Progestogen only pill

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Progestogen Only Pills or Progestin Only Pills (POP) are contraceptive pills that only contain synthetic progestogens (progestins) and do not contain oestrogen. They are colloquially known as mini pills.

Although such pills are sometimes called "Progesterone Only Pills," they do not actually contain progesterone, but one of several chemically related compounds and there are a number of progestogen only contraceptive formulations.

How they work

The mechanism of action of progestogen-only contraceptives depends on the progestogen activity and dose.[1]

Very low dose progestogen-only contraceptives, such as traditional progestogen-only pills (and subdermal implants Norplant and Jadelle and intrauterine systems Progestasert and Mirena), inconsistently inhibit ovulation in ~50% of cycles and rely mainly on their progestogenic effect of thickening the cervical mucus and thereby reducing sperm viability and penetration.

Intermediate dose progestogen-only contraceptives, such as the progestogen-only pill Cerazette (or the subdermal implant Implanon), allow some follicular development but much more consistently inhibit ovulation in 97–99% of cycles. The same cervical mucus changes occur as with very low dose progestogens.

High dose progestogen-only contraceptives, such as the injectables Depo-Provera and Noristerat, completely inhibit follicular development and ovulation. The same cervical mucus changes occur as with very low dose and intermediate dose progestogens.

In anovulatory cycles using progestogen-only contraceptives, the endometrium is thin and atrophic. If the endometrium was also thin and atrophic during an ovulatory cycle, this could theoretically interfere with implantation of a blastocyst (embryo).


The theoretical efficacy is similar to that of the combined oral contraceptive pill (COCP). However, they are taken continuously without any breaks between packets and traditional progestogen-only pills must be taken to a much stricter time every day (within 3 hours vs. a COCP's 12 hours, although in some countries the POP Cerazette has an approved window of 12 hours). The real-life efficacy is therefore dependent upon user compliance.

POPs are not dependent upon gut bacterial flora for their absorption and so are not affected by courses of antibiotics. They will, however, be affected by any episodes of diarrhea or vomiting.


Lacking the oestrogen of combined pills, they are not associated with increased risks of DVT or heart disease. With the decreased clotting risk, they are not contraindicated in the setting of sickle-cell disease. The low dose of progestogen, and absence of oestrogen, make the minipill safe to use during breastfeeding; in fact, it may increase the flow of milk. Like combined pills, the minipill decreases the likelihood of pelvic inflammatory disease.

It is unclear whether POPs provide protection against endometrial cancer and ovarian cancer to the extent that COCP do.

Side effects

  • With no break in the dosage, flow does not initially occur at a predictable time. Most women tend to establish, over a few months, light spotting at approximately regular intervals.
  • May cause mastalgia or mood swings.
  • Weight gain is less commonly experienced than on COCP.

Breast cancer risk

Epidemiological evidence on POPs and breast cancer risk is based on much smaller populations of users and so is less conclusive than that for COCPs.

In the largest (1996) reanalysis of previous studies of hormonal contraceptives and breast cancer risk, less than 1% were POP users. Current or recent POP users had a slightly increased relative risk (RR 1.17) of breast cancer diagnosis that just missed being statistically significant. The relative risk was similar to that found for current or recent COCP users (RR 1.16), and as with COCPs, the increased relative risk decreased over time after stopping, vanished after 10 years, and was consistent with being due to earlier diagnosis or promoting the growth of a preexisting cancer.[2][3]

The most recent (1999) IARC evaluation of progestogen-only hormonal contraceptives reviewed the 1996 reanalysis as well as 4 case-control studies of POP users included in the reanalysis. They concluded that: "Overall, there was no evidence of an increased risk of breast cancer" with progestogen-only contraceptives, but since there was "inadequate evidence", they were "possibly carcinogenic".[4]

Recent anxieties about the contribution of progestogens to the increased risk of breast cancer associated with HRT in postmenopausal women such as found in the WHI trials[5] have not yet spread to progestogen-only contraceptive use in premenopausal women.[1]

See also


  1. 1.0 1.1 Glasier, Anna (2006). "Contraception". In in DeGroot, Leslie J.; Jameson, J. Larry (eds.). Endocrinology (5th edition ed.). Philadelphia: Elsevier Saunders. pp. pp. 2993-3003. ISBN 0-7216-0376-9.
  2. Collaborative Group on Hormonal Factors in Breast Cancer (1996). "Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53,297 women with breast cancer and 100,239 women without breast cancer from 54 epidemiological studies". Lancet. 347 (9017): 1713–27. PMID 8656904.
  3. Collaborative Group on Hormonal Factors in Breast Cancer (1996). "Breast cancer and hormonal contraceptives: further results". Contraception. 54 (3 Suppl): 1S–106S. PMID 8899264.
  4. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans (1999). "Hormonal contraceptives, progestogens only". Hormonal contraception and post-menopausal hormonal therapy; IARC monographs on the evaluation of carcinogenic risks to humans, Volume 72. Lyon: IARC Press. pp. pp. 339-397. ISBN 92-832-1272-X.
  5. Chlebowski R, Hendrix S, Langer R, Stefanick M, Gass M, Lane D, Rodabough R, Gilligan M, Cyr M, Thomson C, Khandekar J, Petrovitch H, McTiernan A (2003). "Influence of estrogen plus progestin on breast cancer and mammography in healthy postmenopausal women: the Women's Health Initiative Randomized Trial". JAMA. 289 (24): 3243–53. PMID 12824205.

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