Estrogen in birth control diminishes sex organs in male rats.

Jan 15, 2010

Mathews, E, TD Braden, CS Williams, JW Williams, O Bolden-Tiller and HO Goyal. 2009. Mal-development of the penis and loss of fertility in male rats treated neonatally with female contraceptive 17alpha-ethinyl estradiol (EE). A dose-response study and a comparative study with a known estrogenic teratogen diethylstilbestrol (DES). Toxicological Sciences 112(2):331-343.


A number of permanent oddities – such as deformed penises and smaller reproductive organs that were caused by exposure to the same estrogen found in birth control pills – contributed to the infertility seen in adult male rats exposed during the time when their reproductive organs were forming.

Recent animal research suggests that women who continue to take birth control pills well into pregnancy may unwittingly skew their boys' reproductive development in ways that could diminish their sons' fertility. Similarly, exposure to environmental chemicals that act like estrogen – such as certain pesticides and industrial chemicals, including bisphenol A – may also affect these organs if the exposure occurs during a sensitive time of development.

Researchers compared the effects of different levels of the estrogen used in birth control pills. Their results are published in the journal Toxicological Sciences.

They found that exposure to low levels of the hormone during development detrimentally affects the reproductive organs and fertility in the male rats tested. The rats have smaller testicles and other reproductive organs if  exposed to the low amount of estrogen a women may use daily in certain birth control pills. Testosterone hormone levels are also reduced. Exposure to just ten times that amount of estrogen permanently deforms penises and causes infertility in the adult animals.

This research is relevant to humans because more than 50 million women worldwide take contraceptive pills. Of those, 3 to 4 percent may take them into the second trimester of pregnancy, the authors say.

In one part of the study, researchers exposed newborn rats to the ethinyl estradiol (EE) – the main estrogen in birth controls pills – for the first week and a half of life. This time of development coincides to the first to second trimester of pregnancy in humans. These are the times when male reproductive organs form in both the rats and in people. The amount of estrogen the baby rats were exposed to varied from the amount a women would use for birth control up to the amount found in previous studies that caused male rat infertility due to severely deformed penises.

The rats have normal penis thickness, length and weight if exposed to estrogen levels found in typical birth control pills. Yet, when the rats are exposed to higher levels – 10 times, 100 times and 1,000 times higher – the penis and testicles are deformed and diminished. Penis thickness, length and weight decrease. Testicle weight decreases, and testicle descent takes longer than normal, which suggests sexual maturity may be delayed.

Sperm counts and fertility also decreased as the amount of birth control estrogen the rats were exposed to increased. At just 10 times the amount of estrogen found in birth control, sperm numbers fell and fertility decreased by 40 percent in male rats.

Researchers also compared male rats that were exposed to either EE or diethylstilbestrol (DES) – a synthetic estrogen drug that was given to pregnant women to help control morning sickness. The authors exposed the rodents to equal amounts of either EE or DES at doses known to deform male rat penises and make half infertile. The DES had similar effects on the rats as did EE – it decreased testicle weight and delayed descent and decreased penis weights, thickness and length. All of the males exposed to DES became infertile.

The results suggest that the kind of estrogen found in oral contraception is as toxic to male reproductive organs as is DES. DES was banned for use as a pharmaceutical in the early 1970s because it caused rare cancers and reproductive deformities in the children of the mothers who took the drug.

In the study, the authors report actual tissue weights, like testicle weight, and also report tissue weights relative to the body weights of the rats. Researchers often use this type of comparison to clarify that treatment-associated differences in tissue weight do not simply reflect differences in body weight. The weight of many male sexual tissues measured in the study decreased as exposure to birth control estrogen increased, in both absolute and relative weight terms. This consistency increases the strength of the study.

Though the penis size of rats is unchanged by exposure to birth control estrogen at doses seen in birth control bills, the fact that penis size decreases as levels of birth control increase is still concerning from a public health perspective.