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Artificial Afterglow:
How SSRIs Might Actually Work

Many of the most popular antidepressants—like Prozac, Zoloft, and Celexa—are classified as selective serotonin reuptake inhibitors, or SSRIs. In the nerve junctions of the brain where the neurotransmitter serotonin is released, it’s typically reabsorbed by nerve cells as a sort of feedback mechanism to regulate the amount present in the synaptic cleft—the space between two neurons. SSRIs act by decreasing this reabsorption of serotonin, which results in a net increase in the amount of serotonin in the cleft.

SSRIs aren’t just used to treat depression. They’re also prescribed for chronic anxiety, and to treat obsessive-compulsive disorder. However, they have significant side effects, the most frequently annoying of which are their sexual side effects. SSRIs typically decrease sexual desire, inhibit sexual arousal—and most frustrating of all, can stop you from being able to attain orgasm. All SSRIs seem to be equally problematic—these sexual effects seem to be tightly bound to their therapeutic benefits.

Over 20 years ago it occurred to me that this might not just be a coincidence, but rather a clue as to the therapeutic mechanism of these antidepressants. I’ve always been intrigued by the mechanism in which birth control pills work. For those of you who don’t know, the reason we don’t have a birth control pill for men is not because of sexism in the health industry—but rather because women happen to have a natural state of infertility, and men don’t. This state of infertility is pregnancy—when ovulation is suppressed by the body in order to preserve the endometrium of the uterus to nourish the fertilized egg that’s implanted there. Birth control pills contain the hormone that promotes gestation, i.e. progesterone—thus imitating the state of pregnancy.

I pondered the array of therapeutic benefits that SSRIs offered—improved mood, decreased anxiety, diminished obsession—and their peculiar sexual side effects, particularly inhibition of orgasm—and it seemed to me that this confluence of effects was more than coincidental. Then it dawned on me that there is in fact a natural state in which we humans exhibit all these phenomena—the refractory stage of sexual response, aka “afterglow.” You know what I mean (or I certainly hope you do)—that time after the act when we probably feel more relaxed, happy, and at peace with the world than any other time in our life. And I wondered if indeed serotonin might just mediate that phase of sexual response. But since that time I haven’t since heard that connection suggested in any psychiatric literature.

As you might expect, SSRIs have been found to exert their influence where serotonin is most prevalent in the brain—which is the raphe nuclei of the pons. This is located in the brainstem just north of the spinal cord—which is nowhere near the higher cognitive centers of the brain. The brainstem is the home of the limbic system, commonly referred to as “the lizard brain”—the seat of our primitive emotions, directing us to choose among any one of the “five F’s” of emotional response: “fight, flee, freeze, feed, or f**k.” And sure enough—along with the hormone prolactin, serotonin has indeed been implicated in mediating the refractory phase of sexual response.

The oldest citation I could find postulating this role of serotonin in sexual response was an archival article that’s currently posted on the website of the National Institute of Health. It’s an article that was first published in the British journal Behavioural Brain Research in 1984—3 years before the release of Prozac, the first SSRI, in 1987. It’s intriguing to me that Prozac was vigorously promoted, by Big Pharma and clinicians, using the unsubstantiated assumption that it was correcting some mythical “chemical imbalance” that was causing depression. For many years we psychiatrists held out hope for the development of an SSRI that didn’t cause these sexual side effects—when the evidence against this possibility was right before our eyes! Nowadays there’s a consensus among sexual response researchers that serotonin functions as a sort of hormonal “brake” applied to the process of orgasm, and that it may trigger release of the hormone prolactin. There is precious little evidence that serotonin has any other role in the control of mood—and numerous studies aimed at identifying any serotonin deficiency in the brains of chronically depressed individuals have failed to do so.

It’s worth noting that only 5% of the body’s serotonin is in the brain—the remaining 95% is in the gastrointestinal tract, where it is involved in the neurological regulation of digestion. This not only accounts for the GI side effects of SSRIs, but is also postulated to explain how we tend to feel our emotions in our guts, and how emotions affect GI function. Anyone who’s ever had a pet cat and moved from one residence to another can testify that this is not a peculiarly human phenomenon. This connection confirms the primitive origins of serotonergic responses, disengaged from the higher cognitive functions that almost certainly have a role in depression.

All this leads me to the conclusion that rather than correcting any underlying chemical imbalance in the brain, SSRIs probably act by creating a chemical imbalance that masks psychiatric symptoms, by triggering the instinctual psychological effects associated with postcoital afterglow—not unlike the way birth control pills trick the female reproductive system into thinking it’s pregnant. Unfortunately, these effects are not experienced with the intensity associated with actual post-orgasmic bliss—perhaps because of the endorphins that are released in intercourse during the plateau period prior to orgasm, and/or the prolactin that is released along with serotonin during the refractory period.

I can’t help but suspect that a whole lot of smart people have been playing dumb about the true nature of serotonin’s role in the brain for many, many years. The evidence of serotonin’s role in sexual response was in plain sight prior to their marketing campaign—so it seems to me that Big Pharma and academic psychiatry chose to pretend that they were fixing something that was broken, rather than acknowledging the likelihood that the efficacy of SSRIs was based on a cheap neurophysiological gimmick. Pursuit of a “healthy balance” is so much more marketable than manufacturing some instinctual delusion of wellbeing. I still prescribe these medications, but I don’t bullshit my patients into thinking that there’s any chemical imbalance to fix.

I am, however, unequivocally concerned about the overuse of antidepressants today. I’m thoroughly convinced that they have undesirable effects that need to be studied further—especially in long term use, and when prescribed to young people. But my overarching concern about antidepressants is the manner in which they are oversold and overutilized as an alternative to actual exploration of feelings and psychosocial stressors—in a manner that ignores the holistic value of sadness, and is dehumanizing to both my profession and its patients. I believe that the thoughtless manner in which antidepressants are used today is a cheap, lazy, and ultimately ineffective way to address the complexities of human existence—the cumulative result of modern psychiatry’s economic and scientific corruption, and a spiritually empty worldview.

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