Genetically Engineered Crops May Produce Herbicide Inside Our Intestines

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Genetically Engineered Crops May Produce Herbicide Inside Our Intestines

http://www.non-gm-farmers.com/news_details.asp?ID=2778

 

- They fail to reveal, however, that after you eat the GM corn, some inactive

herbicide may become reactivated inside your gut and cause a toxic reaction.

In addition, a gene that was inserted into the corn might transfer into the

DNA of your gut bacteria, producing long-term effects.

 

Spilling the Beans, May 2006

Genetically Engineered Crops May Produce Herbicide Inside Our Intestines

By Jeffrey M. Smith

 

Pioneer Hi-Bred's website boasts that their genetically modified (GM) Liberty

Link[1] corn survives doses of Liberty herbicide, which would normally kill

corn. The reason, they say, is that the herbicide becomes " inactive in the corn

plant. " [2] They fail to reveal, however, that after you eat the GM corn, some

inactive herbicide may become reactivated inside your gut and cause a toxic

reaction. In addition, a gene that was inserted into the corn might transfer

into the DNA of your gut bacteria, producing long-term effects. These are just a

couple of the many potential side-effects of GM crops that critics say put

the public at risk.

 

Herbicide tolerance (HT) is one of two basic traits common to nearly all GM

crops. About 71% of the crops are engineered to resist herbicide, including

Liberty (glufosinate ammonium) and Roundup[3] (glyphosate).  About 18% produce

their own pesticide. And 11% do both. The four major GM crops are soy, corn,

cotton and canola, all of which have approved Liberty- and Roundup-tolerant

varieties. Herbicide tolerant (HT) crops are a particularly big money-maker for

biotech companies, because when farmers buy HT seeds, they are required to

purchase the companies' brand of herbicide as well. In addition, HT crops

dramatically increase the use of herbicide,[4] which further contributes to the

companies' bottom line.

 

There are no required safety tests for HT crops in the US - if the biotech

companies declare them fit for human consumption, the FDA has no further

questions. But many scientists and consumers remain concerned, and the Liberty

Link

varieties pose unique risks.

 

Liberty herbicide (also marketed as Basta, Ignite, Rely, Finale and

Challenge) can kill a wide variety of plants. It can also kill bacteria,[5]

fungi[6]

and insects,[7] and has toxic effects on humans and animals.[8] The herbicide is

derived from a natural antibiotic, which is produced by two strains of a soil

bacterium. In order that the bacteria are not killed by the antibiotic that

they themselves create, the strains also produce specialized enzymes which

transform the antibiotic to a non-toxic form called NAG

(N-acetyl-L-glufosinate).

The specialized enzymes are called the pat protein and the bar protein, which

are produced by the pat gene and the bar gene, respectively. The two genes are

inserted into the DNA of GM crops, where they produce the enzymes in every

cell. When the plant is sprayed, Liberty's solvents and surfactants transport

glufosinate ammonium throughout the plant, where the enzymes convert it

primarily into NAG. Thus, the GM plant detoxifies the herbicide and lives, while

the

surrounding weeds die.

 

The problem is that the NAG, which is not naturally present in plants,

remains there and accumulates with every subsequent spray. Thus, when we eat

these

GM crops, we consume NAG. Once the NAG is inside our digestive system, some of

it may be re-transformed back into the toxic herbicide. In rats fed NAG, for

example, 10% of it was converted back to glufosinate by the time it was

excreted in the feces.[9] Another rat study found a 1% conversion.[10] And with

goats, more than one-third of what was excreted had turned into glufosinate.[11]

 

It is believed that gut bacteria, primarily found in the colon or rectum, are

responsible for this re-toxification.[12] Although these parts of the gut do

not absorb as many nutrients as other sections, rats fed NAG did show toxic

effects. This indicates that the herbicide had been regenerated, was

biologically active, and had been assimilated by the rats.[13] A goat study also

confirmed that some of the herbicide regenerated from NAG ended up in the

kidneys,

liver, muscle, fat and milk.[14]

 

More information about the impact of this conversion is presumably found in

" Toxicology and Metabolism Studies " on NAG, submitted to European regulators by

AgrEvo (now Bayer CropScience). These unpublished studies were part of the

application seeking approval of herbicide-tolerant canola. When the UK

government's Pesticide Safety Directorate attempted to provide some of this

information

to an independent researcher, they were blocked by the company's threats of

legal action.[15] The studies remained private.

 

Toxicity of the herbicide

 

Glufosinate ammonium is structurally similar to a natural amino acid called

glutamic acid, which can stimulate the central nervous system and, in excess

levels, cause the death of nerve cells in the brain.[16] The common reactions to

glufosinate poisoning in humans include unconsciousness, respiratory distress

and convulsions. One study also linked the herbicide with a kidney

disorder.[17] These reactions typically involve large amounts of the herbicide.

It is

unclear if the amount converted from GM crops would accumulate to promote such

responses or if there are low dose chronic effects.

 

Perhaps a more critical question may be whether infants or fetuses are

impacted with smaller doses. A January 2006 report issued by the Environmental

Protection Agency's (EPA) Office of Inspector General said that studies

demonstrate

that certain pesticides easily enter the brain of young children and fetuses,

and can destroy cells. That same report, however, stated that the EPA lacks

standard evaluation protocols for measuring the toxicity of pesticides on

developing nervous systems.[18] Scientists at the agency also charged that " risk

assessments cannot state with confidence the degree to which any exposure of a

fetus, infant or child to a pesticide will or will not adversely affect their

neurological development. " [19] Furthermore, three trade unions representing

9,000 EPA workers claimed that the evaluation techniques used at the agency were

highly politicized. According to a May 24, 2006 letter to the EPA's

administrator, the unions cited " political pressure exerted by Agency officials

perceived to be too closely aligned with the pesticide industry and former EPA

officials now representing the pesticide and agricultural community. " [20]

 

Although the EPA may be hampered in its evaluations, research has nonetheless

accumulated which suggests that glufosinate carries significant risks for the

next generation. According to Yoichiro Kuroda, the principal investigator in

the Japanese project entitled " Effects of Endocrine Disrupters on the

Developing Brain, " glufosinate is like a " mock neurotransmitter. " Exposure of a

baby

or embryo can affect behavior, because the chemical disturbs gene functions

that regulate brain development.[21]

 

When mouse embryos were exposed to glufosinate, it resulted in growth

retardation, increased death rates, incomplete development of the forebrain and

cleft

lips,[22] as well as cell death in part of the brain.[23] After pregnant rats

were injected with glufosinate, the number of glutamate receptors in the

brains of the offspring appeared to be reduced.[24] When infant rats were

exposed

to low doses of glufosinate, some of their brain receptors appeared to change

as well.[25]

 

Glufosinate herbicide might also influence behavior. According to Kuroda,

" female rats born from mothers that were given high doses of glufosinate became

aggressive and started to bite each other - in some cases until one died. " He

added, " That report sent a chill through me. " [26]

 

Disturbing gut bacteria

 

If the herbicide is regenerated inside our gut, since it is an antibiotic, it

will likely kill gut bacteria. Gut microorganisms are crucial for health.

They not only provide essential metabolites like certain vitamins and short

fatty

acids, but also help the break down and absorption of food and protect

against pathogens. Disrupting the balance of gut bacteria can cause a wide range

of

problems. According to molecular geneticist Ricarda Steinbrecher, " the data

obtained strongly suggest that the balance of gut bacteria will be affected " [27]

by the conversion of NAG to glufosinate.

 

When eating Liberty Link corn, we not only consume NAG, but also the pat and

bar genes with their pat and bar proteins. It is possible that when NAG is

converted to herbicide in our gut, the pat protein, for example, might reconvert

some of the herbicide back to NAG. This might lower concentrations of

glufosinate inside of our gut. On the other hand, some microorganisms may be

able to

convert in both directions, from glufosinate to NAG and also back again. If the

pat protein can do this, that is, if it can transform NAG to herbicide, than

the presence of the pat protein inside our gut might regenerate more herbicide

from the ingested NAG. Since there are no public studies on this, we do not

know if consuming the pat gene or bar genes will make the situation better or

worse.

 

But one study on the pat gene raises all sorts of red flags. German scientist

Hans-Heinrich Kaatz demonstrated that the pat gene can transfer into the DNA

of gut bacteria. He found his evidence in young bees that had been fed pollen

from glufosinate-tolerant canola plants. The pat gene transferred into the

bacteria and yeast inside the bees' intestines. Kaatz said, " This happened

rarely, but it did happen. " [28] Although no studies have looked at whether pat

genes

end up in human gut bacteria, the only human GM-feeding study ever conducted

did show that genetic material can transfer to our gut bacteria. This study,

published in 2004, confirmed that portions of the Roundup-tolerant gene in

soybeans transferred to microorganisms within the human digestive tract.[29]

 

Since the pat gene can transfer to gut bacteria in bees, and since genetic

material from another GM crop can transfer to human gut bacteria, it is likely

that the pat gene can also transfer from Liberty Link corn or soybeans to our

intestinal flora. If so, a key question is whether the presence of the pat gene

confers some sort of survival advantage to the bacteria. If so, " selection

pressure " would favor its long term proliferation in the gut.

 

Because the pat protein can protect bacteria from being killed by

glufosinate, gut bacteria that take up the gene appears to have a significant

survival

advantage. Thus, the gene may spread from bacteria to bacteria, and might stick

around inside us for the long-term. With more pat genes, more and more pat

protein is created. The effects of long-term exposure to this protein have not

been evaluated.

 

Now suppose that the pat protein can also re-toxify NAG back into active

herbicide, as discussed above. A dangerous feedback loop may be created: We eat

Liberty Link corn or soy. Our gut bacteria, plus the pat protein, turns NAG into

herbicide. With more herbicide, more bacteria are killed. This increases the

survival advantage for bacteria that contain the pat gene. As a consequence,

more bacteria end up with the gene. Then, more pat protein is produced, which

converts more NAG into herbicide, which threatens more bacteria, which creates

more selection pressure, and so on. Since studies have not been done to see if

such a cycle is occurring, we can only speculate.

 

Endocrine disruption at extremely low doses

 

Another potential danger from the glufosinate-tolerant crops is the potential

for endocrine disruption. Recent studies reveal that endocrine-disrupting

chemicals (EDCs) can have significant hormonal effects at doses far below those

previously thought to be significant. The disruptive effects are often found

only at minute levels, which are measured in parts per trillion or in the low

parts per billion. This is seen, for example, in the way estrogen works in

women. When the brain encounters a mere 3 parts per trillion, it shuts down

production of key hormones. When estrogen concentration reaches 10 parts per

trillion, however, there is a hormone surge, followed by ovulation.

 

Unfortunately, the regulation and testing of agricultural chemicals,

including herbicides, has lagged behind these findings of extremely low dose

effects.

The determination of legally acceptable levels of herbicide residues on food

was based on a linear model, where the effect of toxic chemicals was thought to

be consistent and proportional with its dosage. But as the paper Large

Effects from Small Exposures shows, this model underestimates biological effects

of

EDCs by as much as 10,000 fold.[30]

 

In anticipation of their (not-yet-commercialized) Liberty Link rice, Bayer

CropScience successfully petitioned the EPA in 2003 to approve maximum threshold

levels of glufosinate ammonium on rice. During the comment period preceding

approval, a Sierra Club submittal stated the following.

 

" We find EPA's statements on the potential of glufosinate to function as an

endocrine-disrupting substance in humans and animals as not founded on logical

information or peer-reviewed studies. In fact EPA states that no special

studies have been conducted to investigate the potential of glufosinate ammonium

to

induce estrogenic or other endocrine effects. . . . We feel it's totally

premature for EPA at this time to dismiss all concerns about glufosinate as an

endocrine-disrupting substance. . . . Due to the millions of Americans and their

children exposed to glufosinate and its metabolites, EPA needs to conclusively

determine if this herbicide has endocrine-disrupting potential. "

 

The EPA's response was that " glufosinate ammonium may be subjected to

additional screening and/or testing to better characterize effects related to

endocrine disruption " but this will only take place after these protocols are

developed. In the mean time, the agency approved glufosinate ammonium residues

on

rice at 1 part per million.

 

Since glufosinate ammonium might have endocrine disrupting properties, even

small conversions of NAG to herbicide may carry significant health risks for

ourselves and our children.

 

The EPA's response was that " glufosinate ammonium may be subjected to a

dditional screening and/or testing to better characterize effects related to

endocrine disruption "   but this will only take place after these protocols are

developed. In the mean time, the agency approved glufosinate ammonium residues

on

rice at 1 part per million.

 

Since glufosinate ammonium might have endocrine disrupting properties, even

small conversions of NAG to herbicide may carry significant health risks for

ourselves and our children.

 

Inadequate animal feeding studies

 

If we look to animal feeding studies to find out if Liberty Link corn creates

health effects, we encounter what independent observers have expressed for

years-frustration. Industry-sponsored safety studies, which are rarely published

and often kept secret, are often described as designed to avoid finding

problems.

 

If we look to animal feeding studies to find out if Liberty Link corn creates

health effects, we encounter what independent observers have expressed for

years-frustration. Industry-sponsored safety studies, which are rarely published

and often kept secret, are often described as designed to avoid finding

problems.

 

In a 42-day feeding study on chickens, for example, 10 chickens (7%) fed

Liberty Link corn died compared to 5 chickens eating natural corn.  Even with a

the death rate doubled, " because the experimental design was so flawed, " said

bio-physicist Mae-Wan Ho, " statistical analysis failed to detect a significant

difference between the two groups. "   Similarly, although the GM-fed group

gained less weight, the study failed to recognize that as significant. According

to

testimony by two experts in chicken feeding studies, the Liberty Link corn

study wouldn't identify something as significant unless there had been " huge "

changes. The experts said, " It may be worth noting, in passing, that if one were

seeking to show no effect, one of the best methods to do this is would be to

use insufficient replication, a small n, " which is exactly the case in the

chicken study.

 

Without adequate tests and with a rubber stamp approval process, GM crops

like Liberty Link corn may already be creating significant hard-to-detect health

problems. In Europe, Japan, Korea, Russia, China, India, Brazil and elsewhere,

shoppers have the benefit of laws that require foods with GM ingredients to

be labeled. In the US, however, consumers wishing to avoid them are forced to

eliminate all products containing soy and corn, as well as canola and

cottonseed oils. Or they can buy products that are organic or say " non-GMO " on

the

package. Changing one's diet is a hassle, but with the hidden surprises inside

GM

foods, it may be a prudent option for health-conscious people, especially

young children and pregnant women.

 

 

Jeffrey Smith is the author of the international bestseller, Seeds of

Deception. The information in this article presents some of the numerous health

risks

of GM foods that will be presented in his forthcoming book, Genetic Roulette:

The documented health risks of genetically engineered foods, due out in the

fall.

 

References:

 

[1] Liberty Link is a registered trademark of Bayer CropScience.

 

[2] http://www.pioneer.com/canada/crop_management/fsllink.htm.

 

[3] Roundup is a registered trademark of Monsanto.

 

[4] Charles Benbrook, " Genetically Engineered Crops and Pesticide Use in the

United States: The First Nine Years, " October 2004

http://www.biotech-info.net/Technical_Paper_6.pdf.

 

[5] Colanduoni JA and Villafranca JJ (1986). Inhibition of Escherichia coli

glutamine-synthetase by phosphinothricin. Bioorganic Chemistry 14(2): 163-169,

and Pline W A~ Lacy GH~ Stromberg V ~ Hatzios KK (200 I). Antibacterial

activity of the herbicide glufosinate on Pseudomonas syringae pathovar glycinea.

Pesticide Biochemistry And Physiology 71(1): 48-55.

 

[6] Liu CA; Zhong H; Vargas J; Penner D; Sticklen M (1998). Prevention of

fungal diseases in transgenic, bialaphos- and glufosinate-resistant creeping

bentgrass (Agrostis palustrls). Weed Science 46(1): 139-146, and Tada T~ Kanzaki

H~ Norita E~ Uchimiya H~ Nakamura I (1998). Decreased symptoms of rice blast

disease on leaves of bar-expressing transgenic rice plants following treatment

with bialaphos. Molecular Plant-Microbe Interactions 9(8): 762-764.

 

[7] Ahn Y -J, Kim Y -J and Yoo J-K (2001). Toxicity of the herbicide

glufosinate-ammonium to predatory insects and mites of Tetranychus urticae

(Acari:

Tetranychidae) under laboratory conditions. Journal Of Economic Entomology

94(1):

s157-161.

 

[8] Watanabe T and Sano T (1998). Neurological effects of glufosinate

poisoning with a brief review. Human & Experimental Toxicology 17(1): 35-39.

 

[9] Bremmer IN and Leist K-H (1997). Disodium-N-acetyl-L-glufosinate; AE

F099730 - Hazard evaluation of Lglufosinate produced intestinally from

N-acetyl-L-glufosinate. Hoechst Schering AgrEvo GmbH, Safety Evaluation

Frankfurt.

TOX97/014. A58659. Unpublished. (see FAO publication on

www.fao.org/ag/agp/agpp/pesticid/jmpr/Download/98/glufosi3.pdf).

 

[10] Kellner H-M, StumpfK and Braun R (1993). Hoe 099730-14C Pharmacokinetics

in rats following single oral and intravenous administration of3 mg/kg body.

Hoechst RCL, Germany, 01-L42­0670-93. A49978. Unpublished.

 

[11] Huang, M.N. and Smith, S.M. 1995b. Metabolism of [14C]-N-acetyl

glufosinate in a lactating goat. AgrEvo USA Co.Pikeville, PTRL East Inc., USA.

Project

502BK. Study U012A/A524. Report A54155. Unpublished.

 

http://www.fao.org/WAICENT/FAOINFO/AGRICULT/AGP/AGPP/Pesticid/JMPR/Download/98_e\

va/glufosi.pdf.

 

[12] In one study, for example, protein produced from a gene found in E. coli

turned NAG into glufosinate. G. Kriete et al, Male sterility in transgenic

tobacco plants induced by tapetum-specific deacetylation of the externally

applied non-toxic compound N-acetyl-L-phosphinothricin, Plant Journal, 1996,

Vol.9,

No.6, pp.809-818.

 

[13] Bremmer IN and Leist K-H (1998). Disodium-N-acetyl-L-glufosinate (AE

F099730, substance technical) - Toxicity and metabolism studies summary and

evaluation. Hoechst Schering AgrEvo, Frankfurt. TOX98/027. A67420. Unpublished.

(see FAO publication on

www.fao.org/ag/agp/agpp/pesticid/jmpr/Download/98/glufosi3.pdf).

 

[14] Huang, M.N. and Smith, S.M. 1995b. Metabolism of [14C]-N-acetyl

glufosinate in a lactating goat. AgrEvo USA Co.Pikeville, PTRL East Inc., USA.

Project

502BK. Study U012A/A524. Report A54155. Unpublished.

 

http://www.fao.org/WAICENT/FAOINFO/AGRICULT/AGP/AGPP/Pesticid/JMPR/Download/98_e\

va/glufosi.pdf.

 

[15] Ricarda A. Steinbrecher, Risks associated with ingestion of Chardon LL

maize, The reversal of N-acetyl-L- glufosinate to the active herbicide

L-glufosinate in the gut of animals, Chardon LL Hearing, May 2002, London.

(Note: This

work is an excellent summary of the risks associated with NAG conversion

within the gut.)

 

[16] Fujii, T., Transgenerational effects of maternal exposure to chemicals

on the functional development of the brain in the offspring. Cancer Causes and

Control, 1997, Vol. 8, No. 3, pp. 524-528..

 

[17] H. Takahashi et al., " A Case of Transient Diabetes Isipidus Associated

with Poisoning by a Herbicide Containing Glufosinate. " Clinical Toxicology

38(2), 2000, pp.153-156.

 

[18] Ohn J. Fialka, EPA Scientists Pressured to Allow Continued Use of

Dangerous Pesticides, Wall Street Journal Page A4, May 25, 2006,

http://online.wsj

..com/article/SB114852646165862757.html.

 

[19] EPA SCIENTISTS PROTEST PENDING PESTICIDE APPROVALS; Unacceptable Risk to

Children and Political Pressure on Scientists Decried, Press release, Public

Employees for Environmental Responsibility. May 25, 2006,

http://www.peer.org/news/news_id.php?row_id=691.

 

[20] EPA SCIENTISTS PROTEST PENDING PESTICIDE APPROVALS; Unacceptable Risk to

Children and Political Pressure on Scientists Decried, Press release, Public

Employees for Environmental Responsibility. May 25, 2006,

http://www.peer.org/news/news_id.php?row_id=691.

 

[21] Bayer's GE Crop Herbicide, Glufosinate, Causes Brain Damage, The Japan

Times, 7 December 2004.

 

[22] Watanabe, T. and T. Iwase, Development and dymorphogenic effects of

glufosinate ammonium on mouse embryos in culture. Teratogenesis carcinogenesis

and

mutagenesis, 1996, Vol. 16, No. 6, pp. 287-299.

 

[23] Watanabe, T. , Apoptosis induced by glufosinate ammonium in the

neuroepithelium of developing mouse embryos in culture. Neuroscientific Letters,

1997,

Vol. 222, No. 1, pp.17-20, as cited in Glufosinate ammonium fact sheet,

Pesticides News No.42, December 1998, p 20-21.

 

[24] Fujii, T., Transgenerational effects of maternal exposure to chemicals

on the functional development of the brain in the offspring. Cancer Causes and

Control, 1997, Vol. 8, No. 3, pp. 524-528.

 

[25] Fujii, T., T. Ohata, M. Horinaka, Alternations in the response to kainic

acid in rats exposed to glufosinate-ammonium, a herbicide, during infantile

period. Proc. Of the Japan Acad. Series B-Physical and Biological Sciences,

1996, Vol. 72, No. 1, pp. 7-10.

 

[26] Bayer's GE Crop Herbicide, Glufosinate, Causes Brain Damage, The Japan

Times, 7 December 2004.

 

[27] Ricarda A. Steinbrecher, Risks associated with ingestion of Chardon LL

maize, The reversal of N-acetyl-L- glufosinate to the active herbicide

L-glufosinate in the gut of animals, Chardon LL Hearing, May 2002, London.

(Note: This

work is an excellent summary of the risks associated with NAG conversion

within the gut.)

 

[28] Antony Barnett, New Research Shows Genetically Modified Genes Are

Jumping Species Barrier, London Observer, May 28, 2000.

 

[29] Netherwood, et al, Assessing the survival of transgenic plant DNA in the

human gastrointestinal tract, Nature Biotechnology, Vol 22 Number 2 February

2004.

 

[30] Wade V. Welshons et al, Large Effects from Small Exposures. I.

Mechanisms for Endocrine-Disrupting Chemicals with Estrogenic Activity, Table

2,Environmental Health Perspectives Volume 111, Number 8, June 2003.

 

[31]  Glufosinate Ammonium; Pesticide Tolerance, Environmental Protection

Agency, Federal Register: September 29, 2003 (Volume 68, Number 188), 40 CFR

Part

180, ACTION: Final rule,

http://www.epa.gov/fedrgstr/EPA-PEST/2003/September/Day-29/p24565.htm.

 

[32] S. Leeson, The effect of Glufosinate Resistant Corn on Growth of Male

Broiler Chickens, by Department of Animal and Poultry Sciences, University of

Guelph. Report No. A56379; July 12, 1996.

[33] Mae-Wan Ho, Exposed: More Shoddy Science in GM Maize Approval, ISIS

Press Release 13/03/04, http://www.i-sis.org.uk/MSSIGMMA.php.

 

[34] Testimony of Steve Kestin and Toby Knowles, Department of Clinical

Veterinary Science, University of Bristol on behalf of Friends of the Earth,

before

the Chardon LL Hearings of the Advisory Committee on Releases to the

Environment, November 2000.

 

[35] Testimony of Steve Kestin and Toby Knowles, Department of Clinical

Veterinary Science, University of Bristol on behalf of Friends of the Earth,

before

the Chardon LL Hearings of the Advisory Committee on Releases to the

Environment, November 2000.

 

 

 

--

 

© Copyright 2006 by Jeffrey M. Smith.

Source: GMWatch