However, instead of improved health we have seen a decline. People may be living longer but only thanks to hundreds and thousands of dollars worth of prescription medicines that don't cure these diseases but just barely keep us alive and dependent on numerous medications.
Well, a small minority of other researchers are just now beginning to believe that the elevated cholesterol in the setting of disease may not be the cause of disease but may be a sign of the body scavenging cholesterol sulfate to use the needed sulfate elseware. The liver makes plenty of cholesterol every day. But if the body can't get sulfate in the diet directly or by converting sulfur aminoacids, it may scavenge sulfate from healthy tissue.
So, diseases that were once seen as linked to cholesterol toxicity, may instead be related to sulfate and sunlight deficiency. Sunlight catalyzes the sulfation of cholesterol in addition to activating vitamin D.
I can't say that I am convinced one way or another. All I can say is that this war on cholesteol has so far not worked, and I don't believe that God created eggs, milk and butter to be poisons. But that is what the mainstream would have us believe . A proposed experimental treatment for sulfate deficiency would be 1/4 tsp epsom salt twice a day and 20 minutes of sun light.
It is also important to avoid food additives thricalcium phosphate, aluminum phosphate, sodium benzoate as well as certain medicinces like tylenol that deplete sulfate and glutathione.
Chem Biol Interact. 1998 Apr 3;110(3):189-202. The glutathione dependence of inorganic sulfate formation from L- or D-cysteine in isolated rat hepatocytes. Huang J1, Khan S, O'Brien PJ.
The GSH dependence of the metabolic pathways involved in the conversion of cysteine to sulfate in intact cells has been investigated. It was found that hepatocyte-catalysed sulfate formation from added L-cysteine did not occur if hepatocyte GSH was depleted beforehand, but was restored when GSH levels recovered. Furthermore, sulfate formation did not recover in GSH-depleted hepatocytes if GSH synthesis was prevented with buthionine sulfoximine. Thiosulfate formation was, however, markedly enhanced in GSH-depleted hepatocytes. These results suggest that thiosulfate is an intermediate in the formation of inorganic sulfate from L-cysteine and that GSH was required for the conversion of thiosulfate to inorganic sulfate. Much less sulfate was formed if the cysteine was replaced with cysteinesulfinate. Furthermore, sulfate formation from L-cysteine was markedly inhibited by the addition of the transaminase inhibitor DL-cycloserine or the gamma-cystathionase inhibitor DL-propargylglycine. The major routes of sulfate formation from L-cysteine therefore seems to involve pathways that do not involve L-cysteinesulfinate. Similar amounts of sulfate were formed from D-cysteine as L-cysteine. Thiosulfate instead of sulfate was also formed in GSH-depleted hepatocytes. However, sulfate formation from D-cysteine differed from L-cysteine in that it was inhibited by the D-aminoacid oxidase inhibitor sodium benzoate and was not affected by transaminase or gamma-cystathionase inhibitors. These results suggest that thiosulfate is an intermediate in sulfate formation from D-cysteine and involves the oxidation of D-cysteine by D-amino acid oxidase to form beta-mercaptopyruvate.