The most widely used non-nutritive sweetener is aspartame, scientifically known as 1-aspartyl 1-phenylalanine methyl ester. (Alternative Sweeteners, Third Edition. Lyn O’Brien Nabors Ed.).  It was discovered by accident in 1965 by Mr. James Schlatter, a scientist who was working on new drugs to treat ulcers, when he licked his fingers to pick up a piece of paper and accidentally tasted the intense sweetness of the compound he had created. 

Aspartame is 180 times sweeter than sucrose (common table sugar).

www.gnc.com/health_notes/Food_Guide/Non_Nutritive_Artificial_Sweeteners.htm

According to the ADA: “Demand for aspartame in the United States rose from 8.4 million pounds in 1986 to 17.5 million pounds in 1992, a figure that represents more than 80 percent of the world demand. Although soft drinks account for more than 70 percent of aspartame consumption, this sweetener is added to more than 6,000 foods, personal care products, and pharmaceuticals.

Aspartame is approved for use in more than 100 nations. (www.eatright.org/Public/GovernmentAffairs/92_adap0598.cfm). 

It has been sold around the world under various brand names including NutraSweet, Equal, Spoonfuls, Canderel, Bienvia, NatraSweet and Miwon. Its widespread usage has left an extensive trail of complaints and documentation of its negative side effects. Consequently, there is a great deal to be said on the subject of aspartame.

In 1974 the Food and Drug Administration gave its first halting approval to aspartame, then a product of pharmaceutical giant G.D. Searle & Company. Searle owned the original patent on aspartame and did the original laboratory studies on its safety. These studies turned out very badly and remain as some of the most damning evidence against aspartame’s safety.(presidiotex.com/bressler/). Two of Searle’s own scientists, concerned about the safety of the new product, filed a formal objection to try to keep aspartame from coming to the market (www.btinternet.com/~amcbryan/aspartame/comment1a.htm). 

A team from the FDA conducted its own study of Searle’s data and on the corpses of aspartame-poisoned mice, issued a scathing document called the Bressler Report (presidiotex.com/bressler/).  This report, however, did not spell the end for aspartame. 

Following the issuance of the Bressler Report came a period of thickening political intrigue and red tape, wherein two key figures at the FDA failed to press forward with further investigations, only to leave the FDA for jobs with Searle’s law firm, Sidley & Austin. Higher authorities in the FDA quietly consigned the Bressler Report to the archives, and only made it public later, through a Freedom of Information Act Request (presidiotex.com/bressler/).  

While the public remained ignorant, Searle & Co had maneuvered to bring in Donald Rumsfeld, previously the Chief of Staff in the Ford Administration and the then Secretary of Defense, as their new CEO. According to a former Searle employee, Rumsfeld told them that “no matter what, he would see to it that aspartame would be approved. (www.btinternet.com/~amcbryan/aspartame/comment1a.htm).

Searle re-applied for FDA approval of aspartame on the very same day that Ronald Reagan took office in 1980. There were plenty of favors to be called in from within the new Administration, and significant clout was also to be wielded by Robert Shapiro and Utah Senator Orrin Hatch. Senator Hatch has been an outspoken advocate for the sweetener, possibly due to his holdings in Twin Lab, a health supplement company that has used aspartame in a number of their products. (www.btinternet.com/~amcbryan/aspartame/comment1a.htm). 

Between 1981 and 1985, Rumsfeld and Searle began seeing the payoff for their newly-formed subsidiary, the NutraSweet Company. Amidst ongoing controversy, aspartame was slowly, but surely given full FDA approval. Dr. Michael Friedman, then the acting head of the FDA, later accepted a high-level position at Monsanto, the corporation that was to purchase the NutraSweet Company from Searle in 1985. Monsanto has also brought the world such atrocities as Agent Orange, PCBs, dioxins, Recombinant Bovine Growth Hormone (rBGH), Round-Up herbicide and a host of genetically modified foods.

The company has made a fortune off aspartame, at the expense of those who purchase and consume it, and at the hazard of those who actually do the work of producing and handling it. The Material Safety Data Sheet on aspartame (CAS# 22839-47-0) says that to work with the sweetener, one should wear chemical goggles, protective gloves to prevent skin exposure, a chemical apron and a NIOS/MSHA approved air purifying dust or mist respirator. Whatever else one may say about refined white sugar, at least one doesn’t have to wear chemical goggles to work with it!

Problems associated with aspartame consumption are neatly summarized in Nourishing Traditions. “Aspartame. . . is a neurotoxic substance that has been associated with numerous health problems including dizziness, visual impairment, severe muscle aches, numbing of extremities, pancreatitis, high blood pressure, retinal hemorrhaging, seizures and depression. It is suspected of causing birth defects and chemical disruptions in the brain. 

“Researchers at Utah State University found that even at low levels aspartame induces adverse changes in the pituitary glands of mice. The pituitary gland is the master gland upon which the proper function of all biochemical processes depend.

“ When aspartame is digested it breaks down into the amino acids phenylalanine and aspartic acid, plus methanol. Methanol, or wood alcohol, is a known poison. Methanol is also found in fruit juices, and our regulatory agencies have seized upon this fact to assure us that the methanol by-product of aspartame is not harmful. They fail to point out that the methanol content of a diet soft drink is 15 to 100 times higher than that of fruit juices (Fallon, Sally and Enig, Mary G, PhD, Nourishing Tradiitons, NewTrends Publishing, 2001, Washington, DC.).

 

The Environmental Protection Agency (EPA) defines the “safe consumption level” of methanol at 7.8 milligrams per day. One liter of a beverage sweetened with aspartame may contain as much as 56 milligrams of methanol. Other sources also link aspartame consumption with Parkinson’s Disease, Alzheimer’s Disease and the Gulf War Syndrome experienced by U.S. soldiers after serving in Iraq during Operation: Desert Storm (www.aspartamekills.com).

 

According to Dr. Christine Lydon, an accomplished aspartame researcher: “Aspartame’s breakdown products, or metabolites, are even scarier than its components. Phenylalanine decomposes into diketopiperazine (DKP) a known carcinogen, when exposed to warm temperatures or prolonged storage. Even if products are consistently kept at cooler temperatures we are not safe. At cold temperatures, methanol will spontaneously give rise to a colorless toxin known as formaldehyde. Independent studies have shown formaldehyde formation, resulting from aspartame ingestion, to be extremely common. It accumulates within the cells, and reacts with cellular proteins such as enzymes and DNA. This cumulative reaction could spell grave consequences for those who consume aspartame-laden diet drinks and foods on a daily basis.”(www.aspartamekills.com/lydon.htm).

 

Supporters of aspartame claim that the levels of methanol are not high enough to be worrisome and that phenylalanine and aspartic acid are of only limited concern. But there is no argument about the fact that phenylalanine, the largest component of aspartame by weight, is a danger to people who have a hereditary condition called phenylketonuria (PKU). These people must monitor or eliminate their intake of phenylalanine, which also occurs naturally in certain foods. The FDA recommends that pregnant and lactating women, people with advanced liver disease and phenylketonurics avoid products containing aspartame due to concern over metabolizing phenylalanine. The FDA also admits that aspartic acid has the potential to cause brain damage at very high doses, but they assure us that “under normal intake levels, the brain’s mechanism for controlling aspartic acid levels ensures no adverse effects.”(www.cfsam.fda.gov/~dms/fdsugar.html).

This dismissal of phenylalanine and aspartic acid as significant health hazards is a dangerous bit of sleight of hand. According to Dr. Lydon, “Phenylalanine and aspartic acid are amino acids that are normally supplied by the foods we eat; however, they can only be considered natural and harmless when consumed in combination with other amino acids. On their own, they enter the central nervous system in abnormally high concentrations, causing aberrant neuronal firing and potential cell death. The neurotoxic effects of these amino acids, when consumed as isolates, can be linked to headaches, mental confusion, balance problems and possibly seizures.” (www.aspartamekills.com/lydon.htm).

While aspartame has been the subject of hundreds of FDA-approved studies, they clearly have not laid to rest the controversy surrounding its safety. Any adverse reaction to a food item that is regulated under the FDA’s authority is supposed to be reported back to their Adverse Reaction Monitoring System (ARMS). As of 1995, over 75 percent of the adverse reactions reported to the ARMS were due to aspartame (www.holisticmed.com/aspartame/summary.html).

A 1995 report from the US Department of Health and Human Services entitled “Symptoms Attributed to Aspartame in Complaints Submitted to the FDA” (which once again had to be forced into public light through the Freedom of Information Act) lists 92 separate categories of symptoms, including the frequency of each reported claim(aspartametruth.com/92symptoms.html).

In 1997 there was an increase in aspartame users reporting severe toxicity reactions and damage such as seizures, eye damage and vision loss, confusion, severe migraines, tremors, depression, anxiety attacks, insomnia, etc. In the same years, Ralph Walton, MD, Chairman, The Center for Behavioral Medicine showed that the only studies which didn’t find problems with aspartame where those funded by the manufacturer (Monsanto). Given the agreement amongst independent scientists about the toxicity of aspartame, the only question was whether the formaldehyde exposure from aspartame caused the toxicity. That question has now been largely answered because of research in the late 1990s.

The Following Facts Shown By Recent Scientific Research:

Aspartame (Nutrasweet®) breaks down into methanol (wood alcohol). Methanol quickly converts to formaldehyde in the body.  Formaldehyde causes gradual and eventually, severe damage to the neurological system, immune system and causes permanent genetic damage at extremely low doses. Methanol from alcoholic beverages and from fruit and juices does not convert to formaldehyde and cause damage because there are protective chemicals in these traditionally ingested beverages. 

 The most recent independent research in Europe demonstrates that ingestion of small amounts of aspartame leads to the accumulation of significant levels of formaldehyde (bound to protein) in organs (liver, kidneys, brain) and tissues.

Excitotoxic amino acids such as the one, which is immediately released from aspartame likely increases, the damage caused by the formaldehyde.

 

Toxicity Effects of Aspartame Use

Selection of adverse effects from short-term and/or long-Term use

Note: It often takes at least sixty days without *any* aspartame or nutrasweet to see a significant improvement. Improvement in health is also often accompanied by weight loss. Check all labels very carefully (including vitamins and pharmaceuticals). Look for the word “aspartame” on the label and avoid it. (Also, it is a good idea to avoid “acesulfame-k” or “sunette.”) Finally, avoid getting nutrition information from junk food industry PR organizations such as IFIC or organizations that accept large sums of money from the junk and chemical food industry such as the American Dietetic Association

• seizures and convulsions 
• dizziness 
• tremors 
• migraines and severe headaches (Trigger or Cause From Chronic Intake) 
• memory loss (common toxicity effects) 
• slurring of speech 
• confusion 
• numbness or tingling of extremities 
• chronic fatigue 
• depression 
• insomnia 
• irritability 
• panic attacks (common aspartame toxicity reaction) 
• marked personality changes 
• phobias 
• rapid heart beat, tachycardia (another frequent reaction) 
• asthma 
• chest pains 
• hypertension (high blood pressure) 
• nausea or vomiting 
• diarrhea 
• abdominal pain 
• swallowing pain 
• itching 
• hives / urticaria 
• other allergic reactions 
• blood sugar control problems (e.g., hypoglycemia or hyperglycemia) 
• menstrual cramps and other menstrual problems or changes 
• impotency and sexual problems 
• food cravings 
• weight gain 
• hair loss / baldness or thinning of hair 
• burning urination & other urination problems 
• excessive thirst or excessive hunger 
• bloating, edema (fluid retention) 
• infection susceptibility 
• joint pain 
• brain cancer (Pre-approval studies in animals) 
• death 

Aspartame Disease Mimics Symptoms or Worsens the Following Diseases

• fibromyalgia 
• arthritis 
• multiple sclerosis (MS) 
• Parkinson’s disease 
• lupus 
• multiple chemical sensitivities (MCS) 
• diabetes and diabetic Complications 
• epilepsy 
• Alzheimer’s disease 
• birth defects 
• chronic fatigue syndrome 
• lymphoma 
• lyme disease 
• attention deficit disorder (ADD and ADHD) 
• panic disorder 
• depression and other psychological disorders 

 

In 2001, the United Kingdom Food Standards Agency requested that the European Commission Scientific Committee on Food conduct an updated review of the artificial sweetener, aspartame / E951 (FSA 2001a). The Scientific Committee on Food was asked to look at more than 500 scientific papers published between 1988 and 2000 and any other new scientific research not examined previously by the Committee (FSA 2001b). On December 10, 2002, the Scientific Committee on Food published its final report (SCF 2002).

The following is a 2003 response to the Scientific Committee on Foods Report by the Aspartame Toxicity Information Center.  The response will demonstrate that:

Members of the European Commission Scientific Committee on Food have ethical and financial conflicts of interest with the food industry that should have disqualified them from participation on the Committee.

Members of the Scientific Committee on Food did not read some or most of the research papers they cited.

The report ignored independent research related to aspartame and instead relied heavily on and frequently cited articles in books and reviews put together by employees or consultants of the aspartame manufacturers (Monsanto and Ajinomoto). Persons ingesting aspartame are being exposed to significant amounts of formaldehyde that has been shown by independent research to accumulate throughout the body.

Aspartame manufacturer-sponsored studies are designed in a way as to avoid the possibility of finding adverse effects, yet the Committee accepted these studies without any question. In contrast, nearly all independent research on aspartame in humans and animals has found that it can cause problems.

Human studies and clinical reports published in the medical literature linking aspartame use to fibromyalgia, seizures, panic attacks, mania, brain cancer, migraines / headaches, vertigo, symptoms related to depression, memory loss, hives, irregular heart beats, and numerous other symptoms were largely ignored by the Committee.

Food Industry Conflict of Interest and Corruption – Worldwide

On January 9, 2003, The Guardian reported that they obtained a confidential report relating to the food industry experts “infiltrating” the World Health Organization (WHO) Food and Agricultural Organization (FAO) committees (Guardian 2003). The report found that:

Food companies attempted to place scientists favorable to their views on WHO and Food and Agricultural Organization (FAO) committees.

They financially supported non-governmental organizations, which were invited to formal discussions on key issues with the United Nations (UN) agencies.

They financed research and policy groups that supported their views.

They financed individuals who would promote “anti-regulation ideology” to the public, for instance in newspaper articles.

“One industry-led organization, International Life Sciences Institute (ILSI), has positioned its experts and expertise across the whole spectrum of food and tobacco policies: at conferences, on FAO/WHO food policy committees and within WHO, and with monographs, journals and technical briefs.” (Guardian 2003)

The International Life Sciences Institute (ILSI) is an industry group founded in 1978 by Coca-Cola, Pepsi-Cola, Heinz Foundation, General Foods, Kraft Foods (owned by Philip Morris), and Proctor & Gamble. Manufacturers of aspartame, Monsanto and Ajinomoto, have branches in various parts of the world that have separate memberships in the ILSI. Holland Sweetener Company, another company that sells aspartame, is a member of ILSI (ILSI 2003, Guardian 2003). The ILSI funds research on aspartame and other industry concerns. The ILSI Aspartame Committee is made up of the NutraSweet Company, Ajinomoto Co., Coca Cola Co., Pepsico, Inc., Royal Crown Co., Seven-Up, Inc., and other manufacturers of aspartame-containing products [Gordon 1987].  The manufacturer of aspartame threatened to have the ILSI research funding vetoed for one scientist who said negative things about aspartame in public (Wurtman 1987).

Governmental committees are often corrupted by companies and industry trade organizations that are able to get paid consultants or other biased persons on the committee. Monsanto and Ajinomoto of Japan marketed aspartame in Europe in the 1980’s and 1990’s. A confidential memo obtained by GeneWatch demonstrates that Monsanto tries to influence who is put on scientific committees with “scientific outreach”:

“Scientific outreach and Ag Regulatory was instrumental in assuring that key internationally recognized scientific experts were nominated to the FAO/WHO expert consultation on food safety which was held in Geneva this past month. The consultation and final report were very supportive of plant biotechnology, including support for the critical role of substantial equivalence in food safety assessments, antibiotic resistance markers used in these products, and the reservation of animal feeding studies to address specific questions rather than for routine safety” (Monsanto 2000).

Scientific Committee on Food and Obvious Bias

Almost all aspartame studies conducted and funded independently of the aspartame manufacturer (and related trade groups) have linked aspartame to adverse effects or adverse biochemical changes. This includes numerous human studies (e.g., clinical, double-blind) and animal studies (Walton 1996). As discussed throughout this document, the Scientific Committee on Food either ignored many of these independent studies or had negative things to say about almost all of the independent studies that they did mention. An enormous number of reports of serious adverse effects from aspartame are being sent to governmental agencies, scientists, clinicians, and independent organizations (DHHS 1993, Roberts 1988a, Food 1986, Walton 1988, ATIC 1998, ATIC 1997, ACSN 1997, AVSG 2003, NM 2003).

On the other hand, the Committee accepted almost all of the aspartame industry-funded studies without any negative comment. In fact, the Committee relied heavily on and repeatedly cited parts of books and reviews written and compiled by employees of the aspartame manufacturer (e.g., Stegink 1984, Tschanz 1996, Butchko 1994, Butchko 2001).

www.holisticmed.com/aspartame/scf2002-response.rtf

Throughout the Committee’s report on aspartame, there is evidence that the Committee members do not read some or most of the research that they cite. One example will be given in this section.

The Committee cites as evidence, that aspartame does not cause seizures two aspartame industry-funded human studies (Rowan 1995, Shaywitz 1994). Had they read these studies, the Committee would know that nearly 100% of the subjects in these studies were taking anti-seizure medication while the studies were being conducted! Obviously, anti-seizure medication will reduce or eliminate seizures during the study. But the Committee report presented these aspartame industry-funded studies as if they provided legitimate evidence about aspartame use and seizures in the general population. The Committee did not have a negative word to say about these two studies! 

 

There are three possible reasons that the Committee cited these two studies and had nothing negative to say about them:

The Committee did not read the studies.

The Committee is so biased that they will cite any aspartame industry-funded study no matter how irrelevant or absurd it is.

The Committee actually believes that anti-seizure medication doesn’t reduce or prevent seizures, has no effect on the studies, and therefore the studies apply to the general population not taking anti-seizure medication.

It is unlikely that the Committee is completely ignorant about anti-seizure medication. Even though members of the Committee have a conflict of interest, it is hoped that their bias is not so extreme that they would know about the use of anti-seizure medication and still cite these studies as evidence. It is more likely that some or all of the Committee members did not read these studies. There are numerous instances in the report where it becomes clear that the Committee members did not read the research they were reviewing and have only marginal familiarity with aspartame research in general.

Aspartame and Formaldehyde Poisoning

“These are indeed extremely high levels for adducts of formaldehyde, a substance responsible for chronic deleterious effects that has also been considered carcinogenic.

….

“It is concluded that aspartame consumption may constitute a hazard because of its contribution to the formation of formaldehyde adducts.” (Trocho 1998)

 

Aspartame & Formaldehyde Research Ignored by the Scientific Committee on Food

The Scientific Committee on Food appears to be completely unfamiliar with the current research and reviews related to aspartame, formaldehyde, and methanol. The Committee cited and relied solely on a commentary by an aspartame industry researcher (Tephly 1999) and an article in a book put together by aspartame industry researchers (Stegink 1984a) as evidence of safety. In fact, the Committee appears to shy away from the use of the term “formaldehyde” in the report, mentioning it only once when they quote another review (AFSSA 2002). Since the Committee largely ignored the formaldehyde issue, some of the relevant research will be summarized below.

 

Aspartame & Formaldehyde Summary of Research

Methanol is quickly absorbed from aspartame ingestion (Davoli 1986). Methanol is converted into formaldehyde in the body (Kavet 1990). Some of the formaldehyde is converted into formic acid and eliminated by the body (Kavet 1990). However, Trocho (1998) demonstrated that aspartame ingestion at low levels by rodents: 10 mg/kg body weight, lead to formaldehyde accumulation in the liver, brain, kidneys and other parts of the body. The formaldehyde was bound as “adducts” to proteins and DNA. Research in humans demonstrates that adduct formation can occur from formaldehyde exposure (Carraro 1997, 1999).

Setting aside the very serious issue of formaldehyde accumulation from aspartame ingestion and just considering the proven formaldehyde exposure from aspartame, one can see numerous human studies where adverse effects have been reported from chronic, low-level formaldehyde exposure:

 

• Irreversible genetic damage from long-term, low-level exposure (Shaham 1996)
• Headaches, fatigue, chest tightness (Main 1983)
• Sleeping problems, burning skin, fatigue, chest pain, dizziness (Liu 1991)
• Headaches, fatigue, IgE-mediated sensitization (Wantke 1996) 
• Musculoskeletal, gastrointestinal, and cardiovascular symptoms (Srivastava 1992)
• Headaches, tiredness (Olsen 1982)
• Headaches, dizziness, nausea, lack of concentration ability (Burdach 1980)
• Cytogenic effects of blood lymphocytes (Suruda 1993)
• Fertility (adverse effects) (Taskinen 1999)
• Cognitive adverse effects (Kilburn 2000)
• Seizures and neurobehavioral impairment (Kilburn 1994)
• Headaches, skin problems (Proietti 2002)
• Low birth weight (Maroziene 2002)
• Neurobehavioral symptoms (Kilburn 1985)
• Memory problems, equilibrium and dexterity impairment.(Kilburn 1987)

 

Public Relations, Aspartame, Methanol, and Formaldehyde

Before discussing what little the Committee did say related to aspartame and formaldehyde, it is important to answer all of the typical public relations statements from the manufacturer and their consultants who claim there is no problem with aspartame and formaldehyde. 

 

Chart of Aspartame Manufacturer Public Relations Statements

Related to Methanol and Formaldehyde

 

Manufacturer Claim	Independent Response
Methanol is found in fruits and alcoholic beverages at higher levels than in aspartame products.	- Alcoholic beverages contain large amounts of ethanol (a protective factor) which allows methanol to be excreted before much of it is converted into formaldehyde (Leaf 1952, Liesivuori 1991, Roe 1982).  - Fruit juices have protective factors as well that prevent formaldehyde poisoning. Fruit juices produce enough methanol to “qualify as significantly methanol-contaminated liquor” (Lindinger 1997) — more methanol than what causes chronic health problems in occupational exposure (Kazeniac 1970, Kavet 1990, Frederick 1984, Kingsley 1954-55). Since we do not see chronic poisoning from fruit juices, they must contain protective factors as well. Fruit juices have ethanol as well as other possible protective factors.
Blood methanol levels do not increase when aspartame is ingested.	- In every study cited by the aspartame manufacturer, they used a very old methanol measuring method (Baker 1969) that is incapable of registering increases that are less than ~500%. Appropriate methanol testing techniques show as much as a doubling of blood methanol levels when ingesting relatively  small quantities of aspartame (Davoli 1986).
The level of methanol ingested from aspartame is not enough to cause poisoning.	- The manufacturer is referring to levels of methanol that cause death or near-death in one dose. It is the formaldehyde and formic acid (metabolites of methanol) that cause the poisoning from low-level, chronic exposure as described earlier. - The manufacturer sometimes cites Reynolds (1984) where monkeys were given the equivalent of 300 mg/kg of methanol per day for nine months without adverse effects. Methanol and its metabolites are much more toxic in humans than in other animals (Roe 1982). One dose of 300 mg/kg of methanol is potentially lethal in humans (Kavet 1991).
Formaldehyde and methanol is found in the body.	- The levels of formaldehyde and methanol in the body are very tightly controlled so that even very small exposures cause adverse health effects. Exposure to formaldehyde at levels of only ~0.75 mg/day caused adverse health effects (Wantke 1996)
Significant levels of formate (methanol metabolite) are not seen in the blood and urine of persons ingesting moderate doses of aspartame.	- For chronic formaldehyde poisoning “formic acid in urine is not an appropriate parameter for biological-monitoring of low level exposure to formaldehyde.” (Heinzow 1992). Blood formate measurements are not appropriate for chronic, low-level formaldehyde exposure (Osterloh 1996, d’Alessandro 1994)
Higher levels of formaldehyde can be found in some foods.	- Formaldehyde is produced in the body after the methanol from aspartame is absorbed. However, unlike methanol, formaldehyde in foods is not well absorbed: “Ingestion represents a minor route of [formaldehyde] exposure because the dilution factor and the binding to the macromolecules present in food reduce substantially the [formaldehyde] concentration that enters into contact with the gastrointestinal mucos.” (Restani 1991)

Scientific Committee on Food and Formaldehyde Poisoning

The Committee made two comments related to methanol and formaldehyde poisoning in their report:

Referring to the methanol absorbed from aspartame, the Committee stated:

“Methanol is also rapidly metabolized and blood levels are usually not detectable unless large bolus doses of aspartame (>50 mg/kg bw) are administered.” 

They cite Stegink (1984a) as evidence. The second item listed in the chart above details how the manufacturer funded numerous studies using an outdated methanol measuring test (Baker 1969) that was incapable of registering increases that were less than ~ 500%. Why is the Committee relying on an aspartame industry public relations book (Stegink 1984a) when millions of people are getting accurate information from independent sources in the medical literature or on the Internet?

 

Referring to Trocho (1998) where formaldehyde adducts were found to accumulate in the liver, brain, kidneys and other parts of the body after aspartame ingestion, the Committee stated:

“…radiolabelled methanol will be split off and enter the body’s one-carbon pool, with the potential to appear anywhere there is methylation. The Committee therefore agrees with the analysis of Tephly (1999) that formation of DNA adducts has not been demonstrated.”

Formaldehyde is difficult to measure directly. What Trocho (1998) did was radiolabel the methanol portion of aspartame so that it could be tracked in the body. As methanol travels through the body, it is converted into formaldehyde and then at least some of it is converted into formic acid (formate). Trocho (1998) demonstrated with the data that the buildup of radiolabelled material in the brain, liver, kidneys of could not be methanol or formic acid or any other metabolite of methanol — other than formaldehyde bound to protein. 

Trocho (1998) gave a relatively small dose of aspartame to rodents and discovered that formaldehyde from aspartame was binding to protein and DNA (as “adducts”) and accumulating in the brain, liver and other organs and tissues. 

“…. The “alternative” point expressed by Tephly [(1999)], suggesting that aspartame methanol-label goes all the way into formic acid and the C1 pathway was thoroughly refuted by us, using experimental data. There was neither labeled methionine nor thymine in protein and DNA respectively in the rat protein we recovered from rats treated with aspartame. This means–unequivocally– that the label present in DNA and protein adducts was NOT incorporated into amino acids or nucleic acid bases. The only explanation for our data was that the label was in the form of formaldehyde adducts. ….” (Alemany 2002)

If we assume that the Committee read the Trocho (1998) study and actually believes (without any alternate explanation) that it was not formaldehyde accumulating from aspartame ingestion, then the following questions are raised:

Why did the Committee choose not to focus on formaldehyde exposure issues if it was unsure about formaldehyde accumulating from aspartame use? After all, a large number of studies of formaldehyde exposure in humans have shown it causes adverse effects.

Why did the Committee show absolutely no concern about what was accumulating in the body from aspartame ingestion in the Trocho (1998) experiment even if they were not sure it was formaldehyde?

Why didn’t the Committee bring in the researchers from the Trocho (1998) experiment or independent experts on chronic formaldehyde and methanol poisoning to advise them on this issue?

 

Formaldehyde and Excitotoxins: Synergistic Poisoning

The Committee discounted health issues relating to the free-form (unbound to protein) excitotoxic amino acid obtained from aspartame by relying on and citing old and inaccurate information from an aspartame industry book (Stegink 1984a). Because they relied on aspartame industry research (Stegink 1984a) (or perhaps MSG industry research (Walker 2000)) for information about food-based excitotoxins, the Committee was unaware of the need to discuss potential synergistic adverse effects from exposure to formaldehyde and a free-form excitotoxic amino acid.

It is not the goal of this report to provide details about the effects of food-based excitotoxins. Excellent information about both acute and chronic effects from food-based excitotoxins can be obtained from Samuels (1999, 2002), Blaylock (1994), Olney (1984, 1988, 1990, 1994), Science (1972). Samuels (1999) (which is available on the Internet) is a particularly important paper for information about the manipulation of research by the food industry.

After aspartame is ingested, approximately 40% of it breaks down into a free-form excitotoxic amino acid which is quickly-absorbed (as long as it is not given in slow-dissolving capsules) (Stegink 1987a). The sudden absorption can cause a dramatic spike in blood plasma levels of this excitotoxin (Stegink 1987a). It is well known that free-form excitotoxin exposure can cause irreversible damage to brain cells (in areas such as the retina, hypothalamus, etc.) in rodents and primates (Olney 1980, 1994). In order to remove excess, cell-destroying excitotoxic amino acids from extracellular space, glial cells surround the neurons and supply them with energy (Blaylock 1994, page 39, Izumi 2002). This takes large amounts of ATP. However, formate, a formaldehyde metabolite, is an ATP inhibitor (Liesivuori 1991). 

It appears that methanol is converted to formate in the eye (Eells 1996, Garner 1995, Kini 1961). Eells (1996a) showed that chronic, low-level methanol exposure in rats led to formate accumulation in the retina of the eye. Gonzalez-Quevedo (2002) demonstrated that chronic administration of methanol to rodents increased levels of excitotoxic amino acid levels (e.g., aspartic acid) in the retina. Excitotoxic amino acids are believed to be a cause of retinal damage (Romano 1998, Calzada 2002, Kapin 1999, Izumi 2002).

Roberts (1988a) reported that 25% of the aspartame reactors he examined had decreased vision or other eye problems (blurring, “bright flashes,” tunnel vision), 9% had pain in one or both eyes, 8% had decreased tearing, and 3% had blindness. Dr. Morgan Raiford, Ophthalmologist and methanol poisoning expert testified before U.S. Congress regarding aspartame and damage to the eye:

This product has some highly toxic reactions in the human visual pathway, and we are beginning to observe the tragic damage to the optic nerve, such as blindness, partial to total optic nerve atrophy. Once this destructive process has developed there is no return of visual restoration. We are beginning to see and observe another toxic reaction which affects the central nervous system which is related to phenylalanine levels in the central nervous system. These observations are more vague, however, it stimulates the damaging to the brain and the central nervous system, having the manifestations as PKU Neuro Damage. Over 3,000 cases have been reported, and the FDA to date has ignored this existence. 

Human Visual Pathway Damage 

The human visual pathway admits ninety percent of our intellectual input to the brain and central nervous system. All of the learning processes are centered during ones life time. The mechanism of this tragic damage to the human visual system from this product is and has been known for over a decade that visual loss takes place. When this drug enters the digestive tract, largely the upper portion, this aspartame molecule spins off a by- product known as methanol or methyl-alcohol. This product enters the bloodstream and when these portions reach the highly metabolic region of the optic nerve and retina, partial atrophy can and does take place. The vision cannot do without oxygen and nutrition for more than ninety seconds without revealing some damage. Total loss of vision is present and there is no return. In the very early stages in which is referred to as the “wet stage”, treatment can be given and will reserve the destructive pathology to the optic nerve and retina.  In many cases the patient progresses to varying degrees of blindness due to incorrect diagnosis of optic neuritis

The variability of onset of the optic nerve atrophy and symptomatology make accurate diagnosis difficult.  An accurate patient history is critical as well as an understanding of the underlying disease pathology. 

Any portion of the central nervous system can and is affected. Since the chemical phenylalanine can react with other chemicals in the body, symptoms of varying hue are seen in the extremities, sensations of dullness of the intellect, visual shadows, evidence of word structure reversing and some hearing impairment is noted by the individual. This can and will in time cause problems in learning. The medical community must alert itself that we have a problem that has surfaced due to the factor of the drug industry. Parents must be alerted to the side reactions of this toxic product and its reactions. (Raiford 1987) 

 

Aspartame and Migraines / Headaches

Scientific Committee on Food — Ignoring Part of the Evidence and Discounting the Rest

The Committee report cited two independent, double-blind studies demonstrating that aspartame could cause migraines and headaches (Koehler 1988, Van Den Eeden 1994). Like almost all independent studies listed, the Committee quickly discounted these studies as flawed. The report also listed a questionnaire-based study (Lipton 1989) that linked aspartame to headaches. The report did not mention:

1558 headaches reported to the U.S. Food and Drug Administration (FDA) in the first 10 years after aspartame was approved for use in carbonated beverages (DHHS 1993). Reactions reported to the FDA represent less than 1% of adverse reactions experienced according to a former FDA Commissioner (Kessler 1993

Dr. H.J. Roberts reported on 249 cases of aspartame-induced headaches in a questionnaire-based study (Roberts 1988a).

Other case reports of aspartame-induced headache or migraines have appeared in the scientific literature (Johns 1986, Blumenthal 1997, Strong 2000, Watts 1991)

Formaldehyde that is obtained from aspartame is known to cause headaches (Main 1983, Wantke 1996, Olsen 1982, Burdach 1980, Proietti 2002)

Excitotoxic amino acids such as monosodium glutamate (MSG), similar to the excitotoxin obtained from aspartame is known to cause migraines and headaches (Kenney 1972, Ghadimi 1971, Schaumburg 1969, Scopp 1991, Ratner 1984). Note: industry-funded MSG experiments did not find increased headaches because: 

In MSG manufacturer-funded experiments conducted since 1978, aspartame was hidden in the drink mix given to the control groups (Ebert 1991, Samuels 1999); 

The MSG was sometimes combined with a large amount of sugar to completely change the way it is absorbed (e.g., Yang 1997); 

MSG was given in slow-dissolving capsules to reduce typical blood plasma changes (Stegink 1987a, Olney 1994); 

Numerous other experimental design or statistical tricks were employed to avoiding finding adverse effects as discussed by Samuels (1999)).

Chronic headaches (such as those reported from aspartame use) cause impairment of function often worse than that associated with chronic medical conditions such as arthritis and diabetes (Solomon 1993).

 

In summary, all of the scientific and clinical evidence points to aspartame causing migraines and headaches except for one badly flawed, aspartame manufacturer-sponsored study discussed below.

 

Scientific Committee on Food — Industry Studies Accepted Without Question

The Committee based its whole argument on aspartame not causing headaches on a single, one-day, double-blind study that was partially funded by the manufacturer of aspartame (Schiffman 1987). 

The study was partially funded by Monsanto/NutraSweet and conducted at the Searle Center at Duke University. (G.D. Searle was owned by Monsanto.) Susan Schiffman performed her research at the Searle Center at Duke University. The Searle Center was under the guidance of William Anlyan, a former G.D.  Searle director. Schiffman is a former General Foods and G.D. Searle consultant (Gordon 1987, Shapiro 1987). 

 

The Committee report neglected to mention numerous problems with the study including:

The aspartame test was only one day long. In fact almost all manufacturer-sponsored aspartame studies on susceptible population groups are less than 7 days long. The independent, double-blind studies that found that aspartame could cause headaches were four weeks (Koehler 1988) or 14 days (Van Den Eeden 1994) long. A one-day study combined with other major flaws listed below guaranteed that the researchers could report that there were no “statistically significant” adverse effects.

The aspartame was given in a way that even aspartame industry consultants admit is not “bioequivalent” (the same) as aspartame taken in real-world products (Stegink 1987a). The aspartame was given in slow-dissolving capsules. Giving aspartame in slow-dissolving capsules tremendously-reduces the biochemical changes that normally occur from real-world aspartame ingestion. The methanol absorption is slowed tremendously, allowing the body to eliminate more of it before it is transformed into formaldehyde. The absorption of the excitotoxic amino acid is slowed so that the liver can prevent the sudden spike in plasma levels of this amino acid normally seen when aspartame is ingested in liquids (Stegink 1987a, 1987b).

77.5% of the subjects taking the placebo experienced adverse reactions during the one-day period! 45% of the subjects taking the placebo experienced headaches. This is a ridiculously high percentage of subjects reporting adverse reactions to “placebo” in a single day. The number of participants used in this study was “sufficient to ensure that a difference of 33% in the incidence rates of headache” between the aspartame and placebo control groups would be seen as statistically significant. This means that if less than 78% (45% + 33%) of the persons taking aspartame reported headache reactions, it would not be considered statistically significant.

Numerous changes for the subjects. What could cause 77.5% of the subjects taking placebo to experience adverse reactions in a single day? What could cause 45% of the subjects taking placebo to experience headaches? None of the subject had any major medical condition. Unlike the independent double-blind studies on aspartame and headache (Koehler 1988, Van Den Eeden 1994), the following changes were made:

The diet of the subjects was changed from their normal diet to food prepared at the Medical Center. Apparently, the researchers made no attempt to ascertain whether the new diet contained monosodium glutamate (MSG), hidden forms of MSG (e.g., hydrolyzed proteins), or substances that might cause an intolerance reaction. Many of the subjects took off time from their jobs (data processing managers, statistician, CPA, sales director, executive assistants, etc.) and flew in from out of state to stay at the Medical Center for at least 5 days. They were put through numerous laboratory tests during their stay. Diet change reactions, travel stress, taking vacation time from work, laboratory tests, or the combination of all of these things may have led to such a ridiculously-high placebo reaction rate.

No baseline measurements taken. The researchers did not carefully measure the subjects’ normal frequency of headaches while they were on their normal diet and in their normal environment (i.e., baseline measurement). One reason that this is very important is so they would know if the design in the experiment caused an unusual and unintended change in the frequency of headaches reported in both the placebo and aspartame groups. Even though these researchers did not conduct baseline measurements, we can be sure that there was something wrong with the experiment that caused a large number of adverse reactions for the large majority of subjects because: 1) 77.5% of the placebo control group subjects experienced adverse reactions, and 2) the subjects had no major medical conditions that would cause such a high percentage symptoms in a one-day period.  Both independent double-blind studies on aspartame and headaches had baseline measurements (Koehler 1988, Van Den Eeden 1994).

While the Committee briefly alluded to (and quickly discounted) a commentary on and a critique of the Schiffman (1987) research by the Editor of the journal, Headache (Edmeads, 1988), the members of the Committee seem unaware of published criticism of the Schiffman (1987) study by independent researchers:

“Unfortunately, their experimental design was flawed in such a way that their negative results in no way support their conclusion that ‘aspartame is no more likely to produce headache than placebo.’” (Elsas 1988)

“We believe that the study of Schiffman et al had some serious flaws and did not reflect the realities of migraine due to dietary factors.” …. “Persons susceptible to migraine and other vascular headaches should continue to be warned of the possible aggravating role of aspartame.” (Steinmetzer 1988)

 

 

Scientific Committee on Food — Discounting All Independent Studies

Finally, the Committee criticized the Koehler (1988) and Van Den Eeden (1994) studies that found that aspartame can cause migraines and headaches. The Committee stated that these studies did not control the diet during the study itself. That is accurate. The researchers decided to allow the subjects to live their lives in a normal setting and ingest their normal diet. Because both studies performed baseline measurements of the frequency of headaches of their subjects, they could see that only one change that was introduced for part of the experiment, aspartame ingestion (but not placebo), increased the average number of headaches significantly, especially in the longer study by Koehler (1988).

The Committee also criticized the Koehler (1988) study for a high dropout rate. In other words, a number of subjects dropped out of the study. The total study length was 13 weeks (4 weeks for baseline testing, 4 weeks for aspartame testing, 4 weeks for placebo testing, 1 week between the aspartame and placebo testing). The subjects were required to keep a diary of their headaches and dietary intake. It is to be expected that after 13 weeks, many subjects will drop out or will not have done an adequate job keeping their headache and dietary diaries. However, there were still enough subjects left in the Koehler (1988) study to see a rather large and statistically significant increase in headaches in the aspartame group. In addition, there were more subjects left in the Koehler (1988) study than in some aspartame industry studies cited in the Committee report without any mention of the small number of subjects (e.g., Shaywitz 1994, Stegink 1984a). Of course, if would be preferable to conduct a larger independent study with similar subject inclusion / exclusion criteria and similar (or longer) lengths of time on and off aspartame. But at this time, all of the reasonably designed double-blind studies, all of the clinical evidence, and all of the evidence related to aspartame metabolites point to it causing migraines and headaches.

 

 

Aspartame and Seizures

Evidence Listed and Not Listed by the Committee

The Committee should be credited with mentioning in the report an independent, double-blind study, Camfield (1992), that “demonstrated that aspartame could increase the duration of certain types of epileptic seizure in children.” However, that study was only one day long. A longer independent study may have found additional effects related to seizures. The Committee pointed out that Walton (1986) reported one case of seven seizures and mania after high intake of aspartame. Finally, the Committee did cite three independent animal studies demonstrating a connection between aspartame and seizures (Guiso 1988, Maher 1987, Pinto 1988).

 

The following information was not available in the Committee report:

Between 481 and 700 cases of seizures reported to the U.S. Food and Drug Administration (FDA) in the first 10 years after aspartame was approved for use in carbonated beverages (DHHS 1993). (Note: The way the FDA categorizes neurological reactions makes it difficult to determine the exact number of seizures reported.) Reactions reported to the FDA represent less than 1% of adverse reactions experienced according to a former FDA Commissioner (Kessler 1993)

Walton (1988) described eight additional cases of seizures linked to aspartame use.

Dr. Richard Wurtman received 80 cases of seizures linked to aspartame use (Food 1986) and three of those seizure cases were described in a medical journal by Wurtman (1985). 

Eshel (1992) reported two cases of seizure linked to aspartame use. 

In a questionnaire-based study, Roberts (1988a) reported 80 cases of convulsions and seizures linked to aspartame use. 

Seizures have been reported in humans from chronic formaldehyde exposure (Kilburn 1994).

The Committee did not cite all of the other independent animal studies linking aspartame to seizures (or lowering seizure threshold levels) (Diomede 1991, Garrattini 1988, Kim 1988, Pinto 1986, Helali 1996). Nor did they cite the discussion by Wurtman (1988) as to one of many reasons a higher dose in rodents must be used to simulate the biochemical changes from aspartame in humans.

Seizures and other adverse effects from aspartame use by pilots have been mentioned in numerous aviation periodicals (Aviation Consumer 1988, Aviation Medical Bulletin 1988, Pacific Flyer 1988, CAA General Aviation 1989, Aviation Safety Digest 1989, General Aviation News 1989, Plane & Pilot 1990, Canadian General Aviation News 1990, NBAA Digest 1993, ICAS 1995, Pacific Flyer 1995, US Air Force 1992).

 

Overwhelming the Reader with an Long List of References

The Committee quoted the following from the AFSSA (2002) report:

“This causal relationship between aspartame and epileptic seizures has been refuted by a large number of scientists who base their opinions on numerous experimental studies conducted on laboratory animals or on clinical or tolerance studies in humans (Anderson et al., 1996; Gaull, 1985, Rowan et al., 1995; Shaywitz et al., 1994; Tollefson et al., 1992, 1993; Daily et al., 1991; Zhi et al., 1989; Sze, 1989; Tilson et al.,. 1989).”

At first glance, that seems like a very impressive list of 10 studies. 

 

There are only two studies in the list that involve giving aspartame to human subjects (Rowan 1995, Shaywitz 1994):

Nearly all of the subjects in these aspartame industry-sponsored studies were taking anti-seizure medication during the study! Clearly anyone who cites these two studies as safety evidence has not read the scientific literature. 

The Rowan (1995) study administered aspartame for only one day to 18 subjects (16 were taking anti-seizure medication). The Shaywitz (1994) study administered aspartame for only two weeks to 10 children (nine were taking anti-seizure medication). Roberts (1988a) looked at 551 cases and reported that reactions to aspartame appeared anywhere from immediately to more than one (1) year after initial use began. Keeping the studies short helped guarantee that there would be few, if any, adverse reactions.

The aspartame was given in a way that even aspartame industry consultants admit is not “bioequivalent” (the same) as aspartame taken in real-world products (Stegink 1987a). The aspartame was given in slow-dissolving capsules. Giving aspartame in slow-dissolving capsules tremendously-reduces the biochemical changes that normally occur from real-world aspartame ingestion. The methanol absorption is slowed tremendously, allowing the body to eliminate more of it before it is transformed into formaldehyde. The absorption of the excitotoxic amino acid is slowed so that the liver can prevent the sudden spike in plasma levels of this amino acid normally seen when aspartame is ingested in liquids (Stegink 1987a, 1987b).

Please note that the Rowan (1995) study used a susceptible population group — persons who had reported seizures from aspartame use. But by having almost all of the subjects taking anti-seizure medication, administering aspartame for only one day, and administering it in a way that reduces the toxicity, there was little chance that adverse reactions would appear. In addition, the small number of subjects in both studies meant that if there were reactions to aspartame, it would be unlikely that the number of reactions would be considered “statistically significant.” 

Continuing with the studies the Committee listed relating to aspartame and seizures, 

Anderson (1996) is simply a review related to aspartame and seizures in an aspartame industry-compiled public relations book. Gaull (1985) is a Letter to the Editor by a NutraSweet Company physician in response to a Letter to the Editor summarizing several case reports of aspartame-induced seizures (Wurtman 1985). There is nothing wrong with Letters to the Editor, but Gaull’s opinion does not represent a new experimental study as implied by the Committee. Sze (1989) is a review of early animal research related to aspartame and seizures. The review is useful (like most reviews), but it does not contain any original research. Tollefson (1993) is a review of clinical research related to Multiple Chemical Sensitivity and summarizes the same information about aspartame in Tollefson (1992) that the Committee also cited above.

The following three studies cited by the Committee are animal studies related to aspartame and seizures Dailey 1991, Tilson 1989, Zhi 1989). These studies contrast with the many independent animal studies cited above that link aspartame to seizure susceptibility in animals.

This leaves us with one study cited by the Committee that looked at case reports to the U.S. Food and Drug Administration (FDA) related to aspartame and seizures (Tollefson 1992). The author reported that the FDA had received 251 case reports of seizures linked to aspartame. The truth is that the FDA separates “Seizures” from  “Grand Mal Seizures,” “Petit Mal Seizures,” “Complex Partial Seizures” and possibly “Other Neurological” (DHHS 1993). The Tollefson (1992) report focused only on the 251 seizures listed in the “Seizures” category.

Tollefson (1992) then inappropriately classified 13 cases as “highly unlikely to be associated with aspartame” because medical records were not available. A more appropriate category would have been “Unconfirmed Cause.” Another 111 cases was also classified as “highly unlikely to be associated with aspartame” if there was any another possible cause of the seizures or the physician did not agree with the patient that aspartame caused the seizures. Again, a more appropriate category would be “Unconfirmed Cause.”

Of the remaining 127 cases, in 32% of the cases the symptoms (seizures) recurred each time the person consumed different products containing aspartame. In 28% of the cases the symptoms (seizures) recurred each time the person consumed the same product containing aspartame. Despite the unusual way that Tollefson (1992) classified patients, there were still a large number of patients who had clinically-reproducible seizures from aspartame. The full text of this study does not support the Committee’s contention that aspartame does not cause seizures. 

In summary, the Committee ignored much of the independent evidence linking aspartame to seizures. They relied primarily on industry reviews, a manufacturer employee letter, manufacturer-sponsored animal studies, two very short double-blind studies on subjects taking anti-seizure medication, and an analysis that demonstrates that some subjects do have reproducible seizures after ingesting aspartame from the same or different products.

 

Aspartame and Brain Cancer

Evidence Related to Aspartame and Brain Tumors:

In 1996, a group of researchers led by Olney (1996) analyzed brain tumor incidence rates in the United States and other research related to aspartame and brain tumors. They came to the following conclusions:

Within several years after aspartame approval, the incidence of specific types of deadly brain tumors (glioblastomas and anaplastic astrocytomas) increased tremendously in vulnerable population groups (middle aged and elderly). During the same period of time, the incidence of less deadly astrocytoma tumors decreased tremendously. Olney (1996) showed that while the overall brain tumor incidence rate remained somewhat constant, there was a shift in malignancy from the less deadly to more deadly types of brain tumors shortly after aspartame came on the market.

What is very important to understand is that Olney (1996) was not looking at the overall brain tumor rates in the general population. He looked at the conversion of less deadly to more deadly brain tumors (i.e., a “conversion of [existing] astrocytic tumors from a lower to higher grade of malignancy”) in a vulnerable population group (middle age and elderly). This conversion to a higher and more deadly grade of malignancy was seen as a tremendous increase in incidence of glioblastomas and anaplastic astrocytomas shortly after aspartame came on the market and a nearly equal decrease in strocytomas during the same period of time. 

Brain tumors in adults tend to develop over a long period of time before they are diagnosed. If aspartame causes the growth of brain tumors it might take 20 or 30 years (or more) before one would be able to see the increase in the overall brain tumor rates when examining the brain cancer incidence statistics from all age groups of the general population. But Olney (1996) was able to prove that there was a very large change (worsening) of existing malignancies in a vulnerable population group shortly after aspartame came on the market. By itself, the large increase in deadly tumors, shortly after aspartame approval, does not prove that aspartame causes brain cancer or effects existing tumors. But along with evidence in items #2 and #3 below, there is enough evidence to warn people about the possibility.

 

Animals in aspartame pre-approval studies showed an increased rate of the same types of brain tumors.

Aspartame has mutagenic potential in vitro.

The Committee neglected to mention that Hardell (2000) looked at various risk factors for brain cancer. A significant association was found between subjects with higher ingestion of diet drinks and malignant brain tumors. The mean age of the subjects was 50 years old. While the number of subject was very small, it is the only study conducted that looked at an older (vulnerable) population group and aspartame intake.

 

The Committee is Not Familiar with Aspartame and Brain Cancer Research

Any intelligent discussion of the Olney (1996) study and brain cancer data must look at incidence rates of glioblastomas and anaplastic astrocytomas in middle age and elderly population groups. A discussion of overall brain tumor rates is meaningless because Olney (1996) showed that the overall brain cancer rates remain stable due to the drop in less deadly astrocytoma incidence rates.

It becomes clear that the Committee has no familiarity with the Olney (1996) study because they make the following criticisms of Olney (1996) in the report:

The rates of brain cancer was looked at in France and remained relatively stable between 1980 and 1997 (Menegoz 2001). The Committee apparently has no idea that they must look at specific types of brain tumors in vulnerable population groups to see if aspartame may be having an effect on existing malignancies. Had they read Olney (1996), they would not be focusing on overall brain cancer rates.

Gurney (1997) found no link between aspartame and brain cancer in 56 children. Had the Committee read Olney (1996) they would know that the brain cancer increases would be expected to be seen first in vulnerable population groups — middle-aged and elderly for specific types of brain cancer (e.g., glioblastomas and anaplastic astrocytomas). The Gurney (1997) study is not relevant because it combined all types of brain tumors in a relatively small number of children. But the Olney (1996) analysis demonstrated that the large shift to higher-grade brain tumor malignancies was seen first in the middle-aged and elderly population groups (and not in children).

The Committee claimed that the incident rates increased due to better diagnostic methods (Modan, 1992). In the early and mid-1980’s magnetic resonance imaging (MRI) was introduced as a method of detecting brain cancer earlier. However, the types of brain cancer that Olney (1996) showed an increase for in vulnerable population groups was large and easily-detectable without the use of MRI equipment. In fact, the incidence rate of the smaller astrocytomas in the vulnerable population groups went down despite the introduction of MRI technology. One would expect MRI technology to increase the discovery and incidence of smaller, harder-to-detect astrocytomas. Instead, the astrocytoma rate in the vulnerable population group went down. This means that some other factor or factors were a major influence on the changes in brain tumor rates in vulnerable population groups.

The Committee cited several letters and papers that claim the Olney (1996) methodology was flawed (Levy 1996, Linet 1999, Ross 1998, Seife 1999, Smith 1998). Before looking at these references, it is important to know that the scientific journal, The Lancet (1996) reported that the Editor of the journal publishing Olney’s (1996) study was pressured by the NutraSweet Company to publish a rebuttal in the same issue as Olney’s study. The Editor refused, but as soon as he agreed to NutraSweet’s request to publish follow-up correspondence, he received “a blitz of letters.” 

Linet (1999) and Smith (1998) are articles (not related to aspartame) that look at brain cancer incidence in children — not the vulnerable population groups looked at by Olney. Seife (1999) is a letter from a Journalist who disagrees with Olney’s analysis. Both Smith (1998) and Levy (1996) focused much of the criticism on the overall brain cancer rates in all population groups. In fact, Levy (1996) combined population groups rather than looking at the same age ranges from the Olney (1996) study.

Surprisingly, the Committee did not mention a criticism of the Olney (1996) study that can be found in aspartame industry literature (e.g., Butchko 2002). It is sometimes claimed that changes in diagnostic criteria during the mid-1980’s were the cause of the changes in incidence rate for specific brain tumors seen by Olney (1996). As Olney (1996) points out:

“If the shift were artefactual (i.e., assignment of glioblastoma diagnosis to tumors which in the prior era would have been considered astrocytomas), it should cause the < 2 year death rate for glioblastomas to drop substantially, especially in younger age groups in which the characteristic < 2 year death rate is much lower for astrocytomas than for glioblastomas. We found that the < 2 year death rate did not change appreciably from the early period to later period for either astrocytomas or glioblastomas in any of the four age groups. Thus, tumors diagnosed as astrocytomas in either time period behaved as astrocytomas and those diagnosed as glioblastomas behaved as glioblastomas. These results favor the interpretation that the shift reflects a real increase in the rate of conversion of astrocytic tumors from a lower to higher grade of malignancy rather than a mere change in diagnostic assignment practices.”

The Committee referred to pre-approval animal studies that they claim showed that aspartame did not produce brain cancer in rodents. The information they used came from articles written by manufacturer employees and consultants in an aspartame industry public relations book (Koestner 1984, Cornell 1984), and from an FDA Commissioner (FDA FR, 1981-1984). This FDA Commissioner ignored the unanimous vote against aspartame by the independent Public Board of Inquiry (Brannigan 1983) and ignored his own scientists who considered the brain tumor data so worrisome that they could not recommend approval of aspartame (Gordon 1987). This FDA Commissioner left office shortly after he approved the use of aspartame in carbonated beverages and became a high-paid consultant for the aspartame manufacturer’s public relations firm (Gordon 1987 and GAO 1986).

The Committee did not even cite the testimony of Olney (1987) where he addresses the issues surrounding brain cancer seen in pre-approval studies. Dr. Olney is an independent scientist and experienced Neuropathologist. The Public Board of Inquiry (PBOI) that looked at the aspartame and brain tumor issue and other issues convened in 1981 (Brannigan 1983). The only member on the PBOI who was qualified in the area of brain tumors was Peter Lampert, a Neuropathologist and the President of the American Association of Neuropathologists.  Dr. Lampert told Dr. Olney that:

“…[he] had been surprised at the large size of the brain tumors in the Nutrasweet-fed rats. This reinforced his impression that they had been caused by some tumorigenic agent since spontaneous brain tumors are not only rare in laboratory rats but when they do occur they are usually not so large.” (Olney 1987)

The Committee also did not consider the testimony of Dr. Adrian Gross (1985, 1987a, 1987b), the FDA Toxicologists and Investigator who looked carefully at the many of the aspartame pre-approval studies. The Committee simply accepted studies from laboratories where FDA Investigators showed that many of the animals died and mysteriously came back to life several times (Schmidt 1976):

J24HM Found dead 3/21/71 Alive 5/19/71 Dead 5/16/71 Alive 7/14/71 Dead 8/11/71	K18LF Alive 4/22/71 vanished (dead ?) 5/20/71 Alive 6/17/71 vanished (dead ?) 7/15/71	M25CF Found dead 3/6/71 Alive 6/18/71 Dead 7/16/71 Alive 9/10/71 Alive 10/8/71 Dead 11/5/71	H28MF Alive 7/13/71 vanished (dead ?) 8/10/71
H15CF Alive 7/13/71 vanished (dead ?) 8/10/71	G 2HM Found dead 3/10/71 Alive 8/9/71	A15MM Found dead 3/13/71 Alive 5/3/71 Dead 6/1/71 Alive 8/23/71 Dead 9/20/71	G16HM Found dead 3/9/71 Alive 8/9/71 Dead 9/7/71
A 6HM Found dead 2/25/71 Alive 5/3/71 Dead 6/1/71 Alive 8/23/71 Dead 9/20/71	G23HM Found dead 3/7/71 Alive 8/9/71 Dead 9/7/71	E15MM Found dead 1/21/72 Alive 2/25/72	G 8MM Found dead 9/3/71 Alive 11/29/71 Dead 12/27/71
B19HF Alive 6/29/71 vanished (dead ?) 7/27/71 Alive 8/24/71 vanished (dead ?) 9/21/71 Alive 10/19/71 vanished (dead ?) 11/16/71 Alive (?) 2/22/72	B21HF Found dead 2/25/71 Alive 8/24/71 Dead 9/21/71 Alive 10/19/71 Dead 11/16/71 Alive 2/22/72	B14MF Killed 7/30/71 Alive 10/19/71 Dead 11/16/71 Alive (?) 2/22/72	B12HF Found dead 9/2/71 Alive 10/19/71 Dead 11/16/71 Alive (?) 2/22/72
B 4CF Found dead 9/12/71 Alive 10/19/71 Dead 11/16/71 Alive (?) 2/22/72	D30LF Found dead 1/22/72 Alive 2/22/72	B15HF Found dead 1/25/72 Alive 2/22/72	C29LM Found dead 3/29/71 Alive 6/2/71 Dead 6/30/71
C12HM Found dead 8/10/71 Alive 10/20/71 Dead 11/17/71

 

According to Dr. Adrian Gross (FDA Toxicologist and Investigator):

“They [manufacturer] lied and they didn’t submit the real nature of their observations because had they done that it is more than likely that a great number of these studies would have been rejected simply for adequacy. What [the manufacturer] did, they took great pains to camouflage these shortcomings of the study. As I say filter and just present to the FDA what they wished the FDA to know and they did other terrible things for instance animals would develop tumors while they were under study. Well they would remove these tumors from the animals” [FDA Toxicologist and Task Force member, Dr. Adrian Gross (Wilson 1985)]

Apparently the Committee is unaware of the chaos in the manufacturer laboratories for aspartame pre-approval research as detailed in ATIC (1996).

 

Aspartame and Reproductive Effects

Based on the review of summarized pre-approval study data by a World Health Organization committee (JECFA 1980) and the earlier review by the Scientific Committee on Food (SCF 1985), the Scientific Committee on Food stated that:

“…no additional studies were identified which would impact on the no-observed-adverse-effect level (NOAEL) [for aspartame].”

Aside from the chaos that was seen in the manufacturer’s pre-approval studies that led to the criminal investigation of the manufacturer (Merrill 1977), there are several items that the Committee neglected to mention:

The manufacturer employee responsible for reviewing most of the reproduction studies had only one year of prior experience, working on population dynamics of cotton tail rabbits while employed by Illinois Wildlife Service. In order to prepare him for this title of ‘Senior Research Assistant in Teratology’ (fetal damage) the manufacturer bought him books to read on the subject and also sent him to a meeting of the Teratology Society. They claimed that this qualified him to submit 18 of the initial tests to the FDA, in addition to training an assistant and 2 technicians. He certainly must have kept them busy because the manufacturer claimed that 329 teratology examinations were conducted in just 2 days. (Stoddard 1995,  Graves 1984)

The manufacturer’s own consultant, Dr. Gregory Palmer, commented on the poor quality of the pre-approval reproduction studies (Gross 1985):

“Even following the track you did, it seems to me you have only confounded the issue by a series of studies most of which have severe design deficiencies or obvious lack of expertise in animal management. Because of these twin factors, all the careful and detailed examination of fetuses, all the writing, summarization and resummarization is of little avail because of the shaky foundation.”

The Committee did not mention that Dow-Edwards (1989) demonstrated that aspartame administration after conception disrupted “odor-associative learning in newborn guinea pigs. The aspartame dose used was far below the no-observed-adverse-effect level (NOAEL) mentioned in the JECFA (1980) review. Obviously, this study by itself would impact the NOAEL.

As mentioned earlier, The Guardian summarized parts of a confidential report compiled for the World Health Organization which stated that Expert Committees have been infiltrated by food industry consultants (Guardian 2003).

The Committee did not discuss a fairly large body of research related to the reproductive adverse effects of formaldehyde exposure (Thrasher 2001), including a recent paper on low birth weight and formaldehyde exposure in humans (Maroziene 2002)

The Committee made no mention of any reviews or studies related to damage to offspring from ingestion of excitotoxins obtained from aspartame and other chemical sources (e.g., monosodium glutamate) (Olney 1988, Olney 1994, Gao 1994, Fisher 1991, Toth 1987, Frieder 1984). Excitotoxins may be many time more toxic in humans than in rodents and monkeys due to the potential spike in plasma levels after administration (Olney 1994). A discussion of the combined effects of formaldehyde and excitotoxin exposure would have been relevant.

 

Aspartame and Behavior, Cognition, Mood

“Long-Term” Research

For long-term research, the Committee relied on two aspartame industry-sponsored studies when they stated:

“A number of longer term studies with double-blind design involving multiple dosing in healthy individuals also failed to highlight any treatment-related adverse effects on behavior (Spiers 1998, Leon 1989)”

The Committee did not even read the Leon (1989) study because it is not a study on aspartame and behavior. Both studies will be looked at in this report, but a few very important preliminary details must be looked at.

It is important to understand that when the aspartame industry funds studies, the studies are designed in such a way as to make it virtually impossible to find adverse effects. One of many methods that are used is that longer studies will only be conducted only on perfectly healthy subjects. Subjects who have reported adverse effects from real-world aspartame products will be placed in very short studies with other major flaws. For example, Rowan (1995) looked at persons who had experienced seizures from aspartame, but the study was only one day long, almost all of the subjects were on anti-seizure medication, and the aspartame was given in a way as to make it less toxic. Schiffman (1988) looked at persons who reported headaches from aspartame, but the study was only one day long, the aspartame was given in a way as to make it less toxic, and design flaws of the study caused over 75% of the persons on placebo to have adverse effects in a single day. Karstaedt (1993) tested aspartame on Parkinson’s Disease patients, but the study was only one day long and the subjects were given aspartame in a way as to make it less toxic. Hertelendy (1993) studied aspartame in patients with liver disease, but the study only lasted one day.

Sometimes aspartame industry studies on subjects with medical conditions will be longer than one day. Shaywitz (1994) studied epilepsy patients (but not patients who had reported seizures from aspartame) for two weeks, but the subjects were taking anti-seizure medication during the study.

But the longer studies like Leon (1989) and Spiers (1998) will use perfectly healthy subjects who are the least susceptible to reactions from several months of aspartame exposure (but still susceptible to long-term aspartame poisoning from years of use). Even these long studies do not take into account the fact that a large number of persons reporting serious health problems from aspartame use are able to ingest it without clinically-obvious adverse effects for many months or years (Roberts 1988a). Slow poisoning from the formaldehyde exposure in conjunction with the synergistic effects of a free-form excitotoxic amino acid would account for the delays in clinically obvious reactions.

Leon (1989) gave aspartame or placebo to healthy subject for 24 weeks. The aspartame was given in slow-dissolving capsules that reduce its toxicity (as discussed earlier). Even with the use of healthy subjects and a reduced toxicity form of aspartame, there was a > 50% increase in adverse reactions in the aspartame group. However, the researchers split the reactions into 14 small subcategories. They could then claim that within each tiny subcategory, there was no “statistically significant” increase in aspartame reactions. Since Leon (1989) split the reactions into 14 small subcategories, at least 20 times more subjects should have been enrolled in the study to have any hope of seeing statistically significant differences within the tiny subcategories. 

Phase 3 drug trials are used in the U.S. to help determine what adverse effects might be associated with a drug. Enough subjects are enrolled to be able to extrapolate the results to the general population. Several hundred to several thousand patients are enrolled in Phase 3 trials (Nibeuhr 2000, FDA 2001). Patients in clinical trials tend to be more prone to adverse reactions. The Leon (1989) study used healthy patients, less prone to adverse effects from substances and therefore that study should have enrolled even more subjects than typically enrolled in Phase 3 clinical trials.

Leon (1989) had only 50 subjects take aspartame for 24 weeks and 51 subjects take placebo for 24 weeks. With the small number of perfectly healthy subjects and the reactions split into 14 subcategories and a less toxic form of aspartame used, it was inevitable that the researchers could claim no “statistically significant” increase in adverse reactions within each subcategory (even though aspartame caused a > 50% increase in adverse reactions overall).

The Spiers (1998) NutraSweet-funded study is a lesson in how a study can be designed so that there is virtually no chance of seeing “statistically significant” numbers of adverse reactions.

The aspartame was given for only 20 days to perfectly healthy subjects who had a history of aspartame use without reported complaints.

It is important to understand that many people can use aspartame for months or several years without any clinically obvious symptoms appearing. However, the chronic poisoning from aspartame use eventually catches up with most, if not all users.

Under normal conditions, even some healthy subjects would experience immediate reactions to aspartame within a week after first use of the product — probably due to an acute sensitivity to formaldehyde or an excitotoxic amino acid. Roberts (1988a) looked at 551 cases and reported that reactions to aspartame appeared anywhere from immediately to over one (1) year after initial use began. Many of the subjects in the Roberts (1988a) survey repeatedly tested aspartame and found it to cause adverse effects. Some of them (120 subjects) eliminated aspartame and then inadvertently ingested and reacted to a product that they did not know contained aspartame until after they had adverse effects.

The full publication of Spiers (1998) had no information about previous aspartame use of the subjects. But we learn from the original publication of the study in abstract form (Spiers 1993) that the subjects had a “history of aspartame use without reported complaints”. It would be very unlikely, therefore, to see very many adverse reactions with 20 days of additional use. These are the types of subjects who, like the case described above, would be more likely to have chronic health problems develop from aspartame after many months or years of aspartame use. In the Spiers’ own words:

 

“In summary, we made a conscious effort to preselect individuals who we felt would be unlikely to experience any effect from chronic aspartame exposure” (Spiers 1988) 

Not only was the study performed on healthy individuals for only 20 days (a “long” study by aspartame industry standards), but also it was performed on individuals who had not yet experienced clinically obvious adverse effects from aspartame use!

 

Most of the aspartame was given in slow-dissolving capsules that reduce toxicity.

 

As noted numerous times above, even aspartame industry consultants agree that providing aspartame in slow-dissolving capsules is not “bioequivalent” (the same) as real-world aspartame. The biochemical changes from greatly slowing down absorption are reduced significantly.

The combination of the small number of subjects and splitting the reactions into several categories meant seeing a statistically significant change was virtually impossible (especially when combined with the above-mentioned flaws).

Take a look at the most commonly reported adverse effect from aspartame – headaches and migraines (DHHS 1993). Let us assume for the moment that 8 percent of the subjects in the study would begin experiencing aspartame-induced headaches after 20 days of aspartame use. As pointed out above, it would be highly unlikely that even 8 percent of these subjects would report one particular type of adverse effect due to aspartame after only 20 days (especially since that had not yet reported clinically obvious effects from a history of aspartame use). But let us see what would happen if 8 percent of the study population did report aspartame-induced headaches from aspartame use within 20 days.

In fact, there was an 8 percent increase in headaches reported in the aspartame group. However, this increase was not “statistically significant.” When you take a small number of healthy patients and split the reactions into several categories, it is inevitable that within most, if not all of the categories, the reactions will be deemed “not statistically significant.” Combining this problem with the short, 20-day study using a reduced-toxicity administration of aspartame and using subjects who had no chance of reporting immediate effects from first-time use of aspartame, the claimed results of no statistically significant effects was inevitable.

 

 

ADD/ADHD and Behavior Research: Aspartame and Children

The Committee cited numerous aspartame industry-sponsored studies on aspartame and behavior, mood, and learning in children (Shaywitz 1994, Saravis 1990, Wolraich 1994). The first questions the Committee should have asked are: “What is being seen clinically in relation to food and behavior/learning issues in children”? What is working in research and in clinical settings related to food and behavior/learning issues”? Without knowledge of independent studies and clinical aspects related to food and behavior, the Committee is susceptible to accepting any aspartame industry-sponsored study, no matter how irrelevant or poorly designed.

Summarizing the independent research related to food and behavior in children:

Kaplan (1989) reported a > 50% improvement in behavioral measurement and some non-behavioral measurements in a 10-week, blinded crossover study in preschool-age, hyperactive boys. The experimental diet removed monosodium glutamate (MSG), preservatives, caffeine, substances reported by the family to cause reactions. The diet was low in simple sugars and eliminated dairy if the family reported a history of problems with cow’s milk. 

Boris (1994) conducted a study where reactive foods, dyes, and artificial colors were removed from the diets of children with ADHD. In addition, a double-blind, placebo-controlled challenge was conducted. 73% of the children responded favorably to the diet change. 

Carter (1993) designed an elimination diet (removing reactive foods/substances) for 78 children with hyperactive behavior. 59 children improved during the trial period. For 19 of the children, it was possible to disguise certain foods or additives and reliably provoke behavioral problems in a placebo-controlled, double-blind challenge. 

Egger (1985, 1992) found that an elimination diet significantly improved behavior and reduced or eliminated bed-wetting in hyperactive children. Artificial colorants and preservatives were the most common provoking substance, but all of the children reacted to more than just colorants and preservatives. 

Dengate (2002) treated 27 children with a diet that excludes food additives, natural salicylates, amines and glutamates. Their behavior improved significantly. The subjects were then tested by introducing one food additive. A significantly higher percentage of the subjects who took the additive had worsening behavior as compared to when they were ingesting the placebo.

Schmidt (1997) tested an “oligoantigenic diet” (a non-allergenic, simple foods diet) on 49 hyperactive children in a placebo-controlled, double-blind study. In this experiment, only 24% of the children had significant behavioral improvement (relative to the control diet conditions), but the amount of positive changes in behavior was about the same as those who received Ritilan. 

Swanson (1980) gave 20 hyperactive and 20 non-hyperactive children a diet free of artificial food dyes and other additives for 5 days. Large oral doses of food dyes and placebo were then given to the children. The hyperactive children had impaired learning tests compared to the placebo group. 

Conners (1976) conducted a double-blind crossover trial eliminating artificial flavors, colors, and natural salicylates as recommended by the Feingold Association. Fifteen hyperactive children were tested. The teachers noted a highly significant reduction of symptoms on the Feingold diet. Both parents and teachers reported fewer symptoms on the Feingold diet. 

Brenner (1977) tested 59 children diagnosed with hyperactivity and minimal brain dysfunction syndrome. 32 children stayed on the diet. Of those 32 children, 11 improved markedly. While there was no control group or placebo in this study, the researchers stated that “startling changes seen in patients who had been followed for years with other forms of therapy suggest strongly that this improvement was genuine.” 

Salzman (1976) tested 15 hyperactive children with the Feingold K-P diet. “93% responded with improved behavior in areas of over activity, distractibility, impulsiveness and excitability. Sleep and enuresis problems were resolved partially or completely.” 

Rose (1978) tested artificial food colors on two girls who had been on the Feingold K-P diet for 11 months. There was an significant increase in hyperactive behaviors with ingestion of artificial food colors as compared to the placebo.

In a study conducted by the David Hide Asthma and Allergy Research Centre in the UK, 277 children were given a mixture of artificial food colorings or placebo (Foodcomm 2002). While the standardized behavioral tests showed no differences, the parents of the children noticed significant behavioral differences while the children were in their natural environment

Well-known Pediatrician and ADD Expert, Dr. Doris Rapp reports that customized changes to diet, including the removal of various reactions foods and chemicals improves approximately 80% of her patients (Rapp 2002). 

Central Alternative High School in Appleton, Wisconsin reported a large improvement in behavioral problems after removing vending machines (that contain junk food, aspartame- and sugar-containing beverages, etc.) (Appleton 2002). 

It is obvious from independent research and clinical experience that it is the removal multiple offending items (additives, preservatives, colorings, certain sweeteners, monosodium glutamate, foods that cause allergic or intolerance reactions, etc.) that successfully and significantly reduces behavioral problems and even some non-behavioral problems in children.

The aspartame industry designs research on a relatively small number of children who may have behavioral, learning, and mood reactions to a variety of additives, foods, sweeteners (including aspartame) and rather than eliminating all of the offending substances (as seen to work in the independent research and clinical settings), they just manipulate one ingredient (aspartame or sugar). For behavioral issues in children, the manipulation of one ingredient (that the child may or may not have behavioral reactions to after short-term use) will only prove successful in a very small percentage of cases. For the aspartame industry, the small number of children in their tests, the fact that they split adverse effects into multiple categories and use average values on the behavioral and cognitive tests makes it nearly impossible to find any “statistically significant” link between aspartame and behavioral problems.

 

Aspartame and Other Effects

The Committee neglected to report on relief of fibromyalgia symptoms after elimination of aspartame and other dietary excitotoxins (Smith 2001). They did not mention an independent study related to aspartame and dizziness in humans (Gulya 1992). They neglected to mention independent research related to aspartame and memory loss (Orange 1998, Konen 2000). Brief mention was made of the study by Dr. Ralph Walton showing a significant increase in adverse symptoms from aspartame ingestion in patients with depression (Walton 1993). But like all independent studies it was discounted by the Committee for 1) having too few subjects (even though there were more subjects than many of the studies the Committee accepted) and 2) looking at an overall increase in adverse reaction rate rather than splitting the reactions into the 26 separate categories that were recorded.

The Committee also neglected to report on some of the other symptoms reported in the medical literature such as panic attacks (Drake 1986), Lobular Panniculitis (McCauliffe 1991), Granulomatous Panniculitis (Novick 1995), diabetic complications (Roberts 1988b), joint pain (Roberts 1991), vision loss (Roberts 1988a, Raiford 1987), and many other serious adverse symptoms reported from aspartame use in documents written by independent clinicians (Dorway 2003, NM 2003)

The Committee reported that two short aspartame industry-funded studies related to allergic-like effects of aspartame showed no statistically significant effects (Garriga 1991, Geha 1993). The Committee neglected to mention that Kulczycki (1995) declined to take part in the Geha (1993) study due to significant flaws in the study design that “probably tended to discourage the participation of the subjects who were likely to be allergic to aspartame.” Kulczycki (1995) was able to easily find subjects reporting allergic-like effects from aspartame and conducted his own double-blind testing. He found that aspartame caused problems in four of the six subjects he tested with double-blind methodology. There were several other flaws in the Geha (1993) study that were discussed by Kulczycki (1995).

The Committee report mentioned that there were a number of studies focusing on the effects of aspartame on hunger and food intake (e.g., Rolls 1996, Kanders 1996). The Committee mentioned aspartame industry-sponsored studies that claimed no potential negative hunger or food intake consequences, but they did not mention that Lavin (1997) found that females with eating restraint had a higher Calorie intake subsequent to aspartame intake as opposed to sugar or water intake.

 

Conclusion

Persons ingesting aspartame are being exposure to significant amounts of formaldehyde that has been shown by independent research to accumulate throughout the body. Chronic, low-level exposure to formaldehyde (even without accumulation) has been shown in human research to cause irreversible genetic damage, headaches, seizures, neurobehavioral problems, gastrointestinal and cardiovascular problems, fatigue, chest pains, dizziness, etc. Exposure to a free-form excitotoxic amino acid from aspartame would be expected to worsen the adverse effects from chronic formaldehyde poisoning.

Aspartame manufacturer-sponsored studies are designed in a way as to avoid the possibility of finding adverse effects, yet the Committee accepted these studies without any question. In contrast, nearly all independent research on aspartame in animals or humans has found that aspartame can cause problems.

Human studies and clinical reports published in the medical literature linking aspartame use to fibromyalgia, seizures, panic attacks, mania, brain cancer, migraines / headaches, vertigo, symptoms related to depression, memory loss, hives, irregular heart beats, vision loss, and numerous of symptoms were largely ignored by the Committee.

It appears that the Committee obtained most of its information from aspartame industry public relations books that they repeatedly cited (Stegink 1984, Tschanz 1996), published reviews by manufacturer employees (Butchko 1994, Butchko 2001), a report from the French Food Agency (AFSSA 2002) written by some unknown individual(s), and perhaps the occasional published study, primarily manufacturer-sponsored studies. A significant amount of independent research was ignored, and when independent studies were mentioned, they were quickly labeled as flawed. There is evidence that the Committee did not read some or most of the research they cited and is only familiar with aspartame-related research from the aspartame manufacturer’s perspective.

[Gold MD. 2003 Feb. Independent Analysis of the “Opinion of the European Commission, Scientific Committee on Food: Update on the Safety of Aspartame/E951” (SCF 2002)]

 

Tagged as: Food hazards