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Xenobiotics (drugs, -cides, industrial chemicals) combine badly with Poison/"Vitamin A"

What exactly are xenobiotics?  They are defined as relating to or denoting a substance, typically a synthetic chemical, that is foreign to the body or to an ecological system.

As is shown in other places on this website, I have linked (or will link in the future as I have time to go through all the links I have waiting) all of the above in various ways to causing or aggravating or synergizing Poison/"Vitamin A" toxicity.  I found this great paper and thought I'd put it here, highlighting the important parts.  You will have to note that it seems obvious at the start that the author--like so many others--in spite of finding so many problems with Poison/"Vitamin A", still feels the need to try to rescue its reputation as some sort of misunderstood essential nutrient.  It simply isn't one at all, it's just a toxin.

Retinoid-xenobiotic interactions: the Ying and the Yang

The literature provides compelling evidence pointing to tight metabolic interactions between retinoids and xenobiotics. These are extensive and important for understanding xenobiotic actions in the body. Within the body, retinoids affect xenobiotic metabolism and actions and conversely, xenobiotics affect retinoid metabolism and actions.
This article summarizes data that establish the importance of retinoid-dependent metabolic pathways for sustaining the body’s responses to xenobiotic exposure, including the roles of all-trans- and 9-cis-retinoic acid for protecting mammals from harmful xenobiotic effects and for ensuring xenobiotic elimination from the body. This review will also consider molecular mechanisms underlying xenobiotic toxicity focusing on how this may contribute to retinoid deficiency and disruption of normal retinoid homeostasis. Special attention is paid to xenobiotic molecular targets (nuclear receptors, regulatory proteins, enzymes, and transporters) which affect retinoid metabolism and signaling.

Many different linkages between retinoid metabolism and actions and xenobiotic metabolism and actions have been described in the literature. This literature provides compelling evidence that these interactions are extensive and important for understanding xenobiotic actions in the body. It is clear from this literature that retinoids affect xenobiotic metabolism and actions and that conversely xenobiotics affect retinoid metabolism and actions (Figure 1). Many different xenobiotics interact with retinoids including environmental pollutants (toxicants), pharmacologic agents/drugs, and experimental agents used in the study of disease. These will all be considered below. The primary focus of this review will be on interactions in the liver but the reader needs to be aware that these interactions are very important elsewhere in the body, especially in the developing embryo where they contribute to impaired embryogenesis.
Xenobiotic-induced retinoid redistribution from the liver to extrahepatic tissues
The literature clearly establishes that xenobiotic exposure causes a loss of retinyl esters and retinol from hepatic stores. However, alterations in tissue retinoid levels are also observed in other tissues, especially the kidney but also the lung and other tissues. It is important to ask whether this redistribution of tissue retinoids within the body represents a protective response aimed at shielding the body from the toxic effects of xenobiotics or whether this is simply a toxic manifestation of xenobiotic exposure. At present, this is not known.
In studies of CCl4-induced [carbon tetrachloride] liver injury (161,162), pretreatment of rats with relatively large (pharmacological) doses of retinol prior to xenobiotic exposure has repeatedly been shown to potentiate liver injury induced by CCl4. The same conclusion was reached when either allyl alcohol, acetaminophen or galactosamine treatment were used to induce hepatic injury in mice (163-165). In rats, dietary studies involving feeding diets containing high levels of retinol (a daily dose of 250,000 IU/kg body weight) for different time periods prior to administration of a single intraperitoneal dose of CCl4 showed for all treatments equivalent potentiation of CCl4 hepatotoxicity. Although retinol feeding was found to increase concentrations of retinyl palmitate in the liver, a linear correlation was not seen between concentrations of retinyl palmitate and the extent of retinol-potentiated CCl4 hepatotoxicity. Retinol feeding also has been reported to potentiate hepatotoxicity of even minimally toxic doses of acetaminophen, allyl alcohol, and endotoxin. Because each of these agents produces hepatic injury through different mechanisms, it was concluded that retinol potentiates hepatic injury by altering a shared process needed for the progression of hepatocellular injury (166). As an example of this, treatment of mice orally with 3,000 IU retinyl acetate, four times at 12 h intervals, after administration of the hepatotoxin thioacetamide aggravated many parameters that are known to contribute to acute hepatotoxicity (137).

Other studies also have reached a similar conclusion that retinoid supplementation enhances xenobiotic toxicity. In C57BL/6N mice, simultaneous administration, as a single dose consisting of up to 18 µg TCDD/kg body weight and 200 mg ATRA/kg body weight to pregnant dams, dramatically enhances the incidence of cleft palate formation in fetuses. Although both compounds are known teratogens, the combined treatment resulted in a synergistic effect on teratogenic outcome (167).

First, you must know that Poison/"Vitamin A" toxicity during pregnancy is completely associated with causing birth defects (teratogen) all by itself.  Here's the title from a paper way back in 1984: Vitamin A: a newly recognized human teratogen. Harbinger of things to come? Seems like the warning bell was rung a long time ago, right?

If my hypothesis that increasing glyphosate/Roundup toxicity leads to aggravated and accelerated Poison/"Vitamin A" toxicity, which then synergistically interacts with other xenobiotics to increase teratogenic (birth defects) issues like cleft lip and/or palate...can we find evidence that the rates of cleft lips and cleft palates are increasing?  It's not too difficult.

1992:  Incidence of cleft lips, palates rising.

2006:  John Hopkins Medicine website states, "More and more babies in the United States are being born with cleft lip and/or cleft palate, according to a recent report by the Centers for Disease Control and Prevention (CDC)."

There are no coincidences.

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