Does progesterone cause Cancer?

Many, including state authorities, make the mistake that progesterone and the synthetic progestins are one and the same. They are not. Therein lies the root of the misinformation that natural progesterone poses a cancer threat.

Emory University has been studying progesterone for 20 years now and have only found benefits. In fact a study they completed last year on brain trauma victims, found it remarkable at reversing the oedema that formed after the injury, with no adverse side affects. Interestingly 71% of the victims were men.

I do understand your concern, so below you will find links to several research papers on various cancers. Several of these studies show how progesterone actually protects against cancer by activating the gene p53, which is the gene involved in apoptosis. If this gene is inactive cells keep growing.

The hormone oestrogen is a known initiator of heart disease and cancer, progesterone inhibits the production of oestrogen.

There are many, many research papers showing the protective role progesterone plays in the body. It protects against hypertension, lowers blood fats, it prevents coronary hyperactivity, a sign of coronary artery disease, it does not increase breast, endometrial and ovarian cancer risk and can be protective against it, can prevent epilepsy, it improves vasomotor symptoms, it prevents miscarriages and many more.

Here is a paper I wrote to help you get a better understanding of the role of progesterone relative to cancer...

Cancer of hormonally sensitive tissue

There is increasing evidence that 95% of cancers are caused by environmental factors such as pollutants from agriculture and industry, processed food and the misuse of prescription drugs such as oestrogen, whereas only 5% are related to our genes.

Numerous studies show we can alter the way our genes are expressed by changing the factors that influence them, such as those stated above. Continuing research, first started during the 90's, has identified a few genes that help control cell growth by producing substances that regulate cell division. If these genes are damaged by pollutants, by oxidation or by a lack of certain nutrients, the cells multiply rapidly and cancer can be the result.

Homocysteine (H) has been identified as a reliable marker for low levels of certain B vitamins and is indicative of a possible risk for getting over fifty common diseases, amongst them being cancer. There is now evidence that having a high H score adversely affects the rate of tumour growth.

A study reported in Cancer in 2002 found an increase in cancers due to a lack of UV-B and vitamin D3. The researchers believe that mortality rates could be reduced by careful exposure to sunlight and taking vitamin D3 supplements.

It has now been recognised that if a mother has been exposed to high levels of natural or xeno-oestrogens whilst pregnant, the foetus could be affected, leading to breast, ovarian and endometrial cancer in women and testicular, prostate and increasingly breast cancer in men.

Research has shown that the longer a women is exposed to her own natural oestrogen, i.e. a long reproductive lifetime, the greater the chances of her getting cancer. Women with low levels of progesterone have a 5.4 greater chance of getting breast cancer with 10 times a greater chance of dying from all cancers. Breast cancer recurrence after a mastectomy is more likely if the surgery is performed in the first half of the cycle when oestrogen is dominant than in the second half.

The Pill increases the risk of getting cervical cancer, the longer the duration of taking it, the greater the risk.

HRT (hormone replacement therapy), unopposed by progesterone, causes endometrial cancer. 2 studies published in 1995 found that women who had been exposed to HRT for longer than 5 years had a 32% increased risk of getting breast cancer, if combined with a progestin it went up to 41% and for those women who were post menopausal the risk went up to 71%, while the risk of getting ovarian cancer went up by 72%.

The latest evidence of oestrogen and progestin causing problems in women comes from the Women's Health Initiative, which ended in 2003, three years early due to an increase in breast cancer, heart disease and strokes. The FDA has now ordered pharmaceutical firms to include a warning label on HRT boxes stating the increase. By 2004 the latest oestrogen only arm of the WHI was halted due to an increase in the incidents of stroke.

Tamoxifen, a weak oestrogenic drug used in the treatment of breast cancer, is classified as a carcinogen. It causes an increase in both endometrial and liver cancer.

As water is now contaminated with oestrogen from HRT and The Pill, plus those generated by industry, men are increasingly subject to an excess, and with this comes an increase in the oestrogen related cancers, prostate and testicular. If treated with oestrogen for prostate cancer or after transsexual surgery there is an increased risk of men getting breast cancer. The older a man gets the more likely he is to suffer from oestrogen dominance, which causes a decrease in his testosterone levels and an increase in di-hydrotestosterone, this in turn leads to a drop in libido and an increased likelihood of getting prostate hyperplasia or cancer.

There are at least 40 if not more carcinogens to which we are exposed on a daily basis. Of main concern are: alcohol; artificial sweeteners; bleaches used for whitening flour etc; charred food e.g. toast and browned meat; chlorine in drinking water; fluoride; food preservatives; all mineral oil, inc liquid paraffin; oestrogen and xeno-oestrogens; pesticides; industrial chemicals such as dioxin, PCB's and phthalates; plastics; radiation from the sun, nuclear power stations, TV sets, computers and cell phones; refined cooking oil and margarine; tobacco smoke; vehicle exhaust fumes; x-rays.

Additional information

Progesterone: Use between 100-200mg of progesterone daily, this equates to 3-6ml of Natpro. More might be needed, vary the amount used following symptoms as a guide. If radiation therapy is called for put the cream directly on the burn, as it has soothing, pain reducing and regenerative properties. Progesterone is neuroprotective, it prevents lipid peroxidation and confers vascular protection. As an anti-inflammatory agent, progesterone has been shown to reduce the response of natural killer cells as well as other known initiators of inflammation.

Cancer is a mentally stressful disease, stress in turn causes a rise in cortisol and adrenaline. Adrenaline prevents cancer cells from dying, it is also an excitatory hormone. Progesterone counters the rise in adrenaline by activating the GABA receptor sites. GABA is the major calming neurotransmitter in the brain.

Nutrients: Take daily a high level of all the anti-oxidants:1000-6000mg L-arginine; 1000-6000mg N-acetyl cysteine; 10,000-25,000 IU vitamin A; 1-10gm vitamin C; 100-1000 IU vitamin E; 15-50mg zinc and in particular 200-300mcg selenium, which has been found to decrease the risk of getting cancer by nearly 50%, probably because it activates gene p53. 1000-3000 IU vitamin D3; 3-6 capsules probiotics, in particular Lactobacilus acidophilus and L. bulgaricus, these have a remarkable ability to activate the immune system; 100-1000mcg vitamin B12; 400-1000mcg folic acid; 25-100mg vitamin B6; 10-50mg vitamin B2; 8gm L-glutamine, to heal the gut from chemo damage; 1000mg glycine; 500mg methionine; 5-10ml fish oil with EPA and DHA or 15 to 60ml Omega 3 flax oil; 100mg Co enzyme Q10; 1-10gm MSM (methylsulfonyl-methane); 300mg milk thistle extract; digestive enzymes (as directed on label).

It has been calculated that we can reduce our risk of getting cancer by 70% if the above guidelines are followed.

The phytochemicals found in certain plants have been found to be beneficial. A study carried out by the WHO in 50 countries found that hormone related cancers in the West were from 10 to 20 times higher than that found in Asian countries. The low level has been ascribed to their diet high in phytochemicals.

Lignans are phytochemicals. These are cyclic molecules found in the highest concentration in flax seed. These should always be ground before consumption (take 15 to 60ml/day). Lignans have anti-bacterial, anti-fungal and anti-viral properties.

Some therapists recommend alternating enemas of coffee, flax oil and wheat grass. The ‘green foods’, spirulina, chlorella, barleygrass and wheatgrass are not only nutrient dense, but being partly 'digested' are easily assimilated into the gut. Because of damage to the lining of the gut with chemotherapy, nutrient intake is usually far too low in cancer patients on the therapy.

Note: If pregnant or breastfeeding take no more than 10,000IU of vitamin A

Avoid: all forms of oestrogen, the Pill, (change to another form of contraceptive); HRT; Tamoxifen; mammograms; exposure to the above carcinogens; dairy products, red meat and chicken, unless organic, as these often contain oestrogenic growth hormones; sugar and artificial sweeteners, especially aspartame; all forms of processed foods but particularly those containing sugar, i.e. carbonated drinks, including the 'diet' drinks, fruit juices (including freshly squeezed), biscuits, cakes, white breads, canned foods, sauces, sweets, (cancers live off sugar); oxidised fats, (ie margarine, refined oils, deep fried foods); pasteurised milk; smoking; stimulants such as alcohol, coffee, black tea, wheat in any form, and the other gluten containing grains- barley, kamut, oats, rye, spelt, triticale and triticum, also any by-products such as bran, bulgar and couscous.

There is strong evidence that certain peptides (protein fragments) found in gluten interfere with our immune system. Gluten can also damage the lining of the gut, commonly known as leaky gut, found in the majority of people eating a diet high in gluten containing grain. This leads to malabsorption of vital nutrients that the body needs to defend itself against any disease, including cancer. An interesting parallel has been noted between our increased consumption of gluten over the past century and a rise in cancer from 2.5% in 1900 to 33% to date. Please note that all grains are converted to sugar by the body.

References

Cancer Epidemiology Biomarkers & Prevention
17, 614-620, March 1, 2008. Published Online First March 6, 2008;
Reproductive Steroid Hormones and Recurrence-Free Survival in Women with a History of Breast Cancer

British Journal of Nutrition
April 2008, Volume 99, Issue 04, pp 723-731
"Trans-fatty acids induce pro-inflammatory responses and endothelial cell dysfunction"

Diabetes Care 30:561-567, 2007
Prospective Study of Hyperglycemia and Cancer Risk

J. Biol. Chem, March 12, 2007 10.1074/jbc.M611370200
Epinephrine protects cancer cells from apoptosis via activation of PKA and BAD phosphorylation

Breast Cancer Research and Treatment
Volume 101, Number 2, January 2007 , pp. 125-134(10)
Effects of estradiol with micronized progesterone or medroxyprogesterone acetate on risk markers for breast cancer in postmenopausal monkeys

Eur Urol, 2006 Nov; 50(5):935-9.
Testosterone and Prostate Cancer

Cancer Research 65, 54-65, January 1, 2005
Xenoestrogen Action in Prostate Cancer: Pleiotropic Effects Dependent on Androgen Receptor Status

Reproductive Sciences, Vol. 12, No. 4, 285-292 (2005)
Progesterone-Induced Inhibition of Growth and Differential Regulation of Gene Expression in PRA- and/or PRB-Expressing Endometrial Cancer Cell Lines

JNCI Journal of the National Cancer Institute 2005 97(10):755-765
Serum Sex Steroids in Premenopausal Women and Breast Cancer Risk Within the European Prospective Investigation into Cancer and Nutrition

Journal of Steroid Biochemistry & Molecular Biology 97 (2005) 441-450
Pregnancy, progesterone and progestins in relation to breast cancer risk

BIOLOGY OF REPRODUCTION 73, 586–590 (2005)
Carcinogenic Potential of Ovulatory Genotoxicity

JAMA. 2004;291:1701-1712, 1769-1771
Effects of Conjugated Equine Estrogen in Postmenopausal Women With Hysterectomy

International Journal of Cancer Volume 114, Issue 3 , Pages 448 - 454
Breast cancer risk in relation to different types of hormone replacement therapy in the E3N-EPIC cohort

J Endocrinol. 2003 Oct;179(1):55-62.
'Overexpression of wild-type p53 gene renders MCF-7 breast cancer cells more sensitive to the antiproliferative effect of progesterone.'

Oncogene. 2003 Oct 9;22(44):6883-90.
'Progesterone-induced apoptosis in immortalized normal and malignant human ovarian surface epithelial cells involves enhanced expression of FasL'.

BMJ Publishing Group Ltd 2003
'Women need better information about routine mammography'

Clinical Chimica Acta, 2002; vol. 322: 21-8
'Hyperhomocysteinemia is a risk factor for cancer and a new potential tumour marker'

Cancer. 2002 Mar 15;94(6):1867-75
'An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B' radiation.'

J Cell Biochem. 2001;82(3):445-51.
'Apoptosis induced by progesterone in human ovarian cancer cell line SNU-840.'

Anticancer Res. 2001 Nov-Dec;21(6A):3871-4.
'Progesterone induces apoptosis in malignant mesothelioma cells.'

Int J Oncol. 2001 Jul;19(1):31-8.
Steroid receptors and hormones in relation to cell proliferation and apoptosis in poorly differentiated epithelial ovarian tumors.

Cancer 2000, Volume 83, Issue 1 , Pages 111 - 121
Progesterone therapy for endometrial carcinoma reduces cell proliferation but does not alter apoptosis

Chinese Journal of Obstetrics and Gynecology,
2000 Jul;35(7):423-6.
'The effect of progesterone on proliferation and apoptosis in ovarian cancer cell

Molecular and Cellular Biochemistry
Volume 202, Numbers 1-2 / December, 1999 Pages 53-61
Bcl-2, survivin and variant CD44 v7-v10 are downregulated and p53 is upregulated in breast cancer cells by progesterone: Inhibition of cell growth and induction of apoptosis

Journal of the National Cancer Institute, 1998, Vol. 90: 1774-86, No. 23,
Hormonal Etiology of Epithelial Ovarian Cancer, With a Hypothesis Concerning the Role of Androgens and Progesterone

Ann Clin Lab Sci. 1998 Nov-Dec;28(6):360-9.,
'Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53.'

Cancer. 1997 May 15;79(10):1944-50.,
'Progesterone induces apoptosis and up-regulation of p53 expression in human ovarian carcinoma cell lines.'

Cancer. 1995 May 1;75(9):2233-8.
Mutations of the p53 gene in male breast cancer.

J Am Diet Assoc. 1995 Jun; 95(6):693-7.
'Implementing a ketogenic diet based on medium-chain triglyceride oil in pediatric patients with cancer.'

J Am Coll Nutr. 1995 Apri14(2):202-8.
'Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports.'

New England Journal of Medicine 332:1589-1593 June 15, 1995 Number 24
'The Use of Estrogens and Progestins and the Risk of Breast Cancer in Postmenopausal Women'

Web sites

canceractive.com
knowthecause.com
mercola.com

Research papers...

1. Hormonal Etiology of Epithelial Ovarian Cancer, With a
Hypothesis Concerning the Role of Androgens and
Progesterone
Harvey A. Risch

"Progesterone
Evidence for a possible protective role of progesterone in the etiology of ovarian cancer starts with consideration of the increased sex hormone activity during pregnancy. Over the first month of pregnancy, maternal LH and FSH decline strongly with the increase in trophoblast hCG (162). The hCG also stimulates the corpus luteum to continue producing progesterone and not regress (102). After the seventh week, the luteal-placental shift occurs in which the functional capacity of the corpus luteum of pregnancy drops, while the massive placental production of progesterone during pregnancy begins (102). In addition, the placenta extracts maternal (and later, fetal) adrenal androgens, which remain at stable maternal serum concentrations while both production and utilization rates increase; maternal serum estrone and estradiol are made from the adrenal androgens (102). During pregnancy, the placental synthesis thus causes 10-fold increases in maternal circulating progesterone levels (102). Maternal testosterone and androstenedione levels increase some twofold to threefold, although most of the testosterone is bound to the pregnancy-induced higher levels of sex hormonebinding globulin, preventing virilization of female fetuses (102). These maternal ovarian androgens are in any case dwarfed by the huge estrogen and progesterone concentrations. In terms of the pathogenesis of ovarian cancer, we suggest that the additional protective aspect of pregnancy not mediated through suppression of ovulation may be due to the 8–9 months of elevated progesterone. As we have noted, it seems unlikely to be due to the pregnancy estrogens, since most of the evidence relating estrogens to risk of ovarian cancer (as well as to endometrial cancer and perhaps breast cancer) points either to no effect or to increase in risk."

2. Journal of Steroid Biochemistry & Molecular Biology 97 (2005) 441–450
Pregnancy, progesterone and progestins in relation
to breast cancer risk
Carlo Campagnoli £™, Chiara Abb`a, Simona Ambroggio, Clementina Peris

"Abstract
In the last two decades the prevailing opinion, supported by the “estrogen augmented by progesterone” hypothesis, has been that progesterone contributes to the development of breast cancer (BC). Support for this opinion was provided by the finding that some synthetic progestins, when added to estrogen in hormone replacement therapy (HRT) for menopausal complaints, increase the BC risk more than estrogen alone. However, recent findings suggest that both the production of progesterone during pregnancy and the progesterone endogenously produced or exogenously administered outside pregnancy, does not increase BC risk, and could even be protective. The increased BC risk found with the addition of synthetic progestins to estrogen in HRT seems in all likehood due to the fact that these progestins (medroxyprogesterone acetate and 19-nortestosterone-derivatives) are endowed with some non-progesterone-like effects which can potentiate the proliferative action of estrogens. The use of progestational agents in pregnancy, for example to prevent preterm birth, does not cause concern in relation to BC risk."
Conclusion
Available data suggest that progesterone produced during pregnancy does not have deleterious effects on BC risk; conversely, it could have a predominant role in the long term protective effect against BC shown by full-term pregnancies. Even outside pregnancy, the balance of the in vivo evidence is that progesterone does not have a cancer-promoting effect on breast tissue. The greater BC risk related to the use of HRT preparations containing estrogen and synthetic progestins seems in all likelihood to be due to the fact that many of the progestins used have several nonprogesterone like actions that potentiate the proliferative effect of estrogens on breast tissue and estrogen-sensitive cancer cells. Particularly relevant seem to be the metabolic and hepatocellular effects (decreased insulin sensitivity, increased levels and activity of IGF-I, and decreased levels of SHBG), which oppose the opposite effects induced by oral
estrogen. The use of progestational agents in pregnancy, e.g. to prevent preterm birth [107,108], does not cause concern in relation to BC risk. On the contrary, progestational agents could even be protective, especially when they succeed in avoiding preterm delivery, a well documented risk factor for the subsequent development of BC"

3. Int J Oncol. 2001 Jul;19(1):31-8.
Steroid receptors and hormones in relation to cell proliferation and apoptosis in poorly differentiated epithelial ovarian tumors.
Lindgren P ,Bäckström T ,Mählck CG ,Ridderheim M ,Cajander S .
Department of Obstetrics and Gynecology, Umeå University, Umeå, Sweden

4. Cancer Volume 83, Issue 1 , Pages 111 - 121
Published Online: 9 Nov 2000
Copyright © 1998 American Cancer Society
Progesterone therapy for endometrial carcinoma reduces cell proliferation but does not alter apoptosis
Makoto Saegusa, M.D. *, Isao Okayasu, M.D.
Department of Pathology, Kitasato University School of Medicine, Kanagawa, Japan

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