Glyphosate and the Gut Microbiome: Another Bad Argument Annihilated


Glyphosate is a broad spectrum herbicide that was first introduced by the Monsanto company in the 1970s under the brand name Roundup. The already popular product grew even more popular among farmers upon the introduction of various commodity crops which were genetically engineered to resist the herbicide while it killed the surrounding weeds with which the crops would otherwise compete for water and nutrients. Glyphosate went off patent back in the year 2000, and since then many manufacturers have cashed in on its popularity [1]. Although it is of unusually low toxicity, glyphosate receives a level of scrutiny and vehemence of criticism that is disproportionate to its actual established risks [2],[3],[4]. This is attributable in part to its ubiquity in modern conventional farming, but it’s likely even more attributable to its association with Monsanto, against which a large and well-organized counter-movement has emerged [5].

Consequently, many different arguments have been formulated and circulated among this counter-movement and beyond. The purpose of this piece is address one of those arguments in particular. More specifically, on numerous occasions I have heard glyphosate critics argue that glyphosate should be opposed because it might alter the microbiome in humans. In a post on his facebook page, The Mad Virologist discussed a recently published study on the effects of glyphosate on gut microorganisms, and inspired me to unpack the microbiome argument against glyphosate and explain what’s wrong with it.


Glyphosate binds to and inhibits the action of an enzyme known as EPSP synthase, which plants need in order to make three important aromatic amino acids: phenylalanine, tyrosine, and tryptophan via what’s known as the shikimic acid pathway, which occurs in plants, bacteria, fungi, algae and some protozoan parasites [6],[7]

Image c/o Zucko et al 2010 [37].

Glyphosate does this by acting as what’s called an uncompetitive inhibitor. That means that it can only bind to the enzyme-substrate complex – the substrate being shikimate-3-phosphate in this case – and cannot bind the enzyme when the substrate is unbound [8],[9]. Upon binding to the enzyme-substrate complex, glyphosate prevents the complex from forming its product, 5-enopyruvylshikimate-3-phosphate (EPSP). Normally the complex would form EPSP by reacting with another molecule called phosphoenol pyruvate (PEP), but sufficient concentrations of glyphosate reduces the number of units of the enzyme-substrate complex available to form their product. The shikimic acid pathway doesn’t exist in us. Humans and other mammals, for example, can’t make those amino acids at all to begin with, so we get them directly from our food. Plants need those amino acids in order to grow and to make proteins, so if they are unable to synthesize them, they can’t grow, and therefore they die.

Additionally, mammals such as ourselves have lived in co-evolutionary association with myriad microorganisms whose aggregate is referred to as the microbiome. The roles of the microbiome in human health and the effects resulting from changes in its composition are active areas of scientific investigation [33].

Image: retrieved from

However, our collective knowledge of the relationship between the microbiome and human health is still in its infancy. Consequently, the topic is an easy target for exploitation by proponents of pseudoscience who would leverage it as a promotional tool for their own agendas, and/or extrapolate to claims which overstep what the current body of scientific literature actually supports [34],[35],[36].

The Gut Microbiome Argument Against Glyphosate

Keeping that in mind, the reasoning underlying the gut microbiome argument against glyphosate can be summarized as follows:

1. The makeup of a person’s gut microbiome is relevant to human health in ways which are only recently starting to be elucidated.

2. Bacteria possess the shikimic acid pathway and can use it to synthesize aromatic amino acids.

3. Glyphosate inhibits a key enzyme used in the shikimic acid pathway.

4. Therefore, glyphosate might be altering people’s microbiome in detrimental ways.

Simple enough?


Is This Argument Biologically Plausible?

However, the problem is that this argument flies in the face of one of the basic principles of microbiology: that microbes grow in the presence of abundant nutrients. As I’ve explained on several occasions when this has come up in my facebook comment sections, bacteria shouldn’t need to synthesize aromatic amino acids when they are literally bathing in them in the gut, therefore this argument against glyphosate is grasping at straws and not plausible. A recent study tested this more formally (in vivo) [10].

How did I know in advance that this was extremely unlikely to be a major issue before this research? It was because I knew that gut bacteria live in… Wait for it… the GUT!!! Where aromatic amino acids are abundant. That means they will continue to grow if the final product of a given biosynthetic pathway is supplemented to them – which is what we are doing by supplementing them with aromatic amino acids through the food we eat – even in the presence of something that inhibits that specific pathway.

This principle is the basis for experiments that allow scientists to functionally characterize which genes’ enzymes act on which substrates in a given biochemical pathway (called functional complementation analysis), and has been in common use for the last century or so as a method for ascertaining the specific steps of varous metabolic pathways, and/or the genes which code for the enzymes which catalyze each reaction [11],[12],[13],[14].

For an example of how this immersion technique has been used, consider the elucidation of the arginine synthesis pathway in N. crassa fungi by Srb et al 1944 [15]. The authors used radiation to induce mutations in the cells, and then performed a genetic screen to isolate those with mutations relevant to the arginine synthesis pathway. This was accomplished by growing colonies of mutants in a medium which included arginine, and then in one which lacked arginine. Cells which grew in an arginine-containing medium but not without it were deemed incapable of synthesizing their own arginine, and were subsequently grown under four different conditions:

  1. In a medium lacking ornithine, citrulline, and arginine.
  2. The same medium as 1, except supplemented with ornithine only (no citrulline or arginine).
  3. The same medium as 1, except supplemented with citrulline only (no ornithine or arginine).
  4. The same medium as 1, except supplemented with arginine only (no ornithine or citrulline).

The results were as follows: 

Image c/o Biological Science 4th ed [16].

This implied that there were three types of mutants. Some had mutations preventing them from producing functional copies of the enzyme responsible for catalyzing the reaction to produce ornithine from its precursor, some for the enzyme responsible for catalyzing the reaction to produce citrulline from ornithine, and some for the enzyme responsible for catalyzing the reaction to produce arginine from citrulline. This is a simple textbook example, but the point here is that supplementing cells with the end product of a metabolic pathway negates the need for the cell to synthesize it itself through that pathway. This particular example used bread mold, but the same principle applies to bacteria.

Moreover, the Shikimic acid pathway is also metabolically expensive, so it’s not likely that the bacteria are actively using this pathway in the presence of abundant aromatic amino acids (i.e. phenylalanine, tyrosine, and tryptophan), especially when they are in competition with other microbes [17]. So, unless the person (the host) is literally starving to death, then it is far more likely gut bacteria are taking them in the easy way by just absorbing them from their environment.

If the host actually is literally starving to death or suffering from severe malnutrition, then they have far bigger and more urgent problems to worry about than their gut microbiome. Starvation and severe malnutrition themselves cause harm [18]. Consequently, parsing out and identifying harm to the host attributable to malnutrition and distinguishing it from harm to the host due to glyphosate-induced alterations to the microbiome would be problematic, especially considering that any hypothetical problems caused by the latter would be avoided by mitigating or preventing the former.

None of this is new or controversial, which is part of the reason why researchers never bothered with a full blown in vivo experiment until recently on the effects of glyphosate on the microbiome. It is also the reason why the results of the recent study should not be surprising.

Earlier Studies

Earlier studies on glyphosate’s effects on bacteria were either full of methdological problems, and/or not setup in such a way as to test the question of how it affects the microbiome in vivo, where aromatic amino acids are abundant. I’ll start with the lowest hanging fruit before dealing with more credible studies, for which the strengths and limitations are more subtle.

Samsel and Seneff

Computer scientist Stephanie Seneff is an anti-vaccine, anti-GMO, and anti-glyphosate activist who claims that GMO foods cause concussions and suggests that glyphosate in vaccines have contributed to school shootings and the Boston Bombing [19],[20]. Seriously, you can’t even make this shit up, but I digress. She and her co-author, a retired consultant by the name of Anthony Samsel, published a series of papers in a predatory pay-to-play journal (entropy) implicating glyphosate in a whole host of conditions (including celiac disease, MS, Parkinson’s, cancer, and autism), many of which involved convoluted non-sequitur arguments based on glyphosate’s alleged effects on the microbiome [21],[22]. Eric from Skeptoid has meticulously broken down the plethora of flaws and red flags in that paper, which would take way too long to reiterate here [23]. To get an idea of just how terrible that paper is, Thoughtscapism points out that it has actually been used as an example of how to spot bogus science journals: a little factoid I found far too hilarious to omit [24],[22].

Other Earlier Studies

This 1986 study showed significant growth inhibition, but only at glyphosate concentrations on the order of a millimolar or more, which is thousands of times the amounts realistically occurring in the gut from food [25]. To put this into perspective, legumes are the food crop with the highest allowed pesticide residue limit in the US (5.0 ppm) [26]. 5.0 ppm = 5.0 mg of glyph/kg of legumes, and glyphosate has a molar mass of 169.07 g/mol.

So, if we estimate that an average full stomach is roughly 1 L in volume while assuming homogeneous distribution, then we get that millimolar concentrations in the gut would involve (1 L)*(10^-3 mol of glyph/L)*(169.07 g of glyph/mol of glyph)*(10^3 mg/g) = 169.07 mg of glyphosate.

If we then assume the maximum permissible amount of glyphosate on the food crop with the highest maximum allowable glyphosate residue limit, we can calculate that millimolar concentrations in the gut by dividing the mass of glyphosate required to achieve millimolar concentrations by the mass of glyphosate per unit of mass of legumes at the maximum allowable residue limits.

When we do that, we find that it would require ingesting about 33.8 kg of legumes (or about 74.5 lbs).

i.e. (169.07 mg glyph)/(5.0 mg of glyph/kg of legumes) = 33.8 kg of legumes.

This of course assumes 100% absorption, which, as neuroscientist/geneticist/toxicologist, Alison Bernstein (aka Mommy, PhD) explains here, is actually not the case. So, the actual amount of legumes required to reach such concentrations in the gut may actually be many times higher than my sample estimate.

As Thoughtscapism points out, even at those extreme doses, the bacteria were not killed, but rather grew at a slower rate, and even that effect was partially mitigated when the researchers supplemented the bacteria with aromatic amino acids to simulate conditions likely to occur in the gut [27]. This 2010 study suffered from similar limitations [28].

Similarly, the following study showed a significant reduction in colony forming units (CFU) in vitro, but the concentrations were again on the order of a millimolar (and up to 29.5 mM), and no aromatic amino acids were supplemented to any of the test groups, which again means that it cannot be extrapolated to the gut microbiome where aromatic amino acids are abundant [29].

The Danish Study

In the new study, researchers from Denmark mapped the microbiome of Sprague Dawley rats using next generation sequencing techniques both before and after exposure both to high doses glyphosate and a commercial glyphosate formulation [10]. The researchers found that even doses 50 times that European Acceptable Daily Intake value (ADI = 0.5 mg/kg of body mass) had limited effects on microbiome composition over the course of two weeks, and that glyphosate’s effects on prototrophic bacteria growth was highly dependent on the availability of aromatic amino acids in the intestinal environment. If you are thinking that two weeks isn’t very long, you have to consider the fact that the average generational time for bacteria is roughly on the order of about 20-30 minutes (or often even less). That means that two weeks represents something on the order of (2 wks)*(7 days/wk)*(24 hrs/day)*(2-3 generations/hr) = 672–1,008 generations. Given the life expectancy of Sprague Dawley rats relative to humans, this duration is also comparable to roughly a year and a half in the life of a human [30].

What this means is that anyone continuing to promote the wrongheaded argument that glyphosate can affect health by altering the composition of the microbiome will have to hypothesize a completely new mechanism by which this is supposed to occur (preferably a biologically plausible one). This is because the reasoning behind this argument is based on the premise that glyphosate-induced inhibition of the shikimic acid pathway in gut microorganisms should prevent them from growing due to their (wrongly) assumed dependence on it for the synthesis of aromatic amino acids. This hypothesis predicts that hundreds of generations of bacteria should not be permitted to grow normally if this effect is occurring to any meaningful degree. The evidence falsifies this prediction.


The claim that glyphosate harms human health via disruption of the microbiome was never a biologically plausible one, because it only makes sense when the system is not being viewed as a whole. Ironically, glyphosate and GE food opponents like to say that they take a holistic approach, but this is not a holistic argument, because it ignores the environment in which the microbiome exists.

We know that organisms don’t bother synthesizing compounds they can already get from their environment. Knocking out one step of a biochemical pathway and growing microorganisms on different media with various substrates is a tried and true classical method for identifying which substrates are involved in a given pathway and/or the enzymes which catalyze their reactions. We also know that the human gut contains abundant aromatic amino acids alleviating the need for resident microorganisms to synthesize them. Running out of them is not a concern because they are replenished multiple times per day. The exception to this would be cases of starvation or malnutrition, in which case malnutrition would be the problem to address: not glyphosate. Despite this, in vivo research has been done, and reaffirms exactly what theoretical predictions would imply. Gut microorganisms grew and replicated for hundreds of generations, thus contradicting the predictions of the hypothesis under discussion.

In order to continue to argue that glyphosate had some other negative effect on the microbiome which would be undetectable within the first several hundred or more generations, a contrarian would have to either postulate a different mechanism by which this could be rendered into a testable scientific hypothesis, or appeal to vague and unspecified unknowns.

In the former case, this would constitute an abandonment of the original argument in place of a new hypothesis leading to predictions distinct from those of the hypothesis under discussion. Essentially, this would mean conceding (either explicitly or implicitly) that the original claim was false (or at least not supported), and then moving the goalpost to a new claim based on a different mechanism.

In the latter case, such vague and half-baked speculation could be applied just as easily to virtually anything. It makes no specific postulates and thus makes no testable predictions, and is therefore unscientific. It is what we sometimes refer to as “not even wrong” [31].

– Cred Hulk

For more on glyphosate and common myths about it, Thoughtscapism has put together the most comprehensive piece I’ve ever seen on the subject for a general audience [32].


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[3] Hulk, C. (2015). Glyphosate toxicity: Looking past the hyperbole, and sorting through the facts. By Credible HulkThe Credible Hulk. Retrieved 10 December 2017, from

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[5] Millions march against GM crops. (2013). the Guardian. Retrieved 10 December 2017, from

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[7] Starcevic, A., Akthar, S., Dunlap, W. C., Shick, J. M., Hranueli, D., Cullum, J., & Long, P. F. (2008). Enzymes of the shikimic acid pathway encoded in the genome of a basal metazoan, Nematostella vectensis, have microbial origins. Proceedings of the National Academy of Sciences105(7), 2533-2537.

[8] Sammons, R. D., Gruys, K. J., Anderson, K. S., Johnson, K. A., & Sikorski, J. A. (1995). Reevaluating glyphosate as a transition-state inhibitor of EPSP synthase: Identification of an EPSP synthase. cntdot. EPSP. cntdot. glyphosate ternary complex. Biochemistry34(19), 6433-6440.

[9] Alibhai, M. F., & Stallings, W. C. (2001). Closing down on glyphosate inhibition—with a new structure for drug discovery. Proceedings of the National Academy of Sciences98(6), 2944-2946.

[10] Nielsen, L. N., Roager, H. M., Frandsen, H. L., Gosewinkel, U., Bester, K., Licht, T. R., … & Bahl, M. I. (2018). Glyphosate has limited short-term effects on commensal bacterial community composition in the gut environment due to sufficient aromatic amino acid levels. Environmental Pollution233, 364-376.

[11] Hudson, A. O., Harkness, T. C., & Savka, M. A. (2016). Functional Complementation Analysis (FCA): A Laboratory Exercise Designed and Implemented to Supplement the Teaching of Biochemical Pathways. JoVE (Journal of Visualized Experiments), (112), e53850-e53850.

[12] Sohaskey, C. D., & Wayne, L. G. (2003). Role of narK2X and narGHJI in hypoxic upregulation of nitrate reduction by Mycobacterium tuberculosis. Journal of bacteriology185(24), 7247-7256.

[13] Smits, T. H., Balada, S. B., Witholt, B., & van Beilen, J. B. (2002). Functional analysis of alkane hydroxylases from gram-negative and gram-positive bacteria. Journal of bacteriology184(6), 1733-1742.

[14] Salcedo, E., Cortese, J. F., Plowe, C. V., Sims, P. F., & Hyde, J. E. (2001). A bifunctional dihydrofolate synthetase–folylpolyglutamate synthetase in Plasmodium falciparum identified by functional complementation in yeast and bacteria. Molecular and biochemical parasitology112(2), 239-252.

[15] Srb, A., & Horowitz, N. H. (1944). The ornithine cycle in Neurospora and its genetic control. Journal of Biological Chemistry154(1), 129-139.

[16] Freeman, S. (2017). Biological Science (6th ed.). Edinburgh Gate Harlow Essex CM20 2JE England. Pearson Education.

[17] Hibbing, M. E., Fuqua, C., Parsek, M. R., & Peterson, S. B. (2010). Bacterial competition: surviving and thriving in the microbial jungle. Nature Reviews Microbiology8(1), 15-25.

[18] Correia, M. I. T., & Waitzberg, D. L. (2003). The impact of malnutrition on morbidity, mortality, length of hospital stay and costs evaluated through a multivariate model analysis. Clinical nutrition22(3), 235-239.

[19] Seneff Claims GMOs Cause Concussions. (2015). Science-Based Medicine. Retrieved 10 December 2017, from

[20] Who is Stephanie Seneff?. (2017). VAXOPEDIA. Retrieved 10 December 2017, from

[21] Anthony Samsel (n.d.) LinkedIn [Profile page]. Retrieved Dec 10. 2017, from

[22] A guide to detecting bogus scientific journals. (2015). Sci-Phy. Retrieved 10 December 2017, from

[23] Roundup and Gut Bacteria. (2013). Skeptoid. Retrieved 10 December 2017, from

[24] →, V. (2016). 2.-3. Glyphosate and Health Effects A-ZThoughtscapism. Retrieved 10 December 2017, from

[25] Fischer, R. S., Berry, A. L. A. N., Gaines, C. G., & Jensen, R. A. (1986). Comparative action of glyphosate as a trigger of energy drain in eubacteria. Journal of bacteriology168(3), 1147-1154.

[26] (2017). Retrieved 10 December 2017, from

[27] →, V. (2016). 4. Does Glyphosate Harm Gut Bacteria?Thoughtscapism. Retrieved 10 December 2017, from

[28] Ahemad, M., & Khan, M. S. (2011). Toxicological effects of selective herbicides on plant growth promoting activities of phosphate solubilizing Klebsiella sp. strain PS19. Current microbiology62(2), 532-538.

[29] Shehata, A. A., Schrödl, W., Aldin, A. A., Hafez, H. M., & Krüger, M. (2013). The effect of glyphosate on potential pathogens and beneficial members of poultry microbiota in vitro. Current microbiology66(4), 350-358.

[30] Andreollo, N. A., Santos, E. F. D., Araújo, M. R., & Lopes, L. R. (2012). Rat’s age versus human’s age: what is the relationship?. ABCD. Arquivos Brasileiros de Cirurgia Digestiva (São Paulo)25(1), 49-51.

[31] Burkeman, O. (2005). Briefing: Not even wrongthe Guardian. Retrieved 10 December 2017, from

[32] 17 Questions About Glyphosate. (2016). Thoughtscapism. Retrieved 10 December 2017, from

[33] Wang, Y., & Kasper, L. H. (2014). The role of microbiome in central nervous system disorders. Brain, behavior, and immunity38, 1-12.

[34] Germ theory denialism and the magical mystical microbiome – RESPECTFUL INSOLENCE. (2015). RESPECTFUL INSOLENCE. Retrieved 10 December 2017, from

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[36] Gut Check. Probiotics and Metabiome.. (2015). Science-Based Medicine. Retrieved 10 December 2017, from

[37] Zucko, J., Dunlap, W. C., Shick, J. M., Cullum, J., Cercelet, F., Amin, B., … & Long, P. F. (2010). Global genome analysis of the shikimic acid pathway reveals greater gene loss in host-associated than in free-living bacteria. BMC genomics11(1), 628.


The One True Argument™

Anyone who has spent much time addressing a lot of myths, misconceptions, and anti-science arguments has probably had the experience of some contrarian taking issue with his or her rebuttal to some common talking point on the grounds that it’s not the “real” issue people have with the topic at hand. It does occasionally happen that some skeptic spends an inordinate amount of time refuting an argument that literally nobody has put forward for a position, but I’m specifically referring to situations in which the rebuttal addresses claims or arguments that some people have actually made, but that the contrarian is implying either haven’t been made or shouldn’t be addressed, because they claim that it’s not the “real” argument. This is a form of No True Scotsman logical fallacy, and is a common tactic of people who reject well-supported scientific ideas for one reason or another. In some cases this may be due to the individual’s lack of exposure to the argument being addressed rather than an act of subterfuge, but it is problematic regardless of whether or not the interlocutor is sincere.

The dilemma is that there are usually many arguments for (and variations of) a particular position, so it’s not usually possible for someone to respond to every possible permutation of every argument that has ever been made against a particular idea (scientific or otherwise). The aforementioned tactic takes advantage of this by implying that the skeptic is attacking a strawman on the grounds that what they refuted was not the “real” main argument for their position. In comment sections on my page, I’ve referred to this as The One True ArgumentTM fallacy. It’s a deceptive way for the contrarian to move the goalpost while deflecting blame back onto the other person by accusing them of misrepresentation. The argument being addressed has been successfully refuted, but instead of acknowledging that, the interlocutor introduces a brand new argument (often just as flawed as the one that was just deconstructed), and accuses the person debunking it of either not understanding or not addressing The One True ArgumentTM.

Some brands of science denial have brought this to the level of an integrative art form. If argument set A is refuted, they will cite argument set B as The One True ArgumentTM, but if argument set B is refuted, they will either cite argument set A or argument set C as The One True ArgumentTM. If argument sets A, B, and C are all refuted in a row, they’ll either bring out argument set D, or they will accuse the skeptic of relying on verbosity, and will attempt to characterize detailed rebuttals as some sort of vice or symptom of a weak argument (even though the skeptic is merely responding to the claimant’s arguments). I really wish I was making this up, but these are all techniques I’ve seen science deniers use in debates on social media or on their own blogs. Of course, the volume of the rebuttal cannot be helped due to what has come to be known as Brandolini’s Law AKA Brandolini’s Bullshit Asymmetry Principle (coined by Alberto Brandolini), which states that the amount of energy necessary to refute bullshit is an order of magnitude bigger than to produce it.

The argumentation tactics of sophisticated science deniers and other pseudoscience proponents (or even the less sophisticated ones) could probably fill an entire book, but this is one that I haven’t seen many people address, and it comes up fairly often.

For example, many opponents of genetically engineered food crops claim that they are unsafe to eat, and that they are not tested. Often when someone takes the time to show that they are actually some of the most tested foods in the entire food supply, and that the weight of evidence from decades of research from scientists all across the world has converged on an International Scientific Consensus that the commercially available GE crops are at least as safe and nutritious as their closest conventional counterparts, the opponents will downplay it as not being the “real” issue. In some cases they will appeal to conspiracy theories or poorly done outlier studies that have been rejected by the scientific community, but in other instances they will invoke The One True ArgumentTM fallacy. They will claim that nobody is saying that GMOs are unsafe to eat, and that the problem is the overuse of pesticides that GMOs encourage, or that the problem is that the patents and terminator seeds allegedly permit corporations to sue farmers for accidental cross contamination and monopolize the food supply by prohibiting seed saving.

Of course, these arguments are similarly flawed. GMOs have actually helped reduce pesticide use: not increase it, (particularly insecticides) [1],[2],[3], and have coincided with a trend toward using much less toxic and environmentally persistent herbicides [4]. Plant patents have been common in non-GMO seeds too since the Plant Patent Act of 1930, terminator seeds were never brought to market, the popularity of seed saving had already greatly diminished several decades before the first GE crops, and there are still no documented cases of non-GMO farmers getting sued by GMO seed companies for accidental cross-contamination.

However, although the follow up arguments are similarly flawed, the fact is that many organizations absolutely are claiming that genetically engineered food crops are unsafe. I’m not going to give free traffic to promoters of pseudoscience if I can help it, but one need only to plug in the search terms “gmo + poison” or “gmo + unsafe” to see a plethora of less-than-reputable websites claiming precisely that. The point is that it’s dishonest to pretend that the person rebutting such claims isn’t addressing the “real” contention, because there is no one single contention, and the notion that the foods are unsafe is a very common one.

Another example occurred just the other day on my page. I posted a graphic depicting some data showing how effective vaccines have been at mitigating certain infectious diseases. A commentator responded as shown here:

I responded thusly:

Putting aside the fact that information on vaccine ingredients is easy to obtain (they are laid out in vaccine packaging inserts), and the fact that increasing life expectancy and population numbers suggest that, if there is any nefarious plot to depopulate the planet, the perpetrators have been spectacularly unsuccessful so far, the point is that this exemplifies The One True ArgumentTM tactic.

Another common example is when scientists meticulously lay out the arguments and evidence for how we know that global warming and/or climate change are occurring. There are many common contrarian responses to this, some of which employ the One True Argument fallacy, such as when the contrarian claims that nobody actually rejects the claim that the change is occurring, bur rather they doubt that human actions have played any significant role in it.

Of course, the follow up claim is similarly flawed, since we know that climate changes not by magic but rather when acted upon by physical causes (called forcings), none of which are capable of accounting for the current trend without the inclusion of anthropogenically caused increases in atmospheric concentrations of greenhouse gases such as CO2. This is because most of the other important forcings have either not changed much in the last few decades, or have been moving in the opposite direction of the trend (cooling rather than warming). I’ve explained how solar cycles, continental arrangement, albedo, Milankovitch cycles, volcanism, and meteorite impacts can affect the climate with hundreds of citations from credible scientific journals here, here, here, here, here, here, here, here, here, here, here, and here.

 In this instance, although it has become more common than in the past for climate science contrarians to accept the conclusion that climate has been changing but reject human causation, there are still plenty who argue that the warming trend itself is grand hoax, and that NASA, NOAA, (and virtually every other scientific organization on the planet) has deliberately manipulated the data to make money. If you doubt this, all you need to do is enter “global warming + hoax + fudged data” into your favorite search engine to see an endless list of webmasters making this claim. In fact, in one study, the position that “it’s not happening” at all was the single most common one expressed in op-ed pieces by climate science contrarians between 2007 – 2010 [10]. Their abundance even increased towards the end of that time period, so it’s flat out untrue that the push-back against the science has centered only on human causation and/or the eventual severity of the problem. 

The truth is that there was never anything nefarious going on with the temperature data adjustments. Similar adjustments are performed on data in most scientific fields. They were completely legitimate and scientifically justified. There have even been additional studies in which the assumptions and reasoning behind the ways in which the data was adjusted have been scrutinized and compared to data from reference networks, and the same procedures produced readings that were MORE accurate than the raw non-adjusted data: not less [5],[6],[7].[8].[9]. This is nicely explained here, but I digress; the main point here is not just that the follow-up arguments tend to be similarly flawed, but rather that this technique could in principle be used indefinitely to move the goal posts ad infinitum.

It’s easy to see that this also forces a strategic decision on the part of the skeptic or science advocate. Do you nail them down on their use of this tactic? Do you respond to the follow-up argument they’ve presented as the “real” issue? Do you do both? If so, are there any strategic disadvantages to doing both? Would it make the response excessively long? If so, does that matter? If so, how much can it be compressed by improved concision without sacrificing accuracy and/or important details? Disingenuous argumentative tactics like these put the contrarian’s opponents in a position where he or she has to make these kinds of strategic decisions rather than simply focusing on the veracity of specific claims.

As I alluded to earlier, this is not a free license to construct actual strawmen of other people’s positions and ignore their explanations when they attempt to clarify their arguments and their conclusions, because people do that too, and that’s no good either. But the One True ArgumentTM fallacy refers specifically to when a refutation to a common argument is mischaracterized as a strawman as a means of introducing a different argument while trying to construe it as the skeptic’s fault for addressing the argument they addressed instead of some other one. It’s dishonest, it’s based on bad reasoning, you shouldn’t use it, and you should point it out when others do. 


[1] Brookes, G., & Barfoot, P. (2017). Environmental impacts of genetically modified (GM) crop use 1996–2015: impacts on pesticide use and carbon emissions. GM crops & food, (just-accepted), 00-00.

[2] Klümper, W., & Qaim, M. (2014). A meta-analysis of the impacts of genetically modified crops. PloS one9(11), e111629.

[3] National Academies of Sciences, Engineering, and Medicine. (2017). Genetically Engineered Crops: Experiences and Prospects. National Academies Press (pg. 117-119).

[4] Kniss, A. R. (2017). Long-term trends in the intensity and relative toxicity of herbicide use. Nature communications8, 14865.

[5] Jones, P. D., & Moberg, A. (2003). Hemispheric and large-scale surface air temperature variations: An extensive revision and an update to 2001. Journal of Climate16(2), 206-223.

[6] Brohan, P., Kennedy, J. J., Harris, I., Tett, S. F., & Jones, P. D. (2006). Uncertainty estimates in regional and global observed temperature changes: A new data set from 1850. Journal of Geophysical Research: Atmospheres111(D12).

[7] Jones, P. D., Lister, D. H., Osborn, T. J., Harpham, C., Salmon, M., & Morice, C. P. (2012). Hemispheric and large‐scale land‐surface air temperature variations: An extensive revision and an update to 2010. Journal of Geophysical Research: Atmospheres117(D5).

[8] Hausfather, Z., Menne, M. J., Williams, C. N., Masters, T., Broberg, R., & Jones, D. (2013). Quantifying the effect of urbanization on US Historical Climatology Network temperature records. Journal of Geophysical Research: Atmospheres118(2), 481-494.

[9] Hausfather, Z., Cowtan, K., Menne, M. J., & Williams, C. N. (2016). Evaluating the impact of US Historical Climatology Network homogenization using the US Climate Reference Network. Geophysical Research Letters.

[10] Elsasser, S. W., & Dunlap, R. E. (2013). Leading voices in the denier choir: Conservative columnists’ dismissal of global warming and denigration of climate science. American Behavioral Scientist57(6), 754-776.


Genetic Engineering and the Emergence of Herbicide-Resistant Weeds

One of the more common criticisms leveled against Genetically Engineered plants, particularly Herbicide-Resistant (HR) strains, is that they are purported to lead to what critics refer to as “Superweeds.” The term superweeds is not a scientific term, and can be very misleading to people not familiar with the science. What is really meant by the term is the event in which local weeds become resistant to a particular mode of action undertaken by the farmer for the purpose of weed control. For instance, local weeds might evolve a resistance to a particular herbicide is it’s used often in the areas in which they grow. There’s nothing “super” about the alleged superweeds other than the fact that they’ve become resistant to one particular method.

That said, there are legitimate concerns over the evolution of weeds developing resistance to herbicides (such as glyphosate), or for that matter insects building resistance to a particular insecticide (such as Bt), but that’s an issue that affects all methods of pest control. It happens with all herbicides and insecticides, whether they’re organic, synthetic, or naturally produced by the plants, and can occur either via evolution with respect to certain local selection pressures (such as a high usage rate by farmers of a particular herbicide or insecticide), or via horizontal gene transfer. However, anti-GMO activists frequently try to frame the issue of resistant weeds as a uniquely GMO-related problem, (particularly in the case of glyphosate), which shows either ignorance and/or intellectual dishonesty of the anti-GMO movement.

Natasha Gilbert, the author of the following Nature article explains:

But herbicide resistance is a problem for farmers regardless of whether they plant GM crops. Some 64 weed species are resistant to the herbicide atrazine, for example, and no crops have been genetically modified to withstand it.”


As a matter of fact, even tilling weeds by hand can lead to resistant weeds. Indeed, one of the benefits of herbicide resistant crops is it makes it much easier to employ no-till farming, the benefits of which include a reduction in farming-related greenhouse gas emissions and and improved environmental impact quotient, as demonstrated here and here.

One particularly prominent example of herbicide-resistance arising via a combination of selective breeding and mutagenesis is the Clearfield line of plants developed by the BASF company. The Clearfield brand plants are resistant to a class of herbicides called acetolactate synthase inhibitors (or simply ALS inhibitors). ALS is an enzyme involved in the biosynthesis of the branched chain amino acids (leucine, isoleucine and valine) in many plants, fungi, algae, bacteria and yeasts. Resistance to ALS inhibitors has independently arisen multiple times in plants, and has done so by more than one mechanism.

In the case of BASF’s Clearfield line, my understanding of it is that they looked for instances in which a relevant ALS gene mutation had occurred naturally in wild plants sexually-compatible with the crops in which they wished to imbue the trait, and then bred the resistance to ALS inhibitors into their target plants over the course of a few generations, and crossed out any undesired phenotypes which came along for the ride. In cases for which no plants sexually-compatible with the target plant could be found with the desired ALS gene mutation, it was induced via mutagenesis. Mutagenesis is a plant breeding method whereby radiation and/or chemicals are used to speed up the rate of random genetic mutations in hopes that one of them will yield a desirable phenotype, in which case the plant with the desired mutation is kept and selectively bred. This was how ALS resistance was induced in wheat. Chris Barbey, a PhD student in plant molecular genetics and cell biology explains more about the aforementioned process here.

*As a side note, it’s worth keeping in mind that plants created in this manner are extremely common (here’s a registry of them), and are required to undergo no safety or allergy testing whatsoever, despite the fact that the changes induced are random, completely untracked, and the number of genes affected by the process is FAR greater than the number of genes typically altered in the case of modern molecular genetic engineering techniques. In the US, they are even permitted in organic farming (though the same is not true in most European countries). 

Ironically, while anti-GMO activists have been foretelling of the allegedly impending doom of glyphosate-resistant weeds arising from the use of glyphosate resistant GE crops, the number of resistant weeds arising in response to herbicides commonly employed on non-GE crops has been far greater (particularly in the case of the aforementioned ALS inhibitors, as well as triazines) as you can see below.

C/O Weed Control Freaks

c/o (click for the most updated version).

To add insult to injury, Chipotle, the popular restaurant chain which famously announced in 2015 that they’d be going completely GMO-free, used the avoidance of herbicide-resistant weeds as one of their primary justifications for rejecting GE foods. This was an additional irony due to the fact that now the foods they use almost certain to have been grown using pesticides FAR more likely to select for herbicide resistant weeds than the ones they replaced by rejecting GE foods. Their change over appears to have been based on a desire to capitalize on unfounded public trepidation towards genetically engineered foods, and is unlikely to have any positive effect with respect to toxicity, food safety, or the safety of pesticide applicators. Weed scientist, Andrew Kniss explains this development in more detail here.

Moreover, although weed resistance has slightly increased, the RATE at which herbicide resistant weeds have been developing since the rise in glyphosate resistant GMO crops has not increased. In fact, after the introduction of herbicide resistant GE crops, the number of new herbicide resistant weeds actually DECREASED to 11.4 documented cases per year. Practically speaking, the difference in the slopes (which represent the rate at which herbicide resistance develops) of the regression lines between the two time periods are probably not meaningful, but the point is that, based on the best data available, we can be quite certain that adoption of GE crops has NOT increased the rate at which resistant weeds have developed relative to other uses of herbicide.

The following graph presents the chronological increase in unique cases of herbicide resistant weeds. Glyphosate-Resistant GE crops were introduced to the commercial market in 1996, at which time they swiftly became popular. Notice how there is no increase in the steepness of the slope of the graph following their introduction.

Weed scientist, Andrew Kniss goes into greater depth on that here, as does this article here by my friend, Marc Brazeau, creator of Food and Farm Discussion Lab.

Now, it’s all fine and good to highlight the inconsistent logic and lack of adequate analysis of the facts on part of the critics of GE foods, but it seems rather unsatisfactory to merely point out that their criticism is an equally real problem for all crops, but a simple “tu quoque” only rebuts the unique application of the criticism to GE crops, but doesn’t really prescribe any viable means of dealing with the problem.

So what’s the solution?
Well, one crucial component appears to be increasing diversity of weed management protocols. Although there’s a critical caveat with the following recommendations based on recent research (more on that in a moment), according to weed science professors at the University of Wisconsin and Iowa State University, the following practices should help:

These weed management practices avoid the continuous and exclusive use of glyphosate and lessen the potential for developing glyphosate-resistant weeds:

  • Rotate between Roundup Ready® and conventional crops or crops with other types of herbicide resistance.
  • Use Roundup Ready® crops and glyphosate in your crop rotation where they have the greatest economic and management value.
  • Rotate glyphosate with herbicides that have different modes of action.
  • Apply a residual herbicide before glyphosate or tank mix another herbicide with glyphosate.
  • Avoid making more than two glyphosate applications to a field over a two-year period.
  • If glyphosate is used as a burndown treatment and in-crop in the same year, tank mix the glyphosate applied in the burndown treatment with an herbicide that has a different mode of action. The in-crop glyphosate application should still be rotated with other herbicides in other years.
  • Use cultivation and other mechanical weed management practices.
  • In addition, growers should apply glyphosate at labeled rates and at the correct stage of weed and crop growth to reduce the risk of poor control. Also, scout fields regularly, identify the weeds present, and record their locations on maps to allow a quick response to changes in weed populations.”

Here’s the caveat: although it was previously more common to believe that rotating herbicides would be a good strategy to slow the development of herbicide resistant weeds, there is some compelling new research which suggests otherwise. Instead, the superior strategy may be to use a second herbicide with a different mechanism of action concurrently rather than alternating between them. The data actually suggests that rotating them may exacerbate the onset of herbicide resistance.

This may seem counter-intuitive at first, but consider that mutations conferring resistance to a particular herbicidal mechanism of action are relatively rate as it is. If some weeds develop such resistance to one herbicide, then they have a chance to proliferate that trait throughout their population. Later, when the farmer rotates to another herbicide, there’s a chance that a few of the weeds in the local population (some of which already have evolved resistance to the first herbicide) will end up with an additional mutation rendering them resistant to the second herbicide.

Alternatively, if two herbicides with different mechanisms of action are used at once, the likelihood is far less that any weeds in the population will suddenly have not one, but two new mutations that just happen to be the correct mutations to confer resistance to both mechanisms of action simultaneously. If they develop the mutation to resist one or the other, but not both, then the weed just dies. It can’t pass on that trait. This is a bit of an oversimplification, but that’s the basic idea. Importantly, it’s consistent with the data. For a more in-depth explanation, I defer once again to weed scientist, Andrew Kniss’s articles here and here.

So, in conclusion, the issue of resistant weeds is a legitimate one, but since it is neither unique to GE crops, nor any less problematic with non-GE crops, it is not a legitimate criticism of GE foods. There are practices capable of helping farmers manage the problem, but discarding GE technology is not one of them.





About those harsher herbicides that glyphosate helped replace:

One of the common criticisms of commercially available Genetically Engineered (GE) seeds is the idea that they have led to an increase in pesticide use. In actuality, it turns out that they’ve corresponded to a decrease in total pesticide use, but this is attributable primarily to insect resistant GE crops, and critics argue that herbicide resistant crops have led to an increase in herbicide usage. It is true that the rise in popularity of glyphosate-resistant (GR) crops in particular has coincided with an increase in the use of glyphosate, which had already been in use to some degree for a couple of decades before the implementation of glyphosate-resistant crops. However, what critics invariably fail to mention is that its rise in popularity also coincided with the phasing out of other herbicides, most of which were significantly more toxic than glyphosate (about which I’ve written in detail here).

The purpose of this article is not to claim that glyphosate and GR crops are the be all end all of weed control (they’re not), nor is it to claim that they were causally responsible for any and every desirable change we see in herbicide usages patterns. Rather, the purpose of this is to show that when opponents of GE technology and of glyphosate claim that GR crops are bad on the grounds that they increased glyphosate use, they are leaving out critical information that would be highly inconvenient for their narrative.

It’s important to note that the data upon which these usage timeline graphs are based is very USA-centric. Perhaps a timeline and analysis of herbicide usage patterns in other places would be a good topic for another article, but the US is not a bad place to start because we do cultivate a lot of glyphosate-resistant crops here, as well as a lot of GE crops in general.

What were some of these herbicides?

Alachlor was one of them. The EPA states the following about alachlor:

“The greatest use of alachlor is  as a herbicide for control of annual grasses and broadleaf weeds in crops, primarily on corn, sorghum and soybeans.”

Alachlor use

Alachlor: [Source]

According to the EPA’s Water division:

“Some people who drink water containing alachlor well in excess of the maximum contaminant level (MCL) for many years could have problems with their eyes, liver, kidneys, or spleen, or experience anemia, and may have increased risk of getting cancer.”

The EPA and OSHA list alachlor as a Class L1 Carcinogen, which means they consider it likely to be carcinogenic at high doses but not at low doses. With an LD50 of between 930 mg/kg and 1,350 mg/kg in rats, and between 1,910 and 2,310 mg/kg in mice, its acute toxicity is not generally considered to be a big concern (although you may notice that it is still noticeably more acutely toxic than glyphosate which has an LD50 of 5,600 mg/kg). However, its potential for chronic toxicity remains a concern, particularly for the liver, spleen and kidneys (according to its PMEP profile) , and its NOAEL varied depending on the duration of the study in question.

Okay then. What else? How about Cyanazine?

Cyanazine use dropped to zero

Cyanazine use dropped to zero shortly after the rise of GR crops.

Cyanazine has an LD50 of between 182 and 332 mg/kg in rats and 380 mg/kg in mice (far more acutely toxic than glyphosate or alachlor), but its long term effects and NOAEL varied from anywhere around 0.198 to 3.3 mg/kg depending on which study you look at (as you may read more about in this WHO report). Although cyanazine is not known to be carcinogenic for certain, it has been observed to affect the central nervous system upon over-exposure and to increase liver weight while decreasing body weight gain.

Cyanazine was eventually put under special review due to concerns over its possible cancer-causing potential. DuPont voluntarily discontinued it in 1999, and its sale in the US was officially prohibited by 2002.

So, needless to say, cyanazine use went way down rather abruptly. What else?  According to PMEP, Fluazifop “is a selective phenoxy herbicide used for postemergence control of annual and perennial grass weeds. It is used on soybeans and other broad-leaved crops such as carrots, spinach, potatoes, and ornamentals.”

Fluazifop usage

Fluazifop usage

Fluazifop hasn’t gone away completely, but its use did decline quite significantly, possibly thanks in part to the introduction of glyphosate resistant soybeans. How toxic is it though? its LD50 was 3,680 for male rats and 2,451 for female rats, which is only a little bit more acutely toxic than glyphosate, but PMEP notes the following:

“A single dose of the formulated compound (Fusilade 2000) can cause severe stomach and intestine disturbance. Ingestion of large quantities may cause problems in the central nervous system such as drowsiness, dizziness, loss of coordination and fatigue. Breathing small amounts of the product may cause vomiting and severe lung congestion. This may ultimately lead to labored breathing, coma and death.”

So, yeah. There’s that. The good news is that there was no evidence of chronic toxicity in rats under 10 mg/kg per day in 90 day trials.

The next one up is metolachlor.

Technical grade Metolachlor has an LD50 of between 1,200-2780 mg/kg in rats. That’s between twice and 4.67 times the acute toxicity of glyphosate. Additionally, with an NOAEL of roughly 90 mg/kg/day, metolachlor can exhibit chronic toxic effects at doses MUCH smaller than the levels at which it becomes acutely toxic. Symptoms of  human intoxication from metolachlor include abdominal cramps, anemia, shortness of breath, dark urine, convulsions, diarrhea, jaundice, weakness, nausea, sweating, and dizziness.

Okay. Great, but what about Atrazine? In 1996 Atrazine was the #1 herbicide for corn. 2 and 3 were cyanazine and alachalor which, as we just saw, have effectively been zeroed out.

Well, apparently the rise of GR crops has had little to no effect on atrazine usage in the US. This might come as both a surprise and a disappointment to some because atrazine is known to degrade very slowly in soil (often lasting for months) and  has been known to inadvertently end up in drinking water, a fact which contributed to it being banned in the EU. It’s also a suspected endocrine disruptor and is more acutely toxic than glyphosate (with an LD50 of 672 to 3,000 mg/kg in rats). The EPA also classified it as a possible carcinogen, and multiple undesirable biochemical and morphological changes in various organs have been observed in high dose studies of its chronic toxicity. That’s probably not what most of my readers wanted to hear. However, part of being a responsible skeptic is understanding the importance of not cherry picking data. Additionally, we may be able to learn something by asking why this is the case. While at first glance this result is not so exciting, bear in mind that resistant weeds have increased quite a bit without increasing use AND corn production is greatly increased (by about 54%) since 1996, so use per bushel is down (as is use per capita because the population is up in the US by about 50 million people since then). Alright then. That’s not as spectacular as those previous examples, but at least it wasn’t a total bust.

What else? How about Metribuzin?

In 1992, over 2.5 million lbs of metribuzin was used just on soybeans alone. After that, its usage on fruits and vegetables didn’t change too drastically, but we can see that its use on soybeans and its overall use dropped dramatically. It eventually started climbing back up, and there a number of possible reasons for that, but it did initially go down, particularly in soybeans (for which a glyphosate-resistant variety was introduced by Monsanto in 1996). Metribuzin’s LD50 is 1,090 to 2,300 mg/kg in rats, which is about 2.5 to 5 times as toxic as glyphosate. None of the studies looking at chronic toxicity revealed any negative effects at any of the dosages tested.

Another one that was popular in the mid 90s in the US was Nicosulfuron.

Nicosulfuron usage

Nicosulfuron usage

The acute toxicity of Nicosulfuron is not much worse than glyphosate, with an estimated LD50 of in excess of 5,000 mg/kg of body mass. As for chronic toxicity, its NOAEL was found to be about 125 mg/kg/day, and its LOAEL (Lowest Observed Adverse Effect Limit) was found to be 500 mg/kg/day according to the EPA.

If you’ve made it this far, you may be wondering how this data was obtained. The website was created by USGS National Water Quality Assessment (NAWQA) Program.

“The pesticide-use maps provided on this web site show the geographic distribution of estimated use on agricultural land in the conterminous United States for numerous pesticides (active ingredients). Maps were created by allocating county-level use estimates to agricultural land within each county. A graph accompanies each map, which shows annual national use by major crop for the mapped pesticide for each year.

Methods for generating county-level pesticide use estimates are described in Estimation of Annual Agricultural Pesticide Use for Counties of the Conterminous United States, 1992–2009 (Thelin and Stone, 2013) and Estimated Annual Agricultural Pesticide Use for Counties of the Conterminous United States, 2008-12 (Baker and Stone, 2015).  Two different methods, EPest-low and EPest-high, were used to estimate a range of use, with the exception of estimates for California, which were taken from annual Department of Pesticide Regulation Pesticide Use Reports (Baker and Stone, 2015).”

A PDF copy of the entire Thelin and Stone report can be found here, but their quick summary of the data sources is as follows:

“Data sources used to develop EPest pesticide-by-crop use rates and annual pesticide-use estimates by county included the following: (1) proprietary pesticide-by-crop use estimates reported for CRDs; (2) USDA county harvestedcrop acreage reported in the 1992, 1997, 2002, and 2007 Census of Agriculture (, and NASS annual harvested-crop acreage data collected from crop surveys for non-census years (http://quickstats.nass.usda. gov/); (3) boundaries for CRDs and counties; (4) regional boundaries derived from USDA Farm Resource Regions; and (5) pesticide-use information from California DPR-PUR. Each of these sources is described in following sections.”

The USGS also includes this statement on the strengths and limitations of the data:

“Pesticide use estimates from this study are suitable for making national, regional, and watershed assessments of annual pesticide use, however the reliability of estimates generally decreases with scale.  For example, detailed interpretation of use intensity distribution within a county is not an appropriate use.  Although county-level estimates were used to create the maps and are provided in the dataset, it is important to understand that surveyed pesticide-by-crop use was not available for all CRDs and, therefore, extrapolation methods were used to estimate pesticide use for some counties. Surveyed pesticide-by-crop use may not reflect all agricultural use on all crops grown. In addition, state-based restrictions on pesticide use were not incorporated into EPest-high or EPest-low estimates. EPest-low estimates are more likely to reflect these restrictions than EPest-high estimates. With these caveats in mind, including other details discussed in Thelin and Stone (2013) and Baker and Stone (2015), the maps, graphs, and associated county-level use data are critical data for water-quality models and provide a comprehensive graphical overview of the geographic distribution and trends in agricultural use in the conterminous United States.”

Many people never even hear about the herbicides that were phased out in favor of glyphosate simply because they aren’t pertinent to the anti-agricultural biotech narrative, and because their popularity had waned by the time it had become trendy to demonize GMOs and everything remotely associated with them.

I said this before, and I’ll say it again:

“Opponents of glyphosate often seem to hold this unfounded notion that, if they can manage to get glyphosate banned or simply willingly abandoned, then it would mean an improvement in both food and environmental safety, but the truth is it would likely be the exact opposite of that. Weeds are a legitimate problem in farming that has to be dealt with one way or another. In its absence, it would have to be replaced with something else, and it would likely be something more caustic: not less.”


– Credible Hulk.

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I also help run Stop the Anti-Science Movement.


Glyphosate toxicity: Looking past the hyperbole, and sorting through the facts. By Credible Hulk

You may at some point have heard people speak of glyphosate as being “less toxic than caffeine or table salt.” What they’re referring to when they say that is what we call its LD50, which a standard way of quantifying acute toxicity. A substance’s LD50 is the dose at which 50% of the subjects who ingest that amount will die of complications from an acute overdose, and it is measured in units of mass of the substance per unit mass of the subject (usually mg/kg). See, one of the most fundamental principles in all of toxicology is that “the dose makes the poison,” which was famously coined by Paracelsus, the father of toxicology.  Most substances have some amount beyond which they become toxic. Many substances that are benign, beneficial, or even essential to human health in one range of concentration will become harmful if taken in sufficiently large amounts. Even water can be toxic if you drink enough of it. So, you can’t just look at it as though there were some toxic things in the world and some non-toxic things, or that something that is toxic at one dose is bad in any dose, simply because that’s not how toxicology works.

Here you can find a very brief introduction to concepts in toxicology, but for now, suffice it to say that students are generally taught about three main types of toxicity: acute, chronic and subchronic.

By the acute standard of LD50, glyphosate (albeit not necessarily round up brand mind you, which also contains surfactants) is indeed less toxic than either caffeine or table salt.

It has an LD50 of 5600 mg/kg based on oral ingestions in rats, according to EPA assessments, placing it in Toxicity Category III. The EPA ranks chemicals in four categories, I being the most toxic and IV being the least.

To compare, caffeine has a much lower LD50 of 192 mg/kg based on oral ingestion in rats. Similarly, sodium chloride (table salt) has an LD50 of about 3000 mg/kg. Rotenone, which is used on some organic farms (though less so in the US in recent years), has an LD50 162-1500 mg/kg, and Copper sulfate, which also sometimes used on certain organic farms, has an LD50 of  30mg/kg. This is permissible by organic certification due in part to the fact that it is completely naturally occurring, which of course has little to do with its safety or environmental effects. The purpose of these comparison is not to make caffeine and table salt, which most people take for granted as being fairly safe, seem dangerous, nor is it to demonize these other pesticides to make them seem unacceptable; rather, the purpose is to show that idea that glyphosate is this abnormally dangerous toxic substance, a notion popular among many laypeople, simply isn’t accurate.

However, that was only a matter of acute toxicity. Many opponents are willing to concede that the acute risks are fairly minimal, but they worry about the risks of long term low-level exposure. The EPA took that into account as well.  The EPA dealt with this issue by setting maximum safe levels of residues called “tolerances.” The USDA tests crops each year to make sure that herbicide residues do not exceed the permitted tolerance levels. If any crops contain residue amounts higher than tolerance levels, the USDA reports the information to the FDA, who has the regulatory power to recall foods, levy fines and take other actions to prevent the foods from reaching consumers.

In case you’re wondering how these tolerances were arrived at, the EPA tested glyphosate on numerous animal species. They then used the result from the MOST sensitive species tested as the basis for setting the Reference Dose. The RfD represents the level at (or below) which daily aggregate dietary exposure over a lifetime will not pose appreciable risks to human health.

The RfD is determined by using what’s called the “toxicological end point” or the “NOEL” (No Observable Effect Limit) for the most sensitive mammalian toxicological study. The EPA uses an uncertainly factor of 100 in deriving it (which is pretty high in order to be conservative) so as to ensure the sufficiency of the RfD, and based on the assumption that certain segments of the human population could be as much as 100 times more sensitive than the species represented by the toxicology tests. In rat studies on glyphosate, doses of up to 31 mg/kg/day were administered with no observable adverse effects at all, and dog studies have gone as high as 500 mg/kg/day with no negative effects.

The EPA’s assumption about how much people would eat was very conservative. In order to insure you don’t get over 2 mg per kg per day they use a “worst case” dietary risk model of an individual eating a lifetime of food derived entirely from glyphosate-sprayed fields with residues at their maximum levels.

Here are examples of the residues of Glyphosate permitted on our food:

Vegetable, bulb, group 3-07 – 0.20 ppm

Vegetable, cucurbit, group 9 – 0.5 ppm

Vegetable, foliage of legume, subgroup 7A, except soybean 0.2ppm

Vegetable, fruiting, group 8-10 (except okra) 0.10ppm

Vegetable, leafy, brassica, group 5 – 0.2ppm

Vegetable, leafy, except brassica, group 4 – 0.2ppm

Vegetable, leaves of root and tuber, group 2, except sugar beet tops 0.2ppm

Vegetable, legume, group 6 except soybean and dry pea 5.0ppm

Vegetables, root and tuber, group 1, except carrot, sweet potato, and sugar beet 0.20ppm

Note that most are all less than one part per million.

Now to put that in perspective, let’s assume you are a vegetarian and eat a mix that is on the extreme high end and you consume food which is at an average of 5 ppm per day.

So 200 grams of food would yield 1 mg of glyphosate.

You weigh 70 kg or 154 lbs.

To get 2 mg per kg you would need to get 140 mg of glyphosate residue.

So you would need to eat 200 * 140, or 28,000 grams of this 5 ppm produce to get to the 2 mg per kg per day level.

There are 28 grams in an ounce, so that’s 1,000 ounces.

There are 16 oz in a pound, so you would need to eat 62 lbs of produce.

We’re talking about EACH DAY here, and even if you managed that, that would only get you to a level that is 100 times less then the NOEL level in the most sensitive species tested.

Supposing you wanted to do similar calculations on your own upon looking up the EPA tolerances for a particular food item. How would you do that? How about I just derive the formula for you, and you can plug and chug for any given food based on its tolerance (even though, in actuality the residues will seldom be right up at the cutoff level). That way, this formula will apply no matter what the specific tolerances are for the item in question.

Let the Tolerance level of a particular food = x ppm,

which conveniently also equals 1mg/kg,

(which btw is one of the reasons I love the SI system of units).

Let m1= your mass in kg.

We want to see how much of a given food we would have to consume such that our intake of glyphosate residues exceeds 2 mg/kg,

so let m2 = the mass (in kg) of that food you’d have to consume each day to reach 2mg/kg.

So, we have

m2*x = m1*2 mg/kg.

Solving for m2 yields

m2 = 2*m1/x

So, supposing for example that the tolerance of a given crop is 10 ppm, and say you are only 50 kg (about 110 lbs).

Then the mass of that food you’d have to eat every day to exceed 2 mg/kg would be 2*50/10 = 10 kg = 22 lbs per day. Easy, right?

For someone my size, it’d have to be over 52 lbs a day just of that one product, and for an extended period of several years, and even then, only if the farmers were really pushing the limits of what they could get away with, which obviously wouldn’t make much sense from a business standpoint, since that stuff costs them money, and the whole reason they use it is to be more efficient: that is, to get the greatest output for the least input.

Another issue worth addressing is the recent IARC and WHO reclassification of glyphosate as a Class 2A carcinogen. The IARC classification process isn’t designed to serve as a statement on risk analysis, and for that reason, it did not take into account actual common usage practices. They placed glyphosate in the 2A category, which includes “probable” (albeit unconfirmed) carcinogens such as emissions from frying food, hairdresser products and burning wood. It mainly pertains to application protocols rather than minuscule trace amounts in food.

Consequently, banning glyphosate as a knee jerk reaction to its recent classification would be similar to never going out of the house in the daytime because sunlight is carcinogenic. Actually, it would be even less sensible because sunlight is in an even higher class of carcinogen than glyphosate. Think about it. It’s in the same classification as manufacturing glass, burning wood, emissions from high temperature frying, and work exposure as a hairdresser. Alcohol and sunlight are both higher on their carcinogen scale than glyphosate, and neither of those cause cancer with conservative exposure either.

Should proper precautions be taken during application procedures? Of course. Are the trace amounts in food, which are usually on the order of parts per million (ppm) or less even prior to being washed, a threat to consumers? No. The bottom line is that hazard is not the same thing as risk, and the latter is dependent largely upon exposure levels as well as type of exposure.

Moreover, as Kate Guyton, one of the scienists behind IARC’s classification stated:

“I don’t think home use is the issue. It’s agricultural use that will have the biggest impact. For the moment, it’s just something for people to be conscious of.”

Basically, what that means is that it’s the people actually applying the herbicide who are thought to be at increased risk. But applicators have their own set of protocols and certification requirements, and they are generally pretty well-versed in how to properly apply glyphosate.

The Farmer’s daughter USA wrote an informative and easy to understand piece on this. It may also be worthy seeing what various other scientists had to say about the reclassification of glyphosate and what they think it means in this article here.

It’s also worth noting that the IARC also classifies some organic pesticides as carcinogenic, and so do studies at the UC Berkeley.

Does that mean that they cause cancer at in the amounts consistent with actual practical usage?

Not necessarily. But the extreme emphasis some people are putting on glyphosate’s reclassification to the exclusion of the other “natural” compounds is quite a double standard, and double standards are pretty good indication of a strong bias on the part of the people making the most noise about it.

There are legitimate concerns over the evolution of glyphosate-resistant weeds. In fact, it’s one of the few of the common criticisms of glyphosate and GR crops that has any legitimate merit to it, but that’s an issue that affects all methods of weed control (even hand tilling), and although weed resistance has slightly increased, the RATE at which herbicide resistant weeds have been developing since the rise in glyphosate resistant GMO crops has not increased. It has always been an issue, and there are ways of dealing with it, but that’s a discussion for another day.

In closing, the take home message is that glyphosate is not the monumentally dangerous herbicide that its opponents have hyped it up to be. When the proper application procedures are practiced by applicators and usage on food crops are kept within the regulatory parameters, it is fairly innocuous, particularly when compared to many of its more toxic alternatives, many of which were phased out in conjunction with the rise in glyphosate’s popularity. Opponents of glyphosate often seem to hold this unfounded notion that, if they can manage to get glyphosate banned or simply willingly abandoned, then it would mean an improvement in both food and environmental safety, but the truth is it would likely be the exact opposite of that. Weeds are a legitimate problem in farming that has to be dealt with one way or another. In its absence, it would have to be replaced with something else, and it would likely be something more caustic: not less.


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