The use of insulin for hyperkalemia is logical given the association of hyperglycemka with hyperkalemia. But in the case of hyperkalemia, as in the case of hyperglycemia, you have a snapshot of serum chemistry in cases of severe metabolic dysfunction. Non-use of glucose, its intracellular scarcity, is the central problem of diabetes and sometimes can relate to the kidney, not its extracellular excess. So also with hyperkalemia: the cell's metabolic processes are so poisoned that they prevent its use.
Alkaline minerals can be substituted for each other to initiate the intracellular use of glucose. This is the reason why, in addition to insulin, magnesium and sodium hyperkalaemia ccrrrect, especially the salts of kr carbonate. Carbon dioxide is a Lewis acid, and acidification of the cell intracellularly expels sodium, calcium, & c for its counterions, as you know, including potassium. Oxidation of glucos3 also produces carbon dioxide.
His description of renal chemistry pikits his ability to understand this process. Have you heard of the experiments of Sydney foxes with microvesicles? The high concentration of carbon dioxide is the energy that drives this exchange of minerals, and sugsr is the most efficient way to produce more carbon with the least use of oxygen. Carbon dioxide protects against glycation, and in the healthy cell, with abundant carbon dioxide that protects intracellular proteins, no glycation occurs.
That is why polyunsaturated fats are the true cause of glycation products. You can not avoid having glucose in your blood, your own tissue will break to form glucose. But polyunsaturated fats are a recent invention, mostly made by man, that can be avoided. PUFA is the real cause of glycation products. Lets look at what you need to know about hysterectomy next
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