New study explains possible mechanisms of action – Claire Robinson reports
Below is the abstract of the latest paper from Stephanie Seneff and co-authors on mechanisms through which glyphosate-based herbicides like Roundup can exercise their toxicity. This paper, co-authored with Nancy Swanson and Chen Li, shows how glyphosate could act synergistically with aluminium to impair gut function and promote neurotoxicity.
As we’ve said before, regulators routinely ignore such information and only move against pesticides based on long-term animal feeding studies. However, even when toxic effects are found, there is a disturbing trend for industry to delay regulatory action based on the fact that no plausible mechanism exists for the toxic effects. This tactic is being used by industry-affiliated authors with regard to glyphosate-based herbicides.
This is in spite of the fact that no law anywhere in the world, as far as we know, mandates the identification of a mechanism of action before pesticide bans can be enacted. And mechanisms have never been precisely identified for some toxic effects of pesticides, such as DDT causing the thinning of birds’ eggshells. However, DDT was nonetheless banned in many countries. The relatively recent preoccupation with plausible mechanisms of action, which regulators play along with, is an unacceptable framing of the debate by industry. It is worrying because whether something is “plausible” to a regulator often has more to do with their belief systems and world view than with what the data actually says.
Seneff and co-authors’ papers on glyphosate and Roundup provide plenty of plausible mechanisms of action. So while we are currently lacking independent animal feeding studies on Roundup using realistic doses to which you and I could be exposed, we are well ahead with regard to mechanistic knowledge. And certainly, people who want to keep themselves and their families healthy can gain valuable information from these papers on what Roundup might be doing to the human body.
Aluminum and Glyphosate Can Synergistically Induce Pineal Gland Pathology: Connection to Gut Dysbiosis and Neurological Disease
Seneff, S. , Swanson, N. and Li, C. (2015) . Agricultural Sciences, 6, 42-70. doi: 10.4236/as.2015.61005.
http://www.scirp.org/journal/PaperInformation.aspx?paperID=53106&#.VLqOJ3Z5Lta (open access)
Many neurological diseases, including autism, depression, dementia, anxiety disorder and Parkinson’s disease, are associated with abnormal sleep patterns, which are directly linked to pineal gland dysfunction. The pineal gland is highly susceptible to environmental toxicants. Two pervasive substances in modern industrialized nations are aluminum and glyphosate, the active ingredient in the herbicide, Roundup?. In this paper, we show how these two toxicants work synergistically to induce neurological damage. Glyphosate disrupts gut bacteria, leading to an overgrowth of Clostridium difficile. Its toxic product, p-cresol, is linked to autism in both human and mouse models. p-Cresol enhances uptake of aluminum via transferrin. Anemia, a result of both aluminum disruption of heme and impaired heme synthesis by glyphosate, leads to hypoxia, which induces increased pineal gland transferrin synthesis. Premature birth is associated with hypoxic stress and with substantial increased risk to the subsequent development of autism, linking hypoxia to autism. Glyphosate chelates aluminum, allowing ingested aluminum to bypass the gut barrier. This leads to anemia-induced hypoxia, promoting neurotoxicity and damaging the pineal gland. Both glyphosate and aluminum disrupt cytochrome P450 enzymes, which are involved in melatonin metabolism. Furthermore, melatonin is derived from tryptophan, whose synthesis in plants and microbes is blocked by glyphosate. We also demonstrate a plausible role for vitamin D3 dysbiosis in impaired gut function and impaired serotonin synthesis. This paper proposes that impaired sulfate supply to the brain mediates the damage induced by the synergistic action of aluminum and glyphosate on the pineal gland and related midbrain nuclei.