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Correct treatment of Juvenile Diabetes



Correct treatment of Juvenile diabetes

Something is wrong in the treatment of juvenile diabetes (DM-1). But what is it? You delve into books and publications and drown in detail. Medicine is overwhelmed by data which clouds its reasoning. It lacks a consistent framework within which it may define the correct treatment of a disease. I shall now outline a framework for the analysis of juvenile diabetes. Juvenile diabetes (DM-1) is a theory. A theory is a set of statements derived from a small set of axioms which I call atom. Like chemistry and its atom. You may regard elements as different atom states. Juvenile diabetes is such a state with its own atom
.
A theory like chemistry deals only with atoms and ignores anything sub atomic, like quantum mechanics. The same reasoning is applied here to juvenile diabetes. It is a theory whose atom is the beta cell. It ignores all sub atomic statements, e.g. organelles, nucleus or genes
.
Glucose infusion triggers:
1. Insulin secretion (beta cell hypertrophy)
2. Progenitor proliferation (rise of mitotic index)
3. TPU hyperplasia (rising beta cell abundance)
Declining blood glucose:
1. Induces beta cell hypotrophy
2. Reduces progenitor proliferation (hypoplasia)
3. Returns to steady state triggering

I believe that DM-1 (juvenile diabetes) is driven by a chronic virus infection manifested by insulitis. It belongs to the set of childhood diseases driven by chronic virus infections, whose etiology is explained by the Hygiene hypothesis. I maintain that DM1 (juvenile diabetes) and LADA are one and the same disease. They differ by the degree of insulin deficiency. Generally DM1 attains a complete insulin deficiency, while LADA islets continue producing throughout life small amount of insulin. I suspect that like LADA most kids with DM1 might continue secreting small amount of insulin all their life yet are hampered by medical treatment.
False medical treatment contributes to their beta cell deficiency.

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