by Mark D. Gold

Aspartame Toxicity Information Center^*

12 East Side Dr., Suite 2-17

Concord, New Hampshire, 02139 USA

1-603-225-2110

February 3, 2003

*The Aspartame Toxicity Information Center is funded by Mark D. Gold. No funding has been received from the food industry for any work performed by the author or by the Aspartame Toxicity Information Center.

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).

This response will demonstrate that:

In addition to the analysis of the Scientific Committee on Food report, there will be numerous sample aspartame poisoning case reports within the text to give the reader an idea of the clinical effects being reported. The reports will be taken from the medical literature and from the Aspartame Toxicity Information Center listing of cases (ATIC 1997, 1998).

References for this analysis appear at the end of the report.

In the United States, corruption of governmental and scientific committees by the food industry was disclosed in the late 1960’s and early 1970’s. In an article in the journal Science (1972), it was revealed that the National Academy of Sciences (NAS) Food Protection Committee was being funded by the food, chemical and packaging industries. The U.S. Food and Drug Administration (FDA) was relying on the NAS Committee for "independent" information. The Chairman of the NAS Subcommittee investigating monosodium glutamate (MSG) had recently taken part in research partially funded by the MSG manufacturer. Another member of the Subcommittee became a spokesperson for the MSG industry. (Science 1972). Other members of the Subcommittee had ties to the MSG industry. Since that time numerous governmental committees have been corrupted by the placement of food industry-funded consultants on these committees (Samuels 1999, Collins 2000).

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:

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":

Ajinomoto of Japan has benefited tremendously by having key committees corrupted by biased, industry-paid consultants (Samuels 1999)

Members of the European Commission Scientific Committee on Food have admitted to a conflict of interest:

One member of the European Commission Scientific Committee on Food, Ronald Walker, spent seven (7) years as the ILSI’s Chairman of their Scientific Committee on Toxicology/Food Safety in Europe (Walker 2001). Another member of the Committee, W.H.M. Saris, is the chairman of the ILSI Scientific Committee on Nutrition (NUTRIM 2000). At least half of the Committee members have been involved in ILSI projects and/or participated in ILSI workshops (ILSI 1999).

The Scientific Committee on Food (SCF) documents are presented without any information as to the past or current financial ties between the Committee members and the food industry. Despite the efforts by independent organizations, the members of the Scientific Committee on Food do not provide a detailed accounting of their food industry ties even after such ties are discovered (BMA 1997)

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).

In contrast, the Scientific Committee on Food succeeded in banning the sale of the natural sweetener, stevia throughout parts of Europe (SCF 1999). Stevia has been used for centuries in South America and for many decades in Japan and South Korea (AHPA 1991). No adverse reactions have been reported from stevia use (in contrast to an endless flow of adverse reactions from aspartame use). Since stevia is low calorie and diabetic-safe, it would be competition to the manufacturers of aspartame and other artificial sweeteners. A large number of animal studies have been conducted adding to the clinical evidence that demonstrates that stevia is safe (AHPA, 1991, Stevia 2003, HRF 1993, Kinghorn 1988, Kinghorn 1992). Despite the contrast in independent research and clinical reports between stevia and aspartame, the Committee focused on a tiny subset of the stevia animal studies where adverse effects were seen at tremendously-large doses and made a decision that banned the sale of stevia in parts of Europe.

Some medical journals require authors to submit conflict of interest statements and some of those journals will print the relevant conflicts of interest along with the journal article (Krimsky 2001). Scientists who read the article and see a conflict of interest can read it very carefully to see if there are flaws in the experimental design, compare the results with independent research, or even choose to ignore such articles. The Scientific Committee of Food appears to avoid admitting to conflict of interest even after it is discovered (BMA 1997).

Appropriate immediate changes would be as follows:

The immediate changes will not solve the main problem, however, as the Committee reports can still be heavily tainted with food industry bias. The second- step in fixing the problem would be to replace all of the Committee members with scientists who have proven independence, a proven track record of standing up to food industry pressure, and a willingness to thoroughly investigate the matters being studied.

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:

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.

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.

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: 20 mg/kg body weight (acute dose) or 200 mg/kg body weight (chronic dose), 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:

Formaldehyde exposure estimates have been calculated previously by this author based on the intake of aspartame, percentage of methanol derived from aspartame, and the molecular weights of formaldehyde and methanol (ATIC 2000).

Before we discuss 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. The answers provided below will be brief. Much more detailed and referenced answers can be found at ATIC (2001) on the Internet at: [ http://www.holisticmed.com/aspartame/abuse/methanol.html ].

Chart of Aspartame Manufacturer Public Relations Statements

Related to Methanol and Formaldehyde

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

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 (1996) 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, Ophthamalogist and methanol poisoning expert testified before U.S. Congress regarding aspartame and damage to the eye:

To the credit of the Committee, their 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:

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.

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:

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:

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.

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:

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

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):

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."

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.

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:

It is not surprising that the Committee, being somewhat unfamiliar with aspartame research, 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.

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:

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:

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:

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):

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

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

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:

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:

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

I suspect that 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 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.

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.

It appears that there is far too much food industry influence on the Scientific Committee on Food. In fact, it would be unlikely that an unbiased review could be performed on aspartame, stevia or any other controversial food related subjects without refilling the Committee positions from scratch. New Committee members should meet the following criteria:

ACSN 1997. "Transcript of Aspartame Lecture: UT Southwestern Medical School," January 23, 1997, Aspartame Consumer Safety Network, Available at: [ http://web2.airmail.net/marystod/medschol.htm ].

AFSSA 2002. "Assessment Report: Opinion on a possible link between exposition to aspartame and the incidence of brain tumours in humans," Agence Francaise de Securite Sanitaire des Aliments, Maisons-Alfort. Report in French and English, available at [ http://www.afssa.fr/ ].

AHPA 1991. Stevia Petition to the U.S. Food and Drug Administration, October 21, 1991, [ http://www.holisticmed.com/sweet/stv-petition.txt ]. Also, see the petition supplement at: [ http://www.holisticmed.com/sweet/stv-supp.txt ].

Alemany 2002. Letter from Mari Alemany to Rich Murray, September 8, 2002., [ http://groups.yahoo.com/group/aspartameNM/message/864 ].

Anderson, G.M., E.J. Novotny, B.A. Shaywitz, 1996. "Evaluation of seizures," IN: The Clinical Evaluation of a Food Additive: Assessment of Aspartame," Editors: Tschanz, C., H.H. Butchko, W.W. Stargel, F.N. Kotsonis, CRC Press, Boca Raton, New York, London, Tokyo, pages 205-216.

Anthony, H., S. Birtwistle, 1999. "Attention Deficit Hyperactivity Disorder," (letter), Archives of Diseases in Childhood, Volume 81, Page 189, 1999.

Appleton 2002. "A Miracle in Wisconsin," Jon Rappoport, October 14, 2002, StratiaWire, Available at: [ http://www.stratiawire.com/article.asp?id=655 ]. Also, see followup article at: [ http://www.stratiawire.com/article.asp?id=788 ].

ATIC 1996. "Preapproval ‘Research’ and History of Aspartame," Aspartame Toxicity Information Center, [ http://www.holisticmed.com/aspartame/history.faq ].

ATIC 1997. "Aspartame Toxicity Reaction Samples (sent via postal mail)," Aspartame Toxicity Information Center, Available at: [ http://www.holisticmed.com/aspartame/adverse2.txt ].

ATIC 1998. "Aspartame / NutraSweet Toxicity Reaction Samples," Aspartame Toxicity Information Center, [ http://www.holisticmed.net/aspartame/adverse.txt ]

ATIC 2000., "How a Public Relations Campaign Deceives the Public About Formaldehyde Poisoning From Aspartame," Aspartame Toxicity Information Center, 2000. [ http://www.holisticmed.com/aspartame/fm.html ]

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