion, there may be Jello, cereal, gum, and many other aspartame-containing foods. It is important to note that all aspartame-containing products of the same type do not contain the same amount of aspartame. For example, a one liter bottle of diet cola averages aproximately 560 mg of aspartame. However, orange soda contains as much as 930 mg of aspartame per liter (Federal Register 1984). In addition, the Tsang (1985) study showed that there may be an addition 10% or more amount of aspartame in the product than what is claimed by the manufacturer. Neuroscience researcher and Professor of Medicine at the University of California, Dr. William Partridge testified about the intake of aspartame before the U.S. Senate (Pardrige 1987): "The first question is the dosage problem. We are led to believe by the FDA this morning that the typical consumer will have 2 to 4 milligrams per kilogram of aspartame per day; that the 99th percentile intake is 34 milligrams per kilograms per day; and that the advisable daily intake or ADI is 50 milligrams per kilogram per day. "Now, the layperson sitting in the audience is really in no position to analyze these esoteric numbers. But if we put it in a different context and recognize that 50 milligrams per kilogram per day is equal to 5 servings of NutraSweet per 50- pound body weight, we can see that children,owing to their reduced body weight, are at a great risk for overconsumption of NutraSweet. "All one has to do in t his room is look up at that chart and ask yourself if a 50-pound or 60- pound 7 year-old is going to consume 5 or 6 servings of that per day. If they are, then they have consumed 50 milligrams per kilogram per day, or the advisable daily intake. "Now, an 11-year[-old] study in the literature has already shown this, that the average7-to-12-year- old, when made freely available to products like that, consumes 5 servings per 50-pound body weight per day, and up to 77 milligrams per kilogram per day." In the National Soft Drink Association's draft objection to use of aspartame in carbonated beverages it was stated (NSDA 1983): "FDA relied upon an intake value of 34 mg/kg/day in assessing the possible risks of aspartame, describing that level as the '. . . highest obtained from any estimate of potential consumption and exceed[ing] the 99th percentile consumption (25 mg/kg) for all age groups . . .' 48 Fed. Reg. at 31377. For a 30 kg child, however, it would not be unualual for that level to be achieved or, in terms of the effect on plasma PHE (phenylalanine) levels, even exceeded. For example, if a 30 kg child consumed on a warm day after exercise approximately two-thirds of a two- liter bottle of soft drink sweetened soley with aspartame, that child would be consuming 700 mg of aspartame, or approximately 23 mg/kg. This alone roughly equals what FDA considered, the 99th percentile consumption level. If during the day this child consumed other aspartame-sweetened products, the exposure level could quickly [reach] FDA's so called 'loading dose' of 34 mg/kg. 48 Fed. Reg. at 31377." Had the child in the above example consumed two-thirds of a two-liter bottle of aspartame-sweetened orange soda, the values could be as high as 1240 mg of aspartame or 41.3 mg/kg/day for a 30 kg child. Another way to look at intakes is to look at what a child may ingest in a single sitting. At the popular convenience store chain, 7-11, the drinks, "Big Gulp" and "Super Big Gulp" are popular items for both children and adults. A 30kg child purchasing a Big Gulp (32 ounces) of diet soda would ingest 510 mg to 846 mg of aspartame depending upon whether it was diet cola or diet orange. This works out to between 17 mg/kg or 28.2 mg/kg of aspartame in a single sitting! The same child purchasing a Super Big Gulp of diet soda would ingest 700 mg to 1162 mg of aspartame. This works out to 23.3 mg/kg or 38.7 mg/kg of aspartame in one sitting! As an adult who plays basketball outside in the warm whether, I know many people, including myself who can easily drink twice the amount of liquids as found in a Super Big Gulp in one sitting in order to prevent dehydration. What is generally agreed upon when discussing the intake amounts of aspartame is the following: The majority of aspartame users ingest much less than the FDA's Acceptible Daily Intake (ADI). When plotting milligrams per day of aspartame ingested against the percentage of U.S. population, a smaller percentage of the population will ingest the largest amounts. However, a regular, smaller dose of a neurotoxin such as aspartame is not necessarily safe and certainly not health-building. Dr. Roberts found many serious adverse effects from ingestion of aspartame at levels many times lower than the FDA's ADI (Roberts 1990a, page 71-72). The use of aspartame for a lifetime at even very small levels is foolish in my opinion. Looking a studies I have seen in the literature as well as USDA figures for artificial sweetener usage, I would estimate that the average person in the U.S. who ingests aspartame regularly ingests approximately 8 mg/kg per day. This is based on the following estimates: - Approximately 35% of the U.S. population (81 million people -- CIA 1994) are regular aspartame "eaters." Heybach (1988) showed that in adult women (a population likely to have a higher percentage of regular aspartame users than the general population), only 25% ingested aspartame in the survey. Since the survey was only a single day, I will give the NutraSweet Company the benefit of the doubt and assume 35% regular usage for the general population. The FDA submitted an aspartame intake survey to the U.S. Senate which admited that approximately 35% of the survey participants were regular consumers of aspartame (FDA PMS 1987). I do not believe the contrived NutraSweet Company estimates that more than 50% of the U.S. population uses aspartame regularly. - The average weight of regular aspartame users I estimate to be 50kg. This includes many thin women, adolescents, children, and infants who would tend to bring the average way down. - The amount of aspartame used in the U.S. in 1995 I estimate is 28 million pounds. McNamara (1995) stated that 20 million pounds will be sold in the U.S. in 1995. The author probably got that figure from the NutraSweet Company and does not realize that every "fact" spewed out by this company is suspect at best. Figures from the USDA (1988) showed that 7 million pounds were consumed in 1984 and approximately 17.1 million pounds were consumed in 1987 Given that aspartame is now in over 5,000 junk food products worldwide (Geha 1993, Trefz 1994) and was only in hundres of products in 1987, and given that diet beverage sales have increased tremendously in the last 8 years, an estimate of 28 million pounds is quite reasonable (This estimate is probably too low. The actual figure may be as high as 35 million pounds). It is possible to determine the average usage of aspartame in regular eaters using the following formula: (lbs * 1,000,000 mg/kg) / (2.2 kg/lbs. * days/year * # of eaters * kg/person) = 8.6 mg/kg/day for regular eaters. I realize that this is an estimate, but given how ridiculous the "results" of NutraSweet-connected surveys are, an estimate is better than nothing. I believe that at least 10 percent of regular aspartame users ingest at least 20 mg/kg per day. This may amount to over 8 million people in the U.S. I would estimate that nearly 1 percent of aspartame users ingest at least 50 mg/kg per day. This may amount to over 800,000 people. This group would most likely be mostly made up of children and young, adolescent girls due to their low body weight and high intake of junk foods. For many of these people, the warm and hot weather intake will far exceed their Winter intake, such that a person ingesting 20 mg/kg per day in the Winter may ingest 40 mg/kg per day in the hot Summer months. According to Dr. Woodrow Monte, Director of the Arizona State University Food Science and Nutrition Laboratory, a significant number of people in Arizona drink as much as two or three liters of diet soda every day during the Summer (Monte 1995). Even if we accept the FDA's projection that only 1% of the regular aspartame users will consume more than 34 mg/kg/day of aspartame, that still may amount to over 800,000 people. While the national average may be lower than 34 mg/kg/day of aspartame, there are undoubtedly several hundreds of thousands of people who are consuming well over 34 mg/kg/day of aspartame, especially on hot Summer days. NutraSweet researchers sometimes use the following ploy to try and convince gullible listeners that people cannot ingest over 20 mg/kg/day or approach a level of 50 mg/kg/day (despite their own studies which prove them wrong). They compare the amount of one single product that would need to be ingested by an adult male in order to reach these high levels (e.g., Rowen 1995). For exampe, they might say that it takes 100 packets of Equal or 19 cans of diet soda for a 70kg man to reach a dose of 50 mg/kg. First of all, not everyone is a 70kg man. Many people are 50kg women or 20-30kg children where the amount of aspartame required to reach a dose of 50 kg/mg is much less. Secondly, many people who put themselves at risk by ingesting aspartame do so using a wide variety of aspartame- containing "food" products such as soda, puddings, cereal, hot chocolate, coffee, tabletop sweeteners, gum toppings, supplements and pharmaceuticals, fruit drinks, etc. People abusing themselves with aspartame in this way can easily ingest hugh doses. Finally, even doses of only a few mg/kg/day is not safe in the long run. Some researchers try to argue that they can use much less than the current FDA Acceptable Daily Intake (ADI) in their experiments as long as they use a test dosage well above the average intake of aspartame as deterimined by these (flawed) surveys. Stegink states the following (Stegink 1989): "Initial consideration of these projected intakes might lead one to question their validity since 12 oz of aspartame-sweetened beverage ingested by a 27-kg 8-year-old child would account for 7.4 mg aspartame/kg body weight. However, when beverage intake data are examined, the projected aspartame intake values are consistent with these data. For example, Morgan et al reported that 7- to 8-year- old children ingest, on average 6.0 ± 4.2 oz soft drink daily (mean ± SD; value includes both regular and diet beverage) (Morgan 1985). Thus, an average 27-kg 8-year-old child would ingest 3.7 mg aspartame/kg body weight daily if all 6 oz of beverage were sweetened with aspartame. A 27-kg child ingesting beverage at 2 SD above the mean (approximately 97% of expected values) would ingest 14.4 oz of beverage. This would provide 8.9 mg aspartame/kg body weight if all beverage consumed was sweetened with aspartame. Therefore, young children would have to drink unusually large quantities of beverage to ingest much larger quantities of aspartame." What Stegink neglects to mention is the following: 1. The study cited by Stegink (Morgan 1985), does not take into account that, as Dr. Wurtman stated, snacks are commonly forgotten in daily food surveys so that the average ingestion of soft drinks would likely be much greater. 2. The study cited by Stegink uses data from a three-day survey instead of the more accurate seven-day survey. 3. The study cited by Stegink was published in 1985. This study was an evaluation of data from the 1977-78 Nationalwide Food Consumption Survey. Thus, the data was over ten years old when Stegink cited it and is now over 16 years old! Anyone adult in the U.S. who was not in a coma for the last 16 years knows that soft drink consumption has increased tremendously since the late 1970s. 4. Stegink neglects to mention that there are thousands of products with aspartame and that 7- to 8-year-old children can be ingesting significant amounts from foods and beverages other than soft drinks. 5. While the average intake may be relatively low, although much higher than reported by Stegink and not necessary safe, there are undoubtedly a significant number of 7-to 8-year old children who are ingesting large quantities of aspartame by their own choice or by the choice of their parents to avoid sugar. It is ridiculous to use the "average" (even if it was accurately determined) to judge test amounts of aspartame. Conclusion NutraSweet-written survey summaries show a negligable increase in daily aspartame consumption since 1983. Aspartame sales has skyrocketed since 1983. Therefore, the numbers from these surveys which are flawed as described by Dr. Richard Wurtman above, do not make any sense and should be ignored until large, well-designed surveys are conducted separate from the influence of the NutraSweet Company. Until that time, estimates of average consumption for regular eaters at 8 mg/kg/day, 20 mg/kg/day at the 90% level, and over 50 mg/kg/day at the 99% level seem quite reasonable. The NutraSweet Company researchers have begun a concerted effort to convince scientists and laypersons that they are testing high doses of aspartame. This is based on consumer surveys. The reality is that a) the surveys are flawed; b) their own studies show subjects ingesting much higher intakes of aspartame than they use in tests; and c) they are often testing using doses significantly below the FDA's Allowable Daily Intake (ADI). Their efforts to test small doses is a big con job. Don't buy into it. What should be used in experiments is double the ADI of real world aspartame. Any argument for using less should be taken as an admission that the ADI is not a safe amount of aspartame. 3. Serious NutraSweet Research Flaws Before we discuss individual studies, it is important to list common and very serious flaws in all of the research funded by NutraSweet. This is by no means meant to be a comprehensive list of flaws -- simply the most common serious flaws. The flaws I will discuss in this section related to studies after aspartame was approved (post-approval). The pre- approval studies bordered on criminally fraudulent activity in my opinion and will be discussed in a later section. a. Test Material In most of the NutraSweet-funded studies, the test material used was fresh, encapsulated aspartame. This is a major flaw for the following reasons: 1. The chemical makeup of the fresh aspartame used is almost 100% pure aspartame and differs significantly from what is being ingested by the general public. This is discussed thoroughly in the "By-Products and Breakdown constituents" section above. This means that DKP, beta-aspartame, free methanol, and other possible breakdown products are not being tested in these experiments. 2. In 1987, Stegink tested the effect of aspartame taken in liquid as opposed to capsules on plasma phenylalanine, phenylalanine/LNAA, tyrosine, and aspartate (Stegink 1987a). The difference was striking. The plasma phenylalanine and aspartate levels rose very quickly to extremely high levels when ingesting the liquid aspartame mixtures, but the plasma amino acid levels only rose moderately when ingesting encapsulated aspartame. While this experiment compared the effect of aspartame in liquid vs. capsules, it did not test real world liquid aspartame-containing products which would contain significant amounts of DKP, methanol, free amino acids, and other possibly dangerous chemicals. The rise in plasma amino acid levels may be even more striking and sudden with such products due to even faster absorbtion. 3. The experiment conducted by Stegink (1987a) showed that capsule administration of aspartame significantly delayed absorption of aspartic acid and phenylalanine. In fact, with liquid administration, the peak amino acid levels were reached within 32 minutes (average), yet capsule administration led to a gradual rise in amino acid levels and took approximately 2.5 times longer to reach much lower peak levels. Not only is the enormous difference in the plasma amino acid spikes important as discussed above, but the sudden spike that occurs in liquid administration that may also be very important. When a substance is gradually absorbed in a way that causes it to be slightly toxic, the body has a chance to adjust and mount a defense. Sudden absorption of single, potentially neurotoxic amino acids does not give the body a chance to mount a defense. It is also very important to note that delaying the absorption of methanol as would happen when ingesting encapsulated aspartame may reduce the methanol toxicity somewhat since food in the stomach, which also delays methanol absorption, seems to reduce methanol toxicity (Posner 1975). It is interesting to note that as early as 1973, the FDA told the manufacturer of aspartame that there is "No pharmacokinetic data . . . on absorption, excretion, metabolism, half-life; nor bioavailability of capsule vs. food additive administration" (Freeman 1973). It wasn't until 1987, 14 years later, that NutraSweet finally got around to testing capsule administration as compared to liquid administration! There was a striking difference as described above. To this day, there has been no tests comparing the administration of various real-world, aspartame-containing products to capsule administration. The large difference in biochemical reactions produced when ingesting real world aspartame-containing products as opposed to capsules given in the laboratory totally negates the results from experiments which used such capsules and found no adverse effects. When using aspartame-containing capsules, 1) much less aspartame gets absorbed (Stegink 1987a), 2) the absorption is much slower causing the increase in blood levels of aspartame by-products to be much more gradual (Stegink 1987a), and 3) other by-products and breakdown constituents do not get absorbed as they do in real-world products (Tsang 1985). Had real-world, liquid products been used, the number and severity of negative reactions due to aspartame would likely have been much greater. b. Test Product Administration In order to test the effects of aspartame on health it is important to simulate the way the product is taken by the general public. Sometimes aspartame is ingested with full meals. More frequently, however, aspartame is ingested by itself (e.g., diet colas) or with a sugary snack. It is important to test both methods of administration. It is obvious that the biochemical effect of the three original components of aspartame, aspartic acid, phenylalanine, and methanol will be much greater when it is ingested separate from a full meal. (This will be discussed in more detail in later sections.) When taking aspartame with meals the following things occur: i) The aspartame will not be absorbed as quickly leading to less of a rise in plasma aspartate and phenylalanine levels; ii) The other amino acids absorbed from the food will keep the plasma aspartate and phenylalanine levels from rising as high as they would normally; iii) The plasma phenylalanine to large neutral amino acid (LNAA) ratio will not be as large due to the LNAA's in the food. (This will be discussed in detail in a later section.); iv) The food may serve as a protective factor reducing the methanol toxicity as will be discussed in the Methanol section. It is obvious that the acute and chronic effects of aspartame ingestion will be slightly less when it is ingested with full meals. All previous experiments that tested aspartame ingestion with full meals, tested the best-case scenerio and not what is most common in the real world. Therefore, all such research of aspartame with full meals should be regarded as interesting, but not very useful. On the other hand, Yokogoshi (1984) has shown that aspartame ingestion with caloric sweeteners significantly raises to phenylalanine/LNAA ratio to even greater heights than by simply ingesting aspartame alone. Even a NutraSweet-funded, short study on healthy persons using a relatively small amount of aspartame showed a significant further increase in plasma phenylalanine/LNAA ratio when aspartame was ingested with a caloric sweetener (Wolf-Novak 1990). However, it is unclear whether the ingestion of carbohydrates along with aspartame renders the phenylalanine part of aspartame more dangerous. Carbohydrate ingestion lowers the levels of Large Neutral Amino Acids (LNAAs) and therefore the neutral amino acid trasport cites may become unsaturated causing a smaller change in brain chemistry than would otherwise happen with the phenylalanine alone. We will discuss this in more detail in a later section. Therefore, not only should more experiments be done using real-world aspartame products on persons not eating full meals, but experiments should be done on the combination of real-world liquid aspartame (at FDA ADI levels or greater) and caloric sweeteners. Only then will we begin to approach what happens in real-world aspartame ingestion. It is important to note, however, that the ingestion of aspartame with sugar reduces the possible negative effects from the aspartic acid part of aspartame (as will be discussed in the Aspartic Acid section). Such experiments (with caloric sweeteners plus aspartame are very useful, but lack of negative effects does not rule out possible negative effects from the aspartic acid or the aspartic acid plus another breakdown product (i.e., synergy). c. Short Experiments The majority of NutraSweet-funded experiments on humans tested aspartame for one day or less. Although there is a wide variation in when adverse reactions begin, it is usually several weeks or months after use begins before adverse reactions are noticed (Roberts 1990a, page 70). After the adverse reactions begin, regular aspartame use usually causes more frequent adverse reactions. Studies which are not funded by NutraSweet are usually much longer because the researchers are actually interested in testing aspartame. A quality study would be at least six months long, and preferably as long as one year or more. This way, the researchers will be testing adverse reactions that occur due to ongoing use of aspartame -- real world use. One to two year experiments would be ideal. James Scala, the former director of Health Sciences for General Foods Corporation said that most of the early NutraSweet research consisted of short-term studies that ignored possible subtle, long-term effects. Pediatrician and Geneticist Dr. Reubon Matalon stated "Let us say cigarettes were invented today, and you give 20 people two packs a day and after six weeks, no one has cancer, would you say that it is safe? That's what they did with NutraSweet." (Gordon 1987, page 486 of US Senate 1987) All single day or single challenge tests, usually conducted by NutraSweet-connected researchers, should be disregarded. No one is claiming that a single ingestion of even real-world aspartame-containing products represents an imminent health hazard. A single dose of aspartic acid, phenylalanine, methanol, DKP, etc., from aspartame is not acutely toxic in the majority of cases. It is the regular use that represents a extreme hazard. These concerns are not addressed in one-day studies. No reputable researcher would try to extrapolate a lack of negative effects from aspartame in a one-day experiment to a declaration of safety for onging use throughout a lifetime. Unfortunately, this is commonly done by some NutraSweet-supported researchers. It should be noted that some very subtle adverse reactions may be noticed in a single day experiment, especially in vulnerable populations. While a much longer test is necessary, any significant adverse reactions after only a single day test should be a cause for extreme concern. On the other hand, lack of adverse reations after only a single day test does not prove anything. d. Small Test Population The smaller the test population, the more difficult it is to get a statistically significant difference in amino acid and methanol/formate levels in the blood and urine. NutraSweet-funded research usually has such a ridiculously small test population that it is virtually impossible to have a statistically significant difference in measurements. This is especially true when this flaw is combined with other flaws such as capsule administration of aspartame. Another way a small test population can be a problem is if a particular symptom (e.g., seizures) appears in a small percentage of aspartame users -- let's say one out of every 100 regular users, then experiments with small numbers of people would usually not have a seizure victim. This problem is called "lack of statistical power" of the studies and will be dealt with in more detail when the cancer issue is discussed. The technique of using ridiculously small test populations helps to guarantee that reactions that are occurring in the general population do not occur in the test population. e. Irrelevant or Faulty Tests There are numerous NutraSweet-funded research projects which used irrelevant and faulty tests to draw their conclusions. An irrelevant or faulty test is useful only for press releases and convincing scientists who are not intimately familiar with the scientific issues surrounding aspartame ingestion. Performing many such irrelevant or faulty tests allows the researcher to proclaim, "Look! We tested aspartame, performed a whole battery of tests, and found no adverse effects!" When the protocol is examined closely, however, it becomes clear that many of these tests were meaningless or conducted improperly. Many of the improper testing methods appear to be deliberately created and used to avoid negative results. There are many cases of such irrelevant and faulty tests. I will discuss some of those when I get into the details of the research cited in the article. f. Dosage Tested In a number of NutraSweet-funded studies, the aspartame dosage used was much less than it should have been. As discussed in the previous section, NutraSweet's estimates of aspartame intake are obviously flawed. Frey (1976) showed that children can ingest as much as 76 mg/kg/day. In three studies on obese adults, Porikos (1984) showed that the average daily intake of aspartame varied from 8 to 36 mg/kg/day. The FDA's current Acceptable Daily Intake (ADI) is 50 mg/kg/day. NutraSweet researchers have made a significant effort to convince other researchers and the general population that it is okay to test small doses of aspartame. Much of their argument is based on average intake values presented in their ridiculous intake surveys. The fact is that hundreds of thousands of people are consuming amounts of aspartame approaching the FDA's Acceptable Daily Intake level. If the NutraSweet Company actually believes that the FDA's ADI is a safe amount of aspartame, then that is the minimum that should be tested. Either "put up, or shut up" so to speak. In order to have a safety margin, it is preferable to test at least double the ADI using read-world aspartame- containing products in long-term experiments. If they do not want to test at levels at or above the FDA's ADI (using real-world aspartame of course), then we should 1) lower the ADI back to 20 mg/kg/day, 2) label the amount of aspartame on each "food" product that it is in, 3) put a warning on the label stating that no more than 20 mg/kg/day (9 mg/lbs./day) should be consumed, and 4) start proper safety testing in humans at 20 mg/kg/day (or more) using real-world aspartame- containing products. g. Reaction Time Some research ignored certain adverse reactions if they did not occur soon after aspartame ingestion. This is one common way that food industry scientists significantly reduce the number of adverse reactions recorded during the experiment. They simply imply that the suspected reactions are "allergic" (i.e., IgE- mediated) and therefore must occur quickly after ingestion. The fact of the matter is that many food intolerance or toxicity reactions can occur as much as 48 hours after ingestion (Carroll 1992). This use of this flaw has occurred in several NutraSweet-funded experiments. The studies of MSG funded by the International Glutamate Association use this flaw quite often. Independent researchers usually design the experimental protocols to take into account the fact that people often experience delayed reactions. h. Average Values Shown In the publication of many NutraSweet-funded research projects only average values were shown in tables and plotted on graphs. This is fine in studies where there are a large number of participants and the substance being studied has similar biochemical effects on all people. However, most of these studies have very few subjects and it is well-known that there is a wide variation in the biochemical changes caused by methanol, phenylalanine, and aspartic acid. This may also be true with DKP and other breakdown products. If an experiment has six subjects, for example, and two of the subjects show biochemical changes that would be of concern, the significance of those changes would get lost in a listing of averages. Human studies of aspartame conducted by independent researchers often show measurements on an individual basis (not averages) so as not to obscure the possibility of individual susceptibilities (Koehler 1988, Matalon 1988, Van Den Eeden 1994, Walton 1993). Another related technique used by NutraSweet to help hide negative test results is to combine all of the subjects' measurements when they should not be combined. Suppose for a moment that we measure a blood plasma level of aspartate for the first 60 minutes after ingesting aspartame. Below are example values for five different subjects followed by the average values . 0 min 15 min 30 min 45 min 60 min Subject 1 6.0 38.0 32.0 16.0 9.0 Subject 2 5.0 14.0 28.0 51.0 50.0 Subject 3 7.0 8.0 12.0 41.0 12.0 Subject 4 5.0 23.0 41.0 21.0 19.0 Subject 5 6.0 9.0 24.0 37.0 53.0 Mean Values 5.8 18.4 27.4 33.2 28.6 In almost all NutraSweet funded experiments, all that would be shown in publication are the "Mean Values." Notice how the mean values only rise from 5.8 at 0 minutes to a maximum of 33.2 at 45 minutes. When going back to the actual data all of the rises in the subjects were much more extreme than what is apparent by looking only at the mean values. For example, the plasma aspartate level of Subject 2 rose from 5.0 to 51.0 at 45 minutes. Showing only the means values in a chart or a graph will obscure the true rise in blood plasma levels of the substance being measured. This is because some of the subjects reach their peak values at different times, so that when Subject 1 has a peak value of 38.0 at 15 minutes, Subject 3 has a value of only 8.0 at that time -- which brings the mean value at the 15 minutes time period down considerably. The appropriate thing to do would be to list all of measurements for each subject and list the mean starting values and mean peak values: Mean Starting Values = (6.0 + 5.0 + 7.0 + 5.0 + 6.0) / 5 = 5.8 Mean Peak Values = (38.0 + 51.0 + 41.0 + 41.0 + 53.0) / 5 = 44.8 If increases in certain measurements are only moderate, the NutraSweet Company researcher's use of mean values for each time period can sometimes enable the researcher to "prove" that the changes were not statistically significant. Therefore, NutraSweet-sponsored studies which show only mean values for each time period may be hiding some of the negative effects with their statistical games. i. Types of Volunteers Since serious health problems from aspartame seem to develop gradually in many people, it makes sense to conduct very long tests. The NutraSweet Company wants people to swallow this junk for their entire life. Experiments which last a lifetime are obviously impractical. Therefore, it is prudent to conduct relatively long experiments on susceptible populations first so as to get clues as to what will happen to healthy populations after years of use. Most of the studies funded by NutraSweet appears to have been conducted on healthy volunteers (for a very short test period). These experiments had numerous flaws. It seems that the experiments in which unhealthy volunteer were used, the number and seriousness of the experimental flaws increased significantly. The NutraSweet Company wants you to believe that out of the population that is currently allowed to consume aspartame, PKU Heterozygotes (persons who do not have phenylketonuria -- PKU, but have a single gene of PKU) would be the most susceptible to any possible negative effects from aspartame. While this population may be more susceptible than a healthy population, I submit that persons with the following illnesses will be much more susceptible: - Fibromyalgia - Chronic Fatigue Syndrome (CFS) - Chronic Depression - Multiple Chemical Sensitivities - Multiple Sclerosis There are other possibilities, but this is a good start for legitimate tests on susceptible populations. Please note, however, that healthy persons are very susceptible to the damage that can be caused by aspartame, just not quite as susceptible, on average, as persons with the above-mentioned illnesses. j. Animal Tests All three main ingredients in aspartame, methanol, aspartic acid, and phenylalanine have been shown to have much greater toxic effects in humans than in rodents. Methanol and aspartic acid is much more toxic in humans than in monkeys. Methanol tests in rodents are worthless. Methanol tests in rheusus monkeys are also worthless or guesswork at best as discussed in the Methanol section below. Methanol is much more toxic in humans than any other species. Aspartic acid is 5 times more toxic in humans than in rodents and at least 20 times more toxic in humans than in monkeys as discussed in the Aspartic Acid section. Phenylalanine tests in rodents are guesswork at best and probably worthless as discussed in the Phenylalanine section below. Phenylalanine is much more dangerous in humans than in rodents. It is unknown whether DKP, beta-aspartame, or racemized amino acids have different effects in humans as opposed to laboratory animals. Therefore, aspartame tests in animals, especially those which tested for the effects of methanol and phenylalanine in rodents, or methanol and aspartic acid effects in monkeys should be ignored -- as the negative effect in humans would likely have been much greater. It is important to point out that these flaws are not news to the NutraSweet Company. Many people have been pointing out these flaws for years and pushing for legitimate experiments instead of press releases disguised as research. It is also important to note that NutraSweet can make the following claims about their research: "We have studied aspartame in healthy individuals." "We have studied aspartame in diabetics." "We have studied aspartame in persons with liver disease." "We have studied aspartame in adults." "We have studied aspartame in children." "We have conducted acute-dosing tests." "We have conducted chronic use tests [a few weeks only]." etc., etc. However, each one of their experiments had multiple serious flaws, making it virtually useless for anything but a press release. For example, long-term studies often use capsules which were taken with meals and contained numerous irrelevant or poorly conducted tests. Given aspartame's history of what some people consider pre-approval fraud, it does not surprise me that the NutraSweet Company continues to flood the scientific community and the news services with results from badly flawed studies. 4. Methanol From the article: "The presence of small amounts of methanol in aspartame has generated a lot of undue concern. Although large amounts of methanol are harmful, the very small amounts of aspartame-derived methanol are easily handled by the body. "Methanol is a common component of the diet, and is found in many fruits, vegetables, and wines. Furthermore, the amount of methanol from foods far exceeds any contribution from aspartame (Lund 1981). Aspartame-sweetened soft drinks, for example, provide 60 mg of methanol per liter as compared to fruit juices which contain 140 mg of methanol per liter." The excerpt above contains so much NutraSweet Company propoganda, its hard to know where to begin. First, I will discuss how ingesting methanol from aspartame differs from ingesting methanol from alcohol, fruits and vegetables, and fruits and vegetable juices. Alcohol An exhaustive literature search by Monte (1984) showed that all natural products which contain tiny amounts of methanol also contain significant amounts of ethanol. Many alcoholic beverages contain over 200 times more ethanol than methanol. The large ethanol content of alcoholic beverages has served to protect humans from methanol poisoning throughout the ages. Despite the wishful thinking of NutraSweet Company spokespersons (Sturtevant 1985), researchers agree that ethanol serves as a protective factor (Leaf 1952, Liesivuori 1991, McMartin 1980, Posner 1975, Roe 1982). Ethanol protects from methanol poisoning by preventing the conversion of methanol to toxic formaldehyde and formic acid metabolites thus allowing methanol to be excreted through the lungs and urine (Roe 1982, Kruse 1992). Methanol poisoning is treated with ethanol (Kini 1961, Pamies 1993). Leaf (1952) showed that co-administration of methanol with ethanol immediately stopped the conversion of methanol to its toxic metabolites. Fruits and Vegetables Fruits and vegetables do contain methyl ester as part of the pectin. However, human beings do not have digestive enzymes such as pectin esterase to release the methanol (Garrison 1990, page 16, Monte 1984). As Monte (1984) points out: "Fermentation in the gut may cause disappearance of pectin but the production of free methanol is not guaranteed by fermentation (Braverman 1957). In fact, bacteria in the colon probably reduce methanol directly to formic acid or carbon dioxide (Campbell 1978) (aspartame is completely absorbed before reaching the colon)." Microorganisms in the feces can contribute to the production of methanol from pectin, but methanol will not be released in significant amounts unless the pectin sits in the intestines for 72 hours (Siragusa 1988). A couple of grams of pectin (found in an apple, for example) will probably produce only a maximum of 20 mg of methanol provided it stays in the colon fermenting for at least 24 hours. Much of this small amount of methanol is probably used and converted to less harmful substances by intestinal bacteria (e.g., Wolin 1993). Extremely high doses of pectin (i.e., 120 grams over 2 days) by itself can lead to a significant increase in blood methanol (Gruner 1994), but it is not known whether protective factors are absorbed as well. Even if some of the methanol was absorbed and converted to formaldehyde, 120 grams of pectin would amount to eating over 50 small apples (Garrison 1990, page 16). Fruits and Vegetable Juices When certain fruits and vegetables juices are extracted, the pectinmethylesterase enzymes demethylates some of the pectin and liberates methanol. However, the methanol content of most commonly ingested fruit juices do not average 140 mg per liter. The NutraSweet Company has been pushing this fallicy for years even though it has been disproven. The 140 mg/liter figure was obtained from a very old conference paper presented by Francot and Geoffroy (Francot 1956). The authors of this paper state that they did not perform many of the tests and give no original sources for the work except for grape juice and black current juice. No methodology was given although it is certain that in 1956 they did not use the more accurate techniques currently used. The methanol content of fresh juices is probably dependent upon the method used to extract the juice, the type of fruit used (including species), and the time harvested. Lund (1981) showed that the methanol content of fresh orange juice had a mean of 34 mg/liter. Fresh grapefruit juice averaged 27 mg/liter in the Lund study. Sauri (1981) tested fresh orange juice and showed that it contained 33 mg/kg. Nisperos-Carriedo (1990) determined that their sample of fresh orange juice had a mean of 38 mg/liter. The methanol content of processed juices were much less than fresh juices. Lund (1981) showed that orange juice concentrates average about 6 mg/liter of methanol. Grapefruit concentrates average about 2 mg/liter. The reconstituted juices contained no detectible methanol. Nisperos-Carriedo (1990) showed that pasteurized orange juice contained 22 mg/liter and frozen-concentrated orange juice contained 3.4 mg/liter. White (1950) showed that 10.1 kg of apple essence contained 2000 mg of methanol. Since apple essence is a concentration of 150 times that of juice, 10.1 kg of juice contains 132 mg of methanol. However, the author points out that not all of the volatiles were extracted, but we can assume that the concentration in fresh juice is probably less than 200 mg/10.1 kg or 20mg/liter. The most popular freshly-made juices have about one-half (or less) of the concentration of methanol than aspartame. Processed juices contain many times less methanol than aspartame and reconstituted juices contain only trace amounts of methanol. The average juice product ingested in the U.S. probably contains much less than 10 mg/liter if all types of fruits and processing is included since fresh juice is consumed by only a small segment of the population and in relatively small quantities. Some juices have been shown to contain methanol at equal or greater levels than aspartame. Nelson (1969) showed that after extracting the tomato juice and heating it for 30 minutes at 212oF in when enclosed in tin or enamel that the methanol content varied from 127 to 560 mg/liter. However, heating can-sealed tomato juice to extremely high temperatures without inactivating the pectinmethylesterase enzyme would likely increase the creation of methanol tremendously. This is something that is unlikely to happen in commercial or home preparation. Kazeniac (1970) found that blended tomatoes had a methanol content of between 64 and 138 mg/liter depending upon the speed of the blendor and the time blended. The small amounts of methanol in fresh juices or the larger amounts in some fresh juices (such as tomato juice) are probably irrelevant since it is unlikely that the methanol from these natural substances is absorbed and metabolised the same way as methanol from aspartame. The following points lead me to conclude that methanol from natural foods is not absorbed and/or metabolised into formaldehyde and formic acid in significant amounts: a. Alcoholic beverages contain large amounts of ethanol which prevent the large amounts of methanol from being converted to formaldehyde and formic acid. This is a reference point. It proves that we cannot automatically assume that a methanol-containing item will end up producing formaldehyde and formate after ingestion. b. If we can indulge NutraSweet's fantasy for a moment and pretend we find an "average" juice with 140 mg/l of methanol. Suppose that a person drinks 3 liters of this healthy juice per day. For a 50 kg adult woman that would amount to 8.4 mg/kg of methanol per day. Baumann (1979) showed that workers in a printing shop were exposed to methanol concentration in the air between 85 and 134 parts per million (111-174 mg/m3) for an 8-hour day. The total methanol intake of these workers at 60% absorption (twice resting respiration rate) was approximately 8 mg/kg (Kavet 1990). The average blood formate levels nearly doubled (3.2 mg/l to 7.9 mg/l) at this exposure. The urinary formate levels rose from 13.1 mg/l to 20.2 mg/l. Heinrich (1982) showed a similar blood and urinary formate increase for a single work day at a chemical plant at an exposure level of 92 ppm (120 mg/m3). Three liters of fruit juice, leading to a theoretical ingestion of 8 mg/kg of methanol has never been shown to spike urinary and blood formate levels as the experiments discussed above. Such a plasma formate level spike would be highly unlikely to say the least. I would challenge NutraSweet to find any independent research would shows such a spike in formate levels from fruit juice ingestion. c. Under the manufacturer's theory, someone "unfortunate" enough to drink two liters of one of the higher methanol- containing juices such as black current juice (Monte 1984) would be getting about 1.3 grams of methanol (according to NutraSweet claims). The lowest recorded single lethal dose is 15 ml of 40% methanol. This equals 6 ml of methanol or 4.8 grams. (Bennett 1953). 1.3 grams (more than 25% of the minimum recorded lethal dose) of methanol would be an enormous quanity of methanol to ingest every day! God forbid this person would ingest tomatoes which NutraSweet claims is another source of large amounts of methanol (Butchko 1991). Methanol is also found in some cooked foods (Casey 1963). If NutraSweet actually believes its own theories about methanol absorption and metabolism from fruit, they should call for a ban on black currents, tomatoes, and juices with high amounts of methanol. A useful experiment would be to have an independent researcher test the equivalent methanol believed by NutraSweet to be found in 2 liters of black current juice plus a days worth of cooked foods and other methanol-containing foods -- say 1.8 grams per day. The test would be conducted on Monsanto and NutraSweet executives who would ingest 1.8 grams of methanol every day in a single dose with distilled water half way in between lunch and dinner. The experiment would be conducted for two years. Each day that alcohol is ingested would increase the experiment by a day for that subject. Regular blood and urine methanol and formate levels would be tested to make sure that the subjects were getting proper doses. In this way, the company excecutives can see first-hand how "safe" methanol from juices is when taken without the rest of the juice. d. A growing number of people are extremely sensitive to methanol or formaldehyde exposure, hardly being able to tolerate a short exposure in a print shop or chemical plant, but easily being able to drink fresh juice. It would have been relatively easy for NutraSweet researchers to test tomato juice to see if it raises the blood methanol and urinary excretion of formate as does aspartame in the experiments discussed later in this section. Two to three liters of tomato juice given to a 30 kg child could contain the same amount of methanol as was shown in NutraSweet experiments to significantly increase blood methanol levels. Similar equivalent amounts could have been determined to correspond to the NutraSweet experiments which showed a significant increase in urinary formate levels. It's been almost two decades since tests relating to aspartame and methanol have been published and this obviously important experiment has not been conducted or has, more likely, been avoided. At this point, however, the experiment would have to be conducted and funded by corporate-neutral parties to have any validity. The simple fact is that methanol from natural products such as juices is almost certainly not absorbed or metabolised to formaldehyde and formic acid in signficant amounts. Researchers have not taken the time and effort to discover all of the protective factors in juices (similar to ethanol in alcoholic beverages). Juices contain a significant number of volatiles including ethanol, some of which may prevent absorption or metabolism of the methanol. Fructose has been shown to significantly slow methanol oxidation in some species when given in significant quantities (Bradford 1993). Whether this has an effect on humans ingesting small amounts of methanol with fruit juices is unknown. Certain intestinal bacteria have been shown to convert methanol or formaldehyde to acetate (Wolin 1993). It is possible that tiny amounts of methanol from fruit juices may be converted by bacteria in the human digestive tract before it can be absorbed. Some bacteria which convert methanol to acetate are known to do so many times faster in the presence of sodium (Na+) ions (Blaut 1992, Heise 1989). Sodium ions may be found more readily in natural juices than in junky diet sodas. Since methanol toxicity is blocked by ethanol in alcoholic beverages and since inhaled methanol has been shown to spike plasma formate (formic acid) levels, yet similar quantities of methanol from juices has not been shown to spike plasma formate levels, it seems rather ridiculous to automatically assume that methanol from juices would be absorbed and metabolized in the same way as methanol from an artificial sweetener. The high caloric content of fruit and vegetable juices as well as their osmolarity places limits on the quanity of these products ingested on a regular basis (Monte 1984). Monte (1984) shows, using U.S. Department of Agriculture survey figures that the regular juice drinker probably ingests between 1 and 7 mg of methanol per day from these sources. Aspartame, on the other hand, has a low calorie content, leading to the possibility of ingesting large quantities. In fact, in hot whether, it is not uncommon for a person to drink anywhere from 1 to 3 liters of aspartame-containg beverages every day (Monte 1995). Wurtman describes a case of a person who ingested 3.5 liters of diet Coke and a nearly equal amount of diet lemonade every day (Wurtman 1985a). This person was ingesting approximately 350 mg of methanol every day! I know several people who drink well over a liter (i.e., three 12-ounce cans) of diet beverage every day. A person ingesting two to three liters of diet orange soda on a daily basis, for example is ingesting 180 to 270 mg of methanol every day. Fresh juices contain vitamins and minerals which can help protect cells from damage caused by methanol. Folic acid, for example, is an important nutrient which helps break down and eliminate methanol metabolites. It is common that many chemicals in foods protect us from toxic substances in those foods. Remington (1987, page 88) gives a couple of examples of toxic substances causing more damage when not co-ingested with nutrients. In one example, rats which were fasted for six days died at 1/25th the dosage of a toxic substance as compared to rats which ate a normal diet. In the other example, it was shown that giving cabbage and brussels sprouts to rats increased the hydroxylase activity by 100 fold, protecting them from aflatoxin. Diet drinks and other aspartame- containing foods rarely contain significant amounts of nutrients that can protect against methanol damage and often contain other unnecessary and unhealthy chemical additives. In summary, juices usually contain much less methanol than aspartame. Due to the calorie content and osmolarity of juices, much less is ingested on a regular basis. Nutrients such as folic acid serve as protective factors against ingestion of methanol. And most important, it is very unlikely that methanol from juices is absorbed and metabolised in a similar way as methanol from aspartame. Most likely none or only trace amounts from natural juices are converted to formaldehyde. Therefore, NutraSweet's comparison of methanol from aspartame to methanol from natural products is flawed. Methanol Metabolism Methanol from aspartame is released in the small intestine when the methyl group of aspartame encounters the enzyme chymotrypsin (Stegink 1984, page 143). Free methanol rapidly forms in liquid aspartame- containing products at temperatures over 145oF (62oC) (Mullarkey 1992, page 9). Free methanol is absorbed and metabolised somewhat differently than methanol from freshly-prepared aspartame as pointed out by researchers for the NutraSweet industry (Stegink 1983a). Methanol is absorbed in the stomach and more quickly when it is in its free form (Ranney 1976, Monte 1984, Stegink 1981a). There may be a greater toxicity for the quickly absorbed free methanol as discussed by Monte (Mullarkey 1992, page 9). Monte goes on to point out that when people are dieting or have not eaten for a while there is little gut fermentation producing the protective factor, ethanol. Whether absorbed quickly as free methanol or somewhat slower in the small intestine from fresh aspartame, the total amount of methanol absorbed will be approximately 10% of aspartame ingested. The absorbed methanol is then slowly converted to formaldehyde by alcohol dehydrogenase in the liver (DHHS 1993a, Liesivuori 1991). If methanol is co-ingested with a significant amount of ethanol, the methanol conversion is temporarily blocked since ethanol has nine times the affinity for alcohol dehydrogenase as does methanol (DHHS 1993a). This allows the body time to eliminate methanol via the lungs and urine before it gets converted to formaldehyde. The formaldehyde is then converted to formic acid by aldehyde dehydrogenase in the liver, by formaldehyde dehydrogenase in the blood, or through the tetrahydrofolic acid-dependent one-carbon pool (Liesivuori 1991). Methanol Dangers Methanol, also known as wood alcohol, is a deadly poison in small amounts. The toxic effects of methanol vary widely from person to person (Posner 1975, Roe 1982, Tephly 1984). As little as 6 ml (0.2 ounces) of methanol has killed a person (Bennett 1953) although it usually takes as much as 80 ml to 150 ml (2.8 oz. to 5.3 oz.) to cause fatalities in the average adult (EPA 1994). In extremely small amounts and taken without a protective factor (e.g., ethanol), methanol is a cumulative poison, despite the wishful thinking of the NutraSweet Company spokespersons (Sturtevant 1985). The U.S. Environmental Protection Agency published the following about methanol (Cleland 1977): "[Methanol] is considered a cumulative poison due to the low rate of excretion once it is absorbed." After studying workers exposed to formic acid, a toxic methanol metabolite, Liesivuori addressed the issue of it being a cumulative poison (Liesivuori 1986): "The data indicated that formic acid may have a long biological half-life possibly causing an accumulation of the acid in the body. This might constitute a hitherto unappreciated toxicological hazard, as the acid is an inhibitor of oxygen metabolism." Liesivuori later points out that formic acid can accumulate in the brain, kidneys, spinal fluid, and other organs because of the slow excretion from the body (Liesivuori 1991). He also described formic acid's effects at the cellular level: "Exposure to either methanol or formic acid leads to accumulation of acid in the body. Formic acid inhibits cytochrome oxidase, causing decreased synthesis of ATP. This is followed by anaerobic glycolysis and lactic acidosis. At the same time, and also because of acidosis, the generation of superoxide anions and hydroxyl radicals is enhanced leading to membrane damage, lipid peroxidation and mitochondrial damage. This, and the decreased pH in acidosis, allows the influx of calcium into the cells. Although the mitochondrial dysfunction may be secondary to calcium overload in the mitochondria, the final consequence is cell death." While severe acidosis would obviously not likely by a consequence of small amounts of formic acid, the other damaging aspects of formic acid such as the inhibition of cytochrome oxidase and decreased production of ATP are still possible problems. Side Effects The most well-known effect caused by acute or chronic poisoning of methyl alcohol is damage to the optic nerve fibers. However, there are many other symptoms and optic nerve damage is not always one of the symptoms which appear as pointed out by Monte (1984): "Many of the signs and symptoms of intoxication due to methanol ingestion are not specific to methyl alcohol. For example, headaches, ear buzzing, dizziness, nausea and unsteady gait (inebriation), gastrointestinal disturbances, weakness, vertigo, chills, memory lapses, numbness and shooting pains in the lower extremities hands and forearms, behavioral disturbances, and neuritis. The most characteristic signs and symptoms of methyl alcohol poisoning in humans are the various visual disturbances which can occur without acidosis although they unfortunately do not always appear. Some of these symptoms are the following: misty vision, progressive contraction of visual fields (vision tunneling), mist before the eyes, blurring of vision and obscuration of vision." "Chronic occupational exposure to methanol often produces human complaints of neuritis with paresthesia, numbing, prickling and shooting pains in the extremeties." "Methanol is one of the few etiologic factors associated with acute pancreatic inflammation." Many of these symptoms are common in persons ingesting aspartame for long periods of time (FDA 1993). Since the susceptibility of humans to methanol varies greatly and since aspartame provides no protective factors such as ethanol, it is not surprising that many people have experienced methanol poisoning-like symptoms after chronic, long-term aspartame ingestion. The damage is often slow and silent. The following is a letter presented before the U.S. Senate hearings on NutraSweet. It was written by Dr. Margan B. Raiford, M.D., Ps, Msc Med. Ophthalmology (Raiford 1987): "I had the opportunity, in Atlanta, Ga., to see the effects of methyl alcohol toxicity in 1952- 1953 which resulted in visual damage to the optic nerves and retina in over 300 cases and the deaths of over 30 persons. "I examined Shannon Roth on July 7, 1986, along with several other patients [65 cases as of July 10, 1986 (Roberts 1990a, page 136)]. I observed evidence of effects in her eye and the eyes of the other patients that were comparable to the effects observed in the patients who suffered methyl alcohol toxicity in 1952-1953. "There was damage in the central fibers, 225,000 of the total 137,000,000 optic nerve fibers (resulting in optic nerve atrophy) in her case, which would be comparable to that observed from patients suffering methyl alcohol toxicity. The extent of damage to these fibers would explain partial to total blindness. . . . . "But in the kind of chronic low dose exposure to methyl alcohol experienced by Shannon Roth (in NutraSweet consumption) and other NutraSweet consumers, it is likely that they would experience the impact on the optic nerve differently in each eye. "The important point is that the damage observed in Shannon Roth's eye was identical to the damage I observed repeatedly in the eyes of individuals whose eyes have been damaged by methyl alcohol toxicity." The large number of eye disturbances including cases of blindness that are being caused by aspartame led Dr. H.J. Roberts to dedicate an entire chapter to these problem and detail quite a few case histories (Roberts 1990a, page 128). Dr. Roberts surveyed 551 aspartame-reactors (Roberts 1988) and had this to say about eye problems (Roberts 1990a): "Decreased vision was a major complaint in 140 (25.4%), severe pain (one or both eyes) in 51 (9.3%), 'dry eyes' or trouble wearing contact lens in 46 (8.3%), and blindness (one or both eyes) in 14 (2.5%). . . . . "in most of these patients, there was no convincing evidence for underlying glaucoma, occlusion of a retinal vessel, toxic amblyopia (related to excessive alcohol or smoking), or optic neuritis due to multiple sclerosis and other causes that might account for the symptoms. CT scans and MRI studies of the brain or optic nerves generally proved normal in these patients. "Furthermore, that patients had known cataracts, astigmatism, macular degeneration or diabetic retinopathy did not necessarily disprove the role of aspartame . . . especially when vision promptly improved after stopping aspartame products. . . . . "Ophthalmologists and other professionals have told me about dramatic improvement of vision in their patients after the cessation of aspartame products." Susceptibility Folic acid is believed by most researchers to play a large role in protecting from methanol poisoning by increasing the conversion of formic acid to carbon dioxide and water (Roe 1982, Tephly 1984, DHHS 1993a). Persons who have a folic acid deficiency are likely to be much more susceptible to damage from chronic methanol ingestion. Other nutrients may play an important part in protecting from formic acid damage. As Tephly points out (Stegink 1984a, page 114): "Nutritional differences among individuals, such as folic acid deficiency, may play an iportant part in the ability of an individual to metabolize formate. Different degrees of nutritional deficiency may be observed in debilitated and inebriated persons who have not had an adequate diet. In monkeys we observed variability in the metabolism of methanol to formate and carbon dioxide when the animals were studied at different times. Some laboratories have been unable to duplicate results obtained by others. This failure may not be due to differences in experimental design or differences in the procedures of those individual laboratories. Instead, it is possible that animals maintained on the best nutritional regimens may be less susceptible to methanol poisoning, owing to a better hepatic capacity to metabolize methanol and formate to carbon dioxide." In addition to the protective factors of ethanol, folic acid, and possibly other nutrients, Posner (1975) pointed out that the presence of food in the stomach seems to lower the toxicity of methanol. The reason food slightly lowers the toxicity is probably because the food offers protective factors (as does alcohol and juices) and/or the food delays absorption (as does the administration of aspartame in capsules). This does not mean that aspartame in food is safe in long-term use, but probably slightly less toxic. Methanol ingestion may be even more dangerous for persons taking certain pharmaceuticals. The enzyme aldehyde dehydrogenase is believed to play a major role in methanol oxidation and elimination (DHHS 1993a, Liesivuori 1991). The drug disulfiram (trade name Antabuse) inhibits the activity of aldehyde dehydrogenase (Merck 1992, page 2638). Animal experiments have shown a significant increase in toxicity of methanol and a slowing down of methanol elimination when disulfiram was given (Posner 1975). The results are likely to be similar in humans for this particular adverse effect. Antabuse is currently being taken by 400,000 persons in the U.S. and many more are taking generic brands of disulfiram (Roberts 1990a, page 43). Posner (1975) lists research on several pharmaceuticals which shows that ingesting aspartame while on these drugs may present an additional health hazard. Some of these include sulfonylureas (for diabetics), metronidazole (anti-bacterial), and allopurinol (reduces uric acid). There may be other pharmaceuticals which cause adverse reactions when taken with the methanol in aspartame, but few studies have been done. Pilots are another group which may be more susceptible to acute reactions from methanol ingestion. Dr. Phil Moskal, Professor of Microbiology, Biochemistry, and Pathology, Chairman of the Department of Pathology, Director of Public Health Laboratories, discussed one possibility of why pilots may be suffering from dangerous adverse reactions to methanol from aspartame in a letter to George Leighton (Moskal 1990): A. Military studies indicate that a smoking person at sea level is physiologically at 8,000 ft. MSL. Ref. Col. Mauriel Udol. C.O. Ellington AFB, Top Gun - William Tell 1980 B. One (1) ounce of (C2H5OH ) (Ethanol) at sea level doubles in its effects at 10,000 ft. MSL. Ref. AOPA C. (Methanol) (CH3OH) displaces binding sites on the Hemoglobin molecule the same way that Carbon Monoxide (CO) does, reducing O2 (Oxygen) binding sites as CH3OH is acting as a blocking agent to the Oxygen-O2. D. Methanol is metabolized to an aldehyde OHOO - Methal - dehyde which is neuro-toxic (including respiratory, olfactory and ocular nerves. E. Physiology of the human body indicates that an average 170# person's liver metabolizes 1.0 oz. of alcohol/hours. F. Density altitude affects lung performance the same as it affects engine performance. We previously discussed and both know this through personal experience. The FAR's say that the pilot must use supplemental oxygen above 12,500 MSL beyond 30 minutes. As we painfully know, the lung (engine) does not decipher MSL or pressure altitute, only density altitude. AOPA recommends supplemental O2 (oxygen) above 10,000 MSL. That makes sense. However, the FAA doesn't use that rule. Conclusion A through F are additive and if you are 29,000 fee things begin to happen. Low Dosages It is very important to understand that serious health problems can start on a microscopic scale. For example, cancer, atherosclerosis, multiple sclerosis, excitotoxic neural cell damage, and many other diseases can start on a very small scale and build very slowly over the years. Excitotoxic neural cell damage can happen gradually over a lifetime and symtpoms often do not appear until after a large percentage of neural cells in a particular area has died (Blaylock 1994, page 92). The damage caused by these diseases cannot usually be detected until they are much more widespread. By the same token, damage from formic acid and formadehyde, toxic methanol metabolites, may occur very slowly over a long period of time. Even the skeptics agree that laboratory-detectable changes in measurements do not preclude toxic damage. "It is not possible to completely elminate formaldehyde as a toxic intermediate because formaldehyde could be formed slowly within cells and interfere with normal cellular function without ever obtaining levels that are detectable in body fluids or tissues" (McMartin 1978). It is also very important to keep in mind that short, low-level exposure to methanol or its toxic metaboites (e.g., formaldehyde) does not cause laboratory-detectible changes even though longer exposures at those levels do lead to changes and can cause health problems over time. As an example, Schmid showed that persons exposed to a single dose of significant amounts of formaldehyde did not show a statistically significant increase in the excretion of formic acid through the urine (Schmid 1994). Triebig (1989) concurs that formic acid excretion is a "unspecific and insensitive biological indicator for monitoring low-dose formaldehyde exposure." After testing subjects exposed to formaldehyde, Heinzow (1992) stated: "Excretion [of formic acid] in the general population is determined by endogenous metabolism of amino acids, purine- and pyrimidine-bases rather than the uptake and metabolism of precursors like formaldehyde. Hence in contrast to recent recommendations in environmental medicine, formic acid in urine is not an appropriate parameter for biological-monitoring of low level exposure to formaldehyde." A number of investigators have found that a very short, low-level methanol exposure at 200 parts per million (260 mg/m3), the current occupational exposure limit, does not significantly increase the urinary and plasma formic acid measures (average for all subjects) (d'Alessandro 1994, Franzblau 1992, Lee 1992). d'Alessandro found that one subject had a large jump in blood formate levels after exposure to methanol, but this large increase was lost when the average increases were presented (similar to the way the data is usually presented by NutraSweet industry researchers). Kingsley (1954-55) found that workers exposed to a methanol concentrations of 200 to 375 ppm (260-487 mg/m3) when using spirit duplicators experienced adverse reactions such as headaches. Frederick (1984) showed that spirit duplicator exposure caused adverse reactions such as headaches, dizziness, nausea, blurred vision, and behavior disturbances at levels from 365 to 3080 ppm (474-3704 mg/m3). What is important to understand is that most of these workers did not spend most of their day at the spirit duplicator and therefore were breathing in air with a much lower concentration of methanol most of the time. Many of these workers who experienced adverse reactions to intermittant exposures to methanol concentrations as low as 200 ppm (260 mg/m3) probably had been working at the job for a reletively short period of time as compared to a lifetime of methanol exposure from aspartame use. Cook (1991), in a double-blind study, found that after only a 75 minute exposure to 192 ppm (250 mg/m3) of methanol (below the exposure time and level that would lead to a significant change in urinary or plasma formate measurements), the overall results show no changes in some categories, but did show statistically significant changes in other, important measurements. The subjects showed: - slightly greater fatigue from workload - a slight impairment of concentration and memory - a slight change in brain wave patterns in response to light and sound. The amount of methanol absorbed was less than 2 liters of (non-orange) diet soda for a 60 kg adult or less than 1 liter for a 30 kg child. (This assumes 1.3 times resting respiration rate such that 250 mg/m3 * 60% absorption *.6m3/75 minutes = 90 mg of methanol.) One wonders what the results would be had the subjects had this exposure every day for one year, or five years or more, especially if the subjects are more susceptible to the toxic effects of methanol. Unfortunately, it is unlikely that this experiment will be repeated with more participants or for a longer period (e.g., 3 months of regular exposures) to confirm the findings as there is no longer an interest in methanol as a fuel (Cook 1995). Two Russian studies published eight years apart showed that very low levels of methanol exposure affect visual and peripheral olfactory receptors and produced changes in EEG measurements (Kavet 1990). While the experimental protocols were not ideal, these studies seem to agree with Cook (1991) in that minor neurological changes were found for small, short exposures. While it is likely that formic acid is being eliminated when exposed to low levels for a short period of time (although some may accumulate in various organs as discussed earlier), the changes in laboratory measurements may not be statistically significant. However, that does not mean that low levels of formaldehye and formic acid are not causing damage. Getting back to our printing shop analogy, a child who ingests the highest daily amount of aspartame in the study conducted by Frey (1976) will be ingesting nearly 8 mg/kg per day of methanol. In other words, this developing child will be working full-time, 7-days per week in a methanol-laden printing shop (or chemical plant) breathing in methanol fumes (at twice resting respiration rate). A 30 kg child who ingests a two-liter diet cola will be working more than half-days at the printing shop (unless, of course, the child ingests diet orange soda). Please remember that many people will ingest a variety of aspartame-containing "foods" that would be equivalent to 2 liters (or more) of diet soda. Equivalent Weekly Hours Worked at Printing Shop With 140 mg/m3 of Methanol in Air Compared to Aspartame Ingestion Weekly Intake ------------------------------------------------ 2 liters 2 liters six cans soda, cereal diet cola diet orange six Equal packets FDA ADI 30 kg child 26.1 43.4 37.3 33.0 50 kg adult 15.7 26.0 22.4 33.0 70 kg adult 11.2 18.6 16.0 33.0 The formula used to calculate methanol inhaled in the Baumann (1979) study was discussed by Kavet (1990): (140 mg/m3 * 6.67 m3/workday * 5 workdays * 60 absorption rate) / 70 kg = 40 mg/kg/week of methanol. The equivalent weekly hours is calculated with the following formula: ( (mg methanol * 7 days) / kg ) * (40 hours/workweek / 40.0 mg/kg/week) Now NutraSweet may try to make the following claims: a. That only 75% of the methanol gets absorbed from aspartame as discussed by Kavek (1990). This is not certain, but based on industry estimates. If it does turn out to be true then multiply the weekly hours at the methanol-laden printing shop by 0.75. b. That 108 ppm (140 mg/m3) is within environmental exposure limits and therefore "safe." There are several problems with this claim. i. As we can see from the Baumann (1979) and Heinrich (1982) experiments detailed earlier, one would expect quite a significant change in blood chemistry (e.g., plasma methanol levels) in the course of regular, long-term aspartame ingestion. A single dose of aspartame has already been shown to increase urinary formate levels despite numerous experimental errors which would tend to negate the increase (Stegink 1981a). ii. It is quite common for long-term exposure to environmental toxins below the industry limits to cause adverse effects. (Ziem 1989) Occupational exposure limits were set long before chronic methanol testing was done and it had never been done until aspartame came on the market. iii. The toxic load of chemicals including methanol and formaldehyde (toxic methanol metabolite) has increased tremendously over the last 15 years. Methanol is used as a fuel on a small scale (EPA 1994). It is also used in paint strippers, duplicator fluid, model airplane fuel and dry gas. Formaldehyde can be found in carpeting, clothing, glues, adhesives, cements, paste, resins, urea-foam insulation, particle board, plywood, cellulose esters, paint, primer, paint stripping agents, paper, polishes, waxes, disinfectants, cleansers, fumigators, cosmetics, preservatives, medication, mouthwash, inks, sealers, and many other products (Remington 1987, page 89). With aspartame ingestion, we are adding tremendously to this toxic load. iv. As discussed earlier, short term exposures to methanol (i.e., 75 minutes) at levels which would not cause a statistically significant increase in average formate levels has been shown to c