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Glyphosate / Roundup, the herbicide and mineral chelator

Make sure to look at the other thread on celiac's connection to Poison/"Vitamin A" as well.  Glyphosate/Roundup absolutely interacts with Poison/"Vitamin A" in many, many bad ways.  One example of the interaction of glyphosate with the Poison/"Vitamin A" pathway is shown in the papers below, with glyphosate causing the same birth defect issues (teratogenicity) that Poison/"Vitamin A" toxicity does.  The way to avoid this problem is to eat organic, and avoid as much exposure to glyphosate/Roundup in your environment as possible.  The interview with Dr. Stephanie Seneff towards the bottom of this post is great/terrifying, you'll want to read that.

Glyphosate is listed in the state of California as a known carcinogen:

Glyphosate came to market as an herbicide (weed-killer) in 1974.  "Roundup Ready" crops were released in the following years:

  • Roundup Ready Soybeans (first commercialized in 1996)
  • Roundup Ready Cotton (first commercialized in 1997)
  • Roundup Ready Canola (first commercialized in Canada in 1997)
  • Roundup Ready Corn (first commercialized in 1998)
  • Roundup Ready Alfalfa (first commercialized in 2005)
  • Roundup Ready Sugarbeets (first commercialized in 2005)

Note in the below study on "agricultural contaminants [...] altered retinoid concentrations in male bullfrogs from the Yamaska River basin (Québec, Canada) associated with moderate-to-high agricultural activity [...] suggested that a retinoid effect could be implicated in teratogenic mechanisms since the reported deformities resemble those caused by abnormal levels of retinoic acid (RA)".  This means that glyphosate, among other compounds, affected Poison/"Vitamin A" activity and caused those types of birth defects while NOT being actual Poison/"Vitamin A"!

Oxidation of retinoic acids in hepatic microsomes of wild bullfrogs Lithobates catesbeianus environmentally-exposed to a gradient of agricultural contamination

Agricultural contaminants are suspected of contributing to the increased incidence of deformities and the decline of amphibians populations worldwide. Many authors have further suggested that a retinoid effect could be implicated in teratogenic mechanisms since the reported deformities resemble those caused by abnormal levels of retinoic acid (RA). We previously reported altered retinoid concentrations in male bullfrogs from the Yamaska River basin (Québec, Canada) associated with moderate-to-high agricultural activity, and the findings were consistent with a possible effect on hepatic RA oxidation. An in vitro assay was therefore optimized and hepatic microsomal RA oxidation in bullfrogs was found to be quite different from that of other vertebrates. With either all-transRA (atRA) or 13cisRA as the substrate, the major metabolite generated was at4-oxo-RA. The reaction with 13cisRA as substrate, markedly greater compared with atRA, was enhanced in the presence of a reducing agent and inhibited by cytochrome P450 inhibitors in a dose-dependent manner. Hepatic RA oxidation in male bullfrogs showed significant differences between sites with no clear relationship to a gradient of agricultural activity or 13cis-4-oxo-RA quantified in plasma. In contrast, the in vitro RA oxidation in females increased with the levels of contamination and coincided in vivo with higher plasma 13cis-4-oxo-RA concentration. The levels of circulating 4-oxo-derivatives could be influenced by hepatic RA oxidative metabolism as well as isomerization conditions or RA precursor levels.

Glyphosate-based herbicides produce teratogenic effects on vertebrates by impairing retinoic acid signaling.

The broad spectrum herbicide glyphosate is widely used in agriculture worldwide. There has been ongoing controversy regarding the possible adverse effects of glyphosate on the environment and on human health. Reports of neural defects and craniofacial malformations from regions where glyphosate-based herbicides (GBH) are used led us to undertake an embryological approach to explore the effects of low doses of glyphosate in development. Xenopus laevis embryos were incubated with 1/5000 dilutions of a commercial GBH. The treated embryos were highly abnormal with marked alterations in cephalic and neural crest development and shortening of the anterior-posterior (A-P) axis. Alterations on neural crest markers were later correlated with deformities in the cranial cartilages at tadpole stages. Embryos injected with pure glyphosate showed very similar phenotypes. Moreover, GBH produced similar effects in chicken embryos, showing a gradual loss of rhombomere domains, reduction of the optic vesicles, and microcephaly. This suggests that glyphosate itself was responsible for the phenotypes observed, rather than a surfactant or other component of the commercial formulation. A reporter gene assay revealed that GBH treatment increased endogenous retinoic acid (RA) activity in Xenopus embryos and cotreatment with a RA antagonist rescued the teratogenic effects of the GBH. Therefore, we conclude that the phenotypes produced by GBH are mainly a consequence of the increase of endogenous retinoid activity. This is consistent with the decrease of Sonic hedgehog (Shh) signaling from the embryonic dorsal midline, with the inhibition of otx2 expression and with the disruption of cephalic neural crest development. The direct effect of glyphosate on early mechanisms of morphogenesis in vertebrate embryos opens concerns about the clinical findings from human offspring in populations exposed to GBH in agricultural fields.

Increased incidence of severe birth defects in Argentina and Paraguay in areas where GE Roundup Ready crops are widely grown may be linked to the ability of GBHs to increase retinoic acid activity during fetal development [23]4. Glyphosate-contaminated soybean feeds used in the pork industry have also been associated with elevated rates of gastrointestinal-health problems and birth defects in young pigs [32]. Related impacts have been observed in poultry [33].

Gluten or Glyphosate? Part 3 Interview with Dr. Seneff

Dr. Seneff:      Exactly. It won’t work if it’s not activated. On the other hand, the CYP enzymes break down retinoic acid in the liver. Retinoic acid is something that can cause troubles, both in terms of introducing this new condition called eosinophilic esophagitis, which is like an inflamed esophagus, and people have trouble swallowing. It’s a new disease, first identified in the 1990s. I think it’s a direct consequence of glyphosate and excess retinoic acid plays a role in that.

It also plays a role in infertility and in birth defects, and celiac people have an increased risk of infertility and of producing offspring with birth defects, which I think is again due to the fact that there is too much retinoic acid because it can’t be broken down by the CYP enzymes in the liver.

Dr. Osborne:   Basically you end up with vitamin A toxicity.

Dr. Seneff:      Right. Vitamin A toxicity and vitamin D deficiency, and then you have the bile acids, which there are several CYP enzymes involved in producing the bile acids in the liver, which are then sent by the bile duct into the gut, to deal with digesting fats. I think a lot of people are going to have trouble digesting fats because they’re not producing the bile acids because of the CYP enzyme problem in the liver. That’s also associated with celiac disease.

Dr. Osborne:   Just one more fact. I’m going to just repeat that and make sure I hear you correctly. The abnormal function of these liver enzymes responsible for detoxification as well as metabolism, as well as production of bile, are hindered and so what you just said was that bile inhibition leads to fat absorption problems, and so our fat-soluble vitamins like vitamin A and D and E and K, as well as omega-3 fatty acids and other fats, are now at risk for becoming deficient.

Dr. Seneff:      That’s right, and of course messing up the digestive system because the fats don’t get digested.

Dr. Osborne:   Right. Now you have a higher acidic fatty acid component in the gut, and that’s now an increased risk for certain types of cancers.

Dr. Seneff:      Right.

Dr. Osborne:   We’re just talking about one chemical, here, and so far we’ve got glyphosate damaging bacteria, we have glyphosate creating detoxification problems in the liver, creating absorption problems with nutrients. What else do you see in your research? Actually, let me back up. We have it interfering and interrupting tyrosine and tryptophan metabolism, leading to potentially psychiatric disorders and thyroid problems.

One of the things you went into pretty good detail with your paper was the vitamin and mineral deficiencies, and I know we’ve talked about vitamin D and we talked about vitamin A toxicity, but let’s talk about iron and selenium and some of the other things.

Dr. Seneff:      Right. Totally. There are a whole bunch of these minerals, especially the rare minerals like cobalt and molybdenum. These are really critically needed for certain enzymes that do really important things in the body, and you have iron and zinc. All of these minerals are going to be deficient in the food that’s been exposed to glyphosate, as well as in the soil, even, and in the body as well. You’re going to have trouble absorbing them.

Glyphosate chelates these minerals. It forms a cage around them, such that the bacteria can’t get at them even, so the gut bacteria become deficient, and then they die because they can’t get these critical nutrients. Because glyphosate is caged.

Also, the bacteria that are killed are ones that break down phytates, and phytates also bind to these minerals. Because the bacteria are killed that would break it down, the phytates become more abundant and those also chelate these minerals. These things are both working against you that you’re going to have deficiencies in iron and zinc and molybdenum and cobalt and all these things, each of which has a huge number of consequences in terms of your health.

Dr. Osborne:   Cobalt, as an example, in my 13 years of practice, I see more vitamin B12 deficiency than any other nutrient loss. That’s cobalt is vitamin B12 forming.

Dr. Seneff:      Essential for B12 function, yes.

Poison/"Vitamin A" also causes B12 and folate deficiency all by itself.

Zinc deficiency is rampant, and is best treated by utilizing blood tests (so one can get enough, without depleting copper excessively)

Molybdenum is absolutely critical for liver function, and we assess and treat it through hair mineral analysis combined with 4 questions that help to assess molybdenum function.  Molybdenum deficiency is showing up in epidemic numbers on hair mineral analysis, and food sources that used to be able to bring up people's molybdenum levels are NOT working any longer.

By correcting the Poison/"Vitamin A" toxicity, we take great steps towards addressing the main cause of Vitamin B12 and folate deficiencies.

Within a Nutritional Restoration program, we address nutritional deficiencies and excesses, along with the known toxicities.

Dr. Garrett Smith, the "Nutrition Detective"
Licensed Naturopathic Physician (NMD) in Arizona
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