Extraordinary claims… require extraordinary evidence.

247 thoughts on “Extraordinary claims… require extraordinary evidence.”

1. Hi, I posted answers on the Forum to some questions posed on the Forum about the connection between Chlorothalonil and observed problems in vertebrate and insect populations. No one has said anything about the references I found for studies and reviews that say very low levels of pesticides are dangerous to fetuses and children. Or as the Canadian doctors’ review put it “there is no safe level of pesticides for children.” I would think that would likely be true concerning other developing fetuses and young.

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   1. “there is no safe level of pesticides for children”
      Completely idiotic statement and typical of the current lack of understanding of agricultural practices and risk assessment among the masses. The doctors who wrote it should be ashamed. All chemicals whether pesticides or not have a relative toxicity. And exposure also has to be considered. How about sulphur? Registered as a fungicide in most countries around the world. Are you telling me 0.01 ug/kg residue of sulphur on an apple for example isn’t safe. There’s more natural sulphur than that in the same fruit.
      This is an extreme example I admit but there is a sliding scale from this all the way up to a mouthful of DDT every day of your life. Up to a certain point on that scale the harm the pesticide will do to you is less that the harm everything else in day to day life is doing and you’ll die of old age before any effect could be seen.
      Hazard based risk assessments for any chemical are completely pointless. Coffee contains hundreds of carcinogens at concentrations way above pesticide residues in food. And that’s just the chemicals we know about. No-one ever suggests banning coffee on a hazard based assessment or that we don’t know enough about the synergistic toxicities of all these known/unknown coffee chemicals on humans. Instead a sensible risk based approach is used and we all agree that we’re safe.
      Jonathan
      PS How many posts since anyone mentioned Prof Huber. Has he come out and admitted it was all a big joke yet?

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2. This link is to a summary of Dr. Huber’s recent talk in Nebraska. http://www.gmwatch.org/latest-listing/1-news-items/13021-a-hubergmoroundup-update
   In the talk he discussed Parkinson’s disease. In case you are not aware of this aspect of glyphosate, I suggest a Google Scholar search using the keywords “parkinson’s disease” (with quotes) and glyphosate
   Particulary an “in press” paper http://dx.doi.org/10.1016/j.neuro.2011.02.002

   (Please cite this article in press as: Negga R ,etal. Exposure to Mn/Zn ethylene-bis-dithiocarbamate and glyphosate pesticides leads to neurodegeneration in Caenorhabditis elegans.
   Neurotoxicology(2011),doi:10.1016/j.neuro.2011.02.002)

   Apparently this nematode is considered a good test system for Parkinsons studies. The abstract is quite technical. I have the full paper, but I cannot distribute an “in-press” paper. I could not find simple sections to cut and paste in order to make the results clearer.
   The following is listed as the funding source:

   “This work was supported by the National Institute of Environmental Health Sciences[R15ES015628 to VF]and by the Appalachian College Association Colonel Lee B.Ledford
   Endowment Fund[to R.N.,D.R.,N.D.,A.J.andV.F.].”

   For Ewan, the description of the journal is given in the link given here.

   5 year inpact factor 3.126

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   1. So unprotected organisms are susceptible to surfactants.
      Not really surprising or particularly meaningful when compared to organisms which have protection from surfactants (skin)
      More meaningfully studies have been conducted to look at actual relationships in humans between application of various pesticides and incidence of parkinsons disease –
      Here for instance
      Where an odds ratio of 1.0 and 1.1 is given for glyphosate use for parkinsons or incipient parkinsons respectively (ie doesn’t increase risk whatsoever) – it is noteworthy that not all herbicides were indicative of zero risk, which suggests to me that being anti-glyphosate/roundup because of PD risk only makes sense if you’re pro-PD.
      Looking at the rest of the literature it does appear that some herbicides (notably paraquat) do seem to have an actual correlation between use and parkinsons as well as a described mechanism by which they could cause the disease and by which they would make it into the effected tissue.

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      1. Ewan has posted a study that looked at farmers and their spouses:

         Cohort members, who were enrolled in 1993–1997, provided detailed information on lifetime pesticide
         use. At follow-up in 1999–2003, 68% of the cohort was interviewed. Cases were defined as participants who
         reported physician-diagnosed PD at enrollment (prevalent cases, n = 83) or follow-up (incident cases, n = 78).

         and then was published in 2006.
         The study showed that 45 farmers or spouses of that period who had been exposed to Glyphosate had physician-diagnosed PD at enrollment (out of the 83 total that had physician-diagnosed PD at enrollment 1993–1997), and that an additional 49 farmers or spouses had Parkinson’s out of the additional 78 cases reported in the 1999-2003 follow-up.
         After the workup, the Odds Ratios (Table 4 )for glyphosate for the 2 groups were 1.0 and 1.1. Thus they could not pinpoint glyphosate as a cause of Parkinson’s.
         Now let us look at maneb/mancozeb (also Table 4) The odds ratios are also 1.0 and 1.1. THIS IS CONFUSING AS THESE ARE KNOWN CAUSES OF PARKINSON’S DISEASE.
         They then looked at those who completed a supplemental Applicator Questionnaire at enrollment. This information gave Odds Ratios of 1.5 and 2.1 for the 2 groups for the combined Maneb/Mancozeb class.

         Applicators who completed the supplemental Applicator
         Questionnaire provided additional information on some pesticides, including four implicated in PD in previous studies: dieldrin, maneb, paraquat, and rotenone (8–10). When information from the Enrollment and Applicator questionnaires was combined, odds ratios for prevalent PD were 1.3 for dieldrin, 1.5 for maneb/mancozeb, 1.8 for paraquat, and 1.7 for rotenone, and odds ratios for incident PD were 0.9 for dieldrin, 2.1 for maneb/mancozeb, and 1.4 for paraquat; only one incident case had used rotenone. These results were based on 4–10 exposed cases for each pesticide.

         Four pesticides have previously been implicated in the etiology of PD: dieldrin, maneb, paraquat, and rotenone (8–10). We found associations of all four with prevalent PD and of maneb/mancozeb and paraquat with incident PD in the subset of applicators who completed the supplemental Applicator Questionnaire at enrollment. However, only an association of paraquat with prevalent PD was seen in the complete cohort.

         Thus, the situation was too complex to identify either glyphosate or maneb/mancozeb in the complete cohort.

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   2. Just like Phantom of the Opera. ANOTHER NOTE!

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3. Thank you Henry K. That article was extremely interesting. Are there any thoughts on whether there could be a connection between what Dr. Huber has found regarding the new pathogen and the widespread symptoms of fetal hypothyroidism in wild and domestic animals? I have long suspected a glyphosate impact because there is so much used here, but could not find a connection to fetal hypothyroidism, since glyphosate disrupts the retinoic acid, and not thyroid hormones, or at least according to studies I have found. The severe symptoms of fetal hypothyroidism, including spontaneous abortion, premature birth, major developmental malformations and a possible prevalence for cancer and other health problems began here in spring of 1995, but the mothers had to be exposed in 1994, after their normal young were born in spring of 1994. Is there any connection that anyone knows to GMO crops or glyphosate and something new happening in summer of 1994? According to Dr. Huber, speaking about the pathogen, “It could also, and apparently already is, he said, compromising the health and well-being of animals and humans.” Something certainly is. Could the pathogen itself somehow disrupt fetal thyroid hormone function? These are the questions I would like to see answered. Thank you again Henry K.

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   1. Title: The teratogenic potential of the herbicide glyphosate-Roundup in Wistar rats.
      Authors: Dallegrave, Eliane; Mantese, Fabiana DiGiorgio; Coelho, Ricardo Soares; Pereira, Janaina Drawans; Dalsenter, Paulo Roberto; Langeloh, Augusto.
      Authors affiliation: Instituto de Ciencias Basicas da Saude, Department of Pharmacology, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, RS, Brazil.
      Published in: Toxicology Letters (2003), 142(1-2), pages 45-52.
      Abstract: “The aim of this study was to assess the teratogenicity of the herbicide glyphosate-Roundup (as commercialized in Brazil) to Wistar rats. Dams were treated orally with water or 500, 750 or 1000 mg/kg glyphosate from day 6 to 15 of pregnancy. Cesarean sections were performed on day 21 of pregnancy, and no. of corpora lutea, implantation sites, living and dead fetuses, and resorptions were recorded. Wt. and gender of the fetuses were detd., and fetuses were examd. for external malformations and skeletal alterations. The organs of the dams were removed and weighed. Results showed a 50% mortality rate for dams treated with 1000 mg/kg glyphosate. Skeletal alterations were obsd. in 15.4, 33.1, 42.0 and 57.3% of fetuses from the control, 500, 750 and 1000 mg/kg glyphosate groups, resp. The authors conclude that glyphosate-Roundup is toxic to the dams and induces developmental retardation of the fetal skeleton.”
      Google Scholar gives 37 citations for the above paper including one 2011 (with a study of humans). Instead of just using the “anytime” choice, after the initial search of the citing papers, I like to use the “since 2011” choice, than “since 2010” choice, them “since 2009” choice, etc.
      I do not have time now to look at the citing papers in detail.

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      1. Once again the surfactant is the culprit, and in quanitites that are utterly unexpected in humans. As the paper states in the conclusions.
         (This isn’t an unusual effect of feeding surfactants to rats – CTAB apparently does the same thing, as do some tweens and NPs (although not all, and I don’t understand surfactant chemistry well enough to know why exactly that would be))

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      2. As an aside apparently I have a comment that I made while not logged in which is hung in moderation – it’s to Henry’s parkinsons related post – I believe there is a single link hanging it up. (I now can’t see it, probably because I logged in)

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      3. This is the Conclusion section that Ewan is referring to:

         “The developmental retardations of the skeleton
         reported in the present study shows that the effect
         of glyphosate-Roundup† was more marked than
         that of technical glyphosate (WHO, 1994). The
         higher maternal toxicity reported here in comparison
         to that of technical glyphosate is probably
         related to the presence of other components in the
         commercial formulation, such as the surfactant
         polyoxyethyleneamine (Adam et al., 1997; Dallegrave
         et al., 2002). Despite the fact that the doses
         used in this study would never expected to
         correspond to human exposure levels under normal
         circumstances, as reported by Williams et al.
         (2000) for glyphosate and polyoxyethyleneamine in adults or children (margins of exposure/5420,
         3370 and 461 577, respectively), this results shows
         that the commercial formulation poses an increased
         potential risk for the rat skeletal system.
         To better understand this fact, additional studies
         should be carried out to determine the mechanisms
         of effects of the commercial formulation on the
         skeletal system of the fetuses, since humans are
         also potentially exposed to this commercial formulation.”

         H.Kuska comment: Thus they do not attribute the complete effect to the polyoxyethyleneamine It enhances the observed effects. This is not unusual as the polyoxyethyleneamine can help the glyphosate penetrate the rat’s defences.

         According to the following Monsanto paper tests with polyoxyethyleneamine alone found: “No developmental toxicity was observed in the studies with the surfactants”.
         Title: Developmental toxicity studies with glyphosate and selected surfactants in rats.
         Authors: FARMER, D.R., T.A KAEMPFE., W.F. HEYDENS, and W.R. KELCE
         Authors affiliation: Monsanto Company, St. Louis, Missouri.
         Published in: Teratology, 62,(6), page 446, (2000).
         Abstract: “Glyphosate is a non-selective herbicide; it inhibits essential aromatic amino acid synthesis by blocking the activity of a plant specific enzyme. Glyphosate-based formulations are used in over 100 countries in virtually every phase of agricultural and residential weed control and are increasingly used in applications involving genetically modified plants tolerant to glyphosate. This expansive use necessitates a proactive product stewardship program ensuring a wide distribution of the health and safety information for glyphosate. To this end, the results from rat developmental toxicity studies with glyphosate and selected surfactants are presented. Glyphosate (98.7% pure) was administered by gavage to groups of 25 female CD rats at dose levels of 0, 300, 1000, and 3500 mg/kg/day on days 6 through 19 of gestation. Polyethoxylated tallowamine (POEA) and a phosphate ester neutralized POEA were administered by gavage to groups of 25 female CD rats at dose levels of 0, 15, 100 and 300 mg/kg/day and 0, 15, 50 and 150 mg/kg/day, respectively, on days 6 through 15 of gestation. Severe maternal toxicity, including decreased weight gain and mortality (6 of 25 dams), occurred at the excessive dosage of 3500 mg glyphosate/kg/ day and was accompanied by reduced fetal weights, viability, and ossification of sternebrae. The NOEL for maternal and developmental toxicity was 1000 mg/kg/day. No developmental toxicity was observed in the studies with the surfactants. Slight maternal toxicity (decreased food consumption and mild clinical signs) was observed at 100 mg POEA/kg/day. Mortality, clinical effects, and reduced food consumption and body weight gains were observed at the highest doses tested with POEA and the neutralized POEA; maternal NOELs were 15 and 150 mg/kg/day, respectively.”

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      4. Henry – your paper on toxicity states that 360g/L glyphosate was used with 18% w/v POEA.
         To achieve 1000mg/kg body weight one has to additionally give 500mg/kg POEA. To achieve 500 – 250mg/kg POEA – rates which only partically overlap the Monsanto study (to which I lack access – but it does appear in the review of safety “Safety Evaluation and Risk Assessment of the Herbicide Roundup and Its Active Ingredient, Glyphosate, for Humans” (sorry for lack of link – it wouldn’t work due to containing institutional info)that the conclusions were against developmental toxicity of POEA – this seems rather odd to me given that the NOAEL levels are less that 30mg/kg/day for POEA and that maternal toxicity is generally accompanied by fetal abnormalities to some degree (afaik at least) and that the Holson 1990 report suggests a NOEAL for developmental toxicity of 15mg/kg/day (sadly an unpublished report) – however on the weight of evidence provided I’ll back off from completely blaming the POEA and conclude that it does appear that at levels which are utterly unlikely to occur in humans there does seem to be a neffect of POEA which may be enhancing those effects seen at the 3500mg/kg/day level of glyphosate by increasing permeability – thanks for doing the extra legwork to correct that. (I wasn’t aware of the effects at such high doses on development, probably should have been given that I’ve read the paper multiple times, but I have the memory of a wossname)
         It would be prudent however to keep in mind that for a 15mg/kg/day exposure rate a small female (50kg) would have to be exposed to 750mg of POEA a day which would be the equivalent of drinking more than 3ml of concentrated roundup solution (the high % in the initial study) per day for multiple days during preganancy – which isn’t at all likely.

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      5. Ewan stated:

         “Henry – your paper on toxicity states that 360g/L glyphosate was used with 18% w/v POEA.”

         Yes, this was the stock (commercial) solution BEFORE dilution.

         “The Roundup† formulation (lot: BS 1096/98,
         Monsanto of Brazil) consisting of 360 g/l glyphosate
         (N-phosphonomethylglycine) and 18% (w/v)
         polyoxyethyleneamine (the surfactant) was used.
         The solutions of the Roundup† formulation were
         prepared by the addition of appropriate volumes
         of distilled water.”

         All dilutions were made from that. I do not see anywhere in the article (E. Dallegrave et al. / Toxicology Letters 142 (2003) pages 45-52) that they added additional POEA so I do not understand why you are stating the following:

         “To achieve 1000mg/kg body weight one has to additionally give 500mg/kg POEA. To achieve 500 – 250mg/kg POEA …..”.

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      6. The calculation is simple – if the commercial formulation is 360g/L (36%) and 18% POEA then there has to be 50% of the weight in POEA
         I think perhaps my wording was unclear – the additionally there simply means that in addition to 1000mg/kg glyphosate there is 500mg/kg POEA simply as a result – apologies for the lack of clarity.

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      7. Ewan, I was under the impression that the 1000mg was roundup formulation, not glyphosate. I don’t have the paper in front of me, but that’s what I recall. Do they say 1000mg/kg glyphosate?

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      8. The control group
         received distilled water and the experimental
         groups received 500, 750 or 1000 mg/kg glyphosate-
         Roundup† diluted in water. The dosing regimen
         was based on no observed adverse effect level
         (NOAEL) for developmental toxicity in rats
         (maternal and fetal effects), which was 1000 mg/
         kg glyphosate

         To me this suggests dilutions were done such that there was 1000mg/kg glyphosate – it makes sense in that the POEA from this formulation will always scale in a 2:1 manner glyphosate:POEA – but you then have to take this into account when assessing the toxicological effects of POEA in the formulation – given that it has a far lower NOEAL (and apologies if I’m screwing up acronyms here – my box is so small that I can only see 75% of each line) one would expect to see toxic effects at far lower concentrations than the NAEOL of glyphosate alone (ie starting at around 30mg/kg/day if the POEA effect kicks in directly following the lowest NAEOL)

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      9. I’m now looking at the paper and it is not clear to me. They reference their doses as diluted “glyphosate-Roundup”, which suggests formulation to me, then right after that, they say this is based on the previous work of “1000mg/kg glyphosate”, and site Williams, et al. Looking at Williams, they specifically state that when they say “glyphosate” they mean technical grade.

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      10. 1000 mg/kg of the formulation wouldn’t really make much sense though – that’d only be 360mg/kg glyphosate which isn’t remotely in line with anything in the literature.

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      11. Ok, I think I see what you are saying here and what they mean. So essentially, they used 1/360th of a liter of commercial Roundup. This gave them 1000mg of glyphosate. It also contained 500mg of POEA. When they say “1000mg/kg glyophsate-Roundup”, perhaps they mean 1000mg glyphosate as obtained from the Roundup formulation.

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      12. Kinda – they make a solution whereby 10ml will contain 1000mg and then give the rats 10ml per kg by gavage – so I guess 2.7ml of commercial roundup made up to 10ml or scaled up and then gavaged to the rats by weight each day.

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      13. 🙂 Yes, I understood that 🙂 . I should have said “conceptually” not “essentially“. 1/360th of a liter would be a good squirt for a rat. Reminds me of an insult we used to throw around as kids: “up your nose with a rubber hose”, rat! Which, in turn, reminds me why I did not go into the clinical/animal trial end of things.

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   2. Judy: Is there any connection that anyone knows to GMO crops or glyphosate and something new happening in summer of 1994?

      I suspect GM use in 94 was pretty minimal.

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      1. First wide scale use of GM crops was in 96 following commercialization of RR soy – GM crop use in 1994 is as close to zero as to be meaningless (field tests etc)

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      2. So does that mean Judy’s latest attempt to try and implicate GM crops in some poorly characterised environmental problem has fallen flat. Don’t tell me, instead of looking for some other factor from ’94 that may be a cause of her observations she’ll move on to another unrelated statistic from ’96 that she can decide GM is the cause. Its the way the anti GM/antipesicide brigade works.
         Post hoc ad propter hoc-mining they should call it.
         Jonathan

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      3. Is Jonathan’s post going to be removed?

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      4. Why? Unless offensive or threatening language was used I assumed we openly debated any contentious posts on Biofortified. I’ll repy to Judy directly if that’s Ok with you Henry.
         Jonathan

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      5. “Attacks: You may question or argue any ideas but comments that include personal attacks will be removed, and the author may be banned from posting additional comments.
         Conjecture: We aim for fact based discussion. Conjecture, nonsense, and conspiracy theories may be modified or deleted.”

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      6. I don’t see a personal attack. Perhaps you could elucidate.

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

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      8. You honestly think that the content of Jonathan’s post is worthy of either deletion or modification?
         If that’s the case we’d have to delete your phantom of the opera post given that it links to…
         conjecture, nonsense and conspiracy theories.
         I think however that would be a ridiculous enforcement of rules clearly set up to be used judiciously in cases where they’re obviously needed rather than willy nilly whenever the sensibilities of the overly sensitive are tickled.

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      9. The Phantom of the Opera link links to two
         letters that
         Dr. Huber sent (the first with 20 citations to reviewed
         scientific papers).

         1. Letters from Prof Don Huber to US and EU administrations
         2. Letter to Secretary of Agriculture Thomas Vilsack

         Neither I nor the owners of the linked to web
         page made any comments. The first letter
         had not been introduced earlier in this thread.
         The second was introduced in the original
         article in this thread.

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4. Just in case anyone’s interested, Dr. Huber is still singing the same song, apparently very convincingly (to some people, at least). See Latter-Day Luther Nails Troubling Thesis to GM Farm & Food Citadels. I don’t have the energy to point out the issues in this piece, maybe someone else wants to?

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   1. Well, in only a matter of “weeks”, we’ll evidently know what he wants to name this thing…….
      Let’s see if it happens.

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5. Ewan R, thank you for the interesting post and answer to my question. As I said, I can find no connection time-wise or symptom-wise to glyphosate, a retinoic acid disruptor, not a thyroid hormone disruptor in animals, so glyphosate is innocent unless someday proven guilty by new studies by someone. One thing glyphosate apparently does according to the article by Dr. Huber, is “it is also a strong immobilizer (chelator) of essential plant nutrients to impair nutrient uptake, translocation, and physiological efficiency at only a fraction of the labeled herbicidal rate (Ekers, Ozturk, Cakmak, Zobiole, Jolly et al., 2004). Glyphosate is a powerful biocide to harm beneficial soil organisms important for nutrient recycling, N-fixation, nutrient availability, and natural disease control (Kremer & Means, Zobiole et al, Dick et al).” Unless this affect on plants could cause fairly serious malnutrition in the animals eating the plants, I can still find zero connection between glyphosate and the increasing symptoms consistent with fetal hypothyroidism in ruminants, birds, rodents and other animals. I did say the three major factors in causing fetal hypothyroidism according to the studies I could find, are radiation, malnutrition and exposure to thyroid hormone disrupting chemicals and it appears likely that all three factors are involved. One of the symptoms, brachygnathia superior and resultant underbite causes malnutrition, as I think I said on the Forum, thus pregnant females of wild grazing animals with underbite would consequently be very likely to be undernourished. Therefore, one of the symptoms of fetal hypothyroidism in one generation is a likely cause of it in the next generation.
   Jonathan, I thought I explained the symptoms of fetal hypothyroidism fairly well and listed some references on the Forum for studies of fetal hypothyroidism which also described the symptoms at great length and/or listed them, so what exactly do you mean by this statement, “poorly characterised environmental problem?” I do not know where you live, but I am fairly certain that if you would go out to where goats, cattle, horses, llamas or other grazing animals are raised and look at their bite, you would find quite a few with underbite because of underdeveloped upper jaw bones. Or you could go to a taxidermy shop and look at newly killed big game animal heads in the fall when hunting season is on. Just because I am inept doesn’t mean there isn’t a serious environmental problem. I am not antipesticide, I am against unnecessarily killing and/or maiming baby animals during development.

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   1. Sorry I was blunt Judy. Its just assumptions and preconceived ideas have no place in diagnosis of any problem, illness or scientific debate. By ‘poorly characterised’ I meant the cause of what is being observed is poorly characterised. If the problem started in 1994/95 GM cannot be implicated and probably not glyphosate either.
      I stand by my assertion that a wide range of environmental campaigners around the world constantly make assumptions based on post hoc fallacies and in fact go out of their way to find correlations to base such assumptions on.
      Have you now dismissed GMOs/glyphosate from your list of possible causes of hypothyroidism now it is clear it is a problem that began before GM was introduced and at a time when glyphosate was used on a much smaller scale from that presently found? Or is that a line of enquiry you will return to if correlations after GMOs were introduced can be found?
      Jonathan

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   2. I did say the three major factors in causing fetal hypothyroidism according to the studies I could find, are radiation, malnutrition and exposure to thyroid hormone disrupting chemicals

      Have you checked the nutritional status of local deer? Given that skewed sex ratio towards males is indicative of malnutrition (detailed on the forum post) whereas as pdiff points out hormonal disruption skews towards females it would appear that by simple application of Occam’s razor you’d have to go with malnutrition as your culprit until more convincing evidence than has been provided was available.
      At present I’d no more trust Dr Huber on matters of reality than I’d trust Ken Ham on the coexistance of humans and dinosaurs (as traditionally thought of and not the colorful little songsters we know and love today) – his claims on plant disease prevelance and new organisms have apparently zero basis in reality (the first because other plant disease specialists are completely baffled by his claim, the second because he describes an organism that cannot possibly exist (I’m rather concerned as to why the pro-Huber side in this discussion have failed to come up with a rational explanation for this, or at least discarded this bit of obvious fantasy, it remains conveniently ignored, like an elderly relative making socially inappropriate statements)

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      1. The following was stated:

         his claims on plant disease prevelance and new organisms have apparently zero basis in reality (the first because other plant disease specialists are completely baffled by his claim, the second …..

         This plant disease specialist does not appear to be completely baffled by the disease clain:

         Paul Vincelli, a plant pathology professor at the University of Kentucky, said he talked with Huber last fall after he was asked to review a Kentucky researcher’s work on the same topic. Vincelli declined to identify the Kentucky researcher, saying his review was a private consultation, but he said he has seen no evidence to support Huber’s claims linking a new pathogen to crop diseases or animal fertility.
         
         Vincelli said while research has shown the use of glyphosate may make some plants more susceptible to disease, he is not aware of evidence of a new pathogen that increases that risk as Huber claims.

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      2. I refer you to MaryM’s link upthread which shows the view of a soybean expert in phyopathology – descriptive refutation of Hubers outlandish claims – rather than a rather wishy washy non-specific statement that glyphosate use may make some plants more susceptible to disease – hardly the same as Huber’s claims in any way shape or form – I have no doubt that glyphosate application would make many plants more susceptible to disease – non-resistant strains sprayed with sub-lethal doses for instance would be highly stressed and therefore have increased susceptibility – at least Vincelli steps away from Huber’s ultra whacky claims of new pathogens and animal fertility issues.

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      3. Dr. Anne Dorrance’s article was not published in a reviewed scientific journal, nor does it give any literature references to reviewed scientific papers. It does include a graph with data up to (not including) 2006. The data points are scattered. She states (with no documentation)

         “The yield loss recorded for each disease group fluctuates based on the incidence and severity of specific diseases due to the widespread planting of susceptible varieties and/or environmental factors that favor infections.”

         The following is a 2009 Preface (to a special journal issue) with references to reviewed scientific papers:

         Glyphosate interactions with physiology, nutrition, and diseases of plants: Threat to agricultural sustainability?

         Two of the authors are with separate USDA laboratories.
         The table of contents of that special issue is available.

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      4. The following appeared in April 2, 2011 Los Angeles Times:

         “For soybeans, sudden death syndrome has been a serious issue in the Midwest in the last two years. Part of the problem is climate change, said Xiao Bing Yang, a leading expert on the disease at Iowa State University. Soil that is too moist, coming after too cool of a spring, can be a breeding ground for the fungus Fusarium solani f.sp. glycine. It’s the fungus that causes sudden death syndrome, scientists say.
         The effect on soybeans can be dire. At best, a farmer could lose 10% of his crop. At worst, 90% could be wiped out. Once the fungus is in a field, it can remain for years and cause havoc when the environmental conditions are right.
         Last year, after a chilly spring and a very wet summer, soybean sudden death syndrome raced across the Midwest. The hardest hit was Iowa: Yang estimated last summer that up to half of the state’s fields might be infected in varying degrees. The USDA warned in August that “the amount of acreage is becoming a concern.”

         Dr. Yang has a reviewed scientific paper on this subject in which he reports that the application of glyphosate makes the fungus worse in growth-chamber and greenhouse experiments.

         Authors: Sanogo, S., Yang, X. B., and Scherm, H. 2000.
         Title: Effects of herbicides on Fusarium solani f. sp. glycines and development of sudden death syndrome in glyphosate-tolerant soybean.
         Published in: Phytopathology 90: pages 57-66.
         Abstract: Sudden death syndrome of soybean, caused by Fusarium solani f. sp. glycines, is a disease of increasing economic importance in the United States. Although the ecology of sudden death syndrome has been extensively studied in relation to crop management practices such as tillage, irrigation, and cultivar selection, there is no information on the effects of herbicides on this disease. Three herbicides (lactofen, glyphosate, and imazethapyr) commonly used in soybean were evaluated for their effects on the phenology of F. solani f. sp. glycines and the development of sudden death syndrome in four soybean cultivars varying in resistance to the disease and in tolerance to glyphosate. Conidial germination, mycelial growth, and sporulation in vitro were reduced by glyphosate and lactofen. In growth-chamber and greenhouse experiments, there was a significant increase in disease severity and frequency of isolation of F. solani f. sp. glycines from roots of all cultivars after application of imazethapyr or glyphosate compared with the control treatment (no herbicide applied). Conversely, disease severity and isolation frequency of F. solani f. sp. glycines decreased after application of lactofen. Across all herbicide treatments, severity of sudden death syndrome and isolation frequency were lower in disease-resistant than in susceptible cultivars. Results suggest that glyphosate-tolerant and -nontolerant cultivars respond similarly to infection by F. solani f. sp. glycines after herbicide application.

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      5. Dr. Yang also published another paper the next year 2001.

         “Abstract: Three-year field experiments were conducted to assess the development of sudden death syndrome (caused by Fusarium solani f. sp. glycines) in three soybean cultivars, tolerant (P9344 and A3071) and nontolerant (BSR101), to glyphosate following foliar application of four herbicides (acifluorfen, glyphosate, imazethapyr, and lactofen) commonly applied to soybeans in the north-central region of the United States. Cultivar A3071 is resistant to sudden death syndrome, whereas cultivars P9344 and BSR101 are susceptible to this disease. There was no statistically significant cultivar-herbicide interaction with respect to the severity of foliar symptoms of the disease and the frequency of isolation of F. solani f. sp. glycines from roots of soybean plants. Across all herbicide treatments, the level of sudden death syndrome was lower in the disease-resistant cultivar than in the susceptible ones. There was an increase in the disease levels under application of acifluorfen, glyphosate, and imazethapyr compared with nontreated or lactofen-treated plants. The results obtained indicate that the response of glyphosate-tolerant soybeans to sudden death syndrome is not different from the response of conventional soybeans to this disease following application of the selected herbicides, and the resistance of soybean to sudden death syndrome was not changed with application of glyphosate.”

         The abstract seems to be saying 2 opposite things? Fortunately, the link is to the full paper.

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      6. A 2006 USDA paper on the subject of glyphosate application and disease.

         “Abstract: This study tests the effect of glyphosate application on disease severity in glyphosate-resistant sugar beet, and examines whether the increase in disease is fungal or plant mediated. In greenhouse studies of glyphosate resistant sugar beet, increased disease severity was observed following glyphosate application and inoculation with certain isolates of Rhizoctonia solani Kuhn and Fusarium oxysporum Schlecht. f. sp. betae Snyd. & Hans.
         Significant increases in disease severity were noted for R. solani AG-2-2 isolate R-9 and moderately virulent
         F. oxysporum isolate FOB13 on both cultivars tested, regardless of the duration between glyphosate application
         and pathogen challenge, but not with highly virulent F. oxysporum isolate F-19 or an isolate of R. solani AG-4.
         The increase in disease does not appear to be fungal mediated, since in vitro studies showed no positive impact of glyphosate on fungal growth or overwintering structure production or germination for either pathogen. Studies of
         glyphosate impact on sugar beet physiology showed that shikimic acid accumulation is tissue specific and the rate
         of accumulation is greatly reduced in resistant cultivars when compared with a susceptible cultivar. The results
         indicate that precautions need to be taken when certain soil-borne diseases are present if weed management for
         sugar beet is to include post-emergence glyphosate treatments.”

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      7. A very recent study (just arrived this morning)
         Title: Effect of Pesticides on Plant Growth Promoting Traits
         of Greengram-Symbiont, Bradyrhizobium sp. strain MRM6
         Authors: M. Ahemad M. S. Khan (&)
         Authors affiliation: Department of Agricultural Microbiology,
         Faculty of Agricultural Sciences, Aligarh Muslim University, Aligarh, U.P. 202002, India
         Published in: Bull Environ Contam Toxicol (2011), 86 86, pages 384-388.

         “Abstract The aim of this study was to investigate the
         toxicity of herbicides (metribuzin and glyphosate), insecticides (imidacloprid and thiamethoxam) and fungicides (hexaconazole, metalaxyl and kitazin) at the recommended and the higher dose rates on plant growth promoting activities of Bradyrhizobium sp. under in vitro conditions. The Bradyrhizobium sp. strain MRM6 was isolated from nodules of greengram plants. Pesticide-concentration dependent progressive-decline was observed in plant growth promoting
         traits of the strain MRM6 apart from exo-polysaccharides
         which increased consistently on increasing pesticide concentrations.
         Generally, the highest toxicity to plant growth
         promoting characteristics of the Bradyrhizobium sp. strain
         MRM6 was observed when the strain MRM6 was grown
         with three times the recommended field rates of glyphosate,
         imidacloprid and hexaconazole.”

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      8. Sorry, in the last post I gave you the subscriber’s link. Here is the general public link.

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      9. In the Discussion section of the above reviewed published scientific paper by scientists at the Department of Plant Pathology, Iowa State University, Ames, Iowa.

         “Three-year field experiments were conducted to assess the development of sudden death syndrome (caused by Fusarium solani f. sp
         “

         The following was stated:

         Although
         glyphosate has little or no direct effect on
         F. solani (23), this herbicide appears to
         impose some level of stress that may explain
         the higher level of disease in glyphosate-
         treated plants compared with
         nontreated or lactofen-treated plants.

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      10. The above post is referring to the paper mentioned
          by me on
          April 2, 2011 at 7:34 am ·

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      11. Considering, Henry, that we’re discussing Huber’s outlandish claims in a letter (which I’m assuming wasn’t peer reviewed) your constant insistence on everything being peer reviewed is a rather poor show of double standards considering you appear to buy Huber’s rubbish hook line and sinker – Dr Dorrance is an expert specifically in soybean phytopathology and finds Hubers claims that disease has increased in soybean in general outlandish.
          On your other papers – so it appears if you massively over apply herbicides you can increase disease in plants (not surprising – even a glyphosate resistant soybean has a point at which you overwhelm the transgene and the plant will suffer actual herbicide damage – at which point nobody at all would be surprised to see decreased disease resistance) – or, you can investigate effects in a non-field setting and get results probably reflective of your growing conditions etc (there is no opportunity for soil to recolonize with unaffected microorganisms for instance in a pot system in the greenhouse – plants are under utterly different stresses and nutrient regimes) – whereas the field study you show (while admittedly being limited to a handful of cultivars) indicates that the treatment effect of glyphosate on SDS is non-existant. I’ll trust the field data over the greenhouse data.

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      12. The following USDA paper has examined the effect of high moisture and glyphosate applications on Fusarium infections (80% of the isolates were Fusarium oxysporum; F. solani and F. equiseti each comprised 10% of the isolates.) of soybeans.
          In the following (SMC) is “soil moisture content”

          “Our results agree with previous field research that reported increased rhizosphere colonization by Fusarium (a) of soybean with increasing SMCs (Sanogo, Yang, and Scherm 2000; Kremer 2003) and (b) of GR soybean following glyphosate application (Cheng and Schneck 1978; Scherm and Yang 1996; Scherm, Yang, and Lundeen 1998). Glyphosate applied to plants appeared to influence Fusarium through several mechanisms. Glyphosate may increase the quantity and alter the composition of substances released by root exudation and ultimately enhance Fusarium growth in the rhizosphere (Greaves and Sargent 1986; Kremer, Means, and Kim 2005). Host plant defenses may be weakened from reduced phytoalexin production, caused by interruption of the shikimate pathway by glyphosate, and allow increased root colonization by Fusarium (Johal and Rahe 1988). Also, glyphosate may be translocated to roots, released into the rhizosphere, and selectively stimulate Fusarium growth and root colonization (Wardle and Parkinson 1992b; Krzys´ko-Lupicka and Orlik 1997; Kremer, Means, and Kim 2005). The combined effects of glyphosate with optimum to high soil moisture that led to increased Fusarium populations (root colonization) in this study may help explain the Fusarium disease epidemics documented in GR soybean fields during wet growing seasons, notably in 1997, the first year of widespread GR soybean production (Wrather, Stienstra, and Koenning 2001). High root colonization rates by Fusarium species under optimum soil moisture also leads to reduced root biomass (Ortiz-Ribbing and Eastburn 2004). Thus, decreases in root mass by glyphosate may be augmented by coincident enhancement of Fusarium colonization, leading to reduced plant productivity.”

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      13. More evidence that greenhouse application of glyphosate increases fusarium colonization – still no field data.
          You don’t have to keep flogging a dead horse – it appears conclusive that under greenhouse conditions it’s best not to spray glyphosate on soy – I’m sure greenhouse growers of soy across the globe will take heed.

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      14. The increased levels of fusarium had no effect on above ground biomass in the glyphosate treated plants. That suggests a protective effect that minimizes the impact of fusarium infection on biomass and presumably yield.
          Kills weeds and protects against biomass reductions from fusarium infection? Sounds like another benefit of glyphosate.

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      15. <

          blockquote>”The first growing season of widespread cultivation of GR soybean in 1997 was unusually wet in the midwest United States, which contributed to severe epidemics of soybean sudden death syndrome (SDS) caused by the soilborne fungal pathogen Fusarium solani f. sp. glycines (Wrather, Stienstra, and Koenning 2001). Glyphosate-resistant varieties were more frequently identified with SDS than conventional varieties (Myers et al. 1999). These observations suggested that Fusarium infection was related to soil moisture content (SMC) and to the increased use of glyphosate with GR soybean. Our recent field studies revealed inconsistent colonization of roots by Fusarium between growing seasons, partly due to contrasts in seasonal rainfall patterns (Means 2004). Studies on soil moisture relationships with root colonization of GR soybean by Fusarium species are very limited. Thus, our research objective was to determine the impact of different SMCs on root colonization of glyphosate-treated soybean by Fusarium species.”</blockquote

          >”The combined effects of glyphosate with optimum to high soil moisture that led to increased Fusarium populations (root colonization) in this study may help explain the Fusarium disease epidemics documented in GR soybean fields during wet growing seasons, notably in 1997, the first year of widespread GR soybean production (Wrather, Stienstra, and Koenning 2001). High root colonization rates by Fusarium species under optimum soil moisture also leads to reduced root biomass (Ortiz-Ribbing and Eastburn 2004). Thus, decreases in root mass by glyphosate may be augmented by coincident enhancement of Fusarium colonization, leading to reduced plant productivity.”

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      16. I’ll see you one comment based on a conference presentation/poster (apparently – can’t find the Myers reference anywhere – perhaps you have a source?) and raise you one peer reviewed paper released at a later date (2003) which utilizes a multi-year, multi-location, multi-maturity group design concluding that…
          Fsg and SDS leaf symptoms did not significantly increase following the application of glyphosate.
          I await your next greenhouse/growth chamber study with baited breath.

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      17. Dr. Robert Kremer, microbiologist with the USDA-ARS Cropping Systems and Water Quality research unit in Columbia, Mo. presented the 22nd annual David W. Staniforth Memorial Lecture, “Glyphosate Interactions Beyond Weed Control: Current State of Knowledge”, Thursday at Iowa State University, Ames, Iowa.
          The summary is here.

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      18. The actual video of Dr. Robert Kremer’s talk and the slides used can be downloaded from the following link:
          http://talk.newagtalk.com/forums/thread-view.asp?tid=229510&mid=1740205#M1740205

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      19. Here’s a question for the weekend everyone….
          What causes a bigger increase in a crop’s susceptibility to disease?
          (a) use of glyphosate to control weeds?
          (b) organic farming of the crop?
          Answers below and please show your working.
          Have a good one all,
          Jonathan

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6. Thank you Henry K. Jonathan, no offense taken.
   In 1996, I alerted the proper authorities, the Montana Department of Fish, Wildlife and Parks and Health Departments of what I was seeing, provided data and photos on a small sample of 10 accident killed yearling male deer from various areas of Ravalli County, MT, 9 of which had no or half a scrotal sac, with one also misaligned. The MDFWP said the impact with a vehicle just caused the deer to just look malformed to an inexperienced observer, which I guess included their own biologists, two of which said the deer were malformed.
   While I may seem over zealous, this quote from the most recent article about Dr. Huber that was posted says it all concerning what I have always tried to do.This is the quote and it pretty much says it all. I do appreciate any and all help and criticism too.
   “If someone is making a new discovery, they normally want someone to know about it and if this was an important environmental or agricultural problem, you would want to engage other people in finding what the causes of the problems are.”
   The article was at http://dailycaller.com/2011/04/01/biotech-letter-gets-notice-online-but-is-it-true/#ixzz1IHeknFVq
   Ewan R., the goat herds in our area have a prevalence of over 60% with brachygnathia superior and judging by comments and photos on goat related websites, this malformation is quite common all over the U.S. I checked the mouths of 20 newborn goats from four herds in four different parts of our county in 2009. The mother goats were well fed, so malnutrition in the mother does not seem to be a factor in the goats. I collected 13 one and one half year old butchered beef steer heads all except two from the same ranch, were from different ranches. The beef steers were butchered for the ranchers, so were likely for their own use. Of the 13, 9 had underbite and 4 had a normal bite. The beef cattle are well fed here in winter while the fetal calves are developing. Pregnant mares on horse ranches were well fed between 1996 and 2003 when I was keeping much better track of what was happening with foals. Again online websites have quite a lot of chatter about underbite on foals now.
   While malnutrition is very likely a significant factor in fetal hypothyroidism in wild ruminants, I can find no connection to malnutrition with the high prevalence of fetal hypothyroidism symptoms in the well fed animals. The same with wild birds. The parents and the hatchlings appear to be well fed, even though the hatchlings of a variety of bird species rescued from nests that are blown down in wind storms or swallow hatchlings in nests that fall down by accident or are deliberately knocked down by miscreants have brachygnathia superior or other symptoms of thyroid hormone disruption during development. Also, what puzzles me is prior to 1995, we never saw brachygnathia superior or malformed genitalia on newborns after very hard winters that killed lots of big game animals because they died of malnutrition. Where I live, we have not had a winter with deep snow all winter for many years, but the brachygnathia superior and other symptoms appear to be increasing. Also, most puzzling, snow levels during the winter do not seem to correlate with increases observed or documented scientifically in the brachygnathia superior and other fetal hypothyroidism symptoms on newborns of either wild or domestic mammal -same for birds but they are very hard to track. I am not saying that malnutrition is not involved. I am saying it historically did not cause brachygnathia superior and brachygnathia superior is prevalent on young of well fed ruminants. I also really think we need to find the cause of this because a lot of jobs and businesses depend on the affected animals.

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   Reply

   1. http://www.miller-mccune.com/environment/more-evidence-linking-pesticides-and-malformations-30560/

      “Meanwhile, Hoy is preparing a paper for publication and has found a collaborator of sorts in a 14-year-old whose involvement grew out of a school project.
      Samantha Crofts read Rachel Carson’s Silent Spring before enrolling in Brett Taylor’s freshman science class at Missoula’s Sentinel High School. Taylor requires all students develop a research project suitable for presentation at a science fair. He knew something of Hoy’s research and suggested Crofts visit Hoy at her rehabilitation center.
      After talking with Hoy, Crofts decided to research the incidence of underbite on domestic goats — in the Bitterroot Valley. She has visually observed 43 goats and has found 60 to 70 percent of them have the condition known as brachygynathia, similar to Hoy’s recent findings when observing Bitterroot fawns. (“Goats aren’t my favorite animal,” Crofts admitted. “I’m scared of them, to tell you the truth.”)
      Crofts plans to continue the study by determining the probability that genetics is behind the malformations; her control will be drawn from two baseline studies with a population of 39,000 animals.”

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7. Seralini et al. have a new paper:
   Genetically modified crops safety assessments:
   present limits and possible improvements

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   1. No doubt, there will be a lot to say on this, however, I have to ask Seralini, where’s the beef? He is claiming evidence of kidney disease from Bt maize. He also admits that Americans eat more GM, including maize, than anyone else. So why haven’t American renal disease (ESRD) rates changed? For females, the rates are even plateauing.
      See: ESRD Plot. The reference is at 1994, where GM was introduced.
      Looks like a Failure to Fail…..

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      1. PDF modified (4/4/11) to show adjusted rates per million and age classes.

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8. Another attempt to post. The 2003 field study soybean paper with a Monsonto author that found no effect on SDS used glyphosate

   “Treatments consisted of glyphosate-sprayed and a nonsprayed control.
   At the V3 growth stage (Fehr et al., 1971), the treated subplots were sprayed
   with 1.12 kg a.i. ha 1 glyphosate.”

   while the 2001 field study paper that I had presented used
   the commercial formulation Round-Up.

   “Four herbicides were tested in this study: acifluorfen
   (Blazer), glyphosate (Roundup Ultra),
   mazethapyr (Pursuit 2AS), and lactofen
   (Cobra 2EC). The recommended field
   application rates”

   The statement was made in the Round-Up paper that:

   “Although glyphosate has little or no
   direct effect on F. solani (23), this herbicide appears to
   impose some level of stress that may explain
   the higher level of disease in glyphosate-
   treated plants compared with
   nontreated or lactofen-treated plants.”

   If the explanation that the Round-Up introduced some level of stress, one can
   understand why the 2003 results could be different as without the
   “spreader sticker” not much glyphosate may be
   absorbed into the plant.
   Although the Monsanto paper was published in 2003, it did not reference
   the 2001 field Round-Up paper that I referenced (it did reference the

   same authors’ 2000 greenhouse study).

   That the use of the formulated product could be important is illustrated by another Monsanto publication:
   Fungicidal Effects of Glyphosate and Glyphosate Formulations on Four Species of Entomopathogenic Fungi
   W. E. MORJAN,1 L. P. PEDIGO,2 AND L. C. LEWIS3Environ. Entomol. 31(6): 1206Ð1212 (2002)

   Click to access IND23312192.pdf

   “Differences in fungicidal activity between glyphosate
   and different formulations are not surprisingsince
   some of the inert ingredients in formulations may
   increase or reduce the toxicity of the pesticide to specific organisms (Ware 1994).”

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   1. New Dr. Huber related post with additional information.
      http://www.agprofessional.com/show_story.php?id=1318206

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      Reply

9. Dr. Huber’s letter was meant to be Internal and Confidential, so going into great detail about all the evidence he should have provided is not fair. It was a letter outlining a general situation, not a paper submitted for publication and/or peer review. It was not meant to be a press release or public at all. The recipient would be expected to contact Dr. Huber for more information. The entire point of the letter was to give a basic outline of an existing problem to get just such a reaction (more research)from the government. Our 10 chickens went from 2-3 eggs a day total to one a day each within a week when we switched from commerical (GE corn) poultry feed to mixing our own organic feed. It was cheaper too. You don’t need a PhD to observe what is happening.

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   1. According to my sources, he emailed the letter to anti-GE groups, and gave permission to post it online. So it does not seem to be true that it accidentally leaked out. He is now talking about it in a speaking tour as well – it is entirely fair to criticize such an action without going through the peer review process.

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   2. Our 10 chickens went from 2-3 eggs a day total to one a day each within a week when we switched from commerical (GE corn) poultry feed to mixing our own organic feed.

      Otherwise nutritionally the same, or a completely different diet?
      Extraordinary claims and all that.

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      1. I do have to wonder about methionine levels, etc in the two different feeds.

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      2. And of course levels of all other micro and macro nutrients – given a more than 200% increase in productivity one would have to assume that the egg industry would be all over this new formulation.
         Congratulations on your newfound riches Sea.Palm.

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   3. “Our 10 chickens went from 2-3 eggs a day total to one a day each within a week when we switched from commerical (GE corn) poultry feed to mixing our own organic feed.”
      Hmmm… makes sense. Many agronomists agree that organic is less productive.

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      1. 2-3 per 10 compared to 10 a day per 10 methinks – I thought the same as you initially Eric, but a more attentive parsing tells a rather different story

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10. I can’t find where the more recent posts are going, they aren’t here.
    Judy Hoy

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    1. Did you try to leave a comment and it didn’t appear? If so please let me know. We have been having problems with comments getting lost.

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       1. I’ve found that the best way to get a comment lost is to fill in the blank for ‘Website’ when submitting.

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11. Dear Karl,
    My comment is up, so did not get lost, but I was sent the following comment automatically and clicked on the link. I looked everywhere for where it was posted by Henry, but I couldn’t find it. I thought there may be some discussion about how serious Chlorothalonil is to exposed frog tadpoles. And there may be some discussion concerning the high prevalence of underbite on all ages, sexes and species of goat that Samantha Crofts examined for her science project. I couldn’t find Henry’s post or any discussion about it. By the way Henry, thank you ever so much for posting this, even if I can’t find it on the Biofortified website.
    Author: Henry Kuska
    Comment:
    http://www.miller-mccune.com/environment/more-evidence-linking-pesticides-and-malformations-30560/

    “Meanwhile, Hoy is preparing a paper for publication and has found a collaborator of sorts in a 14-year-old whose involvement grew out of a school project.
    Samantha Crofts read Rachel Carson’s Silent Spring before enrolling in Brett Taylor’s freshman science class at Missoula’s Sentinel High School. Taylor requires all students develop a research project suitable for presentation at a science fair. He knew something of Hoy’s research and suggested Crofts visit Hoy at her rehabilitation center.
    After talking with Hoy, Crofts decided to research the incidence of underbite on domestic goats — in the Bitterroot Valley. She has visually observed 43 goats and has found 60 to 70 percent of them have the condition known as brachygynathia, similar to Hoy’s recent findings when observing Bitterroot fawns. (“Goats aren’t my favorite animal,” Crofts admitted. “I’m scared of them, to tell you the truth.”)
    Crofts plans to continue the study by determining the probability that genetics is behind the malformations; her control will be drawn from two baseline studies with a population of 39,000 animals.”

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    1. A 14-year-old?
       There’s an 11-year-old child prodigy out there who’s at least as good on the topic of GMOs as the levitating dance teacher:

       I think Birke Baehr is actually better than Smith. In presentation, that is. Smith is too cadaverous to be appealing. Between Smith and Baehr, the scientific accuracy of their offerings is roughly equal.
       Enjoy! Run time is 6 mins, 25 secs.

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    2. Ah, I found the comment – it is way up there – search for one of the key words in the comment to find it. (Ctrl + F) This thread is getting pretty long!

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12. At least the claims are not much more extraordinary than people leveraging talking points like drinking cups of Roundup, and whether that’s lethal.
    MDV

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13. Interesting that most favor

    peer review

    while dissecting Dr. Huber’s letter. Have any of the scientists posting here actually looked at the research Dr. Huber has conducted or will you simply rely on

    debunking

    Dr. Huber’s letter?
    I know that Anastasia views Dr. Huber (rather derogatorily), as an “aging scientist” -she spells it out on another website. Perhaps she would like to leave her ad homs parked and actually look at his research and not critique a letter. I would like to point out, once again, it was not a peer reviewed article. It was a letter to the head of the USDA from a well respected and well known scientist that has worked in the field of emerging pathogens for 20+ years. I am quite sure that had Tom Vilsak asked for the scientific research that Dr. Huber conducted to reach his conclusions, Dr. Huber would have (or did, as far as anyone here knows) supply it; we may never know as most of the emeging pathogen research is classified or is not available to the average researcher.
    Of course, peer review is essential. Duh. However, I am equally confident that an experienced scientist of Dr. Huber’s caliber would not make such claims if there were no scientifically based reason. So, rather than using your superior mental intellect to deride a letter to a head of a government agency suggesting that government approval of questionable practices should be reconsidered, you will toil over the research actually performed; or, better yet: do it yourself. That is, if Monsanto will fund you. Which leads to the dearth of information and research performed on these types of organisms. To say that the major corporations funding the research has an agenda would be an understatement. To wit: has anyone posting here ever heard of Dr Robert Van den Bosch? Of course, that will be dismissed as old science from an aging, cranky scientist.
    Perhaps when Anastasia gets awarded her doctorate, she will be in more of a qualified position to call an experienced researcher and scientist, essentially, a washed-up, old-fart of a has-been.
    I truly hope that, as a doctoral candidate, Anastasia’s future career will not be placed in jeopardy because of her own knee-jerk reaction.

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    1. By the way, science is not decided on authority – evidence comes before anything else. And none has been provided other than the self-contradictory claims in this letter. Being a Ph.D. or not really doesn’t matter when it comes to deciding if there is enough evidence to reach this conclusion, and seasoned scientists can make mistakes as well.

       Of course, peer review is essential. Duh. However, I am equally confident that an experienced scientist of Dr. Huber’s caliber would not make such claims if there were no scientifically based reason.

       Your argument depends upon trusting that Huber is being completely genuine in his statements about this ‘new’ organism. Would your position of trust change if you discovered that he was being disingenuous in these public statements? I’m curious.

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    2. Perhaps you’d care to link any of the peer reviewed research which backs Hubers claims rather than simply stating that it should be looked at?
       Why critique a letter? Because that’s all we have. It sparked a firestorm. It is full of utter nonsense.
       It’s also amusing that you focus on Anastasia’s Ad Hom (which I presume resides elsewhere, the above post details Hubers experience and a quick skim through doesn’t appear to be a smear on him for being washed up or an old fart (it questions the position he held in a given organization) and it does take a look at Hubers research (one would assume that being retired the guy isn’t actually actively doing research – I’m guessing Emeritus professors tend not to pull in research grants) rather than addressing any of the actual points made. It’s almost as if you’re commiting precisely the same (or at least a deceptively similar) logical fallacy – you are failing utterly to address the points brought up here and instead are relying on smearing Anastasia’s entire post based on what you categorize as a knee-jerk reaction. Doubly amusing as your entire post appears to be little more than a knee-jerk reaction (see screed about failing to address any of the issues)

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    3. I didn’t use the word “aging” in this post or my other post about Dr. Huber’s letter. If I did use it elsewhere (if you’d provide a link that would be nice), I would not use “aging” in a derogatory way. Do not put words in my mouth. If you have a problem with elders continuing to work and be productive, that’s you, not me. I did mention in this post that Huber has a solid record of publication: “we can say that he is a well published scientist that has published relevant subject matter in some fairly reputable journals for his field… Dr. Huber appears to have relevant and recent expertise on the subject of the effects of glyphosate on mineral uptake and disease resistance.”
       Dr. Huber chose to put controversial ideas that are not substantiated by any evidence out into the world. Those ideas have been picked up by people all over the world as some sort of proof even though there is no evidence. Critiquing those ideas ≠ knee jerk or ad hom. You might want to think a little bit more about what a knee jerk reaction is, because you seem to have some symptoms of that yourself. To be blunt, I wonder if you even read this post at all or if you just assumed that I was saying Huber was an old fart because I disagree with his unsubstantiated claims until they are substantiated.
       This post was about Huber’s claims that are not substantiated in peer-reviewed literature. I did consider the literature about glyphosate and crop mineral uptake in my followup post. I have intentions to write an additional post summarizing the literature about crop-fungus-glyphosate interactions, however I am restricting the time I spend on blogging at the moment because this is an unpaid extracurricular activity and I must focus on writing my thesis and other commitments. If you or someone you know would like to submit a post on the subject that is substantiated with references from peer-reviewed literature, please find instructions for doing so here.

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       1. You tell it sister! I considered stealing a bit of your thunder, and I’m glad I didn’t.

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14. the whole point of Genetic Engineering is to move a gene from one species to another via both GE bacteria and a viral promoter which is supposed to turn off and doesn’t.
    If you would kindly research GE, first, before trying to investigate a military threat investigator’s legitimacy based on no background of GE.

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15. I did not see any tweet or info on this news article. I thought I would post it here.
    “A former Purdue University professor says it will be a few more months before he can support his claim that Roundup Ready technology is responsible for the proliferation of a previously unknown microscopic organism he says causes plant diseases and livestock abortions.
    A sample of the organism was sent to a lab in March for sequencing so the organism could have its characteristics clearly identified, said Don Huber, the retired Purdue professor.
    However, a contaminant was found in the sample, “so we had to take more time to get the material that is required,” Huber said.”
    http://www.capitalpress.com/idaho/se-Roundup-claims-072211
    “Huber said that during a trip to Washington, D.C., last week, he had “some pretty receptive ears” and he was encouraged to submit grant proposals to study the issue further.”

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    1. There are lots of ways to get research funding, and Huber’s approach is one of them.

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    2. Some of Huber’s quotes in this story suggest that he already has his conclusion in mind and is trying to find evidence to support it. Anyone notice how the sequencing effort for this organism is fraught with delays, yet when a brand new E. coli was discovered in Germany, is took all of 3 days to sequence and assemble the entire thing? And this is supposed to be smaller than an E. coli.

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       1. Didn’t you mean he has his “hypothesis” in mind. Of course he does.

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       2. You are right in that it is just a hypothesis. However from following his promotion of this mystery pathogen and from talking directly to him he has no evidence that it is actually linked to GE, yet, he says, it must be due to GE because in his view, that is the ‘only thing that has changed’. He has already made a conclusion, and is actively promoting that explanation. Scientists with hypotheses say they are just hypotheses and also offer alternate explanations.

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16. A former Purdue University professor says it will be a few more months before he can support his claim that Roundup Ready technology is responsible for the proliferation of a previously unknown microscopic organism he says causes plant diseases and livestock abortions.

    One would expect then that it would be a few more months before we hear anything about it – surely nobody of his stature would go around making unsuppor… oh wait, I remember this thread! Nevermind!

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17. I have heard Dr. Huber has been contacted by 60 mins. and they are planning a hit piece on RU and GMO’s some time in Dec. I was also pondering if Dr. Huber’s position here is being tainted in some way do to the fact he is a devout Mormon?

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    1. That’s the first time I’ve heard that he had any religious affiliation at all, so I don’t believe that has anything to do with it.

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18. Hello,
    I have been a very busy little bee, so haven’t posted for a while. Here is the reason, the doi for our new study Observations Of Brachygnathia Superior in Wild ruminants in Western Montana, USA
    J.A. Hoy1, G.T. Haas2, R.D. Hoy1 & P. Hallock3,*
    Wildl. Biol. Pract., 2011 December 7(2): ..-.. doi:10.2461/wbp.2011.7.13
    I think you will find it of interest.
    Thank you,
    Judy Hoy

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    1. Hi Judy. This could be interesting, but doesn’t relate to the post. You might get a better response if you start a topic in the forum so people could discuss this item.

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19. A friend of mine has stopped eating soy, beef and corn because of Dr. Mercola’s claims here: http://www.goodfoodworld.com/2011/12/dr-huber-expert-in-microbial-ecology-discusses-the-effects-of-genetically-modifying-plants/
    I would appreciate an analysis.

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    1. I don’t understand. This post is the analysis of the claims that there is a new microorganism. In short – no one has shown any evidence that one exists.

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    2. My analysis suggests your friend is a fool for changing any sort of habits on the advice of Mercola.
       Plus what Anastasia said.

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20. A&E,
    What I’d appreciate is information/opinion on the level of credibility Dr. Huber should be afforded re this video (and PT-2): it’s looong and full of shocking assertions that should be testable/corroborable, just like the “µfungus” issue. For example, he claims that glyphosate works by chelating Manganese, that crops subjected to it are non-healthy, non-healthful, non-nutritious, dangerous, that it bio-accumulates, etc. I didn’t have time to closely attend to the whole video, but I think claims of livestock infertility were in there, whether still attributed to the mystery organism or not.
    Dr. Mercola is seen as a populist hero, like Oprah, but I am somehow neither knowledgeable nor familiar with his material.

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    1. I think some of that is covered above – claims that glyphosate works by chelating Manganese are simply wrong – it can chelate manganese (as far as I know) but its mode of action is well established – it inhibits EPSPS which is an enzyme in the pathway which synthesizes various amino acids – block this and the plant dies – stick in the same enzyme but modified such that glyphosate doesn’t inactivate and the plant doesn’t die (if the MoA was Mn chelation then RR crops wouldn’t work)
       Although from what I remember of Huber he didn’t make that claim, his claim was that glyphosate also chelates Mn and as such leads to health issues – which I believe Henry and I went on, and on, and on about above (or elsewhere)
       From what I recall the infertility claims were around the micro-organism (the impossibly small one, the fungus that’d be smaller than its constituent organelles) – again part of the fantastic nature of the claims, not only was the organism claimed impossibly small, but it also had cross-kingdom impact.
       Oddly Huber still hasn’t published on this matter – odd that as we’re approaching 1 year since this post was made and thus a little longer since the claims themself were made – surely nobody would be making such outlandish claims without at least having the evidence in order and somewhat close to being able to publish. It’s almost as if he just made it all up.

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21. In the video, at 4:40, Dr. Huber explicitly attributes herbicide activity, specifically glyphosate’s, to chelation. By 8:00 he’s implied that it has the same effect in US. At 10:16 he is explicit that “critical micronutrients” are reduced (by 80-90%) for animal nutrition. The idea is then flogged by Mercola (including “animal fertility”). Then they go on to discuss the serious damage glyphosate supposedly causes to soil, soil microorganisms and nitrogen fixation. And then on to it causing increases in plant diseases, including botulism(!).

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    1. How glad I am then that I don’t watch videos!
       If that is his explanation for the herbicidal activity he is dead wrong – that hypothesis is killed utterly by the simple fact that adding in the enzyme which glyphosate binds to, but without the binding (or whatever the difference is… I think it lacks a binding site – whatever it is you end up with more activity) leads to survival. Also one of the mdoes of glyphosate resistance in weeds is massive overexpression of EPSPS – again, if Mn chelation was the culprit this wouldn’t explain why the weeds survive.
       The micronutrient piece of the puzzle is getting massively overblown – from memory there may be issues in Mn depleted soil (as glyphosate does bind some Mn for sure) – but in Mn replete soil the issue is non-existant – all claims appear to be similarly overblown.
       This isn’t unexpected with Mercola – he’s a quack extraordinaire.

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22. At 22:50, “glyphosate accumulation”
    I would comment that the molar quantity of a given ion is vastly greater than that of the chelator (glyphosate) present, then how can the chelator have any significant effect at all?

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23. I’m curious, have any farmers contributed to this discussion? How many of you who have contributed have grown fruit/vegetable/grain crops or used GM crops in anything other than a home garden or a trial?

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24. Pingback: ‘Genetic Roulette, the movie’ a review | Jim's Kitchen Lab
25. Pingback: Anti-, problems with, etc GMO foods - Page 6 - Homesteading Today

26. SO I see Anastasia, Ewan and Karl are all at it again. Haven’t you all figured out that all the universities where you are learning are bought and paid for by BIG AG, and Monsanto? Who do you think provides your curriculum? BIAS!!!! Its been 20 years since horizontal gene transfer has been played with and while you have made progress in so far as exact placement of a gene, it still stands that you don’t know everything and you never will… your big college words will not change the fact that the Human Genome project completed in 2002 failed dramatically to identify one gene for every one protein in the human body, forcing researchers to look to epigenetic factors — namely, “factors beyond the control of the gene” – to explain how organisms are formed, and how they work.. Im sure by now you are taught that that any gene can give more than one protein and that inserting a gene anywhere in a plant eventually creates rogue proteins. Some of these proteins are obviously allergenic or toxic.” Well here is some scientific evidence, Im sure you’ll try to poke as many holes as possible, but, ultimately, you guys should open your eyes.
    http://www.mdpi.com/1099-4300/15/4/1416
    Glyphosate’s Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases
    Anthony Samsel 1 email and Stephanie Seneff 2,* email
    1 Independent Scientist and Consultant, Deerfield, NH 03037, USA 2 Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge, MA 02139, USA
    * Author to whom correspondence should be addressed.
    Received: 15 January 2013; in revised form: 10 April 2013 / Accepted: 10 April 2013 / Published: 18 April 2013
    (This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
    PDF Full-text Download PDF Full-Text [518 KB, uploaded 18 April 2013 14:15 CEST]
    Abstract: Glyphosate, the active ingredient in Roundup®, is the most popular herbicide used worldwide. The industry asserts it is minimally toxic to humans, but here we argue otherwise. Residues are found in the main foods of the Western diet, comprised primarily of sugar, corn, soy and wheat. Glyphosate’s inhibition of cytochrome P450 (CYP) enzymes is an overlooked component of its toxicity to mammals. CYP enzymes play crucial roles in biology, one of which is to detoxify xenobiotics. Thus, glyphosate enhances the damaging effects of other food borne chemical residues and environmental toxins. Negative impact on the body is insidious and manifests slowly over time as inflammation damages cellular systems throughout the body. Here, we show how interference with CYP enzymes acts synergistically with disruption of the biosynthesis of aromatic amino acids by gut bacteria, as well as impairment in serum sulfate transport. Consequences are most of the diseases and conditions associated with a Western diet, which include gastrointestinal disorders, obesity, diabetes, heart disease, depression, autism, infertility, cancer and Alzheimer’s disease. We explain the documented effects of glyphosate and its ability to induce disease, and we show that glyphosate is the “textbook example” of exogenous semiotic entropy: the disruption of homeostasis by environmental toxins.

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