12. Scientific Research or Public Relations? The manufacturer of aspartame, Monsanto/NutraSweet, has literally flooded the scientific community with fatally flawed "scientific" studies. The number of studies are in the hundreds. Unfortunately, the trickle of a few independent studies per year gets lost in the NutraSweet- propogated "research." The company literally controls the "scientific" opinion of aspartame (much the same way the Glutmate Association controls scientific opinion on MSG and food-based excitotoxins) since it can afford to fund 10 flawed studies to "disprove" every single study by an independent researcher who finds problems with aspartame. There is almost no money available for independent researchers to perform studies despite researchers pleading to the U.S. Congress for money to study aspartame. Here's an excerpt that discusses this issue (Lisa 1994): Dr. Richard Wurtman, Director of the Clinical Research Center and Professor at Massachusetts Institute of Technology, in April 1988 urged the FDA to issue warnings to physicians that aspartame may be associated with a syndrome including severe headaches, and in some cases, grand mal seizures. Wurtman had received over 1,000 complaints at M.I.T. directly into his department . . . . . Wurtman tried for over a year to get support for his research [to study aspartame and seizures], to no avail. He said, "The present system, in which the companies that sell our synthetic foods--like NutraSweet--fund virtually all of the studies, FDA- mandated or not...is too vulnerable to misuse...when outside investigators propose studies that might yield the 'wrong' answer, a large bag of 'dirty tricks' is available for derailing those studies." Looking at the NIH Current Research Information System (CRISP), one can see that in 1995, there are essentially no indenpendent studies on the health effects of aspartame. The chance of NIH funding an independent study on aspartame (or MSG) are almost zero. The chance of getting funding for a quality, long-term study (i.e., over one year) is zero. Therefore, based upon the horrendous quality of studies put out by industry researchers as discussed in this document and upon the lack of independent studies, we are at the mercy of whatever NutraSweet wants to convince us about aspartame. Researchers are continuing to put out badly flawed studies such as: 1. Stokes (1991) and Stokes (1994) published studies purporting to show that aspartame had no effect on the cognitive performance of pilots. Selected Flaws -------------- a. The 1991 study was only a single dose study. No one is suggesting that a single dose of aspartame in a lifetime is going to lead to major brain chemistry changes. Unfortunately, many industry experiments are worthless single-day studies when the major concern is the ingestion of aspartame for months and years. This is especially the case when considering the phenylalanine from aspartame since it is believed by some researchers to cause a gradual change in brain chemistry. The 1994 study was slightly better in this regard, but still only 9 days long. This can hardy be regarded as "chronic" aspartame dosing. I would not even consider it a medium length experiment. It is closer to an acute dosing study. On the other hand, if it didn't have all of the major flaws discussed below, it might be an acceptable acute dosing study. b. The aspartame was given in capsules. This was a particularly bad mistake. Stegink (1987a) showed the major differences between ingesting aspartame in liquid form and in capsules. The plasma phenylalanine spikes to extremely high levels when ingesting aspartame in liquids, but the spike is much lower when ingested in capsules. Since the hypothesis involved the concern for spiking the plasma phenylalanine levels, this mistake, by itself, renders this test questionable at best, and probably worthless. c. The tests given the pilots started 45 minutes after aspartame capsule ingestion. The Stegink (1987a) experiment cited above shows that plasma phenylalanine levels do not peak (using capsules) until 123 minutes (average) and it takes as much as 240 minutes until it peaks in some persons. In addition, simply because the plasma phenylalanine level has peaked, does not mean that enough time has passed for a) small changes in brain chemistry to take place and b) slight changes in neurotransmission (from the single dose of aspartame). d. Substances were given with aspartame that are likely to reduce any possible biochemical changes and toxicity from the aspartate and the methanol. The aspartame was mixed with orange juice which would help prevent any problems from low-level methanol effects such as that shown in Cook (1991). One hypothesis (discussed earlier in the Methanol section) presented by Dr. Phil Moskal is that the high altitude may potential the negative effects of methanol from aspartame, causing it to bind to hemoglobin (like carbon monoxide) and thereby inducing hypoxia (Moskal 1990, Stoddard 1994). A small amount of sweet product was given with the aspartame and orange juice, allegedly to increase the phenylalanine/LNAA ratio. The sweetener would likely cause some or all of the aspartic acid to be converted to alanine before absorption. Therefore, two of the three major constituents of aspartame (methanol and aspartic acid) were not even being tested! e. Fresh aspartame was used, eliminating the possibility that DKP, beta-aspartame, or other breakdown products might cause or contribute to a degradation of pilot cognitive performance. Therefore, these protocol designs carefully eliminated any possibility of problems with aspartame's breakdown products. The protocols seemed to be designed to avoid finding problems with aspartame. f. The study was funded by two organizations that have had a history of turning their backs on the dangers of aspartame -- the FDA (see history section) and the Federal Aviation Administration (FAA) (Stoddard 1995a, page 19). In fact, the Transportation Secretary under the Bush Administration was none other than Samuel Skinner, the former U.S. Attorney who negotiated and took a job with G.D. Searle's law firm while he was supposed to be preparing to present fraud cases against G.D. Searle for their aspartame pre-approval studies. In addition, Harriet Butchko of the NutraSweet Company had some unknown role in support. I find it difficult to believe that protocols could have been this poorly designed without the imput of the NutraSweet Company. Conclusion ---------- It is sad to see that the FDA and the FAA would ignore the seriousness of the aspartame problem for so long and then turn around and fund protocols this poorly designed. 2. Four studies were presented at the "Aspartame: Cognitive, Behavioral, and Electrophysiological Aspects Conference" (Spiers 1993a). While the introductory paragraph claimed that the studies were conducted by "independent" investigators, that was definately not the case. Three of the four studies (De Sonneville 1993, Benninger 1993a, and Shaywitz 1993) had researchers who have conducted flawed research funded by the NutraSweet Company (e.g., Trefz 1994, Shaywitz 1994b). The Trefz (1994) study involved the same exact set of investigators (Trefz, de Sonneville, Matthis, Benninger, Lanz-Englert, and Bickel), had the same protocol as the combination of the de Sonneville (1993) and Benninger (1993a) studies, and appeared to have been conducted around the same time period! The Trefz (1994) study was funded in part by the NutraSweet Company. How these researchers could be considered "independent" investigators is beyond me. The Shaywitz (1994b) study also involved the same exact investigators as their purportedly "independent" investigation presented at this conference, Shaywitz (1993) (B.A. Shaywitz, C. Sullivan, Anderson, Gillespie, B. Sullivan, S. Shaywitz). The protocol for boths studies appears to be the same. The Shaywitz (1994b) study was funded by the NutraSweet Company. I suspect that the abstracts presented at this conference from "independent" researchers were from studies funded by the NutraSweet Company and published in full form at a later date. It seems clear that some researchers who get their money from the NutraSweet Company are attempting to convince people that they are "independent" researchers. Without going into detail about each study, which might be impossible anyhow since they were only published in abstract form, they seem to repeat many of the same standard aspartame industry experimental errors discussed throughout this document. It is very disappointing that Paul Spiers and Richard Wurtman conducted such a short study on relatively healthy individuals using what appears to be (as far as I can determine) capsule administration of fresh aspartame. It is even more disappointing that these individuals would pretend that the research presented at this conference was "independent" when, in fact, it was performed by industry-supported researchers. 3. Trefz (1994) published a study testing neuropsychological and biochemical responses to aspartame in heterozygotes for phenylketonuria. Forty- eight adult subjects were given either 15 or 45 mg/kg/day of aspartame or placebo for 12 weeks. The researchers found no difference in EEG analyses, urinary organic acid concentrations, or adverse experiences between the aspartame and placebo periods. Selected Flaws -------------- a. The aspartame was given in capsules. Once again, as shown in Stegink (1987a), this significantly reduced the spikes on plasma amino acid levels. This is obviously one reason that the plasma phenylalanine measurements showed no change at 15 mg/kg/day and only a minor change at 45 mg/kg/day. It is hard to believe that these NutraSweet-funded investigators did not know of this fact. b. "Coincidentally," the aspartame doses were given near mealtime (7 a.m, 1 p.m., and 7 p.m.). This would further reduce the spikes in the plasma amino acid levels and lessen the toxicity from the methanol (Posner 1975). A protocol seemingly designed to reduce reactions. c. Fresh aspartame was used. So much for testing breakdown products! d. The phenylalanine measurements were taken at 1 and 3 hours after dosing. Stegink (1987a) showed that while the time for phenylalanine to reach its peak varies considerably, the average time when aspartame was taken with capsules is 123 minutes or ~ 2 hours. Therefore, the investigators took the measurements at the wrong time further contributing to an apparent lower spike in phenylalanine levels. e. Averages measurements for all of the subjects were presented a each time period. This is a common NutraSweet flaw discussed earlier in this document. f. The dosages given was very low in one group and barely passable in the other group (45 mg/kg/day). The researchers cite Butchko's ridiculous review of aspartame consumption surveys to claim that the study tested 20 times the average intake. g. The length of the study was only 12 weeks. Had the other major flaws not been part of the protocol (and real indepedent investigators conducted the study), 12 weeks may have just barely been long enough to notice significant neuropsychological effects from aspartame ingestion. 4. Shaywitz (1994b) conducted an experiment to test the effects of aspartame on children with Attention Deficit Disorder (ADD). Aspartame capsules containing approximately 34 mg/kg/day of aspartame were given to children each morning in either week 1 or 2 and week 3 or 4 of the study. No significant difference was found between the aspartame and placebo weeks except for a small difference in the activity category. Selected Flaws -------------- a. The aspartame was given in capsules. Once again, as shown in Stegink (1987a), this significantly reduced the spikes on plasma amino acid levels. This is obviously one reason that the plasma phenylalanine measurements showed only a moderate change 1 hour after aspartame administration. b. "Coincidentally," the aspartame doses were given near mealtime (i.e., breakfast). This would further reduce the spikes in the plasma amino acid levels and lessen the toxicity from the methanol (Posner 1975). Another protocol seemingly designed to reduce reactions. c. Fresh aspartame was used. So much for testing breakdown products! d. The methanol testing was reprehensible at best. The outdated methanol test that was used had no possibility of finding changes in blood methanol levels. Researchers who are actually interested in looking for such changes (e.g., Cook 1991, d'Alessandro 1994) use proper tests that are sensitive enough to find such changes. e. The blood was drawn at improper times to test for high levels of formate -- 1 hour, 2 hours, and 24 hours after aspartame administration -- rather than 12 to 16 hours after administration. The timing of this formate test was far worse than the aspartame industry's earlier studies. f. The phenylalanine measurement was taken at 1 hour after dosing. Stegink (1987a) showed that while the time for phenylalanine to reach its peak varies considerably, the average time when aspartame was taken with capsules is 123 minutes or ~ 2 hours. Therefore, the investigators took the measurements at the wrong time further contributing to an apparent lower spike in phenylalanine levels. g. Averages measurements for all of the subjects were presented a each time period. This is a common NutraSweet flaw discussed earlier in this document. h. The dosages given was too low considering that Frey (1976) showed that children, due to their low body weight, can ingest as much as 76 mg/kg/day of aspartame. The researchers cite Butchko's ridiculous review of aspartame consumption surveys to claim that the study tested 10 times the average intake. i. The length of the study was only 2 weeks (on aspartame). Had the other major flaws not been part of the protocol (and real indepedent investigators conducted the study), 2 weeks would probably still be much too short to notice major differences in the aspartame and placebo group. From time to time researchers for the NutraSweet Company will publish "reviews" of the scientific literature, always concluding by proclaiming the "safety" and "harmlessness" of aspartame. 1. Fernstrom (1994) published a review in the Journal of the American Dietetic Association where he discussed both the MSG and aspartame issue. Selected Flaws -------------- a. Dr. Fernstrom did not divulge is strong ties to the aspartame and MSG industries thereby conning unsuspecting dieticians into believing that he was performing an unbiased review. b. Dr. Fernstrom had the nerve to cite the Reynolds (1976), Reynolds Stegink (1975), and Reynolds (1980) studies on the lack of effects of glutamate and aspartate on monkeys even though these studies were hopelessly flawed at best and bordered on fraud at worst as discussed in an earlier section of this document. He must have known the problems with these studies as 1) he participated in an MSG industry workshop three years earlier (MSG 1994) where some of the problems were discussed; and 2) Dr. Olney had submitted his statement to FASEB outlining these problems in 1993, one year before this publication (Olney 1993). c. Dr. Fernstrom neglected to point out that a couple of industry studies have shown a significant increase in plasma aspartate after administration of aspartame (see Stegink 1987a, for example), but instead, pointed to a study which is likely flawed. d. Dr. Fernstrom neglected to point out that numerous industry studies have shown enormous increases in plasma glutamate levels when MSG was taken with water, broth, soup, or food. He simply cited a single study which did not find such an enormous increase most likely because of flaws. e. Dr. Fernstrom states that "aspartame ingestion has been found to produce no adverse effects" even though almost all independent research has shown that aspartame does produce adverse effects as discussed earlier. 1. Lajtha (1994) put together a work of art (NutraSweet PR) which would convince almost any uninformed scientist that aspartame is safe. Unfortunately, the whole review is based on flawed studies, half-truths and totally inaccurate information. Selected Flaws -------------- a. Methanol i. Lajtha cites a NutraSweet study claiming that methanol is three times more prevelent in fruit juices than in aspartame even though he also cites Monte (1985) which points out the flaws in that argument and which lists more recent research showing several times less methanol in fruit juices. ii. Lajtha tries to confuse the issue by comparing methanol doses required for severe acute poisoning to methanol from aspartame ingestion even though slow, chronic toxicity from methanol is the issue. Chronic toxicity from methanol, formaldehyde and formic acid has been discussed in the scientific literature, but this is rarely, if ever, mentioned by NutraSweet researchers. iii. Lajtha cites single-dose experiments to back up his claim that blood formate is not raised from aspartame ingestion. He neglects to mention that 1) a tiny number of subjects were tested, 2) average values at each time period were used, 3) formate measurements were not made at an appropriate time as discussed in Liesivouri (1986), 4) in many cases a single dose would not raise blood formate levels significantly, but regular doses would as seen in methanol and formadehyde experiments, 5) formic acid can accumulate in the organs, 6) the average base formate levels for the aspartame subjects was suspiciously high and probably helped prevent a significant increase from the single exposure, and 7) the aspartame was often given with gruit juice which may reduce the absorption of methanol and/or prevent or delay the conversion of methanol to formaldehyde. iv. Lajtha cites four studies which he claims show no increase in plasma methanol levels at a dose of 2/3 the FDA Allowable Daily Intake. The methanol tests he cited represent incompetance at best (as discussed in the methanol section) or scientific fraud at worst, since an inappropriate testing procedure was used. v. Lajtha admits that as little as 8% of the FDA Allowable Daily Intake of aspartame led to a statistically significant increase in blood methanol. He passed it off as being with the "normal" range of individual variation. But one person's "normal" range may be dangerous to another person over time. It is difficult to understand how Lajtha can believe that small doses increase plasma methanol levels, yet larger doses cause no change. vi. Lajtha claims that an extremely high blood methanol concentration is required for measurable formate formation even though single-dose experiments of aspartame have shown measurable formate formation (excreted through the urine) at blood methanol levels many times less than he claims. In addition, continuous environmental exposure to low levels of methanol or formaldehyde raises formate levels significantly as discussed in the Methanol section. He also neglects to consider that symptoms from chronic methanol exposure may be caused by different mechanisms than the severe acidosis which is present in acute poisoning. b. Aspartic Acid i. Lajtha mentions that the blood brain barrier (BBB) excludes excess aspartate, but neglects to focus the discussion on the areas of the brain unprotected by the BBB which are extremely sensitive to excitatory amino acids. He also neglects to mention that the BBB can be damaged in a number of diseases and that the infant BBB may not be fully formed. ii. Lajtha mentions the dosages at which aspartic acid causes brain lesions in rodents. He neglects to mention that humans concentrate glutamate 5 times more than rodents in their blood and the same is expected with aspartate. This would decrease these values by a factor of five. He also neglects to mention that at 1/4 the toxic doses, significant changes in hormone output has been seen. Finally, he neglects to mention that these are single-dose studies and the regular ingestion of months or years -- constantly spiking the aspartic acid levels -- may be causing gradual damage, especially when one considers the cumulative effects of aspartic acid plus glutamic acid (MSG). iii. Lajtha uses a couple of experiments purporting to show the lack of increase in plasma glutamate and aspartate after ingesting MSG or aspartame. He neglects to mention that there are a number of studies showing large increases in plasma glutamate after ingesting MSG with water, soup, or meals, and that there are several aspartame studies showing a significant increase in plasma aspartate. In particular, the Stegink (1987a) study showed an increase in plasma aspartate as much as 18 times that of the baseline measurement from a single dose. iv. The experiment conducted purporting to show that aspartic acid cannot cross the placental barrier was done in the third trimester when the barrier tends to be more impervious to free amino acids. Several studies have demonstrated that excitotoxic amino acids can cross the placental barrier as discussed in the Aspartic Acid section. d. Phenylalanine i. Lajtha confuses the issue of ingesting free phenylalanine in aspartame by using phenyalalnine in foods as a comparison. Phenyalalnine in aspartame spikes the plasma phenyalalnine to high levels, unlike when a high protein meal is ingested. ii. Lajtha seems to be attempting to demonstrate the ability of the brain to tolerate higher concentrations of phenylalanine by pointing out that some areas of the brain have much higher concentrations than other areas. The problem is that areas of the brain have certain concentrations for a reason. Raising the concentration of phenylalanine in an area that is supposed to have a low concentration is not necessarily safe and almost certainly not health-building. iii. Lajtha cites studies where encapsulated aspartame was used (and where averages at each time period were the only values presented) to discuss plasma phenyalalnine. He ignored Stegink (1987a) and Matalon (1988) where realistic amounts of liquid aspartame spiked plasma phenylalanine to extremely high levels. This renders his whole discussion based on plasma phenylalanine and doses required to obtain these levels flawed and pointless. iv. Lajtha cites the absurd Hjelle (1992) NutraSweet study attempting to convince readers that it takes only two to six times the dose of phenylalanine in rats to obtain a similar effect as occurs in humans. The reality is that independent researchers have found that it takes at least 60 times the dose in rats to cause a similar change in plasma phenylalanine/LNAA ratio as occurs in humans. v. Lajtha cites the Koeppe (1991) study which showed a slight decrease in blood brain barrier amino acid transport rates after the administration of 34 mg/kg of aspartame. Lajtha states that there will be "little measureable transport change" at levels "under average (50th percentile) dietary use." He neglects to mention that, in reality, the equivalent of approximately a dose of 17 mg/kg was tested (as discussed in the Phenyalalnine section). Also, it is a gradual change in brain chemistry which causes extreme concern. vi. Lajtha cites a number of low-dose studies in rats showing no effect of aspartame on monoamine levels of the brain. He neglected to mention that independent studies using a more appropriate dose and looking at certain specific brain areas found changes in levels of monoamines (Coulombe 1986, During 1988). e. DKP i. Lajtha states that DKP is metabolized in the gut to aspartic acid, but then later admits that 5% is excreted in the urine and the rest is "probably metabolized." It is clear that no one is sure what happens to the DKP and wishful speculation does not equate to food safety. ii. Lajtha claims that the 90th percentile consumption of DKP is 0.6 mg/kg/day. However, it is clear that persons consumer the FDA Allowable Daily Intake of 50 mg/kg/day of aspartame can ingest 12 mg/kg/day of DKP or more based on the Tsang (1985) study discussed earlier. f. Aspartame Dosages i. Lajtha uses the same laughable "surveys" discussed in an earlier section to try to convince readers that a much lower dose of aspartame is being consumer than any sensible estimate would predict. He also cites a Canadian study saying that it measured "consumption in a single day," when Butchko (1994) clearly states that it was a 7-day survey. Are we to believe that Canadians went on a wild, seven-day binge of aspartame corresponding to this survey or, much more likely, the survey cited by NutraSweet researchers are flawed to the point of being worthless. g. Pregnancy i. Lajtha points out that the maximum recommended level of plasma phenylalanine is 360 umole/liter, yet he uses flawed studies to show that aspartame doses do not raise the plasma phenylalanine to near these levels. The Stegink (1987a) and Matalon (1988) studies show that it is quite possible for even healthy women to approach this level of plasma phenylalanine. Women who are phenylketonuric heterozygoes may have even a higher risk of damaging their child. In addition, regular consumption of aspartame during pregnancy would spike the phenylalanine constantly, not just one time, causing the phenylalanine levels in the fetal brain to be regularly spiked to extremely high levels. As discussed earlier in the Phenylalanine section, some researchers believe that smaller changes in the plasma phenylalanine levels during pregnancy have important clinical effects. ii. Lajtha obscures the concern about constantly spiking the phenylalanine level by discussing phenylalanine derived from food source. When ingesting food, the protein is broken down gradually, the phenylalanine is aborbed gradually and other Large Neutral Amino Acids (LNAAs) are absorbed along with the phenylalanine. h. Seizures i. Lajtha neglects to mention that one of the original studies on aspartame in monkeys showed that it caused seizures. ii. Lajtha uses all of the NutraSweet-funded, flawed seizures studies (as discussed earlier) to back up the claim aspartame does not cause seizures. Independent examinations of the aspartame and seizure issue almost always show problems. Seizures are one of the most frequently reported reactions to aspartame. There are so many people who have gotten rid of their seizures by going off aspartame, that all that is lacking for final proof are real experiments from independent scientists. There are many other problems with the Lajtha review, but they are too numerous to mention here. Suffice it to say that the review is a masterful whitewash of the evidence of aspartame's danger. The food industry has formed organizations that fund flawed studies in order to convince government and private organization as well as scientists of the "safety" of their product. The International Glutamate Technical Committee (IGTC) is one such organization which funded "sutdies" that abused the scientific process as was discussed in the Aspartic Acid section. The International Life Sciences Institute (ILSI) is another such organization supported by food companies which has no interest in funding studies which have any possibility of finding problems with their supporter's products. ILSI consists of approximately 154 member companies and 12 to 14 technical committees, one of which is the Aspartame Committee (Dews 1987). The Aspartame Committee is made up of NutraSweet Company, Ajinomoto Co., Coca Cola Co., Pepsico, Inc., Royal Crown Co., Seven-Up, Inc., and six other manufacturers of aspartame-containing "food" products (Gordon 1987, page 488-489 of US Senate 1987). According to a 1987 United Press International (UPI) investigation, the ILSI's Executive Director is Jack Filer, the researcher who has conducted numerous "studies" for NutraSweet and who was found to have a conflict-of-interest judging the "safety" of MSG while receiving money from the companies marketing the junk as discussed earlier in the Aspartic Acid section (Gordon 1987, page 486 of US Senate 1987). During the 1980s, ILSI denied funding to researchers who were independent at the time, Dr. Louis Elsas and Richard Wurtman and instead, funded researchers who had a long-standing relationship with industry groups (Elsas 1987; Gordon 1987, page 485-486, 488 of US Senate 1987). ILSI- funded studies are basically no different from the countless manufacturer-funded studies, except, judging from ILSI's aspartame studies, the protocol designs are actually worse! Industry Arguments ------------------ Monsanto/NutraSweet or ILSI will fund these horribly flawed studies purporting to show the "safety" of aspartame. Soon after the study is published, a press release is pushed onto the unsuspecting media. The media then propogates the results from these flawed studies without critically examining the "information" and without discussing the design of the experiments with independent experts on the subject. As long as the study has an image of respectiability (i.e., conducted at a well-known university), the media can easily be manipulated by these big companies. The industry will argue that these studies are "peer- reviewed," implying that they are examined closely by experts in the field and therefore properly conducted (Shapiro 1987, page 425-426 of US Senate 1987). First of all, almost all of the post-approval studies funded by Monsanto/NutraSweet discussed throughout this review were "peer-reviewed." These studies represent an abuse of the scientific method, yet they were still made it through "peer review" and were published. Secondly, many tobacco companies studies which also represented an abuse of science were peer reviewed. It is abundantly clear that the peer review system does not prevent deceptive and worthless studies from being published. Author Cynthia Crosen (Crossen 1994, page 178) had the following to say about the peer review system: "But the peer review system is stretched thin. The sheer volume of biomedical journals--some 15,000 journals publish about 250,000 articles a month-- puts insupportable demands on the system. Peer reviewers are unpaid volunteers, and they can't take the time to scrutinize the raw data, let alone replicate the research. The specialization of medicine means the pool of people capable of doing any particular review is diminishing. Whatever the outcome of the peer review, the editor of the journal may decide to accept or reject the article for editorial or personal reasons. Scientists say that peer reviews are increasingly done by graduate students or postdoctoral fellows who do not have enough breadth of experience and that peer reviewers compete with teh authors for research money, possibly biasing their opinions. Critics also say peer review is biased in favor of well-known professors from prestigious schools--the so-called halo effect-- and those who use 'current fashionable approaches.' And what scientist wants to break the news to another scientist that he or she has just wasted years on a poorly designed piece of research? "Even regular contributors to journals decry the state of the peer-review system. 'Despite this system, anyone who reads journals widely and critically is forced to realize that there are scarcely any bars to eventual publication,' wrote Drummond Rennie, professor of medicine at the University of California at San Francisco. 'There seems to be no study too fragmented, no hypothesis too trivial, no literature too biased or too egotistical, no design too warped, no methodology too bungled, no presentation of results too inaccurate, too obscure and too contradictory, no analysis too self-serving, no argument to circular, no conclusions too trifling or too unjustified, and no grammar and syntax too offensive for a paper to end up in print.'" Conclusion ---------- "Corporate control of NutraSweet testing continues at Monsanto, torturing the ethics of academic medicine" (Constantine 1995). Much of the food safety research has become a no-rules, public relations playground for food companies. These companies help to fund and design hundreds of fatally flawed studies. Poorly-designed studies, guaranteed to put a particular product in a good light are certainly not limited to the aspartame and glutamate industries. These industries, however, seem to be capable of designing the most worthless and deceptive "research" which rivals some of the research done in the past by the tobacco companies.