Wednesday, May 27, 2015

How to Cause Alzheimer's with Glyphosate 1: The Microbiome Route.

In my previous post I showed that the increase in Alzheimer’s disease (AD) could not be attributed solely to an increase in the elderly population (pointing to some environmental factor), and why glyphosate was a possible candidate for that factor.

But no matter how much circumstantial evidence you can produce, no account of a previously-unknown process is complete without showing a possible mechanism by which that process could be brought about.  Although there was evidence for continental drift, nobody would believe Wegener because he was unable to say how it could have happened.  Although there was evidence for the mortality of normal human cells, no-one—initially—would believe Hayflick when he said they underwent programmed death.  Hayflick was luckier than Wegener.  He lived to be able to demonstrate the function of telomeres.

At present, the cause of AD remains completely unknown.  Indeed, when I started to look at the AD literature, I was shocked to see (a) how many different possible explanations had been advanced and (b) how many of those explanations were mutually incompatible.  I would also have been shocked, if I had been as naïve as some GMO advocates are (or pretend to be), at (c) the failure of most papers to even mention that there were alternative explanations to theirs.  In the real world of science, hardly anyone does that; to paraphrase the immortal words of Truman Capote, “A boy has to hustle his theory”.  So the most anyone can do here is show some plausible routes by which glyphosate might cause AD.

How is glyphosate supposed to work?   According to Monsanto, “Glyphosate inhibits an enzyme that is essential to plant growth; this enzyme is not found in humans or other animals, contributing to the low risk to human health.”  That enzyme, 5-enolpyruvylshikimate 3-phosphate (EPSP) synthase, “is the sixth enzyme on the shikimate pathway, which is essential for the synthesis of aromatic amino acids and of almost all other aromatic compounds in algae, higher plants, bacteria, and fungi”.

Bacteria?  We’re full of them!  The human gut contains more than a thousand species, so that to say, as some RoundUp labels do, that “Glyphosate targets an enzyme that is found in plants but not on people or pets” is simply false, hence the subject of a false-advertising lawsuit just opened in Los Angeles.  Indeed, they’re not just found in us, there’s a full-scale symbiosis going on—they’re a functional part of us.  According to one source, although “Mechanistic studies linking alterations in microbiota to the etiopathology of disease are relatively few”, “The human microbiome appears to modulate the regulation of multiple neurochemical pathways through a complex series of highly interactive and symbiotic host-microbiome signaling-systems that mechanistically link the gastrointestinal tract to the central nervous system, the enteric nervous system and the neuroendocrine and immune systems.”

So how could this work?  Many members of our gut microbiota have positive consequences, but some don’t.  But we don’t yet even know what all of them are, still less what they all do.  And I haven’t so far found any studies showing whether a skewed distribution of biota is found in AD patients as compared with age-matched healthy individuals, still less whether a similar skewed distribution correlates with glyphosate residues or other biomarkers of exposure to glyphosate.  “Mechanistic studies…are relatively few” is, if anything, an understatement.  And a situation that ought to be amended, pdq.

But we have an unlikely source for the likely result: chickens.

Yes, an article dealing with the effects of glyphosate on poultry gut biota shows that “the highly pathogenic bacteria as Salmonella Entritidis, Salmonella Gallinarum, Salmonella Typhimurium, Clostridium perfringens and Clostridium botulinum are highly resistant to glyphosate. However, most of beneficial bacteria as Enterococcus faecalis, Enterococcus faecium, Bacillus badius, Bifidobacterium adolescentis and Lacto-bacillus spp. were found to be moderate to highly susceptible.”  All very well, you say, but how can chickens tell you what’s going on in the human gut?  Very easily.  As its name tells you, Salmonella Gallinarum is found exclusively in chickens.  But all the other bacteria named here are found also in the human gut.  If glyphosate kills or spares them in chickens, it does exactly the same in humans.

How might changes in the balance of microbiota trigger AD?  Well, Bifidobacterium adolescentis and Lacto-bacillus species are among those susceptible to glyphosate, and “Lactobacillus, and other Bifidobacterium species, are capable of metabolizing glutamate to produce gamma-amino butyric acid (GABA), the major inhibitory neurotransmitter in the CNS; dysfunctions in GABA-signaling are linked to anxiety, depression, defects in synaptogenesis, and cognitive impairment including AD.”  In other words, if you kill off beneficial bacteria, you can’t produce a chemical that is essential for your brain to keep running.

So that’s one route, but by no means the only possible route.  There are at least two more. But in order to discuss them, it’s necessary to know what the AD literature says about the causation of AD.  And as I said earlier, what the AD literature says is still a mess.  

But as I was preparing this, I got a very clear view of the way science works, and an equally clear view of the way the pro-GMO version of science is supposed to work.   They turn out to be very different ways.  And these two interlocking pictures, the Alzheimer’s controversy and the views of science it so clearly demarcates, will form the topic of my next post, “Real Science versus GMO Fantasy Science”.


  1. " If glyphosate kills or spares them in chickens, it does exactly the same in humans."


    The paper however doesn't show that glyphosate kills them in chickens, but that it kills them in a test tube. This is a reasonably important distinction. It also doesn't actually show that glyphosate kills a damned thing, given that they use roundup ultramax rather than glyphosate (and thus a mixture of glyphosate and surfactants)

    Second, the paper rather nicely (with the obvious problem that this is in vitro, and thus conditions are wildly different) demonstrates minimum inhibitory concentrations for each bacterial species tested. Worst case scenario, for a single species, this value was 0.075mg/ml - for all other species tested 0.075 was not inhibitory and the 0.15mg/ml concentration then comes in to play (for 6 more species) etc etc.

    Even if we take worst case scenario of 0.075mg/ml we need to put this into perspective. The human stomach has a capacity of about a liter, stretchable to about 4. So we'll take just this portion of the GI tract as our start point, and go conservative with 1L. so 1000ml, which would require 75mg of glyphosate in order to reach MIC for the most sensitive bacterium tested.

    The EPA allowable glyphosate residue on soybean is 40ppm, which is 40mg per kg of soybean - so one would have to consume about 2kg (or 4.4lbs) of straight up soybean at max allowable residue in order to achieve enough to hit this 75mg/ml level. Already the math gets a little... against your theory - because the 1000ml we started with now contains 2000ml of soybean (approximately) - making it a literal impossibility to consume enough soybean to increase concentrations to levels that would be of issue (40ppm = 40mg/kg - 1kg of soy takes up approximately 1L of volume).

    It isn't, therefore, possible to eat enough food containing glyphosate to reach levels that would impact gut bacteria, even the most sensitive of these.

    So we are left with a situation where we haven't actually tested glyphosate itself, but a mix of glyphosate and its surfactants in roundup ultramax, and even if we take the results as holding true into the guts of humans (or indeed even chickens) we are left with a scenario where it is not plausible that anyone would ingest the quantity of food required to raise concentrations to levels which would have a minimum inhibitory effect.

  2. I'd also take umbrage with the GABA comment

    "n other words, if you kill off beneficial bacteria, you can’t produce a chemical that is essential for your brain to keep running."

    This isn't remotely true - humans can synthesize their own GABA in situ and don't require bacteria to provide it.

  3. Decent scientists don't just jump to the conclusion of junk science or cherry-picking. But they are confronted with it in such a large assortement of low-quality publications that they are capable of calling junk junk.

    I didn't accuse the former physict/graph drawer of cherry picking because I don't like her results. I am only saying that that is the logical conclusion. It makes it a low quality work that isn't worth spending time or treasure refuting in better study. It's not wrong, it's flawed. It's flawed in such a fundamental way that either it is intentional, or the work of incompetence. You decide, but without actual

    Butg instead of going for the hard stuff, you simply attacked me (by implication) for something I did not do. I did not dismiss the study because of inconvenient results. On the other hand, I do believe you are accepting it based on convenient results.

    Come on, do the hard stuff and explain why the data sets are left incomplete. Why only compare certain GMO stats with certain disease stats. Prove me wrong.

    I'm not a real scientist, but real scientists don't sit idly by when clearly flawed studies are purported to prove or imply something they do not. The critique and criticisize. It is not always in formal responses, or in rebuttal studies.