Thursday, January 16, 2014

If humans were rats...

Monsanto GMO safety test assures... half would be dead *
the rest would suffer from  kidney and liver disease in under 90 days...

Veterinary Medicine Perspectives 

I Can't Get No Satisfaction**


400 rats...

 test results published for as few as 4 ?!

First Red Flag:  Ns (number of rats) in all Tables in this study should add to  200/sex -400 TOTAL 

“Results of a 13 week safety assurance study with rats fed grain from glyphosate tolerant (Round-Up-Ready) corn." 

Hammond B, Dudek R, Lemen J, Nemeth M.
Food Chem Toxicol. 2004 Jun;42(6):1003-14

Dear Food and Chemical Toxicology: shouldn't you retract Hammond's study-- rather than Seralini's ? 

Food and Chemical Toxicology, the journal which recently retracted the  infamous  Seralini study- reporting  kidney & liver disease, as well as unexpected breast canceralso published four safety assurance studies by Hammond et al.  

Seralini  was crucified in the popular media: " Commentators variously claimed the study to be "biased", "poorly performed", "bogus", "fraudulent", "sub-standard", "sloppy agenda-based science", "inadequate" and "unsatisfactory". Séralini was said to have "sought harm" for the rats, the experiment was dismissed as "inhumane" and the research group was called "partisan". France was outed as "the most anti-science country in anti-science Europe" and vociferous GM supporters"  

The reason for the retraction was simply bizarre. The study that replicated Monsanto's 90 day safety test on Round Up Ready Corn (NK603) by Hammond et al  was retracted because the results were found  to be inconclusive : "Ultimately, the results presented (while not incorrect) are inconclusive, and therefore do not reach the threshold of publication for Food and Chemical Toxicology" 
If this standard was applied to other studies in any field of science, 90% of studies would have to be retracted. But of the two studies, Hammond's suffers from far worse, indeed- catastrophic flaws.  

Agricultural GM cheerleaders who lobbied aggressively for retraction of Seralini's life-long rat study, made darn sure that Hammond's study which triggered Seralini's study-never ever ever never drew any attention. 

Read and understand this study- representing a standard safety test on the most prevalent transgenic crop in the food supply. 

Full text of the study is linked above-  take this opportunity to read the study linked --few GMO studies are OPEN ACCESS. In fact the majority are neither peer reviewed nor published. 

Consider checking off the boxes as you go along

The study is a safety assessment to ensure that the RoundUp Ready corn (NK 603) is as safe as conventional corn involving two components. Firstly, it is an evaluation of safety of the newly introduced trait- Round Up Resistance conferred by the Round Up Ready transgene (CP4 EPSPS). Secondly, it is an assessment for possible toxicity due to unintended pleiotropic effects resulting from the insertion of the trait (transgene). [*] 

But it appears this study does not provide robust evidence to support either claim, is even less  conclusive than Seralini- and should likewise be retracted. 

The following dissection should clarify the reasons why  it fails to live up to its title- Safety Assurance Study- a very bold claim, unsupported by evidence. 

DATA is reported for HALF and sometimes fewer animals: Selection Bias

Elementary school arithmetic for non-scientists.  Number of experimental animals (N) in Tables should be 20 because there were 20 rats/sex/group.

If you add the experimental and control rats in any category, test  results should be available for  400 rats.  Let see what happens when you try this exercise for bilirubin, in the table posted above, as an example.  For male rats (Table 4)  bilirubin is reported for 4-6 experimental and 36 control rats, while for females (Table 5) it's reported for 7-8 experimental and 49 control rats.  
So results are reported for  (4 to 6 + 36) + (7 to 8 + 49) = 96 to 99 rats. 

          Where are the remaining 301 to 304 rats......on vacation ?   

And what does a result on 4 to 6 mean, anyways? Was it four, five, or six rats? 

Don't feel too bad if you aren't finding it easy, because the "esteemed"  scientists and editors at  Food and Chemical Toxicology, as well as regulators---   flunked elementary school arithmetic. 

The reason blinding has been used for hundreds of years in research is to prevent just this type of biasScientists often want a particular outcome from an experiment, and it is  possible to choose the animals to test in such a way as to achieve desired results.

 In a non-blinded experiment, where the researchers know which animals are exposed to which food, and test results are published for less than half the rats ( N 4-10, instead of 20 in Tables 2,3,4), the researchers are free to cherry pick the rats based on overt clinical signs.  

If the transgenic corn was engineered with a metabolite toxic to the kidneys, the most  affected rats would be identifiable, as they would be drinking excessively and urinating excessively. Rats with liver disease could likewise be avoided for sampling  because their white skin would glow yellow  due to jaundice. 

But beyond just that-- biochemistry and hematology are reported for half as many rats as were necropsied-dead-thus the data literally says, only half of the rats were analyzed because the other half died. Laboratory rats rarely to never go on  Caribbean vacations.

 Bias does not have to be due to deliberate deception- human nature makes scientists vulnerable to confirmation bias...which is the reason blinding is used in good experiments to mitigate bias. 

 Data and conclusions of a non-blinded experiment missing data for more than half the animals should be declared invalid by design.

  •  I could stop right here..this study is  "inconclusive" based on this fact alone.... 

 but I shall go on...because there is so much more.

Safety of introduced CP4 EPSPS trait


of Round Up Ready (CP4 EPSPS)  transgene protein

 NOT Ruled Out 

Committees of global experts have created decision trees largely based on assessment of IgE-mediated food allergenicity for risk assessment.[8] The WHO guidelines state that a transgene with greater than 6 (continuous) amino acid homology to a known allergenic epitope or > 35% of (discontinuous) sequence , should be further screened on 25 individual serum samples with high IgE titers to that air borne or food borne allergen.
[2] CP4 EPSPS protein has homology of SEVEN amino acids  to a known and prevalent allergen- dust mite allergen (der p 7).[1] 
Hammond cites Harrison et al, a study on digestibility of CP4 EPSPS protein as evidence for lack of  allergenicity of the introduced transgene. While digestibility is a preliminary step in screening novel proteins, it is not a substitute for immunologic studies. Hammond also cites studies on Round Up Ready soybeans as evidence of lack of allergenicity. However, studies on  Round Up Ready soybeans are not a substitute for studies on Round Up Ready corn.  Moreover, a targeted analysis on serum from patients with dust mites allergies was not performed  on 25 serum samples in the studies.  The largest inhibition ELISA on CP4 EPSPS was reported for Round Up Ready soybeans on a trivial sample of 4 [9]  and thus the studies would not uncover cross reactivity  between Cp4 EPSPS and der p 7  in soybeans.  

Research to verify lack of cross-reactivity is not cited by Hammond et al, and a literature search failed to uncover such studies on 25 serum samples with high levels of IgE to dust mites.[9]   Inhibition ELISA studies can and should  be conducted to assess for the presence of allergenic cross-reactivity between the EPSPS CP4 protein in corn and der p 7 to definitively rule out allergenicity [10] This is a minimal standard of risk assessment for known allergens, while everyone accepts that even this standard leaves large gaps since not all allergies are IgE mediated.  

 This meticulously conducted  independent proteomics study on a different variety of genetically engineered corn [4] also shows a well known allergen.  This 2DE gel  detected 50KD gamma zein, a latent allergen expressed after the genome was disrupted by biolistics (gene gun).

Non-targeted “omics” profiling studies might be able to  detect unintended and unexpected changes  that targeted compositional analysis underpinning the current risk assessment by Hammond et al would not-- by revealing novel toxins or allergens; making GMO safety studies more conclusive   [11]   However omics are not part of the regulatory risk assessment and are not published for commercialized GMOs, but proper safety assessment must include profiling, because without them  safety studies are inconclusive.

  • Failure to rule out allergenicity  makes the study inconclusive ...but I shall go on.. .there is more

Toxicity due to pleiotropic effects resulting from insertion into the corn genome [*]

Random integration of a transgene may cause gene disruptions leading to sequence changes, production of new proteins or formation of new metabolites or altered levels of existing metabolites that could compromise safety. This includes the potential production of new allergens or toxins.[5] For example, a  proteomics study on maize demonstrated that 43 proteins were up- or down-regulated in transgenic seeds with respect to their controls specifically related to the insertion of a single gene into a maize genome by particle bombardment.[4]

Kidney and liver would most likely be some of the metabolic organs affected by novel metabolites or inflammatory proteins. And it turns out inflammation is reported in this study in both  liver and kidneys on histopathology of these rats. 


 Sprague Dawley rats suffer from spontaneous kidney disease, chronic progressive nephropathy (CPN) which confounds toxicology studies.

Blood tests associated with kidney function (BUN, creatinine)  are not significantly elevated until advanced stages of disease, which makes the “normal”  tests reported in Tables 4 & 5 meaningless. 
A urinalysis does indicate progression and loss of renal function by declining urine specific gravity, elevated levels of urine protein/ albumin, and casts- prior to elevation of blood tests.

 These inexpensive and crucial functional tests are not published in this study nor any Hammond et al feeding trial.

  • Absence of basic renal function tests makes this study inconclusive. I could stop right here, but I shall go on...because there is more. 

The  findings reported in Table 7 are vague and not descriptive of the specific histopathological changes.  The earliest lesions of CPN in young rats are convolutions of a single proximal tubule showing basophilia and crowded nuclei, representing simple tubule hyperplasia, with thickened basement membrane (especially of  the Bowman's capsule),  which is not reported in this study. 
The study instead reports mononuclear cell infiltrate, which is  generally a feature of inflammatory/ immune mediated processes. However, CPN is not an inflammatory or vascular disease, and it has no immunological or autoimmune basis. [6]

 Regeneration is reported in 17/20 rats, which is disproportionately high to the number of animals in whom degeneration is reported, while these processes occur simultaneously. Thus without a  review of histopathology slides by independent pathologists assurances of absence of reno-toxicity can not be made.  

Furthermore, pathologists recommend histopathological grading on a scale of 0-4 (kidneys graded by the study pathologist as minimal = 1 (less than 25% of renal tubules affected); mild = 2 (T 25–50%); moderate =3 (T 50–75%); or marked = 4 (T 75%); [7] [6] which likewise was not done in this study, making a valid comparison of severity between the groups impossible.

In any case, sample sizes of 9-10 for whom results are published are too low to parse toxic  effects  from confounding  spontaneous kidney disease - unless the potential  toxin has a very strong effect  in a very short period of time. 

So, if you recall the main, and I believe,  valid  criticism of Seralini as having sample sizes too small  to draw conclusions, the same is the case with this study. The sample size is too small to rule out kidney toxicity, separate and apart from the  other flaws I list.  GMO toxicity would be masked by spontaneous kidney disease which doesn't  manifest until more than 75% of renal function has been destroyed.  

  • Failure to rule out reno-toxicity makes this study inconclusive. I could stop right here, but I shall go on... because there is more.

Liver toxicity 

Tables 2,3,4  report normal liver enzymes which would suggest that the corn is not hepatotoxic. Unfortunately they do not. 

Liver enzyme tests are not liver function tests-they are tests of inflammation.  In fact, liver enzymes can appear relatively normal in the face of liver failure.  Bilirubin is a marker of jaundice most often associated with hepato-biliary disease.   In cats the most common form of liver disease is known as hepatic lipidosis or  fatty liver disease. The same disease is recognized  in rats and in  people, and it is called  non-alcoholic fatty liver disease (NAFLD).
 Its prevalence rate  is rising- especially among kids.

 I present an illustrative  case report   with  blood work and a urinalysis in a cat with imminent liver failure, in whom liver enzymes were nearly normal.  The test most crucial for diagnosis was serum and urine bilirubin. 

Recall at the very beginning of this post there is a table that shows that Total bilirubin (t.bili) in Table 4 is reported for 4-6 out of 20 male rats (and 7-8 out of 20 female rats.) Bilirubin values in the urine are not published for the rats at all. 

The study reports multifocal chronic inflammation in most of the rats in Table 7 which is histopathological indicator of  chronic inflammatory hepatitis. Histopathological inflammation is usually associated with elevation of liver enzymes, interestingly reported to be within normal ranges, which doesn't make sense.  The clinical test veterinarians usually perform to assess animal liver function ( in contrast to inflammation) is the bile acid test  - available for rodents, but wasn't performed.

The liver represents a suitable model for monitoring  effects of a diet, due to its key role in controlling the whole metabolism.

 A study examining effects of Round Up Ready soy diet were studied on liver of  female mice in order to elucidate possible interference with ageing.  Several proteins belonging to hepatocyte metabolism, stress response, calcium signalling and mitochondria were differentially expressed in GM-fed mice, indicating a more marked expression of senescence markers in comparison to controls. Moreover, hepatocytes of GM-fed mice showed mitochondrial and nuclear modifications indicative of reduced metabolic rate. The study demonstrated that GM soybean intake can influence some liver features during ageing while liver enzymes (the tests reported by Hammond et al) were not afffected at all.  The mechanisms remain unknown, underlining the importance of  investigating  long-term consequences of GM-diets and the potential synergistic effects with ageing, xenobiotics and/or stress conditions. [12] [13]

  • Failure to rule out liver toxicity make this study inconclusive...

I could stop here... but there is more. 


Type II Error

Tables 2-4 do not report precise number of rats. Means and standard deviations cannot be calculated for ranges (for example 4-6 or 9-10) of rats. 

A balanced experimental design would consist of 200 experimental and 200 control rats. Instead there are only 80 experimental rats raising risk of type II Error-- Not Finding Deleterious Organ Effects associated with chronic diseases that this experimental crop caused-liver such as NAFLD, bowel such as inflammatory bowel diseases and dysbiosis,  kidney toxicity and kidney stones or allergies for which this rat strain makes an inappropriate model. Due to brevity, 90 day trial design and long lag time between exposure and development, also-- cancer-- whether breast tumors or blood, kidney or other organ.  

Statistics make the study inconclusive.

Invalid reference groups.

The experiment was conducted on 400 rats fed two doses of corn (11% & 33%). A balanced experimental design using 400 rats would consist of 50 rats/sex/dose on transgenic corn compared to 50 rats/sex/dose of its isogenic parent line grown side by side-  agronomic factors (soil, fertilizers), and environmental influences (location, weather, stress) are all factors that must be considered during “GE versus non-GE” evaluations. [3]  Environment has been shown to play a prominant effect in the protein, gene expression and metabolite levels in plants- in one maize study 5 proteins, 65 genes and 15 metabolites were found to be differentially expressed.[5]  Approximately 100 total proteins were differentially expressed as a consequence of  environmental influence in a different independently conducted proteomics study. [4]   

Yet,  Hammond's reference/control groups A-F are grown in random geographic locales such as Indiana, Iowa and Colorado, while the genetically engineered corn was grown in Ohio! Thus reference/ control  A-F in Table 1  not grown in Ohio--are inappropriate reference groups used to establish invalid reference ranges. Shrinking 

  • I could stop right here. If the reference ranges for non-GE corn are invalid, it isn't possible to compare GE and non-GE for statistical differences within 2 standard deviations as the study does, which makes this study inconclusive   But I shall go on...because there is more. 

Baseline lab-work should have been obtained at the beginning of the experiment,  repeated mid-point and at the end of the experiment, in order to measure trends. A single lab test recorded at one time point is highly unlikely to parse differential effects on physiology of experimental and control rats, when no effort is made to measure and record  trends. Absence of metabolic trends makes this study inconclusive

I hope I've clarified  why this study by Hammond et al does not meet its stated goal of reassuring me of safety of this crop to rats. The other three studies linked above relied on  the same flawed experimental design.  By definition, no study on rats can meaningfully show safety to a human, since many adverse effects of food additives and drugs are often discovered only when large randomized epidemiological studies are performed on humans. 

In spite of  lack of  " conclusiveness"  factor  I outlined above, this study has not been retracted,  which suggests that the agricultural biotechnology science establishment is promoting GROSS and inexcusable scientific double standards. This is scandalous for many distinct reasons, not the least of which is that science is uncovering multiple mechanisms  which could have caused the rats in Serallini's study to develop breast cancer

So, the next time you read a GMO booster criticize Seralini, please direct them here to justify every one of Hammond's egregious flaws, as well as the fact that these safety studies haven't  been replicated long term--for a lifetime of a rat, which is the duration of time animals and people are expected to eat them. 

My hope is that unwrapping one study for readers will open your eyes to the fraud that is GMO safety testing. 

This, as well as the other 3 short term studies by Hammond et al, linked above, were cited by this  "long-term" review by Snell et al   which  claims to show long term GMO absurd claim!!!

"Some of my concerns with GMOs are “just” practical ones. I have read numerous GMO risk assessment applications. These are the documents that governments rely on to ‘prove’ their safety. Though these documents are quite long and quite complex, their length is misleading in that they primarily ask (and answer) trivial questions. Furthermore, the experiments described within them are often very inadequate and sloppily executed. Scientific controls are often missing, procedures and reagents are badly described, and the results are often ambiguous or uninterpretable. I do not believe that this ambiguity and apparent incompetence is accidental. It is common, for example, for multinational corporations, whose labs have the latest equipment, to use outdated methodologies. When the results show what the applicants want, nothing is said. But when the results are inconvenient and raise red flags, they blame the limitations of the antiquated method. This bulletproof logic, in which applicants claim safety no matter what the data shows, or how badly the experiment was performed, is routine in formal GMO risk assessment.
To any honest observer, reading these applications is bound to raise profound and disturbing questions: about the trustworthiness of the applicants and equally of the regulators. They are impossible to reconcile with a functional regulatory system capable of protecting the public." Dr. Latham

I could go on and say more ....but  I won't.   Hopefully, I've given  you enough food for thought. 


  1.BMC Structural Biology Screening of transgenic proteins expressed in transgenic food crops for the presence of short amino acid sequences identical to potential, IgE – binding linear epitopes of allergens Gijs A Kleter  and Ad ACM Peijnenburg

   2.Evaluation of  Allergenicity of Genetically Modified Foods Report of a Joint FAO/WHO Expert Consultation on Allergenicity of Foods Derived from Biotechnology  January 2001 Food and Agriculture Organization of the United Nations (FAO) Rome, Italy

8/29/2014 Edit: Snap! The WHO  link went dead. Try  :

       3. ISB NEWS REPORT • MAY 2010 Molecular Profiling Techniques as Tools to Detect Potential Unintended Effects in Genetically Engineered Maize. Eugenia Barros.

   4.  J Proteome Res. 2008 May;7(5):1850-61.doi:10.1021/pr0705082. Epub 2008 Apr  Proteomics as a complementary tool for identifying unintended side effects occurring in transgenic maize seeds as a result of genetic modifications. Zolla L, Rinalducci S, Antonioli P, Righetti PG.

5. Comparison of two GM maize varieties with a near isogenic non-GM variety using transcriptomics, proteomics and metabolomics.  Eugenia Barros,Sabine Lezar, Mikko J. Anttonen,, Jeroen P. van Dijk, Richard M. Röhlig, Esther J. Kok3, and Karl-Heinz Engel

6.Toxicologic Pathology, 32:171–180, 2004A Contemporary Overview of Chronic Progressive Nephropathy in the Laboratory Rat, and Its Significance for Human Risk Assessment


7. Toxicol. Sci. (2012) 128 (2): 346-356. Chemically Exacerbated Chronic Progressive Nephropathy Not Associated with Renal Tubular Tumor Induction in Rats: An Evaluation Based on 60 Carcinogenicity Studies by the National Toxicology Pgram Ronald L. MelnickKathleen M BurnsJerrold M. Ward and James Huff  

8. Environ Health Perspect. 2003 Jun;111(8):1114-21.
Clinical and laboratory investigation of allergy to genetically modified foods.


Yonsei Med J. Aug 31, 2006; 47(4): 505–512. doi:  10.3349/ymj.2006.47.4.505 
Evaluating the Allergic Risk of Genetically Modified Soybean

10. Clinical and Molecular Allergy 2007; 5:2 Assessment of allergen cross-reactivity Rob C Aalberse

11.Molecular profiling — a tool for addressing emerging gaps in the comparative risk assessment of GMOs Jack A. HeinemannBrigitta Kurenbach,, David Quist

12.   2008 Nov;130(5):967-77. Epub 2008 Jul 22.
A long-term study on female mice fed on a genetically modified soybean: effects on liver ageing.

13.  2002 Aug;27(4):173-80.Ultrastructural morphometrical and immunocytochemical analyses of hepatocyte nuclei from mice fed on genetically modified soybean.


[*] The study as designed by Hammond et al  does not permit evaluation for  pleotropic effects since there is a confounding factor that has not been segregated out. The corn was treated with Round Up- a mixture of glyphosate, AMPA and proprietary adjuvants. The authors  state that glyphosate wasn't detected at 250 ppb, however, the methodology isn't listed. Typically residues are measured by High Pressure Liquid Chromatography in tandem with Mass Spectrometry or ELISA. Since methods weren't published reported glyphosate residues are questionable. If indeed the levels of glyphosate were <250ppb they might not represent field conditions, and if greater-these additional chemicals make it  impossible to tease away any potential  metabolic toxicity caused by transgene insertion on the genome  from chemical toxicity of Round Up and its adjuvants. It is also the reason that Seralini in his retracted paper came up with the  "complicated design"  separating rats into groups exposed to transgenic corn alone ( to evaluate effects of transgene insertion on the genome in isolation of Round Up)  and those exposed to Round Up in the drinking water. 

*When I say NK603 killed half the rats-- it is literally what  DATA indicates.  Post mortem (necropsy or  autopsy)  histopathology in this study was done on rats who were dead, while biochemistry and hematology was reported for half of the animals necropsied.

**Scandalous! GMO safety studies are not designed, interpreted or reviewed by doctors in veterinary medicine-the only animal health professional with expertise  to interpret veterinary tests- even while the majority of GMO safety studies are performed on animals using  clinical veterinary tests. 


  1. Although I can’t say you are incorrect, I can definitely say you are not right.
    First, the reason Hammonds study was not picked apart was because he both followed OECD guidelines as well as made sounds conclusions based on his data.
    Second you claim on the lack of validity due to not enough study of CP4 EPSPS is not incorrect, but neither is it correct. This study didn’t thoroughly test variable x is not enough to mean the study should be retracted.
    Third, you seem to act like this single study is the single piece of evidence that the FDA looks at to decide to deregulate a crop. You couldn’t be farther from the truth! We go through years of toxicity testing, allergenic testing, feeding trials, yield trials, seed purity tests. And then and only then after years of work and countless tests are ran, do we have enough information to take a brief to seek deregulation.
    Fourth you claim RR soy and RR corn are not the same, why? It’s the same trait. How can you say the same trait is not the same. Its like saying my DNA is different when I am inside vs outside. The DNA doesn’t change just because of where it is!
    Fifth you mislead readers into assuming that the locations of grown corn are different, when they are not all different, there are three controls of corn grown from Ohio just like the GM corn that you seemed to have excluded from you review, accidentally, I’m sure!
    Sixth, you seem to take issue and claim researched acted in a bias way because they knew which rats urinated more? Are you telling me you are claiming researchers watched these rats for 24 hrs a day and charted which ones urinated the most and also were always 100% sure they could tell all these random rats from one another??? I apologize if I have to say that is ludicrous!
    Now, I could and will stop there. I see your train of thought, present half truths and explain why they should negate the study. Well, like I said before, the little bits you pulled out of the study are not Incorrect, but are no where near correct.
    I understand you don’t think this study was done perfect. Maybe it wasn’t, but just because it does fit your reasoning, does not negate its findings. I’m sorry you can’t see the difference between Hammond’s and Seralini’s study.
    To me, them seem as plain as day.

    1. Hello Ben. Our opinions are so far apart I am not sure we can bridge the gap, but here goes.

      1. OECD guidelines for an unscientific experimental design are not an excuse for a poorly designed study. It is akin to saying that you jumped off a cliff because your friends told you to. The report is authored by Hammond et al (employees of Monsanto), They are accountable for the study's strengths and liable for its weaknesses. A study titled a safety assurance study must provide the data for a reader to reach that conclusion. It fails. If the OECD is your excuse, Monsanto needs to take it up with the OECD, not the reader of the study, because from my perspective it looks like an exercise in shifting responsibility.

      1.b "as well as made sounds conclusions based on his data" the DATA in the study does not support the conclusion the corn is safe. At a minimum the data shows that the corn disappeared half the experimental animals, and the rest of the DATA is insufficient to rule out allergenicity, renotoxicity or hepatotoxicity.

      2. Sorry, I don't understand this statement. Please clarify it.

      3. The study has to be self-contained and provide all the data required to support the conclusions either in the body of work or in supporting citations. It does neither. See 1B
      The other studies the FDA evaluates or does not evaluate are hearsay and rhetoric rather than science.

      4.You are mistaken if you believe it is the same trait-this corn was transformed with two different cassettes.

      "Nucleotide sequencing indicated that the sequence of the CP4 EPSPS gene within the second (3' proximal) cassette differed by two nucleotides from the inserted sequence. This gave rise to a single amino acid substitution at position 214 of the expressed protein (leucine --> proline; variant protein referred to as : (CP4 EPSPS L214P)"

      Not only is it not the same trait, which is the reason the trait in the corn is titled CP4EPSPSL214P, but each insertion event is completely unique regardless of the trait being inserted, because biollistics inserts the trait randomly causing rearrangements at the site of insertion and genomic disruptions elsewhere unique to each transformation event.

      "In addition to a complete copy of the introduced DNA, the insert also included a 217 bp fragment (50 bp of polylinker sequence + 167 bp of the enhancer region of the rice actin promoter) inversely linked to the 3' terminus of the introduced DNA.

      Analyses of specific PCR products from the 3’ terminus of the inserted DNA revealed that an additional segment comprising 305 bp of chloroplast DNA had been co-integrated. Bioinformatics analysis indicated that this sequence corresponded to a portion of the maize DNA-directed RNA polymerase alpha-subunit and ribosomal S11 protein. The source of this DNA was believed to be the chloroplast of the transformed cell"

      Thus each individual event needs to be tested individually, let alone testing a completely different species of plant.

      5. I didn't mislead my readers-the study is linked in the title for anyone to reach their own conclusions. Table 1 clearly shows superfluous and inappropriate reference groups.

      6. I am claiming that one of the reasons this study is unreliable is that it wasn't blinded. If you want to argue against the utility of blinding in reducing bias, you'll need to take it up with the entire medical establishment.

      The study does not assure me, a veterinary medical doctor, that the corn is safe for rats to eat. Let alone dogs, cats or people. Your expectation that I will conclude it be safe based on rhetoric assurances from the FDA or the OECD is not much different than telling me the Pope said the corn is safe, in the expectation of suspension of scientific skepticism and developing a conclusion on what amounts to a religious belief.

      I appreciate your engagement-thanks for your comment.

      Cheers, Ben

  2. Ben, are you suggesting that Seralini did not follow OECD guidelines? If so, which OECD guidelines did Seralini not follow?