The Oxygen Model of Insulin Toxicity
Majid Ali, M.D.
A Course on Hyperinsulinism
Hyperinsulinism is a state of excess insulin activity in the body as determined by raised blood insulin levels (hyperinsulinemia). measured by in which cells are resistant to actions of insulin. The blood insulin levels rise when the pancreas gland releases increasing amounts of insulin to overcome the resistance of cells to the action of insulin hormone. To explain the primary metabolic role of insulin hormone on cells, in 2000 I proposed a crank-crank-shaft analogy in insulin is visualized as a crank—a device that transmits rotary motion—and the insulin receptor protein as a crank-shaft embedded in the cell membrane.
The cell membranes become resistant to insulin when they become chemicalized—plasticized, so to speak, by toxicities of foods, environment, and thoughts (disappointments, chronic anger, and mental health issues) —and hardened. Cell membrane plasticization immobilizes insulin receptors embedded in the membranes. The insulin receptor is a protein that criss-crosses the cell membrane like a cord. One of the consequences of grease buildup on cell membranes is that insulin receptor becomes turned and twisted, literally and figuratively. In a previous paper, I offered the analogy of a crank and a crank-shaft to explain insulin resistance. I visualize insulin as a crank—a device that transmits rotary motion—and the insulin receptor protein as a crank-shaft embedded in the cell membrane.
The insulin resistance can then be seen as a “rusted” crank-shaft of insulin receptor which is impacted in a hardened cell membrane, and so cannot turn the insulin crank. Insulin cannot function well when cell membranes are greased, matrix is gummed, and mitochondria are gutted—conditions created by disturbances in oxygen function. The pancreas tries to compensate for it by over-producing insulin. The greater the production of insulin, the thicker the grease buildup and deeper the problem of insulin resistance.
My Oxygen Model of Hyperinsulinism is an extension of my Oxygen Model of Health and Disease. It is a unifying model that explains all aspects of insulin resistance—causes, clinical course, consequences, and control—on the basis of disturbed oxygen function. The most important among these compromised and/or blocked functions are:
(1) oxygen signaling;
(2) oxygen’s ATP energy generation;
(3) oxygen’s detergent functions;
(4) oxygen’s cellular detox functions;
(5) oxygen-regulated cell membrane and matrix functions;
(6) oxygen’s cellular repair roles.
The Oxygen Model of Hyperinsulinism provides a simple model that allows physicians to reduce complexities of diverse clinical syndromes into a workable simplicity. This model predicts that ongoing research will reveal that components of acidosis (excess acidity), oxidosis (increased oxidative stress), and CUD (clotting-unclotting dysequilibrium) will be found to play important roles in the pathology and clinical features of hyperinsulinism .
- The crucial importance of the Unifying Oxygen Model of Hyperinsulinism is that it:
- Explains the scientific basis of hyperinsulinism in the body;
- Sheds light how altered insulin functions can be restored by addressing all oxygen-related issues;
- Elucidates how toxicities of foods, environments, and thoughts cause buildup of cellular grease on cell membrane and lead to insulin resistance; and
- Reveals the mechanisms by which various detox therapies work in freeing up insulin receptors and restoring insulin function.
Since hyperinsulinism and insulin resistance are essentially two terms for the same insulin disorder, my Oxygen Models of Hyperinsulinism and Insulin Resistance are the same.
It is important to recognize in this context that oxygen is the primal detergent which removes cellular grease and allows cells to breathe freely.
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