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Got Hormones?

By Jeffrey M. Smith, author of 'Seeds of Deception'
December 1, 2004

The Controversial Milk Drug that Refuses to Die

"Effective December 1, 2004, as a current customer, you will have access to an increased supply of POSILAC."1 This news from Monsanto to its customers was disappointing for those around the world who understood its consequences. Back in January, the company announced that they would reduce their supply of the drug by 50%, after FDA inspectors discovered unacceptable levels of contamination. Many people hoped that Posilac would quietly disappear altogether. "If Monsanto gives this stuff up, it would be a godsend to both cows and people,"2 said Rick North who heads up the campaign by Oregon Physicians for Social Responsibility to fight the drug. But on October 8, 2004, Monsanto announced it would be increasing its supply back up to "at least 70%."

Posilac is a genetically engineered drug that increases milk production in cows by 10-15%. It is also known as recombinant bovine growth hormone, rbGH, Bovine Somatotropin, BST, and "Crack for Cows." Its controversial history has left fifteen years of frustrated whistleblowers strewn in its wake.

Early casualties were scientists at the Food and Drug Administration (FDA) during the drug's evaluation. Chemist Joseph Settepani, in charge of quality control for the approval process of veterinary drugs at the Center for Veterinary Medicine (CVM), testified at a public hearing about threats to human safety. Soon after, he was reprimanded, threatened, stripped of responsibilities, and relocated a trailer at an experimental farm. In later testimony before a congressional subcommittee, Settepani said, "Dissent [atCVM] is not tolerated if it could seriously threaten industry profits."3

Division director Alexander Apostolou wrote in an affidavit, "Sound scientific procedures for evaluating human food safety of veterinary drugs have been disregarded. I have faced continuous pressure from my CVM superiors to reach scientific conclusions favorable to the drug industry. . . . In my time at CVM I have witnessed drug manufacturer sponsors improperly influence the agency's scientific analysis, decision-making, and fundamental mission."4 Apostolou was forced out after he began to express his concerns.

FDA Veterinarian Richard Burroughs said that agency officials "suppressed and manipulated data to cover up their own ignorance and incompetence."5 He also described how industry researchers would often drop sick cows from studies, to make the drug appear safer. Burroughs had ordered more tests than the industry wanted and was told by superiors he was slowing down the approval. He was fired and his tests canceled.

The remaining whistle-blowers in the FDA had to write an anonymous letter to Congress, complaining of fraud and conflict of interest in the agency. They described one FDA scientist who arbitrarily increased the allowable levels of antibiotics in milk 100-fold. This was necessary before approving rbGH. Since the drug increases the chance of udder infections, farmers inject cows with more antibiotics. This leads to a higher risk of antibiotic resistant diseases in cows and humans. According to the letter, Margaret Miller authorized the increased levels. She had formerly conducted research on rbGH while with Monsanto and then moved into the FDA department that evaluated her own research.

Dr. Samuel Epstein, Professor at the University Of Illinois School Of Public Health, cited numerous potential or theoretical health dangers from rbGH, including "hormonal and allergic effects . . . premature growth and breast stimulation in infants," and possibly cancer in adults.6 Epstein also received an anonymous box of stolen files from the FDA. Documents revealed that in order to show that rbGH injections did not interfere with fertility, industry researchers allegedly added cows to the study that were pregnant prior to injection. Also, blood hormone levels skyrocketed by as much as a thousand-fold after injections.7

Monsanto tried to silence Epstein. Their public relations firm created a group called the Dairy Coalition, which included university researchers whose work was funded by Monsanto, and selected "third party" experts and organizations. Representatives of the Dairy Coalition pressured editors of the USA Today, Boston Globe, New York Times and others, to limit coverage of Epstein.

 Got Hormones? [continued]

Hormones in Your Milk

Several claims made by FDA scientists in defense of rbGH have not held up under scrutiny. For example, they said that bovine growth hormone does not increase substantially in milk from treated cows. The study they cited, however, shows a 26% increase in the hormone. Furthermore, researchers injected cows with only a 10.6 mg daily dose of rbGH compared to the normal 500 mg bi-weekly dose used by farmers. In fact, they didn't even use Monsanto's rbGH, but rather another version that was never approved. They then pasteurized the milk 120 times longer than normal in an apparent attempt to show that the hormone was destroyed during the process. They only destroyed 19% of the hormone.8 They then spiked the milk with powdered hormone-146 times the naturally occurring levels-heated that 120 times longer than normal, and were then able to destroy 90% of the hormone. FDA scientists reported that 90% of the hormone was destroyed during pasteurization.9

The hormone most critics are concerned about, however, is insulin-like growth factor 1 (IGF-1). Natural milk contains IGF-1. Milk drinkers increase their levels of IGF-1.10 Studies suggest that pre-menopausal women below 50 year old with high levels of IGF-1 are seven times more likely to develop breast cancer.11 Men are four times more likely to develop prostate cancer.12 IGF-1 is also implicated in lung and colon cancer. Milk from cows treated with rbGH has significantly higher levels of IGF-1.13 (No comprehensive study has evaluated a direct link between rbGH and human cancer.)

This potential link between rbGH and cancer was one of the many controversial topics to be covered in a four-part investigative news series at a Tampa-based Fox TV station. But four days before the series was to air, Fox received a threatening letter from Monsanto's attorney. They pulled the show. The station manager reviewed it, approved the content, and scheduled it for the following week. A second letter arrived from Monsanto's attorney, this time threatening "dire consequences for Fox News."14 The show was postponed indefinitely. Jane Akre and Steve Wilson, the award winning investigative reporters who had created the report for Fox, say that they were offered hush money to leave the station and never speak about the story again. They declined. So Fox's corporate attorney led them in a series of rewrites, attempting to soften the language and apparently appease Monsanto. Six months and 83 rewrites later, the reporters were ultimately fired for refusing to write in the script that the milk from treated cows was the same as normal milk. The reporters argued that that Monsanto's own research showed a difference, such as the increased IGF-1 levels, and even the FDA scientists had acknowledged this.

The reporters sued. Akre was awarded $425,000 by a jury that agreed that Fox "acted intentionally and deliberately to falsify or distort the plaintiffs' news reporting on BGH,"15 and that Akre's threat to blow the whistle was the reason she was fired. But an appeals court overturned the verdict on the grounds that the whistle-blower's statute only protects people who threaten to report a violation of a law, rule, or regulation. Distorting TV news, evidently, is not technically illegal. Akre and Wilson now have to pay a combined $196,500 to cover some of Fox's legal costs. This is on top of the $200,000 - $300,000 they already spent on their case.

Attacks on rbGH whistleblowers are not limited to the US. In 1998, six Canadian government scientists testified before the Senate that they were being pressured by superiors to approve rbGH, even though they believed it was unsafe for the public. Their detailed critique of the FDA's evaluation of the drug showed how the US approval process was flawed and superficial. They also testified that documents were stolen from a locked file cabinet in a government office, and that Monsanto offered them a bribe of $1-2 million to approve the drug without further tests. (A Monsanto representative went on national Canadian television claiming that the scientists had obviously misunderstood an offer for research money.) The Canadian scientists later described how their superiors retaliated against them for testifying. They were passed over for promotions, given impossible tasks or no assignments at all, one was suspended without pay. Three of the whistleblowers, who also spoke out on such controversial topics as mad cow disease, were ultimately fired on July 14, 2004.

Most industrialized nations have banned rbGH. Within the US, many school systems have also banned it and several dairies refuse to use it. Oakhurst Dairy of Portland, Maine, for example, requires its suppliers to sign a notarized affidavit every six months. The Oakhurst label stated, "Our Farmers' Pledge: No Artificial Growth Hormones." But on July 3, 2003, Monsanto sued the dairy over their labels. Oakhurst eventually settled with Monsanto, agreeing to include a sentence on their cartons saying that according to the FDA no significant difference has been shown between milk derived from rbGH-treated and non-rbGH-treated cows. The statement is not true. FDA scientists had acknowledged the increase of IGF-1 in milk from treated cows. Nonetheless, the misleading sentence had been written years earlier by the FDA's deputy commissioner of policy, Michael Taylor. Prior to becoming an FDA official, Taylor was Monsanto's outside attorney. He later worked at the USDA on biotech issues, and later became vice president of Monsanto.


  1. POSILAC® SUPPLY UPDATE October 8, 2004

  2. Emailed correspondence

  3. Craig Canine, "Hear No Evil: In its determination to become a model corporate citizen, is the FDA ignoring potential dangers in the nation's food supply?" Eating Well, July/August 1991

  4. Craig Canine, "Hear No Evil: In its determination to become a model corporate citizen, is the FDA ignoring potential dangers in the nation's food supply?" Eating Well, July/August 1991

  5. Craig Canine, "Hear No Evil: In its determination to become a model corporate citizen, is the FDA ignoring potential dangers in the nation's food supply?" Eating Well, July/August 1991

  6. Samuel Epstein, "Growth Hormones Would Endanger Milk.," op-ed piece, Los Angeles Times, July 27, 1989

  7. Samuel Epstein and Pete Hardin, "Confidential Monsanto Research Files Dispute Many bGH Safety Claims," The Milkweed, January 1990

  8. Robert Cohen, Milk, the Deadly Poison, Argus Publishing, Englewood Cliffs, New Jersey, 1998

  9. Judith C. Juskevich and C. Greg Guyer, "Bovine Growth Hormone: Human Food Safety Evaluation," Science, 1990, vol. 249, pp. 875-884

  10. Robert P. Heaney and others, "Dietary changes favorably affect bone remodeling in older adults." Journal of the American Dietetic Association, vol. 99, no. 10, October 1999, pp. 1228-1233 and "Milk, Pregnancy, Cancer May Be Tied," Reuters, September 10, 2002

  11. S. E. Hankinson, and others, "Circulating concentrations of insulin-like growth factor 1 and risk of breast cancer," Lancet, vol. 351, no. 9113, 1998, pp. 1393-1396

  12. June M. Chan and others, "Plasma Insulin-Like Growth Factor-1 [IGF-1] and Prostate Cancer Risk: A

  13. Prospective Study," Science, vol. 279, January 23, 1998, pp. 563-566

  14. C. G. Prosser and others, "Increased secretion of insulin-like growth factor-1 into milk of cows treated with recombinantly derived bovine growth hormone," Journal of Dairy Science, vol. 56, 1989, pp. 17-26; and Peter Montague "Milk, rbGH, and Cancer," Rachel's Environment and Health News, no. 593, April 9, 1998

  15. BGH Bulletin, Target Television Enterprises Inc.,


Genes Are Not Immune to Context

By Craig Holdrege
In Context #12
Fall, 2004

Examples from Bacteria

One of the most widespread misconceptions concerning the nature of genes is that they have a defined and fixed function that allows them to operate the same in all organisms and environments. We have the picture of the robust gene determining all the characteristics an organism has. And this gene will do the same thing in a bacterium as in a corn plant or human being. It doesn't care where it is. The gene carries its set of instructions with it wherever it goes and strictly carries out its duty.

This picture informs genetic engineering. Take a gene from bacteria and put it into a plant and the plant will produce its own pesticide or become resistant to a herbicide. Since such transgenic plants exist, the proof is evidently in the pudding. Genetic manipulation works; genes are faithful workhorses. But does genetic manipulation work the way we imagine with our schematic pictures? What else may be occurring that doesn't fit into a neat mechanistic scheme?

It's somewhat ironic that precisely within the last ten to fifteen years—the period in which genetically modified crops have been developed and commercialized in the U.S. and some other countries—a wealth of research on genes in relation to environmental effects has been carried out, showing that genes are anything but automatic instruction programs immune to their context. This research has significant implications for the way we assess genetic engineering. Unfortunately, it often seems that the results of this basic research have little effect on the minds and pocket books supporting the global drive to manipulate organisms genetically. In this article I'll discuss some examples of the contextual gene in bacteria.

The Interactive Gene

With the widespread use of antibiotics in our culture, many bacteria have become resistant. They thrive even when subjected to high doses of antibiotics. As a rule, the resistance comes at a cost, since the resistant bacteria tend to grow slowly. But when they are grown in laboratory cultures, some of these resistant bacteria will experience so-called compensatory mutations—they stay resistant, but change genetically in a way that allows them to grow fast like wild, nonresistant strains. Others mutate back to the wild form and lose their resistance altogether.

The question arises whether such mutations (changes in genes or in higher-order genetic structures) are in any way dependent on the environment. The traditional view, rooted deeply in the Neodarwinian theory of evolution, holds that genes mutate spontaneously and independently of the environment. The classical experiment with bacteria by Luria and Delbrück in the 1940s gave clear evidence that such spontaneous, milieu independent mutations exist (Luria and Delbrück 1943). For decades this experiment (along with other evidence) served as the rock solid "proof" that genetic mutations, except for extreme cases involving irradiation or exposure to chemical toxins, are not influenced by their environment. But more recent research shows that mutations do in fact arise in response to changing environmental conditions.

A group of biologists in Sweden investigated whether the above-mentioned compensatory mutations and the reversion to the wild form in bacteria are influenced by the environment (Björkman et al. 2000). They grew antibiotic-resistant bacteria—in the absence of antibiotics—as laboratory cultures (in petri dishes) and also inoculated mice with the same bacteria. The researchers monitored the mutations that occurred in the bacteria in these two different habitats. They found that compensatory mutations occurred in both habitats, but, to their surprise, they discovered that the way the genetic material changed differed significantly depending upon the environment. In the case of streptomycin-resistant bacteria in mice, they found ten cases of identical compensatory mutations within the resistance gene. In contrast, this gene never mutated in the lab-cultured bacteria, where they found fourteen compensatory mutations in genes outside the resistance gene. Evidently, the environment had everything to do with what kind of mutations occurred. "Mice are not furry petri dishes," as the title of a commentary article put it (Bull and Levin 2000).

The authors conclude that the mutations are "condition-dependent" and suggest that some unknown "mutational mechanism" limited the mutations in the mice to a specific part of the resistance gene while also increasing its mutation rate. Whatever the details of cell physiology turn out to be, it is clear that the genome of the bacteria changes in relation to a specific kind of environment. The bacteria—down into their genes—interact with and evolve in relation to their environment.

Adaptive Mutations

In another recent study (Bjedov et al. 2003), a research group in France gathered wild strains of the bacterium E. coli from a wide variety of environments—the large intestines of humans and different animals, soil, air, and water. In the end they collected 787 different strains. These strains were given optimal conditions in lab cultures and began to grow and multiply rapidly, mimicking ideal conditions in nature where bacteria reproduce quickly. But in nature, bacteria are also exposed to times of dearth, where the substrate they live upon, for example, is suddenly used up. To mimic these conditions, the researchers withheld nutrients for a seven-day period. Most bacteria survive under these conditions, but they no longer grow and divide.

The scientists measured the rate of mutations occurring in the cultures the first day after withholding nutrients and then again at the end of the seven-day period. During this time the mutation rate increased on average sevenfold. In other words, the mutation rate increased dramatically when the bacteria no longer received adequate nutrition. The bacteria switch, in the words of the authors, "between high and low mutation rates depending on environmental conditions" (p. 1409).

Such a stress-induced increase in mutation rate has been discovered in many laboratory strains of bacteria. Does this increase in mutation rate serve the bacteria, or is it a kind of last gasp, a dissolution of the bacteria before they die of starvation? The answer is clear: the bacteria produce unique kinds of mutations during such periods of physiological stress, some of which help the bacteria survive under specifically those conditions. One speaks of "adaptive mutations." (See Wirz 1998 and Rosenberg 2001 for good overviews of the research and literature.)

For example, there are strains of E. coli that have lost the capacity to utilize the sugar lactose as a source of energy. If such a strain is cultured in a starvation medium with lactose as the only energy source, most of the bacteria remain in a stationary phase until they die. But under these conditions some of the bacteria begin to hypermutate, which means they rapidly create a large number of mutations and among these are ones that allow them to live from lactose. The bacteria with this ability survive, multiply and form new colonies. In at least some cases such adaptive mutations arise only in the specific medium—that is, the mutations allowing bacteria to utilize lactose don't occur when bacteria are grown in a medium with sugars other than lactose.

In other instances, E. coli bacteria do not hypermutate, but find another way to deal with the environmental challenge. Some of the bacteria in the medium with lactose produce multiple copies of the gene related to their inability to live from lactose. This gene amplification seems at first absurd. But scientists found that E. coli strains unable to grow when they only receive lactose as a nutrient do form enzymes that break down lactose, but in inadequate amounts. When the bacteria amplify the defective lactose enzyme gene, the cumulative effect is that they produce enough enzymes to break down a sufficient amount of lactose to grow slowly and survive - a remarkably active and meaningful genetic adaptation. This amplification occurs in no other genes in the bacteria. It is specific to the lactose enzyme gene and clearly induced by the environment.

Transfer of Resistance

Bacteria have a further way of adapting to new conditions. I have already mentioned antibiotic-resistant bacteria. Cholera bacteria, for example, are normally susceptible to different antibiotics. After 1993 antibiotic-resistant cholera bacteria rapidly spread around the globe. How could this occur? Scientists discovered that these bacteria are simultaneously resistant to at least five different antibiotics. They found that the genes related to this resistance were all grouped together and formed a "packet" of genes that can move from bacterium to bacterium.

A research group at Tufts University in Boston recently discovered conditions that facilitate this movement and uptake of genes (Beaber et al. 2004). When bacteria are grown in cultures with concentrations of antibiotics that are not sufficient to kill them, they go through physiological changes similar to what happens to bacteria in a starvation medium. Part of this transformation is called an SOS response. It comes about when DNA is damaged and involves DNA repair and duplication. The Tufts scientists found that during the SOS response the bacteria also increased the transfer of the resistance gene clusters to other bacteria. Evidently, the use of antibiotics promotes the spread of antibiotic resistance among bacteria. In this way, once resistance is anchored in mobile genetic elements, it can spread rapidly.

The examples I have described show how strongly the en-vironment influences the activity of genes, induces changes within genetic structures (mutations), and stimulates the movement of genes between bacteria. Bacteria are in continual interplay with their environment, actively responding to changing conditions. And this responsiveness and flexibility includes genes. If we release genetically engineered bacteria into the environment, there is little doubt that in time they will be passing their genes to other bacteria, as well as receiving genes from other bacteria and mutating according to changing circumstances. Whether the manipulated foreign genes they carry will be exchanged, or how they may affect or be affected by the dynamics of genetic responses to changing environments is completely open. But two things we can know for sure: these genes will not function immune to the changing circumstances and things will happen that no one expects or can foresee. I'm not saying this to promote fear, but to dissolve the illusion that we can keep under control what we have released into the world in this way. Genes are robust, but they are also part of the world.


  • Beaber, John W. et al. (2004). "SOS Response Promotes Horizontal Dissemination of Antibiotic Resistance Genes." Nature vol. 427, pp. 72-74.

  • Bjedov, Ivana et al. (2003). "Stress-Induced Mutagenesis in Bacteria." Science vol. 300, pp. 1404-1409.

  • Björkman, J. et al. (2000). "Effects of Environment on Compensatory Mutations to Ameliorate Costs of Antibiotic Resistance." Science vol. 287, pp. 1479-1482.

  • Bull, James and Bruce Levin (2000). "Mice Are Not Furry Petri Dishes." Science vol. 287, pp. 1409-1410.

  • Luria, S.E. and M. Delbrück (1943). "Mutations of Bacteria from Virus Sensitivity to Virus Resistance." Genetics vol. 28, pp. 491-511.

  • Rosenberg, Susan M. (2001). "Evolving Responsively: Adaptive Mutation." Nature Reviews Genetics vol. 2, pp. 504-515.

  • Wirz, Johannes (1998). "Progress Towards Complementarity in Genetics." Archetype Sept (No. 4), pp. 21-36. Available online:


Europe Still Resisting GMOs

By Lim Li Ching
December 2004

The authorisation of Bt 11 sweet maize for food use in May this year marked the end of Europe's de facto moratorium on GM approvals. However, there is by no means consensus on GMOs in Europe. Lim Li Ching explains how approvals can still occur despite objections.

On 29 November 2004, an EU regulatory committee once again failed to reach a qualified majority to support a proposal by the European Commission for the import of Monsanto's GM maize (MON863 and MON863 x MON810 hybrids). The Scientific Panel on GMOs of the European Food Safety Authority (EFSA) had earlier this year pronounced MON863 "safe". Nonetheless, the maize has been controversial, as concerns have been raised regarding the results of a feeding study that showed suspected adverse effects in the blood and kidneys of rats fed the GM maize. These effects were unobserved in rats fed conventional maize.

Earlier, on 20 November, the committee postponed a formal vote on Monsanto's application, to seek clarification and more information. At the Commission's request, EFSA's GMO Panel reviewed an evaluation report on MON863 that was submitted by Germany, as well as retrospectively evaluated some of the scientific data that were causing concern. On 20 October, the GMO panel issued a statement saying, "there is no evidence… that changes the conclusions already reached by the GMO Panel earlier this year". Despite the reassurances, only eight countries (133 votes) voted in favour of approving MON 863, while 12 countries (123 votes) voted against and five abstained (65 votes). The Council of Environment Ministers must now decide on the proposal to approve MON863, within three months.

This is just the latest in a string of GM applications to meet strong resistance from European countries. It was the ninth failed attempt by the Commission to win support for a GMO or GM product, as health and environmental concerns over these GMOs have been raised by scientists and regulators from various countries.

Under current EU law, when an application is made by a company to market a GMO or GM product in a Member State, and there is no consensus among other Member States, then the Commission steps in. It seeks advice from the European Food Safety Authority (EFSA), which provides the various scientific panels that carry out environmental risk and human and animal health assessment. Lack of scientific consensus has sometimes occurred at this stage. If EFSA supports an application, the Commission drafts and adopts a proposal to approve the GMO or GM product concerned.

This is then transmitted to the appropriate regulatory committee, depending on the intended use of the GMO or GM product concerned. The committees comprise representatives of the 25 Member States. Decisions are made by a 'qualified majority' vote. The votes are weighted among the Member States according to their size. A certain percentage of the weighted votes (232 out of 321 votes) are required to reach qualified majority.

If the regulatory committee cannot reach a qualified majority to adopt or reject a Commission proposal, the next decision level is the Council of Ministers (comprising of environment or agriculture ministers from the 25 Member States, depending on the intended use of the GMO or GMO product). A qualified majority is needed to either approve or reject the proposal.

However, in the absence of a qualified majority and according to the so-called 'comitology' procedure, the Commission can take the final decision. This means that 'approval' of a GMO in the EU can occur despite continuing objections by a number of Member States. In addition, such 'approval' goes against the wishes of most European citizens, who overwhelmingly reject GMOs.

The following is a list of the failures to reach qualified majority at either the regulatory committee or Council stages since December 2003:

  • 8 December 2003: Vote on Bt 11 sweet maize for food use at the Standing Committee on Food Chain and Animal Health. Result: no qualified majority. 6 countries in favour; 6 against; 3 abstentions.
  • 18 February 2004: Vote on NK 603 maize for import and use in feed and industrial processing at the Standing Committee of Release of GMOs into the Environment. Result: no qualified majority. 9 in favour; 5 against; 1 abstention.
  • 26 April 2004: Vote on Bt 11 sweet maize for food at the Council of Agriculture Ministers. Result: no qualified majority 6 in favour; 6 against; 3 abstentions. The decision thus reverted to the Commission, which approved Bt 11 sweet maize for food use on 19 May 2004, ending the EU's de facto moratorium. However, Syngenta later said the product would not be commercialised in Europe, for now, due to strong consumer resistance.
  • 30 April 2004: Vote on NK 603 maize for food use at the Standing Committee on Food Chain and Animal Health. Result: no qualified majority. 8 in favour; 5 against; 2 abstentions.
  • 16 June 2004: Vote on GT 73 oilseed rape for import and use in feed and industrial processing at the Standing Committee of Release of GMOs into the Environment. Result: no qualified majority. 9 in favour; 12 against; 4 abstentions. GT 73 will go to the Council of Environment Ministers for a vote.
  • 28 June 2004: Indicative vote on NK 603 maize for import and use in feed and industrial processing at the Council of Environment Ministers. Result: no qualified majority. 11 in favour; 9 against; 3 abstentions. The decision thus reverted to the Commission, which on 19 July 2004 approved NK 603 for import and processing for use in animal feed or for industrial purposes. However, imports for this use can only commence once the equivalent approval has also been granted for food use.
  • 19 July 2004: No official vote, so no decision at the Council of Agriculture Ministers on NK 603 maize for food use. This was after it became clear that no qualified majority could be reached, as Member States had not changed their positions from when the Standing Committee met on 30 April. The proposal reverted to the Commission on 13 October 2004, which approved NK 603 for food use on 26 October; this means that imports of NK 603 are now allowed into Europe.
  • 20 September 2004: Formal vote on MON863 and MON863 x MON810 hybrids postponed, to seek clarification and more information, after concerns were raised.

In other developments, on 8 September 2004, the Commission approved the inscription of 17 varieties derived from MON 810 maize in the Common EU Catalogue of Varieties of Agricultural Plant Species. MON 810 has been authorised in the EU since 1998, under previous weaker legislation, but this is the first time GM varieties have been added to the Common Catalogue.

The move allows farmers to commercially grow the GM varieties across the whole of Europe. Before this decision, the 17 varieties seeds only had national authorisations - 6 are on the national catalogue in France, 11 in Spain – so only farmers in those countries were able to buy and plant the seeds. There is an on-going Europe-wide campaign to "Stop the Crop", being co-ordinated by the Friends of the Earth Europe (see And opposition is not just coming from NGOs; fifteen of the 25 EU member states have also criticised the Commission's decision. In addition, Poland's environment and agriculture ministries want to have continued national restrictions on the cultivation of MON 810.

The Commission however was unable to reach consensus on a proposal to set maximum levels of GMO contamination in seeds. A draft decision was due to be adopted by Commissioners, proposing a 0.3% threshold in maize and oilseed rape, before triggering labelling. Critics, including farmers, trade unions, environmental groups, and seed producers, deem this threshold as too high and have campaigned for it to be set at 0.1%, the current lowest technically feasible level. Moreover, Austria has had a workable and feasible seed purity law since 2002. It adopted a 'zero-tolerance' policy, prohibiting contamination of seeds with GM varieties above the detection level of 0.1%.

The decision on seed thresholds was postponed pending more information on the economic impact of the proposed threshold. The issue will now come before the newly appointed Commission. The new agriculture commissioner, Mariann Fischer Boel, had campaigned for a 0.1% threshold in her native Denmark, and has told the European Parliament that the seed thresholds should be set at the lowest possible level.

The national bans on GMOs held by a number of European countries are currently being challenged. The European Commission also asked countries to vote on 29th November at the regulatory committee meeting, on whether each country that has a national ban should lift its embargo or not. Such bans are the subject of the complaints against the EU brought to the WTO by the US, Canada and Argentina, with those countries claiming that they are trade barriers. However, the national bans were not overturned and the proposals to lift the bans will now be forwarded to the Council of Environment Ministers. It is clear that the GM fight will continue in Europe. But resistance remains strong at all levels.



  2. "European Ministers Split on Monsanto's GM Maize NK 603," Third World Network Biosafety Information Service, 30 June 2004.

  3. "Monsanto GM Maize Not Authorised by EU Commission," Friends of the Earth Press Release, 28 June 2004.

  4. "Civil Society Urges EU Commission to Reject GM Seed Contamination," Press Release from Save Our Seeds, Kampffmeyer Mühlen Hameln, EFFAT, Greenpeace, Friends of the Earth Europe, EEB, IFOAM EU, EURO COOP, Confederazione nazionale COLDIRETTI, Coordination Paysanne Européenne CPE, Coordinadora de Organizaciones de Agricultores y Ganaderos of Spain, 8 September 2004.

  5. "Inscription of MON 810 GM Maize Varieties in the Common EU Catalogue of Varieties," European Commission Press Release IP/04/1083, 8 September 2004.

  6. "EU Urged to Exercise Caution on GM crops," Environment Daily 1750, 19 October 2004.

  7. "EU Commission Drops Decision on GMO Seed Labels," Reuters, 8 September 2004,

  8. "Austria's No GE Seed Contamination Regulation Working Well," Third World Network Biosafety Information Service, 19 June 2003.

  9. "Safety Fears and Secrecy: Greenpeace Challenges New GMO Application," Greenpeace, 17 September 2004

  10. "Europe Halts Monsanto Maize," Friends of the Earth Europe, 20 September 2004.

  11. "Don't Let Bush and the WTO Win: Help Stop the European Commission From Backing Down on GM foods," Friends of the Earth Europe, October 2004.

  12. "EU Experts Fail to Authorise New Biotech Maize," by Jeremy Smith, Reuters, 30 November 2004.

Lim Li Ching, Senior Fellow at The Oakland Institute, works with the biosafety programme at Third World Network (TWN), an international NGO based in Malaysia. TWN is involved in efforts to bring about a greater articulation of the needs and rights of peoples in developing countries; a fair distribution of world resources; and forms of development which are ecologically sustainable and fulfill human needs.

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