Hypothesis of Auto-Immune Disease Part-4 of 8

Hypothesis of Auto-Immune Disease Part-4 of 8


Diabetes: I believe diabetes does not start out as a high blood glucose problem, I believe that is only the internal adjustment. I believe it is a disruption in the metabolism of (ATPs) cellular energy that the internal systems perceive to be a low glucose problem. The internal systems are triggered that not enough ATPs are available so they assume the glucose used to make the ATPs is low, so this triggers the release of all glucose to the blood to serve as fuel to make the ATPs. But glucose is not the problem it is the acids disrupting the cellular metabolism process. So when homeostasis still cannot be achieved the body perceives that there is a glucose scarcity, and secretes human growth hormone (hGH). hGH functions to decrease glucose up take, and retard glucose use for ATP production by most body cells, in order to spare glucose for neurons' use. Add this to the fact that human growth hormone is also activated in the 2nd stage of the stress, response, and glucose becomes excessive.

This persistent high blood glucose concentration stimulates the pancreas to continually secrete insulin. Such excessive stimulation, if it lasts for weeks or months may cause "beta-cell burnout". "Beta-cell burnout" means the capacity of the pancreatic beta cells to synthesize and secrete insulin is greatly decreased. Thus, in time, excess secretion of hGH may cause diabetes mellitus (lack of insulin activity).

The excessive glucose that cannot be utilize eventually exceeds the proteins' ability to transport, other words exceeds its transport maximum ™ . When the transport ability is exceeded then the glucose spills over into the urine keeping water with it causing larger than normal urine volumes. Thus this would account for the excessive urine volumes in diabetics. The cell starvation would not allow the "I'm satisfied" (satiety center) trigger to be stimulated so the diabetic would feel hungry all the time as well as people with eating disorders..

(This disruption could well be the answer to the obesity epidemic going on). The metabolism of cellular energy (ATP) is the function by which metabolic water is produced. Lack of metabolic water leads to dehydration and dehydration triggers the thirst sensation. In the presence of excessive glucose the cells that line the blood vessels shrink and pull apart to open up gaps, which increase permeability of the filtration membrane in the kidney (endothelial-capsular membrane).

Increased permeability of the endothelial-capsular membrane permits proteins to escape from blood into urine.. This is called proteinuria or the Nephrotic syndrome. This disruption results in the loss of albumin which decreases the ability for small particles to be suspended in the blood (blood colloid osmotic pressure: colloid is a factor in thyroid hormone storage). Proteinuria results in edema, high blood levels of cholesterol, phospholipids, and triglycerides.. So I ask why couldn't diabetes be a nutritional deficiency?


BONE DISEASES: Imbalances between bone formation and bone reabsorption underlie nearly every disease that influences the adult skeleton.. bone disorders are caused by an imbalance in the osteoclast and the osteoblast. An insufficient secretion of PTH results in inactivity of the osteoclasts. And Calcitonin works antagonistically to the PTH and inhibits osteoclast activity and promotes osteoblast activity.


Most common skeletal disorders are excessive destruction and inhibited formation. I feel because of the PTH disruption, what is happening is the newly formed bone is already in a weakened state due to a loss of too much calcium and the Vit.D deficiency, would be creating bones in an already partially destructed state. And since the old bone is not being destroyed to be replaced by new bone then the old bone is just deteriorating from old age.. Plus oxygen deficient lysosomes become fragile and rupture releasing destructive enzymes and disrupt their ability to carry off debris and that can cause arthritic conditions. Plus excess glucose can form irreversible cross links in adjacent proteins causing stiffening and loss of elasticity..


The excessive long term activation of the stress response releasing cortisol and suppressing the production of IL-1 completely disrupts the T and B cell immune responses. The activation of the T cells is inhibited because IL-1 is the costimulator. The B cell are only antigen-presenting cells, so they can only prepare the exogenous antigens for removal from the fluid. If the IL-1 is not present to activate the helper T cell then the helper T cells cannot be stimulated to start releasing IL-2. IL-2 is he stimulator of cell division, so at this point the IL-2 positive feedback system is disrupted.

IL-2 is needed for virtually all immune responses. IL-2 is the prime substances that triggers and enhances activation and proliferation of T cells, B cells, and natural killer cells.. IL-1 is also necessary to activate the helper T cells to stimulate the secretion of IL-4, gamma-interferon, and transforming growth factor beta (TGF-B)…IL-2 is the stimulator of cell division.. IL-2 binds to IL-2 receptors on neighboring helper T, cytotoxic T, or B cells and if they have already bound an antigen, it serves as a costimulator to activate them.

The cytotoxic T cells: Must have the IL-2 or other cytokines produced by helper T cells to be able to lyse cells. The B cells can secrete the antibodies: But the helper T cell has to be activated to produce the IL-2 costimulator that activates the B cells and to stimulate the machrophages to secret the IL-1 that enhances B cell proliferation and differentiation into plasma cells…

If the B cells do not differentiate they remain as memory B cells, ready to respond more rapidly and forcefully at the antigen. B cells can respond to unprocessed antigen dissolved in lymph or interstitial fluid and are able to perform immune adherence called opsonization, by coating the microbes in antibodies (immunoglobulin), but the helper T cells have to be activated by the IL-1 to activate IL-2 and more IL-1 to costimulated B cell proliferation and differentiation into plasma cells.

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