Molecular biologist, Dr. Ben Formby of Copenhagen, Denmark and Dr. T.S. Wiley at the University of California in Santa Barbara researched two genes, BCL2 & P53, and their effect on formation of cysts, tumors, 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. This hormone turned on the BCL2 gene, causing the cells to grow rapidly and not die on time. Then, progesterone was added to the cell cultures. Cell reproduction stopped and the cells died on time (apoptosis).

This methodology was applied to all types of female-specific cancers and prostate cancer.

Transdermal estrogen (estradiol) increased the cell proliferation rate by 230%, while transdermal progesterone decreased the cell proliferation rate by >400%!

A combination estradiol/progesterone cream maintained a normal proliferation rate (apoptosis).

This is direct evidence that estradiol (a potent estrogen) stimulates hyper-proliferation of ovarian & breast tissue cells (inhibiting apoptosis) and progesterone mediates hyper-proliferation (normalizing apoptosis), validating the following conclusions:

• The BCL2 gene, stimulates the growth of these reproductive cells (inhibiting apoptosis) increasing the growth of cysts, tumors & cancer.
• The P53 gene promotes highly desirable apoptosis or “programmed cell death“ reducing the formation of cysts, tumors & cancer.
• Estradiol upregulates or stimulates the production of the BCL2 gene, while progesterone upregulates or stimulates the production of the P53 gene (normalizing apoptosis).

In order for natural 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 natural progesterone from occupying the receptor site.

Synthetic progesterones not only fail to produce the P53 gene but prevent it’s production by blocking natural progesterone from occupying the progesterone receptor, dramatically increasing a woman’s risk for the formation of cysts, tumors and female-specific cancers.

Clearly, a primary, underlying cause of PCOS, fibrocystic breast disease, prostate cancer, breast & ovarian cancer is too much estrogen and its production of the BCL2 gene, relative to an insufficiency of bio-identical progesterone and its production of the P53 gene.

This is Good News!

Why? Progesterone, applied topically will stimulate apoptosis, supporting your body’s own natural ability to stop unchecked cell growth.

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

• The American Cancer Society Journal
• The Journal of Clinical Endocrinology
• The American Journal of Pathology
• International Journal of Cancer
• The Journal of the American Medical Association (JAMA)
• Fertility and Sterility – Journal of the American Society For Reproductive Medicine