Progesterone

Progesterone

the Master Hormone in Women

Role of the P53 Gene

How Do Estrogen & Progesterone Influence
Breasts & Ovaries?

the following also applies to the prostate

Influences of Estrogen & Progesterone on Breasts & Ovaries

What Effect do Hormones Have?

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.

The Research

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).

The Measured Effect

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).

Birth Control: What Influence on Breast Cancer?

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.

What if if one’s cancer cells are progesterone-receptor positive?

This is Good News!

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

Conclusion

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

References

There are 7 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:

  1. Progesterone induces apoptosis and up-regulation of p53 expression in human ovarian carcinoma cell lines –
    The American Cancer Society Journal
  2. Antagonism between estradiol and progestin on Bcl-2 expression in human endometrial carcinoma cells –
    The Journal of Clinical Endocrinology
  3. Estrogen receptor, progesterone receptor, and bcl-2 are markers with prognostic significance in CIN III–
    The American Journal of Pathology
  4. Clinical Observations and Molecular Variables of Primary Vascular Leiomyosarcoma (Cancer)–
    The Journal of the American Medical Association (JAMA)
  5. Expression of steroid receptors and proteins related to apoptosis in endometrial carcinoma –
    Journal of the American Society For Reproductive Medicine
  6. Bcl-2 expression on fine-needle aspirates from primary breast carcinoma –
    The American Cancer Society Journal
  7. p53 mutations and expression in breast carcinoma in situ –
    The American Journal of Pathology