A friend was recently diagnosed with stage zero & stage one breast cancer.  She was scared, so opted for a double mastectomy.  While the two tumors were removed (the symptom was treated) the underlying causes were not addressed. She received no dietary/lifestyle modification guidelines.  Her risk of reoccurrence has not been reduced!

Molecular biologist, Dr. Ben Formby of Copenhagen, Denmark and Dr. T.S. Wiley at the University of California in Santa Barbara have researched two genes, BCL2 and P53, and their effect on female-specific cancers and prostate cancer.

Cells of breast, endometrium, ovary and prostate, were grown in the laboratory. Estrogen (estradiol) was added to the cells. The estradiol turned on the BCL2 gene, causing the cells to grow rapidly and not die (blocking apoptosis). Then, progesterone was added to the cell cultures. Progesterone turned on the P53 gene. The result? Cell reproduction stopped and the cells died on time (apoptosis).

What is the result of cells not dying on time? Cysts, benign tumors, malignant tumors…

This methodology was applied to all the above types of cancer. The BCL2 gene, therefore, blocks apoptosis, stimulates the growth of these cells and the risk of cancer. Conversely, the P53 gene promotes apoptosis or programmed cell death and thereby, reduces the risk of cancer.

Estradiol upregulates or stimulates the production of the BCL2 gene, while progesterone upregulates or stimulates the production of the P53 gene.

Further investigation revealed transdermal estradiol increased the cell proliferation rate by 230%, while transdermal progesterone decreased the cell proliferation rate by >400%.

A combination estradiol/progesterone cream maintained the normal proliferation rate. This is direct evidence that estradiol (a potent estrogen) stimulates hyper-proliferation of breast tissue cells and progesterone mediates hyper-proliferation.

In his best selling book, “What Your Doctor May Not Tell You About Breast Cancer” Dr. John Lee states, “estrogens promote breast cancer, progesterone prevent breast cancer.”

A second study by noted researcher Bent Formby, Ph.D. was just published with more insightful results. To determine the biologic mechanism of why progesterone inhibits the proliferation of breast cancer cells, a variety of cancer cell lines with different receptors and different expression of genes were exposed to progesterone.

The results: Exposure to progesterone induced a maximal 90% inhibition of cell proliferation in T47-D breast cancer cells and no measurable response to MDA-231 progesterone-receptor negative breast cancer cells. An impressive 43% of the T47-D cancer cells had undergone apoptosis (programmed cell death) within 24 hours after exposure to progesterone.

Further analysis showed that in the presence of progesterone, the genetic expression by T47-D cancer cells of the BCL-2 gene was down regulated, and that of the P53 gene (tumor suppressor gene) was up regulated. Since the P53 gene expression induces cell apoptosis and the BCL-2 gene when expressed inhibits apoptosis, if one’s cancer cells are progesterone-receptor positive, then progesterone as part of one’s therapy appears to be very important. However, 50% of breast cancer cell lines have mutant or no P53 oncogene expression, so in this instance, genistein therapy might be helpful.

In order for body-identical progesterone to stimulate the production of the P53 gene it must attach itself to progesterone receptors found in abundance in breast, ovarian, and endometrial cells.

If a woman is taking birth control pills or any other form of synthetic progesterones (progestins, progesterone acetate, medroxy-progesterone acetate) these synthetic progesterones will occupy progesterone receptors and prevent body-identical progesterone from occupying the receptor site.

There are 12 references to tests on BCL2 and P53, and how they are affected by progesterone & estrogen. This information has been published, in part, in the following journals:

Clearly, from the above information, we can conclude that primary underlying causes of breast cancer are too much estrogen (BCL2 gene) relative to too little of the helpful benefits of the P53 gene, stimulated by the presence of body-identical progesterone. This increased risk for breast cancer is especially so in the presence of trans fatty acids (hydrogenated fats).