GMOs and Health: The Scientific Basis for Serious Concern and Immediate Action - Page 2

GMOs and Health: The Scientific Basis for Serious Concern and Immediate Action

Epidemiological studies have suggested an association between chronic glyphosate exposure and certain cancers.  One study, done in Sweden, found that those diagnosed with non-Hodgkin's Lymphoma were 3.04 times more likely to report a history of glyphosate exposure compared to those without cancer, suggesting that glyphosate may increase the risk of this disease[16].  Another study, using populations in Iowa and North Carolina, suggested a possible association between glyphosate exposure and multiple myeloma[17].

Glyphosate also appears to be a potent endocrine disruptor with pronounced effects on testosterone production in males.  Studies on male rats demonstrate the glyphosate inhibits testosterone related enzymes and decreases the levels of testosterone in a dose-dependent manner[18].   Compared to control rats, those exposed to the highest dose of glyphosate produced only ½ of the testosterone.  Another rat study utilized doses of glyphosate which have been found in samples of human urine (1 ppm) and demonstrated that this dose reduces testosterone production by 35%[19]!  The same study showed that higher doses cause testicular cell death.  A study on human reproductive cell lines demonstrated that endocrine disrupting effects start at a dose of 0.5 ppm.  Genotoxic effects started at a dose of 5 ppm and cytotoxic effects started at 10 ppm[20]. The glyphosate residual that is allowed by federal regulations is 400 ppm in animal feed, 200 ppm in spearmint and peppermint tops, 85 ppm in sunflower and safflower seeds, 30 ppm in barely and cereal grains like rice, 30 ppm in molasses, 20 ppm in soybean, and 5 ppm in corn, legumes and quinoa, just to name a few[21].  Assuming that the average person has 5 liters of blood, one could experience blood levels of glyphosate at 0.5 ppm from eating 125 grams (or roughly 4.4 ounces) of soybeans or 29 grams (1 ounce) of sunflower seeds (note that small bags of sunflower seeds are often 5 ounces or more).

In addition to glyphosate toxicity, we should be concerned about possible toxicity from other GMO associated pesticides like Bt (bacillus thuringiensis) toxin.  The effects of ingesting this GMO crop produced pesticide have hardly been studied.  I found only one study, an in vitro study on human cells, and the results indicate the Bt toxins Cry1Ab and Cry1Ac do trigger cell death at moderate concentrations[22].  Additionally, these pesticides appear to interact with glyphosate (which often accompanies them on food) with unpredictable consequences.

The issue of interaction effects in toxicology is a very serious one that is poorly studied or not studied at all.  Of 80,000 chemicals in production, very few have been studied in combination, let alone the extremely common combinations that are found in the environment and in various products.  For instance, glyphosate is rarely used alone, yet studies still evaluate its toxicity alone.  Glyphosate products contain adjuvants or surfactants that enhance its herbicidal activity.  One study did, in fact, look at the effects of glyphosate and its adjuvants (like POE-15) on human cell lines.  The results showed that the combination was much more toxic than glyphosate alone[23]!

It needs to be mentioned that the levels of glyphosate exposure from food and the complexity and doses of pesticide combinations (and their interactions) are likely to increase as a result of progressing glyphosate resistance.  Just like antibiotic resistance among pathogenic bacteria, the target plants (i.e. weeds) for glyphosate are rapidly evolving a resistance to the pesticide as a result of its intensive use[24].  In order for glyphosate to work on these plants, higher and higher doses are needed, or additional pesticides must be applied simultaneously. Currently there are 24 weed species listed with resistance to glycine pesticides, the pesticide class of glyphosate[25].

To be fair, internal studies done by Monsanto (the owner and producer of glyphosate) in the early 1980's show glyphosate to be relatively non-toxic.  These are the studies submitted to regulatory agencies for approval and then used to set regulatory limits on public exposure and environmental contamination.  For example, the EPA uses this 30 year old data for its Integrated Risk Assessment System (IRIS).  These reviews often take 10-20 years to complete due to inadequate EPA funding, making them outdated the moment they are published!  Again, no one is out there protecting our health.  You can browse the EPA glyphosate review here if interested: http://www.epa.gov/iris/subst/0057.htm

Environmental and ecosystem effects of agricultural GMOs:

In addition to the possible harm of GMOs and GMO associated pesticides on the microbiome, cells, and physiology of humans and other mammals, there is concern about environmental effects (which always end up affecting the health of the environment's inhabitants as well). These environmental effects involve the same or similar mechanisms as those above.  For example, GMO genes can transfer to environmental (soil and aquatic) microorganisms as well as native plants (like grasses) and possibly other food crops (like organic corn and soy, the fields of which may become contaminated with GMO seeds)[26].  

Additionally, GMO associated pesticides or toxins may negatively impact helpful insects (like predator or carnivorous arthropods) as well as target insects, selecting for the emergence or immigration of new, more resistant, pests[27].  Similarly, intensive use of glyphosate may kill plants which support critical pollinators.  For instance, glyphosate use has reached levels which are now killing milkweed, thus jeopordizing the monarch butterfly habitat and leading to a decline in their numbers.

Additionally, glyphosate and Bt toxin accumulate in the soil due to serial applications, leading to escalations in soil contamination, and glyphosate has been shown to contaminate most agricultural watersheds[28],[29]

The environmental effects of GMOs and GMO associated pesticides have barely been studied and the consequent effects on biodiversity and groundwater (drinking water) are uncertain. 

Don't Throw the Bathwater Out With The Bathwater

To be fair, I need to mention the supposed intentions behind GMO agriculture promoted by the industry.  Clearly, there is a profit motive as there exists a powerful synergistic feedback cycle in the consumption of proprietary pesticides and proprietary pesticide resistant seeds.  However, GMO advocates sincerely, I believe, also hope that the technology can do good in the world.

For instance, "Golden Rice" is genetically modified rice which possesses the genes to produce beta-carotene.  Beta-carotene is the precursor to vitamin A in humans, and in regions of Africa and Asia, vitamin A deficiency is extremely common (causing a number of severe problems such as blindness).   Therefore, this rice could effectively reverse the epidemic of vitamin A deficiency.  Such medical and public health applications of GMO technology do appear to be much more reasonable than the pesticide resistant varieties (which are largely admired because they make agriculture more simple).  However, the potential health implications of medical or public health oriented GMO technology are largely the same as all other GMO technology with regard to gene transfer and insertional mutagenesis. 

Even more relevant, however, is that the vitamin A deficiency in much of the world can be remedied in several other ways, many of which will have additional health benefits than just supplying beta-carotene.  The vitamin A deficiency in much of the world is a result of a subsidized grain (largely rice) diet, which is a product of World Bank, World Trade Organization, and UN economic incentives and agreements aimed at increasing the economic output of developing nations.  If the people of these nations were growing food for themselves and not for export, they would likely grow more diverse plant foods.  Beta-carotene is widely abundant in the plant kingdom.  Basically any plant food with a yellow, red, orange, and dark green color is likely to contain significant amounts of beta-carotene.  Essentially, rice is not the solution to the vitamin A deficiency, it is the cause of it.  This is a larger problem and a more difficult one to reverse, for sure, but we need to recognize the difference between real solutions which address the root problem and superficial solutions which simply compensate for one consequence of the problem.  Failure to do so will accelerate our decline down the slippery slope of unintended consequences.

For additional research on GMOs on the GreenMedInfo.com database: Health Guide: GMO Research


[1]. de Vendômois JS, Cellier D, Vélot C, Clair E, Mesnage R, Séralini GE. Debate on GMOs health risks after statistical findings in regulatory tests. Int J Biol Sci. 2010 Oct 5;6(6):590-8.

[2].  Gilles-Eric Séralini, Dominique Cellier, Joël Spiroux de Vendomois . New analysis of a rat feeding study with a genetically modified maize reveals signs of hepatorenal toxicity. Arch Environ Contam Toxicol. 2007 May;52(4):596-602. Epub 2007 Mar 13.

[3].  de Vendômois JS, Roullier F, Cellier D, Séralini GE. A comparison of the effects of three GM corn varieties on mammalian health. Int J Biol Sci. 2009 Dec 10;5(7):706-26.

[4].  Carl-Alfred Alpert, Denis D G Mater, Marie-Claude Muller, Marie-France Ouriet, Yvonne Duval-Iflah, Gérard Corthier. Worst-case scenarios for horizontal gene transfer from Lactococcus lactis carrying heterologous genes to Enterococcus faecalis in the digestive tract of gnotobiotic mice.Environ Biosafety Res. 2003 Jul-Sep;2(3):173-80.

[5].  M Gruzza, M Fons, M F Ouriet, Y Duval-Iflah, R Ducluzeau. Study of gene transfer in vitro and in the digestive tract of gnotobiotic mice from Lactococcus lactis strains to various strains belonging to human intestinal flora. Microb Releases. 1994 Jul;2(4):183-9.

[6].  Aris A, Leblanc S. Maternal and fetal exposure to pesticides associated to genetically modified foods in Eastern Townships of Quebec, Canada. Reprod Toxicol. 2011 May;31(4):528-33. doi: 10.1016/j.reprotox.2011.02.004. Epub 2011 Feb 18.

[7].  Shehata AA, Schrödl W, Aldin AA, Hafez HM, Krüger M. The effect of glyphosate on potential pathogens and beneficial members of poultry microbiota invitro. Curr Microbiol. 2013 Apr;66(4):350-8. doi: 10.1007/s00284-012-0277-2. Epub 2012 Dec 9.

[8].  Krüger M, Shehata AA, Schrödl W, Rodloff A. Glyphosate suppresses the antagonistic effect of Enterococcus spp. on Clostridium botulinum. Anaerobe. 2013 Feb 6. pii: S1075-9964(13)00018-8. doi: 10.1016/j.anaerobe.2013.01.005. [Epub ahead of print]

[9].  F Mañas, L Peralta, J Raviolo, H García Ovando, A Weyers, L Ugnia, M Gonzalez Cid, I Larripa, N Gorla. Genotoxicity of AMPA, the environmental metabolite of glyphosate, assessed by the Comet assay and cytogenetic tests. Ecotoxicol Environ Saf. 2009 Mar ;72(3):834-7. Epub 2008 Nov 14.

[10].  Benachour N, Séralini GE. Glyphosate formulations induce apoptosis and necrosis in human umbilical, embryonic, and placental cells. Chem Res Toxicol. 2009 Jan;22(1):97-105. doi: 10.1021/tx800218n.

[11]. Taetzsch T, Block ML. Pesticides, Microglial NOX2, and Parkinson's Disease. J Biochem Mol Toxicol. 2013 Feb;27(2):137-49. doi: 10.1002/jbt.21464. Epub 2013 Jan 24.

[12]. Wang G, Fan XN, Tan YY, Cheng Q, Chen SD. Parkinsonism after chronic occupational exposure to glyphosate. Parkinsonism Relat Disord. 2011 Jul;17(6):486-7. doi: 10.1016/j.parkreldis.2011.02.003. Epub 2011 Mar 2.

[13].  Barbosa ER, Leiros da Costa MD, Bacheschi LA, Scaff M, Leite CC. Parkinsonism after glycine-derivate exposure. Mov Disord. 2001 May;16(3):565-8.

[14].  Gui YX, Fan XN, Wang HM, Wang G, Chen SD. Glyphosate induced cell death through apoptotic and autophagic mechanisms. Neurotoxicol Teratol. 2012 May-Jun;34(3):344-9. doi: 10.1016/j.ntt.2012.03.005. Epub 2012 Apr 4.

[15] Samsel A, Seneff S. Glyphosate's Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases. Entropy. 2013; 15(4):1416-1463.

[16].  Lennart Hardell, Mikael Eriksson, Marie Nordstrom. Exposure to pesticides as risk factor for non-Hodgkin's lymphoma and hairy cell leukemia: pooled analysis of two Swedish case-control studies.Leuk Lymphoma. 2002 May;43(5):1043-9

[17].  Anneclaire J De Roos, Aaron Blair, Jennifer A Rusiecki, Jane A Hoppin, Megan Svec, Mustafa Dosemeci, Dale P Sandler, Michael C Alavanja. Cancer incidence among glyphosate-exposed pesticide applicators in the Agricultural Health Study. Environ Health Perspect. 2005 Jan ;113(1):49-54.

[18].  R M Romano, M A Romano, M M Bernardi, P V Furtado, C A Oliveira. Prepubertal exposure to commercial formulation of the herbicide glyphosate alters testosterone levels and testicular morphology. Arch Toxicol. 2010 Apr;84(4):309-17. Epub 2009 Dec 12.

[19].  Clair E, Mesnage R, Travert C, Séralini GÉ. A glyphosate-based herbicide induces necrosis and apoptosis in mature rat testicular cells in vitro, and testosterone decrease at lower levels. Toxicol In Vitro. 2012 Mar;26(2):269-79. doi: 10.1016/j.tiv.2011.12.009. Epub 2011 Dec 19.

[20]. Gasnier C, Dumont C, Benachour N, Clair E, Chagnon MC, Séralini GE. Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines. Toxicology. 2009 Aug 21;262(3):184-91. doi: 10.1016/j.tox.2009.06.006. Epub 2009 Jun 17.

[21] U.S. Code of Federal Regulations.  Accessed 3-15-13 at: http://www.ecfr.gov/cgi-bin/retrieveECFR?gp=1&SID=4f4321356131eb0fa7347ec95e9f11df&ty=HTML&h=L&r=SECTION&n=40y25.0.1.1.28.3.19.131

[22].  R Mesnage, E Clair, S Gress, C Then, A Székács, G-E Séralini. Cytotoxicity on human cells of Cry1Ab and Cry1Ac Bt insecticidal toxins alone or with a glyphosate-based herbicide. J Appl Toxicol. 2012 Feb 15. Epub 2012 Feb 15.

[23].  R Mesnage, B Bernay, G-E Séralini. Ethoxylated adjuvants of glyphosate-based herbicides are active principles of human cell toxicity. Toxicology. 2012 Sep 21. Epub 2012 Sep 21.

[24].  Green JM, Owen MD. Herbicide-resistant crops: utilities and limitations for herbicide-resistant weed management. J Agric Food Chem. 2011 Jun 8;59(11):5819-29. doi: 10.1021/jf101286h. Epub 2010 Jun 29.

[25]. Heap I. The International Survey of Herbicide Resistant Weeds; available at http://www.weedscience.com, 2010, accessed April 15, 2010.

[26]. María L Zapiola, Carol A Mallory-Smith. Crossing the divide: gene flow produces intergeneric hybrid in feral transgenic creeping bentgrass population. Mol Ecol. 2012 May 24. Epub 2012 May 24.

[27]. Astrid T Groot, Marcel Dicke . Insect-resistant transgenic plants in a multi-trophic context. Plant J. 2002 Aug;31(4):387-406.

[28]. Richard H Coupe, Stephen J Kalkhoff, Paul D Capel, Caroline Gregoire. Fate and transport of glyphosate and aminomethylphosphonic acid in surface waters of agricultural basins. Pest Manag Sci. 2012 Jan ;68(1):16-30. Epub 2011 Jun 16.

[29]. Dani Degenhardt, David Humphries, Allan J Cessna, Paul Messing, Pascal H Badiou, Renata Raina, Annemieke Farenhorst, Dan J Pennock. Dissipation of glyphosate and aminomethylphosphonic acid in water and sediment of two Canadian prairie wetlands. J Environ Sci Health B. 2012 ;47(7):631-9.

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.

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GMOs and Health: The Scientific Basis for Serious Concern an



The very basic requirement is proper consumer information on all products, in this case GMO must be boldly printed on all labels of products containing or deriving directly or indirectly from GMO products. If the government requires sugar, for example, to not only be included on the labels but their concentration, why is GMO exempted!? I am surprise California voted down GMO labeling requirement recently. Deep pocket won again. One begs the question: Why is Monsanto fighting to resist GMO labeling?

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