The male version of the birth control pill could contain something other than hormones.
Equality for men may be on the horizon, contraceptive equality, that is. For just over a half century, women have been able to pop a pill to prevent pregnancy, but a pharmaceutical alternative has never emerged for men.
Now, research to interfere with the body's ability to use vitamin A is showing some promise, because, in men, vitamin A is necessary for the production of sperm.
One recent study found that a compound that interferes with the body's ability to use vitamin A rendered male mice sterile while they were receiving 8- or 16-week courses. But once the mice were taken off the compound, they resumed making sperm. Significantly, the researchers found no side effects, and the testosterone levels of the mice stayed normal, meaning no fluctuations in mousey libido.
"Our mice, they mate quite happily, so that is not something we have interfered with," said Debra Wolgemuth, one of the study researchers and a professor of genetics and development at Columbia University Medical Center. [Top 10 Aphrodisiacs]
The female birth control pill uses hormones — chemical signals — to short circuit the release of a mature egg, known as ovulation. A similar approach can work in men, using hormones like progestins and testosterone, to suppress the production of sperm.
Although effective techniques have been developed, none have received approval by the Federal Drug Administration, according to Diana Blithe, a program director for contraceptive development at the Eunice Kennedy Shriver National Institute for Child Health and Human Development.
"The reality is we could get a product out there very quickly if companies would aggressively take on the process of making it happen," she said.
Hormones don't suppress sperm production in a small number of men; however, these men could easily be identified and advised to use a different method, she said [5 Myths About the Male Body]
Some researchers, like Wolgemuth and her colleagues at Columbia, are exploring nonhormonal methods to interfere with the production or function of sperm.
When you consume vitamin A, your body converts it into the metabollically active form, retinoic acid, which binds to a protein in your cells called a retinoic acid receptor. Then, the receptor protein can initiate the expression of genes necessary for the creation of sperm, if you are a man.
The compound Wolgemuth's team tested blocks the retinoic acid from binding to the receptor and so prevents the formation of new sperm.
"The long and short of what we know is vitamin A and its metabolite are absolutely essential for the production of male germ cells, or sperm," she said.
A high bar
Other research is looking at ways to use this pathway to render men temporarily sterile. Dr. John Amory, a professor of medicine at the University of Washington, has been working with a drug that interferes with the action of an enzyme that converts vitamin A to its biologically active form in the testis.
One of the barriers to the development of a pharmaceutical contraceptive for men is a high bar for safety, according to Amory.
"For women the small risks of birth control have been always been justified by the larger risk of pregnancy or unintended pregnancy," he said. For instance, hormonal contraception carries a risk of blood clots that is dwarfed by the risk created by pregnancy.
"You can't use the same justification for a male contraceptive," he said.
The work by the team from Columbia supports the idea that interfering with the retinoic acid pathway can render male animals temporarily sterile, he said. Even though side effects have yet to show up in their work with the compound, he said: "The concern I have as a clinician about their approach is retinoic acid has multiple functions in multiple tissues so blocking the activity by blocking the receptor, I have concerns that could cause side effects."
Retinoic acid is important for vision, a healthy immune system and other functions.
The Columbia team's latest work is scheduled for presentation today (June 4) at the conference for endocrinologists, ENDO 2011, in Boston.