Page 19 - Summer 2017 Journal

an insignificant p-value of 0.19. Although correlation does not always imply causation, it is surprising and noteworthy when a factor presumed to be causative is not correlated with the disease.
In comparison, there is a very strong and highly significant correla- tion between hyperlipidemia and glyphosate application to corn and soy crops (R = 0.97, p < .000018), as shown in the second figure. Glyphosate application rates have steadily increased over time due to the widespread appearance of glyphosate-resistant weeds growing among the crops that are increasingly engineered to be Roundup Ready. Serum lipids have risen in tandem with the increase in glyphosate use, despite the increase in statin drug prescriptions. As the second figure suggests, it is not unreasonable to propose that glyphosate is causal in hyperlipidemia.
Glyphosate disrupts CYP enzyme activity in the liver, which can explain the contribution of glyphosate to hyperlipidemia.19 A rat study assessing the impact of glyphosate, clofibrate (a cholesterol-lowering drug) and two phenoxyacid herbicides on liver function showed that glyphosate reduced the activity of CYP enzymes in the liver much more than the other substances investigated.19 Multiple CYP enzymes are needed to produce bile acids,20 which facilitate digestion and absorption of lipids and regulate cholesterol homeostasis. Bile acids normally export a large amount of cholesterol via the digestive system. Impeded bile acid synthesis due to a defective CYP7A1 gene produced neonatal cholestasis (blocked bile ducts) and hypercholesterolemia (specifically, elevation in serum LDL) in mice fed a normal chow diet.21
Given that eNOS is a CYP enzyme, it is entirely plausible that glyphosate disrupts eNOS’s ability to synthesize sulfate. We would expect eNOS exposure to glyphosate in the red blood cells, because glyphosate
export via the kidney requires transit through the vasculature. Disrupted synthesis of cholesterol sulfate will necessitate an increase in the syn- thesis of LDL particles to transport cholesterol in its unsulfated form, because cholesterol is not water-soluble and therefore must be stored inside a lipid particle for transport.
ATHEROMA AS ALTERNATIVE SUPPLIER OF CHOLESTEROL SULFATE
In another Entropy publication, my coauthor and I suggested that when red blood cells produce cholesterol sulfate while traversing the surface veins, catalyzed by sunlight, they release the cholesterol sulfate to the tissues in the capil- laries.22 This refurbishes both the cholesterol and the sulfate supply to the endothelial wall, maintaining vascular health.
The glycocalyx is a complex mesh of sul- fated sugar chains that lines the interior wall of all blood vessels and is important for vascular health. Heparan sulfate proteoglycans (HSPGs) in the glycocalyx play many important roles,23 mediating cellular signaling mechanisms and promoting uptake of various nutrients, including LDL clearance by liver cells.24 Perhaps the most important role of cholesterol sulfate in the capil-
FIGURE 2: Graph of incidence of hospital discharge diagnoses of hyperlipidemia (ICD 272.0-4), available from the CDC, and the rate of glyphosate application to corn and soy crops, obtained from the U.S. Department of Agriculture.
SUMMER 2017
Wise Traditions 19