Dear Food & Chemical Toxicology: RETRACT HAMMOND'S Study, NOT Seralini's!

Dear Food & Chemical Toxicology: RETRACT HAMMOND’S Study, NOT Seralini’s!

Dear Food & Chemical Toxicology: RETRACT HAMMOND'S Study, NOT Seralini's!
MEET AIXA: Aixa Ponce Cano was BORN in the small town of Avia Terai in rural Argentina WITH TUMORS on her back and moles covering her body. Her mother, like most other people in Avia Terai, LIVES NEAR GMO Soybean Fields that are Sprayed with PESTICIDES:

Veterinary Medicine Perspectives

If Humans Were Rats…

Monsanto’s Own GMO Safety Test by Hammond Assures that HALF would be DEAD…

*the Rest would suffer from KIDNEY & LIVER DISEASE in UNDER 90 Days…

?1st Red Flag:


But Results Published for… Few as 4?

We see can the study initially began with 400 Test Subjects…



What Happened to the Rest?!

 Column ‘N’ = # Test Subjects


Click Here for “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


Food & Chemical Toxicology, the journal which recently retracted*** the infamous Seralini study- reporting kidney & liver disease, as well as unexpected breast cancer, also 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 The study that replicated Monsanto’s 90 day safety test on Round Up Ready Corn (NK603) by Hammond et al was retracted*** because the results were supposedly found to be inconclusive : “Ultimately, the results presented (while not incorrect) are inconclusive, and therefore do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 were 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. First, it is an evaluation of safety of the newly introduced trait- Round Up Resistance conferred by the Round Up Ready transgene (CP4 EPSPS). Second, 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.



Emails Reveal Role of Monsanto in Seralini Study Retraction

Seralini’s Team Wins Defamation and Forgery Court Cases on GMO and Pesticide Research

Republication of the Séralini Study: Science Speaks for Itself


The following dissection clarifies 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 MERELY HALF & 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 301-304 Rats…… on Vacation???

And what does a result on 4-6 mean, anyway?  Was it 4, 5, or 6 rats??  Don’t feel bad if you aren’t finding it easy, because the “esteemed” scientists and editors at Food & Chemical Toxicology, as well as regulators—  apparently flunked elementary school arithmetic. 

The reason blinding has been used for hundreds of years in research is to prevent just this type of bias. Scientists 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 & Conclusions of a Non-Blinded Experiment Missing Data for More than Half the Animals Should be Declared Invalid by Design.

…this study is inconclusive based on this fact alone…. 

Safety of Introduced CP4 EPSPS Trait

ALLERGENICITY 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 forknown 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 Renders the Study Inconclusive.

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 Renders this Study Inconclusive.

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 Renders this Study Inconclusive.


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 both 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 aging.  Several proteins belonging to hepatocyte metabolism, stress response, calcium signaling 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 aging while liver enzymes (the tests reported by Hammond et al) were not affected at all.  The mechanisms remain unknown, underlining the importance of  investigating  long-term consequences of GM-diets and the potential synergistic effects with aging, xenobiotics and/or stress conditions. [12] [13]

?Failure to Rule Out Liver Toxicity Renders this Study Inconclusive

Other Experimental Design Flaws

Invalid reference groups.

The experiment was conducted on 400 rats fed 2 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 prominent 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 the experimental group to 80 (20/sex/dose)  while increasing the control group to 320 animals serves to increase type II error (false negatives), reducing sensitivity of detecting adverse health effects.

?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, rendering the Hammond study INCONCLUSIVE.

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 Renders this Study Inconclusive.


Statistics are Invalid

?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 study with four times as many control reference animals (N=320) as experimental (N=80) is intuitively grossly imbalanced. Poor Math Skills and Statistics render the 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 crap I mean 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’ve 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.

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 safety… an absurd claim!!!

As another researcher, Dr. Latham aptly describes the flawed testing:

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.
Hear Dr. Latham’s podcast here: GMO Scientist speaks on GMO concerns



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: 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 LRinalducci SAntonioli PRighetti 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 PgramRonald 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.
Bernstein JABernstein ILBucchini LGoldman LRHamilton RGLehrer SRubin CSampson HA.


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
Sang-Ha Kim,1,* Hyun-Mi Kim,1 Young-Min Ye,1 Seung-Hyun Kim,1 Dong-Ho Nahm,1 Hae-Sim Park,corresponding authorSang-Ryeol Ryu,2 and Bou-Oung Lee3

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.  Histochem Cell Biol. 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.

Malatesta MBoraldi FAnnovi GBaldelli BBattistelli SBiggiogera MQuaglino D.

13. Cell Struct Funct. 2002 Aug;27(4):173-80.Ultrastructural morphometrical and immunocytochemical analyses of hepatocyte nuclei from mice fed on genetically modified soybean.
Malatesta MCaporaloni CGavaudan SRocchi MBSerafini STiberi CGazzanelli G.



[*] 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 hese 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 the 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 ONLY 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.