I never used to write much about genetically modified organisms (GMOs) before. I still don’t do it that often. For whatever reason, it just hasn’t been on my radar very much. That seems to be changing, however. It’s not because I went seeking this issue out (although I must admit that I first became interested in genetic engineering when I was in junior high and read a TIME Magazine cover article about it back in the 1970s), but rather because in my reading I keep seeing it more and more in the context of anti-GMO activists using bad science and bad reasoning to justify a campaign to demonize GMOs. Now, I don’t have a dog in this hunt, (Forgive me, I have no idea why I like that expression, given that I don’t hunt.) I really don’t. I was, not too long ago, fairly agnostic on the issue of GMOs and their safety, although, truth be told, because I have PhD in a biomedical science and because my lab work has involved molecular biology and genetics since I was a graduate student in the early 1990s, I found the claims of horrific harm attributable to GMOs not particularly convincing, but hadn’t bothered to take that deep a look into them. It was not unlike my attitude towards the the claims that cell phones cause cancer a few years ago, before I looked into them and noted the utter lack of a remotely-plausible mechanism and uniformly negative studies except for a group in Sweden with a definite ax to grind on the issue. Back then, I realized that there wasn’t really a plausible mechanism by which radio waves from cell phones could cause cancer in that the classic mechanisms by which ionizing radiation can break DNA molecular bonds and cause mutations don’t apply, but I didn’t rule out a tiny possibility that there might be an as-yet unappreciated mechanism by which long term exposure to radio waves might contribute to cancer. I still don’t, by the way, which has gotten me into the odd kerfuffle with some skeptics and one physicist, but I still view the likelihood that cell phone radiation can cause cancer as being just a bit more plausible than homeopathy.
As was the case for the nonexistent cell phone-cancer link, there has now been a steady drip-drip-drip of bad studies touted by anti-GMO activists as “evidence” that GMOs are the work of Satan that will corrupt or kill us all (and make us fat, to boot). Not too long ago, I came across one such study, a truly execrable excuse for science by Gilles-Eric Séralini at the University of Caen purporting to demonstrate that Roundup-resistant genetically modified maize can cause horrific tumors in rats. I looked at the methods and conclusions and what I found was some of the worst science I had ever seen, every bit as bad as the quack “science” used by the antivaccine movement. It wasn’t for nothing that I made the comparison, because the anti-GMO movement is very much like the antivaccine movement and the cranks who claim that cell phone radiation causes cancer. As if to demonstrate that very point, last week I came across an article by the all-purpose crank to rule all cranks, Mike Adams, at NaturalNews.com entitled GMO feed turns pig stomachs to mush! Shocking photos reveal severe damage caused by GM soy and corn:
If you have stomach problems or gastrointestinal problems, a new study led by Dr. Judy Carman may help explain why: pigs fed a diet of genetically engineered soy and corn showed a 267% increase in severe stomach inflammation compared to those fed non-GMO diets. In males, the difference was even more pronounced: a 400% increase. (For the record, most autistic children are males, and nearly all of them have severe intestinal inflammation.)
The study was conducted on 168 young pigs on an authentic farm environment and was carried out over a 23-week period by eight researchers across Australia and the USA. The lead researcher, Dr. Judy Carman, is from the Institute of Health and Environmental Research in Kensington Park, Australia. The study has now been published in the Journal of Organic Systems, a peer-reviewed science journal.
It sounds pretty damning, doesn’t it? It sounds truly horrific, just as the Séralini study did. Adams is useful in that he takes the messages of anti-GMO activists (well, actually, he takes the messages of just about all cranks and quacks) and, as they said in This Is Spinal Tap, turns them up to 11. On the surface, it does, anyway. But what about the actual study. There was really only one thing for me to do, and that’s the same thing I did with the Séralini study: Go and see for myself. So I did.
What hath Judy Carman wrought?
Judy Carman’s study was, fortunately, published in an open access journal, and there was a direct link to the study itself. The first thing I did was to look at the journal. I had never heard of it before. The journal seems to cater to the organic crowd, being sponsored by groups like the Organic Federation of Australia and CSAFE, while the guidelines for authors state that “topics are to be consistent with current principles of organic farming and its associated industries, especially those in Australia, New Zealand, Asia, and the Pacific Islands.” The journal itself appears not to be indexed on PubMed, which tends to indicate either that it’s a new journal or not a very good journal. On the other hand, to be fair, there are plenty of CAM journals indexed in PubMed, and many of them are pure pseudoscience; so I can no longer conclude that lack of indexing in PubMed automatically means a journal is dodgy. It is, however, often an indication that it is. Moreover, if you wander over to Judy Carman’s website, gmojudycarman.org, you’ll see that it’s chock full of anti-GMO activism.
After having seen this study, I think that the editors of this open access journal have made a massive mistake and have, either wittingly or unwittingly, allowed their journal to become a tool of anti-GMO activist groups, a couple of which which gleefully announced the results of the study with press releases (for example here and here) calling the study “groundbreaking,” asserting that it was evidence of “adverse effects” due to GMO feed, and claiming that the results show “…clear evidence that regulators need to safety assess GM crops containing mixtures of GM genes, regardless of whether those genes occur in the one GM plant or in a mixture of GM plants eaten in the same meal, even if regulators have already assessed GM plants containing single GM genes in the mixture.”
Here’s a hint: It’s none of the above.
As I read the study itself, the first thing that became apparent to me is that it’s a massive fishing expedition. What do I mean by that? I mean that there’s no clear hypothesis. Basically, the only seeming hypothesis was “GMOs bad,” and the study was designed to find bad things associated with GMOs. At first glance, the design seems simple enough. The investigators used 168 just-weaned pigs at a commercial piggery in the US. The pigs were fed a standard diet, but half the pigs were fed widely used varieties of GM soy and GM corn, while the control group fed an equivalent non-GM diet. Basically, one protein made the plant resistant to a herbicide and two proteins were insecticides. The specific GM varieties used were as follows:
The corn used in this study contained 90% DK 42-88 RR YG PL (a triple stack of NK603, MON863 and MON810 genes) with the remainder being equal quantities of Pannar 5E-900RR (containing NK603), Pannar 4E-705RR/Bt (a double stack of NK603 and MON810) and Producers 5152 RR (containing NK603). Therefore, the GM corn that was used was genetically modified to produce three new proteins. Two were Bt proteins that protected the plant against insect attack, while the third protein provided the plant with tolerance to the herbicide glyphosate (Testbiotech, 2012; Monsanto, 2012). Because Roundup ReadyTM (RR) soy is predominant in the GM soy market, this was used. This crop contains a gene that provides tolerance to the herbicide glyphosate. GM DNA analysis (Genetic ID, Fairfield, Iowa, US) confirmed that the GM corn contained a combination of NK603, MON863 and MON810 genes (expressing the CP4 EPSPS, Cry 3Bb1 and Cry 1Ab proteins respectively), that the RR soy was 100% RR soy (expressing the CP4 EPSPS protein), that the non-GM feed contained a median of 0.4% GM corn and that the non-GM soy contained a median of 1.6% GM soy. Such GM contamination of apparent non-GM material is common in the US.
So the investigators fed piglets a diet of GMO grain versus non-GMO grain, let the pigs mature according to the normal methodology, and then after slaughter looked at a variety of outcomes. Worse, the authors measured these variables without any sort of control for multiple comparisons. Of course they found differences! Actually, what surprised me is how few differences they found between the groups, not how many. I’m going to hone in on the main finding of the paper first. It’s the finding that seemed the most dramatic and was the most highly publicized, the one mentioned by Mike Adams in his breathless description of he results, as though it was slam-dunk evidence that GMOs are evil. I’m referring, of course, to the claim that more stomach inflammation was observed in the pigs fed a GMO diet, specifically a 267% increase in severe stomach inflammation in the GMO group, with a whopping 400% increase in male pigs. It’s the result that produced pictures like this one in the paper (and, not surprisingly the same picture posted to many an anti-GMO website):
These images certainly look striking, but what do they mean? Well, not much. First of all, as many have pointed out, the photos chosen are deceptive in that not enough of the groups are shown, nor can we be sure that these are representative. Also, as Mark Hoofnagle points out, the assay for inflammation in the gastric mucosa of the piglets was only based on gross pathology. Basically, there was no histological study and pathological examination of the tissue to detect and quantify actual inflammation. Basically, the assay was based just on a gross visual inspection of the the tissue by a veterinarian (not even a veterinary pathologist even, as far as I can tell). Unfortunately, such inspections can be highly misleading, particularly after animals have been slaughtered in an abattoir, as described by Professor Robert Friendship, University of Guelph:
Dr. Robert Friendship, a professor in the Department of Population Medicine at the Ontario Veterinary College, University of Guelph and a swine health management specialist, reviewed the paper [see reference below]. He concluded that ‘it was incorrect for the researchers to conclude that one group had more stomach inflammation than the other group because the researchers did not examine stomach inflammation. They did a visual scoring of the colour of the lining of the stomach of pigs at the abattoir and misinterpreted redness to indicate evidence of inflammation. It does not. They would have had to take a tissue sample and prepare histological slides and examine these samples for evidence of inflammatory response such as white blood cell infiltration and other changes to determine if there was inflammation. There is no relationship between the colour of the stomach in the dead, bled-out pig at a slaughter plant and inflammation. The researchers should have included a veterinary pathologist on their team and this mistake would not have happened. They found no difference between the two experimental groups in pathology that can be determined by gross inspection.’
What I found particularly suspicious was Table 3. Notice how the level of inflammation is divided into no inflammation, mild inflammation, moderate inflammation, severe inflammation, erosions, pin-point ulcers, frank ulcers, and bleeding ulcers. This is not really a standard way of scoring inflammation. I don’t know about pigs, but in humans there are a variety of scoring systems for the endoscopic assessment of inflammation (for example, this one), particularly chronic gastritis (which is what we’re talking about, although such redness as described would, if associated with gastritis, be more associated with acute gastritis). Worse, gross visual assessment of gastric mucosa is subject to high inter-observer variability, and, although the personnel caring for the pigs and doing the autopsies were blinded to the experimental group (which is good), I don’t see any attempt to control for inter-observer variability, and, again, no control for multiple comparisons.
I also note that the difference between pin-point ulcers, frank ulcers, and bleeding ulcers is rather arbitrarily defined and not entirely clear. Also notice how twice as many pigs had no inflammation in the non-GMO group and that there was actually a lower risk of mild and moderate inflammation, as well as erosions and pin-point ulcers. Of course, the p-values are all non-significant, except for one: that for severe inflammation. In fact, on the entire table, the only “statistically significant” result is for “severe inflammation.” In fact, as Mark Lynas points out, many more pigs fed non-GMO feed had stomach inflammation than those with GMO feed.
Lynas also points out that the data are all over the place with respect to reported levels of inflammation, asking the very apt question, “If GMO feed is causing the severe inflammation, why is the non-GMO feed causing far more mild to moderate inflammation?” One also can’t help but notice that for “moderate” inflammation, there was a difference favoring the non-GMO feed, and I echo the question, “Do Carman et al perform a test for statistical significance to see if GMO feed has a protective effect on pigs stomachs? Of course not – that’s not the result they are after.” Exactly. Even worse, they used the wrong statistical analysis to analyze categorical data. When the data are analyzed more appropriately, there appears to be no statistically significant difference between the groups, just as there was no real statistically significant difference in the tumor burden of the rats in the Séralini study. Come to think of it, Carman’s study resembles the Seralini study in that it basically looks at a whole lot of outcomes in a fairly arbitrary fashion and cherry picks the inevitable “positive” result. In fact, if you take all the groups together, there actually appears to be a non-statistically significant trend towards less stomach inflammation in the GMO group. Yes, less. As Karl Haro von Mogel put it, the authors appeared to be “trying to shoe-horn individual categories that aren’t binary data into a statistical test designed for binary data is the wrong approach.” Basically, however you look at it, there’s just no “there” there. Analyzed correctly, there is no statistically significant (or, no doubt, biologically significant) difference in stomach inflammation in this study. As for the reported increase in uterus weights, as Professor David Spiegelhalter, Winton Professor of the Public Understanding of Risk at the University of Cambridge points out, “There are also 19 other reported statistical tests, which means we would expect one significant association just by chance: and so the apparent difference in uterus weight is likely to be a false positive.”
There’s another aspect of this paper that’s very troubling, and it is that these animals were all very sick. Indeed, I have to wonder how they were being cared for. Over half the animals are reported in Table 3 to have pneumonia, defined as “consolidating bronchopneumonia of the cranial ventral lung lobe(s) and/or caudal lobes.” That is just not normal, and it doesn’t sound like a minor pneumonia. True, this pneumonia wasn’t histologically verified either, as far as I can tell, although pneumonia can be viewed grossly if it’s bad enough. It is, after all, basically puss mixed with mucous in the alveolae and bronchial passages. As has been pointed out in multiple discussions of this study, such a high percentage of animals with pneumonia is an indicator of very bad animal husbandry, indeed. The bottom line is that there are many, many problems with this study, the totality of which are more than enough to render its results meaningless. There is no dose-dependent mechanism for the effects reported, no rhyme or reason consistent with a mechanism that would explain why GMOs would affect just the stomach (and then only to cause severe inflammation) and uterus size. The study was a fishing expedition and not hypothesis-driven. It’s not surprising that it found something. I’d be shocked if it hadn’t. In the end, this study abused a fairly large number of innocent pigs to produce no useful data. She might try to defend it against criticism, but she basically fails. In particular, one notes that she can’t seem to defend against the charge of a lack of hypothesis and that she didn’t even try to defend the criticism that she didn’t bother to look at stomach histology to verify that there really was inflammation in the gastric mucosa, despite Carman’s touting that the “authors have over 60 years of combined experience and expertise in medicine, animal husbandry, animal nutrition, animal health, veterinary science, biochemistry, toxicology, medical research, histology, risk assessment, epidemiology and statistics.” Sad that they didn’t use all that experience to produce a paper whose results are believable and useful.
This isn’t Judy Carman’s first time…
In reading this study, I couldn’t help but notice the corresponding author: Judy Carman. I had heard that name before. But where? Oh, yes. I remembered. I had encountered her making some truly ridiculous claims about GMOs, so ridiculous that I think it’s worth bringing up now. She didn’t write the commentary I’m about to describe, but she voiced support for its findings, providing tactical air support to its author, Jack Heineman. I had wanted to write about it at the time I came across it, but, for whatever reason, didn’t manage it. So now’s as good a time as any. In brief, Carman appears to be an anti-GMO activist who, along with another anti-GMO activist, Professor Jack Heinemann at the University of Canterbury’s Centre for Integrated Research in Biosafety, made some truly nonsensical claims about GMOs. I first encountered these nonsensical claims in the blog of a homeopath named Heidi Stevenson, who claimed that genetically modified wheat may damage human genetics permanently.
Stevenson prefaces her article with this scary paragraph:
The Australian government, in the form of its science research arm, is joining Agribusiness profiteering by designing a GM wheat that could kill people who eat it & be inherited by their children.
Scared yet? Does Stevenson have your attention? Who are these nefarious scientists, and why would they want to make genetically modified wheat that would do these things? They wouldn’t, of course, but, like the Frankenstein that anti-GMO activists think scientists are, it’s a matter of messing with nature resulting in unintended consequences. In fact, the hilarity is such that I think it’s worth quoting a decent sized chunk of the first part of Stevenson’s article:
We have not yet seen the worst damage that genetic engineering may do. Australia’s governmental agency, Commonwealth Scientific and Industrial Research Organisation (CSIRO), is developing a wheat species that is engineered to turn off genes permanently.
Professor Jack Heinemann at the University of Canterbury’s Centre for Integrated Research in Biosafety has studied the wheat’s potential. Digital Journal reports that he says1:
What we found is that the molecules created in this wheat, intended to silence wheat genes, can match human genes, and through ingestion, these molecules can enter human beings and potentially silence our genes. The findings are absolutely assured. There is no doubt that these matches exist.
The implications are clarified by Professor Judy Carman of Flinders University:
If this silences the same gene in us that it silences in the wheat—well, children who are born with this enzyme not working tend to die by the age of about five.
Silencing the equivalent gene in humans that is silenced in this genetically modified wheat holds the potential of killing people. But it gets worse. Silenced genes are permanently silenced and can be passed down the generations.
Yes, that’s the very same Judy Carman who published this awful “stomach inflammation” study that I just discussed.
Basically, Carman’s claim here is that a variety of genetically modified wheat under development by the CSIRO will kill your children. I kid you not. And Judy Carman has not only promoted this idea but amplified it by emphasizing that she thinks children could die. Of course, Stevenson apparently doesn’t see the contradiction between saying that this GM wheat will kill your children but that its gene-silencing effects will also be passed down the generations. Neither does Carman, who continued:
As a result, there is a chain of evidence to show that there is a risk that the dsRNA from this GM wheat may survive digestion, enter the tissues of people that eat it and silence a gene or genes in those people. There is also evidence that any genetic changes so produced may be stable and become established in many cells of an organ. Furthermore, there a possibility that these changes may be passed-on to future generations.
In any case, I could recognize some amazing speculation and fear mongering right off the bat; so it’s time to explain.
Gene “silencing” means what the name implies: Shutting down the activity of a gene so that it stops making its gene product. Of course, gene silencing is not an all-or-nothing phenomenon. Like other forms of gene regulation, silencing happens on a continuum from zero to complete silencing, depending on the level and activity of the silencing agent. In this case, the silencing agent that is being turned into the bogeyman du jour is RNA. Specifically, it’s a type of RNA-mediated gene silencing called RNA interference (or RNAi), also known as post transcriptional gene silencing (PTGS). The idea is that the CSIRO is apparently engineering a strain of wheat that produces a short RNA molecule designed to silence specific genes in the wheat. Most of the time, when we talk about RNA, we talk about messenger RNA (mRNA), the RNA that is the intermediary between DNA and protein. However, back in the late 1990s, it was discovered that there are other RNA molecules that actually regulate gene expression by binding to complementary sequences on mRNAs. These molecules include classes of RNAs called microRNAs, as well as double-stranded RNA molecules known as short interfering RNA (siRNA), that can participate in cellular pathways that contribute to gene silencing, most commonly through binding to complementary sequences and inducing the degradation of different mRNAs in a sequence-specific manner. In fact, siRNAs were first discovered in plant genetics and only later was it discovered that short RNAs serve as a gene regulatory mechanism in mammalian cells as well.
An excellent video explanation of RNAi can be found, courtesy of Nature:
So what’s the problem? Heinemann and Carman are apparently worried that the siRNA that will be used to silence two genes in wheat called SEI and SEII. Heinemann apparently did an analysis based on the sequence of the SEI and SEII genes, comparing them against the human genome and looking for matches. He found them in the gene for the enzyme mentioned by Judy Carman. In humans, the equivalent gene is known as glucan (1,4‐alpha‐), branching enzyme 1, abbreviated GBE. Based on some similarities he found between SEI and GBE, Heinemann sounded an alarm through an anti-GMO activist group known as the Safe Food Foundation & Institute. Humans store carbohydrates as glycogen, and GBE makes branches in glycogen. There is a consequence to not being able to branch one’s glycogen, although not branching it in wheat could be useful for decreasing its glycemic index. There is a disease known as glycogen storage disease IV, which leads to damage to the liver over time. That’s the disease that Judy Carman was referring to.
Of course, the problem with Dr. Heinemann’s highly speculative analysis is that he didn’t know the actual siRNA sequences that were going to be used. Without that information his analysis was pretty pointless. At the very best, it was highly speculative. At the worst, it was ideologically and politically motivated.
So how could this possibly matter? After all, it’s RNA. It’s really unstable, isn’t it? Well, not exactly. Single stranded RNA is very unstable. It can’t survive long outside of the cell. However, dsRNA can be quite stable, even outside of a cell. But that still leaves the question of whether dsRNA from a plant that is eaten can have any effect. To do that, the siRNA would have to survive digestion, be absorbed into the bloodstream, enter other cells, and act on gene expression. Heinemann notes that such a phenomenon can be observed in insects and worms.
But can it happen in humans? Well, there is one paper that Heinemann latched on to because he thinks it demonstrates that the same phenomenon can happen in humans. It’s a paper by Zhang et al. published in Cell Research that showed that showed that a plant-derived microRNA (miR-168a) from rice can be found in human serum after ingesting rice and that it can actually bind to the mRNA for low-density lipoprotein receptor adapter protein 1, thus inhibiting the expression of this protein. It’s an interesting observation, but there are a number of questions. For one thing, although the microRNAs are detectable in serum they circulate at a really low concentration, namely the femtomolar range (10-15 mole/Liter). News stories describing the study at the time were quite credulous, but a better discussion can be found at Sandwalk. In any case, the exceedingly low concentration of microRNA observed in the bloodstream leaves a huge question in that there is no known mechanism by which such a low concentration could have such an effect. When I first read the study, I thought it plausible, but the more I think about it the more I agree with the Sandwalk commenter who says it screams “artifact” to him. Or this commenter:
There is probably 10 fM of everything in the blood. Sheesh, that’s less than 4×10^9 molecules per whole body consisting of about 7×10^12 cells and containing no more than 7×10^10 hepatocytes. That’s less than 0.1 miRNA per liver cell in the best possible scenario. What are these RNAs, totally magic?
Maybe they’re homeopathic, although admittedly fM concentrations are far and away greater than the concentrations of most homeopathic remedies (i.e., zero). In any case, stoichiometry is your friend when figuring these things out. Personally, I’ll wait for some confirmation that this happens from other groups before I buy it. True, another group has reported finding miR-168a, but it also reported a huge variety of microRNAs in the serum from a variety of sources, including bacteria and fungi as well as from other species, such as various insects. Basically, we’re awash in microRNAs from other species that we come into contact with. So far, the only evidence that they have any effect whatsoever is that one study suggesting that miR-168a might regulate one gene, even though it’s hard to figure out by what mechanism it could possibly accomplish this. Add to that the utter lack of evidence that any circulating microRNA can not only silence a gene in human cells but actually induce epigenetic changes, and Professor Heinemann’s speculation becomes ever more…speculative. This is true particularly in light of the fact that we regularly eat plants that make many siRNAs and microRNAs. Why would GM wheat siRNAs be any different or more dangerous, particularly given the very low concentrations involved?
Let’s put it this way. For Heinemann and Carman’s fear mongering to be a real concern, any siRNA or microRNA from genetically modified wheat would not only have to be made in sufficient quantity at least to equal the normal concentration of miR-168a in rice, but also be stable enough to pass through stomach acid and the gut lining undigested, and get into the bloodstream at a high enough level to affect gene expression. That’s leaving aside the question of whether there is even enough sequence match that the siRNA could even target the human GBE mRNA in the first place, which is impossible to say because we don’t know the actual sequence of the siRNA being used. It’s true that Heinemann has updated his “report.” However, that update doesn’t really show anything new or contribute to the plausibility of Heinemann’s concerns. In fact, it trashes the plausibility even more because the homology (in laymen’s terms, match) to the glycogen enzyme that Heinemann was promoting pretty much disappears in this reanalysis. (In fact, if you look at it in depth, it wasn’t even there to begin with, and it’s questionable whether he even used the right wheat sequence in his BLAST analyses.) Even in the reanalysis, the only areas of match appeared in introns, which, as Biofortified put it:
However, all of the matches he highlights are either to introns – which would not matter for the mechanism of action that is the issue here. Or they are in the genome desert areas, thousands of bases away from anything that appears to be a gene.
Result: Take a deep breath. The GMO wheat that forms the basis of this claim will not kill your children or permanently alter your genome.
More interestingly, I decided to check back and see if the human GBE gene is still sticking with this sequence switcheroo. The main fear-based claim was that the GBE gene would be suppressed and children with a disorder of this can die by the age of 5. So let’s see–let’s do an analysis of this new sequence and compare it to GBE. If you perform a BLASTn at NCBI with these two sequences and default settings as Jack says he does, what do we get?
The result? No significant similarity found.
That’s right. The entire foundation of the fear–the match to GBE–is gone. Evaporated. Vanished. Nada. Zip.
No wonder Australian and New Zealand regulators have rejected the concerns.
Add to that the enormous lack of likelihood that, even if the siRNAs and microRNAs in GM wheat could actually make it into the bloodstream in concentrations sufficient to alter gene expression, it’s incredibly unlikely that such RNAs could actually induce “permanent” epigenetic changes to justify the fear mongering.
There might be questions about GMOs, but by and large they are not issues of safety. Rather, they are issues of intellectual property; i.e., how large companies developing GMOs behave. Hysteria of the like generated by the likes of Jack Heinemann and Judy Carman and parroted by useful idiots like Heidi Stevenson generate heat, but no light. Nor does the latest round of attempts to generate hysterical fear mongering based on Carman’s latest study. Both Heinemann’s speculations and Carman’s most recent bit of data mining are of a piece. They are not designed to provide a dispassionate analysis of the true potential risks and benefits of GMOs. They are designed to be propaganda to produce fear, uncertainty, and doubt about GMOs, just like Andrew Wakefield’s studies about the MMR vaccine, just like Mark and David Geier’s studies of thimerosal in vaccines, just like the studies of any variety of antivaccine cranks. It is the equivalent of shouting “fire!” in a crowded theater.
Unfortunately, the pseudoscience is metastasizing. GMO Pundit points out the next frontier of anti-GMO fear mongering.:
Yes, because a new flu vaccine Flublok is made in “insect cells” (specifically, the baculovirus system, a very common system of expressing mammalian proteins for use in genetically engineered products), it is now a “GMO product” and to be feared as much as GMO-derived foods. In actuality, Flublok should end up being safer than the old flu vaccine because it doesn’t include all those extraneous proteins, such as egg protein, just the three hemagglutinin, or HA proteins, of the most common flu strains circulating in any given year.
What’s next? Telling diabetics that they shouldn’t take insulin derived from genetic engineering because the protein is made in—gasp!—bacteria or yeast?
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