Contraception

It is established practice that contraception is required until the age of 55 unless it is certain that the person has reached their final menstrual period^1,2. There is not, unfortunately, a test that will definitively establish that the final menstrual period has passed and that the person will not ovulate again: elevated serum follicle stimulating hormone (FSH) does NOT exclude future ovulation.

Some people who have or have had breast cancer do not need to think about contraception because, for example, they have been sterilised, their only partner assigned male at birth has had a vasectomy, or they have only partners who were assigned female at birth.

In addition, contraception is not required if an individual:

• is aged 55 years or over^1,2
• has had a hysterectomy, both ovaries removed or has been sterilised (note that endometrial ablation does not reliably prevent pregnancy)
• has been naturally amenorrhoeic for a year after age 50^1,2 (this does not include people who are amenorrhoeic while using hormonal contraception or people who become amenorrhoeic because of chemotherapy or use of tamoxifen).

Younger people who have a period of natural amenorrhoea, and people who become amenorrhoeic following medical treatment that affects ovarian function could later regain some ovarian activity and should be advised to use contraception.

• had a serum FSH >30 IU/L prior to chemotherapy or hormone therapy for breast cancer, which was taken when they were aged ≥50 and was taken over a year ago. Younger people with elevated FSH and people with elevated FSH after chemotherapy frequently regain ovarian activity and should be advised to use contraception^1,2.

Note that tamoxifen, aromatase inhibitors and GnRH analogues affect ovarian function but are not reliably contraceptive. Additional contraception should be advised during use.

It is recommended that (regardless of the receptor status of the breast cancer) hormonal contraception should generally be avoided by people who have or have had breast cancer^2,3. This is because of concern about the effect of contraceptive hormones on the breast cancer, its risk of recurrence and future occurrence of another breast cancer. Effective non-hormonal contraceptive options should be recommended first line.

Highly effective non-hormonal contraceptive methods

• Copper intrauterine device (Cu-IUD). About 99% effective for contraception for at least 5 years (some devices are effective for 10 years). Reversible^3,4,5.
• Female sterilisation. About 99% effective for contraception. Permanent^3,4,5.
• Male sterilisation. > 99% effective for contraception. Permanent^3,4,5.

Less effective non-hormonal contraceptive methods

• With typical use of condoms, the contraceptive failure rate is estimated at about 13-18% in the first year of use. With perfect use of condoms, contraceptive failure rate is lower^3,4,5.
• Diaphragm with spermicide. Contraceptive failure rate in the first year of use is estimated at about 12-17%^3,4,5.

Note that withdrawal is not an effective method of contraception. Natural family planning methods including contraceptive apps vary widely in terms of effectiveness, are highly user-dependent, and are not suitable for people with irregular cycles or using hormone treatment after breast cancer^6,7.

All other effective contraceptive methods contain progestogen hormones, either alone (progestogen-only contraceptives), or in combination with oestrogen (combined hormonal contraceptives).

Many people are very happy using non-hormonal contraceptive methods. These methods might, however, be less acceptable if the person:

• already has heavy, painful periods (the Cu-IUD can exacerbate this)
• wants to avoid a medical procedure
• has more than one partner
• wants contraception that is more effective than a barrier method. This is of particular importance during treatment for breast cancer. Achieving highly effective contraception is crucial during use of any treatment that is teratogenic².

There are not robust direct data to inform the effect of use of contraceptive hormones after any type of breast cancer on risk of recurrence or risk of a further primary breast cancer. The limited (indirect) evidence that we do have comes from studies of the general population (rather than people who have already had breast cancer).

Combined hormonal contraception. The evidence (from observational studies) has, for a long time, indicated that there is an association between use of combined hormonal contraception (which contains both oestrogen and a progestogen) and a small increased risk of developing breast cancer^8-33. For that reason, it is established practice and an ongoing recommendation that combined hormonal contraception (which includes the combined contraceptive pill, transdermal patch and vaginal ring) is avoided after breast cancer^{2, 34}.

Importantly, combined hormonal contraception is also associated with significantly increased risk of thrombosis³⁴.

Progestogen-only contraception. Recently published observational evidence⁹ indicates an association between progestogen-only contraceptives and increased risk of developing breast cancer similar to that with combined hormonal contraception. After adjusting for confounders, when compared to non-use of hormonal contraception, the data indicate that current or recent use of progestogen-only contraceptive methods is associated with increased risk of breast cancer in the general population.

It is noted that contrary to what is often suggested, the recent evidence indicates that the levonorgestrel-releasing intrauterine devices (e.g., Mirena^®, Levosert^®, Benilexa^®, Kyleena^®, Jaydess^®) with their low systemic progestogen exposure are no safer than any other progestogen-only contraceptive in terms of effect on risk of occurrence of breast cancer⁹.

The very limited evidence relating directly to use of the 52mg LNG-IUD by individuals who have had breast cancer³⁵ is inadequate to inform any robust recommendation regarding effect of use on risk of breast cancer recurrence, occurrence of a new breast cancer or how benefit of the 52mg LNG-IUD for endometrial protection during use of tamoxifen weighs against its effect on breast cancer risk³⁶.

The current evidence base is inadequate to make any recommendation as to whether, after a breast cancer, different progestogen-only contraceptives affect risk of recurrence or occurrence of a new breast cancer differently.

All hormonal contraception should normally be avoided after breast cancer. In consultation with the individual and their breast cancer specialist, and taking into consideration the characteristics of the person’s breast cancer and its treatment a clinician might (on an individual patient basis) consider offering a progestogen-only contraceptive after breast cancer only if:

• the effective non-hormonal contraceptive options described above are not acceptable
• the person has a significant additional gynaecological indication for using a progestogen-only contraceptive (e.g, very heavy, painful menstrual bleeding, severe endometriosis)
• the person has unscheduled bleeding during use of tamoxifen. Erratic bleeding during tamoxifen use requires endometrial investigation because tamoxifen increases risk of endometrial hyperplasia and endometrial cancer².

An opinion should be sought from a specialist in contraception if required. For further information refer to the FSRH guidance.

It is recommended that people using hormonal contraception at the time of breast cancer diagnosis should be supported to switch to effective non-hormonal contraception as soon as possible, but without leaving them at risk of pregnancy².

Users of combined hormonal contraception at the time of breast cancer diagnosis should be supported to make an immediate switch to alternative effective contraception that does not contain oestrogen. This reflects both the potential effect of oestrogen on the breast cancer and the combined hormonal contraception-associated risk of thrombosis at a time of already increased risk of venous thromboembolism. For some individuals this might involve an initial switch to a progestogen-only contraceptive as a short-term measure to maintain effective contraception until the person is able to make definitive choices about ongoing contraception².

Copper intrauterine device (Cu-IUD)

After unprotected sex, the copper IUD is the most effective method of emergency contraception and should always be offered when emergency contraception is requested if the strict criteria for insertion are met. This is time-critical and requires immediate urgent referral to an IUD provider.

A copper IUD can be inserted for emergency contraception:

• within 5 days after the earliest likely date of ovulation (this can be estimated ONLY if the person has regular natural menstrual cycles and is not using any hormone treatment); OR
• within 5 days after the first unprotected sex in a natural menstrual cycle, OR
• if a high sensitivity urine pregnancy test is negative AND all unprotected sex in the last 21 days took place in the last 5 days.

A copper IUD inserted for emergency contraception can be retained to provide effective ongoing contraception.

Oral hormonal emergency contraception

If a copper IUD is not suitable or is not acceptable, the only other alternative for emergency contraception is oral hormonal emergency contraception. Oral emergency contraception is much less effective than the copper IUD and is ineffective if the individual has already ovulated.

It is considered that the benefit of occasional use of oral emergency contraception after unprotected sex outweighs any potential adverse effect on breast cancer risk. Either levonorgestrel or ulipristal acetate oral emergency contraception may be offered.

• Levonorgestrel 1.5mg po stat (3mg if the person has weight > 70kg or BMI > 26kg/m2) can be offered up to 96 hours after unprotected sex
• Ulipristal acetate 30mg po stat can be offered up to 120 hours after unprotected sex.

Please see FSRH guideline Emergency Contraception for emergency contraception decision-making algorithms.

Note that oral emergency contraception is not a substitute for regular effective contraception.

1. FSRH Clinical Guideline: Contraception for Women Aged over 40 Years (August 2017, amended July 2023) FSRH Clinical Guideline: Contraception for Women Aged over 40 Years (August 2017, amended July 2023) - Faculty of Sexual and Reproductive Healthcare (accessed 30/10/2023)
2. FSRH CEU Guidance: Supporting Contraceptive Choices for Individuals Who Have or Have Had Breast Cancer (November 2023) FSRH CEU Guidance: Supporting Contraceptive Choices for Individuals Who Have or Have Had Breast Cancer, Faculty of Sexual and Reproductive Healthcare (FSRH).
3. Faculty of Sexual and Reproductive Healthcare (FSRH). UK Medical Eligibility Criteria for Contraceptive Use April 2016 (Amended September 2019). 2019.
4. Trussell J, Aiken A, Micks E, Guthrie K. Efficacy, safety and personal considerations in: Contraceptive Technology 21st Edition. 21st Editi. New York, NY: Ayer Company Publishers, Inc.; 2018.
5. Center for Disease Control. Contraception [Internet]. [cited 2023 Oct 13]. Available from: https://www.cdc.gov/reproductivehealth/contraception/index.htm
6. Peragallo Urrutia R, Polis CB, Jensen ET, Greene ME, Kennedy E, Stanford JB. Effectiveness of Fertility Awareness-Based Methods for Pregnancy Prevention: A Systematic Review. Obstetrics and gynecology. 2018 Sep;132(3):591–604.
7. Faculty of Sexual and Reproductive Healthcare (FSRH). Fertility Awareness Methods. 2015.
8. Mørch LS, Skovlund CW, Hannaford PC, Iversen L, Fielding S, Lidegaard Ø. Contemporary Hormonal Contraception and the Risk of Breast Cancer. N Engl J Med. 2017 Dec;377(23):2228–39.
9. Fitzpatrick D, Pirie K, Reeves G, Green J, Beral V. Combined and progestagen-only hormonal contraceptives and breast cancer risk: A  UK nested case-control study and meta-analysis. PLoS Med. 2023 Mar;20(3):e1004188.
10. Iversen L, Sivasubramaniam S, Lee AJ, Fielding S, Hannaford PC. Lifetime cancer risk and combined oral contraceptives: the Royal College of  General Practitioners’ Oral Contraception Study. Am J Obstet Gynecol. 2017 Jun;216(6):580.e1–580.e9.
11. Gierisch JM, Coeytaux RR, Urrutia RP, Havrilesky LJ, Moorman PG, Lowery WJ, et al. Oral contraceptive use and risk of breast, cervical, colorectal, and endometrial  cancers: a systematic review. Cancer Epidemiol Biomarkers Prev. 2013 Nov;22(11):1931–43.
12. Iodice S, Barile M, Rotmensz N, Feroce I, Bonanni B, Radice P, et al. Oral contraceptive use and breast or ovarian cancer risk in BRCA1/2 carriers: a  meta-analysis. Eur J Cancer. 2010 Aug;46(12):2275–84.
13. Cibula D, Zikan M, Dusek L, Majek O. Oral contraceptives and risk of ovarian and breast cancers in BRCA mutation  carriers: a meta-analysis. Expert Rev Anticancer Ther. 2011 Aug;11(8):1197–207.
14. Moorman PG, Havrilesky LJ, Gierisch JM, Coeytaux RR, Lowery WJ, Peragallo Urrutia R, et al. Oral contraceptives and risk of ovarian cancer and breast cancer among high-risk  women: a systematic review and meta-analysis. J Clin Oncol. 2013 Nov;31(33):4188–98.
15. 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. 1996 Jun;347(9017):1713–27.
16. Kahlenborn C, Modugno F, Potter DM, Severs WB. Oral contraceptive use as a risk factor for premenopausal breast cancer: a  meta-analysis. Mayo Clin Proc. 2006 Oct;81(10):1290–302.
17. Zhu H, Lei X, Feng J, Wang Y. Oral contraceptive use and risk of breast cancer: a meta-analysis of prospective  cohort studies. Eur J Contracept Reprod Health Care. 2012 Dec;17(6):402–14.
18. Vessey M, Painter R. Oral contraceptive use and cancer. Findings in a large cohort study, 1968-2004. Br J Cancer. 2006 Aug;95(3):385–9.
19. Poosari A, Promthet S, Kamsa-ard S, Suwanrungruang K, Longkul J, Wiangnon S. Hormonal contraceptive use and breast cancer in Thai women. J Epidemiol. 2014;24(3):216–20.
20. Hannaford PC, Selvaraj S, Elliott AM, Angus V, Iversen L, Lee AJ. Cancer risk among users of oral contraceptives: cohort data from the Royal  College of General Practitioner’s oral contraception study. BMJ. 2007 Sep;335(7621):651.
21. Charlton BM, Rich-Edwards JW, Colditz GA, Missmer SA, Rosner BA, Hankinson SE, et al. Oral contraceptive use and mortality after 36 years of follow-up in the Nurses’  Health Study: prospective cohort study. BMJ. 2014 Oct;349:g6356.
22. Vessey M, Yeates D, Flynn S. Factors affecting mortality in a large cohort study with special reference to  oral contraceptive use. Contraception. 2010 Sep;82(3):221–9.
23. Wingo PA, Austin H, Marchbanks PA, Whiteman MK, Hsia J, Mandel MG, et al. Oral contraceptives and the risk of death from breast cancer. Obstetrics and gynecology. 2007 Oct;110(4):793–800.
24. Familial breast cancer: collaborative reanalysis of individual data from 52  epidemiological studies including 58,209 women with breast cancer and 101,986 women without the disease. Lancet. 2001 Oct;358(9291):1389–99.
25. Marchbanks PA, McDonald JA, Wilson HG, Folger SG, Mandel MG, Daling JR, et al. Oral contraceptives and the risk of breast cancer. N Engl J Med. 2002 Jun;346(26):2025–32.
26. Gaffield ME, Culwell KR, Ravi A. Oral contraceptives and family history of breast cancer. Contraception. 2009 Oct;80(4):372–80.
27. Chen S, Parmigiani G. Meta-analysis of BRCA1 and BRCA2 penetrance. J Clin Oncol. 2007 Apr;25(11):1329–33.
28. Mavaddat N, Peock S, Frost D, Ellis S, Platte R, Fineberg E, et al. Cancer risks for BRCA1 and BRCA2 mutation carriers: results from prospective  analysis of EMBRACE. J Natl Cancer Inst. 2013 Jun;105(11):812–22.
29. Antoniou A, Pharoah PDP, Narod S, Risch HA, Eyfjord JE, Hopper JL, et al. Average risks of breast and ovarian cancer associated with BRCA1 or BRCA2  mutations detected in case Series unselected for family history: a combined analysis of 22 studies. Am J Hum Genet. 2003 May;72(5):1117–30.
30. Begg CB, Haile RW, Borg A, Malone KE, Concannon P, Thomas DC, et al. Variation of breast cancer risk among BRCA1/2 carriers. JAMA. 2008 Jan;299(2):194–201.
31. Gadducci A, Biglia N, Cosio S, Sismondi P, Genazzani AR. Gynaecologic challenging issues in the management of BRCA mutation carriers: oral  contraceptives, prophylactic salpingo-oophorectomy and hormone replacement therapy. Gynecol Endocrinol. 2010 Aug;26(8):568–77.
32. Cibula D, Gompel A, Mueck AO, La Vecchia C, Hannaford PC, Skouby SO, et al. Hormonal contraception and risk of cancer. Hum Reprod Update. 2010;16(6):631–50.
33. Davidson BA, Moorman PG. Risk-benefit assessment of the combined oral contraceptive pill in women with a  family history of female cancer. Expert Opin Drug Saf. 2014 Oct;13(10):1375–82.
34. Faculty of Sexual and Reproductive Healthcare (FSRH). FSRH Clinical Guideline: Combined Hormonal Contraception [Internet]. 2019 [cited 1BC Oct 13]. Available from: https://fsrh.org/standards-and-guidance/documents/combined-hormonal-contraception/
35. Trinh XB, Tjalma WAA, Makar AP, Buytaert G, Weyler J, van Dam PA. Use of the levonorgestrel-releasing intrauterine system in breast cancer  patients. Fertil Steril. 2008 Jul;90(1):17–22.
36. Romero SA, Young K, Hickey M, Su HI. Levonorgestrel intrauterine system for endometrial protection in women with  breast cancer on adjuvant tamoxifen. Cochrane Database Syst Rev. 2020.