Of the advances in medical science, the ongoing quest to develop a male contraceptive pill is perhaps the most persistent. Unfortunately, many of the efforts have simply led to loose ends. Now, researchers from the University of Melbourne and the University of Leicester have collaborated on a study that they suggest could feasibly lead to the world’s first pill for men.

What makes this study unique compared to prior attempts is its treatment of the male’s sperm. Where others have sought to inhibit the sperm’s fertilization with the egg, or more popularly, destroy sperm altogether with a cocktail of hormones, the present study involves some logistical mix of the two. Scientists discovered that two key proteins along the smooth muscle cells, α1A-adrenoceptor and P2X1-purinoceptor, which mediate sperm transport, made the sperm’s “launch” during ejaculation impossible.

"Previous strategies have focused on hormonal targets or mechanisms that produce dysfunctional sperm incapable of fertilization,” said study researcher Dr. Sab Ventura in a statement, “but they often interfere with male sexual activity and cause long term irreversible effects on fertility.”

Blocking the triggering transport system in mice models could enable scientists to develop contraceptive options for men that bypass hormone treatments. These methods often employ a combination of testosterone and desogestrel, a synthetic steroid found in the female pill, which temporarily inhibits sperm production. The problem, frequently, is that hormonal options can create feelings of moodiness, depression, and even loss of sex drive.

The latest research claims to have avoided such side-effects with short-term infertility and long-term health of the sperm. "We've shown that simultaneously disrupting the two proteins that control the transport of sperm during ejaculation causes complete male infertility,” Ventura said, “but without affecting the long-term viability of sperm or the sexual or general health of males. The sperm is effectively there, but the muscle is just not receiving the chemical message to move it.”

The cycle of research bubbling up, appearing hopeful, only to flat line later has made some people skeptical of new innovations. One of these skeptics is the father of the female version of the pill, himself, the eminent Stanford University chemist, Dr. Carl Djerassi. Djerassi noted in an essay for Wired in early November that he believes the male version of the pill is all but a fantasy.

He wrote:

A young woman will not ask whether continued use of her Pill would affect her fertility at 45 or 50, whereas many 20-year-old men would require a guaranteed answer. To provide an epidemiologically valid answer to a young man would be expensive, time-consuming (thus cannibalizing most of the potential patent life) and open to lawsuits, since men may blame their Pill for age-related erectile dysfunction and prostate-gland problems.

Despite Djerassi’s speculations, a 2005 survey suggests the demand is there. Some 55 percent of more than 9,000 male respondents on four continents said they’d be receptive to male fertility control (MFC). The one caveat researchers mentioned, however, was that such decisions are often made jointly between partners. And if they’re made by one person, it will often be the female. “This strong influence of females with regard to contraceptive choices,” the researchers conclude, “requires that the attitudes of women toward contraception in general, and MFC in particular, be more explicitly assessed in future studies of this nature.”

In the meantime, Ventura suggests the next avenue for exploration is developing the pill itself, given the immense success he and his colleague observed in their mice models. "This suggests a therapeutic target for male contraception,” he said. “The next step is to look at developing an oral male contraceptive drug, which is effective, safe, and readily reversible."


Source: White C, Choong Y, Short J. Male contraception via simultaneous knockout of α1A-adrenoceptor and P2X1-purinoceptors in mice. PNAS. 2013.