Before we can go further, I have to answer the multiple objections to the whole Alzheimer’s scenario raised by my two most faithful commentators, Mike W. and Ewan R. (sorry you continue to lurk behind screen names instead of putting yourselves squarely behind your remarks, but if you don’t mind the implications of that, it’s your choice). Only when the issues they raise have been fully and thoroughly dealt with can I go on to connect the dots and show direct links between glyphosate and the mechanisms that underlie Alzheimer’s (AD).
Let’s begin with what seems at first sight the most damaging evidence: the apparent absence of any time-lag between the steep rise of glyphosate use/GE R-R crops and AD statistics. Ewan himself inadvertently gave me the answer to that:
“Herbicide use on corn in the years prior to HT corn (1998 being year of release) 1994 - 170,221,000 lbs 1995 - 167,642,000 lbs 1996 - 186,977,000 lbs 1997 - 164,051,000 lbs 1998 - 177,012000 lbs.” In other words, massive use of herbicides predated the emergence of glyphosate as the major herbicide.
When did I ever claim that glyphosate was the only herbicide that caused chronic disease? Neither Swanson nor I did this. Indeed Swanson specifically states that “We do not imply that all of these diseases have a single cause as there are many toxic substances and pathogens that can contribute to chronic disease.” We focused on glyphosate because of its present-day ubiquity, but there’s no reason to doubt that similar chemicals used in a similar way would have had similar effects. So the steep rise in levels of AD and other chronic diseases in the 1990s reflects mostly exposure to previously-used pesticides, from 1970 (when Roundup was introduced) to the ’90s when it became dominant, giving just the predictable time-lag for AD. After all, even industry representatives were congratulating themselves (and still do) on having substituted glyphosate (“the pesticide of the century”, as GMO advocate called it) for the more dangerous pesticides that preceded it.
As for attributing chronic diseases to obesity, that fails on a number of grounds. For instance Hawaii, which has a shot at most-sprayed-state-in-the-union status, has a chronic kidney disease rate 30% higher than the natural average, yet in 2013 had the second-lowest incidence of obesity. Moreover, as will be shown in subsequent posts, the mechanisms that cause obesity are the same as those involved in the etiology of chronic disease. One thing we’ve learned (or should have) in the last few years is that the old one-size-fits-all medical model is hopelessly at variance with the facts. People are vulnerable in different ways, simply because we all differ in our genetic make-up, so the same chemical (whether cure or poison) may have quite different effects on different people. What effect a pesticide might have will then tend to vary from person to person, although a cascade effect is likely in some cases—pesticide-triggered hormonal dysfunctions precipitating obesity which in turn leads to diabetes, which in turn leads to AD, and so on. But it follows too that at some stage a saturation point will be reached—only a certain proportion of the population will be likely candidates for obesity, and once that point is reached you’ll see the kind of leveling off you’d like to seize on to show that glyphosate is not what’s doing the harm.
Note that the same argument I made about the supposed “AD time-lag” applies equally to the 80’s rise in obesity that began before massive glyphosate use—other pesticides could have started what glyphosate, for all the touting of its “safety”, simply continued. I’m not claiming that the Swanson case might not have been more effective if this point had been seen and emphasized. But obviously something in the environment started to change in the last quarter of last century. If not pesticides, then what? Change in lifestyles? People don’t want to be obese. If they did, how could the weight-loss industry be as big as it is? How could new fad diets emerge almost daily? You’d think all this publicity (even including TV shows like “The Biggest Loser”) would send rates plummeting. And if better diet and more exercise could cure it, you’d surely think they would. But they don’t. Obesity rates creep on up no matter what people do.
But there are much broader issues involved in Mike’s and Ewan’s remarks. For instance, Ewan made a big deal of the fact that atrazine, contrary to what I suggested, is a selective pesticide. I would have thanked him for this—no-one is readier than me to admit when I’m wrong or more grateful for any addition to my knowledge—if he had not started so immodestly crowing over it. The fact that I got this wrong was to him a clear indication that I could not even grasp “the simple stuff” and was therefore clearly incapable when it came to “the hard stuff”.
Sorry, Ewan, that’s not how science works. It may be how science education works, by slowly accumulating factoids into solid chunks of what currently passes for knowledge, but I suspect that’s exactly why science education in the U.S. is so ineffective. Science isn’t like that. First of all it advances through argument. If you retracted from science journals all the papers that weren’t arguing one opinion against another, those journals would be two-thirds empty. So contrary to normal practice in pro-GMO circles, you do not treat your opponents as ignorant idiots (or “fear-mongers”, if it comes to that). Second of all, you don’t need to learn “the simple stuff” in order to learn “the hard stuff”--especially if, as in this case, the simple stuff is in one branch of science and the hard stuff is in a quite different branch.
Atrazine and its properties form part of weed science. As I’m the first to admit, I don’t know weed science, and I’m sure Ewan does. But weed science is just a small branch on the great tree of biology, and if you’ve been following that over the last decade or two you’ll know that there’ve been great changes—changes that produced whole new biological fields such as evo-devo and niche construction theory. These changes have already turned biology into something a lot less friendly to the whole GMO/pesticide nexus than the “one gene = one protein = one trait”, “genes rule”, “genes are like Lego blocks” biology of the Dawkins era. Now we know that genes are pleiotropic as well as collaborative, so that to talk about “the gene for X” where X is any behavioural trait is at best misleading. GMO researchers had to find this out the hard way; what they seldom admit is that “implanting the gene for X” fails far more often than it succeeds. (Occasionally even the staunchest GMO advocate can let this slip out: “There are probably fifty different genes that have been engineered into citrus trees, most of them don't work or show little promise”—Kevin Folta.) Far from genetic engineering being a precise and well-understood process, its procedures are just hit-and-miss trial and (mostly) error.
With the new biology we know the ease with which, especially given the ideal circumstances, resistance to any threat can evolve. GMO enthusiasts have provided those ideal circumstances. “Ecological theory predicts that the large-scale landscape homogenization with transgenic crops will exacerbate the ecological problems already associated with monoculture agriculture.” Artificially breed resistance to a particular herbicide in a crop, grow that crop over as large an area as possible, use that herbicide over that whole area, and you are just doing evolution’s job at a faster rate. You are actively selecting for herbicide-resistant weeds, because you are killing off all their competition--the non-resistant weeds--and leaving a vacuum for the “superweeds” to fill (just like the asteroid strike cleared the field for us mammals 65 million years ago). Monsanto didn’t know this—their propaganda in the nineties said there was little likelihood that glyphosate would create resistance—but anyone with up-to-date scientific knowledge could have predicted it.
Now we further know that environmental inputs can have massive effects on development from foetus to adult, modifying gene expression, upregulating or downregulating proteins, guiding not only individual development but the future evolution of species. This new knowledge has already proved fatal to the canon on which all GMO undertakings are based—“The dose is the poison”, the dictum of a sixteenth-century alchemist/astrologer, and surely the last piece of sixteenth-century science to survive into the twenty-first century. All pesticide safety testing is aimed at detecting acute effects, whereas the main dangers from pesticides are chronic effects that can be caused by much lower doses, but only become apparent after long periods. (Don’t forget how they told you for years that smoking was safe, and to be sure, nobody ever collapsed as a consequence of smoking a pack.) Chemicals can no longer be assumed to have monotonic dose-response curves, leading the Endocrine Society (who should surely know about toxicity, if anyone does) to call for a complete change is safety-testing methods.
That is what I meant and will continue to mean by the “hard stuff” that GMO advocates refuse to deal with. I can only assume it’s because there’s no way they could. And this explains why they have to pounce every time a GMO opponent misstates some trivial factoid about pesticides--it's the only way they can maintain the myth that they know science and the other side doesn't. It also explains why, when I began quite recently to learn about GMOs, my first reaction was “There’s no way, in the second decade of the twenty-first century, that anyone could call this stuff scientific!”