Women have been popping pills for years to prevent them from getting knocked up, and for almost as many years there have been attempts at coming up with an equivalent for men. Even though a recent breakthrough show promises, challenges up ahead are yet to be bested.
The latest research on mice shows that it’s possible to prevent males from ejaculating, but translating this discovery to a pill for human males would require years of further testing for safety and effectiveness.
Compared with female birth control, the male version is somewhat of a biological challenge. Rather than stopping one single egg, male birth control would have to block each of the 1,500 sperm cells men produce every second.
Earlier tests with hormones have proven to be clumsy and causing too many side effects. Attempts at halting the rapid production of sperm is just as difficult, in part because a natural barrier between the blood and the testis, the area where sperm is produced, keeps drugs out.
Temporarily ending this process is just half the battle, though. The other half is making sure that the method finally used is reversible, and without long-term damage to sperm cells.
Scientists at the Sabatino Ventura of Monash University in Australia have taken a different route: Instead of blocking the production of sperm, researchers are now trying to block its transport.
When a man ejaculates, smooth muscle propels the sperm out of the epididymis through a tube called the vas deferens, into the urethra and out of the body. The muscle is controlled by hormonal signals that tell the muscles to expel the sperm from the body.
These receptors, known as 1A-adrenoceptors and P2X1-purinoceptors, have been successfully blocked in the past, but the method used led to decreased male fertility, but not entirely. Male mice with blocked receptors could still father offspring about half the time.
Older studies focused on blocking one of the two receptors, which may have caused the unblocked receptor to be beefed up to compensate.
In the new study, the researchers bred mice that lacked both 1A-adrenoceptors and P2X1-purinoceptros. Female mice could still reproduce as normal. Males pursued the females and mated as usual but it never led to babies.
The males were producing sperm that was viable for artificial insemination, but the muscle responsible for ejecting sperm was not contracting, as it should, suggesting that the lack of receptors stopped ejaculation.
This discovery may lead to a future pill that would block both receptors, and possibly put an end to the discussion of who will sleep on the wet spot.