Global scientists assess homeopathy-funded Séralini study claiming all GMO tests 'contaminated'

Gilles-Éric Séralini's latest study on GMOs–“Laboratory Rodent Diets Contain Toxic Levels of Environmental Contaminants: Implications for Regulatory Tests”--was published on PLOS ONE on July 2, 2015 more than two weeks after its originally scheduled release.

  • GLP has an analysis of the latest Séralini study here.
  • GLP has a profile of Séralini and his research here.

Journalists had been supplied with an embargoed version of the original paper in mid June. The final version contains two significant changes.

Séralini had not disclosed that his laboratory and the professor himself has received significant funding from Sevene Pharma, a French company that promotes "cures" using homeopathy, which mainstream scientists consider pseudo-science. Sevene sells homeopathic remedies but is also paying Séralini to research atrazine and glyphosate risks. Sevene markets “detoxification” homeopathy products to treat the alleged toxic effects of glyphosate and atrazine "contamination", which is the focus of Séralini's research, a clear conflict of interest the professor has apparently been forced by PLOS to now acknowledge.

Séralini has been a long time consultant for Sevene. According to an article on the French professor (published in French here, but translated and excerpted here by geneticist David Tribe), he also spends a significant part of his time promoting so-called detoxification products, for example at a training seminar organised by Corinne Lepage’s CRIIGEN, with lectures organized by Sevene and at symposiums on alternative medicine, some sponsored by Sevene. Séralini's research team includes a former director from Sevene. A translation of the French article--"The "dark side" of Professor Séralini--is available here.

The final PLOS version of the study also eliminated a section from the abstract:

The high background rate of pathologies in laboratory rodents could be due to die- tary contaminants. This invalidates the use of external controls (historical data) in regulatory tests, consisting of comparisons of toxicological effects to control rats from other experi- ments, because these control rats are fed different mixtures of pollutants. This also ques- tions the use of 50 rats per group in carcinogenicity studies to increase the statistical power lost due to the elevated pathological background.

Scientists react

Two organizations, the Science Media Centre in the UK and Washington, DC based GENeS--Genetic Expert News Service--an independent, foundation funded NGO--solicit expert opinions from independent researchers on breaking genetics stories. Both organizations have posted analyses on their respective websites. The GLP summarize a few key reactions here, but we urge readers to visit those websites directly for extended comments.


Dr. Richard E. Goodman, Research Professor in the Food Allergy Research and Resource Program, University of Nebraska (webpage):

The authors are using a controversial method of estimating cumulative risks (Hazard Quotients) of minor contaminants in animal feeds that have not been validated to demonstrate realistic risks, with biological proof of harm at levels of contamination that the authors found in this PLoS ONE study. As far as I know, there have not been publications demonstrating that the method of cumulative hazard assessment, even though referenced by a paper by the US EPA and one in the EFSA Journal (11:3313), have suggested this approach might be useful for understanding risks of mixtures of chemical toxicants including pesticides, dioxins and heavy metals have accurately predicted risks or outcomes.

The fact is that no studies I am aware of, other than the authors’ previous retracted study in Food and Chemical Toxicology in 2012 on NK603 maize and glyphosate, has shown high levels of tumors, cancers or other deleterious effects in control animals fed normal commercial rodent diets. The authors have not cited published studies that have shown high levels of adverse effects in control animals fed commercial rodent diets.

It seems the authors are trying to prove that their earlier reported tests with high tumor incidence in the 2012 study was due to “incidental contamination of control diets” rather than the genetic strain of rats used in their 2 year study.  Or that they want to invalidate the safety tests on many GM crops.  Yet the same tests and lab chow has been used safely to demonstrate convincing risk or safety of a number of pharmaceuticals, pesticides and other compounds.

Dr. Frédéric Y. Bois, Professor at Sorbonne UTC, and Research Director at L'Institut National de l'Environnement Industriel et des Risques (INERIS)(webpage):

Not too surprisingly, rat diet, like most of ours by the way, is contaminated with those chemicals. It would actually be interesting to compare those results with the producers' records.

Whether the exposed rats are likely to suffer serious damage from such exposures is not clear though. The hazard indexes computed by the authors use acceptable daily intakes (ADI) calculated for humans. Those do not really apply to rats, because safety factors are used in their derivations to specifically protect humans (assumed to be more susceptible than animals), and among humans infants etc.  Furthermore the hazard indexes for various chemicals were summed to get an estimate of the effect of the multiple exposures.

Using hazard indexes and summing them maybe a reasonable conservative procedure for protecting human public health. However, when assessing the actual impact of food contaminants on the health of lab animals (which is a matter of scientific precision, not of rat health protection) they are likely to overestimate the risks.

The question also of the number of chemicals whose safety evaluation has been biased by the presence of food contaminants in lab animal diets needs to be addressed with precaution, without jumping too fast to conclusions. At least the authors should be congratulated for tackling an interesting question, which, by the way, also extends to the analysis of epidemiological cohorts.

Dr. Carl Winter, Cooperative Extension Food Toxicologist, University of California, Davis (webpage):

The authors contend that since the maximum dietary intake of the pesticide pirimiphos-methyl in seven of the diets exceeds the Acceptable Daily Intake, that animals fed such diets are being fed toxic levels of pirimiphos-methyl.  This conclusion is not supported for two reasons

1) The maximum dietary intake represents an exaggeration of the true dietary intake.

2) (More important) Comparing maximum dietary intake with the Acceptable Daily Intake is not appropriate to demonstrate risk. A more appropriate comparison would be the No Observed Effect Level (NOEL) from long-term animal toxicology studies, which represents the maximum amount given to laboratory animals on a daily basis that does NOT cause any noticeable toxicity.

For all of the other seven pesticides detected, exposure at the exaggerated maximum dietary intake level was still below the ADI levels, (commonly 100 times lower than NOEL levels from animal studies), so it is difficult to make a valid case as to how such exposures would cause effects in the animals consuming feed containing pesticide residues.

Science Media Centre

Prof Maurice Moloney, CEO of the Global Institute for Food Security, Canada (An Institute of the University of Saskatchewan)

The underlying hypothesis of this paper is the contention that the development of tumorous growths and carcinomas on the widely used Sprague-Dawley rat is the result of the toxicological effects of contaminants carried over into the feed pellets of lab animals from agricultural cultivation. Special emphasis is placed on the GM nature of some of the source materials and to one particular herbicide, glyphosate, or when formulated ‘RoundUp’. If this hypothesis were upheld, the authors believe that it means that most of the toxicological studies using this strain of rats are invalid, because of the intrinsic pernicious nature of the feed itself rather than the chemical (or other treatment) being tested. The previous study from this group was retracted from the Journal of Food and Chemical Toxicology, based on serious flaws identified after publication that should have been corrected in peer review, but which rendered the work inconclusive. The current work is no less inconclusive than the previous study, but nevertheless does offer some new data not heretofore published.

In summary, if this paper is an attempt to support the previous (now retracted) study by this group, it falls far short of doing so. The new paper suggests we ought to doubt an entire testing system but does not provide the evidence to back up such doubt.

By analogy, this is like a football team that is consistently disallowed goals, because they fall prey to an offside trap, calling into question all the laws of football. They do this rather than simply imposing discipline on their strikers not to move until the ball is in play. This paper lacks discipline in its discussion of the data, even though in the case of organophosphates and heavy metals, it might have discovered something that warrants further investigation. Food with minimal known toxin residues would help to ensure that test animals are treated ethically. For Sprague-Dawley rats, an ethical prerequisite is to use them only as intended for 90 day trials. Beyond that, as we saw in the revoked paper in the Journal Food and Chemical Toxicology, the test animals are subjected to significant distress, most likely due to a well-known genetic predisposition to form tumours.

Prof Cathie Martin, Group Leader, John Innes Centre

Seralini et al conclude that one cannot trust historical control data, but the tumour incidence of Sprague Dawley rats was published several decades ago (CANCER RESEARCH 33, 2768-2773, November 1973), when the contamination values for rodent chow were likely to be very different. Reports of the high cancer incidence of Sprague-Dawley rats were made long before the advent of GMO crops, so it cannot be concluded that GMOs are the cause of the high tumour incidence. The high tumour incidence in Sprague Dawley rats, which underpins the recommendation that they should not be used for studies beyond 18 months old, is most likely their high level of inbreeding.

It is strange that the conclusion of Seralini et al is that one cannot trust any experiments done with ‘control’ rats because of dietary contaminants.  A more reasonable conclusion would be that no one can trust data purporting to show that glyphosate and glyphosate resistant corn cause tumors in Sprague-Dawley rats, when they have a high inherent incidence of tumors in animals older than the recommended 18 months (whatever the cause).

Prof Tamara Galloway, Professor of Ecotoxicology, University of Exeter

The chemical analysis has been performed by accredited laboratories and appears robust and of good quality. The authors found that a number of the test diets contained residues of pesticides, metals and industrial chemicals, and this is perhaps unsurprising given their widespread use, but it is reassuring to see that the concentrations of these compounds are below regulatory limits.

... the authors have calculated a hazard quotient, which they then compare with acceptable daily intakes (ADI) calculated for human consumption. Since the ADI is calculated using a safety factor of 100, a direct comparison of the two estimates could give the wrong impression, since the safety factor is not taken into account.

The authors do not measure the biological or health effects of the food and hence it is not possible to say anything from the paper on the likelihood that food contamination might have a role to play in the high incidence of health problems in laboratory rodents, as speculated by the authors. The discussion speculates beyond the evidence presented in the paper.

Prof Alan Boobis, Professor of Biochemical Pharmacology, Imperial College London

The paper of Mesnage et al provides a useful survey of the levels of a number of contaminants present in the feed of laboratory rodents. However, I believe the title is potentially misleading in the use of the term “toxic levels”. Firstly, in general the levels of individual contaminants are extremely low. Note that a hazard quotient (HQ) of 1 would represent exposure at 1% of the critical no observed adverse effect level (NOAL). Secondly, it is assumed that these low levels would all exhibit dose additivity (HQs were summed), regardless of mode of action or potential site of effect. This is contrary to the approach that EFSA, and others, recommend for risk assessment of combined exposures. However, even in this situation, the summed HQs are in all cases less than 100, indicating that total exposure is below the NOAEL.

Prof Tony Dayan, Emeritus Toxicologist:

It appears to have been assumed that the samples of diets were representative samples which had not been contaminated prior to analysis. It may be more important that the quality of the feed provided for animals in regulatory tests has to comply with legally binding Good Laboratory Practice regulations (GLP), which include regular analyses to demonstrate amongst other things that contamination with heavy metals, pesticides and other substances is kept below strict limits. No information is provided to show that the batches reported in the new work were of a quality compliant with GLP and so might have been used in carcinogenicity or other formal tests.

Professor Mesnage and colleagues make many comparisons between their findings and ADI (‘Acceptable Daily Intake’) and HQ (‘Hazard Quotient’) values, suggesting that the results may indicate risks to rodents. Those concepts and the calculated values are empirical factors derived and successfully employed over many years specifically to assess potential risks to humans. There is no experimental justification or experience to apply them to rodents as done here.

Dr Graham Tobin, Technical Director, Harlan Laboratories, Europe/ROW


The argument is flawed on the following basis:

1. No data or compelling literature support was presented to demonstrate the contaminant levels found in the diets will contribute to these specific pathologies within rats.

2. The safety assessment was predicated on human ADI levels that are not properly scaled to assess safety risks in rodents.

3. The argument is too simplistic, ignoring other factors such as genetic predisposition, and practical experience. It overlooks the well-established effect of dietary restriction to improve survival and reduce pathology; this beneficial effect occurs in the absence of a reduction in contaminant intake per unit body weight.

This paper addresses an important subject, but does a disservice to laboratory animal science by inflating the potential risk of typical dietary contaminant levels through use of an inappropriate metric.  On the basis of the evidence presented it certainly seems inadvisable and unwarranted to apply the adjective ‘toxic’ to the levels of contaminants reported here.

This report was compiled by the Genetic Literacy Project using data provided by GENeS and the Science Media Centre.


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