* Door: Mark D. Gold *Aspartame Toxicity Information Center*
12 East Side Dr., Suite 2-18
Concord, New Hampshire, 02139 USA
1-603-225-2110
http://www.holisticmed.com/aspartame/

Vertaling: Ed Gunneweg

Onafhankelijke analyse van het "Oordeel van de Europese Commissie, wetenschappelijk comité voor de voeding: Update over de veiligheid van aspartaam / E951" (SCF 2002)

* "Aspartame Toxicity Information Center" werd opgericht door Mark D. Gold. Er werd geen subsidie ontvangen van de voedingsindustrie voor enig werk verricht door de auteur of door het 'Aspartame Toxicity Information Center'.

INHOUDSOPGAVE

Introductie *

De invloed van de aspartaamindustrie en de wetenschappelijke Commissie voor de voeding *

Het Wetenschappelijk committee voor de voeding leest geen onderzoek *

Aspartaam en Formaline vergiftiging *

Aspartaam en Migraine / Hoofdpijn *

Aspartaam en Epilepsie *

Aspartaam en Hersentumoreen *

Aspartaam en invloed op de voortplanting *

Aspartaam en Gedrag, Kennis, Stemming *

Aspartaam en andere Effecten *

ADD/ADHD en gedrags onderzoek: Aspartaam and kinderen

Conclusie *

DEEL DRIE

Aspartaam en hersentumoren

A. Bewijs voor aspartaam en Hersentumoren

In 1996 analiseerde een groep wetenschappers onder leiding van Olney (1996) de cijfers van het voorkomen van hersentumoren in de Verenigde Staten en ander onderzoek m.b.t. aspartaam en hersentumoren. Zij kwamen tot de volgende conclusie:

1. Binnen enkele jaren na de goedkeuring van aspartaam was het aantal dodelijke hersentumoren (glioblastoma's en anaplastische astrocytoma's) enorm in aantal toegenomen bij de zwakkere groepen zoals middelbare leeftijd en bejaarden). Gedurende de zelfde periode verminderde het aantal minder dodelijke astrocytoma's. Olney 1996) toonde aan dat hoewel het globale aantal hersentumoren ongeveer gelijk bleef er een verschuiving plaats vond in kwaadaardigheid van de minder dodelijke naar de meer dodelijke soorten hersentumoren, kort nadat aspartaam op de markt was gekomen.

Wat hierbij zeer belangrijk is, is dat Olney (1996) niet zocht naar de totale hoeveelheid hersentumoren onder de bevolking. Hij keek naar de wisseling van de minder dodelijke naar de meer dodelijke hersentumoren (dat is: een verandering van [bestaande] tumoren in astrocyten van een mindere vorm naar een ernstiger graad van kwaadaardigheid") bij zwakkere groepen zoals middelbare leeftijd en bejaarden). Deze wisseling

Hersentumoren bij volwassenen hebben de neiging zich over een langere periode te ontwikkelen voordat de diagnose gesteld wordt. Als aspartaam de groei van hersentumoren zou veroorzaken kan het 20 tot 30 jaar (of mee) duren voordat de toename van het totale aantal hersentumoren zichbaar zou worden wanneer men hersentumoren statistieken zou onderzoeken in alle leeftijdsgroepen. Maar Olney (1996) kon aantonen dat er een zeer grote verandering (verslechtering) was van bestaande kwaadaardigheid bij een gevoelig bevolkingsgroep, kort na de goedkeuring van aspartaam. Op zichzelf toont de grote toename van dodelijke tumoren, kort na de goedkeuring van aspartaam, niet aan dat aspartaam hersentumoren veroorzaakt of uitwerking heeft op bestaande tumoren. Maar samen met bewijs in onderdeel #2 en #3 is er genoeg bewijs om mensen te waarschuwen voor de mogelijkheid.

2. Proefdieronderzoek vóór de goedkeuring van aspartaam vertoonde een verhoogd aantal van dezelfde types hersentumoren.

3. Aspartaam kan in de reageerbuis genetische verandering veroorzaken.

Het kan geen verrassing zijn dat het Committee, dat enigszins onbekend is met aspartaam onderzoek, vergat te vermelden dat Hardell (2000) de verschillende risicofactoren voor hersentumoren had bekeken. Er werd een belangrijke overeenkomst gevonden bij personen die meer light limonade gebruikten en kwaadaardige hersentumoren. De gemiddelde leeftijd van deze persoen was 50 jaar. Terwijl het aantal personen zeer klein was, is het het enige onderzoek dat gehouden is bij een oudere (meer kwetsbare) bevolkingsgroep en het gebruik van aspartaam.

B. Het Committee is niet bekend met aspartaam en hersentumor onderzoek

Ieder intelligente discussie van het onderzoek van Olney (1996) en hersentumoren moet het voorkomen van de hoeveelheid glioblastoma's en anaplastische astrocytoma's bij mensen van middelbare leeftijd en ouderen bekijken. Een discussie van het totaal aantal hersentumoren is zonder enige betekenis, omdat Olney (1996) aantoonde dat het totaal aantal hersentumoren gelijkt bleef door verminderen van het aantal dodelijke astrocystoma's.

Het is duidelijk dat het Committee geen kennis heeft van het onderzoek van Olney (1996) omdat ze de volgende kritiek uitten over Olney (1996) in het rapport:

1. Er was naar het aantal gevallen van hersentumoren gekeken in Frankrijk en die bleven in verhouding stabiel tussen 1980 en 1997 (Menegoz 2001). Het Committee had er klaarblijkelijk geen idee van dat ze moesten kijken naar een speciaal soort hersentumor bij een kwetsbare bevolkingsgroep om te zien of aspartaam een effect konhebben op bestaande kwaadaardigheid. Als ze Olney (1996) hadden gelezen dan zouden ze zich niet hebben geconcentreerd op het totaal aantal hersentumoren.

2. Gurney (1997) vond geen link tussen aspartaam en hersentumoren bij 56 kinderen. Als het Committee Olney (1996) hadden gelezen dan hadden ze geweten dat het meerdere voorkomen van hersentumoren het eerst zou worden gezien bij kwetsbare bevolkingsgroepen -- middelbare leeftijd en ouderen voor specifieke soorten hersentumoren (b.v. glioblastoma's en anaplastische astrocytoma's). Het onderzoek van Gurney (1997) is niet relevant omdat het alle soorten hersentumoren combineerde bij een relatief klein aantal kinderen. Maar de analise van Olney (1996) demonstreerde dat de grote omslag naar een groter aantal kwaadaardige tumoren het eerst werde gezien bij mensen van middelbare leeftijd en oudere bevolkingsgroepen (en niet bij kinderen).

3. Het Committee beweerde dat het aantal gevallen vermeerderde door de betere diagnostische methoden Modan (1992). In het begin en midden van 1980 werd de Magnetic Resonance Imaging (MRI) geïntroduceerd als een methode om hersentumoren eerder te ontdekken. De types hersentumoren waarvan Olney (1996) een verhoging aantoonde bij kwetsbare bevolkingsgroepen was groot en gemakkelijk te ontdekken zonder gebruik van MRI apparatuur. In feite ging het aantal kleinere astrocytoma's naar beneden, ondanks de introductie van de MRI technologie. Je zou verwachten dat de MRI technologie het aantal van de kleinere, moeilijker te ontdekken astrocytoma's zou verhogen. Het tegenovergestelde was waar, de hoeveelheid astrocytoma's bij kwetsbare bevolkingsgroep ging naar beneden. Dit betekend dat andere factoren een belangrijke invloed hadden op de verandering in het aantal tumoren bij kwetsbare bevolkingsgroepen.

4. 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 followup correspondence, he received "a blitz of letters."

Linet (1999) and Smith (1998) are articles (not related to Aspartaam) 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 Aspartaam 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 Aspartaam did not produce brain cancer in rodents. The information they used came from articles written by manufacturer employees and consultants in an Aspartaam 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 Aspartaam 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 Aspartaam (Gordon 1987). This FDA Commissioner left office shortly after he approved the use of Aspartaam in carbonated beverages and became a high-paid consultant for the Aspartaam 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 Aspartaam 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 Aspartaam 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):

De misdaad in beeld gebracht

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

Alleen zo kon aspartaam goedgekeurd worden

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 Aspartaam pre-approval research as detailed in ATIC (1996).

Aspartaam 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 Aspartaam]."

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:

1. 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)

2. 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."

3. The Committee did not mention that Dow-Edwards (1989) demonstrated that Aspartaam administration after conception disrupted "odor-associative learning in newborn guinea pigs. The Aspartaam 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.

4. 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).

5. 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)

6. The Committee made no mention of any reviews or studies related to damage to offspring from ingestion of excitotoxins obtained from Aspartaam 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.

Aspartaam and Behavior, Cognition, Mood

A. "Long-Term" Research

For long-term research, the Committee relied on two Aspartaam 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)"

I suspect that the Committee did not even read the Leon (1989) study because it is not a study on Aspartaam 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 understen that when the Aspartaam 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 Aspartaam products will be placed in very short studies with other major flaws. For example, Rowan (1995) looked at persons who had experienced seizures from Aspartaam, but the study was only one day long, almost all of the subjects were on anti-seizure medication, and the Aspartaam was given in a way as to make it less toxic. Schiffman (1988) looked at persons who reported headaches from Aspartaam, but the study was only one day long, the Aspartaam 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 Aspartaam on Parkinson’s Disease patients, but the study was only one day long and the subjects were given Aspartaam in a way as to make it less toxic. Hertelendy (1993) studied Aspartaam in patients with liver disease, but the study only lasted one day.

Sometimes Aspartaam 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 Aspartaam) 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 Aspartaam exposure (but still susceptible to long-term Aspartaam 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 Aspartaam 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 Aspartaam or placebo to healthy subject for 24 weeks. The Aspartaam 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 Aspartaam, there was a > 50% increase in adverse reactions in the Aspartaam 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 Aspartaam 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 thousen 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 Aspartaam 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 Aspartaam used, it was inevitable that the researchers could claim no "statistically significant" increase in adverse reactions within each subcategory (even though Aspartaam caused a > 50% increase in adverse reactions overall).

"A 27-y-old female television producer drank 3 cans of Aspartaam-containing soft drinks a 1 glass of presweetened iced tea daily for 2 y[ears]. She suffered pain in both eyes, severe headaches, tingling of the extremities, heart palpitations, nausea, and marked frequency of urination. She also had difficulty wearing contact lenses. A CT scan of her brain and various eye tests proved normal. Her complaints improved shortly after she stopped using Aspartaam. The remission had persisted many mo[nths] when she completed the questionnaire." (Roberts 1988a)

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.

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

It is important to understen that many people can use Aspartaam for months or several years without any clinically obvious symptoms appearing. However, the chronic poisoning from Aspartaam use eventually catches up with most, if not all users. Here is a case described by an a person who had ingested Aspartaam for approximately 6-8 months before symptoms had begun to appear (ATIC 1998):

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