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GENETICALLY ENGINEERED CROPS MAY PRODUCE HERBICIDE INSIDE OUR INTESTINES
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By Jeffrey Smith
June 7, 2006
NewsWithViews.com
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”[31] 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.
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.[32] Even with 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.”[33] 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,[34] 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,”[35]
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.
Footnotes:
1, Liberty Link is a
registered trademark of Bayer CropScience
2, Pioneer
Brand hybrids with the LibertyLink1 gene
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
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.
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.
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
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.
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
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,
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,
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
32, S.
Leeson, The effect of Glufosinate Resistant Corn on Growth of Male Broiler
Chickens, by Department of
33,
Mae-Wan Ho, Exposed: More
Shoddy Science in GM Maize Approval, ISIS Press Release
13/03/04
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.
© 2006 Jeffrey M. Smith- All Rights
Reserved
Jeffrey M. Smith
is working with a team of international scientists to catalog all known
health risks of GM foods. He is the author of Seeds of Deception, the
world's bestselling book on GM food, and the producer of the video, Hidden
Dangers in Kids' Meals.
Website: www.seedsofdeception.com
E:Mail: [email protected]
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