Slap on a condom, get an irreversible snip, or abstain. For a sizable number of men, two of those three male contraceptive methods aren’t viable options. The good news is that several new developments aim to change that.
There’s the so-called "dry orgasm" or "clean sheets" pill, a combination of two drugs no longer on the market, phenoxybenzamine and thioridazine, which block the release of sperm while still allowing ejaculation. Researchers hope to eventually produce a pill that will be taken a few hours before sex, with effects that wear off after a day. Then there’s gamendazole, which stiffens sperm so they can’t reach the egg – think of it like trying to swim for land if you can’t bend any of your joints. Or JQ1, which puts the brakes on BDRT, needed for the production of sperm.
But why is nothing commercially available yet when birth-control pills for women have been around for so long? Halting the production of sperm is apparently quite a bit harder than stopping ovulation once a month. Pharmaceutical companies have also been reticent to pursue unpalatable, inconvenient (despite women using the very same methods) and therefore unprofitable treatments.
And some of the solutions proposed thus far turn out to be ineffective or just flat-out dangerous.
Whatever the reason, just be happy that this bar was set early: Any male contraceptive should be reversible, and have no adverse effect on libido or performance. In The Male Pill: A Biography of Technology in the Making, Nelly Oudshoorn quotes one wry medical-report writer in 1989: “Loss of libido and the inability to attain erection would obviously constitute an effective birth-control measure.” Stand down, sir. Anyhow, here’s a quick spin through some of the field’s flops.
Steroids (testosterone and progesterone), 1958
How it was supposed to work: In a similar manner to the female pill, hormones adjust the messages the body sends itself to produce sperm (or eggs, in the case of females).
Why it didn’t: Although it did shut down the spunk factories, the test subjects, prisoners at Oregon State Penitentiary, lost all sexual desire and had trouble getting it up and making (non-sperm-laced) semen. Research into hormone treatments continued, increasing in the 1990s as pharmaceutical companies got involved. See Norplant below.
Bis(dichloroacetyl) diamines, 1961
How it was supposed to work: Another study conducted at Oregon State Penitentiary (jeez) and published by Dr. Carl Heller found diamines stopped the production of sperm without affecting inmates’ horniness.
Why it didn’t: When tests were conducted on people who weren’t incarcerated, it transpired that they couldn’t hold their liquor—in other words, taking the pill with even half a beer made them violently sick. (Dr. Heller then went on to bake balls with radiation—what a guy).
How it was supposed to work: A 1929 study in China proposed a link between cooking with raw cotton-seed oil and infertility. The Chinese government (with the support of the World Health Organization) began a large-scale study of 10,000 men in 1972 and found that gossypol effectively stopped the creation of sperm.
Why it didn’t: There was the small problem of gossypol’s impact on our body’s ability to take in potassium (and we sort of need that). There were also toxicity issues and, oh yeah, a significant section of test subjects couldn’t get the baby-making factories back online again. Research continued, but the WHO kiboshed it in 1998.
How it was supposed to work: In 1992, Dr. Susan Benoff began to investigate a couple’s infertility problem, and reasoned it may have something to do with a drug the man was taking for high blood pressure. The patient switched medication, and the couple successfully conceived. The current understanding is that nifedipine hardens sperm, leaving it unable to fuse with an egg.
Why it didn’t: Put on your tin-foil hat before reading: It is claimed that further research was hampered by big pharma’s fear of lawsuits (infertility was a possible side effect) and a desire to retain the profitability of the blood-pressure drug. You may remove your tin-foil hat now. An unrelated study of a similar drug published in 1997 reported that two gents who took it didn’t shoot blanks and later became fathers.
Enzyme inhibitor, 1996
How it was supposed to work: Using a derivative of sugar, Dr. Joseph C. Hall “blinded” sperm by covering them in an sugary enzyme found on the layer of the egg. Once the sperm binds with the fake enzyme, it can’t penetrate the real thing.
Why it didn’t: Although the National Institutes of Health funded research in 2005, all is quiet on the sugar-pill front.
How it was supposed to work: Research on this existing medication, used to treat a genetic disease, found it caused abnormalities in mouse sperm but left little Mickey with a normal sperm count and undiminished libido. After doses were discontinued, everything went back to normal.
Why it didn’t: Further research concluded it did nothing to other mammals, including us.
Norplant (probably), 2002
How it was supposed to work: Amid the pharmaceutical industry’s apparent unwillingness to develop a commercially available male pill, Schering AG and Organon announced they were joining forces to produce a “male pill” to hit shelves in five to ten years. The trial drug was reportedly a variation of Norplant, found in the female pill, that scrambled the message the body sends to the testes to crank up sperm production.
Why it didn’t: Organon and Schering called off the partnership in 2006. As with most hormonal options, regular injections were needed to mitigate some of the side effects, and the pair thought it too onerous to catch on. The World Health Organization and other bodies have continued the research, so if you don’t mind numerous appointments with needles, there may still be hope.