If you record noise, you don’t get music – you get nonsense.

Many women, no Cry by Marcel Kuntz 29 April 2011

A recent publication by Aziz Aris and Samuel Leblanc in the journal Reproductive Toxicology (Maternal and fetal exposure to pesticides associated to Genetically Modified Foods in Eastern Townships of Quebec, Canada) claims to have detected traces of:
herbicides (used on herbicide tolerant ‘genetically modified’ plant varieties) or their major metabolite,
and the insecticidal protein Cry1Ab (produced by certain varieties called Bt-resistant insect pests)
in the blood of Canadian women, pregnant or not pregnant, and in umbilical cords.
Th[e Kuntz] site will publish any credible information about the validity of these claims and this article will be updated periodically.
A publication lacking credibility
Only claims of Aris and Leblanc on Cry1Ab are discussed here for the time being.
The Cry1Ab protein is produced by some Bt cotton and corn (e.g. MON810).
Aris and Leblanc claim they detected this protein in 93% of pregnant women and 69% of non-pregnant women tested and believe that this is linked to the consumption of foods derived from Bt varieties, which in Canada must mean corn rather than cottonseed oil.
Surprisingly, the authors do not consider that the origin of Cry1Ab could be food from organic farming (which sprays Cry1Ab, or bacteria producing it, on fruit or vegetable crops) or from its use in gardening (CryA1b is part of available “natural insecticide” formulations).
If we examine the possibility of a Bt corn food origin for Cry1Ab, since these proteins do not bioaccumulate, it is necessary to consider recent consumption.
First question: do 93% of pregnant women in Canada actually consume corn almost daily?
Second question: are the values in blood reported by Aris and Leblanc consistent with the levels present in Bt corn kernels?
The answer is no. Here is why:
The authors reported average values of 0.19 nanograms per milliliter (ng / ml) of blood from pregnant women. Knowing that, in corn MON810 for example, levels of Cry1Ab in the grain are between 190 and 390 ng / g fresh weight, assuming that 1% will pass into the blood (which is on the high side taking into account losses during corn storage, cooking, gastric digestion and the intestinal barrier), this would require a woman of 60 kg to consume 120 g of corn (for the mean blood value of 0,19 ng / ml, assuming a plasma volume of 2.5 liters) and about 1.5 kg (for the maximum reported blood values of 2.28 ng / ml), which seems unrealistic … And even more if one takes into account all extracellular fluids (10 liters, which would imply an average consumption of 490 g of corn and 5.8 kg in order to reach the maximum value in blood).
Third question (which follows logically the above-mentioned findings): is the Cry1Ab detection method used by Aris and Leblanc reliable?
Note first that the test used, marketed by Agdia is claimed to detect the protein Cry1Ab from 1 ng / ml (read the introduction to this article).
While Aris and Leblanc claim to have detected average concentrations lower than the detection limit, e.g. 0.04 ng / ml in umbilical cords!
One can cite the publication by Lutz et al. (J. Agric. Food Chem. 2005, 53 (5) :1453-6) showing that the ELISA test used by Aris and Leblanc is not sufficient to guarantee the identity of positive signals (« to avoid misinterpretation, samples tested positive for Cry1Ab protein by ELISA should be reassessed by another technique »).
Note that Aris and Leblanc did not discuss this issue, nor the results of Chowdhury et al. (J. Animal Sci., 2003, 81:2546-2551) which indicate that these ELISAs do not work for blood (from pigs)…
Moreover, they do not cite the publication by Paul et al. (Analytica Chimica Acta 2008, 607: 106-113) that discusses the validity of the tests available on the market…(Provisional) answers to the questions that arise: in the absence of the validation of the detection of Cry1Ab, it is likely that the authors, incorrectly, conclude that any signal was indicative of the presence of the Cry1Ab protein, whereas they most likely correspond to false positives.
A possible validation, which surprisingly is lacking in the work of Aris and Leblanc, is the electrophoretic separation of plasma proteins and immunodetection of the protein Cry1Ab (‘Western blot‘, a common laboratory technique).
It therefore appears that this publication, in its present state, is of unsufficient quality to be convincing. It has not undergone a proper review process according to the standards of a scientific journal, which would have required the validation of the results and their discussion in relation to available literature.

FSANZ response to study linking Cry1Ab protein in blood to GM foods Accessed 30 May 2011

There has been some media speculation about a recent paper published by Aziz Aris and Samuel Leblanc titled ‘ Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada’ [Reproductive Toxicology, in press, 2011].
What is the paper about?
The paper deals with two herbicides, glyphosate and glufosinate ammonium that are sprayed on both genetically modified (GM) and non-GM crops, and an insecticidal protein Cry1Ab that is produced by the naturally occurring soil bacterium Bacillus thuringiensissub sp.kurstaki (Btk). The gene encoding this protein has been used to genetically modify some crops so that they contain the protein and are thus protected against certain insect pests. The protein is also extensively used in organic and conventional farming as a direct application pesticide
The authors of the study claim to have detected the Cry1Ab protein in the blood of pregnant and non-pregnant Canadian women, and in umbilical cord blood of foetuses.
What are the concerns about the paper?
A number of methodological and interpretive limitations of this paper limit the relevance of the reported findings and conclusions about food safety. The key limitations include insensitivity of the assay method used and unsubstantiated and invalid assumptions regarding the source of the Cry1Ab protein in the diets of test subjects. Media speculation arising from this paper has also presented conclusions about the human health relevance of this paper which are not supported by either the paper itself or the broader scientific literature.   These issues are discussed in more detail below.
The assay method
The assay method (ELISA) used for Cry1Ab protein was not tested (validated) for its suitability to measure Cry1Ab in human blood. Other reports in the scientific literature have shown that the ELISA assay is not suitable for this purpose.
In mammals, the Cry1Ab protein is degraded in the stomach. If any fragments of the Cry1Ab protein were to pass through into the blood stream, they would be present at levels much lower than could be quantified by the assay method used in the study.
The assumption that GM foods are the source of the Cry1Ab protein
The authors do not provide any evidence that GM foods are the source of the protein. No information was gathered on the diet of any individual in the study so the assertion that the detection of Cry1Ab is linked to ingested GM food is, at best, speculative.
Several insecticidal formulations (e.g. Delfin, Dipel) contain a blend of crystallised proteins, (including Cry1Ab) and livingBtkspores that germinate into the bacterium that then produces the proteins. These formulations have been applied worldwide, including in Australia, for decades. They are applied to crops such as broccoli, cauliflower, celery, melons, potatoes, spinach, tomatoes, cucumbers, turnip, grapes, kiwi-fruit, citrus, avocados. They are used both commercially and by home gardeners and are permitted for use on organically-certified crops.
In comparison, the consumption of food derived from GM corn containing the Cry1Ab protein (no other currently commercialised GM crop species contain this gene) is recent and relatively minor. The corn lines containing the Cry1Ab protein are mostly used for animal feed and for processing into refined products such as corn syrup and corn starch which, because of processing, contain negligible levels of any protein. None of the GM corns produced so far are popcorn or sweetcorn lines and are therefore not consumed directly. Therefore, ingestion of Cry1Ab by humans via GM corn is not likely to be significant compared to conventional and organic produce sources.
Interpretation by the media that Cry1Ab protein is a human safety issue
There have been claims in the media that the paper is proof GM foods are not safe for human consumption.
However, the paper does not discuss the safety implications of finding Cry1Ab in the human body and the authors make no mention of any abnormalities in either the subjects or, in the case of those who were pregnant at the time of the study, the subsequent process of birth or the health of the mothers and babies postpartum.
The Cry1Ab protein, whether ingested via Btk-sprayed conventional or organic crops or GM corn products containing the protein, is safe for human consumption at the levels likely to be found in these sources.
For more information, see this report , prepared under the auspices of the World Health Organization. It is about Bacillus thuringiensis, the organism used in the spray formulations, and from which various genes have been isolated for use in genetically modified crops. Chapter 7 deals with a whole range of exposures to the organism (and hence, the proteins produced by it) and their effects in humans.
See also later post: Many sources of Bt in addition to GM crops

88 thoughts on “If you record noise, you don’t get music – you get nonsense.

  1. Here’s a question that begs for an answer: is it possible for a person to gain a degree in science without knowing the fundamentals of designing a meaningful experiment?
    If the answer is ‘no’, then people like Aziz Aris and Samuel Leblanc, and studies like this, are concocting propaganda in their labs.
    There is of course another interpretation. Likely we all remember the work Losey did with Bt and Monarch butterflies. Come up with scary crap and more funding for research arrives post haste. Which would mean there’s something fundamentally wrong with how research funds are allocated.
    Unfortunately, Greenpeace is known to pay for research, and to get the results they pay for. Which is also quite bad. Seralini et al junk science results from activist funding.

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    1. Absolutely – particularly in areas in which they aren’t trained (Molecular biologists doing toxicology, as an example)

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  2. The following was stated by David Tribe in the introduction:

    “The Cry1Ab protein is produced by some Bt cotton and corn (e.g. MON810). Aris and Leblanc claim they detected this protein in 93% of pregnant women and 69% of non-pregnant women tested and believe that this is linked to the consumption of foods derived from Bt varieties, which in Canada must mean corn rather than cottonseed oil.”

    The actual statement in the paper (in the introducion) is.

    A foodmarket-basket, representative for the general Sherbrooke population, contains various meats, margarine, canola oil, rice, corn, grain, peanuts, potatoes, fruits, and vegetables, eggs, poultry, meat and fish. Beverages include milk, juice, tea, coffee, bottled water, soft drinks, and beer. Most of these foods come mainly from the province of Quebec, then the rest of Canada and the United States of America. Our study did not quantify the exact levels of PAGMF in a market-basket study. However, given the wide spread use of GM foods in the local daily diet (soybeans, corn, potatoes, . . .), it is conceivable that the majority of the population is exposed through their daily diet [31,32].”

    Please note that the actual article does not state that all of the Bt came from directly eating only corn.

    “However, given the wide spread use of GM foods in the local daily diet (soybeans, corn, potatoes, . . .), it is conceivable that the majority of the population is exposed through their daily diet [31,32].”

    Thus, the argument by David Tribe that it could not have come from direct eating of only Bt corn is what is known as setting up a “straw man”.

    It does state in the Discussion Section the following :

    “(1) that these toxins may not be effectively eliminated in humans and (2) there may be a high risk of exposure through consumption of contaminated meat.”

    I interpret point number one as indicating that the authors feel that the Bt may have accumulated from a number of food sources.

    The second possibility listed is that it came from contaminated meat, I feel that that possibility needs a literature citation. I did a quick check of the beef Bt literature, and it appears that a good case could be made (from existing literature) that it did NOT come from eating beef.

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    1. I spent some time examining their statement about the contaminated meat, and they mean contaminated by food in the gut of the cattle – akin to meat contaminated by gut bacteria.
      Remember that the paper is examining several substances, one of which is Cry1Ab (the test they used also tests for Cry1Ac which they did not mention).
      Also, you misrepresented what the article said, it did not say that the authors claimed that it came directly from eating corn – but that it must have come from corn if true.

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    2. Please note that the actual article does not state that all of the Bt came from directly eating only corn.

      “However, given the wide spread use of GM foods in the local daily diet (soybeans, corn, potatoes, . . .), it is conceivable that the majority of the population is exposed through their daily diet [31,32].”

      Thus, the argument by David Tribe that it could not have come from direct eating of only Bt corn is what is known as setting up a “straw man”.

      No, it’s absolutely not a straw man. There’s a reason why he focused only on corn & cottonseed oil: they are the only things of relevance here since only corn and cottonseed have commercial cultivation of varieties expressing BT proteins (currently commercially cultivated soybean GMO’s express various herbicide resistance traits and likewise there are no commercial BT potatoes). Also, you might have a wrong impression of how widespread GM crops are, at this point in time, if you think GM potatoes are common (they might be at some point but that was definitely not the case as of the time of the writing of that article).

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    3. Henry, I think you are missing the point that the only GM crop that the Bt could have come from was corn, as there were no other crops using the Bt transformation event at the time but corn and cotton, and people don’t eat cottonseed meal. But plenty of Bt is used in organic food production, and there is no way to determine from this study whether that could have accounted for the exposure, if any.

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  3. Hmm. I’ll have to look again later, but at first glance I can’t seem to find the controls. You know, other proteins from plants that you’d want to compare in the blood samples.
    I saw the blank, and the spiked stuff, but I mean other proteins in the blood to help us understand the amount getting through to the blood.

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    1. MaryM, is it possible that daedalus2u idea about if there was 100% detection that would mean a strong possibility of false positives is why the Editor/reviewers did not insist on a further test for false positives. i.e. was the fact that there were human blood samples that tested negative sufficient to rule out that another human blood protein was responsible?

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  4. Regarding Karl Haro von Mogel statement:

    “Also, you misrepresented what the article said, it did not say that the authors claimed that it came directly from eating corn – but that it must have come from corn if true.”

    Yes, that is what David Tribe is saying, but he is discussing an actual article that does not make that statement. I put in quotes what the actual article states. David Tribe seems to be assuming that no GM products are imported. The original authors are making the reasonable assumption (for Canada) that the pregnant woman were exposed to

    “However, given the wide spread use of GM foods in the local daily diet (soybeans, corn, potatoes, . . .), it is conceivable that the majority of the population is exposed through their daily diet [31,32].”

    Regarding Karl Haro von Mogel’s statement

    “I spent some time examining their statement about the contaminated meat, and they mean contaminated by food in the gut of the cattle – akin to meat contaminated by gut bacteria.”

    Yes, thank you, they do state that

    “However, trace amounts of the Cry1Ab toxin were detected in the gastro intestinal contents of livestock fed on GM corn [38–40], raising concerns about this toxin in insect-resistant GM crops.”

    I did not understand the part of the statement

    “raising concerns about this toxin in insect-resistant GM crops”

    Since, of course the toxin would be in the GM BT crop. What they probably should of said (as you suggest) “raising concerns that the BT in the GM Bt food in the gut could contaminate the meat”. Again, thank you.

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  5. The following was stated:

    “Note first that the test used, marketed by Agdia is claimed to detect the protein Cry1Ab from 1 ng / ml (read the introduction to this article). While Aris and Leblanc claim to have detected average concentrations lower than the detection limit, e.g. 0.04 ng / ml in umbilical cords!”

    H.Kuska comment: Neither the Agdia web page for this test nor the actual manual mentions a 1 ng / ml detection limit.
    From the Agdia manual for this test the following was stated:

    “Measure the optical density of the testwells on a plate reader at 650 nm or visually. Wells in which a blue color develops indicate positive results. Wells in which there is no significant color development indicate negative results. Test results are valid only if positive control wells give a positive result and buffer wells remain colorless.”

    Thus it appears reasonable to me that the fact that another lab could not detect a color change below 1 ng / ml, would only apply if the same optical detection system and method was used.

    The article states

    “A standard curve was prepared by successive dilutions(0.1–10 ng/ml)of purified Cry1Abprotein.”

    I would assume that if the standard curve had a point for 0.1 ng / ml that they actually detected it.

    Also please notice that the 0.04 was an average. From Table 3 the actual numbers are:
    Range of detection (ng/ml)
    nd to 1.50 and nd to 2.28
    AND
    Mean ±SD (ng/ml)
    0.19±0.30 and 0.13±0.37
    Please note, the means are much higher than the stated .04 average.

    It appears (to me) that the .04 average included the zero values.

    I am willing to give the authors credit that they observed signals (positives) above the background level. My main question is how do they know that they were not “false positives”? A water blank is not sufficient. Ideally they would need to run the tests on women who ate the same diet but with no GM Bt food and that these tests came out negative. i.e. there may be other molecules that will react positive in something as complex as a human system. (This may be similar to what MaryM is saying.) One this point I agree with David Tribe with the change of his “likely” to “possible” and his “most likely” to “may”:

    “(Provisional) answers to the questions that arise: in the absence of the validation of the detection of Cry1Ab, it is likely that the authors, incorrectly, conclude that any signal was indicative of the presence of the Cry1Ab protein, whereas they most likely correspond to false positives.”

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  6. Correction. Please disregard the 0.04 average discussion regarding Table 3. The .04 “average” is a “mean” from Table 2. Sorry.

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  7. As part of the example of setting up a “straw man” argument. One of the points that the original authors made (approved by the reviewers and the editor) is:

    “that these toxins may not be effectively eliminated in humans”

    yet David Tribe states in setting up his “corn only” analysis the following:

    “since these proteins do not bioaccumulate, it is necessary to consider recent consumption”

    .
    No reference(s) is/are given.
    It is possible that the reason that the original authors used the words “in humans” is because transfer from the gut may be species dependent. For example “A very low frequency of transmittance to visceral tissue was confirmed in pigs, but not in sheep.”
    In addition to pertaining to the bioaccumulate question, this last quote opens up the possibility that the woman were exposed to Bt when consuming contaminated pork.

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  8. Regarding the statement:

    “It has not undergone a proper review process according to the standards of a scientific journal, which would have required the validation of the results and their discussion in relation to available literature.”

    This is what the Journal states:

    “Out of 44 journals in the Agriculture, Multidisciplinary category, Journal of Agricultural and Food Chemistry is the #1 journal in total citations (56,340), #2 in ISI® Impact Factor (2.469), and #1 articles published (1,588). Journal of Agricultural and Food Chemistry is also the #1 ranked journal in total citations in Applied Chemistry and Food Science and Technology. *
    James N. Seiber, Editor of the Journal of Agricultural and Food Chemistry, and formerly Director of the USDA Western Regional Research Center, is current chair of the Department of Food Science and Technology at the University of California, Davis. He continues as the Editor of JAFC, and the JAFC editorial office remains in the Environmental Toxicology Department at the University of California, Davis, where Dr. Seiber is an emeritus Faculty member.”

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  9. Henry, the Agdia test is qualitative, it is a presence/absence test. The method as described in the manual is not a quantitative method. There is no discussion of using a calibration curve and fitting absorbance readings and then interpolating the results. The authors did not follow the Agdia protocol for the test they used and they used it for something it was not designed to do.
    The way the assay works is that there is an antibody that binds the Bt protein to the container. Then another antibody linked to an enzyme is added which binds to the Bt protein now bonded to the container. Then another reagent is added that the linked to enzyme causes to produce a color change. The container needs to be rinsed carefully, and the time for the enzyme to generate the color change needs to be correct. The time the directions call for is to generate a presence/absence test, not to generate a color signal proportional to the quantity of peroxidase enzyme present.
    The assay is designed for testing plant materials, seeds and leaves, not animal materials like blood or plasma.
    If there are proteins in blood that bind non-specifically to the Cry1Ab antibodies, or to the container, or proteins in blood that act as peroxidases (like hemoglobin, SOD, myeloperoxidase for example), there could easily be false positives. That essentially every sample was positive indicates to me they were very likely false positives.

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  10. I agree with the above comments – especially those from deadalus2u. Almost all their signals were extremely weak, and they give no indication that they did any validation of the assay as they used it. (Interestingly, they report limits of detection for all four GC-MS assays, but none for the ELISA).
    Some of their numbers from Table 2 make me even more skeptical. They report that 24 of 30 fetal cord serum samples were positive for Cry1Ab. In their methods, they say they used a standard curve from 0.1 – 10 ng/mL. Ordinarily, you wouldn’t attempt to quantify any samples that gave a response lower than the lowest standard. You certainly shouldn’t do that if you haven’t verified the LOQ of your assay.
    But even if all 24 supposed positives were right at the lowest standard of 0.1, then the group average would have been 0.08 ng/mL (24×0.8/30). Instead, they report a group average of only 0.04 ng/mL. That means that many of those 24 “positives” must have had numeric values well below 0.1, and even below 0.05.
    That sort of thing makes it even harder to have much confidence in the validity of their results.

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    1. Very good point. That dissection of the math had not occurred to me yet, as my own analysis has chiefly focused on whether they were above the limit of detection. Limit of detection or not, you cannot use a data point that is outside the range of standards used in your standard curve to quantify anything, let alone outside the linear portion of your standard curve.

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      1. Karl Haro von Mogel stated:

        “Limit of detection or not, you cannot use a data point that is outside the range of standards used in your standard curve to quantify anything, let alone outside the linear portion of your standard curve.”

        H.Kuska comment. It is my understanding that the reason that a calibration curve is used is because detectors are not linear. Also, see my comment about the use of the blank as part of the calibration curve.

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  11. daedalus2u, of course, it is being used as you describe but it can be used as part of a quantitation determination as the authors used it (David Tribe in the lead article gave a reference where this particular kit was used as part of an attempted quantitative determination of Cry1Ab protein.)

    I looked at the manual to see if it gave a minimum sensitivy value. I did not expect any as the color intensity can be detected by many spectrospic techniques which vary in sensitivity (in my day a Fourier transform optical spectrometer was probably state of the art sensitivity wise).

    Your statement:

    “That essentially every sample was positive indicates to me they were very likely false positives.”

    H. Kuska comment: I am confused about what you are basing the above statement about “every sample” on. This is what I read:

    “On the other hand, Cry1Ab toxin was detected in 93% and 80% of maternal and fetal blood samples, respectively and in 69% of tested blood samples from nonpregnant women.”

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  12. The following was stated:

    “Ordinarily, you wouldn’t attempt to quantify any samples that gave a response lower than the lowest standard. You certainly shouldn’t do that if you haven’t verified the LOQ of your assay.”

    H.Kuska comment. I do not know if they used the blank for a .00 extrapolation point. I think that one would have to look at the actual calibration curve to see if the lower concentraions were linear and intersected the blank at zero concentrations (or produced a curve with a very high r(squared) (confidence) value). I would think that they had to determine the LOQ (limit of quantitation – concentration at which quantitative results can be reported with a high degree of confidence) as they did conclude that some readings had to be reported as as “not detectable”. I agree it would of been nice if they had presented more raw data and more detail about the data work up but as I mentioned in another thread:

    “H. Kuska comment: I do not know what is happening today regarding complete presentation of supporting statistical data. In my day authors could sometimes provide this type of additional information to the editor for examination by one or more of the reviewers either on their own or by request. Sometimes there would be a note that additional data were available by request or in a repository.”

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    1. Anastasia Bodnar, I did not find in this thread any comments from you concerning which of the findings you feel merits frustration. Perhaps if you present them, I and/or someone else may either explain why they said what they did or benefit from your points.

      This is their Conclusion section.

      5. Conclusions. To our knowledge, this is the first study to highlight the presence of pesticides-associated genetically modified foods in maternal, fetal and non pregnant women’s blood. 3-MPPA and Cry1Ab toxin are clearly detectable and appear to cross the placenta to the fetus. Given the potential toxicity of the seen vironmental pollutants and the fragility of the fetus, more studies are needed, particularly those using the placental transfer approach [41]. Thus, our present results will provide base line data for future studies exploring exploring an a new area of research relating to nutrition, toxicology and reproduction in women. Today, obstetric-gynecological disorders that are associated with environmental chemicals are not known. This may involve perinatal complications( i.e. abortion, pre-maturity, intrauterine growth restriction and preeclampsia)and reproductive disorders(i.e. infertility, endometriosis and gynecological cancer).Thus, knowing the actual PAGMF concentrations in humans constitutes a cornerstone in the advancement of research in this area.

      The Editor/reviewers allowed

      “3-MPPA and Cry1Ab toxin are clearly detectable”.

      They are the independent experts and had the ability to correspond with the authors on unclear points and material not appearing in the manuscript. The established scientific way to challenge an article is to send in a follow-up article or communication/letter to the same journal. This allows the editor and original authors a chance to either explain whatever points you feel are deficient or to agree with them.

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  13. Another odd part which seems to get no mention – it appears that pregnancy eliminates glyphosate from the blood. This then warrants no further mention – when you look into it only 2 of the non-pregnant women had detectable glyphosate despite the mean being 73.6 and the standard deviation being 28.2 – this would suggest monsterously high levels of glyphosate in 2 of the subjects (greater than 1ug/ml – which is what one would expect if exposed to 400mg/kg glyphosate orally within the last 24 hours (or last 10 minutes..) – which amounts to 24g of glyphosate for an average woman) – the numbers are also funky – I can’t see how one would get an SD of only 28.2 in a group of 39 subjects with a mean of 73.6 where only two subjects had non-zero values (of ~1500) – the SD should be in the region of 200+
    The other notable mention in the paper is that the levels they detect show absolutely no correspondance with levels which induce issues in rats – it strikes as somewhat odd that they therefore do not conclude that there should be no worries, what with the detected levels being vastly below what might be expected to cause harm – rather the conclusion is that their own levels should be used as reference points – which may well be the case, but if so it should be made explicit that in all the literature regarding adverse effects of the chemicals studied their reference levels would have turned out as having no effects.
    On limits of detection and calibration curves – it is simple standard practice not to report results lower than your lowest concentration on a calibration curve – regardless of whether you have a blank of 0 and an apparently linear graph, if you end up with lower concentrations one would think you’d simply redo your calibration curve to cover the actual range you find.

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    1. Concerning Ewan R’s May 2, 2011 at 8:37 am comments about the glyphosate part of the paper. It was my understanding that David Tribe was discussing only the Cry1Ab part of the paper at present.

      “Only claims of Aris and Leblanc on Cry1Ab are discussed here for the time being.”

      Ewan R’s May 2, 2011 at 8:37 am comment about exposure in a short time seems to also be assuming no bioaccumulation as did David Tribe in the original article. I requested documentation for that assumption but have not received any. I did provide documentation for Cry1Ab being detected in pig muscle.

      Concerning Ewan R’s May 2, 2011 at 8:37 following comment:

      “The other notable mention in the paper is that the levels they detect show absolutely no correspondance with levels which induce issues in rats.”

      H.Kuska comment. Unfortunately the mode of action, results, etc. cannot always be predicted from rat or mice studies. In fact sometimes the rat and mice studies are not supportive of each other. (Another example of Nature is complex).

      The following Ewan R’s May 2, 2011 at 8:37 comment:

      “On limits of detection and calibration curves – it is simple standard practice not to report results lower than your lowest concentration on a calibration curve – regardless of whether you have a blank of 0 and an apparently linear graph, if you end up with lower concentrations one would think you’d simply redo your calibration curve to cover the actual range you find.”

      H.Kuska comment. No documentation was given for the above “standard practice” The reviewers and editors accepted the procedure and I am not aware of of this inability to use the zero concentration point in a calibration cure using the “protections” that I mentioned earlier. Of course one could not do this if there was reason for suspecting a phase transition, dimer formation, etc. in the range below .10 and .00, but it appears that neither the authors, reviewers, nor editor felt that something like that applied.

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      1. comments about the glyphosate part of the paper. It was my understanding that David Tribe was discussing only the Cry1Ab part of the paper at present.

        Consider the discussion expanded. The paper is full of erroneous nonsense, I decided to discuss another aspect.
        Bioaccumulation in my post refers to glyphosate, so references to cry in this are meaningless.
        Unfortunately the mode of action, results, etc. cannot always be predicted from rat or mice studies.
        Editors and reviewers for toxicological studies repeatedly accept rat data, I would suggest perhaps you write a letter to the various toxicological journals expressing your incredulity that they’d continue to use rat models. I await the results with trepidation.

        No documentation was given for the above “standard practice”

        Because it is standard. It has been highlighted above that this was unexpected. Given the other absolute howlers that made it into the paper I think we can expect that the editors and reviewers were not on their A game the day this paper came to light, your persistent return to the “but the editors and reviewers…” is disingenuous, tiring, and a block to any sort of discussion.

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      2. Regarding standards using the blank data. This is from A google search:

        “[PPT] Standardization and Calibration – 1:29pmFile Format: Microsoft Powerpoint – Quick View
        Normally, one uses a calibration blank + at least 3 standards to prepare a curve . You want the standard concentrations to bracket the analyte concentration …
        employees.oneonta.edu/schaumjc/CHEM361/chapter5.ppt – Similar”

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  14. I have a question (actually a couple):
    Is there any reason to assume that the Bt-originated protein is anything other than inert in humans? That it has a particular effect on certain insects does not, to me, indicate that, to humans, it is a “toxin.” (I hate the use of “scare words,” and the language of this study, along with its particular choice of human subjects, seems intended to create emotional impact.)
    Also, if some proteins can enter the circulation from the gut, other than this Cry, it seems a pretty ordinary result, not worthy of words like “contamination” or “[high risk of] exposure” since those terms are very likely to be understood differently in everyday speech than in a technical discussion. I’m willing to bet that many other proteins or peptides of plant, animal and bacterial origin also cross the barriers, and we don’t freak-out about that normal occurrence. Again, what’s so special about Cry that we should especially worry about it? I believe that the use of it (or related proteins) directly as a pesticide has received quite a bit of attention; if it’s been found to be unconcerning in that context, then why should it be concerning in this one? (David touched on this at the beginning of the original post.)
    What about all those unexamined and unknown proteins from the test subjects’ gut bacteria, from the yogurt, meat and vegetables they eat, and worse, what if there was an accidental leaf from a not-recognized-as-edible weed that accidentally got included in someone’s green salad?

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    1. The question was asked:

      “Is there any reason to assume that the Bt-originated protein is anything other than inert in humans? “

      H.Kuska comment. The following very recent paper does not yet appear on Google Scholar. It does suggest that the Bt protein may not be inert.
      I cannot paste the abstract or pertinent sections) here as for some unknown reason I have lost the ability today to copy and paste from a PDF document. Here is the full scientific reviewed publication in PDF form.
      Please use your PDF “Find” command (not your browser’s Find command) with the keyword “human”.
      http://www.jstage.jst.go.jp/article/bbb/75/2/305/_pdf

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      1. Which leads us to a section which tells us that there is a similar fold utilized by proteins for various things with varying substrate specificity, one of which proteins is human – tells us nothing about the inertness or otherwise in humans (whereas the literature is replete with instances where Bt proteins have no adverse effect)
        Setting up straw men Henry?

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  15. Ewan R I am sorry that you do not interpret that my cited paper is indicating what I stated:

    “It does suggest that the Bt protein may not be inert.”

    I should have added “in humans”. Since that was the topic I apparently did not feel it necessary.

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    1. The only piece about humans says nothing about whether or not it would be inert – it highlights an interesting aspect of Cry protein structure in that there are folds which are represented across various binding proteins with different specificities.

      Like

  16. Part of Ewan’s original comment on May 2, 2011 at 8:37 am was:

    “The other notable mention in the paper is that the levels they detect show absolutely no correspondance with levels which induce issues in rats.”

    H.Kuska comment. If this is a non Cry1Ab based point, then I will not discuss it further in this Cry1Ab thread. If it is a Cry1Ab point, please provide a reference for the rat studies that you are referring to.

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    1. It’s about roundup, the post in general is about the study, only in the linked post (so your disparaging David Tribe is a marvellous straw man as you should be disparaging Kuntz) is the discussion limited to cry proteins – I was simply reinforcing that the study itself is clearly flawed by looking at another aspect. You could simply not respond rather than attempting to weasel your way out of a response on a technicality that makes no sense in a situation where a broader topic is clearly open for discussion (ie the fact that the paper is full of holes)

      Like

      1. The following was stated:

        “You could simply not respond rather than attempting to weasel your way out of a response on a technicality …..”

        H.Kuska comment. The forum Comment Policies states:

        “Conjecture: We aim for fact based discussion. Conjecture, nonsense, and conspiracy theories may be modified or deleted.”

        I.E. I did not state that I could not respond. Please only discuss what I actually state.

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      2. Writing fail I guess. When I stated “you could not respond” I meant rather that you could take a course of simply not responding, rather than implying that you physically couldn’t respond to the point.

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      3. Actually the word failure was mine. Your actual statement included the word “simply” which should have made the meaning clear to me. The reason I brought up the “Conjecture, nonsense, and conspiracy theories rule” is the rest of your statement

        “rather than attempting to weasel your way out of a response on a technicality”

        I am honoring what I feel is the author’s restriction/wish. It had nothing to do with an “attempting to weasel”

        “–verb (used without object)
        6. to evade an obligation, duty, or the like; renege (often followed by out ): That’s one invitation I’d like to weasel out of.
        7. to use weasel words; be ambiguous; mislead: Upon cross-examination the witness began to weasel.
        8. Slang . to inform.”

        My earlier statements were:

        “Concerning Ewan R’s May 2, 2011 at 8:37 am comments about the glyphosate part of the paper. It was my understanding that David Tribe was discussing only the Cry1Ab part of the paper at present.”

        I then quoted the following notice at the beginning of the thread (by whoever the actual author is):

        “Only claims of Aris and Leblanc on Cry1Ab are discussed here for the time being.”

        AND later
        I stated:

        “If this is a non Cry1Ab based point, then I will not discuss it further in this Cry1Ab thread.”

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      4. This part of the discussion is getting silly. I did not read Ewan’s comment as being a statement that you were unable to respond, instead it was a suggestion that you had the option of not responding. Second, the reference to comment policy is outright silly here.
        The statement about “Only claims of Aris and Leblanc on Cry1Ab are discussed here for the time being.” is from the original article by Kuntz and is not an instruction to only talk about Cry1Ab in the thread. Also, Marcel Kuntz name is clearly posted at the top of the pasted article, so there should be no confusion as to who wrote what.

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      5. Karl Haro von Mogel stated:

        “the reference to comment policy is outright silly here.”

        H.Kuska reply. Well, you are an administrator and if comments like

        “rather than attempting to weasel your way out of a response on a technicality”

        and your above comment are considered appropriate in this scientific discussion based forum, then I am leaving this forum.

        “silly
        –adjective
        1. weak-minded or lacking good sense; stupid or foolish: a silly writer.
        2. absurd; ridiculous; irrational: a silly idea.
        3. stunned; dazed: He knocked me silly.”

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  17. I had stated

    :”Unfortunately the mode of action, results, etc. cannot always be predicted from rat or mice studies.”

    Ewan commented:

    “Editors and reviewers for toxicological studies repeatedly accept rat data,…..

    The following very recent review appears to address this question:
    A Critical Review of the Effectiveness of Rodent Pharmaceutical Carcinogenesis Testing in Predicting for Human Risk”
    Unfortunately, only the abstract is available to the public Here is some quotes from the full paper:

    “An early example of the latter is the realization that a positive response in the rodent cancer assay is a poor predictor of human cancer risk for compounds with robust CYP450 enzyme induction.”

    “Equally critical is the assessment of biological plausibility, including consideration of rodent-specific mechanisms and
    consideration of the biologic attributes of the test article (DNA
    reactivity, hormonal modulation, chronic tissue injury, immunosuppression, and cell cycle or growth perturbation).”

    “Of these 78 drugs, 32 (41%) had tested positive in
    the rodent bioassay and 12 had tested negative. Thus, the
    false-negative rate for drugs of enhanced concern was 15%”

    “Out of all the drugs examined, most drugs that tested positive in rodents were listed without recognition of enhanced human risk. As mentioned previously, 161 tested positive in rodents, out of
    which only 32 were indicated to be of enhanced human concern,
    for a hypothetical false-positive rate of 80%.”

    “Several molecules were tested in multiple rodent
    cancer studies, sometimes using different test systems, including
    benzoyl peroxide, levofloxacin, penicillamine, pimecrolimus,
    and tretinoin. When tested repeatedly, most molecules,
    including dapsone, metoprolol, sirolimus, and pimecrolimus,
    had conflicting test results; this was considered evidence of
    poor test reproducibility.”

    “The carcinoid response in rats to proton pump inhibitor
    treatment is generally recognized as irrelevant for
    human cancer risk”

    “The hypothetical false-positive rate was determined by taking the number of APIs that had positive rodent test results and were not of enhanced human carcinogenicity concern (129) and dividing that number by the number of APIs that had positive rodent test results (161), for a hypothetical false-positive rate of 129/161 ¼ 80% (Fig. 1).”

    “Positive predictivity was determined by taking the number of APIs that had positive rodent test results and were of enhanced human carcinogenicity concern (32) divided by the number of APIs that had positive rodent test results (161), for a positive predictivity value of 32/161 ¼ 20%.”

    “The false-negative rate of the rodent carcinogenicity
    tests in this review of labels was 15%. This substantial
    incidence of false-negative responses is not generally
    recognized.”

    I could give many more but this is probably already too long. Of course one could say that this only applies to cancer studies, but in my general reading this has happened in many areas of toxicological testing. If someone wishes to cite documentation(s) that my statement is incorrect, please do and I will examine it/them.

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    1. It would be a grave error to believe that rats are ‘little humans’ when it comes to performing experiments.
      Live humans would be better, but testing things on humans is, in some settings, considered unethical.
      For instance, there was the test of GM lactoferrin rice to combat diarrhea-related dehydration which used children (in Peru?) who actually had acute diarrhea. If I recall aright, a doctor or two were exiled from the country in lieu of criminal proceedings.
      There are similar problems with the Golden Rice situation: it’s far enough along that it would be possible to feed it to children going blind, etc., from vitamin A deficiency to see if it’s efficacious. That, too, is considered unethical.
      When you keep bumping your head against these issues, rats looks like pretty much your main option.

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  18. The mode of action of Cry Bt proteins is well established for insect pests. If they worked similarly in the human gut, you’d get symptoms similar/identical to stomach ulcers. This is beating a dead horse.

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    1. Eric’s statement includes “If they worked similarly in the human gut,”
      H.Kuska comment. But is there sufficient evidence to be confident that the Cry Bt proteins will act similarly in both insects and humans to satisfy the requirements of a government safety assessment? I would not expect that a statement containing the word “if” would not be sufficient.
      I still cannot cut and paste from the article, please see what it states on page 311 about small animals.

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      1. please see what it states on page 311 about small animals

        Small soil dwelling animals. Like nematodes. One would think that as this is a Cry5 piece of information you’d keep it out of a discussion on Cry1Ab, consistency y’know?
        The literature is replete with information on the mode of action of Cry1Ab – it is labile in the acid environment of the mammalian stomach, it requires cleavage by insect proteases under alkaline conditions found in the insect midgut, and binds to specific insect midgut proteins causing pore formation and perforation (which is either what directly kills the insect, or which leads to systemic infections as Eric has alluded to – this would indeed appear to be the reason that Bt does what it does – rather interesting method of spreading ones progeny)

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      2. I worked with Bt constructs in a previous life. My understanding is that these proteins are active at high pH (as in the gut of Leps and Coleops). They are inactive in humans due to the acidic nature of the gut.

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  19. Sorry, please remove one of the “not” in: “I would not expect that a statement containing the word “if” would not be sufficient.”

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  20. To put some published paper details on the record, I am pasting here some direct quotes from the papers referred to by Marcel Kuntz’ original post:
    Chowdhury EH et al. (2003). Detection of corn intrinsic and recombinant DNA fragments and Cry1Ab protein in the gastrointestinal contents of pigs fed genetically modified corn Bt11. J Animal Sci. 81:2546-2551, 2003. “However, because the ELISA or immunochromatography kits and immunoblot did not work for blood samples, the present trial could not determine whether Cry1Ab was absorbed into the blood.”
    Lutz, Bodo, Steffi Wiedemann, Ralf Einspanier, Johann Mayer, and Christiane Albrecht (2005)Degradation of Cry1Ab Protein from Genetically Modified Maize in the Bovine Gastrointestinal Tract. J. Agric. Food Chem., 2005, 53 (5), pp 1453–1456. “Two independent sets of gastrointestinal samples revealed the apparent discrepancy between the results obtained by ELISA and immunoblotting, suggesting that the antibody used in the ELISA reacts with fragmented yet immunoactive epitopes of the Cry1Ab protein. It was concluded that Cry1Ab protein is degraded during digestion in cattle. To avoid misinterpretation, samples tested positive for Cry1Ab protein by ELISA should be reassessed by another technique.”
    Paul Vijay Kerstin Steink and Heinrich H.D. Meyer (2008) Development and validation of a sensitive enzyme immunoassay for surveillance of Cry1Ab toxin in bovine blood plasma of cows fed Bt-maize (MON810). Analytica Chimica Acta 607:106–113, 2008.doi:10.1016/j.aca.2007.11.022
    “A number of ELISA [21–25] and commercial kits (QuantiPlate kit for Cry1Ab/Cry1Ac, Envirologix and DAS ELISA kit for Bt-Cry1Ab/1Ac protein, Agdia) are already existing for the detection and quantification of Cry1Ab protein expressed in GM crops and their by-products. These commercial kits have been also used in various livestock feeding studies on GMO for the surveillance of transgenic protein in the animal tissues and gastrointestinal contents [17–20,26]. Though the commercially available Cry1Ab protein ELISA kits(QuantiPlate kit for Cry1Ab/Cry1Ac, Envirologix and Agdia)were reported to detect Cry1Ab protein down to 1ngmL−1 of spiked blood [L. Petit, F. Baraige, Y. Bertheau, P. Brunschwig, A. Diolez, K.Duhem, M.N. Duplan, P. Fach, A. Kobilinsky, S. Lamart, A.Schattner, P. Martin, J. AOAC Int. 88 (2005)654.], however, the study missed the most important assay validation part. Further, in another study [E.H. Chowdhury, H. Kuribara, A. Hino, P. Sultana, O. Mikami, N. Shimada, K.S. Guruge, M. Saito, Y. Nakajima, J. Anim. Sci.81 (2003) 2546.] the same ELISA kit (Envirologix) did not work for the analysis of blood plasma for the surveillance of transgenic protein. Hence, such commercial kits designed for transgenic protein (Cry1Ab or Cry1Ac) quantification in plant materials warrants for a proper assay validation before used for protein analysis in animal systems.”
    “4. Conclusions [Paul et al.]
    A sandwich ELISA based on immuno-affinity purified polyclonal native capture and biotin-labeled detection antibody has been developed for the Cry1Ab toxin determination at low levels (CCbeta, 2.3 ngmL−1) in bovine blood plasma. The developed ELISA satisfied the performance and validation criteria laid down by Commission Decision 2002/657/EC. The immunoassay performed well with the spiked plasma samples and recoveries ranged from 89 to 106% (mean value of 98%). When applied for the surveillance of transgenic Cry1Ab toxin from Bt-maize in blood plasma of cows fed transgenic ration for a short-term, no sample was positive for the presence of Cry1Ab protein. Further work can be carried out to apply and validate this ELISA for surveillance of Cry1Ab toxin in blood plasma and other matrices like milk, urine and faeces collected from the animals fed for long-term on transgenic ration. Most probably it could answer questions like digestive fate of transgenic protein and possible entry into the blood stream, if successful in breaking the digestive barrier of animals fed for long-term on GM plant and plant by-products.”

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  21. There’s a really bizarre post on Rodale about the Aris paper: Genes from GMO Food Do Wind Up in People, Study Shows
    Nevermind that the paper wasn’t about genes…. Here’s the money quote (emphasis added):

    The study, in press in the journal Reproductive Toxicology, contradicts that biotech companies are either misleading or inaccurate when they repeatedly reassure the government and public health organizations that genes and bacteria inserted into GM crops cannot survive the digestive tract.

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  22. As an employee of Agdia, Inc. I want to say that these two papers are very well done. I could not have done a better job. Our Bt diagnostic tests were developed and intended for use in plants period. Any other use is simply not valid and certainly not endorsed by our company.

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  23. Hey y’all, I just found a critique of this post on GM Watch, written by an anonymous scientist.
    http://gmwatch.org/latest-listing/1-news-items/13450-scientists-rebut-of-critique-of-bt-toxin-in-human-blood-supply
    It completely misses the mark on the issue of whether the kit that was used was appropriate. As indicated by even an employee of the company that made the ELISA kit, it was not designed for use on blood, serum, or anything like that, but instead plants.

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  24. Thank you Karl. It never ceases to amaze me how tenaciously even highly educated people will hold to a scientifically untenable point of view. What really worries me is that the mass media might just pick this up and run with it. I find that many times the mass media does not seem care about the truth either.

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  25. As someone who has been involved in these issues for over 30 years (and was at the meeting of the Codex Labeling Committee when first word of this study came around and this UN agency adopted GE food labeling guidelines after 18 years of contention), the ONLY public policy issue of note is that neither governments nor industry cares to fund studies to replicate this or any other experiments that have indicated dangers. Yet the Codex documents on biotech foods(agreed to unanimously–ie, including both the US and Canada) call for risk assessments and the use of precaution. The failure to follow such a clear and sane public policy is an abuse of science, not somehow a “gotcha” moment.

    Like

    1. Hi Phil, thanks for stopping by. It would indeed be good to replicate a study such as this, particularly to address its shortcomings. There would need to be a control group of people who were not likely exposed to GE maize, and the tests would have to have been used properly, such as using the correct buffer solution for the standard curve for the ELISA. In contrast to your statement, this study did not indicate dangers of any kind with regard to Bt. It argued it, however the “positive” data was indistinguishable from zero. That’s not an indication of danger. That’s the point of this post, and current and future followups. Not sure what you mean by a gotcha moment in this context – more of a “junk science” moment.

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  26. I have to agree with Eric Baumholder in the very first comment on this. I would also like reinforce what daedalus2u said. Agdia’s test is a qualitative test for plants period. It is not to be used for any other purpose. I also doubt very strongly that this test is sensitive down below 1ng/mL especially when background noise is considered although it is true that I have found that Agdia’s small protein tests tend to be more sensitive than its tests for the viruses. I have in fact run quite a few quantitative ELISA’s over the years here at Agdia. I should have some knowledge of this. I have been developing tests here at Agdia since ’91 and I can in fact claim that I either developed or redeveloped the majority of Agdia’s plant pathogen tests. I developed the bottles A&B ELISA protocol that Agdia uses. I have developed the GEB2, GEB3 and RUB6 buffers. And we have an entirely new ELISA protocol in the wings that I cannot tell you about. So I think I do know a little something about this matter.

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  27. Despite all of the scientists arguing technical points here, the study is of great importance from a policy point-of-view. For years the industry has been arguing that there are not ill health effects because digestion destroys the engineered constructs. (of course, they never offerred published studies to support their self-serving claims). This study is a warning signal for any sane public health system–maybe the engineered material is NOT destroyed. Experiments should be done to see further what is going on–and the onus is on the industry, under both the Cartagena Protocol and the Codex guidelines. So “bring it on”.

    Like

    1. This study is a warning signal for any sane public health system–maybe the engineered material is NOT destroyed

      Well, no, it isn’t, at best this is a warning signal to properly check the materials and methods section before publishing an article – thorough peer review in this case would have seen the data thrown out – a phone call to Agdia asking the question “Yo, can this kit be used to reliably look for Cry proteins in human blood” would have yielded the answer “hells to the no” at which point you’d write a letter to the authors to the tune of “my dearest colleagues, please redo all your experiments with kits that’ll work, then we’ll take a look at your results”
      At which point, if results had come back suggestive of something, the onus would be on the industry to investigate further.
      You don’t investigate further based on bad science, you say “oh look, this is bad science” and leave it at that.

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      1. Good points, Ewan. Badly-performed science should never be used to base policy off of. I completely disagree with Phil on this count, and further add that there have been many studies that demonstrate the rate at which Bt is digested and its safety, in multiple animal models. David Tribe has been adding many links to these studies, which contradicts Phil’s claim that studies were never produced. I understand that this study has been very important from an advocacy point of view, but that doesn’t make it important for sound policy.
        I’m hoping, Phil, that you would be willing to answer a direct question about the Aris and Leblanc study we are discussing here:
        Have you read the study, analyzed its methods, and do you conclude that the study was conducted properly to be able to reliably conclude that Bt proteins were indeed present and detected in the blood samples examined?
        Let’s not beat around the bush and talk about policy implications. I’m asking for your professional scientific opinion of the methods employed in this study. Did they have the evidence necessary to reject the null hypothesis? I look forward to your answer.

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    2. These are the gut digestion analyses that Phil Bereano says have never been proferred, and addressing issues of Bt protein digestion in the gut:
      (Oh and by the way, testing of Bt proteins in GMOs for rapid digestion in simulated gastric juices is a regulatory requirement, Note in the insect the midgut is ALKALINE, not acid.)
      Thes may be “technical points” =factual specifics, but they are essential and relevant technical details.
      *Development and validation of a sensitive enzyme immunoassay for surveillance of Cry1Ab toxin in bovine blood plasma of cows fed Bt-maize (MON810)
      Vijay Paula,, Kerstin Steinke,, Heinrich H.D. Meyer analytica chimica acta 6 0 7 ( 2 0 0 8 ) 106–113
      QUOTE In situ studies
      in bovine rumen showed the time-dependent degradation of
      transgenic recombinant protein (Cry1Ab protein) from Bt176
      corn [17]. Nevertheless, trace amounts of the Cry1Ab toxin
      were detected in the gastrointestinal contents of the livestock’s
      fed on GM corns [18–20]. However
      [17] S. Wiedemann, B. Lutz, H. Kurtz, F.J. Schwarz, C. Albrecht, J.
      Anim. Sci. 84 (2006) 135.
      [18] E.H. Chowdhury, N. Shimada, H. Murata, O. Mikami, P.
      Sultana, S. Miyazaki, M. Yoshioka, N. Yamanaka, N. Hirai, Y.
      Nakajima, Vet. Hum. Toxicol. 45 (2003) 72.
      [19] E.H. Chowdhury, H. Kuribara, A. Hino, P. Sultana, O. Mikami,
      N. Shimada, K.S. Guruge, M. Saito, Y. Nakajima, J. Anim. Sci.
      81 (2003) 2546.
      [20] B. Lutz, S. Wiedemann, R. Einspanier, J. Mayer, C. Albrecht, J.
      Agric. Food Chem. 53 (2005) 1453.
      Also a recent one:
      Effects of Feeding Bt MON810 Maize to Pigs for 110 Days on Peripheral Immune Response and Digestive Fate of the cry1Ab Gene and Truncated Bt Toxin.
      Walsh MC, Buzoianu SG, Rea MC, O’Donovan O, Gelencsér E, Ujhelyi G, Ross RP, Gardiner GE, Lawlor PG.
      PLoS One. 2012;7(5):e36141. Epub 2012 May 4.
      Teagasc, Pig Development Department, Animal and Grassland Research and Innovation
      Centre, Moorepark, Fermoy, County Cork, Ireland.
      … Pigs were sacrificed on day 110 and digesta and organ samples were
      taken for detection of the cry1Ab gene and the truncated Bt toxin. On day 100,
      lymphocyte counts were higher (P<0.05) in pigs fed Bt/isogenic than pigs fed Bt
      or isogenic. Erythrocyte counts on day 100 were lower in pigs fed Bt or
      isogenic/Bt than pigs fed Bt/isogenic (P<0.05). Neither the truncated Bt toxin
      nor the cry1Ab gene were detected in the organs or blood of pigs fed Bt maize.
      The cry1Ab gene was detected in stomach digesta and at low frequency in the ileum
      but not in the distal gastrointestinal tract (GIT), while the Bt toxin fragments
      were detected at all sites in the GIT. ..

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      1. Has anyone done a study re: Bacillus thuregensis or its resultant toxins/genes in the gut, blood, etc? Or is that unreasonable for some reason?

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      2. Well humnan sure, but I was thinking of any animal study looking at good ol’ organic type bt material, not GE bt material. How can we evaluate what GE is doing without knowing what the background from ‘traditional’ bt is?

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      3. Safety and Advantages of Bacillus thuringiensis-Protected Plants
        to Control Insect Pests
        Fred S. Betz, Bruce G. Hammond, and Roy L. Fuchs
        Regulatory Toxicology and Pharmacology 32, 156–173 (2000)
        Contains large tables listing dozens of studies on safety of Bt proteins.

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      4. Thanks. That somewhat answers the question. Blood cultures for the bacteria were negative after oral ingestion (human), although we don’t know about the presence of Bt proteins themselves. One thing I found interesting: 50% of the subjects showed viable cultures from stool samples …. 30 days after ingestion. Seems like that might upset some people to know these things were hanging around in their gut for a full month, potentially producing all those nasty Bt toxins. I wish they’d label Bt treated stuff so we could make a choice about these things.
        An open copy of the article cited above: Safety and Advantages of Bacillus thuringiensis …

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      5. I am not sure I understand your comment, “potentially producing those Bt toxins.” The only way more toxins would be produced would be if there are live Bacillus theringiensis in the food product. This is never the case. One other point that people seem to miss is that these bacteria are natural to the environment. They are everywhere. In fact most microbes produce toxins of one sort or another. Thank God for penicillin. I think we should all stay inside, continuously disinfect, wash our hands frequently and be fearful all the time. (tongue in cheeck) You see I don’t think all this fear that people keep trying to incite makes logical sense when you take time to understand the science.

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      6. I think Pdiff is making the point that as Bt (the bacterium) has been demonstrated to survive the human digestive tract people who are scared of GMOs because of handwaving something or other handwaving should also be scared of crops which utilize the bacterium rather than a transgenic approach – you can’t prove 100% that all the bacteria die and don’t end up getting consumed, therefore these things should be labeled for consumer choice.
        (illustrating the vapid arguements around labeling GMOs rather than seriously thinking these things should be labeled also)

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  28. I guess Ewan and others don’t understand the major difference betw using Bt SPRAY on organic crops (only on the leaves and above-ground portions of crop, washes off in the rain in a few days, etc) and Bt GE– the construct is in every cell of the plant (incl the roots were a huge number of organisms are exposed to it–totally novel situation) and is permanent. Thus, facile comparisons are merely industry propaganda blurbs, designed to lull the public into somnolence. Comments here should have more precision

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    1. I guess you don’t understand sarcasm and the explanation thereof. Thus facile poking at what people do or do not understand makes you look just a tad silly.

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    2. <

      blockquote cite=””> … Bt SPRAY on organic crops (only on the leaves and above-ground portions of crop, washes off in the rain in a few days, etc) and Bt GE– the construct is in every cell of the plant (incl the roots were a huge number of organisms are exposed to it–totally novel situation) and is permanent.

      <

      blockquote cite=””>
      On the contrary, I do understand that quite well. I also understand that it does not necessarily “wash off in the rain”. Who says it will always rain? And where do you think it goes when it does? (The answer is into the soil where all those roots are 🙂 ). As I understand it, Bt is naturally a soil organism and transporting it to leaves and above ground parts is quite unnatural and, I assume, a great deal of organisms in that niche are therefore exposed to it and possibly the toxins when they normally would not be. You know, in a “totally novel situation”. Just exactly how do you imagine it is “permanent”? Nothing in this world is so. Perhaps that’s what you meant, but I was expecting you to be precise in your comment.
      Dr. William Pdiff

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      1. Har, hadn’t considered it that way – but yes… the absolute novelty of Bt toxins to soil organisms is quite clearly a blatant fallacy (although for clarity some of the artificially jiggered with Bt toxins would be somewhat novel, although not, I would suspect, to the degree that they’d make the damndest bit of difference).
        It would seem, infact, that you are utterly off the mark about what happens with Bt spores which reach the soil
        http://aem.asm.org/content/50/6/1496.short
        http://www.ncbi.nlm.nih.gov/pubmed/17973155
        Really Phil, shouldn’t you be more precise? Or at least less y’know, false?
        Particularly when you aren’t just kidding about?

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    3. I would like to add that Phil is drawing a distinction between Bt crops and Bt-bacterium-based forms of pest control that is not as clear as he makes it out to be. For instance, There is no guarantee that 100% of the bacteria will be washed off of the plant. There are all kinds of papers that demonstrate the presence of bacteria on – and in – food crops although they are only exposed to them on the surface.
      Moreover, it is becoming increasingly common in organic agriculture to inject LIVE Bt bacteria INTO the plants to control the same pests. In sweet corn, this involves injecting Bt bacteria suspended in oil into the developing ear. No doubt, eaters of fresh sweet corn will be exposed to Bt. Here is a PDF file at Johnny’s Selected Seeds that explains the practice.
      Indeed, organic researchers are trying to put live Bt bacteria in more crops than just sweet corn. I attended an organic ag lunch discussion where a researcher was talking about injecting Bt bacteria into the stems of squash plants, to get them living inside the vascular tissue of the plants to protect them from insect pests. They complained that it is difficult to inject all the plants individually. So I suggested, “why not fill a shotgun shell with tiny beads coated with live bacteria and shoot all the plants at once?” They laughed, but loved the idea. I missed the opportunity for the perfect followup: “Wait, why not coat the beads with just the Bt gene so the plants produce it themselves?” (Because that would be genetic engineering!) It is simply amazing that two processes could be so alike, yet so mutually exclusive.
      If Phil Bereano feels that Bt proteins inside the tissues of plants are a concern, then he should be concerned about these organic practices.

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  29. I believe most the people commenting here do understand perfectly that the construct is in the DNA of every cell of the plant. Not only that on many occasions there is an additional marker gene such as the NPT II gene. I believe a good percentage also understand that as well. I fail to see the reason to be fearful of something that is completely natural and found in nature everywhere. For example, the fear of vegetables that contain the coat proteins of plant viruses. The coat proteins give the plant immunity to the virus. People don’t realize that you cannot eat a salad without there being some plant viruses in there with their coat proteins. A fear of this is unreasonable.

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  30. I find it interesting that you never mention the benefits of Bt crops. I find that lying by omission is a common practice in the press now days. http://www.greenspirit.com/logbook.cfm?msid=62
    “By using Bt cotton in 2000 in Shandong province alone, the reduction of pesticide use was 1,500 tons. It not only reduced the environmental pollution, but also reduced the rate of harmful accidents to humans and animals caused by the overuse of pesticides.” Patrick Moore – co-founder of Greenpeace The natural insect population began to rise followed by the bird population. A good thing for the overall natural environment.

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  31. You guys are so funny with these old stale arguments.
    **
    URL: http://www.thaindian.com/newsportal/world-news/gm-crops-no-longer-safe-from-pests_100625921.html
    DATE: 21.06.2012
    GM CROPS NO LONGER SAFE FROM PESTS
    SUMMARY: “Genetically modified crops may no longer be safe from the scrouge of pests, underscoring the importance of closely
    monitoring and countering pest resistance to biotech crops, according to a new discovery. […] researchers have exposed cotton
    bollworm populations to Bt toxins in controlled lab experiments and studied the genetic mechanisms by which the insects adapt.
    ?We found exactly the same mutation in the field that was detected in the lab,? Tabashnik said. ?But we also found lots of other
    mutations, most of them in the same gene and one in a completely different gene.?”
    TITLE: TROUBLE ON THE HORIZON FOR GM CROPS?
    SOURCE: University of Arizona, USA
    AUTHOR: Press Release, by Daniel Stolte
    URL: http://www.uanews.org/node/47788
    DATE: 19.06.2012
    SUMMARY: “Pests are adapting to genetically modified crops in unexpected ways, researchers have discovered. […] Resistance of
    cotton bollworm to insect-killing cotton plants involves more diverse genetic changes than expected, an international research
    team reports in the journal Proceedings of the National Academy of Sciences. […] In the first study to compare how pests
    evolve resistance to Bt crops in the laboratory vs. the field, researchers discovered that while some the of the lab-selected
    mutations do occur in the wild populations, some mutations that differ markedly from those seen in the lab are important in the
    field.”

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    1. Phil, please read our comment policy about posting entire articles in the comments. It takes up excessive space, and may also run into copyright issues. I have removed the text of the comment and kept the links so those who have not already read these stories can still read them.

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    2. You guys are so funny with these old stale arguments.

      Rather have stale arguments which withstand the litmus test of being actually truthful, than stale arguments which are lies.
      You know, like the ones you made about Bt above?
      Is there a particular reason that the anti-GM crowd never acknowledges being caught in a lie? (I had a similar run in with Wow over on denialism, there was no acknowledgement at any point that he was flat out making stuff up despite it being abundantly obvious that he was) I mean, you could just acknowledge you were wrong, not doing so just makes it look more like you’re perfectly aware that you are lying through your teeth. Which is hardly good form.
      Also…
      way to shift the goalposts
      We were discussing your egregious dishonesty – perhaps we can finish that particular discussion before moving on to the interesting, but currently minor (and hardly unexpected unless you’re some kind of creationist) issue of resistance (an issue which isn’t really even pertinent to the current discussion or any sub discussions which have developed – which is indicative that the current debate is won due to the fact Phil has seen fit to move the goalposts so very, very far away (and reshape them no doubt))

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  32. The Precautionary Principle appears twice in the Cartagena Protocol and is embedded in the Codex guidelines for doing risk assessments of GE foods.
    I am no longer going to participate in this chat, given the personal invective. I have better things to do than waste my time on a bunch of school-boy name-callers.
    Over and out.

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    1. Ewan’s last comment was a little over the top and unnecessary. It is enough to know that several things said today were demonstrably false. It is quite obvious however, Phil, that you were engaging in trolling behavior with your comments as well. You insulted Ewan’s intelligence, and then made an obviously false claim. You then proceeded to try to make fun of those you disagreed with and called opinions you didn’t like propaganda, without answering the criticisms made against your arguments. It is difficult to moderate a discussion where neither party wants to be more civil.
      However, I really hope you will take the time to answer my question about whether or not you believe the study was conducted properly. You care about this topic deeply, indeed, we are having a discussion on a year-old post. You clearly consider this study to be worthy enough to defend, do you in fact defend its methods and conclusions as sound?
      Hope to hear from you.

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    2. As Karl alludes, you started it! (there’s some schoolboy tactics for you)

      I guess Ewan and others don’t understand the major difference betw using Bt SPRAY on organic crops

      and

      facile comparisons

      but flouncing when you’ve been called out as a liar is pretty much par for the course – there is no personal invective here (yet… don’t worry, it’s coming – other than “school boy name callers” and I’m pretty sure that originated at your own fingers.)
      The issue here of course is actually that what I write comes across with bad tone (who cares?) but substantial content, whereas all you have is bad tone (again, who cares?) and the sort of content normally only found in the ileum of a male specimen of Bos taurus. So why not grow up a bit (again, you’re the one who brought up school-boy name calling, so back the hell down before getting all puffed up that someone dare fire back with the same ok?) and address content rather than tone. You can even throw in some name calling if you like, it may even make you feel better – and ellicit some cheers from the peanut gallery.

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    3. Hey! Guys! There was a ball around here somewhere. Did someone take it home? I wanted to play!
      .
      No matter, I brought my own:
      From the Grand Cartagena Protocol, Annex 3 (Risk Assessment), Part 4

      4. Lack of scientific knowledge or scientific consensus should not necessarily be interpreted as indicating a particular level of risk, an absence of risk, or an acceptable risk.

      In other words, if you can’t use “science” to specify all possible outcomes that we may dream up, we can throw your case out. We can always claim there aren’t enough studies or find a handful of scientists who disagree with you to claim a lack of consensus. This is exactly why the Precautionary Principle, as a pure concept, is completely useless. We not only have to prove a negative, we have to prove all possible negatives.

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