GM crop may produce herbicide inside intestines !!

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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

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.

 

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.

 

 

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The Institute for Responsible Technology is working to end the genetic

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[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_eva/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_eva/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.

 

 

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© Copyright 2006 by Jeffrey M. Smith.

 

 

 

 

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