Also see:
Hormonal profiles in women with breast cancer
PUFA Increases Estrogen
Radiation Increases Breast Cancer Incidence
PUFA Inhibit Glucuronidation
PUFA Promote Cancer
Maternal PUFA Intake Increases Breast Cancer Risk in Female Offspring
Estrogen and Bowel Transit Time
Progestin and Cancer
Study: Acquired Breast Cancer Risk Spans Multiple Generations
Ray Peat, PhD on Thyroid, Temperature, Pulse, and TSH
Pre and Postmenopausal Women: Progesterone Decreases Aromatase Activity
Endometriosis and Estrogen
Ray Peat, PhD on the Menstrual Cycle
“Women and other mammals that are deficient in progesterone, and/or that have an excess of estrogen, have a higher than average incidence of cancer. Animal experiments have shown that administering progesterone could prevent cancer. Cells in the most cancer-susceptible tissues proliferate in proportion to the ratio of estrogen to progesterone. When the estrogen dominance persists for a long time without interruption, there are progressive distortions in the structure of the responsive organs–the uterus, breast, pituitary, lung, liver, kidney, brain, and other organs–and those structural distortions tend to progress gradually from fibroses to cancer.
As a result of the early studies in both humans and animals, progesterone was used by many physicians to treat the types of cancer that were clearly caused by estrogen, especially uterine, breast, and kidney cancers. But by the 1950s, the drug industry had created the myth that their patented synthetic analogs of progesterone were medically more effective than progesterone itself, and the result has been that medroxyprogesterone acetate and other synthetics have been widely used to treat women’s cancers, including breast cancer.
Unfortunately, those synthetic compounds have a variety of functions unlike progesterone, including some estrogenic and/or androgenic and/or glucocorticoid and/or antiprogesterone functions, besides other special, idiosyncratic side effects. The rationale for their use was that they were “like progesterone, only better.” The unpleasant and unwanted truth is that, as a group, they are seriously carcinogenic, besides being toxic in a variety of other ways. Thousands of researchers have drawn conclusions about the effects of progesterone on the basis of their experiments with a synthetic progestin.” -Ray Peat, PhD
Progesterone protects against cancer and supports pregnancy and child birth. Synthetic progesterone, known as progestin, acts more like estrogen in that they do not support progestation (which is why they are used in contraceptives), and they have been shown to be carcinogenic while promoting the effects of estrogen.
Resources:
J Steroid Biochem Mol Biol. 2005 Jul;96(2):95-108.
Progestins and progesterone in hormone replacement therapy and the risk of breast cancer.
Campagnoli C, Clavel-Chapelon F, Kaaks R, Peris C, Berrino F.
Controlled studies and most observational studies published over the last 5 years suggest that the addition of synthetic progestins to estrogen in hormone replacement therapy (HRT), particularly in continuous-combined regimen, increases the breast cancer (BC) risk compared to estrogen alone. By contrast, a recent study suggests that the addition of natural progesterone in cyclic regimens does not affect BC risk. This finding is consistent with in vivo data suggesting that progesterone does not have a detrimental effect on breast tissue. The increased BC risk found with the addition of synthetic progestins to estrogen could be due to the regimen and/or the kind of progestin used. Continuous-combined regimen inhibits the sloughing of mammary epithelium that occurs after progesterone withdrawal in a cyclic regimen. More importantly, the progestins used (medroxyprogesterone acetate and 19-Nortestosterone-derivatives) are endowed with some non-progesterone-like effects, which can potentiate the proliferative action of estrogens. Particularly relevant seem to be the metabolic and hepatocellular effects (decreased insulin sensitivity, increased levels and activity of insulin-like growth factor-I, and decreased levels of SHBG), which contrast the opposite effects induced by oral estrogen.
Cancer Lett. 2005 Apr 18;221(1):49-53.
Effects of progesterone on ovarian tumorigenesis in xenografted mice.
McDonnel AC, Van Kirk EA, Isaak DD, Murdoch WJ.
Circumstantial evidence indicates that progestins reduce the risk of epithelial ovarian cancer. We report that the tumorigenic capacity of human ovarian carcinoma (SKOV-3) cells inoculated into the peritoneal cavity of athymic mice is suppressed by pretreatment with subcutaneous progesterone-releasing pellets. Numbers of tumor implants on the intestines/mesentery and invasiveness into underlying host tissues were reduced at 6 weeks following exposure to progesterone. Progesterone prevented tumors from forming on the liver. Life spans of progesterone-treated animals were prolonged. There was no beneficial effect of administration of progesterone if initiated after ovarian tumors had become established on organ surfaces. Our findings implicate a role for progesterone in ovarian cancer prophylaxis.
Am J Epidemiol. 1981 Aug;114(2):209-17.
Breast cancer incidence in women with a history of progesterone deficiency.
Cowan LD, Gordis L, Tonascia JA, Jones GS.
In order to investigate the nature of the association of involuntarily delayed 1st birth and breast cancer risk, 1083 white women who had been evaluated and treated for in fertility from 1945-65 were followed prospectively through April 1978 to ascertain their breast cancer incidence. These women were categorized as to the cause of infertility into 2 groups, those with endogenous progesterone deficiency (PD) and those with nonhormonal causes (NH). Women in the PD group had 5.4 times the risk of premenopausal breast cancer as compared to women in the NH group. This excess risk could not be explained by differences between the 2 groups in age at menarche or age at menopause, history of oral contraceptive use, history of benign breast dieases, or age at 1st birth. Women in the PD group also experienced a 10-fold increase in deaths from all malignant neoplasm compared to the NH group. The incidence of postmenopausal breast cancer did not differ significantly between the 2 groups.
