Science 

Reinventing the Pill: Male Birth Control

In the late 1950s near Salem, Oregon, scientists started testing a birth control drug called WIN 18,446 in male prisoners. Men took responsibility for most birth control then, so a male contraceptive seemed a natural fit for American society. WIN 18,446 worked well, too: The prisoners felt fine and seemed quite healthy, except that their sperm was suddenly stunted and feeble. Unfortunately, when clinical trials shifted to the general population, men started getting sick—vomiting, sweating, headaches, blurry vision. They seemed poisoned. After some digging, scientists pinned down the culprit: alcohol. Because prisoners couldn't drink, no one had realized at first that WIN 18,446 did not mix well with liquor. The drug was abandoned, and 60 years later, no one has gotten any closer to the “male pill.”

WIN 18,446 is a perfect example of why creating the male pill is so hard. It did exactly what it was supposed to do—stopped sperm production in everyone who took it—and it was reversible. Sperm levels returned to normal after men stopped taking it. Yet it failed anyway as a drug because of an arguably minor side effect.

Male contraceptives are held to high standards partly because the calculus for male and female birth control is different. For example, taking the female pill increases a woman's chances of developing blood clots. But because pregnancy increases the chances of blood clots by 10 times more, the pill's side effects seem worth the risk. With men, there's no counterbalancing risk of pregnancy, so the tolerance for side effects drops to zero. That's especially true because “you're dealing with healthy people, not people with an illness, and you'd have to use [the pill] for long, long periods,” says Diana Blithe, a program director at the U.S. National Institute of Child Health and Human Development (NICHD) in Bethesda, Maryland, which funds research into male contraception

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Plugs. Hormones. Special underwear. Autoimmune attacks. The “dry orgasm.” There's no shortage of approaches to male contraception (see diagram, p. 319). But all share the same goal: slowing down the relentless proliferation of sperm in men and holding sperm counts to about 1 million per milliliter of ejaculate. Even the reduced concentration “may sound like a lot,” says John Amory, a doctor and reproductive biologist at the University of Washington, Seattle, “but that's a pretty good, effective contraceptive” that will reduce fertility by 99%.

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Still, the prize could be worth the risk. “Female oral contraception is one of the most important medicines ever developed,” Bradner says. The male counterpart could be in the same league worldwide, and the identification of testes-specific genes and enzymes makes scientists guardedly optimistic that the time for a safe, effective, targeted, and so on, male pill might be nigh. Blithe says: “To say it's a year off or 5 years off isn't accurate. [But] I suspect that if one gets out there, a lot more will follow.”