Proceedings of the Green Ireland Conference • Kilkenny Castle, 16-18 June 2006

First speech by:

Dr. Stanley Ewen

Dr. Stanley Ewen is a Consultant Histopathologist with Grampian University Hospitals Trust in the UK. He is also a member of the Independent Science Panel (www.indsp.org), an international transdisciplinary network of scientists working for the public good. He and Dr. Arpad Pusztai's paper on the health risks of GM food was published in The Lancet.

This is the verbatim transcript of a video recording of the first of two speeches which Dr. Ewen made at this Green Ireland conference, including all of the slides from his PowerPoint presentation entitled Potential adverse human health effects of GM foods.

The PowerPoint presentation can also be downloaded separately as a 4.7 MB ppt file. Dr. Ewen's second speech may be found here.

Numbers in the text refer to the endnotes below the main text. These endnotes, (together with the notes between round brackets in the main text) are by the conference chair, Michael O'Callaghan.

Transcript:   download as printer-friendly 1.3 MB pdf file

Dr. Stanley Ewen:

I'm very happy to be here and thank you very much indeed Michael, for inviting me. I've been greatly impressed so far with all your efforts. Tell me, if the UK includes Ulster, is that not a thorn in your flesh? Isn't the wind going to blow from the wrong way?

Michael O'Callaghan (conference chair):

We absolutely need (GM policy) co-ordination across the border, and I can just partially answer your question very quickly by saying that two or three years ago I got a phone call from (Professor Robin Grove-White,) a member of the UK Agriculture and Environment Biotechnology Commission [1] that was under statutory orders to be consulted in the formulation of the UK policy on GM issues - it's the same group that Dr. Sue Mayer was part of [2]. He was at a meeting in Belfast to talk with the government people up there on GM policy. And they had invited people from the Department of Agriculture here in the Republic. And he phoned me up to say "I just want to warn you that the people from your Department of Agriculture are woefully ignorant about the subject, and you need to bring them up to speed on it"! [3]. So we do need to coordinate both at the governmental and grassroots level, between companies and businesses and food producers across the border in order to have a viable policy on this island [4].

Dr. Stanley Ewen:

Absolutely! But it seems a bit theoretical too. Poland is GM-free, but what about the country next door? [5]

Slide 1: Potential adverse human health effects of GM foods

Slide 2: Affiliation • Retired from Aberdeen University. • Presently - National Health Service Histopathologist. • No present or past involvement with commercial food production. • Member of Independent Science Panel (ISP) • Co-author in peer-reviewed paper on carrageenin and colonic ulceration.

Well as I said, it's great to be here! I'm just a humble pathologist; I'm still practicing although I'm sixty-seven. They should have pensioned me off long ago, but the University of Aberdeen got rid of me - or at least I got rid of them - when things got very tough.

I retired from the University of Aberdeen because they didn't like the GM story that I was involved in at all. I had been working with Dr. Arpad Pusztai at the Rowett Research Institute [6] since around 1990, and we had been doing all sorts of exciting experiments.

This GM story was in fact one at the end of a great long line of experiments looking, hopefully, to show that GM food was no different from normal parent food. But in fact we found the opposite. And at that point they didn't like me! So I changed over to the National Health Service as a histopathologist. I'd like to say that I have no present or past involvement with any commercial food production, because there are so many people who masquerade.

I'm a member of the Independent Science Panel [7] and I will just put this last comment in: I've been interested in food and food ingredients for a number of years, and I was a co-author in a peer-reviewed paper on carrageenan [8]. Now carrageenan doesn't strike a chord, I know, but it is a food additive. And we showed some ten or fifteen years ago that it causes ulceration - ulcerative colitis - in guinea pigs [9]. But I can assure you that to this day you can buy it in various preparations, mainly from Danone, and it's still available in their little pots of food today. Nobody paid any attention to the research then, so why should they pay any attention to my research now? Before that, by the way, I was involved with Diabetes mellitus and nitrosamines in smoked food; smoked food is a bit like eating the smoke that you inhale from a cigarette: it can be bad for you!

Let me get on with the main burden of what I want to say.

This paper that I want to present to you is in fact a formulation that I drew up last october for presentation to the FAo - the United Nations Food and Agriculture organisation - in Rome [10]. That was my second meeting with a UN organisation. My first was with the WHo (World Health organisation) in Geneva; where I laid my case on the table to speak at the meeting, the person next to me happened to be the chairman of ACNFP - the UK Food Standards Agency Advisory Committee on Novel Foods and Processes [11], and when he found it was me who was sitting next to him he moved his seat! So this is just to say that I am still reviled.

Slide 3: Assessment of potential adverse human health effects • Classical toxicological methods cannot be used to assess food safety due to compositional complexity, thus substantial equivalence has prevailed. • A physiological, nutritional or structural approach is more appropriate but acceptable animal studies, reported in quality journals, are few. • Some of the relevant available evidence in the public domain will be outlined.

The problem with food is that classical toxicological methods cannot be used to assess food safety, mainly due to compositional complexity and thus "substantial equivalence" has prevailed [12]. This word "substantial equivalence" is a problem. It's a term developed from GRAS - which stands for Generally Recognised as Safe. That was the original concept, and from that grew up this notion of "substantial equivalence". But nobody has defined it. How many substantial deviations are possible? What is the sort of deviation from the mean that is permitted? Nobody has defined it, I'm afraid.

I believe that a more physiological and nutritional approach is appropriate. But unfortunately, when we come to look for animal studies, properly refereed in quality journals, there are very very few indeed.

Part of the problem may be - and we've heard a great deal of discussion about the American viewpoint (see speeches by Percy Schmeiser [13] from Canada and Deborah Koons Garcia [14] from the USA) - and perhaps to put the record straight, we must say that the American regulatory process is of course voluntary.

There is no incumbency at all on any biotech company to submit their product to the FDA (the US Food and Drug Administration) [15]. And therefore, in fact, the FDA has not formally approved a single GE crop for human consumption!

I'm quoting from Freeze and Schubert who wrote a most interesting chapter in a book [16] which reads like a novel, and I commend it to everyone here because it is full of what I consider to be the truth.

Just to put that perspective in front of everyone: so here (i.e. in the USA), on one hand we have a voluntary system - mainly voluntary because in the early 1990s, when set up by father Bush and Reagan, it was thought that this aided competitiveness! [17]

One of the problems is then, and I want, in essence, I'd like to develop the use of animals, but the question is, and when I was invited to give the talk in Rome, I had to put both sides of the argument. Because the argument is that foods will, normal foods will contain toxins etc., so you have to put both sides of the coin.

Slide 4: Are the animal results helpful in assessing potential health effects? • Do the transgenic products survive animal digestion? • Is there variability in survival of transgenic products in human GI tract? • Do the transgenic products bind to human gut cells? And one of the questions was, "are animal results helpful in assessing health changes?" And therefore I tried to make three headings in this talk: • Do the transgenic products survive animal digestion? • Is there variability in survival of transgenic products in the human GI (gastro-intestinal) tract? • And do the transgenic products bind to the human gut cells? obviously if they don't bind, they go whistling straight through.

So first of all, looking at binding of normal food: these are substances that we are eating every day. We have to obviously mention right at the very beginning that many of the transgenic products [18], once they are cooked, become relatively harmless. I'm really concerned about the next generation of GE products which will be eaten raw. So we have to bear that in mind

Slide 5: Binding of normal food and transgenic products to animal gut

Slide 6: Binding of normal food components to mammalian gut? • The usual "food" components that can bind are lectins, adhesins and toxins. • Lectins will bind to specific sugars along the gut and many resist digestion and will reach colon - some are mitogenic. • Bacterial adhesins attach to sugars and may reach colon to bind to blood group substances in caecum. • BT produces an AB toxin and the B subunit binds to cells surfaces.

So first of all, looking at normal food products and their binding to animal gut.

The usual food products that bind to the human gut, or any gut in fact, are lectins [19], which you find in plants, they are ubiquitous; adhesins [20], which are bacterial products very similar to lectins; and toxins [21].

Of course lectins will bind to specific sugars, which are present along the gut, and many of these lectins resist digestion and will reach the colon (i.e. the lower and last part of the digestive tract) without change. But bear in mind that some lectins are mitogenic (in other words, they cause the gut to proliferate and grow), and some will be in fact anti-mitogenic.

Bacterial adhesins, on the other hand, adhere to, attach to sugars and may reach the colon to bind to blood group substances in the caecum [22], and for example, E. coli 0157 [23] - that's the situation that it binds to blood group substances in the caecum, and causes a right-sided colitis [24].

Bt - that's Bacillus thuringiensis [25] - produces an AB toxin, and the B subunit binds to cell surfaces. (Bacillus thuringiensis is a soil bacterium that produces small quantities of toxins to poison its predators. About 40 per cent of all GM crops currently on the market are the so-called Bt crops - i.e. modified by insertion of DNA from these bacteria - so that every cell of such crops produces the insecticide, and does so all the time and in larger amounts than do the soil bacteria. As a result, the entire genetically modified Bt plants producing this toxin are classified as insecticides in the USA!)

Now just to give you an example, here's wheat germ agglutinin [26] fed to a 100 gm rat for ten days.

Slide 7: Wheat germ agglutinin fed to 100g rat for 10 days. IC with antibody to WGA

Slide 8: Rat jejunum crypt and villus length (μm) 10 d normal food
	Crypt	Villus
PHA	246 (6)	548 (11)
SBL	180 (3)	512 (9)
SB meal	133 (3)	512 (9)
GNA	94 (2)	509 (22)
Egg albumen	118 (3)	579 (14)
Lactalbumin	103 (2)	607 (16)

This is immunocytic chemistry - and by the way, this is pure microscopy, I hope you have some knowledge of microscopy. Have any of you never seen down a microscope before? OK, right, thank you.

Slide 9: Jejunal crypt of rat (100g) fed high dose Galanthus nivalis agglutinin for 5 d. IC stained with antibody to GNA

Here then we have the villus. The vilus is the main part of the digestive system [27]. once you have amino acids etc. [28], then they are absorbed by the villus. And this finger-like projection is actually part of the small intestine. As you know the gastro-intestinal tract is divided up into stomach, small intestine, and colon. Most of the digestion happens in the small intestine (i.e. the jejunum).

Slide 10: Jejunal crypt of rat (100 gm) fed PHA for 5 days. Freeze substitution plastic embedding

Here then the wheat germ agglutinin in the small intestine, at a fixed distance from the pylorus, the stomach, always at a 10 cm fixed point so everything is directly comparable (we have to be comparing apples with apples). And there then is the staining which shows - notice the dark staining on the surface, and notice as well these particles within the cytoplasm: so the wheat germ agglutinin has actually entered your body at this point.

Now of course, the small intestine turns itself over. These cells come up from the base of the crypt - and I'll be showing you that in a moment - and move up and are rejected or ejected from the tip of the villus in five days. So anything happening, being caused by the adhesin, doesn't matter, because it's going to be turned over in five days - no problem. So that's a normal substance, wheat germ agglutinin, which you could eat raw.

Slide 8: Rat jejunum crypt and villus length (μm) 10 d normal food
	Crypt	Villus
PHA	246 (6)	548 (11)
SBL	180 (3)	512 (9)
SB meal	133 (3)	512 (9)
GNA	94 (2)	509 (22)
Egg albumen	118 (3)	579 (14)
Lactalbumin	103 (2)	607 (16)

Now, this may be slightly redundant and I wonder if I shouldn't just carry on quite quickly, but suffice it to say that if you look at it at surface level, here then is red kidney bean (PHA), this is soya bean lectin (SBL), this is soya bean meal (SB meal), and this is GNA which stands for Galanthus nivalis agglutinin (i.e. snowdrop lectin), and egg albumen; lactalbumin was the control protein that we used.

So this is the normal depth of the crypt (103 μm) [29]. The crypt is the part that generates cells for the rest of the villus - the finger-like structure in the small intestine.

But notice this one here: Galanthus nivalis agglutinin, which is the snowdrop lectin, actually causes a reduction in height (94 μm) compared to the normal (103 μm).

Whereas this one up here (246 μm), and including soya bean lectin (180 μm) by the way, these two, raw, will cause an elongation, whereas this one here (GNA at 94 μm) caused a shortening. And for that reason we selected it for our model GM product.

(Re. slide 9:) And just to say that whereas most of the absorption takes place in the finger-like process, which is up here, notice that the binding will also occur at the base of the crypt - the generative part - so it binds here and also enters the cells down here to control the whole process of generation and cell turnover time in the small intestine.

(Re. slide 10:) And there's the proof there, by the way, that it's also entering the cells of the crypt.

Slide 11: Animal GM feeding experiments need further investigation: • As a pathologist, I suggest that chronic toxicity, carcinogenesis and teratogenesis of GM products are seriously under-investigated. • Feeding a single GM food to an experimental animal is representative of diets in Africa. • This is a neglected area and animals ought to be used to determine the safety of a GM product. • Two "historical" experiments remain valid.

Now looking at the whole process here, as a pathologist I suggest that chronic toxicity, carcinogenesis (production of cancer) and teratogenesis (production of congenital malformations or birth defects) of GM products are seriously under-investigated.

Some criticism was levelled at the experiments that we did. At least, I didn't do them, it was Arpad's idea (i.e. Dr. Arpad Pusztai) [30] - he was the brains behind it.

As I say, pathologists and hospital situations tend to be reactive; you know, "here's a disease, you find out what caused it". In the same way, he wanted to know were there any changes in the gut - structural changes - and I was able to answer that for him, over several years.

One of the criticisms was that you cannot feed a single food to a rat as a model of human food consumption: you're taking a different series of ingredients as food. But in fact, if you consider it, feeding a single GM food to an experimental animal is quite representative of diets in Africa - particularly, for example, in Somalia, where you saw just now recently on the television that they are eating perhaps just a porridge-like thing once a day, and it's one product only. So in a sense humans do sometimes eat only one food. And I believe there's a greatly neglected area, and animals ought to be used to determine the safety of a GM product.

And I wanted to just mention two historical experiments now which I believe still remain valid.

Slide 12: Published (1998 & 1999) raw GM-potato micro
Authors	Fares et al.	Ewen & Pusztai
Species	male mouse	male rat
Age	4 wk	6 wk (84 g)
Feeding time	14 days	10 days
Inserted gene	B. thuringiensis	Galanthus n.ag
Examination	ileal villus planimetry	jejunal crypt image anal.
Result	+ 21.7%	+ 57.8%

Suffice it to say that although Ewen and Pusztai published in The Lancet [31], we were actually pipped to the post by Fares [32], an Egyptian who worked with potatoes; he fed his raw GM potatoes to mice, and the result was an increased growth of almost 22 per cent. Whereas when we measured it in the rat, there was an almost 58 per cent increased size of the crypt. And that really was unexpected in a "substantially equivalent" foodstuff! [33].

Slide 13: Jejunum
Raw GM GNA potato fed 10d to rat (starting weight 84g). HE	(same distance from pylorus) Raw parent potato

And here is the photographic evidence. This was, by the way, before I did all my digital photography. The bit that we are really looking at is the bit here in the lower part. This is the crypt down here. This is the finger-like structure that does the absorption. And notice this great elongation of the crypt: this is what really disturbed me. The raw GM product had caused this elongation that we could never have predicted!

And I think you might agree that there are little black cells here in the mucosa [34], and when you do a formal count, they too are increased; these are the intra-epithelial lymphocytes - the inflammatory cells that respond to virus infection.

Now of course, as you know and as Michael said, "why should I have to eat virus (DNA)?" Well the point about the virus is that the way in which the cassette (i.e. the package of transgenic DNA from other species that is inserted into a recipient organism in order to modify its genetic code) is driven in GM food is to put a driving mechanism - something that promotes the expression of the gene right beside it, and that's the infectious part of a virus, not the whole virus - just this promoter. And that of course comes in this instance from the Cauliflower mosaic virus (known as the CaMV promoter gene) [35].

So in other words, looking at these photographs, the virus seems to have caused an inflammatory change, a mild inflammatory change, this hyperplasia - excess growth - and we recorded that in The Lancet in 1999 [36].

And one of the responses was that this paper was "a heap of steaming horse manure" - that's what one commentator said; he didn't use the word "manure", by the way!

Slide 14: comparison of colon of rats fed on GM potato (left) and ordinary potato (right)

Now the thing was, of course, what happened further down the gastro-intestinal tract? And here we have the colon. And you can see here is the normal and here is the one that has been fed the raw GM. So it is doing something to the colon as well. It hasn't been digested. We can go into the reasons for that later, but I'll speed on.

Slide 15: Jejeunal changes in rats fed on GM potatoes (D' Mello 2003)
	Parent raw	Parent raw + GNA	Raw GM
Crypt cell count	15.8 (1.5)	17.0 (1.6)	20.3 (1.8)
Mitoses (10 crypts)	5.8	5.2	7.5
		p <0.0005	p <0.0005

I quantified all this. It has been written up in D' Mello's book on food safety [37], and if you do a formal count, you find that the number of cells in the crypt is increased with the raw feeding of potatoes that are genetically modified to express the snowdrop lectin. This is the parent, by the way, and this is the raw. So there's the difference: the number of mitotic divisions [38] in the cell has increased, and these are all very highly significant results.

Slide 16: IEL /100 epith. cells raw or boiled GM/parent potatoes
Jejeunum	raw	boiled
Parent	13.2 (2.9)	4.6 (0.3)
GNA-GM	21.4 (3.9)	10.3 (0.3)
	p < 0.01	p < 0.01

And then the number of inflammatory cells has also increased in the raw. There's the parent - that's the background number - whereas in the genetically modified potato you can find the inflammatory cells have risen, per unit, and the unit is 100 epithelial cells up there. You count 100 epithelial cells and then count the number of lymphocytes, and you find that's the number. So that's my evidence for saying that there is some sort of reaction to the virus (material) that is incorporated into the GM food. And this is what they are supposed to do.

Slide 17: Intraepithelial lymphocytes in small bowel mucosa • Usually between villus cells and believed to be suppressor/cytotoxic T lymphocytes. • Surveillance function for damaged or virally infected cells. • Greatly reduced in germ free animals. • Greatly increased in coeliac disease.

These inflammatory cells are usually situated between the villus cells and are believed to be suppressor / cytotoxic T lymphocytes - all highly technical. And they have a surveillance function; they are greatly reduced in germ-free animals, and greatly increased in coeliac disease [39], which is quite common in Ireland.

Slide 18: The effect of cooking on GM products • Experiments should test raw against cooked GM produce (DNA denatured at 95C for 5min). • Ewen & Pusztai did demonstrate that raw GM potatoes produced unexpected hyperplasia. • Boiling of GM potatoes almost completely reduced the hyperplastic effect on rat mucosa.

If you cook the potatoes, of course, or cook any GM food, as I have said already, we must always test raw against cooked. And by the way, DNA is denatured - destroyed - by heating for five minutes at 95 degrees centigrade.

The summary is that Ewen and Pusztai did demonstrate that raw GM potatoes produced unexpected hyperplasia [40]. Boiling of the potatoes almost completely reduced the effect.

Slide 19: Uncooked GM products • We assume that uncooked GM potatoes contain an unidentified growth factor. • Fruit and vegetables may be consumed raw (up to 40% of diet) and thus the availability of dietary transgenic DNA would be maximised. • Pusztai's 110 day cooked GM potato feeding displayed significant differences in organ weights (no histology taken).

Now we assume that the uncooked GM potatoes contain some unidentified at present growth factor, although in my talk tomorrow [41]. I'll try and explore that slightly further, because I think the unidentified growth factor almost certainly is the cauliflower mosaic virus gene.

Now in a sense it doesn't really matter if cooking is involved, or processing. All soya is heavily processed. But I am concerned about the eating of fruit and vegetables which may be consumed raw - up to 40 per cent of the diet, or even more if you're a vegetarian. Thus the availability of dietary transgenic DNA will be maximized. The point is to bear in mind that even at 110 days, although I didn't get histology [42], he could still show differences in the cooked GM potato in the organ weights. Everything was very carefully scrutinised in these animals and Pusztai weighed every single organ in the rat's body.

Slide 20: Example from the past • The first commercial safety test was on GM tomato: • Feeding trial of tomato fruit (protein and energy content cannot support growth). • 15 ml/kg of tomato homogenate to 5 female or male rats -haematology and wt gain similar between groups. • But starting weight of animals very wide (+/- 23%) cf. Ewen & Pusztai 84g +/- 1g.

Now just to say that of course in the past, we can understand from the regulatory process such as it is in America, that this was a tomato - by the way, the first commercial safety test was on a tomato; the feeding trial was a tomato fruit - and notice that the protein and energy content of a tomato is insufficient to support growth, so something else has to be given.

Anyway, what they found was that 15 ml per kilogram of tomato homogenate was given to five female or male rats and the haematology [43] and weight gain was similar between the groups. But, as bedevils so many of these experiments, they are not actually done by the biotechnology groups, they are actually put out to some firm, sub-contracted to some other firm that will do the experiments for them. And the difficulty with these particular experiments was that the starting weight of the animals was very wide indeed, and you couldn't really draw any conclusion from it. It was like they deliberately designed the experiment to fail. The figures of course are that the weights are plus or minus 23 per cent, whereas in our animals they were all 84 grammes, plus or minus one gramme.

Slide 21: Detailed results of safety test • 28 day histology study (gavage). • Urea and electrolytes not different. • Treatment related erosions in gastric mucosa of 4 female rats (increased to 7 by histopathological experts). • No lesions in male group or controls. • Erosions can cause severe haemorrhage in human equivalent - these rat lesions deemed "not related to GM ingestion" 7 of 40 eating GM died at 2wk (cause of death not specified).

The detailed results: just to say maybe we can skip some of this, as I'm very aware of the time.

In the gastric mucosa then, there were erosions. We mustn't downplay these gastric erosions because a gastric erosion in humans could be fatal because of haemorrhage (internal bleeding). There were no lesions in the male groups. And there is the story there about severe haemorrhages.

Slide 22: Murine liver and pancreatic changes after GM soya • Animals not pair fed and zone of EM hepatic sample not specified. • Findings; nuclei and nucleoli irregular in GM fed suggestive of increased metabolic rate. • Reduced digestive enzyme synthesis in pancreas possibly due to reduced post transcriptional hnRNA processing. – Liver has a vast reserve capacity but could hepatoma be accelerated in areas of hepatitis?

Now there were other changes in other experimental situations. More recent work was by Malatesta (Manuela Malatesta and colleagues in the Universities of Pavia and Urbino in Italy) [44 & 45], and I deliberately included this because it describes changes in the murine liver - mouse liver - after ingesting GM soya. There are objections to some of the protocol, but just to say that some of the nucleoli were changed in the GM-fed animals, suggestive of an increased metabolic rate. Something was occurring in the GM-fed animals.

Slide 23: Pancreatic ultrastructural changes in mice fed GM soybean • 4 groups of 3 female mice fed for 1,2,5 or 8 months on 14% GM soyabean. • Significant reduction in amylase labelling over zymogen granules in all 4 groups of GM fed mice consistent with stimulation of secretion. • Soya is associated with adenoma formation but not with ductal adenocarcinoma.

And when I spoke to her at the end concerning this experiment here - this is also Malatesta's work - once again changes were seen: and this time it was the zymogen granules [46]. And when I spoke to Malatesta after the meeting, she said that they also had, in the same university, results that were very similar to ours. But the dean of the university concerned had suppressed the publication of the findings [47].

So at all levels, at all places, there's what I would call corruption of the truth [48].

Slide 24: Monsanto 863 maize • Contract rat study using 460 animals. • Significant increases in WBC and lymphocyte counts in males and reduced retic. count in females were considered within normal range. • But a government commissioned report by AJP indicates possible differences in interpretation of the findings. • Histology was not taken from normal control rats for comparative quantitative measurements.

I don't need to discuss this, I don't think [49].

Slide 25: Animal model - human diseases; discrepancies? • Rodent stomach - upper third squamous. • The rat caecum is large and the colon produces faecal pellets. • The use of rodents has been grossly underused in food safety testing. • In vitro data cannot determine safety for human consumption unless tested in animals • Inter group differences revealed by sophisticated tests on comprehensive animal trials with substantially equivalent GM crops are meaningful.

One of the problems, I think however - once again trying to be fair to both sides - is that animals and humans are different. For example, the rodent stomach is different because it's got a squamous lining [50], whereas ours is a mucous lining. The rat caecum is large, and the colon produces faecal pellets whereas ours is a continuous stream of faeces.

Nevertheless, despite these minor adjustments, I think the use of rodents has been grossly underused as a food safety-testing device.

Slide 26: Simulated gastric juice digestion of DNA and protein • Simplistic studies with artificial gastric juice and pepsin are inadequate in the human situation. • Recombinant proteins are relatively easily destroyed by HCl + pepsin - use of toxin from GM plant should be obligatory. • Babies and up to 2/5 of adults (PPI) have greatly reduced gastric acidity thus transgenic DNA survival in human gut could be facilitated. • Especially as plant DNA is surrounded by lignin.

The other main criticism I have with GM food and what biotechnology has tried to convince us of, is the fact that studies so far are rather simplistic. They use artificial gastric juice and pepsin, which are the basic components of gastric digestion, but there is a problem because the proteins that they use are recombinant (i.e. mass produced in a laboratory) - they are not the proteins from the (GM) crop: it's cheating. Because generally speaking, these recombinant proteins are much more easily broken down. And they also use a far higher level of HCL (hydrochloric acid) than exists in the human stomach.

So a lot of the work that's been reported and that is part of the submission to the regulatory bodies is bogus, in my opinion [51].

Now just to say that babies of course, and up to two fifths of adults have altered gastric juice. I'm not going to do a count of how many people in this room are taking PPIs (Proton Pump Inhibitors), but I do, for one. So the effect of taking treatment means that the acid in your stomach is greatly reduced, and therefore the digestion of, say, a GM protein, is greatly reduced, therefore more gets down to the colon.

And this is one of the fallacies, I think, in which much of the food story is based. There is an assumption that we all have a "normal" gastro-intestinal tract. And that is not true, of course. Many of us will have lesions in the gastro-intestinal tract that we don't know about. We may have acid reflux [52] up our oesophagus (i.e. the alimentary canal from the mouth to the stomach). We may have Helicobacter pylori [53]; we may have a polyp in the colon [54]. And it is this problem, I think - the person with early disease - that I am speaking up for.

Slide 27: Binding and survival of transgenic products in humans

Binding.

Slide 28: "Historical" GM deaths • Tryptophan (dietary supplement), produced by recombinant DNA, caused a completely new illness - eosinophilia myalgia syndrome (EMS). • In or around 1989 there were 38 deaths recorded as a result of EMS. • One or more toxic impurity caused the deaths but no animal model or in vitro test has been developed to identify the case-associated impurity in a relatively simple problem although deviant metabolism in some GM organisms is likely.

This is historical [55], in a sense, and we can skip over that, and maybe focus on plant DNA and the human gastro-intestinal tract.

Slide 29: Plant DNA and the human GI tract • First human study of GM soya ingestion (Netherwood et al.). • 3 of 7 ileostomy patients contained CaMV 35S promoter before study had started. • All 7 passed excreta containing GM DNA after test meal ("surprised that any could survive"). • Faeces of 12 volunteer controls contained no CaMV (were they age and sex matched?)

This is time it's human: this was a study, and you know it was the Newcastle study (by Netherwood at al.) [56]. But notice: three of the seven ileostomy patients - these are people, by the way, with a side passage (the small intestine is simply discharging out onto the surface, so you can give them food up here and look at the contents of the ileostomy bag; a nice little experiment) - but notice that three of the seven people actually contained cauliflower mosaic virus (CaMV) 35S promoter before the study started. So interestingly enough, they must have eaten, somewhere, GM food, and that's in Newcastle!

And interestingly enough, all seven passed excreta containing GM DNA after the test meal. And the authors were surprised that any could survive. I wasn't surprised; I fully expected it from my results in the colon of the rats.

The faeces of the twelve volunteers who passed the food - of course, per rectum - contained no CaMV. But were they age and sex matched to the seven ileostomy people? The ileostomy people must have had their colon removed for some reason, but we were not informed. So like many papers, there are referee faults. The referee should have been much stricter, before this paper was allowed to be published.

Slide 30: Unanswered questions concerning Netherwood et al. • We are not informed about the reason for resection of colon (not terminal ileum as stated) - was the disease colonic malignancy or inflammatory bowel disease which could affect remaining small bowel function? • If unprocessed GM food was to be ingested possibly much more transgenic DNA would access, and be released into, the normal colon. • Fate of stoma excreta - septic tank to aquatic life?

So the unanswered questions are: Why was the colon removed? Was it for malignancy or for inflammatory bowel disease? And the other question is, if unprocessed GM food was to be ingested, much more DNA would access, and be released into, the normal colon. And of course the question is, what happens to stoma excreta (i.e. faecal matter) when it gets into the septic tank, or aquatic life, it's then just passed on into the river, obviously.

I'm going to go rather quickly because I'm running out of time. My actual business is of course to show you human material, and to say that there are certain lesions there in the human gastro-intestinal tract that are pre-neoplastic (Neoplasia is the correct, scientific term for diseases commonly called "cancer", "tumor" or "growth". Neoplasms can be benign or malignant lesions.)

Slide 31: DNA does persist in gut? • GM soya bean survived the whole length of remnant ileum when fed to humans with an ileostomy. • Thus transgenic DNA could be taken up by small bowel bacteria. • Transgenic DNA does survive to pass into human colon. • In pigs, DNA is transferred to duodenal juice, lymphocytes and liver (Chowdury, J. anim.sci. 2003).

Slide 32: Cell survival and vulnerability • Popular belief - "the cells of the gut have a rapid turnover thus the chances of adverse consequences are highly unlikely". • This is true in the human small intestine but malignancy affects stomach and colorectum. • Dysplastic cells are transformed or immortalised and have an extended lifespan.

Slide 33: Unstable lesions in human GIT • Lesions of OGJ occur usually as a result of obesity-induced reflux. • Step 1 - metaplasia from squamous to columnar small bowel type mucosa. • Step 2 - binding of lectin (Bt) to columnar epithelium with endocytosis. • Step 3 - growth factor effect.

Slide 34: oesophagus - diseased v. normal Above: diseased in 77 year-old male • Below: normal in 63 year-old female

This is the normal situation. This is a control biopsy in a female, 63 years. This is a male of 77. I know it's not age-matched, but you can't organise things for taking photographs all that well. But notice that at the same point in the human gastro-intestinal tract this normal mucosa has changed into this. And this is an absorbite mucosa, therefore if there is any carcinogens, any product from a GM food, it will be absorbed. And this is one of the areas at the present time where there is a known increase in rate of malignancy. The oesophagal-gastic junction is increasing in cancer incidents.

Slide 35: unstable lesion (2) • Helicobacter pylori (HP) organisms infect 40-50% of stomachs by 50 yr. • HP produces intense inflammation with ensuing intestinal metaplasia. • Binding of transgenic Bt toxin occurs with growth factor effect. • Possible accelerated transition to dysplasia and neoplasia.

Unstable lesion 2: stomach, after infection with Helicobacter pylori organisms.

Slide 36: Stomach: diseased v. normal Above: normal stomach in 63 year-old female Below: diseased stomach in 52 year-old male

There's the normal (second image above): you can see it's quite nice, but there (image directly above) you can see it's changed into small intestinal mucosa. And that's the effect of the microorganism. Now we don't know we've got that (infection), but if there's binding here, and a variety of hydroplastic agents [57] going in here, my concern is that this might speed up the formation of stomach cancer. Now I've no direct evidence for that, except to say we've observed this hyperplasia [58] in the small intestine.

Slide 37: unstable lesion (3) • Colorectal cancer common in Scotland. • Multi centre study (1985) revealed 60%, 45% and 13% autopsy incidence (all ages) in NE Scotland, Tromso and Kuopio resp. • Could the transgenic DNA growth effect speed up the interval between oncogene activation and invasive malignancy?

And thirdly, the story of polyps in the colon. What happens here is that the polyp goes through a variety of stages before it becomes malignant, and I have shown - I hope - that the GM food does get down to the colon, it will cause hyperplasia, and speed up the growth of this sequence. And that's my other concern then about GM food.

Slide 38: other possible unexpected effects of GM products in humans

Difficulties with GM food: we're not going to be able to measure sudden death by eating GM food, no, but I do believe that it is capable, because of a growth factor - which I believe to be the cauliflower mosaic virus - I do believe that it's capable of causing increased growth, perhaps, in the wrong sort of tissue, that we don't know about in our body. I'll be expanding about this, by the way, tomorrow [59].

Thank you very much.

NOTE: Dr. Ewen did not have time to show and comment on the final 10 slides of his 48-slide presentation, but these are included below:

Slide 39: Carcinogen formation by GMOs • "Genetic modification can cause deregulation of the synthesis of low MW toxins, mutagens and carcinogens and this has the potential to be the single greatest long term health risk". • Plants will synthesize substances similar to cycasin from which azoxymethane is a short step. • The metaplastic epithelium of Barrett's or stomach are almost certainly absorptive.

Slide 40: Beta glucuronidase • Steroids, toxins and drugs are detoxified by liver to glucuronide. • Normal small intestine almost sterile thus bacterial deglucuronidation limited. • But GUS gene-derived β-glucuronidase could amplify deglucuronidation in the small intestine resulting in higher circulating levels of toxins, steroid and drugs (M. Hill personal commun.)

Slide 41: Allergy • Allergic reaction in larynx and pharynx is possible producing angioneurotic oedema before entering gastrointestinal tract. • Many food allergens are stable to digestion. • The longer an allergen is present in gut the more likely it is to lead to sensitisation • Present testing uses pepsin and acid with recombinant bacterial surrogates that may have lowered function and heat denaturation also. • pH levels in human stomach may be much higher permitting longer allergen survival.

Slide 42: GM crop herbicide safety • Formulations may cause synergistic, and dose dependent, delay of cells into M-phase. • S. Richard June 2005 (Env.health perspect 113,716) has shown that glyphosate is very toxic to cytotrophoblast (JEG3 cells from choriocarcinoma) at levels "100 times" lower than agricultural levels. Those housed next to fields are at great danger from abortion (farmers should be obliged to identify pregnant women nearby).

Slide 43: Areas for expeditious investigation Freese and Schubert believe that the plant GM we eat is virtually untested and argue very persuasively for 6 test screens viz. 1. Carcinogenesis/mutagenesis with Ames test. 2. Metabolic profiling. 3. Teratogenesis over several generations. 4. DNA chip analysis. 5. Animal feeding - acute and chronic. 6. Comprehensive allergenicity testing.

Slide 44: Urgent human investigations • The in vitro binding ability of GM products to normal human gut mucosa is required. The tissues should be from healthy adults as well as children and those with known morbidity. • Consideration should be given to in vivo ingestion with biopsy sampling.

Slide 45: Considerations for Safety Assessment (1) • Parent and transformed lines must be grown and harvested under identical conditions • Analysis of protein, starch, lipid also proteomics and "transcriptomics". • Stability to degradation by acid, pepsin or other proteases of GM products has to be established in animal stomach and intestines. • The morbid state of the human recipient should be fully considered (PPI, immunosuppression, co-morbidity).

Slide 46: Considerations for Safety Assessment (2) • Immunocytochemistry for presence or absence of GIT mucosal binding (lectins or BT toxin) including colon. • Biological, immunological, hormonal properties and allergenicity should be establishes with GM crop product (not recombinants from E. Coli). • Young growing animals should be used to reveal unexpected effects on metabolism, organ development and immune system.

Slide 47: Considerations for Safety Assessment (3) • Animal testing must use iso-proteic and iso-energetic diets most of the protein being derived from the GM crop. • Obligatory - pair feeding & daily weighing. • Blood samples before, during and at end of period for immune, hormonal and haematological studies. • At PM weights of organs (wet and dry) and samples at identical sites for quantitative histology.

Slide 48: Conclusions • Possible effects on health must be answered before any long-term benefits of GM products can be recommended without reservation. • Additional sound science is essential to avoid unnecessary human health effects. • Processing and cooking GM products reduces, but does not completely prevent, long term changes in rats. • Raw GM products, such as fruit and vegetables, will make up to 40% of human diet in the future.

1.

The UK Agriculture and Biotechnology Commission was the British Government's strategic advisory body on biotechnology issues affecting agriculture and the environment. Following an independent review, the Commission was wound up at the end of April l2005. Its website (www.aebc.gov.uk) continues to exist but is no longer updated.

2.

Dr. Sue Mayer is also the Director of GeneWatch UK, www.genewatch.org .

3.

Personal communication to Michael O'Callaghan from Prof. Robin Grove-White, Professor of Environment and Society and Director of the Centre for the Study of Environmental Change at Lancaster University in the UK. He is also a former Director of Greenpeace UK.

4.

As of September 2006, there are serious conflicts between the Irish and UK draft strategies for the so-called "co-existence" of GM crops with conventional and organic farming.

The conflicts between the Irish and UK draft Irish strategy for "co-existence" include, inter alia, that the UK plan (see below) intends to keep the locations of GM crops secret, and also that the Irish plan does not recommend any final separation distance for GM oilseed rape crops because of their high risk of cross-contamination (pending further research).

In 2003, the EC issued a non-binding and legally flawed EC Recommendation for EU Member States to establish national strategies "to ensure to co-existence of GM crops with conventional and organic farming", despite global evidence that so-called "co-existence" is impossible because GM seeds and crops inevitably contaminate conventional and organic varieties, as well as wild plants.

For an updated list of contamination incidents in 39 countries, see the GM Contamination Register at www.gmcontaminationregister.org. See also Impossible co-existence: Seven years of GMOs have contaminated organic and conventional maize: an examination of the cases in Catalonia and Aragon (published by Greenpeace in June 2006). The report shows that the EC's strategy for "co-existence" is a recipe for widespread contamination. This report can be downloaded as a 928 kb pdf file from www.gmfreeireland.org/coexistence/Greenpeace/impossible-coexistence.pdf.

In December 2005, the Irish Agriculture Minister Mary Coughlan published Ireland's draft strategy "Report on co-existence of GM and non-GM crops" which is available for download at www.gmfreeireland.org/coexistence/DAF/strategy/draft/index.php. This report was finally published a year after a changed deadline which prevented the majority of invited stakeholder groups from participating in a related public consultation process which also excluded 86% of the stakeholders who will be materially affected by the policy! This clearly violates the legal requirements for public participation in environmental decision-making required by the Aarhus Convention on Access To Information, Participation, and Justice In Environmental Decision-Making, which has been transcribed into EU law. The Minister said she plans to finalise the strategy by end of 2006 or early 2007 pending negotiations with the Department of Finance on a compensation fund for contaminated farmers. A full dossier about the failed consultation process, including stakeholder submissions, is available at www.gmfreeireland.org/coexistence/index.php.

More information about the Aarhus convention may be found in the speech by Michael Ewing at the Green Ireland Conference in June 2006, which is available online at www.gmfreeireland.org/conference/trans/mewing.php. For additional information on the Aarhus Convention and on the Access Initiative to examine Environmental Democracy in Ireland see www.gmfreeireland.org/conference/trans/mewing.php.

In July 2006, the UK published its draft strategy on "co-existence" which was widely described as a farce. Notable among its blunders is a recommended separation distance of 35 meters for GM rapeseed, despite scientific evidence that wind-blown pollen from GM rapeseed has contaminated conventional crops 26km from its source, a voluntary system of compensation for ruined non-GM farmers, and permission for GM crops to be grown at secret locations (rejecting a public register of sites sanctioned by EU law)! If approved, the UK strategy is a recipe for irreversible GM contamination of Irish food and farms across the border with Northern Ireland.

5.

Poland - the largest agricultural producer in the EU - extended its nationwide blanket ban on GMO seeds and crops with a two-year deadline announced on 22 July 2006 for biotech companies to prove that the use of GM animal feed is safe for humans, animals and the environment or face a total ban on further imports of GM feed into Poland.

For details see http://www.gmfreeireland.org/news/2006/july.php#poland.

6.

The Rowett Research Institute is a research centre for studies into food and nutrition located in Aberdeen, Scotland. It was instructed by Tony Blair in 1998 to suppress publication of research by Dr. Arpad Pusztai and Dr. Stanley Ewen which found evidence that GM potatoes caused health problems in laboratory animals. For details see notes 30 and 31 below.

7.

The Independent Science Panel (www.indsp.org) is an international transdisciplinary network of scientists committed to science for the public good. Its many publications include the excellent report The Case for a GM-free Sustainable World, which explains how the biotech lobby's pseudo-scientific claims that GMOs are safe are based on the outdated reductionist paradigm which ignores 30 years of new scientific insights in molecular biology, ecology, complexity theory, and the emergent properties of complex systems. There is no need for "new scientific evidence" to prove the health and environmental risks of releasing GMOs. You can download the report as a 408kb pdf file from

www.gmfreeireland.org/documents/science/A GM-Free Sustainable World.pdf.

8.

Carrageenans are a family of linear sulphated polysaccharides extracted from red seaweeds. Gelatinous extracts of carrageen seaweed (also known as Irish moss) have been used as food additives for hundreds of years. When used in food products, carrageenan has the EU additive E-number E407. They are widely used in the food and other industries as thickening and stabilizing agents. There is evidence from animal studies, performed on rats, guinea pigs and monkeys, which indicates that degraded carrageenan (poligeenan) might cause ulcerations in the gastro-intestinal tract and gastro-intestinal cancer. A scientific committee working on behalf of the European Commission has recommended to limit the amount of degraded carrageenan (defined as carrageenans with a molecular weight of less than 50 kDa) to at most 5% of total carrageenan mass.In addition, carrageenan is claimed to inhibit absorption of certain minerals (e.g. potassium), and to induce gastro-intestinal discomfort in some people.

9.

Marcus SN, Marcus AJ, Marcus R, Ewen SWB, Watt J. The pre-ulcerative phase of carrageenan-induced colonic ulceration in the guinea-pig. Int J Exp Pathol 73:515-526 (1992).

10.

Workshop on Safety of Genetically Modified Foods held at FAo Headquarters, Rome, 13 - 14 october 2005: ftp://ftp.fao.org/es/esn/food/meetings/2005/gm_workshop_info.pdf.

11.

See the GM foods section of the UK Food Standards Agency web site at www.food.gov/uk/gmfoods . The Board of the Food Standards Agency stated in June 2000 that it was satisfied that the safety assessment procedures for GM foods are sufficiently robust and rigorous to ensure that approved GM foods are as safe as their non-GM counterparts, and posed no additional risk to the consumer.

12.

The economic argument that GM foods are "substantially equivalent" to their conventional counterparts is used by the agbiotech industry in their global strategy to try to force countries to open up their markets to GM food and farming. That's because governments which sign the WTO's World Trade Agreement must agree in principle to avoid any impediments to trade in so-called "like products" - regardless of differences in the process and production methods used to produce them. But from scientific point of view, GM crops and food are substantially different from their conventional counterparts because they are, by definition, transgenic - i.e. they are modified to contain mixtures of genetic material from various species which could not possibly occur in nature. Moreover, the controversial patents on GMO seeds and crops - which provide the legal means for the GMO patent owners to demand crop patent royalties and to file patent infringement lawsuits against contaminated farmers - are specifically based on the transgenic genes they contain.

The transgenic DNA in GM crops results in novel proteins which have never existed before in nature, and which our immune systems may be unable deal with or unable to recognise. This causes one class of health risks posed by GM foods.

In May 2003, the US, supported by Canada and Argentina, launched a WTO trade dispute against the EU concerning the EU authorisation regime for GMOs, alleging the EU's de facto moratorium on approvals of GM foods between 1999-2003 violated the requirement that GMO authorization requests be processed without "undue delay" under the WTO's Agreement on Sanitary and Phytosanitary Measures (SPS Agreement). The WTO also agreed with the co-complainants that marketing or import bans on GMO products in six EU member states - France, Germany, Austria, Italy, Luxembourg, and Greece - were in violation of WTO rules. The WTO's secretive and undemocratic trade dispute panel, however, said the co-complainants failed to prove that the EU's assessment procedures were not appropriate in relation to the actual risk posed by GM products, that there was insufficient scientific evidence to justify its assessment procedures, and that the EU failed to apply its procedures in a consistent manner by subjecting biotech products and products produced using biotech processing aids to different approval requirements. The panel also refused to rule on whether GM foods are generally safe or not. For details see www.gmfreeireland.org/wto.

For more on GMO crop patents follow links in notes 13 and 14 below.

13.

Speech by Percy Schmeiser at the Green Ireland Conference: www.gmfreeireland.org/conference/trans/pschmeiser.php.

14.

Speech by Deborah Koons Garcia at the Green Ireland Conference: www.gmfreeireland.org/conference/trans/dgarcia.php.

15.

The US Food and Drug Administration (FDA) has been heavily criticised for its revolving door policy with the agbiotech industry it is supposed to regulate, and for its total failure to contain the spread of GMO pharmaceutical crops in the USA. For a good exposé, see note 16 below.

16.

Seeds of Deception: Exposing Corporate and Government Lies about the Safety of Genetically Engineered Food. By Jeffrey M. Smith, with a foreword by Michael Meacher. Published by Green Books, UK, 2004: tel + 44 (0)1 803 863 260 o www.seedsofdeception.com .

17.

The notion that governments must accept the legalisation of GM crops in order to maintain "competitiveness" is a principal argument of the agbiotech corporate spin doctors, and is fully embraced by the current (2006) governments of Ireland and the UK. However, given the reality that GM foods are refused by the vast majority of EU consumers, rejected by the 60 largest food brands and food retailers in the EU, the argument violates the basic economic principle of supply and demand, and makes no sense whatsoever. Countries which are concerned about retaining access to the European market for safe food are banning GM crops. For details, see www.gmofree-europe.org.

18.

Transgenic products are those resulting from crops which have been genetically modified. The term is used to specify the fact that genetically modified organisms differ from conventional organisms because their genetic codes contain DNA from other species.

19.

Lectins are a type of receptor protein of non-immune origin that specifically interact with sugar molecules (carbohydrates) without modifying them. These proteins recognise and bind specifically to monosaccharides and are classified by which sugar they recognise. Most lectins recognise either N-acetylneuraminic acid, N-Acetylglucosamine, N-Acetylgalactosamine, galactose, mannose, or fucose. Lectins are found in a variety of species from plants to insects to man. There are two proposed biological roles for lectins in plants. The first is as an intermediary in the symbiosis between some plants and bacteria by aiding in the attachment of nitrogen-fixing bacteria to legumes. The second proposed role is in the protection of plant seedlings against pathogens such as fungi, viruses, and bacteria by binding to the surface of the microorganisms via sugar residues and inhibiting their growth.

While the function of lectins in plants is believed to be the binding of glycoproteins on the surface of cells, the role in animals also includes the binding of soluble extracellular and intercellular glycoproteins. For example, there are lectins found on the surface of mammalian liver cells that specifically recognise galactose residues. It is believed that these cell-surface receptors are responsible for the removal of certain glycoproteins from the circulatory system. Another example is the mannose-6-phosphate receptor that recognises hydrolytic enzymes containing this residue and subsequently targets these proteins for delivery to the lysosomes. They serve many different biological functions from the regulation of cell adhesion to glycoprotein synthesis and the control of protein levels in the blood. Lectins are also known to play important roles in the immune system by recognising carbohydrates that are found exclusively on pathogens, or that are inaccessible on host cellsÖ

The real function of lectins in plants is still to be found - they are not necessary for rhizobia binding as mentioned above (ruled out with lectin-knockout transgene) and cell adhesion function as their sole purpose in plants also questionable. Large presence in seeds (from which lectins are usually isolated) decreases with growth is suggesting a great role in plant's germination and perhaps in the seed's survival itself.

Lectins are considered as direct predecessors to the immune system and they have still great role in it - lectin complement activation pathway, Mannose binding lectin, S,P,E lectins, etc. For more information see http://en.wikipedia.org/wiki/Lectins.

20.

Adherence is often an essential step in bacterial pathogenesis or infection, required for colonizing a new host. To effectively adhere to host surfaces, many bacteria produce multiple adherence factors called adhesions. For example, nontypeable Haemophilus influenzae expresses the adhesins Hia, Hap, oap and a hemagglutinating pili.

Adhesins are attractive vaccine candidates because they are often essential to infection and are surface-located, making them readily accessible to antibodies.

The effectiveness of anti-adhesin antibodies is illustrated by studies with FimH, the adhesin of uropathogenic Escherichia coli (UPEC). In animal models, passive immunization with anti FimH-antibodies and vaccination with the protein significantly reduced colonisation by UPEC. Moreover, the Bordetella pertussis adhesins FHA and Pertactin are components of 3 of the 4 acellular pertussis vaccines currently licensed for use in the U.S. For more info see http://en.wikipedia.org/wiki/Adhesin.

21.

A toxin is a poisonous substance produced by living cells or organisms. Toxins are nearly always proteins that are capable of causing disease on contact or absorption with body tissues by interacting with biological macromolecules such as enzymes or cellular receptors. Toxins vary greatly in their severity, ranging from usually minor and acute (as in a bee sting) to almost immediately deadly (as in botulinum toxin).

Biotoxins vary greatly in purpose and mechanism, and can be highly complex (the venom of the cone snail contains dozens of small proteins, each targeting a specific nerve channel or receptor), or relatively small protein.

22.

The caecum is a pouch connected to the ascending colon of the large intestine and the ileum. It is separated from the ileum by the ileocecal valve (ICV) or Bauhin's valve, and is considered to be the beginning of the large intestine.

23.

Escherichia coli (E. coli) is one of the main species of bacteria that live in the lower intestines of mammals. They have also been located on the edge of hot springs. They are necessary for the proper digestion of food and are part of the intestinal flora. Its presence in groundwater is a common indicator of fecal contamination. It belongs among the Enterobacteriaceae, and is commonly used as a model organism for bacteria in general. One of the root words of their family's scientific name, "enteric", refers to the intestine, hence "gastroenteritis" (from 'gastro-', stomach, 'entero-' intestine, '-itis', inflammation). "Fecal" is the adjective for organisms that live in feces, so it is often used synonymously with "enteric".

The number of individual E. coli bacteria in the feces that one human passes in one day averages between 100 billion and 10 trillion. All the different kinds of fecal coli bacteria and all the very similar bacteria that live in the ground (in soil or decaying plants, of which the most common is Enterobacter aerogenes) are grouped together under the name coliform bacteria. Technically, the "coliform group" is defined to be all the aerobic and facultative anaerobic, non-spore-forming, Gram-negative, rod-shaped bacteria that ferment lactose with the production of gas within 48 hours at 35ƒC (95ƒF). In the body, this gas is released as flatulence. E. coli cells are elongated, 1-2 µm in length and 0.1-0.5 µm in diameter.

24.

Colitis is a digestive disease characterized by inflammation of the colon. There are several types of colitis, including ulcerative colitis, Crohn's colitis, diversion colitis, ischemic colitis, infectious colitis, chemical colitis and atypical colitis.

A well known subtype of infectious colitis is pseudomembranous colitis, resulting from infection by a toxigenic strain of Clostridium difficile. Parasitic infections can also cause colitis.

Any colitis which has a rapid downhill clinical course is known as fulminant colitis. In addition to the diarrhea, fever, and anemia seen in colitis, the patient has severe abdominal pain and a clinical picture similar to septicemia with shock is present. Approximately half of those patients require surgery.

Irritable bowel syndrome is a separate disease which has been called spastic colitis or spastic colon. This name causes confusion since colitis is not a feature of irritable bowel syndrome.

Autistic enterocolitis is a disputed medical entity but refers to a type of colitis found in patients with autism.

25.

Approximately 40% of all GMO crops currently on the market are the so-called Bt crops, which are modified with genes from the soil bacterium Bacillus thuringiensis. Specific strains of Bacillus thuringiensis produce slightly different types of Bt toxin which are damaging to certain species of insects including the European corn borer, southwestern corn borer, tobacco budworm, cotton bollworm, pink bollworm and the Colorado potato beetle. Bacillus thuringiensis is also used as a biological control agent by organic farmers.

Genetically modified Bt crops including Bt cotton, Bt corn, and Bt potatoes are being grown in the United States, Canada, Argentina, South Africa, France, and Spain.

See Possible Health Hazards of Genetically Engineered Bt Crops: Comments on the human health and product characterisation sections of EPA's Bt Plant-Pesticides Biopesticides Registration Action Document, by Michael Hansen, Ph.D., Consumer Policy Institute/Consumers Union, Presented to the EPA Science Advisory Panel Arlington, VA, USA, october 20, 2000: http://www.organicconsumers.org/ge/btcomments.cfm.

In India, Bt cotton has lead to massive crop failures, including 68% lower incomes for farmers (www.gmwatch.org/archive2.asp?arcid=6444), thousands of farmer suicides: www.hindu.com/thehindu/holnus/002200609070310.htm, and reports of sheep deaths.

In May 2005, an illegal shipment of 2,546 tonnes of illegal genetically modified Bt10 maize was unloaded at Greenore, Co. Louth. For details see www.gmfreeireland.org/scandal.

In September 2006, leading scientists issued the following statement on the potential allergenicity of the Bt toxin, Cry1AC:

Scientists' statement from
Professor Ian F. Pryme
Professor Gilles-Eric Seralini
Dr. Christian Velot

5 September 2006

We, the undersigned, note with concern the recent discoveries of contamination of rice [1] and rice products, including baby food [2], with an experimental genetically engineered (GE) rice. The GE rice contains a gene for the Cry1Ac protein, or possibly for a fusion Cry1Ab/Cry1Ac protein with similar immunogenic properties to Cry1Ac3. Cry1Ac has not been approved for human consumption in any food crop and there is concern over its potential allergenicity.

Research [4] into the gene for Cry1Ac has found that

1. Cry1Ac protoxin is a potent immunogen.

2. The protoxin is immunogenic by both the intraperitoneal (injected) and intragastric (ingested) route.

3. The immune response to the protoxin is both systemic and mucosal.

4. Cry1Ac protoxin binds to surface proteins in the mouse small intestine, and this could induce mid or long-term effects on mammalian health.

Therefore, we urge the developers and regulatory authorities of this GE rice to proceed with caution with the use of the gene for the Cry1Ac in any part of the genetic construct within the GE rice. It is possible that humans, in particular sub-populations such as infants and small children could be exposed to immunogenically-significant amounts of Cry proteins contained in foods.

A thorough evaluation of its food safety prior to any import, consumption, approval or further development of this GE rice would be necessary as rice is a staple food crop. Studies following the steps recommended by the FAo/WHo expert consultation [5] to evaluate allergenicity should be conducted by independent scientists, and their results published in peer-reviewed journals to allow evaluation of food safety. In addition, further studies into the potential allergenicity of Cry1Ac and other Bt proteins should be undertaken as a matter of the utmost urgency.

Signed

Pr. Gilles-Eric Seralini
President du Conseil Scientifique du CRII GEN
Universite de Caen
France

Pr. Ian F. Pryme
Dept. of Biomedicine
University of Bergen
Norway

Dr. Christian Velot
Conseil Scientifique du CRII GEN
Institut de Genetique et Microbiologie
Universite Paris-Sud France

Notes:

1. Zi, X. (2005) GM rice forges ahead in China amid concerns over illegal planting. Nature Biotechnology 23: 637.

2. www.greenpeace.org/china/en/press/releases/20060314-heinz-rice-cereal.

3. Tu, J., Zhang, G., Datta, K., Xu, C., He, Y. Zhang, o., Khush, G. & Datta, S.K. (2000) Field performance of transgenic elite commercial hybrid rice expressing Bacillus thuringiensis-endotoxin. Nature Biotechnology 18: 1101-1104.

4. Moreno-Fierros, L. Garcia, N. Gutierrez, R. Lopez-Revilla, & R. Vazquez-Padron, RI.(2000) Intranasal, rectal and intraperitoneal immunization with protoxin Cry1Ac from Bacillus thuringiensis induces compartmentalized serum, intestinal, vaginal and pulmonary immune responses in Balb/c mice. Microbes Infect 2: 885-90; Vazquez-Padron, R.I, Moreno-Fierros, L. Neri-Bazan, L, de la Riva, G.A & Lopez-Revilla, R. (1999) Bacillus thuringiensis Cry1Ac protoxin is a potent systemic and mucosal adjuvant. Scand J Immunol 49: 578-584; Vazquez-Padron, R.I Moreno-Fierros, L. Neri-Bazan, L, de la Riva, G.A & Lopez-Revilla, R. (1999) Intragastric and intraperitoneal administration of Cry1Ac protoxin from Bacillus thuringiensis induces systemic and mucosal antibody responses in mice. Life Sciences 64: 1897-1912; Vazquez-Padron, R. I., Moreno-Fierros, L. Neri-Bazan. L. MartÌnez-Gil, A.F., de la Riva, G.A. & Lopez-Revilla, R. (2000) Characterization of the mucosal and systemic immune response induced by Cry1Ac protein from Bacillus thuringiensis HD 73 in mice. Braz J Med Biol Res 33: 147-155; Vazquez-Padron, R. I., Gonzales-Cabrera, J., Garcia-Tovar, C. Neri-Bazan, L., Lopez-Revilla, R., Hernandez, M., Moreno-Fierros, L. & de la Riva.G.A. (2000) Cry1Ac protoxin from Bacillus thuringiensis sp. kurstaki HD73 binds to surface proteins in the mouse small intestine. Biochem Biophys Res Comms 271: 54-58. Guerrero, G. G., Dean, D.H. & Moreno-Fierros, L. (2004) Structural implication of the induced immune response by Bacillus thuringiensis Cry proteins: role of the N-terminal region. Molecular Immunology 41: 1177-1183.

5. FAo/WHo 2001. Evaluation of allergenicity of genetically modified foods. Report of a joint FAo/WHo expert consultation on allergenicity of foods derived from biotechnology, 22 - 25 January 2001. Rome, Italy.

26.

Wheat germ agglutinin is a lectin that was noted to agglutinate (clump) red blood cells together. This was observed before the overall understanding of lectins that bind to specific sugar molecules was fully worked out.

27.

Villi (singular: villus) are tiny, finger-like structures that protrude from the wall of the intestine and have additional extensions called microvilli (singular: microvillus) which protrude from epithelial cells lining villi. In all humans, the villi and microvilli together increase intestinal absorptive surface area 30-fold and 600-fold, respectively, providing exceptionally efficient absorption of nutrients in the lumen. This increases the surface area of the intestine to around the area of a small parking lot or a tennis court. There are also enzymes on the surface for digestion. Villus capillaries collect amino acids and simple sugars taken up by the villi into the blood stream. Villus lacteals collect absorbed fatty acids.

In short, villi are small projections shaped like fingers extending into the interior of the small intestine. They increase the absorptive area of the intestinal wall. Digested nutrients (including sugars and amino acids) pass into the villi. Circulating blood then carries these nutrients away.

28.

In chemistry, an amino acid is any molecule that contains both amine and carboxylic acid functional groups. In biochemistry, this shorter and more general term is frequently used to refer to alpha amino acids: those amino acids in which the amino and carboxylate functionalities are attached to the same carbon, the so-called α-carbon. These amino acids are used as the basic components of proteins. There are twenty "standard" amino acids used by cells in protein biosynthesis that are specified by the general genetic code. A list of standard amino acids describes their chemical structures and basic physical and chemical properties.

An amino acid residue is what is left of an amino acid once a molecule of water has been lost (an H+ from the nitrogenous side and an oH- from the carboxylic side) in the formation of a peptide bond, the chemical bond that links the amino acid monomers in a protein chain. Each protein has its own unique amino acid sequence that is known as its primary structure. Just as the letters of the alphabet can be combined in different ways to form an endless variety of words, amino acids can be linked together in varying sequences to form a huge variety of proteins. The unique shape of each protein determines its function in the body.

29.

μm is the scientific symbol (established by the International System of Units) for micrometre (i.e. one tenth of a millimetre).

30.

Dr. Arpad Pusztai is one of the world's most widely respected protein scientists. In 1995, the Scottish office of the UK Government Department of Agriculture Environment and Fisheries commissioned a three-year multi-centre research programme into the safety of GM food, co-ordinated by Dr Pusztai at the Rowett Research Institute in Aberdeen. At the time there was not a single publication in a peer-reviewed journal on the subject. The scientists' primary task was to establish credible methods for the identification of possible human/animal health and environmental hazards of GM food and feed. The idea was that the methodologies that they tested would be used by the regulatory authorities in later risk assessments of GM crops. For the first time, independent studies would be undertaken to examine whether feeding GM potatoes to rats caused any harmful effects on their health, bodies or metabolism. But by late 1997, the first storm clouds were brewing at the Rowett. Preliminary results from the rat-feeding experiments revealed totally unexpected and worrying changes in the size and weight of the rat's body organs. Liver and heart sizes were getting smaller, and so was the brain. There were also indications that the rats' immune systems were weakening. Finally in August 1998, Pusztai expressed his growing concerns in a 150 second interview on the BBC World in Action programme during which he said:

"We're assured that this is absolutely safe: we can eat it all the time; we must eat it all the time; there is no conceivable harm which can come to us. But as a scientist looking at it, actively working in the field, I find that it's very, very unfair to use our fellow citizens as guinea pigs. We have to find guinea-pigs in the laboratory." Dr Pusztai also said the effect of feeding GM food to rats "was slight growth retardation and an effect on the immune system. One of the genetically modified potatoes, after 110 days, made the rats less responsive to immune effects".

He continued: "If I had the choice, I would certainly not eat it till I see at least comparable experimental evidence which we are producing for our genetically modified potatoes. I actually believe that this technology can be made to work for us. And if the genetically modified foods will be shown to be safe, then we have really done a great service to all our fellow citizens. And I very strongly believe in this, and that's one of the main reasons why I demand to tighten up the rules, tighten up the standards."

On the evening of the broadcast, the head of the Rowett Professor James congratulated Pusztai on his TV appearance, commenting on 'how well Arpad had handled the questions'. The following morning a further press release from the Rowett noticed that a 'range of carefully controlled studies underlie the basis of Dr Pusztai's concerns'. But following two phone calls from UK Prime Minister Tony Blair, Dr. Pusztai and his wife and co-researcher Dr. Susan were told to hand over their data. All GM work was stopped immediately and Pusztai's team was dispersed. His three PhD students were moved to other areas. He was threatened with legal action if he spoke to the media. His phone calls and emails were diverted.

Although banned from talking to the press, he was not banned from talking to other scientists outside the Rowett. In February 1999 30 international scientists from 13 countries published a memo supporting Pusztai that was published in the Guardian which sparked a media frenzy over GM.

A week after the international scientists backed Pusztai, a secret cross-departmental government committee formed to deal with the crisis, called MISC6, met to counter the growing alarm over GM. Contrary to reassurances by the government that GM food was safe, the minutes show the committee knew the reassurances were premature. It 'requested' a paper by the Chief Medical officer (CMo) and the Chief Scientific Advisor (CSA) on the 'human health implications of GM foods'. That very same day - 19 February - The Royal Society publicly waded into the Pusztai controversy saying it was going to review the evidence on GM.

On 18 May 1999, the Royal Society issued its damning verdict against Pusztai, at a press conference. The report said that Pusztai's work was "flawed in many aspects of design, execution and analysis and that no conclusions should be drawn from it". The same day, 18 May, the House of Commons Science and Technology Select Committee attacked Pusztai too.

On 21 May, just three days after The Royal Society and Select Committee published - Jack Cunningham stood up in the House of Commons: "Biotechnology is an important and exciting area of scientific advance that offers enormous opportunities for improving our quality of life."

Cunningham then laid his killer punch: "The Royal Society this week convincingly dismissed as wholly misleading the results of some recent research into potatoes, and the misinterpretation of it - There is no evidence to suggest that any GM foods on sale in this country are harmful".

31.

Dr. Pusztai and Dr. Stanley Ewen published a study about the potential dangers of genetically modified potatoes in The Lancet in 1998: Ewen SWB, Pusztai A (1999): Effect of diets containing genetically modified potatoes expressing Galanthus nivalis lectin on rat small intestine. Lancet 354:1353-1354. According to The Lancet editor, Richard Horton, the former Vice-President and Biological Secretary of The Royal Society and President of the Academy of Medical Sciences Professor Lachmann phoned him during the peer review process threatening that his job would be at risk if he published Pusztai's paper, and called Horton "immoral" for publishing something he knew to be "untrue". After the article was published, the biotechnology industry and The Royal Society again attacked Horton and The Lancet. But 24 independent scientists later confirmed the accuracy of Pusztai's research. See www.gmwatch.org/archive2.asp?arcid=1132 and Dr. Pusztai's homepage at http://www.freenetpages.co.uk/hp/a.pusztai for details.

32.

Fares NH, El-Sayed AK. 1998: Fine structural changes in the ileum of mice fed on delta-endotoxin-treated potatoes and transgenic potatoes. Nat Toxins. 6:219-33.

33.

This refers to the WTO concept of "substantial equivalence". See note 12 above.

34.

The mucosa is the innermost layer of the gastro-intestinal (GI) tract, surrounding the lumen, or space within the tube. The mucosa layer comes in direct contact with the food (or bolus), and is responsible for absorption and secretion, important processes in digestion.

35.

The 35S CaMV promoter gene (taken from the Cauliflower Mosaic virus) is closely related to human hepatitis B virus, and less closely, to retroviruses such as the AIDS virus. It is used in most GM crops to boost very high levels of expression of the other foreign genes with the desired traits which are introduced as the genetically modified "gene expression cassette." The CaMV promoter can drive the synthesis of related viruses. It is active in all living systems from bacteria to higher plants. Two kinds of potential hazards exist: the reactivation of dormant viruses, and recombination between the CaMV promoter and other viruses, dormant or otherwise, to generate new, super-infectious viruses or viruses with broadened host-range.

It has been claimed that the 35S promoter is plant-specific and would not be active in mammalian cells, and hence would not pose risks linked to the consumption of GE food and feed in the event that plant DNA fragments are taken up from the mammalian gastrointestinal tract. However, this claim has not been supported by experimental data.

On the contrary, there have already been published reports indicating that this assumption might be incorrect, for example, previous research has indicated the potential of the 35S promoter to be active in mammalian systems. More recently, direct evidence that the 35S promoter is active in mammalian cell cultures has been presented.

of particular importance are the cells lining the intestinal wall, given that the gastrointestinal tract will be the first site of exposure to GE food and feed.

In a recently published paper, scientists have demonstrated that the 35S CaMV promoter was able to drive the expression of two reporter genes (gfp and luc) in the human cell line Caco-2, which share a number of characteristics with human enterocytes (cells lining the intestinal wall).

While the protein expression levels were modest compared to results obtained with strong mammalian promoters, the significant observation remains that the 35S CaMV promoter, generally assumed to be plant specific, initiated significant protein expression levels in host cells that share important characteristics with those lining parts of the human gastrointestinal tract.

These results, taken together with other published papers, leads the scientists to conclude that the 35S CaMV promoter is capable of initiating gene expression in some mammalian cell lines under a range of different conditions and circumstances. Computer based searches further indicate that transcriptional activation by the 35S promoter may be stronger in other human and animal cell types than those investigated so far.

This research clearly warrants further serious investigation, including by in vivo means.

Whether there are GE food safety implications would be linked to the process of foreign DNA uptake from the human gastrointestinal tract. The uptake of food-derived DNA fragments from the intestines into the blood stream and some organs has already been demonstrated in various animal species and recently also in humans.

Given the potential for the 35S promoter to initiate gene expression in some mammalian cells, if the intact 35S promoter is taken up, the biological consequences are potentially great (for example, inappropriate expression of genes may occur).

For more information see: www.gmwatch.org/archive2.asp?arcid=5945.

See also: The CaMV 35S Promoter - Government and Corporate Scientific Incompetence: Failure to assess the safety of GM crops. By Ricarda A. Steinbrecher. ExoNexus Briefing, December 2002: www.econexus.info/pdf/ENx-CaMV-35S-Promoter-B-2002.pdf.

See also: The 35S CaMV plant virus promoter is active in human enterocyte-like cells European Food Reseach and Technology (2005), DoI 10.1007/s00217-005-0154-3 Marit R. Myhre (2, 4), Kristin A. Fenton (4), Julia Eggert (3), Kaare M. Nielsen (3) and Terje Traavik (1, 2).

36.

See note 31 above.

37.

Food safety, contaminants and toxins. Edited by J.P.F. D'Mello. Published by CABI, Oxford in 2003 (Pusztai, Bardocz and Ewen p. 347).

38.

Mitotic is the adjective derived from the Greek work meiosis, which is the scientific term for cell division.

39.

Coeliac disease is an autoimmune disorder of the small bowel that occurs in genetically predisposed individuals in all age groups after early infancy. Symptoms may include diarrhoea, failure to thrive (in children) and fatigue, but these may be absent and associated symptoms in all other organ systems have been described. It affects approximately 1% of Caucasian populations, though it is significantly underdiagnosed. A growing portion of diagnoses are being made in asymptomatic persons as a result of increasing screening.

Coeliac disease is caused by an abnormal reaction to gliadin, a gluten protein found in wheat (and similar proteins in barley and rye). Upon exposure to gliadin, the body's immune system cross-reacts with the enzyme tissue transglutaminase, causing a inflammatory reaction that leads to flattening of the lining the small intestine, which interferes with the absorption of nutrients. The only effective treatment is a diet, lifelong in principle, from which gluten is absent.

This condition has several other names, including: cúliac disease (with ligature), c(o)eliac sprue, non-tropical sprue, endemic sprue, gluten enteropathy or gluten-sensitive enteropathy, and gluten intolerance.

40.

Hyperplasia (or "hypergenesis") is a general term for an increase in the number of the cells of an organ or tissue causing it to increase in size. It may be due to any number of causes including (but not limited to) increased demand, chronic inflammatory response, hormonal dysfunctions, or neoplasia. For more info see http://en.wikipedia.org/wiki/Hyperplasiae.

41.

Dr. Stanley Ewen's second talk at the Green Ireland Conference may be found at www.gmfreeireland.org/conference/trans/sewen2.php.

42.

Histology is the study of tissue sectioned as a thin slice, seen through a microscope. It is used for accurate diagnosis of cancer and other diseases.

43.

Haematology is the branch of internal medicine and pediatrics that is concerned with blood, the blood-forming organs and blood diseases. Hematology includes the study of etiology, diagnosis, treatment, prognosis, and prevention of blood diseases.

44.

Manuela Malatesta and her colleagues have published five papers 2002-2004. Abstracts of the papers can be found here: www.agbioworld.org/biotech-info/articles/agbio-articles/GMfeedsafetypapers.html.

45.

Mangiare OGM non fa differenza? Non proprio. The original full paper in Italian may be found at www.greenplanet.net/Articolo9833.htm. The study was a preliminary study not yet peer-reviewed and published by the author. But her results were so worrying to independent scientists that dissemination became imperative. See Jeffrey Smith: fully referenced article in "Spilling the Beans," Oct 2005: www.seedsofdeception.com/utility/showArticle/?objectID=299 .

46.

A zymogen (or proenzyme) is an inactive enzyme precursor. A zymogen requires a biochemical change (such as a hydrolysis reaction revealing the active site, or changing the configuration to reveal the active site) for it to become an active enzyme. The biochemical change usually occurs in a lysosome where a specific part to the precursor enzyme is cleaved in order to activate it. The amino acid chain that is released on activation is called the activation peptide.

Very often the suffix "-ogen" can be added to the name of the enzyme to indicate that it is in the precursor form. Examples of zymogens are trypsinogen, chymotrypsinogen, pepsinogen, most of the proteins of the coagulation system, some of the proteins of the complement system, the caspases.

Zymogen is another term for a pro-enzyme. Some enzymes have a pro- prefix to denote their inactive status eg. Proalbumin which is converted into albumin.

47.

Personal communication from Manuela Malatesta to Dr. Stanley Ewen in October 2005 at the FAO meeting in Rome.

48.

Regarding corruption of the truth on the health and environmental risks of GM food and crops, see Seeds of Deception: Exposing Corporate and Government Lies about the Safety of Genetically Engineered Food. By Jeffrey M. Smith, with a foreword by Michael Meacher. Published by Green Books, UK, 2004: tel + 44 (0)180 386 3260 o www.seedsofdeception.com .

49.

Monsanto 863 maize scandal: in May 2005, GM-free Cymru (GM-free Wales) revealed the the full extent of a conspiracy by UK and EC officials which has, against the public interest, enabled a highly damaging study on the safety of GM maize to be held on a secret dossier and which has gagged scientists who have seen it.

The study, into the effects of feeding rats for 90 days on Monsanto's MoN863 maize, was requested by various EU countries as part of the MoN863 assessment process, and was completed in September 2003. The results showed "statistically significant" changes to blood and to certain vital organs in the rats fed on the GM maize, as compared with those in the control group, and immediately alarm bells started to ring in scientific circles throughout Europe. The French authorities tried to cover up the scientific debate about the study (1). In the autumn of 2004 concerns were expressed about the study findings by a number of other national regulatory bodies, including Belgium and Germany. Germany actually commissioned an evaluation of the rat feeding study from Dr Arpad Pusztai, but Monsanto would not allow its 1,139 page research dossier to be examined without the signing of a "declaration of confidentiality." Incredibly, the EC and the German authorities acceded to this demand, which means that their key officials are now bound by a secrecy agreement. This would not be so bad if it were not for the fact that Dr Pusztai's evaluation was highly critical of both the methods and the findings of the study, indicating that MoN863 maize by no means has a "clean bill of health." Subsequent leaks (2) from France, Germany and Belgium suggest that the maize variety may indeed be unsafe for animal or human consumption, and that a major cover-up is under way, designed to protected the corporate giant Monsanto and the regulatory authorities who have prematurely advised that MoN863 is perfectly safe.

For details see www.gmfreeireland.org/resources/documents/science/scandals/GMfreecymru1.php.

50.

Squamous cells are flat cells which form the surface of an epithelium (such as skin or mucous membranes).

51.

This view that many GM health risk assessments submitted to the regulatory bodies in the USA and Europe are bogus is widely shared by observers around the world.

For details of how regulatory bodies in the USA collude with the biotech industry's false safety claims, see Seeds of Deception: Exposing Corporate and Government Lies about the Safety of Genetically Engineered Food, by Jeffrey M. Smith, with a foreword by Michael Meacher M.P. Published by Green Books, UK, 2004: tel + 44 (0)1 803 863 260, www.seedsofdeception.com.

The European Food Safety Authority (EFSA) has been widely criticised for failing to conduct comprehensive studies of the health risks of GM foods, and for relying on the risk assessments provided by the biotech companies it is supposed to regulate.

Friends of the Earth published a detailed critique of the EFSA and its work on GM foods in November 2004 entitled "Throwing caution to the wind". (See www.foeeurope.org/GMOs/publications/EFSAreport.pdf).

On 6 October 2005, consumer, environmental and health groups across the EU then challenged the EFSA to fulfil its legal obligations to take into regard the long term safety and scientific uncertainties of GM foods, to review it scientific panels to make them impartial and independent from industry, and to improve its transparency. (See: www.efsa.eu.int/stakeholder_stakeholder_consultative_platform).

In 2005 a German court effectively said that EFSA failed to protect the public health by accepting a Confidential Business Information (CBI) classification on research and DNA information in the case of the contamination scandal with Monsanto's GM maize MON863. After many months of delay, EFSA was shown to have acted against the public interest, and Monsanto was forced to open up its research dossier for public scrutiny.

Ten demands for the reform of the EFSA are supported by the European Public Health Alliance, Eurocoop, the European Environmental Bureau, Greenpeace and Friends of the Earth. See www.foeeurope.org/publications/2005/EFSA_stakeholders_challenge.pdf .

in April 2006, under the Austrian Presidency of the EU, Member States' Environment Ministers, called for greater transparency in the EU approvals process on GMOs and also called into question the validity of risk assessment procedures used by the EFSA. The EFSA has come under fire from member states and NGOs for failing to fully take account of national safety concerns. EC Environment Commissioner Stavros Dimas broke Brussels ranks by unleashing further criticism and accusing EFSA of depending too much on information supplied by the biotech industry, when making risk assessments. "There is the question of whether scientific opinions relied solely on information supplied by companies which produce GMOs," said Dimas. "The EFSA cannot deliver a sound scientific opinion on GMOs. They only examine short term effects and they do not take into account the opinions of member states." For related media coverage see http://www.gmfreeireland.org/news/2006/april.php.

On 18 September 2006, GM-free Cymru revealed that EFSA was involved in a cover-up of Bayer CropScience's illegal American long-grain GM rice LL601 by claiming that it might be safe to eat while refusing to release 30 pages of information submitted by the seed owner that might well show that LL601 is genetically unstable and dangerous.

52.

Gastroesophageal Reflux Disease (GERD or GoRD) is defined as chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. In adults, the major symptom is heartburn. In children and infants, symptoms may include repeated vomiting, effortless spitting up, coughing, and other respiratory problems. Inconsolable crying, failure to gain adequate weight, refusing food and bad breath are also common. Children may have one symptom or many - no single symptom is universally present in all children with GERD.

53.

Heliobacter pylori (HP) organisms infect 40-50% of stomachs by 50 yr. HP infection produces intense inflammation with ensuing intestinal metaplasia.

Helicobacter pylori is a bacterium that most often infects the mucus lining of the stomach and duodenum. Many peptic ulcers, and some types of gastritis are caused by H. pylori infection. It is estimated by some researchers that approximately 50% of the world's population is infected, although most humans who are infected will never develop symptoms. This bacterium is the only known microorganism that can thrive in the highly acidic environment of the stomach. Its helix shape (hence the name helicobacter) is thought to have been designed to penetrate the mucus lining to colonise.

54.

A polyp is an abnormal growth of tissue (tumor) projecting from a mucous membrane. Polyps are commonly found in the colon, stomach, nose, urinary bladder and uterus. They may also occur elsewhere in the body where mucous membranes exist like the small bowel.

55.

There is growing scientific evidence of deaths and disease attributable to GM food in laboratory animals, livestock and the human population.

A leaked European Commission document submitted to the World Trade organisation admits "there is no unique, absolute, scientific cut-off threshold available to decide whether a GM product is safe or not". For details, download the report Hidden uncertainties - What the European Commission doesn't want us to know about the risks of GMOs published by Friends of the Earth Europe and Greenpeace in April 2006: www.foeeurope.org/publications/2006/hidden_uncertainties.pdf .

A January 2001 report from an expert panel of the Royal Society of Canada said it was "scientifically unjustifiable" to presume that GM foods are safe. A 2002 report by the UK's Royal Society said that genetic modification "could lead to unpredicted harmful changes in the nutritional state of foods," and recommended that potential health effects of GM foods be rigorously researched before being fed to pregnant or breast-feeding women, elderly people, those suffering from chronic disease, and babies.

There is growing evidence of allergenic and toxic effects of GM food. Three separate studies of the health risks in 2005 have triggered fresh demands for GM components in human food and animal feed to be banned immediately, and have also led to accusations of criminal negligence aimed at the Irish and UK Governments and the European Commission. For details, see the press release issued in November 2005 by Dr. Brian John of GM-free Cymru, which is included at www.gmfreeireland.org/health/ .

Article 14 of European food safety legislation (EC/178/2002) calls for the assessment of the long term effects of GMOs and effects of subsequent generations. However, to date the long term effects of eating or growing GM foods seem to be completely ignored.

For more on the health risks of GM foods, see

a. Center for Food Safety: www.centerforfoodsafety.org

b. Econexus: www.econexus.info

c. GeneWatch: http://www.genewatch.org

d. Independent Science Panel on GM: www.indsp.org

e. Norwegian Institute of Gene Ecology: www.genok.org/english/default.asp

f. Seeds of Deception: www.seedsofdeception.com

g. Union of Concerned Scientists: http://go.ucsusa.org

h. GM-free Ireland Network: www.gmfreeireland.org/health/.

56.

The Newcastle feeding study (published 2003) involved a small portion of GM soya fed to just seven ileostomy patients: www.foodstandards.gov.uk/news/newsarchive/statement. See also www.gmwatch.org/archive2.asp?arcid=990 and comments by Dr Michael Antoniou at www.gmwatch.org/print-archive2.asp?arcid=143.

57.

Hyperplastic agents stimulate epithelium (lining) cells to grow (under control). This is seen as an increased length of the small intestinal crypt where the cells are generated (normally the cells move up the villus to be shed into the lumen but in precancer this orderly movement stops eg. in a colonic polyp or metaplasia of stomach).

58.

Hyperplasia - see note 40 above.

59.

Dr. Stanley Ewen's second talk at the Green Ireland Conference may be found at www.gmfreeireland.org/conference/trans/sewen2.php.

Sponsored by Global Vision Corporation

© 2003 - 2006 Global Vision Consulting Ltd • updated 22 September 2006
Privacy policy
For enquiries contact mail@gmfreeireland.org
URL of this page: www.gmfreeireland.org/conference/proceedings/trans/sewen1.php