Here's How That New Sex Pill for Women Actually Works

Illustration for article titled Here's How That New Sex Pill for Women Actually Works

Yesterday, the FDA voted to approve flibanserin, a new drug to treat women with hypoactive sexual desire disorder, or lack of desire for sex. The drug, marketed as Addyi, has been touted as “female Viagra,” in the sense that it helps bring sex back into these women’s lives. But flibanserin doesn’t actually work like Viagra.


Viagra, and drugs like it, act on the erectile tissue inside the penis, to increase blood flow in men with circulatory system problems. Men who use erectile dysfunction drugs don’t have a problem desiring sex; their bodies just don’t respond to that desire.

Women with HSDD–about 8-9% of women between the ages of 30 and 60–have a very different problem. There’s nothing physically wrong with their genitalia: they can become aroused and have intercourse, even orgasm, but they feel no motivation to have sex. For some reason scientists still don’t understand, the “desire circuits” inside their brain aren’t turning on, either for their partners or even for their own fantasies. Flibanserin, developed by Sprout Pharmaceuticals, acts on the brain, and claims to help some women turn those circuits back on. Here’s how it works.

The Neuroscience of Desire

Women with HSDD seem to experience erotic situations differently than women with normal sexual function.

Some researchers think this happens because they can’t easily dial down the activity of certain parts of the brain. One 2009 study of women with HSDD found that the parts of their brains that were responsible for monitoring internal emotional states were overactive when they watched erotic videos–as if their brains were focused on judging whether their reactions were appropriate, instead of living in the erotic moment. Flibanserin helps to change the balance of active circuits in the brain by acting on the neurons that are normally controlled by two neurotransmitters: serotonin and dopamine.

Neurotransmitters are the chemicals that neurons use to send signals to other neurons. They’re released after an electrical signal moves through a neuron: When the signal reaches the end of a neuron’s axon, it releases the chemicals into a tiny gap between neurons called the synaptic cleft. Neurotransmitters diffuse across the gap and latch onto specific receptors on the neighboring neuron. When neurotransmitters dock into receptors, they start chains of chemical reactions that can help get an electrical signal moving through the new neuron.


Or not. Neurons aren’t simple on/off switches. Some neurotransmitters excite the neurons they dock to and push them toward firing, but others damp down electrical reactions. Every neuron is constantly receiving both types of signals from its neighbors—and the sum of the signals determines whether the neuron fires or not. The interplay between excitatory and inhibitory signals is one of the things that makes brain function so complex, because it allows the same circuits to react differently to a variety of different situations.

Neurons can even change how they react to the neurotransmitters that are released by their neighbors, by adding or removing receptors for specific chemicals to their surface. A neuron can become more sensitive to dopamine, for example, by adding more dopamine receptors to its surface.


What’s more, each neurotransmitter can bind to a family of related receptors, and each one can be tied to a different set of chemical reactions. A neurotransmitter on one type of receptor can excite or depress the cell a different amount than if it was docked at a different receptor.

That distinction is important, because this new drug, flibanserin, can act on two different types of serotonin receptors. When it binds to a 5-HT1a receptor, it has the same affect as a serotonin molecule. But when it latches onto a 5-HT2a receptor, it blocks the normal effect of serotonin. Serotonin normally inhibits neurons, which means flibanserin tends to reduce neuron activity in areas rich in 5-HT1a receptors and increase it in neurons that have 5-HT2a receptors. Researchers assume that women with HSDD aren’t making enough serotonin in their brains in general, but flibanserin only mimics the neurotransmitter’s effect on one subset of neurons—the ones that have 5-HT1a receptors.


So Does It Really Work?

The net result? Flibanserin quiets neurons in a part of the brainstem called the dorsal raphe nucleus and the memory-and-emotion hippocampus—but it seems to have its strongest quieting effect on the cerebral cortex, where all that ‘self-judging’ activity is taking place.

Illustration for article titled Here's How That New Sex Pill for Women Actually Works

And because the brain is a network, changing the activity of one set of neurons can also change the behavior of the neurons in the rest of their circuit. The downstream effects of flibanserin aren’t entirely clear, but one study in rats showed that it can make neurons in the cortex release both noradrenaline and dopamine, neurotransmitters that typically kick motivation into gear. It’s possible that a rise in available dopamine, paired with the drug’s mild effects on one type of dopamine receptor, bumps up the activity of the brain’s reward circuits and makes the prospect of sex more exciting.


But the drug’s effects are subtle. This is not a miracle sex drug that makes women pant for more. In fact, because the drug’s main effect is to restore the brain’s ability to inhibit the parts of the brain that normally suppress ‘desire’ circuits, it won’t even work on most women—their inhibitory circuits work just fine, thank you. Flibanserin only works on HSDD sufferers who have low serotonin levels. And even for those women, Sprout Pharmaceuticals’ clinical trials have shown a complex and fairly modest effect.

And like any other drug that affects brain function, flibanserin can have side effects. According to Sprout Pharmaceuticals’ FDA briefing document, 9 to 11% of women taking the drug in the clinical trial experienced dizziness, fatigue, and nausea (as opposed to 2 to 5% of the women on a placebo). The drug can also interact with other substances that have a depressive effect on the brain, such as alcohol, and amplify their effect.


Earlier this year, the FDA’s advisory committee recommended approval of the drug, so long as it is tied to a risk evaluation and mitigation strategy (REMS) that helps doctors prescribe it correctly, and keep a close eye on any side effects. The FDA has now decided that flibanserin’s benefit for the subset of women it works on outweighs its side effects. It remains to be seen whether that group of women is large enough to recoup Sprout’s 50 million dollar investment in the drug.

[Borsini et al. 2002 | Cooper er al. 2003 | Jovanovic et al. 2008 | Montgomery 2008 | West et al. 2008 | Arnow et al. 2009 | Invernizzi et al. 2009 | Stahl et al. 2011 ]


This post originally appeared on Throb in June, 2015. It has been updated.

Top image AP Images. Body image Sprout Pharmaceuticals | FDA briefing document

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Okay. I’m seeing a few kinds of comments here. I dislike all of them. Here we go.


Men statistically have naturally higher libidos, and women have cultural pressure to be less horny. Do the math. Women, right now at this point in time and history, need more help having their brains let them have lots of sex, compared to men. Also, Viagra helps many men have the confidence to have more sex, since men have a huge issue with “oh shit my boner is going to deflate and then I will be humiliated.” Women don’t do the same thing per se, unless there is a massive fear of dryness (at which point some lube will do the trick easily, men don’t have an auto-boner device...except Viagra or a pump).


No, we’re addressing the actual pathology of having your mind just never *subconsciously* want a thing you *consciously* really really want. Compare this to “I want to be happy but my brain chemistry won’t let me so I’m depressed.” (And yes, I have chronic depression, yes, this is simplifying, don’t even bother pointing that out.) This pill is for women who want to desire and can’t manage it through non-pharmaceutical means, just like Viagra is for men who desire and their erections just don’t happen. I don’t see you telling thse guys that they’re not allowed to be unhappy with their level of boner. Also, as I have said in basically every thread ever about people being elitist over taking the easy way out...humans ALWAYS look for the easiest way out. If they want a pill to help themselves, why the fuck are you complaining? You use technology every day.


No. See above. If looking at your favorite hunk du jour or eating some chocolate or drinking a glass of wine would do it for you, you are not the group of women this pill is targeting. Again, it’s like Viagra in that effect — if you could get a boner by looking at a dirty mag, you don’t need Viagra.


So you’re going to kick the women who want this pill in the nads because you’re scared society’s men will go apeshit and start saying they’re only going to date their girlfriends any longer if their girlfriends jack up their libidos artificially to suit said men? Well, for one, this pill *can’t* do that, as it said before. It’s not a magic pill that makes you one step hornier than you were. Two, this is an awful view of men in general, damn, there’s such a thing as *compatibility* and men have enough of a brain to seek out someone with a compatible libido. Three, this is an awful view of women, because it implies women can’t dump their sorry asses and go find men that will accept them as they are fine being. If you don’t let science do a thing on the grounds that society may cause an issue, then science doesn’t get to do anything, because EVERYTHING causes issues. Humans are great at doing that.


Okay that would be an actual problem. Selling a product that doesn’t work sucks. Although, I expect that, like any other new drug type altogether, the first few products in this area won’t be that amazing. Like any branch of a tech tree, gotta start small, yeah?