Uterine Fibroids

This protocol addresses the treatment aspects of uterine fibroid tumors. Uterine fibroids are masses which often develop in women with a history of compromised health.

The conventional treatment for Uterine Fibroid Tumors is hysterectomy which removes the fibroids and with the uterus. Removal of the uterus preempts future fibroid development, but often creates persistent hormone dysregulation, which invites prolonged hormone instability.

Fibroid tumors often become quite large. They generally occur within the uterus, and infrequently develop into a malignant status.

Infrequent malignant transition likely results because uterus, womb, is the foci of template energy, and the strong energetic template which protects the fetus from energetic interference, tends to inhibit parasitic deviation in undifferentiated cells. This topic is discussed in more detail in Malignancy Cofactors.

Uterine fibroids are the apparent result of mycelial junction of the endothelial uterine tissue, likely precipitated from uterine lymphatic stagnation.

The electro-energetic junction between triggers a healing response which similar to a fetus, triggers proliferation of undifferentiated fibroblastic tissue, which unchecked developes into a significant and prolific pathogenic mass.

Fibroblastic tissue cannot differentiate because it is "self". This tissue is protected from immunological targeting by several likely mechanisms:

• It is self, hence tends not to activate "invader" immunological response;
• It is in the womb, and hence enjoys energetic protection by the mother which protects a fetus.

Individuals with immunological or subacute pancreatic suppression tend to develop fibroids. The likely cause results from sub-acute pancreatic performance fails to maintain sufficient systemic enzyme levels, which would provide tissue stress on the fibroid growth, resulting in sub-acute limitation or natural elimination.

During normal pregnancy, hormone signals suppress pancreatic production enabling implantation, and embryo development until about the end of the first trimester. Hormonal pancreatic suppression explains gas, and weakened digestion during the first trimester.

Individuals with otherwise weakened pancreatic response tend to lack the auto-defensive ability to "digest" fibroid artifacts as a part of the normal autoimmune process which naturally prevents fibroid development. This suppression explains the unique differential tendency of some individuals to develop fibroids.

In simple terms, individuals with chronic susceptibility to "flatulence", or pancreatic insufficiency are more likely to develop fibroid growths than those without. Gas is a telltale for chronic compromised pancreatic performance, typically resulting from undiagnosed sub-acute pathology.

Protocol Model

The protocol model selectively targets fibroid cells following factors. Fibroid Growth:

• Initiation results from parasitic development resulting from overgrowth of parasitic organisms;
• Development is enabled by chronic suppressed levels of pancreatic enzymes;
• Anaerobic in nature;'
• Survive on glucose like a parasite and hence present dexorotatary proteins, like a fetus or other anaerobic parasite;
• Are metabolical-hosted similar to a fetus.

Hence likely present vulnerabilities common to anaerobic/parasitic organisms/tissue:

• Stressed by therapeutic titers of dexorotatary enzymes;
• Stressed by oxygenic minerals which tend to force activation aerobic metabolism;
• Vulnerable to nutrient conditions which precipitate pregnancy termination;
• Preferential absorption of lipids which enable dexorotatary cell membranes;
• Vulnerable to deficiency in glucose.

Protocol Components

This protocol addresses the several vulnerabilites to fibroid growths:

1. Therapeutically elevated enzyme levels;
2. Cellular targeted nutrients which trigger transition to aerobic metabolism;
3. Locally targeted supplements which disable glucose uptake;
4. When possible triggering of cellular electroporation to accelerate uptake of therapeutic agents..

The recommended protocol uses supplements and suppositories, preferably intra-uterine, which create a therapeutic concentration of the elements which naturally limit fibroid development.

Probable Response

Normal localized applicaton of Beta Glucans to glucogenic tissue triggers terminal stress response with 48 hours. Likewise, application of metabolic sulfur to anaerobic cells triggers acute stress with 24-36 hours. Enzymatic response requires more time, but provides backup, in case both of the other methods fail to provide the necessary response.

The normal exit path for uterine artifacts is passage or absorption. Most individuals tend to pass artifacts, similar to abortion or miscarriage. Generally, the larger the artifiact mass, the greater the tendency for bulk passage.

After passage, the uterus will likely enter a post-birth menstration cycle, and potential heavy prolonged bleeding, similar, if not identical to miscarriage or post-pregnancy..