Page 18 - Summer 2017 Journal

in the skin, catalyzed by sunlight. Therefore, in accordance with my unifying theory, one would expect sunny climates to reduce heart disease risk. Indeed, geographical data show an inverse relationship between cardiovascular disease and annual sunlight availability.6 France and Spain have much lower rates of death from heart attacks than the United Kingdom. In a study conducted in the British Isles, mean annual sunshine hours accounted for 49 percent of the variance in mor- tality from coronary heart disease.7
Despite related studies showing that vitamin D deficiency is associated with cardiovascular disease risk,8 placebo-controlled trials have failed to demonstrate any benefit from vitamin D3 supplementation.9 Why? My coauthors and I suggest that, where heart disease is concerned, the benefit of sunlight comes from cholesterol sulfate synthesis rather than vitamin D3 synthe- sis. In a 2012 article in Entropy,10 we proposed that sulfate is produced from reduced sulfur sources in the skin, catalyzed by sunlight.
The enzyme that likely carries out this func- tion is endothelial nitric oxide synthase (eNOS), the same enzyme that produces nitric oxide to relax the artery wall. The enzyme eNOS is a member of the cytochrome P450 (CYP) super-
family of enzymes, which metabolize drugs and synthesize cholesterol, steroids and other lipids. I hypothesize that the overuse of sunscreen has played a dual damaging role, suppressing sunlight catalysis but also actively disrupting eNOS’s sulfate-producing function due to sunscreen’s aluminum content.11 Many other environmental chemicals also disrupt CYP enzymes, including mercury12,13 arsenic,14 cadmium12 and glypho- sate,15,16 the active ingredient in the pervasive herbicide Roundup. When aluminum or other toxic chemicals disable eNOS, it is unable to make enough sulfate to supply the needs of the endothelial cells, creating a systemic sulfate deficiency problem.
It is well established that eNOS produces superoxide as well as nitric oxide, but biologists have always viewed this as a pathology.17 At the same time, the fact that RBCs contain abundant eNOS baffles biolo- gists, because nitric oxide would disrupt hemoglobin’s ability to transport oxygen.18 Viewing eNOS superoxide synthesis as an alternative function to oxidize sulfur offers an explanation for both of these puzzles.
GLYPHOSATE AND HYPERLIPIDEMIA
Getting back to coronary artery disease, most people assume that
elevated serum lipids (hyperlipidemia) are a causal factor. Tens (if not hundreds) of millions of people receive advice from their doctor to take a statin drug to protect them from heart disease because their serum lipid levels are high. Therefore, one would expect a plot over time of the hospital discharge rates for hyperlipidemia to be highly correlated with a similar plot for coronary artery disease. This is not the case, however. As the figure below shows, the correlation coefficient value is a weak 0.39 (whereas greater than .70 would indicate a strong correlation), with
FIGURE 1: Graph of incidence of hospital discharge diagnoses of hyperlipidemia (ICD 272.0-4) and ischemic heart disease (ICD 410-414) over time from 1998 to 2010, available from the CDC.
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Wise Traditions SUMMER 2017