I searched the term PCOS & was a bit surprised, rather I should say, disappointed to find the following:

 

Since the beginning of 1995 I have had the privilege of assisting hundreds of thousands of women to identify the causes of hormonal imbalances, and safely correct the relevant underlying factors. Many have given us feedback for which recommendations worked best. With that in mind, let’s break down what PCOS is.

First, the acronym stands for polycystic ovary syndrome.

It is important to note that a “syndrome” is a term given to a common set of symptoms for which a known, identifiable etiology (cause or causes of disease) has not been identified. When a syndrome is eventually paired with a clearly defined cause, it is given a new name, a “Disease”!

Second, obviously, “ovary” simply refers to the affected organs.

Third, “polycystic” is taken from the word poly, meaning many or multiple and the word cystic inferring a cyst.

Simply stated PCOS is the growth of multiple cysts in one or both ovaries.

First, let’s identify and define a normal part of healthy cell life called apoptosis. It is defined as a form of “programmed cell death” and is a normal, healthy, bodily process. When apoptosis fails to function properly, cells form cysts, benign tumors & eventually, malignant tumors.

So the most relevant question is “What negatively influences normal, healthy cell apoptosis? And, what effect do hormones have on cell apoptosis?

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 & 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. Then, progesterone was added to the cell cultures. Cell reproduction stopped and the cells died on time (apoptosis)!

This methodology was applied to all the above types of cancer. The BCL2 gene, therefore, stimulates the growth of these cells and the risk of cancer. On the other hand, 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!

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 (apoptosis).

Since the P53 gene expression induces 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 a very important component of a woman’s treatment.

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 and in the presence of excess estradiol, dramatically increase a woman’s risk for female-specific cancers!

Clearly, from the above information, we can conclude that primary underlying causes of ovarian cysts, breast cancer, prostate cancer and more, are too much estrogen (BCL2 gene) relative to too little progesterone and the benefits of the P53 gene, stimulated by the presence of natural progesterone. This increased risk for breast cancer is especially so in the presence of prolonged stress and EDC’s.

Take a look at the brief whiteboard animation below:

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:

• 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
• Supplemental Research