The Male Pill: Are We There Yet?
Condoms. The Pill. Implanon. IUD’s. Diaphragms. Contraceptive injections. Vaginal rings. Sterilisation.
We women really are spoiled for choice.
Contraception is, for many women in heterosexual relationships, an everyday part of life. Whether it’s setting a daily alarm for your pill, or squeezing a condom over a banana in 9th grade, we’ve all crossed paths with it at least once. And we’ve all probably pondered the same thing: Why women?
The male pill is something that crops up in the media every now and then. We’ve all seen the headlines: “Scientists one step closer to Male Birth Control!” And we’ve all probably thought: Jeez, they do seem to be taking their time with it, don’t they?
The First Attempt
Believe it or not, the first attempt at a male pill occurred in the late 1950s. The drug was named WIN 18,446 (catchy, right?) and was tested initially on male prisoners (Look, it was the 1950s). There seemed to be no side effects. Better yet, it was totally reversible. Success, right?
When tested on the general population, men were hit with a wave of sweating, vomiting, headaches and even blurred vision. The problem? Prisoners aren’t allowed alcohol. Something in WIN 18,446 reacted with alcohol consumed by the general population, and so the drug was dropped. 60 years later, we’re finally starting to try again.
Halting Sperm in their Tracks
It’s 2013. “What does the Fox Say” is blasting on the radio. “Twerk” has been added to the dictionary. I have braces. Scientists are deleting rat genes to make them infertile.
A team at Monash University felt that the problem with making male birth control was that researchers were targeting hormones – which can open up a whole world of side effects. Instead of halting sperm production, they sought a different route – halting sperm in their tracks.
Quite literally, the aim was to block sperm transport. During ejaculation, sperm is propelled by the vas deferens. Smooth muscle cells around the vas deferens contract due to activation of (bear with me here) P2X1-purinoceptor ligand-gated channels and (good grief) α1A-adrenergic G protein-coupled receptors. Let’s just call them channels and adrenoreceptors.
They thought that by knocking out the channels and adrenoreceptors through deleting genes, they could render male rats infertile. However, there was hesitation – the same receptors and channels occur throughout the body, and help control blood pressure homeostasis.
Surprisingly, knocking out the channels and receptors rendered the male rats 100% infertile, and with no side effects. Sperm still functioned normally, but could not be transported outside the body. The rats did not appear negatively affected in any way, and demonstrated normal sexual behaviour, including – yes, this is from a real scientific article – “pelvic thrusting with appropriate vigour.”
The study opens up avenues to non-hormonal treatments. Even better, a blocker for adrenoreceptors already exists – it’s called tamsulosin, and is used to treat chronic prostatitis. This means that only a safe means off blocking the channels is required.
A Real Pain in the Butt
Perhaps in 2016 you remember scrolling past a headline about contraceptive injections. This was a study that started recruiting participants back in 2012, and its main goal was to hormonally suppress spermatogenesis – the formation of sperm. For up to 26 weeks, men received 2 gluteal injections every 8 weeks, of hormones aimed to reduce sperm count.
The men in the study had to have a normal sperm count, have been in a monogamous relationship with a woman for at least a year and – importantly – have no intention of ending the relationship during the study. Not only would that be awkward for everyone involved, but it’d mess with the results.
Semen samples were provided at 8 and 12 weeks, and then fortnightly. The threshold for infertility was 1 million/ml. Yes, that still seems like a dangerous amount to me, but to be fair, it’s a lot less than the 1.2 billion usually released during ejaculation. Once sperm count was below 1 million/ml, the real test of the study came into play.
The couples were asked to rely solely on the injections for birth control.
The results? Four out of 266 couples fell pregnant. BUT, when you do the maths, that’s a success rate of 98.5% – the female pill has a success rate of 99% (when used correctly). Unfortunately, there were side effects, so much so that they had to stop recruiting participants. These side effects included mood disorders and depression, decreased libido, acne, muscle pain, and in one case, an increased heart rate following the injection.
Effective contraception? Technically. But perhaps injections aren’t the way to go.
Where are we now?
It was March of 2019 when a potential male birth control pill passed safety tests. The pill is called 11-beta-methyl-19-nortestosterone dodecylcarbonate (ok, this is just getting ridiculous).
The pill mimics progesterone and testosterone throughout the body, reducing the side effects of low testosterone, but doesn’t provide enough testosterone in the testes to support spermatogenesis. The goal? Reduce sperm production but maintain libido.
Participants did, of course, experience some side effects that many women are already familiar with– fatigue, acne, headaches, a slight decrease in sex drive, and a few had mild erectile dysfunction. But notably, no participant stopped taking it and the safety tests were all passed. The next step is larger studies on sexually active couples.
We’re getting closer and closer with each study. A male pill could be available in as little as 10 years. In the meantime, women will keep swallowing our pills, inserting painful devices into our cervixes, and weird rods into our arms, waiting for the day we can finally remind the men in our lives, “Honey, don’t forget to take your pill.”