Friday, May 22, 2015

Who’s Got the Science? An Answer to Mike and Ewan.




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!”

16 comments:

  1. RE: Swanson time lag

    So, if we're seeing time-lagged effects of pre-glyphosate pesticides, then Nancy's graphs and R^2 values are meaningless. The best conclusion in the exercise was that so many correlations with relatively high R^2 values couldn't be coincidence. Based on Derek's explanation, this conclusion is now null.

    And we still don't know why she omitted data.

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    1. Why do the disease rates get even higher years after the other herbicides have been mainly phased out, if the work is "null" or "meaningless"?

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  2. Re: Central Dogma

    It's not dead. There are other things going on. That doesn't mean that the idea of the fundamental flow of information from DNS to RNA to protein is flawed. But, the other things do matter, and that's one of the reasons it takes a while to get a GMO to work. You have to grow out and look for unforseen consequences.

    It's done in the plant world all the time, even without mad scientists driving it. And we aren't plagued with dangerous hybridizations every growing season. Random crossing shuffles and jumbles a lot of genes.

    Further, Kevin Folta's statement is being totally murdered here. He is not saying that there are 50 ideas that they know would work, but can't get to work. He's saying that not every idea works. Not everythign is a one protein solution. When all you have to do is give corn a gene to make the BT protien, you can pretty easily add a trait that kills caterpillars that eat any part of that plant. Trying to add a trait that may introduce disease resistance from something like spinach to something like a tree ca be a different story. You can't always just get one protein into a plant and viola, all bacteria die. If you could, you probably wouldn't want to. So you find ways to add resistance - ways to help the plant survive. Not as simple of a solution.

    This doesn't mean when a GE solution to add reisatance doesn't work, that it's because of a fundamental misunderstanding of genetics.

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  3. “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)”

    Not quite sure what on earth this has to do with anything. My internet ‘nym has been Ewan R since approximately 2008/9 when I was uncertain that I wanted my full name associated with what I was posting, but too uncreative to come up with a handle less close to my actual name. The only implications that I can see behind it are that someone not conversant with how the actual internet works (as in common usage, rather than technical) might read some sort of nefarious purpose behind it, but I’m not overly concerned about what such people think. It is pretty easy, however, to get to my actual details if one is even remotely interested in doing so (not sure why one would be, I’m not overly interesting at all) – I’ve had two individuals contact me at work with nothing more than a couple of blog responses to go on (both were entirely civil and awesome, which shatters all preconceptions about the internet) – posts on Pharyngula and Respectful Insolence if I recall correctly. (Hell Derek, we share a group membership on facebook, I’m really not that hidden at all, can’t speak for Mike though..)
    “Ewan himself inadvertently gave me the answer to that”
    There was nothing inadvertent there. I was literally establishing that prior to glyphosate use essentially (when it comes to corn at least) exactly the same quantities of herbicides were used.

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  4. “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.”
    Which chemicals are we claiming are similar to glyphosate here exactly?
    If we’re going to assume that previously used herbicides (similar or not) to glyphosate had what you are claiming are similar effects then doesn’t this make your use correlation, regarding glyphosate, utterly meaningless? If previously used chemicals had the same effect then the correlation with glyphosate has to be meaningless (given the lack of a time lag where one would expect it we can, I think, discard the correlations as meaningless anyway) – thus the entire foundation on which you’re building this blog is removed.

    “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.”

    So by your own admission the smoking gun has left the building. It is no more. It has shuffled off this mortal coil. This gun is not smoking, it is an ex-gun. It is not pining for the fjords.
    “As for attributing chronic diseases to obesity, that fails on a number of grounds.”

    And yet all of the diseases covered are, in the medical literature, associated with obesity. The data you presented were for the US as a whole, not for a single state – one would not expect the link to be 100% (Hawaii is a very different place than California, or Texas, or Alaska) in that those states with the highest rates of obesity/overweight should follow the same rank order – that there was a subsequent uptick in rates of obesity related diseases a decade or so after the nation as a whole went through a massive shift towards being more likely to be overweight or obese is mechanism enough to explain the bulk of the shift seen in the Swanson data.

    Also, by your own criteria Swanson fails here also – if Hawaii is the most sprayed state, and if one must see a fixed correlation (highest obesity must equal highest kidney disease or attribution fails) then given that Hawaii does not have the highest obesity rate in the US… well, you do the math – I don’t believe this, alone, would be grounds for failure, but if we’re going to go by that criteria then I suggest we go disease at a time and check that Hawaii is number one, if it isn’t (and given the obesity data it can’t be…) then by your own logic we can discard the Swanson paper and be done.

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    1. In t hat case you could easily produce correlations with obesity that are as good or better than Swanson's. Why not do that, if you dispute her results?

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    2. Because, Derek, I reject the notion that one must see a fixed correlation. That appeared to be your stance. If it is the stance you hold then your support of the Swanson paper is undermined by the Hawaii data as much as my obesity link to the various diseases is. If not then your opposition on these grounds is moot.

      I'm suggesting your opposition is moot, not that the correlation must behave this way.

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    3. Are you denying that correlation must always accompany causation? Of course there are plenty of correlates that aren't causes, but the obverse is, I should have thought, irrefutable. But if there is a correlation, AND enough of the Bradford Hill postulates are confirmed, there is is an irrefutable case for concluding, NOT that the correlated factor MUST BE the cause, but that it is a highly probable cause and must therefore be thoroughly investigated. That's all Swanson is saying and it's all I'm saying. You're saying it's not, because X and because Y, but X and Y are never big enough to justify saying that NO IT CAN'T BE THE CAUSE. That's the difference between a scientist and an activist. In a nutshell.

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    4. "Are you denying that correlation must always accompany causation?"

      I'm not sure where you'd get that idea from. I have clearly caused confusion by speaking less than clearly above.

      I shall attempt to lay out the conversation as I see it, hopefully to illustrate what I'm waffling about.

      You initially stated that

      "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. "

      I rejected that simply because for a single data point the correlation didn't hold (correlations with low R2 values will still follow from causative factors - particularly in multifactorial situations) that one could not hold obesity up as a plausible mechanism for the bulk of the diseases covered.

      You appear to have taken this as me saying that correlation somehow disproves causation, which would indeed be an odd stance for anyone to take.

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    5. " But if there is a correlation, AND enough of the Bradford Hill postulates are confirmed, there is is an irrefutable case for concluding, NOT that the correlated factor MUST BE the cause, but that it is a highly probable cause and must therefore be thoroughly investigated."

      Lets take a look at Bradford Hill criteria then.

      1. Strength: A small association does not mean that there is not a causal effect, though the larger the association, the more likely that it is causal.

      There is certainly a strong association. I don't think anyone could refute that.

      Consistency: Consistent findings observed by different persons in different places with different samples strengthens the likelihood of an effect.

      I'm not sure this has been covered - do we have multiple consistent findings by different groups in different locations which support all the connections Swanson makes?

      Specificity: Causation is likely if a very specific population at a specific site and disease with no other likely explanation. The more specific an association between a factor and an effect is, the bigger the probability of a causal relationship.

      Swanson data lacks specificity given that it covers the US as a whole. This does however leave a lot of cherry picking that one can fall back on, so there's hope for you there.

      Temporality: The effect has to occur after the cause (and if there is an expected delay between the cause and expected effect, then the effect must occur after that delay).

      This kills the case against Glyphosate as causative. Dead and buried. The correlation lacks the temporal offset one would expect. Sure, you can shift your attention elsewhere, that's fine. The Swanson paper is, however, very specific about glyphosate, and your own blog is entitled the gmosmokinggun - because of the link between glyphosate and gmos, so if glyphosate is not causative then both Swanson and your own stance can be cast aside - could other agrichemicals be causative in certain diseases? Quite possibly (this makes the case, in my mind, for glyphosate rather than against it though, assuming it replaces causative chemicals, but as we fail to see a decline in these diseases it would appear that whatever is causative has simply not been removed, and thus the blame can hardly fall on the chemistries that glyphosate has replaced)


      Biological gradient: Greater exposure should generally lead to greater incidence of the effect. However, in some cases, the mere presence of the factor can trigger the effect. In other cases, an inverse proportion is observed: greater exposure leads to lower incidence.

      Dose response? Do applicators of glyphosate have increased rates of these diseases? (it would appear that urbanization is one of the higher predictors of autism, thus moving away from application zones where high exposure would be expected is not related to increased rates of autism, so one might question whether autism was a relevant one here, although given that rural areas tend to have overall poorer life expectancy than urban many of the other correlations may still hold here)




      Plausibility: A plausible mechanism between cause and effect is helpful (but Hill noted that knowledge of the mechanism is limited by current knowledge).

      Arguably still no plausible mechanism. A one liner in a far larger piece from a scientific society does not constitute scientific evidence.

      Coherence: Coherence between epidemiological and laboratory findings increases the likelihood of an effect. However, Hill noted that "... lack of such [laboratory] evidence cannot nullify the epidemiological effect on associations".[1]

      There is no coherence here at all - one does not see signs of any of the numerous diseases in lab studies of glyphosate exposure.

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    6. Experiment: "Occasionally it is possible to appeal to experimental evidence".
      The experimental evidence, as discussed above, doesn't support the correlation at all.

      Analogy: The effect of similar factors may be considered.

      One would here have to justify the similar factors to be considered.

      y"ou're saying it's not, because X and because Y, but X and Y are never big enough to justify saying that NO IT CAN'T BE THE CAUSE."

      With regards to glyphosate the time lag is, categorically, enough to justify saying it cannot be the cause. Effect cannot precede cause, if you're going to postulate that other pesticides were causative and that glyphosate is also causative then you're left having to provide evidence

      a) that other pesticides actually were causative (this may well be the case)
      b) that glyphosate is also causative (and the Swanson paper here provides zero evidence given the need for cause to precede effect)

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    7. One could, of course, apply the BH criteria to the link between obesity and said diseases also...

      In which case one through eight are fully supported by a massive amount of data, and nine is largely irrelevant (I'm not even entirely sure what would be analagous to obesity, although no doubt such things exist)

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  5. Part the third
    “other pesticides could have started what glyphosate, for all the touting of its “safety”, simply continued”

    But now you completely lack data, if you’re going to switch the blame to other pesticides (as you must in order to explain the time lag and still blame pesticides) then your smoking gun (regarding GMOs) is gone as all Swansons correlations are rendered meaningless by the pesky 4th dimension.

    “But obviously something in the environment started to change in the last quarter of last century. If not pesticides, then what? Change in lifestyles? “

    If only there was any science looking at this…

    http://www.sciencemag.org/content/280/5368/1371.abstract?ijkey=f5e4dea012900c2b67dcb5aff6105a2ba42bbc4d&keytype2=tf_ipsecsha

    http://epirev.oxfordjournals.org/content/29/1/6.full#ref-69

    “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.”

    You so brashly make statements of fact on trivially researched matters that the inability to be right on the simple stuff belies an unwillingness to research ones statements beyond ones preconceived ideas. Being so glaringly wrong about multiple aspects of agriculture is indicative that, when it comes to ag, you’re much like Jon Snow.

    “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. “

    Are you a time traveler? Do you come here from 1990? Lewontin introduced niche construction theory in the early 80’s. Evo-devo is about as central to biology of the past 50 years as one can get.

    “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.”

    It would appear you’re as unfamiliar with biology as you are with Dawkins as you are with agriculture in general.

    I studied biology in the late 90’s. The gene to protein to trait model was, even then, a simplistic view of how biology worked, in first year lectures we were literally told that hey, this is sort of how it works, but this is insanely simple, and if you take second year biology classes you’ll start to see why it is simple, if you’re a chemist taking bio because it’s easy… well, just remember it isn’t this simple – much like, every topic covered in first year biology (and then we moved to second year, and learned about pleiotropy (acknowledgement of pleiotropy is as old as genetics, given that Mendel noted a pleiotropic trait) and that (importantly) it exists for some genes, and not for others).

    So, rather than exciting new changes in the past decade that invalidate all that comes before them… you’re essentially bringing up foundational pieces of biology that were learned by all 2nd year bachelors students in the late 90’s and certainly in the decade preceding that – it is astonishingly unsurprising that highly qualified molecular biologists, plant physiologists and so on actually are completely well aware of these things. But hey, why not live in the pretense that biologists are actually completely clueless about biology, because clearly angry internet warriors are far more likely to be keyed in to the most recent trends in biology. Even those who mistake advances made in the past 30-100 years as having come in the past decade or two.

    Alas I shall return at some point to deal with the rest, work calls and all that.

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  6. Don't tell me about the recent history of biology. Tell Clifford Tabin, Chair of Genetics at Harvard Medical School, because he seems to be equally ignorant:

    "When we thought about such things, say, 20 years ago, one had to assume that the genes to make a fruit fly would include instructions for wings, genes that we didn't need. And, conversely, that we'd have genes dedicated to making a human limb or human heart that a fly would never have. The stunning finding was that, to a first approximation, the same genes are present in both and are being used in both."
    (http://www.pbs.org/wgbh/nova/evolution/what-evo-devo.html).

    As for niche construction, the three founders of the theory acknowledge Lewontin as one who anticipated a few of its ideas, but even L. himself would never claim that he'd "introduced it".

    As the Scriptures have it, "Pluck the mote from thine own eye..."

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    1. No, I don't believe that I have to tell Clifford Tabin that he is equally ignorant.

      Dr Tabin gave that interview 6 years ago. Thus his 20 year timeframe takes us back over 25 years, which exceeds the last decade or two. Tabin was involved in the discovery of the sonic hedgehog gene (and other hedgehogs in humans) in the very early 90's (the work was published in 93, still over 2 decades ago) which is, essentially, his stunning finding (thus, had we taken our DeLorean back to 2009 perhaps your timeframe would be correct taken to an extreme, but here in 2015 you're incorrect) - at exactly the same time other labs were making similar discoveries of homologous genes (wingless for instance, being part of a transcription factor family that included a number of human oncogenes). Thus, the biology of the last 2 decades has not been ignorant of pleitropic effects, or of evo-devo, but has, instead, been soundly grounded in same. Assuming one has greater than an intermediate high school level understanding of biology (where the newest discoveries are unlikely to become part of the syllabus for quite some time, and even then likely to be glossed over somewhat given time constraints and level of understanding required)

      "As for niche construction, the three founders of the theory acknowledge Lewontin as one who anticipated a few of its ideas, but even L. himself would never claim that he'd "introduced it"."

      Perhaps you should take this up with Dr John Odling-Smee, Prof Kevin N. Laland and Prof Marc Feldman who state in no uncertain terms that

      "The niche-construction perspective was introduced to evolutionary biology in the 1980s through a series of seminal essays by Harvard evolutionary biologist Richard Lewontin (1-3), and has gathered momentum over recent years."

      http://lalandlab.st-andrews.ac.uk/niche/Evolution.html

      Odd that, as a brief look at what is out there on niche theory suggest that these 3 are top proponents of niche construction theory today, which rather suggests that rather than considering the mote in my eye, you might want to deal with the beam in thine own and then you may well, one imagines, see clearly to attend to any perceived motes.

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    2. You said: "Evo-devo is about as central to biology of the past 50 years as one can get."

      Look in any history of evo-devo and you'll see something like this:
      "It was fully realized only in the 1990’s, that our understanding of both evolution and development would greatly benefit from the partial merging of the two above-mentioned disciplines into what is called today Evolutionary Developmental Biology (EVO-DEVO)."
      (http://www.lanevol.org/LANE/Evo-Devo.html)

      If you had been watching biology through the 1980s , you would have registered that Lewontin was regarded as well outside the biological mainstream of his day and his ideas got very little traction until the three you mention (btw, I know all of them personally, Laland I have corresponded with on several occasions, and Odling-Smee has been a friend of mine for over ten years--we even at one stage seriously considered co-authoring a book, since I know so little biology--and I'm sure you will be sorry to learn that he suddenly and quite recently became completely blind) formed his ideas into a coherent body of theory and very generously credited him with being their forerunner.

      Of course, your remarks on the history of biology were no more than a distraction, typical GMOer strategy when you can't answer the hard stuff. The hard stuff is explaining why the new biology is,if not more, at least as friendly to genetic engineering as the old biology.

      But that, predictably, you haven't dealt with. The sad part is, you couldn't even get the facts about the history right.

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