GM crop may produce herbicide inside intestines !!

[Jagannath Chatterjee]

GM WATCH daily
http://www.gmwatch.org
---
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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[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.

"Our ideal is not the spirituality that withdraws from life but the conquest of life by the power of the spirit." -  Aurobindo.

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