Hypothesis of Auto-Immune Disease Part-7 Of 8

Hypothesis of Auto-Immune Disease Part-7 Of 8


Fever would normally be present at an inflammation or infection to intensify the healing effects. But interleukin-1 is the hormone that regulates the immune response that activates fever, and interleukin-1 production is suppressed by the excessive amount of cortisol that is being released in the 2nd stage stress response that is triggered by the "cell starvation".

Metabolic dysfunctions and malnutrition created by the lack of oxygen in the cellular metabolism process, causes a reduced temperature. Plus the disruption in the thyroid, affects the fever process. All these disruptions lead me to feel that the fever process itself is trapped in a fight or flight response. A nurse once told me that most people did not have the 98.6 temperature. There was no reason for her to lie and I took her at her word, so what has happened that lowered peoples' normal temperature, I wonder.. Could it be the lack of nutrition leading to a disrupted metabolism process?


One of the major disruptions caused by acidosis is it inhibits the (functional proteins): antibodies [gamma globulins] / hormones / transport proteins: hemoglobin, cholesterol, iron transporters, and other substances / contractile proteins which underlie movements in the body such as muscle contractions, cell division , and sperm propulsion / and catalysts enzymes which are essential to virtually every biochemical reaction in the body and increase the rates of chemical reactions by at least a million fold. These functional proteins become unable to perform their physiological roles.

Functional proteins depend on intramolecular bonds, particularly hydrogen bonds, to maintain their structure. And their function depends on specific arrangements of atoms called active sites. These active sites allow them to interact chemically with other molecules. Hydrogen bonds are fragile and easily disrupted by excessive acidity. A disruption in the intramolecular bonds allows the separation of the atoms and this destroys the active sites.

And functional proteins such as antibodies and transport proteins are disrupted: Example, hemoglobin becomes totally unable to bind and transport oxygen when blood pH becomes to acidic.


With the starvation in the cells the fight or flight response is activated this translates into the SYMPATHETIC NERVE PATHWAY being activated. And the activation of the sympathetic system inhibits the secretion by the Brunner's gland which is the thick mucous secreting glands. This is what protects the mucosa from digestion by the acidic chyme and gastric juices. So why couldn't this disruption be the beginning point of ulcers?


Collagen is an albumin type of protein. So if the inflammation reaction leads to cell permeability due the excess histamine, and this cell permeability allows Albumin to become deficient because it passes out of its normal place into the urine, why wouldn't it have a disrupting effect on collagen balance?


GLYCOGEN serves as nourishment for the early embryo…Glycogen availability is inhibited due to the fact that the oxalic and phytic acids block the metabolism of ATPs thus causing a deficiency in the storage of glycogen and so there would not be an ample supply of glycogen to nurture the embryo…. / The fetus and newborns naturally acquired passive immunity would be disrupted by the inhibited Immunological memory process, in the mother.

The baby’s resistance stems mainly from the IgG antibodies. Immunological memory arises during proliferation and differentiation of antigen-stimulated B and T cells. The deficiency of the IL-1 caused by the stress activated cortisol would cause an incomplete primary response. Thus there would be a deficiency in the IgG antibodies from a secondary response that afford the naturally acquired passive immunity protection.


The cell starvation caused by these two acids will not allow the satiety "satisfied" center to be stimulated.. So it just stands to reason people would be hungry all the time eating and getting obese.



Excessive oxalic and phytic acids and excessive phosphates create excessive insoluble iron complexes. Combined this with the fact that the malfunctioning dying cells are releasing iron inhibitors and the result is a deficiency in usable iron. So as the availability of usable iron declines so does the availability of sufficient oxygen. When there is not sufficient oxygen in the cellular metabolism process then cell energy (ATP) cannot be produced.



The 2nd stage stress response called the "resistance reaction” is a long-term reaction. And since homeostasis cannot be brought back to the body (without intervention) then the hormones released in this response would accumulate and become excessive. These hormones cause long-term secretion of cortisol and hGH. Excessive hGH causes diabetes. Excessive cortisol disrupts the negative feedback system that regulates the immune response.


The helper T cell aids in all immune responses and that is inhibited by the stress response. I feel the calcium in the insoluble calcium salts creates and inability for the immune system to view them as foreign substances so they are not being targeted for removal. Thus they are allowed to build up and create the malfunction in the nutritional pathway. And when the cells began to destroy themselves because they think they are infected with a virus, no virus is there, because the culprits (the insoluble calcium salts) do their dirty work from a distance..


The metabolism shift caused by the starving cells that are dying, attempting to protect surrounding cells, along with excessive oxalic and phytic acids and excessive phosphates creates inhibited, and insoluble iron complexes, which leads to an iron deficiency. An iron deficiency leads to deficient oxygen in the cellular respiration electron transport chain, which disrupts the metabolism of ATPs and creates many major disruptions including excessive hydrogen which results in acidosis..
Also the deficient oxygen causes cell garbage disposals (lysosomes) disruption. When the lysosomes are deficient in oxygen, they become fragile rupture and burst and release nerve cell destroying enzymes. Stem cells are one of the cells destroyed in this disruption.

Hormonal disruption :

Inhibited Pth leads to deficient activation of Vit. D, which leads to decreased synthesizes of the Calcitriol hormone creating a deficiency…aka 1, 25-dihydroxycholecalciferol or 1, 25-dihydroxy vitamin D3.

Nutrient disruptions:

Inhibited PTH would cause excessive phosphates, deficient Calcium, deficient Mg+, deficient activation of Vit. D leading to the deficiency in Calcitriol hormone. Reduced calcium causes elevated levels of phosphate.

Excessive Aldosterone: leads to major ion disruptions: excessive water, excessive Na+, excessive Cl- because it follows Na+ passively, .deficient K+ and this disrupts the regulation of pH

Osmotic gradient disruption: disrupted with the disruption in the Na+ which is its regulator..

Disruption in the Anions: Because the exchange of Cl- for HCO3- maintains the correct balance of anions in ECF and ICF.

Imbalance in the HCI: Excessive Cl- and H+ disrupts the balance of hydrochloric acid..

Disruption in pH regulation: deficient K+ and excessive H+ disrupt the H+ shift exchange.

Neuromuscular and cardiac functions disrupted: when K+ is deficient. Resting membrane potential and repolarization phase of action potentials in muscles disrupted: by deficient K+.

Fluid volume in cells disrupted: by deficient K+.

Disruption in the electrochemical gradient: the ion disruption caused mainly by the excessive aldosterone but also by the def. calcium and excessive phosphate disrupts the anion, the negatively charge and the cations positively charge in the cells and the ECF..

Disruption of the CSF and its functions such as protecting the brain and spinal cord from chemical and physical injury and its role in maintaining homeostasis : imbalances in the chemical composition

Negative feed back systems activated: The Renin -angiotensin system in regulation of blood pressure and therefore glomerular filtration rate….the efferent arterioles constrict to increase glomerular blood, hydrostatic pressure, secretion of aldosterone causes retention of Na+, Cl-, and water to increase blood volume, the thirst center signals increased thirst when angiotensin II is increased, thus increased water intake leads to increased blood volume, and the increased ADH causes water retention to increase blood volume.

The negative feedback regulation of glomerular filtration rate by the juxtaglomerular apparatus (JGA): the low blood pressure causes a decrease in the net filtration pressure and the glomerular filtration rate. The JGA decrease secretion of vasoconstrictor substances causing the afferent arteriole to dilate which increase blood flow through glomerulus.

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