PROGESTERONE PROMOTES APOPTOSIS
PROGESTERONE’S EFFECT AT THE GENE LEVEL
The following article was not written by Dr. Lee, but is drawn from information that he presented in his lectures.
- Breast Cancer and Programmed Cell Death (Apoptosis)
- Progesterone Promotes Apoptosis; Estrogen Turns it Off
- Breast Cancer Cells Need Apoptosis In Order To Die
- Can You Cure Cancer if You Can Control Apoptosis?
- Progesterone Upregulates the Gene that Causes Cancer Cells To Die; Estrogen Upregulates the Gene that Cause Cancer Cells to Not Die
- References to tests on BCL2 and P53, and the difference between progesterone and estrogen.
Breast Cancer and Programmed Cell Death (Apoptosis)
Breast cancer is considered to be a hormone dependent cancer, which means that hormones have something to do with the growth and development of breast cancer. About two years ago, Time magazine had an article referring to apoptosis in reference to looking for something that would work against cancer. In the 1/28/98 issue of the Journal of the American Medical Association (JAMA), there was a reference to apoptosis in reference to cancer.
Almost all the cells in your body are being created, live a certain length of time, and then die to make place for the new cells coming along. White blood cells last only two days. Red blood cells last 120 days. Your skin cells are being made new all the time. They are the ones that flake off when you take a bath and make a ring in your tub. If you’ve had your arm in a cast for 6 weeks, when you take the cast off you can flake off a lot of old, dead cells. They die on their own. It is a planned cell suicide. They are designed to do this because the new cells are coming.
What has been discovered is that the cells that become cancer cells are not only those that are multiplying rapidly, because the white blood cells multiply rapidly, and they don’t become cancer cells. It’s the ones that don’t die on time; they don’t go through this programmed cell suicide. Programmed cell suicide is called apoptosis. It means “without dropping away.” Ptosis means “dropping.” If you have one eyelid that won’t go up; that’s called ptosis. The dropping away refers to the programmed cell suicide.
Progesterone Promotes Apoptosis; Estrogen Turns If Off
Research has looked into what it is that makes a cell do this. It is not told to by some other cell. It is built into the DNA of the genes of that cell. It’s designed that way. It turns out that there’s a gene that will block apoptosis and try to get the cell to live longer. That gene is called BCL2. It leads to the cell becoming a cancer cell.
Breast Cancer Cells Need Apoptosis In Order To Die
The cancer cell doesn’t think of itself as a bad cell. It thinks of itself as a cell that outsmarted you, and it is going to live on. You might die, but it is going to try to live on. But the gene that normally functions to cause that cell to commit programmed cell suicide is the gene called P53.
In the 1/28/98 issue of the Journal of the American Medical Association (JAMA) is an article entitled “To Die or Not to Die.” They are not talking about your life, though they well could be. They are talking about the cell and what controls and determines if it dies on time as it ought to. They refer to gene P53 as the gene that tells the cell to die on time, and BCL2 is the gene that blocks this. So if BCL2 is the dominant one you’ll develop cancer. If P53 is the dominant one you won’t.
Inside your breast you have skin cells that line the milk ducts. You have miles of milk ducts in your breasts. These cells are like skin cells. They are being made; then they are supposed to die, and the specialized blood cells (macrophages) go and eat them up, because new cells are coming along all the time. Imagine that they didn’t die on time, and your breast just retained all these cells that are being made all the time. Pretty soon your breasts would be dragging on the ground. The only way you keep normal size breasts is to have last month’s cells die, because this month new cells are coming along. This doesn’t happen to brain cells or muscle cells, but in all the other cells in your body this goes on all the time. What keeps you young and healthy is the new cells coming along.
Can You Cure Cancer if You Can Control Apoptosis?
What they are admitting in the JAMA article is that the war on cancer has been a failure. The war on cancer has been trying to find medicine that stops rapidly growing cells from multiplying so rapidly, but in the process they are stopping your own white blood cells, your hair follicles and everything else. So if they give you a medicine strong enough to kill the cancer cells, they are in the process killing you. They admit that chemotherapy is a failure, except for some leukemias and lymphomas in young children. Young children that have a real strong immune system will survive the chemotherapy and come back. But for those of us who are adults, the chemotherapy strong enough to kill the cancer would have to be strong enough to kill us first. So now, the new treatment goal is how to control apoptosis to bring on cell death of the cancer cells. “New cancer therapies that aim to induce apoptosis, specifically in cancer cells and cells becoming cancer, are the source of much excitement and renewed hope for cure.” You can cure cancer if you can control apoptosis.
Progesterone Upregulates the Gene that Causes Cancer Cells To Die; Estrogen Upregulates the Gene that Cause Cancer Cells to Not Die
Last year Dr. Ben Formby and Dr. T.S. Wiley at the University of California in Santa Barbara proved how to do that very thing. Dr. Ben Formby is from Copenhagen, Denmark. He is a molecular biologist who has learned how to build cell cultures, and how to tell the products of specific genes like BCL2 and P53. So he took the cell cultures of breast, endometrium, ovary and prostate, and he grew them in culture. On some he added a little estrogen (estradiol). Guess what happened? The estradiol turned on BCL2, and the cells grew rapidly and didn’t die. Then he added some progesterone to it. Guess what happened? They stopped growing so rapidly; they died on time, and the cancer all disappeared. He did that for all these types of cancer.
What do we have? The gene BCL2 stimulates the risk of cancer. Gene P53 decreases the risk of cancer. Estradiol upregulates BCL2. Progesterone upregulates P53. Therefore, progesterone decreases cancer. Unopposed estradiol causes the cancer. Simple. Estrogen dominance is the cause of the cancer growing and the inability of the body to cure it.
Progesterone and Estrogen Functions in Breast Cancer Supported by Major Medical Journals
The critics are saying that they don’t see anything about this in the medical journals that they read. Maybe they aren’t reading the correct journals. There are 12 references to tests on BCL2 and P53, and the difference between progesterone and estrogen. Here are some of the places these articles have occurred:
- The American Cancer Society
- 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
PROGESTERONE DECREASES CELL PROLIFERATION
NATIONAL CANCER INSTITUTE’S SYMPOSIUM ON ESTROGEN AS A MAJOR CAUSE OF CANCER
The following article was not written by Dr. Lee, but is drawn from information that he presented in his lectures.
Progesterone Decreases Cell Proliferation: Estrogen Increases It so If You Want To Increase Cell Proliferation Use Estrogen; If You Want To Decrease Cell Proliferation Use Progesterone
Progesterone Levels At Time of Breast Cancer Surgery Affect Survival Rates
Method of Measuring Cell ProliferationProgesterone Levels at the Time of Surgery
Estrogen a Major Cause of Cancer
National Cancer Institute’s Symposium on EstrogenEstrogens as Endogenous Carcinogens in the Breast and ProstateProgesterone Decreases Cell Proliferation: Estrogen Increases It
The Fertility and Sterility Journal article that we mentioned in Part 1 of this article was particularly interesting, as it was the first double blind, placebo controlled, randomized study using transdermal progesterone and transdermal estrogen (estradiol) on real women (40 of them) who were having breast biopsies. They had one at the beginning of the study and another biopsy 13 days later, and were able to check on several interesting things.The first thing of note was that even though the estrogen and the progesterone did not show up in the serum, it showed up in the breast tissue at over 100% increased levels above the placebo cream.The most interesting finding was what happened to cell proliferation during this 13 day test. The following chart shows two ways of measuring cell proliferation. The PCNA (proliferating cell nuclear antigen) is the most accurate, but both methods were used.Based on PCNA numbers (these tend to be the most accurate measurement) the numbers in the following chart showing increase or decrease of cell proliferation showed up in only 13 days. Translated into percentages the following three sentences summarize it.
Topical Progesterone reduced cell proliferation by 410%
Topical Estrogen increased cell proliferation by 223%
Topical Estrogen/Progesterone combination reduced cell proliferation by 16%
Method of Measuring Cell Proliferation Placebo Progesterone Estrogen
Estrogen &Progesterone
Mitosis per 1000 Cells 0.51 0.17 0.83 0.52 PCNA 7.8 1.9 17.4 6.5 The numbers on this chart were excerpted from the Fertility and Sterility Journal, Vol. 63, No. 4, April, 1995. The exact reference is: Chang KJ, Lee TTY , Linares-Cruz G, Fournier S, de Lignieres B. Influences of percutaneous administration of estradiol on human breast epithelial cell cycle in vivo. Fertility and Sterility 1995; 63; 7865-7891.
If You Want To Increase Cell Proliferation Use Estrogen; If You Want To Decrease Cell Proliferation Use Progesterone
The conclusion seems to be: if you want increased cell proliferation, use estrogen. If you want decreased cell proliferation, use progesterone. The entire study is worth reading, and is an excellent affirmation that what Dr. John Lee has been saying and writing is correct. This is not secret information, but it is being denied to the typical doctor of conventional medicine, even though similar information is in the Journal of the AMA. It is Dr. John Lee’s contention that progesterone prevents breast cancer, and if you already have breast cancer progesterone protects you against reoccurrence or late metastases. In his medical practice he treated many women who had had mastectomies. In the 20 years since he started recommending the use of progesterone, not one of the hundreds of women he treated has died of breast cancer. Think about what the odds are on that number when you compare it to normal post mastectomy figures.
Progesterone Levels At Time of Breast Cancer Surgery
Affect Survival Rates
In 1976 Dr. Mohr started a test at two major hospitals in London that did breast surgery. He requested that every time they had a breast surgery that they take a blood test and save it so that he could test the progesterone level at the time of surgery. He tested testosterone, progesterone and estrogen. He found that progesterone level at the time of surgery was correlated with better survival. The survival record was reviewed 18 years after breast cancer surgery in node positive patients: this means that the cancer had already spread, was already metastasizing.
Summary of Dr. Mohr’s Findings
Progesterone Level at the Time of Surgery Survival Percentage After 18 Years
Adequate Progesterone (4ng/ml or more)62%
Low Progesterone (less than 4 ng/ml)30%
This was written up in the British Journal of Cancer in 1996. The title of the article is: “Serum Progesterone and Prognosis in Operable Breast Cancer.” This is over a 100% improvement just by having adequate progesterone levels at the time of surgery. There is no treatment that provides that degree of benefits. Progesterone is the treatment.
Estrogen a Major Cause of Cancer
Dr. Ercole Cavalieri is the head of cancer research at the University of Nebraska Medical Center (also one of the speakers at the National Cancer Institute program shown below). He calls estrogen the angel of life, the angel of death. It is necessary at the beginning to create a successful pregnancy, and if you have estrogen dominance later in your life it is the angel of death. When the body tries to metabolize estradiol and estrone it is possible to end up in this pathway which ends up in cancer. This is real human estrogen, and the body is trying to get rid of it. If the body does it correctly it methylates it, and it is safely excreted. But if the person has been eating margarine or transfatty acids, things that are not real and are missing the essential fatty acids it falls into another pathway. If the same person is not getting the sulfated amino acids like methionine and cysteine that is in garlic and beans, it continues on in this pathway and binds to DNA, causes a mutation, and creates cancer and kills the person.National Cancer Institute’s Symposium on Estrogen as a Cause of CancerEstrogen is the cause of the cancer that women fear, and yet there are many doctors still giving them unopposed estrogen. The recent National Cancer Institute symposium on March 16-17, 1998 basically states that estrogen is the cause of the cancer that is killing women. If you look at the following program to see some of the major medical research organizations stating this in their presentations, it sort of makes you wonder why we didn’t hear any of this on the news in any of the major media. It makes you wonder why unopposed estrogen is still being so widely used. Look at the following program. The content of the seminar fully supports Dr. Lee’s assertion of the link between cancer and estrogen. Read the information below on their program, and you will find both the introduction and the titles of the presentations enough to make you pause before taking estrogen. Also, listening to Dr. Lee’s tapes will give you a good insight into some of the material presented at this symposium.
Estrogens as Endogenous Carcinogens in the Breast and Prostate
This symposium has been planned to explore the role of endogenous estrogens in the etiology of human breast and prostate cancer. An international group of scientists will share viewpoints and construct a more holistic understanding of the way estrogens induce cancer. Topics will include metabolic activations of estrogens to carcinogenic forms, deactivation of carcinogenic metabolites, and the role of estrogen receptor-mediated processes in tumor induction. One of the goals of this symposium is to provide the attendees with an overview of the direction of research on estrogen-induced cancer. Another goal is to identify biomarkers that can be useful in studies of cancer risk among humans and in the future development of preventive strategies. The overview of the role of estrogens in cancer obtained from this symposium will be useful for scientists engaged in a variety of cancer-related studies, as well as for epidemiologists, health planners, journalists and members of advocacy groups for breast and other human cancers.