The relationship between progesterone and cancer is multifaceted, varying significantly based on the specific type of hormone, its use, and individual circumstances. It is not a simple matter of whether progesterone causes cancer, but rather how different forms of this hormone influence risk in various bodily systems.
The Role of Progesterone in the Body
Naturally occurring progesterone is a steroid hormone produced primarily by the corpus luteum in the ovaries after ovulation, and by the placenta during pregnancy. This hormone prepares the uterine lining (endometrium) for the implantation of a fertilized egg by stimulating the growth of blood vessels and glands. If pregnancy occurs, progesterone levels remain elevated, helping to maintain the uterine lining, prevent uterine contractions, and support the development of the fetus.
The term “progesterone” specifically refers to the hormone chemically identical to what the body produces, often called “bioidentical progesterone” when administered externally. In contrast, “progestins” are synthetic compounds that mimic some of progesterone’s effects but have different chemical structures. These structural differences can lead to varying interactions with the body’s receptors and distinct physiological outcomes.
Progesterone, Progestins, and Breast Cancer Risk
The Women’s Health Initiative (WHI) study provided significant insights into the link between hormone use and breast cancer risk. This large-scale clinical trial demonstrated that combination hormone therapy, specifically estrogen combined with a synthetic progestin (medroxyprogesterone acetate or MPA), was associated with an increased incidence of breast cancer. The increased risk for women taking this combined therapy persisted after discontinuing use.
It is important to differentiate the effects of synthetic progestins from bioidentical progesterone in this context. Some research suggests that regimens combining estrogen with natural micronized progesterone may not carry the same increased breast cancer risk as those using certain synthetic progestins, or may even be associated with a lower risk. The duration of hormone therapy also influences risk, with longer periods of use generally linked to a greater potential for increased breast cancer incidence.
Impact on Endometrial and Ovarian Cancer
Progestins play a different role in endometrial cancer. Estrogen, when used alone in hormone therapy, can stimulate excessive growth of the uterine lining, leading to endometrial hyperplasia and increasing the risk of endometrial cancer. Progesterone or progestins are administered alongside estrogen therapy to counteract this effect, preventing the over-thickening of the endometrium and thereby reducing the risk of endometrial cancer. This protective action is why progestins are included in menopausal hormone therapy for women who still have a uterus.
The relationship between progesterone, progestins, and ovarian cancer is less straightforward and a subject of ongoing research. Historically, progesterone has been viewed as a protective factor against ovarian cancer, largely due to observations that hormonal contraceptive use and pregnancy, both states of elevated progesterone, correlate with a lower risk of ovarian cancer. However, some more recent preclinical studies suggest that ovarian progesterone might actually contribute to the development of certain aggressive ovarian cancer subtypes, particularly high-grade serous ovarian cancer. Despite these newer findings, hormonal contraceptives, which often contain progestins, are still associated with a reduced risk of epithelial ovarian cancer.
Context of Hormone Use
The risk profile of progesterone and progestins depends on the medical context. In menopausal hormone therapy (MHT), the aim is to alleviate menopausal symptoms. For women with an intact uterus, estrogen is combined with a progestin to prevent endometrial overgrowth. The type of progestin, dosage, and duration of MHT can all influence the associated cancer risks.
Progestins are also used in hormonal contraceptives, including birth control pills, injections, implants, and intrauterine devices (IUDs). While these formulations primarily prevent pregnancy, they also have varying effects on cancer risk. For instance, some contraceptives have been linked to a small, temporary increase in breast cancer risk that typically declines after discontinuation. Conversely, hormonal contraceptives reduce the risk of endometrial and ovarian cancers. The age of the user and the specific progestin type and dosage contribute to the overall risk-benefit assessment in contraceptive use.