In the 2004 film, Eternal Sunshine of the Spotless Mind, a heartbroken man played by Jim Carrey undergoes an experimental treatment to erase memories of his ex-girlfriend, played by Kate Winslet, following their painful breakup. When the film came out, using drugs or other technologies to meddle with memory, especially as a way of healing from a traumatic relationship, was not exactly feasible in the real world.
Early this year, though, a real-life technique for memory modification in response to heartbreak hit the newsstands. The coverage centered on Alain Brunet, a psychiatrist and expert in post-traumatic stress disorder at McGill University in Montreal, Canada. In his lab, Brunet works with victims of what he calls “romantic betrayals.” These can range from harassment by a former lover to sudden abandonment by a long-term partner. He uses a technique known as reconsolidation therapy, which combines a drug-based treatment with practical exercises to change the emotional content of disturbing recollections. “We don’t treat the symptoms,” Brunet says of his method, “we treat the memory.”
Unlike the fictional staff of Lacuna, Inc., the memory-erasure firm in Eternal Sunshine of the Spotless Mind, Brunet and his collaborators stop short of trying to “delete” traumatic memories altogether. “You don’t forget your memory,” Brunet stresses, asking, “Who would want to forget their love story?” Rather, the goal of the therapy is to keep the memory intact while removing its traumatic aspects. Here is how this works:
An hour before a therapy session, the patient is given a dose—between 50 mg and 80 mg—of a beta-blocker called propranolol, and is asked to write a summary of the traumatic experience, following a strict format: a first-person text in the present tense that describes at least five physical sensations felt at the time of the event. By reading the summary out loud, the patient “reactivates” the memory, and does so over four to six weekly sessions, under the influence of propranolol. At every reading, the memory is “recorded again” while the drug suppresses the pain it contains.
The therapy has a good success rate. More than 70 percent of participants in a 2018 study conducted by Brunet and his colleagues reported meaningful relief from their breakup-related stress. Following treatment, many patients said reading through the details of their memory felt like “reading a novel.” In other words, the narrative remained, but the pain was gone.
Love and heartbreak often go together. Sometimes, the suffering that comes with the end of a relationship helps us grow. It can force us to slow down, reflect on what happened, and learn to avoid repeating past mistakes. But other times, the suffering just crushes our soul. The pain becomes too much to bear, and it prevents us from moving on with our lives or opening ourselves up to positive relationships.
If we can use the tools of medicine, including drugs and psychotherapy, to treat the trauma of a broken heart—could we use it to cure ourselves of unrequited love or a love gone bad?
According to the philosopher Carrie Jenkins, love has a “dual nature.” One aspect is psychosocial: love as we experience it, subjectively, within a particular cultural and historical context. This is where art, literature, music, philosophy, and poetry shed light on love. The other aspect is biological: Love as it is rooted in our animal nature, emerging from the mating and bonding mechanisms that drive our species to reproduce. Science can help us make sense of this dimension.
Modern neuroscience traces the biological side of love to the brain specifically. In 2008, one of us (Julian) along with our good friend and colleague Anders Sandberg, published the first-ever discussion of the science and ethics of chemically enhanced love and relationships. This account focused on the potential use of biochemistry to help maintain a good and worthwhile relationship that might otherwise needlessly break down. The following year, writing in Nature, the neurobiologist Larry Young raised the possibility of pushing love in the opposite direction with a chemical cure.
As Young sees it, love is essentially “a cocktail of ancient neuropeptides and neurotransmitters.” He argues that “drugs that manipulate brain systems at whim to enhance or diminish our love for one another may not be far away.” Although we agree with Young’s general point, we think it would be better to say that the biological dimension of love is an emergent property of an ancient chemical cocktail, whereas the psychosocial dimension of love emerges from practices, cultural norms, and institutions embedded in societies. With this clarification in mind, what kinds of drugs could be added to the biological cocktail to bring about the effects Young speaks of?
To make sense of the different options, let’s organize them around three distinct brain systems that some researchers argue form the biological building blocks of romantic love: lust, attraction, and attachment. Each of these is thought to serve a different evolutionary purpose, and each can (and does) function somewhat independently in humans and other mammals.
Drugs acting on the lust system are already available. They include antidepressant medications, androgen blockers, and oral naltrexone. We can also add a few household examples, namely tobacco and alcohol. And then there is a range of other drugs with libido-weakening effects among their potential outcomes. These include almost all blood pressure pills, pain relievers containing butalbital as well as opiates such as morphine and hydrocodone, statin cholesterol drugs, certain acid blockers used to treat heartburn, the hair loss drug finasteride, and seizure medications including gabapentin and phenytoin. With the exception of androgen-reducing drugs used specifically for chemical castration (sometimes applied to serious sex offenders), the negative effects of these substances on a person’s sex drive are typically neither intended nor desired. Yet that doesn’t have to be the case.
It’s a real-life technique for memory modification in response to heartbreak.
What is the mechanism of these drugs? Basically, it is regulation of testosterone. Focusing on this hormone as one important biological factor behind sexual desire and behavior, a number of studies have measured the effects of reducing testosterone on problematic sexual thoughts or activities—mostly in men—such as intrusive erotic fantasies or compulsive exhibitionism (like flashing random strangers in the park). One study, for example, reported that cutting testosterone levels led to a reduction in pedophilic sexual fantasies and urges among some men. Likewise, the neuroscientist Till Amelung looked at the combined effects of androgen deprivation therapy and group psychotherapy on a small sample of “self-identifying, help-seeking pedophiles,” and reported a reduction of inappropriate sexual behaviors, an increase of risk awareness and self-control, and a dampening of thoughts that tend to correlate with pedophilic actions.
Side effects are a huge problem with these drugs. In one study, antiandrogen drugs were given to hospitalized patients struggling with a range of paraphilic conditions. These included pedophilia, voyeurism, public masturbation, compulsive hiring of prostitutes (or sex workers) and use of peep shows, “tendency to commit rape,” and unwanted masochistic desires. The researchers reported positive outcomes in a number of cases and concluded that one of the drugs they used “shows promise as a treatment for paraphilias.” But complications occurred in each of the 12 cases described: one patient experienced nausea and vomiting; some lost the ability to ejaculate or have an erection altogether; others showed a complete absence of sexual feeling or interest and became severely depressed; and every patient subjected to prolonged treatment suffered bone mineral density loss, putting them at risk for osteoporosis.
Another problem with anti-androgen drugs is that their effect on a person’s libido is typically global rather than selective. Imagine that you wanted to reduce only harmful or ill-directed lust—toward a prepubescent child, for example, or an adult who was tempting you away from your well-considered monogamous commitment. You would likely be disappointed. Current biotechnology is not sensitive enough to reliably deliver on these sorts of person-specific goals.
Anti-attraction drugs are a bit trickier. For one thing, interventions into the attraction system are less studied than those that primarily affect libido. Some blunt chemical instruments currently exist, but the nature of what makes a partner attractive in the first place is little understood and is likely to be highly variable. Insofar as they could be shown to work, anti-attraction drugs would probably reduce the obsessive thoughts characteristic of early-stage romantic relationships, or the chance that an initial spark of attraction would lead to longer-term attachment.
Donatella Marazziti is an Italian neuroscientist based at the University of Pisa. She has been trying to find out whether serotonin might play a role in early-stage romantic attraction. Her hunch came from observing that this all-consuming period, characterized by obsessive thought patterns and nervous preoccupation with the tiniest of details (similar to what can happen with jealousy as well), might have more than a passing resemblance to obsessive-compulsive disorder, or OCD, which has already been linked to low levels of serotonin. The idea was that the “same lack of serotonin that results in an OCD patient’s believing that touching a door five times upon entering can guarantee safety may also be behind the way you constantly, compulsively think about a new squeeze when you are in the honeymoon phase of a relationship.”
As she predicted, participants who had recently fallen in love—still in the intense first stage of a relationship but prior to having sex—had levels of serotonin similar to those of a sample of OCD patients, both groups having lower levels than healthy controls. As Marazziti and her coauthors conclude, “It would suggest that being in love literally induces a state which is not normal.” Indeed, retesting the lovers at 12 to 18 months revealed that serotonin levels had returned to baseline, at which point their “obsessive ideation regarding the partner” had disappeared as well.
Given the findings of Marazziti and colleagues, one possibility is that drugs used to treat OCD could dampen at least the obsessive aspects of a nascent amorous relationship. As it happens, patients with OCD respond most reliably to selective serotonin reuptake inhibitors (SSRIs), that same class of antidepressants whose ability to diminish the sex drive is now well known. SSRIs can also sometimes lead to “emotional blunting” of higher-level feelings involved in romantic attraction and relationships generally: 80 percent of SSRI-using patients in one study “reported less ability to cry, worry, become angry or care about others’ feelings.”
Again, if you’re trying to maintain a relationship, not caring about your partner’s feelings is a lousy idea. If you’re trying to end a relationship or keep it from developing into something more, however, maybe this type of treatment could grease the wheels.
Finally, anti-attachment interventions. There isn’t a whole lot of concrete evidence that existing technologies could completely sever a long-term human pair bond, although breakdowns in attachment obviously happen on their own all the time (just ask anyone who has gotten over their ex). There is, however, compelling evidence for such a possibility in other mammals with analogous mating habits—namely, voles. Studies have shown that injecting the brain chemical oxytocin, which is crucial to forming the attachment bond between parents and their infants as well as between adult mating partners, could foster a pair bond in at least one species of vole without any actual mating. And crucially for our purposes, this kind of effect could be reversed.
In one study, injecting female prairie voles with either an oxytocin or a dopamine blocker caused them to lose their monogamous tendencies; that is, they failed to show any partner preference as a function of copulation. As Larry Young put it: “They will not bond no matter how many times they mate with a male or how hard he tries to bond. They mate, it feels really good, and they move on if another male comes along.” Likewise, pair-bonded male prairie voles injected with a dopamine blocker—at a specific site in the brain known as the nucleus accumbens—failed to show characteristic mate-guarding behaviors and became more receptive to interactions with novel females.
Being in love literally induces a state which is not normal.
Most scientists who study human attachment believe that something like the prairie-vole bonding mechanism is preserved in mammals over evolutionary time and shows up in our species as well. Nevertheless, we are not aware of any scientists who have injected blockers for oxytocin, dopamine, or any other neurochemical into the brains of human subjects to find out what happens to their romantic attachments. Not only would this be hard to justify to a university ethics committee; it would also presumably not inspire many volunteers.
There may be a way around this scientific hurdle. Consider a 2019 headline from VICE magazine: “How to Bio-Hack Your Brain to Have Sex Without Getting Emotionally Attached.” The author, Sirin Kale, writes about an “an all-too-familiar situation for many people: You decide to have sex with someone whose personality you find repugnant, whom you have no interest in dating, only to find yourself bizarrely attached to them in the morning.” Now, one thing you could do to avoid this situation is to think twice about going to bed with someone whose personality repulses you. But suppose it’s too late for that, and you’re already deep in the ardent throes of your dubious decision. Can you somehow immunize your brain against its own tendency to form a sex-based emotional attachment?
According to Young, you can. The trick is to avoid eye contact with your partner during sex. Research shows that prolonged eye contact causes the release of oxytocin in the brain; this, in turn, increases the chance of forming a bond. “When you’re having sex with someone,” Young explains, “you’re making an intimate connection with their face and eyes particularly. This is going into your brain, and it’s inherently rewarding. Love and attachment are very much like addiction. They have a lot of the same chemicals. So if you can divert that information from coming in by not having that eye contact, that will help.”
Certain illicit drugs may “help” as well. According to Young, cocaine and methamphetamine boost dopamine secretion, which is also involved in pair bond formation. If you take a drug to raise your dopamine levels “prior to an intimate moment,” he says, “it won’t have the same impact later. The specialness of the sex, and the differential caused by the dopamine release won’t be so high.”
People are afraid of pathologizing love and relationships.
Finally, alcohol can foster attachment-free sex (which might be one of the reasons why they often go together). But the disruptive effect of alcohol on pair bonding seems to be different for males and females. At least, that is how it seems in the case of voles. “When male voles drink alcohol they become promiscuous and it prevents them from bonding,” Young says. For female voles, it is exactly the opposite. Alcohol “increases the likelihood they will bond prematurely.” Voles in the wild are not usually big on alcohol. So you can guess that these findings come from a lab.
Another, more speculative lead for an attachment-dissolving intervention comes from a medical condition known as Capgras’s delusion. In this tragic delusion, an individual reports believing that a spouse, sibling, or close friend has been replaced by an impostor who shares identical visual features. Patients suffering from this condition are able to recognize faces, but the automatic emotional connection to familiar faces that most of us experience just doesn’t come online. That lack of emotional connection leads to the belief that the person must be an imposter.
One explanation for this phenomenon is that neuroanatomical pathways responsible for responding to familiar visual stimuli have become damaged or degraded. This account fits nicely with the oxytocin-dopamine model of attachment, which involves combining social-identity cues (such as the physical features of a person) with a network of positive emotions.
Anti-attachment interventions of the future, then, might mirror the Capgras syndrome—ideally without inducing its delusive aspects—by interfering with this integration in a targeted way.
Taken together, these findings suggest that it may soon be possible to block or diminish lust, attraction, and/or attachment using pharmacological strategies. In fact, it is already possible to achieve some of these effects, if in a blunt and haphazard way. One question this raises, then, is whether these current, messy drugs should ever be used to affect relationships, notwithstanding the risk of various side effects and the fact that most of these uses would be off-label.
The ethics of prescribing drugs off-label is tricky. Sometimes the evidence concerning appropriate doses, benefits, and risks has changed since the manufacturer’s label was finalized. If you’re prescribing a drug for the purpose it was originally intended for, in a way that is consistent with the best available evidence, and the evidence just happens to have changed since the label was printed, hardly anyone would seriously object.
On the other hand, if you’re prescribing a drug for a purpose it was not originally intended for, the most likely scenario is that there won’t be enough high-quality evidence concerning the effects of the drug for that use. You might then be exposing the patient to unknown harms, which weighs against the practice.
However, the drugs we currently use for individualized symptoms are already affecting our relationships, but in ways and under conditions about which we are mostly clueless, because the evidence base consists primarily of case studies and anecdotes. Sure, you can approach treatment for someone dealing with extreme jealousy, as one psychiatrist reportedly did, “as if” the patient had OCD—and cross your fingers that he stops haranguing his wife. So long as you have a plausible on-label use for the drug that just happens to be associated with a person’s relationship difficulties, you are probably good to go. But we should be going about this in a much more cautious, scientific way.
Why aren’t we? What’s stopping us from deliberately researching the interpersonal effects of common medications, both good and bad? One reason is that people are afraid of pathologizing love and relationships. Since doctors are only allowed to prescribe drugs that society regards as medicine, and since medicine is typically used to treat patients who have some kind of disease or disorder, the fear is that prescribing a drug to help someone’s intimate relationship would imply that the relationship is pathological—when maybe it’s just down to hard times.
This fear is understandable given the current paradigm. But the paradigm needs to change. Drugs are just chemicals. You can call them medicine, but chemicals don’t know if you have a disease they’re supposed to be treating (so that they can somehow confine themselves to acting only within the definition of that disease). Instead, they just do whatever they do, whether you intended them as a cure for a pathology or just believe they could improve your life.
We should be open to the idea that certain chemicals can increase people’s happiness or well-being, on balance and under the right conditions, without our first having to invent a disease for those chemicals to be addressing. One particularly promising area for this idea concerns the recent explosion of scientific and medical research into psychedelic drugs (like “magic” mushrooms) for both treatment and enhancement purposes. On the treatment side, there is growing evidence that psychedelic-assisted psychotherapy can help some people with otherwise incurable PTSD get their lives back. And on the enhancement side, such therapy has had positive effects in healthy individuals who then feel better able to navigate the vagaries of life. In the case of improving relationships, the idea is not to subsume yet another domain of ordinary human existence under the disease labels of medicine so that people can gain access to certain drugs. Instead, it would be to take certain drugs out of the domain of disease labels and ask whether they could improve certain aspects of relationships.
Brian D. Earp is the associate director of the Yale-Hastings Program in Ethics and Health Policy at Yale University and the Hastings Center, and a research fellow in the Uehiro Centre for Practical Ethics at the University of Oxford.
Julian Savulescu holds the Uehiro Chair in Practical Ethics at the University of Oxford and directs the Oxford Centre for Neuroethics.
Excerpted from Love Drugs: The Chemical Future of Relationships, by Brian D. Earp and Julian Savulescu, published by Stanford University Press, ©2020 by Brian D. Earp and Julian Savulescu. All Rights Reserved.
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