Genetically Engineered Food - Part 2

This is a continuation from the very long thread: Genetically Engineered Food. Last post from that one follows:

Member posted 07-13-99 01:39 AM

[Transcript of letters sent by me to Europe. Some really good questions!]

Copy of letter sent 6/30/99 to EuropaBio, the biotech association in Europe*

To: Paul Muys, Communication Manager EuropaBio
CC: Editor, The Independent, UK

Dear Paul:

On June 20, 1999, the UK newspaper “The Independent” printed a headline article entitled “World’s top sweetener is made with GM bacteria.” That article mentioned that several UK MPs were “hunting” around for GM processes used in food production. Yet according to the article, the GM process to produce an enzyme was not even being used in the UK, but only in the US.

Upon reading this headline, it occurred to me that the UK public (and MPs) must be completely unaware that most of the world’s cheese is produced using the enzyme chymosin, a product of genetic engineering. Indeed, tracing back many months through all the UK press debate, I have found no headline story revealing the truth in this respect. I find it quite shocking (as I think others would) that this issue hasn’t been discussed at this point, particularly considering chymosin has some solid benefits – there aren’t enough calves to go around to make the alternative rennet, for example. How can an organization like EuropaBio neglect to inform the public that the cheese supply depends on a GM enzyme, particularly since the theme of the “GM food” campaign has been the “right to know”, rather than of food safety (which has been well established)? How can cheese be excluded – is it simply because it hasn’t been mentioned in the press? This is ridiculous.

In a related case, I find it astounding that the UK is importing herbicide-tolerant soybeans (DuPont “STS”) through US Archer Daniels Midland Co., which are being sold in the UK as “GM-free”, simply because they are genetically modified using a process different than those used in Monsanto beans, and this happens to let them slip through US FDA policy (the trick is, they leave the US as “identity preserved” and are re-labeled later). Surely, these beans contain genes for herbicide tolerance – just like the Monsanto beans. This is particularly vexing since I’ve noted “herbicide tolerance” as an issue of concern which often comes up for European customers (for example, Greenpeace brings this up as a key point). Therefore, how can the “debate” in Europe concerning these products neglect to mention that consumers will still be eating beans with genes for herbicide tolerance, when campaigners told them “GM-free” implied this wouldn’t be the case? There are around ten million acres of these beans being grown, by the way. This is no small matter.

I have written a letter to The Independent (attached below), informing them of these issues. They have not yet published my letter, probably since they too find my information shocking. Nevertheless, I think it is important that these two issues be brought into the UK debate, however uncomfortable that may be at this point. In fact, I plan on contacting folks in the UK until these issues are heard, or bringing my information to prominence on the Internet. That is of course, unless these issues are on the EuropaBio agenda – please contact me as soon as possible with any plans you have in this regard.

Dan Spillane
Seattle, WA USA

*** Unpublished letter follows ***
(Sent 06/21/1999)

To: Editor, Independent (UK)

“GM Hunting”

Your recent headline “World’s top sweetener is made with GM bacteria” (June 20) made it all the way to the US, believe it or not. It’s not that Americans find this so surprising, given that many products here are made this way. Rather, what we find surprising is how you are hunting on our side of the Atlantic – while you still have some hunting left to do on your own side. It seems if you are looking for “secret” GM projects, you only need to look in any UK grocer:

  1. Almost all UK cheeses (about 90 percent) are produced using GM enzymes, made in a way similar to how Monsanto’s sweetener is made. This is according to several sources in the UK, including your own government. Why has this “secret” not made headlines in any of your newspapers yet? Are all these cheeses labeled “GM”, since you say it is the customers “right to know”? How can cheeses be treated differently if they are made with GM? Could there be a "cover up’?

  2. Many soybeans now being imported into Europe are being sold and labeled as “GM-free” – it should make you happy these aren’t the Monsanto kind. But does the UK know they are still getting soybeans genetically modified to be herbicide-tolerant, just like the Monsanto beans? These soybeans are labeled “GM-free”, simply because they get around US FDA policy. That policy states, “The agency has not required labeling for other methods of plant breeding such as chemical- or radiation-induced mutagenesis, somaclonal variation, or cell culture.” Who can assume “chemical- or radiation- induced mutagensis” – or any other science – is safer than what is done to Monsanto beans, especially when no one in the US has found any more testing data for these beans than the Monsanto ones?

Dan Spillane
Seattle, WA USA

Carry on!

Re: Antibiotic resistance in bacteria and insects
Thankyou for your reply, Eric. Unfortunately, I think I may have mis-stated some things in my original post. Essentially, the porblem was that I was using what little I do know (i.e. bacterial antibiotic resistance) to speak about a related but different topic, (i.e. insect antibiotic resistance). Actually, I was talking about insect antibiotic resistance when I said that interbreeding might form more antibiotic-resistant strains (also, is an insecticide like Bt toxin properly called an “antibiotic?” I don’t know).
Anyways, it is interesting to remark, although I’m sure you already know this, that some bacteria also undergo a form of “breeding,” or at least sexual DNA transfer. For example, some populations of E. coli harbour both F plasmid positive and negative cells, and a copy the plasmid can be transferred from the “male” F+ to the “female” F- cells (this “male/female” terminology isn’t actually used, I think, but what good is science if you can’t sprinkly your conversation with neologisms and jargon:P)
Anyways, that’s beside the real topic here, which is the question of whether Bt toxin and the actual Bacillus thuringiensis spores will have a different effect in regards to development of antibiotic resistance. I think it likely that the spores are more likely to produce resistance than the transgenic plants… of course I could be wrong.
I also though perhaps I should get on a self-rigteous high horse and complain about the amount of newspaper article posting that goes on in this group… really, I mean, most people can read a paper themselves, and would far rather hear the ideas of the poster, backed up by a few choice quotations if necessary. But, again, about this I may also be wrong.
-Alex Kennedy

NYTimes July 20, 1999 Stalked by Deadly Virus, Papaya Lives to Breed Again


Healthy genetically altered papaya plants thrived on the right in 1996 as the traditional plants, at left, withered.

For better or worse, genetic engineering comes to the rescue of Hawaiian farmers.

[Note: This message has been edited by JillGat

Professor Michael Lipton
University of Sussex
12 July 1999
Genetically Modified Crops Already Diminishing Undernutrition

Sir, Dr Alok Bhargava (Financial Times, Letters, June 14) alleged that my “argument that (genetically) modified foods will reduce undernutrition is . . . premature”. But GM staple foods are doing so already. The gains would be greater if they received more than the present 5-10 per cent of GM research. The Nuffield report on GM crops documents varieties that have improved yield and stability - often by better tolerance of fungi, viruses or soil poisons - for example, for rice in China, potatoes in Peru and sweet potatoes in Kenya.

Yes, GM foods need long-term health monitoring, though they have been grown commercially in the US since 1994, and on well over 1m hectares in China, with no reported health damage. The Nuffield report suggests that new aid should help developing countries to design and implement appropriate, open procedures to regulate, improve and monitor the health and environmental impact of specific GM varieties. However, as the World Health Organisation and the UN Food and Agriculture Organisation agree, a huge source of health damage is undernutrition and underemployment due to risky and unproductive varieties of staple food crops. Hence caution demands not only regulation and monitoring but also a big increase in the present dismally low share of GM research that tests or spreads improved varieties of food staples.

Finally, Dr Bhargava stated that my arguing for GM foods as a weapon against undernutrition “would even seem disingenuous to those who see it as a conspiracy to experiment with dangerous products on the most vulnerable”. “Those who see it” that way are making groundless charges of disingenuousness and callousness. I see no ethical grounds for denying Vitamin A-enhanced GM rice to children at risk of eye damage but I accept the good faith of those who do. “Those who” unreasonably attack others’ good faith, especially if also failing to address the substance of a controversy, merely demonstrate the weakness of their own case.

Michael Lipton,
professor of economics,
Poverty Research Unit,
Sussex University,
and member, working party on GM crops,
Nuffield Council on Bioethics,
Falmer, Brighton, Sussex BN1 9SJ

[Is this fascism in action? A farmer in the UK compares this kind of thing to the Nazi book burnings.]

Monday, July 26, 1999 Published at 12:25 GMT 13:25 UK
GM crop destroyed in green protest

[Note, this test was to specifically show an environmental benefit. Naturally, Greenpeace targets any experiment that might show the truth.]

[Note: This message has been edited by JillGat]

You ask “whether Bt toxin and the actual _Bacillus thuringiensis_spores will have a different effect in regards to development of antibiotic resistance.”

Development of or toxin resistance in insects, just like antibiotic resistance in microbes, is concentration dependant. With exposure to low levels of the toxin the population as a whole will gain resistance; the mechanism is fairly straight forward - the insects that aren’t as naturally susceptible will live the others won’t and the population expresses that gene to a greater extent. My initial impression is it won’t matter which you use, as far as resistance development, but the concentration that you use them in. My research into this area has not been extensive though so this may not be the case.

As an aside, sorry for the article posts, I felt that they would contribute to the dialogue and give some more information to those who wished it.

The articles posted have been interested and relevant for the most part, but unfortunately verbatim repostings of entire articles are a violation of copyright and are not permitted on the SDMB. Please paraphrase articles or include links. Later today I will delete the above articles.

Thanks for the reply. Actually, it wasn’t so much articles in particular, or your articles in particular, about which I was complaining… it was more a plea for moderation when posting (i.e. some people here seem to post astoundingly long messages to put forth fairly simple points, for some odd reason).
Anyways, the reason I would suspect a different amount of antibiotic resistance to appear with spores than with constitutively expressed toxin, I take from analogy with bacterial antibiotic resistance. When a low level of antibiotic is presented to a population, weakly resistant strains are not killed off, as you know. This gives time for various genetic factors (we all know, I’m sure, that evolution of antibiotic resistance doesn’t seem to occur on a “accumulation of single helpful mutations” type of scale… although I may be wrong about this, and am interested in what you think) to strengthen resistance. If a large dose of toxin is given, however, weakly resistant strains are also killed, meaning resistance does not develop (unless there are strongly resistant strains already in the population). So I would suspect that the spores, which give a small one-time dose of toxin would be less effective at preventing resistance than the constitutively expressed plant-produced toxin.
The only problem with this is that I’m looking at it from the perspective of gradualistic ideas of evolution that I was (sort of) taught in school, which I’m now starting to think might not show the whole picture. Please, I beg any criticism of my analysis here.

During my research into this topic, I have found that there are primarily 2 strains of bacillus used as microbial insecticides: Bacillus thuringiensis kurstaki (Btk), and Bacillus thuringiensis aizawai (Bta.). Of these strains, Btk was used primarily. Btk produces a crystalline toxin CryIA that binds to the gut epithelial cells of the target insect, killing it. Resistance to Btk spores is widespread and thought to be the result of decreased CryIA binding. Btk can produce 5 different crystalline toxins including 3 types of the CryIA toxin. Bta. can produce the same three CryIA toxins and as well as 2 different toxins. Since there is resistance to CryIA, a switch to Bta. may not effective. There are really three points to consider here.

First, resistance to the CryIA toxin already exists in high levels in the populations of the pests we’re trying to control.

Next, the resistance the insects have is to the toxin itself. That means that the genetically engineered plants may not fair much better - I don’t know this yet, I’m not aware of the specific toxin that the plants excrete.

Finally, when the Bt spores transform into viable Bacillus thuringiensis bacterium, they will continue to produce the toxin until they are killed. This means that a low number of spores ingested may result in a high level of the toxin in the insect.

To continue the line of reasoning from my last post, the thing that really maters as far as resistance, is not the specific delivery system (assuming the plant produces CryIA), but the concentration that is delivered. The insects will show susceptibility at some point and the closer the delivered concentration is to this point, the more problems I would expect to see with increased resistance.

As far as the gradualistic evolutionary approach, it works fine under most circumstances. There are specific times where it breaks down but normally I prefer it to the punctuated approach.

You make a good point about the resistance to a similar toxin already existing in the population, and an even better point about persistance of toxin production given the germination of B. thurigensis (sp? I can never remember :o). Of course, the aim is to kill those insects who are eating the corn (presumably corn borers), and we don’t have anything against insects elsewhere. Presumably, if there’s a certain concentration of toxin in the corn the insects are eating, then the insects will die after eating a certain amount of corn.

I wonder about your comment about succeptibility levels… do you mean more resistance will arise the lower the level of toxin, down to the point where the toxin in no longer leathal? If so, I obviously agree.
I’m just trying to point out (as I’m sure you know) that the toxin itself does not “create” resistance. Using huge amounts of toxin is not any more likely to create resistance than small amount; in fact, it’s less likely to do so, since borderline resistants are killed off. Anyways, I’ve said this before, and you seem to agree with me… think of this paragraph as a recap :stuck_out_tongue:

I did mean that the lower the concentration of the toxin you use the higher the likelyhood of acquired resistance to that concentration becomes. We seem to be in agreement about this.


I agree- we’re in agreement. This is horrible! It’s no fun to write on a board where everyone’s of one mind. Maybe some creationists could pop up here, or something…

Millions of children to be saved from blindness and illness

[An interesting story from the EU government which didn’t make headlines – not copyrighted.]

European Commission
05 August 1999
‘Yellow Rice’ To Prevent Vitamin A Deficiency

A project funded by the European Union - Carotene plus - has successfully incorporated the production of B-carotene into rice. This major scientific achievement, which incidentally turns the rice grains yellow, will help prevent severe vitamin A deficiency in countries relying on rice as a staple food.

Vitamin A deficiency is a public health problem in 118 countries. Not only does it cause xerophthalmia the leading cause of childhood blindness in developing countries but it also has broader consequences in terms of child morbidity and mortality by leading to greater susceptibility to various diseases such as respiratory infections, diarrhoea and measles. According to the World Health Organisation (WHO), between 140 and 250 million pre-school children are deficient in vitamin A world-wide . Improving the vitamin A status of pre-school children reduces mortality by 23%, measles mortality by 50% and diarrhoeal disease mortality by 33%. It also reduces the severity of childhood infectious diseases, in particular diarrhoea and measles. Another report suggests that improved vitamin A intake would prevent 1.25-3.5 million of the nearly 8 million late infancy and pre-school-age child deaths that occur each year in the highest-risk developing countries.

However, as supplements are difficult to distribute effectively, and costly to administer, an alternative way to defeat severe vitamin A deficiency is to introduce it directly into the diet via rice, for example, which is the major staple food for over two billion people.

A breakthrough in pathway engineering

The “Carotene plus” research project has succeeded in modifying rice by genetic engineering to make it produce B-carotene (provitamin A) which is converted to vitamin A by humans. As a result of the carotene content the rice is yellow. This rice can be considered as a functional food a new category of food products providing specific health benefits. It contains enough B-carotene to meet total vitamin A requirements in a typical Asian diet.

The strategy used was to introduce the genes corresponding to the complete biosynthesis pathway into the rice genome, so that B-carotene could be produced in the rice endosperm. Technically the work consisted of isolating the genes coding for the enzymes required to produce B-carotene. Four plant genes, namely phytoene synthase, phytonene desaturase, zeta carotene desaturase and lycopene cyclase are theoretically required. However, by using a bacterial phytoene desaturase capable of replacing the two plant desaturase genes, only three genes were finally necessary to achieve B-carotene production. The two plant genes were from Narcissus pseudonarcissus (daffodil).

Like any other plant, rice is capable of synthesising B-carotene in its green parts. However, the edible part of rice grains the so-called endosperm is carotenoid-free. The use of endosperm-specific promoters, regulating the activity of the B-carotene biosynthesis genes ensures B-carotene production in this specific tissue leading to a yellow appearance of the milled grains. Rice grains are traditionally consumed in the milled form, a process in which the outer layers are removed thereby also discarding many compounds with high nutritional value. The reason for milling is to remove a fat-rich outer layer that rapidly turns rancid during storage, especially in tropical and sub-tropical climates.


The responsible action of the scientists involved means that the plants have been grown in full compliance with EU and national legislation, i.e. using contained facilities. No application has yet been made to release the plants into the environment under the Deliberate Release Directive or their safety for human consumption assessed under the Novel Foods Regulation . Furthermore, no transfer of the technology to developing countries will be made until full compliance with all European safety legislation has been ensured.

A continuing effort

The “yellow rice” now available must be further developed. Using traditional breeding techniques, the trait will be transferred to rice varieties adapted to local conditions. Once the nutritional and environmental properties have been carefully examined, free access to the seed is to be given to subsistence farmers in developing countries.

The “Carotene plus” project also provides for the introduction of B-carotene biosynthesis into tissues that are carotene-free in other crops, including many other cereals, the aim being to develop functional foods by adding compounds known to have a positive effect on human health due to their antioxidant properties and their provitamin A character.

This project is currently funded by the European Commission through its FAIR programme and its initial phase was supported by the Rockefeller Foundation.