Select Committee on Food Standards First Report


Submitted by Dr Helen Fullerton, Farming and Livestock Concern UK

  I am a retired agricultural chemist who now researches on matters of human and animal health, particularly nutrition. I have contributed to the consultations on Professor Philip James's Food Standard Agency proposal and to the White Paper "A force for Change". Farming and Livestock Concern UK is a network of farmers and allied interests.


  Genetically modified organisms (GMOs) were not identified in the White Paper nor in the consultation on draft Legislation for the Food Standard Agency (FSA), nevertheless it is now recognised they will be a major concern. I draw attention to clause 19(2) of the Food Standards Bill: "The Agency shall take into account of:

    (a)  the nature and magnitude of any risks to public health, and or risks, which are relevant to the decision (including any uncertainty as to the adequacy or reliability of the available information);

    (b)  the likely costs and benefits of the exercise or non-exercise of the power or its exercise in any manner which the Agency is considering."

  Also I draw attention to the Guiding Principles 3—"The Agency's decisions should be proportionate to the risk; pay due regard to costs as well as benefits to those affected by them and avoid over-regulation."

  I put the case that GMOs are an unacceptable risk because their effects are unpredictable with respect both to food safety and security of food supply.


  In risk assessment it is only required that the amounts of known components (usually restricted to nutrients, toxins and allergens) be the same as that in a comparable non-GMO foodstuff and devoid of the inserted DNA for it to be declared "substantially equivalent" with respect to safety, and it will be approved for marketing by the Advisory Committee on Novel Foods and Processes (ACNFP). For "fast track approval" (60 days) the foodstuff must also be devoid of the protein product, as in the case of soya oil derived from GM-soya [1 paragraph 673]. The EU Commission and the Government propose that "only products where the transgene or its product are detectable should be labelled" [2 paragraph 137]. This means that if either are present below a certain threshold of detectability the foodstuff:

    (a)  would not need to be labelled; and

    (b)  would be considered substantially equivalent. At present the detectable limit for GM is 0.1 per cent.

  The Lords suggest an agreed EU threshold of 2 per cent [2 paragraph 142]. This may lead to import disagreements, invoking the WTO: in US and Canada labelling is only required to identify the presence of potential health or safety risks and where there are significant changes to the compositional or nutritional value when compared to non-engineered food [2 paragraph 126].

  Labelling is seen in the EU and UK as necessary to win consumer confidence and provide consumer choice rather than as an essential safeguard, enabling identification in case something goes wrong. Traceability is deemed too difficult and costly and best left to supermarkets [2 paragraph 117]. It is recommended to be replaced by monitoring.

  Monitoring involves both risk assessment and post-marketing surveillance. ACNFP identifies any injurious protein product of inserted genes by monitoring, using databases of toxic and allergic sequences. If one of these is present in the known protein product e.g., the enzyme conferring resistance to a herbicide or pest, or if the foodstuff contained higher levels of toxicity than a comparable non-GM, it would not be given market approval [1 paragraph 724]. The EU Directive proposes that the seed company perform the monitoring. The Lords demurred, recommending that it be done by an independent body, funded by the applicants [2 paragraph 102].

   The value of tests to detect the presence of transgene DNA is to check whether or not the food or ingredient has been genetically engineered, e.g., for purposes of labelling. DNA is detected via polymerase chain reaction (PCR) amplification. Costs escalate as levels become low as in processed food. Protein product and metabolite analysis is rarely undertaken, because antibodies must be raised against the protein and few are available. [1 Memorandum of the Laboratory of the Government Chemist Ltd pp. 358-66].

  Despite all the cautious measures, the entire edifice of risk assessment and its dependence on the concept of substantial equivalence is unsafe. It takes no account of any risk that might arise from the presence of an unpredictable, unknown protein or metabolite produced by the genetic manipulation, or of a changed behaviour of the protein product. Examples follow.


  Professor Arpad Pusztai, a leading expert in lectins (a type of glycoprotein) was concerned that incorporation of the snowdrop (Galanthus nivalis) gene into potato tubers might be injurious to health. He believes that experiments are not being done to find out if the genetic modification induces unpredictable nutritional effects on the consumers of GM crops. World wide only one peer-reviewed paper has examined this question (Pusztai pers.comm). In 1995 the Scottish Office Agriculture, Environment and Food Department (SOAEFD) commissioned a three year multicentre project whose main objective was "to identify genes encoding anti-nutritional factors which will be suitable for transfer into plants to enhance their resistance towards insects and nematode pests, but will have minimum impact on non-target beneficial organisms, the environment, livestock fed on those plants and which will present no health risks for humans either directly or indirectly through the food chain."

  There is much interest in the snowdrop lectin (GNA) gene since it is expected its product will be toxic to sucking insects particularly in rice crops, and to nematodes in root crops, by interfering with the pests' digestion. When the gene was introduced into potato tubers the lectin comprised up to a maximum of 0.5 per cent of the total root protein and led to a reduction in nematode females of 80 per cent.3 These benefits must be set against the risks. Researchers at the Scottish Crops Research Institute (SCRI) found its incorporation into the potato leaf led to lowered fertility and lifespan of the ladybirds feeding on the aphid larvae.4. Professor Pusztai who co-ordinated research at the Rowett Research Institute (RRI) found5:

    (i)  The starch and glucose content of the transgenic GNA potatoes were different to those of the parent potatoes, as were the level of potato lectin, and of trypsin and chymotrysin inhibitors. In one line the raw or baked transenic contained nearly 20 per cent less protein than its parent. SCRI scientists had already found a decreased foliar glycoalkaloid content.6 Pusztai commented: "The results clearly indicate gene silencing, suppression and or somaclonal variation as a result of gene insertion . . . the GNA-GM potato lines were not substantially equivalent to the parent tubers".

    (ii)  10-day feeing experiments on rats showed that digestion and absorption of a transgenic potato-based diets were retarded in comparison with parent potato diets, and there was a reduction in weight of most organs. This, together with a partial liver atrophy on feeding boiled transgenic potato diets and enlargement of jejunum, pancreas and testes on feeding raw GNA-GM potato diets suggested a lack of equivalence of the metabolic consequences between feeding GM and parent potatoes.

    (iii)  Potatoes spiked with the snowdrop lectin did not show these abnormalities. The abnormalities were thus a consequence of the genetic manipulation.

    (iv)  Lymphocytes from rats given transgenic potato diets were almost always less responsive to mitogenic stimuli, indicating immuno-suppression. In contrast, snowdrop lectin-spiked potato diets in some instances stimulated the immuno-response.

  Many plants contain lectins, notably the legumes. They are in the tomato and widespread in seeds and storage organs where they may have a protective function against pests but are benign to the mammal. No doubt when asked for their approval ACNFP would have consulted their data base to see if the snowdrop lectin contained a toxic sequence similar to the kidney bean lectin. If it did not, as indeed the rats fed the GNA—spiked potatoes suggest, would it have been given approval?

  After his appearance on World in Action 10 August 98, Professor Pusztai was dismissed from the Rowett 14 August and forbidden under the terms of the BBSRC staff code (chapters 11, 12) from speaking or publishing in defence of his research. His report [5] was suppressed and the embargo only lifted under media pressure 17 February 1999. The team has been disbanded and the research quietly discontinued, despite that many questions remain to be answered. One can only conclude the project was abandoned under pressure from GMO interests, particularly Montsanto who have already given £240,000 to the Rowett for research. If GM companies were required to do pharmacological toxicity testing as above, it would not only be expensive, but might give uncomfortable results as in the case of bovine somatotropin (BST).


  It is often claimed there is no scientific evidence that transgenic crops are not substantially equivalent. There is little proof because:

    (a)  it is not looked for; and

    (b)  if found, the matter is buried in the literature or else hushed up.

  Also hushed up is the nature of GM technology itself. Pusztai attributed his transgenic results to "gene silencing and/or somaclonal variation." Nowhere in the House of Lords Report [2] is there mention of either, nor did those giving evidence draw attention to them. The single exception was the account given by Dr Michael Antoniou on behalf of Greenpeace [1 Greenpeace memorandum, Appendix 2 pages 36-39]. Since their occurrence is unpredictable and the risks cannot be quantified, this can be the only reason that the Government's advisors neglected to inform the Lords about them, except by obliquely emphasising "it is not the gene that matters, but how it behaves."

    (i)  Gene silencing: When a foreign gene is inserted into an organism, the DNA—like other tissues—can recognise self from non-self [7] and attempts to inactivate the intruder by silencing or suppressing the gene, usually by attaching a methyl group to the DNA. The gene will not be expressed and the looked-for characteristic e.g., insect resistance, cold tolerance, etc., will not appear, or may fail to appear in the progeny. More significantly, plant genes with a similar sequence may also inadvertently be switched off.

    (ii)  Somaclonal variation: this is the rearrangement of plant genetic material during tissue culture and plant regeneration from a single cell [8]. All GM plants are grown from cells cultured in a dish. Conventional breeders use the same technique, but without the added complication of the "foreignness" of the gene. The results are totally unpredictable. Genes do not work in isolation but in an interdependent network, their expression determined by the activities of the cell, the reactions of the organism and environmental influences. The rearrangement may mean that proteins are expressed in different cells, enzymes work faster or more slowly, or are switched on at inappropriate times. These in turn as one may surmise in Pusztai's rats can affect the nutritional quality of the food, introduce unknown toxins or alter metabolism [9].


    (i)  A transgenic yeast engineered for an increased rate of sugar fermentation with multiple copies of one of its own genes resulted in the accumulation of a metabolite methyl glyoxal 30 times higher than in the original strains. The authors pointed out that these levels could be mutagenic and suggested the concept of substantial equivalence for the safety assessment of genetically engineered food was not always applicable to genetically engineered microbes [10].

    (ii)  The most famous case is that of a GM tryptophan genetically engineered in bacteria to produce a cheap food supplement of this essential amino acid by a Japanese company Showa Denko. In 1989 in USA 5,000 people became ill with eosnophilia myalgic syndrome. Thirty-seven died and 1,500 were permanently disabled. The disaster was eventually traced to the engineered tryptophan and the presence of a toxin at a concentration of less than 0.1 per cent of the product. It has never been ascertained whether the toxin was produced by the genetic manipulation or in the production process [11]. But we note that:

    (a)  since the product was not labelled "GMO" it was indistinguishable from the natural tryptophan on the shelves.

    (b)  At a concentration of 0.1 per cent it would today be considered below the threshold limit and classified as substantially equivalent.

    (iii)  In a field experiment, the mainly self-pollinating Arabidosis thuliana had been engineered to be resistant to the herbicide chlorsulphuron via a mutation in the enzyme acetolactate synthase. It should have been substantially equivalent to a mutant wild type expressing the same mutation. The plants are insect-pollinated and it was found that the wild weed growing along side the test plants was 20 times more likely to be fertilised by the transgenic plant than by the mutated one, i.e., it as 20 times more likely to confer herbicide resistance to the native and create a super weed [12]. Although not directly relevant to food, this case is analagous to the differing effects on rats of Pusztai's GNA-GMO potatoes and GNA-spiked potatoes. In both cases it was the genetic manipulation that created the changed and unwanted properties.

    (iv)  We do not know whether the widespread crop failures in transgenic cotton (see below) were due to gene silencing and/or to the pressure of a new environment on the GMO.


  Another matter that is hushed up is the "construct", aptly described by Professor Mark Williamson as the scaffolding [1 paragraphs 519-20], necessary to ferry the transgene into position and provide it with an on-switch (the promoter), an off-switch (the terminator), and a marker for identifying those cells that have been modified and will be grown into plants. The most popular promoter is cauliflower mosaic virus. A major worry in genetic engineering is that a fragment of viral DNA or RNA will combine with other fragments or with a benign virus to cause a virulent disease in crops, beneficial insects, animals or humans. Given the multiplicity of virus used and the scale, it may be only a matter of time.


  The FSA has no remit for the environmental impact of GMOs. Nevertheless there is a link here with the security of food supplies. Bearing in mind that even low probability events will occur if scale and time increase, foreseeable problems include:

    (i)  The development of pest resistance. The most widely used toxin conferring protection to crops is the product of the Bt gene extracted from Bacillus thuringiensis. Commercial releases include transgenic maize, potatoes, cotton, tobacco and leafy vegetable crops. Montsanto's cotton boll-guard Bt-cotton bred in California lost resistance to bollworm in the droughty climate of the southern states and had to be sprayed to save it. Australian farmers were up in arms last year when they too lost their cotton crop or had to spray it. In the laboratory it was found that the diamond back-moth, a major pest of cabbages developed resistance in a few generations against four strains of Bt via a genetic change in a single gene [13].

    (ii)  The destruction of pest predators and of pollinators. Already ladybirds [4], lacewings [14] and pollinators including our precious bees [15] have been shown at risk. Crop yields in recent years have already declined due to the destruction of pollinators by chemical sprays [16].

  Should there be crop failures around the globe, due to the scale and uniformity of GM planting it will not be a matter of unsafe food but of food scarcity.


  The FSA should avoid over-regulation and intrusion into the freedom of the public to choose its own food. Examples of unwarranted interference include the attempt to restrict the availability of vitamin B6, the attempt to ban unpasteurised milk and the imposed ban on beef on the bone. The issue of GMOs is exactly the opposite. Here we have a hazardous technology foisted on the public by commercial interests and the desire of government not to jeopardise UK competitiveness "by any undue delay, cost or burden [2 paragraph 171] . . . or to impede scientific progress" [2 paragraph 123]. The role of the FSA should be to protect and inform the public, not to "reassure" it. As a safeguard it must insist on labelling, traceability, monitoring and post-market surveillance of all GM foodstuffs including derived products. The Lords rejected the idea of an outright moratorium on commercial releases [2 paragraph 98], on the grounds it would allow our competitors to get ahead, and that only large scale trials give information as to how transgenic crops interact with the environment. A moratorium would enable us to discover some of the problems from the releases already occurring on a continental scale. In US with only 10 per cent of its land in agriculture the impact of GMOs on ecosystems is less damaging than on the patchwork agrisystems of Europe. A moratorium would give us time to pause and think: should we go down that road?

  Nuclear energy was once considered safe and cheap. We now know the costs of decommissioning and of nuclear accidents make it neither safe nor cheap and could burden future generations with pollution. GMO releases are similarly irreversible. A safe and adequate food supply can be ensured for all if research funds were diverted into ecologically sound agricultural technologies; if land and income were sufficient for the poorest to grow or buy their food; and if food sovereignty were guaranteed by international law against the take-over of our food supplies by global corporations and their legal arm the World Trade Organisation (WTO).

  Our advisory bodies do not have the remit to ask the questions: are the risks of GMOs necessary? are the benefits long-term? are there alternatives? Everyone of us and every MP should ask them. Our health and the future of our beautiful country may depend on how we answer.

March 1999


  1 House of Lords Select Committee on the European Communities. EC Regulation of Genetic Modification in Agriculture. Session 1998-1999. 2nd Report. Evidence. HMSO 1998.

  2 Ibid Report.

  3 Jung C et al Engineering nematode resistance in crop species. Trends in Plant Science 1998; 3:266-271.

  4 Gledhill M and McGrath P Call for a spin doctor. New Scientist. 1 November 1997 p. 4.

  5 Pusztai A SOAEFD Flexible Fund Project RO 818. Report of Project Co-ordinator on data produced at the Rowett Research Institute. October 1998.

  6 Interim SCRI Report FF 818 April 1998.

  7 Siva P K et al. Genome intruder scanning and modulation systems and transgenic silencing. Trends in Plant Science 1998; 3:97-105.

  8 Kappeli O and Auberson L. How safe is safe enough in plant genetic engineering? Trends in Plant Science 1998; 3:276-281.

  9 Ho W M Genetic Engineering—Dream or Nightmare? chapter 8 pp. 102-123. Bath; Gateway Books 1998.

  10 Inose T and Murata K Enhanced accumulation of toxic compound in yeast cells. Int J Food Science and Technology 1995; 30:141.

  11 Mayeno A N and Gleich G I Eosinophilia myalgia syndrome and tryptophan production: a cautionary tale. Trends in Biotechnology 1994; 12:346-352.

  12 Bergelson J et al. Promiscuity in transgenic plants. Nature 1998; 395:25

  13 Jonathan Beard reporting in New Scientist 8 March 1997 p. 5.

  14 Hillbeck A et al. Effects of transgenic Bacillus thuringiensis corn-fed prey on mortality and development time of immature. Chrysoperla carnea. Environmental entomology April 1998 p. 480.

  15 Charlene Crabb reporting in New Scientist 16 August 1997 p. 12.

  16 Gordon A W et al. The potential consequences of pollinator declines on the conservation of biodiversity and stability of food crop yields. Conservation Biology 1998; 12:8-17.

previous page contents next page

House of Commons home page Parliament home page House of Lords home page search page enquiries

© Parliamentary copyright 1999
Prepared 12 April 1999