Female sexual dysfunction (FSD) is a medical condition affecting thousands of women. Women with FSD experience problems with sexual desire or response that can occur at any time in life. Several factors contribute to this condition, including physical, hormonal, and psychosocial. One common cause not often discussed is oral contraceptive pills (OCPs). OCPs have several known side effects, some of which can be life threatening. The hormonal changes induced by oral contraceptive pills can lead to female sexual dysfunction.
Female Sexual Dysfunction
Sexual desire and response in a woman is multifactorial, involving physiology, emotions, experiences, beliefs, lifestyle, and nature of relationships. Disruption of any of these components can affect sexual drive, arousal, or satisfaction. There is more than one type of female sexual dysfunction. Types include1:
- Low sexual desire. A diminished libido, or lack of sex drive.
- Sexual arousal disorder. The desire for sex might be intact, but there is difficulty or an inability to become aroused or maintain arousal during sexual activity.
- Orgasmic disorder. A persistent or recurrent difficulty in achieving orgasm after sufficient sexual arousal and ongoing stimulation.
- Sexual pain disorder. There is pain associated with sexual stimulation or vaginal contact.
The cause of female sexual dysfunction is often difficult to pinpoint, and more than one cause may be present. The health of a relationship, anxiety, depression, fatigue, insomnia, body image issues, and religious and cultural beliefs can all lead to issues with sexual function in women. Medical conditions play a role, especially physical conditions such as arthritis, urinary or bowel difficulties, pelvic surgery, headaches, pelvic pain, and neurological disorders. Medications contribute to FSD, as do hormones. Women often experience sexual problems postpartum, during perimenopause, and transitioning into menopause. One often overlooked link to FSD is the use of OCPs.
Oral Contraceptive Pills
Many patients and even physicians are not aware of the sexual side effects caused by hormonal contraceptives. A commonly used Web-based resource (UpToDate) does not mention mood or sexual side effects in its list of the adverse effects of oral contraception.2 Sexual and mood side effects are one of the main reasons that women discontinue the use of oral contraceptives (OCs).
In a prospective study of 76 women in stable committed relationships, 1 year after starting OCs, only 38% continued with the original brand of OCs, 47% had discontinued the medication, and 14% had switched to another OC. Emotional and sexual side effects were the best predictors of discontinuation and switching OCPs.3
The mechanism of how oral contraceptives affect sexual function are well documented. Combined oral contraceptives reduce levels of androgen, especially testosterone, by inhibiting ovarian and adrenal androgen synthesis and by increasing levels of sex hormone-binding globulin (SHBG). Recently a meta-analysis was performed to evaluate these effects on women. A total of 151 records were identified by systematic review and 42 studies with a total of 1495 healthy young women (aged 18–40 years) were included in the meta-analysis. Pooling of the results derived from all the included papers showed that total testosterone and free testosterone levels significantly decreased during combined estrogen plus progestin oral contraceptive use. Levels of SHBG significantly decreased.4 This study also differentiated between types of oral contraceptives and found that pills containing 20 to 25 µg ethynylestradiol (EE) had similar effects on total and free testosterone compared with OCPs with 30–35 µg EE. In addition, suppressive effects on testosterone levels were not different when comparing different types of progestins.4 However, there were differences in relation to the effect on SHBG. OCPs containing the older second-generation progestins verses the newer third- and fourth-generation progestins were found to have less impact on SHBG concentrations. Also, OCPs with lower estrogen doses (20–25 µg EE) compared with higher doses had less impact on SHBG concentrations.4 This study suggests that OCPs with lower amounts of EE (20–25 ug) and with second-generation progestins may have less an impact on androgen levels in women.
Low testosterone in women as a result of OCP use may in part contribute to female sexual dysfunction. Testosterone deficiency is associated with many undesired effects, including diminished well-being and quality of life, mood changes, loss of energy, cognitive disturbances, interference with optimal sexual function, declining muscle mass and strength, and lowering of bone mass and bone density.5
It is clear that oral contraceptives affect women's hormone levels, but do these changes lead to problems in sexual function? In regard to desire, studies are mixed. In fact, one study showed that, despite the changes to androgen levels, women who used OCPs had an increase in sexual desire.6 In this small study, 49 women were randomized into two groups to receive pills containing EE 30 mcg and levonorgestrel (LNG) 150 mcg or EE 20 mcg and LNG 100 mcg, for six cycles. Sexual function was assessed using a standardized questionnaire (Female Sexual Function Index [FSFI]). The results showed that the pill with EE30/LNG150 decreased plasma androgen levels, but there was no impairment in sexual desire; on the other hand, sexual desire score increased with in women taking the pill with EE20/LNG100.6
Another study using the same questionnaire had very different results. This study looked to investigate the relationship between oral contraception and female sexual dysfunction in female German medical students. This study did not measure androgen levels but looked at signs and symptoms of FSD in relation to OCP use. The FSFI was used, with additional questions on contraception, sexual activity, and other factors that may influence sexual function. 1086 questionnaires were included in the analyses after screening. The results showed that hormonal contraception was associated with lower total FSFI scores and lower desire and arousal scores than no contraception and nonhormonal contraception only.7
The majority of studies do indicate that women who use oral contraceptive pills have problems with sexual desire and libido. In a cross-sectional, community-based study of sexual function in Australian women, Davison and colleagues described that OC use was associated with a significantly lower incidence of sexual thoughts, interest, and days of sexual activity per month than reported by nonusers of OCPs.8 Female sexual dysfunction includes more than sexual desire and arousal problems. Pain with intercourse and changes to female sexual organs are part of FSD. Oral contraceptives also play a role in sexual pain disorders.
More Than Desire
In addition to the hypoactive sexual dysfunction discussed above, OCPs have also been associated with increased incidence of sexual pain disorders such as vulvar vestibulitis (VV), causing dyspareunia and vulvadynia. A study of 138 women showed that women who have ever used OCPs have a greater risk for developing VV than women who have never used OCPs. The likelihood of developing VV was highest in women with the longest duration of pill use and in those who initiated use of OCPs at a young age.9 The proposed mechanism linking OCPs and VV is the changes that OCPs induce in the vulva and vagina.
Oral contraceptive pills, through their interaction with hormone receptors in the vestibule, may alter the vulvar mucosa, which may in turn become more vulnerable to external exposures or irritants and eventually increase local inflammatory response, pain at touch, and dyspareunia.10 In a study of female OCP users, the labia major thickness and vaginal introitus tissue were evaluated along with sexual function via a questionnaire. After 3 months of using an OCP containing 30 µg EE and 3 mg drospirenone, the labia minora thickness and the vaginal introitus area significantly decreased in comparison with the baseline values. The OCP use decreased the number of acts of intercourse per week, and the frequency of orgasm during intercourse. Pain during intercourse worsened after OCP use as well.11
Other studies confirm the link between OCP and vulvadynia and dyspareunia. In a prospective study, Bazin et al. showed that women who started taking OCPs before age 17 were 11 times more likely to develop vestibulodynia than women who had never taken OCPs.12 A recently published case study in Sexual Medicine showed that 50 consecutive women developed vestibulodynia while taking OCPs. The women were treated by having them stop OCPs and by applying a compound that contained topical estrogen and testosterone to the vestibule. On average their vestibular pain dropped from 7.5 to 2 on a 10-point pain scale after 3 months of treatment. Although this was not a placebo-controlled study, the results are compelling enough to suspect that OCP use is linked to sexual pain disorders.13
Not all women who take oral contraceptives develop female sexual dysfunction, but many do and often go undiagnosed. Patients should be asked about sexual dysfunction during routine office visits. Clinicians should screen patients for depression and other medical conditions that might impact sexual function and address interpersonal issues such as relationship quality. For women who complain of pain with intercourse, clinicians should also complete a detailed physical examination to deterimine the exact location of pain. Other causes of sexual pain must be ruled out before assuming that the discomfort is related to OCPs. Women who believe that their OC has led to sexual dysfunction may benefit from a trial of another method of contraception.
Dr. Marchese is the author of 8 Weeks to Women's Wellness: The Detoxification Plan for Breast Cancer, Endometriosis, Infertility, and other Women's Health Conditions. She graduated from the National College of Naturopathic Medicine in 2002. She maintains a private practice in Phoenix, Arizona, and teaches gynecology and environmental medicine at Southwest College of Naturopathic Medicine. She lectures on topics related to women's health and environmental medicine throughout the US and Canada.
1. Female sexual dysfunction [Web page]. Mayo Clinic. http://www.mayoclinic.org/diseases-conditions/female-sexual-dysfunction/basics/definition/con-20027721. Accessed December 26, 2014.
2. UpToDate [website]. Waltham, MA: UpToDate Inc; 2000. www.uptodate.com. Accessed December 26, 2014.
3. Sanders SA et al. A prospective study of the effects of oral contraceptives on sexuality and well-being and their relationship to discontinuation. Contraception 2001;64(1):51–58.
4. Zimmerman Y et al. The effect of combined oral contraception on testosterone levels in healthy women: a systematic review and meta-analysis. Hum Reprod Update 2014;20(1):76–105.
5. Traish A, Guay AT, Spark RF. The Testosterone Therapy in Women Study Group. Are the Endocrine Society's clinical practice guidelines on androgen therapy in women misguided? A commentary. J Sex Med. 2007;4:1223–1235.
6. Strufaldi R et al. Effects of two combined hormonal contraceptives with the same composition and different doses on female sexual function and plasma androgen levels. Contraception. 2010;82(2):147–154.
7. Wallwiener CW et al. Prevalence of sexual dysfunction and impact of contraception in female German medical students. J Sex Med. 2010;7:2139–2148.
8. Davison SL, Bell RJ, LaChina M, Holden SL, Davis SR. Sexual function in well women: stratification by sexual satisfaction, hormone use, and menopause status. J Sex Med. 2008;5(5):1214–1222.
9. Bouchard C et al. Use of oral contraceptive pills and vulvar vestibulitis: a case-control study. Am J Epidemiol. 2002;156(3):254–261.
10. Keller JM, Gaba ND. Sexual function and oral contraceptives. Female Patient. 2010;35:28–32.
11. Battaglia C et al. Sexual behavior and oral contraception: a pilot study. J Sex Med. 2012 Feb;9(2):550–557.
12. Bazin S et al. Vulvar vestibulitis syndrome: an exploratory case-control study. Obstet Gynecol. 1994;83:47–50.
13. Burrows LJ, Goldstein A. The treatment of vestibulodynia with topical estradiol and testosterone. Sex Med. 2013;1:30–33.