What do your dainty eyeteeth mean for your love life?
Human behavior varies a lot. As compared with other primates, we’re heavily influenced by culture, religion, family upbringing, and so forth. As a consequence, it’s logical to conclude that our fitful monogamy is purely culturally induced and not instinctual. (On the other hand, we readily seem to accept that promiscuous tendencies are wired into our brains.)
In fact, we are programmed to pair bond—just as we’re programmed to add notches to our belts. By programmed, I mean that our brains are set up so that we engage in these behaviors with a lower threshold of enticement than we would otherwise. Both these programs serve our genes, as does the tension between them. For example, on average, we stay bonded long enough to fall in love with a kid, who then benefits from two caregivers. Then we may easily grow restless and seek out novel genes in the form of another partner. Italian research, for example, reveals that our racy “honeymoon neurochemistry” typically wears off within two years.
Pair bonding is not simply a learned behavior. If there weren’t neural correlates behind this behavior, there would not be so much falling in love and pairing up across so many cultures. The pair-bonding urge is built-in and waiting to be activated, much like the program that bonds infants with caregivers. In fact, these two programs arise in overlapping parts of the brain and employ the same neurochemicals.* The Coolidge Effect (that sneaky tendency to habituate to a familiar sex partner and yearn for a novel one) is also a program. The fact that these programs often dominate one another doesn’t alter the fact they both influence us.
Even when we override inclinations like these, they lurk. So it is that mates must often grit their teeth if they choose to remain faithful in the face of urges to pursue novel partners. And most humans are wired with powerful parent-child bonding impulses, even if they choose not to have children. It is a rare mother who does not bond with her kids (although it can happen if, for example, drug use has interfered with her neurochemistry). Similarly, people may choose never to engage in sex and orgasm, but groups of interconnected neurons are ready to give them a powerful experience if they do.
Again, such programs are present because of the physical structures in the brain—especially those that make up “the reward circuitry.” This mechanism is activated by a neurochemical called dopamine (the “I gotta have it!” neurochemical). This is why falling in love, sex, nurturing a kid, and often pursuing a novel partner all register as rewarding.
Without this neurochemical reward, pair bonders wouldn’t bother to pair bond. They’d settle into the usual, promiscuous mammalian program, in pursuit of its rewards. Predictably, there is evidence of unique brain activation in pair-bonding voles (compared with the non-pair-bonding variety). And there is data showing similar brain activity in pair-bonding primates. See: Neural correlates of pairbonding in a monogamous primate. Although more research is needed, it may be that pair-bonding mammals (unlike non-pair-bonding bonobos, for example) share similar neural correlates: neural networks, receptor type and specific neurotransmitters, etc. Neuroendocrinologist Sue Carter expressed this view: “The biochemistry [of bonding] is probably going to be similar in humans and in animals because it’s quite a basic function.”
While all mammals find sex rewarding, pair bonders also register the individual mate as rewarding. Thanks to this hidden pair-bonding program, our brains light up so we become infatuated. And our hearts ache when are parted from our sweetheart. Pair-bonding voles, too, show signs of pining when separated from a mate.
Need more evidence? Consider the hellish fury that arises when we are jilted for someone new. A cow, on the other hand, is quite indifferent if the bull that fertilized her yesterday does his duty with her neighbor today. Lacking the requisite neural correlates, she is not a pair bonder.
Why should we care that we’re pair bonders?
Given the fact that the urge to switch partners so often overrides our pair-bonding inclinations, shouldn’t we continue to give this unreliable program scant attention? Maybe not. Even though our pair-bonding urge is clearly not a guarantee of living happily ever after with a lover, a better understanding of it may furnish important clues for relationship contentment, and even greater well-being. We don’t have to conform to our genes’ friction-prone agenda.
Let’s consider some oft-ignored aspects of this program:
First, we may have come from a long line of pair bonders. A recent fossil find suggests that pair bonding could be the opposite of a superficial cultural phenomenon. The discovery of upright early human Ardipithecus (4.4 million years old) means that our line and the chimp line diverged long ago. Some researchers hypothesize that, because Ardipithecus males and females were about the same size, and the specimens do not have large, sharp canine teeth, it’s possible that the fierce, often violent competition among males for females in heat that characterizes gorillas and chimpanzees was absent.
This could suggest that the males were beginning to enter into somewhat monogamous relationships with females—possibly devoting more time to carrying food (which would favor walking on two legs) and caring for their young than did earlier ancestors. See: Did Early Humans Start Walking for Sex? In short, promiscuous bonobo chimps, our nearest living relatives, are really not so close. As non-pair bonders, they may have little to teach us about contented love lives.
Second, a happy pair bond offers humans sensations of deep, health-promoting satisfaction. When researchers measure happiness factors, a contented pair bond registers as one of the most important determinants of happiness. This may be a function of our pair-bonder wiring. Research shows that warm, comforting touch between mates appears to be protective of health and longevity. “Increasing warm touch among couples has a beneficial influence on multiple stress-sensitive systems.”
Affectionate contact between pair-bonding mates is apparently an exaptation of the same soothing contact that bonds infants and caregivers. Many popular articles emphasize that frequent orgasm benefits mates. Yet that assumption overlooks that we’re wired to benefit from bonding and closeness themselves, quite apart from whether orgasm occurs. Clarity on this point can make staying in love more effortless than we thought.
* [From Speaker Summary of talk by Larry Young, PhD entitled, “Neurobiology of Social Bonding and Monogamy”]
Prairie voles, like humans, are highly social and form long-lasting pair bonds between mates. This is in contrast to 95 percent of all mammalian species, which do not appear capable of forming long lasting social bonds between mates. Studies examining the brain and genetic mechanisms underlying pair bonding have revealed an important role for a few key chemicals in the brain in establishing social relationships. Oxytocin and vasopressin appear to focus the brain’s attention to the social signals in the environment. During pair bond formation, these chemicals interact with the brain’s reward system (e.g. dopamine) to establish an association between the social cues of the partner and the rewarding nature of mating. So why are some species capable of forming social bonds while others are not? Research comparing the brains of monogamous and non-monogamous species reveals that it is the location of the receptors that respond to oxytocin and vasopressin that determines whether an individual will be capable of bonding. For example, monogamous male prairie voles have high concentrations of vasopressin receptors in a ventral forebrain reward center that is also involved in addiction. Non-monogamous meadow voles lack receptors there. However, if receptors are inserted into this reward center in the non-monogamous meadow vole, these males suddenly develop the capacity to form bonds. These studies also suggest that pair bonding shares many of the same brain mechanisms as addiction. Genetic studies have revealed that DNA sequence variation in the gene encoding the vasopressin receptor affect the level of receptor expression in certain brain regions and predict the probability that the male will form a social bond with a female.
Recent studies in humans have revealed remarkable similarities in the roles of oxytocin and vasopressin in regulating social cognition and behavior in vole and man. Variation in the DNA sequence of the human vasopressin receptor gene has been associated with variation in measures of romantic relationship quality. In humans, intranasal delivery of oxytocin enhances trust, increases gaze to the eyes, increases empathy and enhances socially-reinforced learning. Indeed it appears that stimulating the oxytocin system in humans increases the attention to social cues in the environment.
Are brains that fall in love more sensitive?
In Human Brains Are Built to Fall in Love we looked at the neurochemical reality that lies behind our instincts to fall in (and out of) love. We saw that our ancestors may have been pair bonders for a very long time, implying that pair bonding serves important ends for our species. We observed that the same bonding behaviors that effortlessly strengthen our pair bonds also reduce stress and increase well-being.
In this article we’ll look at a hidden pair-bonder vulnerability that causes misery both in and out of the bedroom. Namely, the tendency to pursue excess. This hazard came to light when scientists offered amphetamines to two vole species. The species are apparently identical but for one characteristic. One pair bonds, while the other is cheerfully promiscuous. (Think human and bonobo. Our limbic brain possesses the “gear” for pair bonding while the bonobo’s doesn’t.)
Which species used more of the drugs and showed higher brain levels of dopamine (the “I gotta have it” neurochemical)? The pair-bonding species.
Apparently, they have lots of a specific type of dopamine receptor called “D2” in the reward circuitry of their brains. Think of D2 as the “craving” receptor.
In contrast, the non-pair-bonders have more “D1” receptors. D1s play a little-understood role in easing cravings for intense stimulation. When flooded with enough dopamine, these D1 receptors deliver the message, “Okay, I’ve had enough of this drug, this alcohol, or this crazy rat humping me. Think I’ll get on with my day.” *
Sex may be fun for chimps, but falling in love (the urge to pair bond) is such an important factor in our species’ genetic success that, for us, the phenomenon may rival a drug trip. The experience has been known to launch a thousand ships, destroy political careers, and make priests break vows. By the same token, when a pair bond breaks, it can motivate the abandoned partner to grab a cleaver and hack off an appendage.
Let’s not underestimate our pair-bonding program. After all, it’s probably an exaptation of a far older mammalian program, the one that bonds infants and caregivers. Parents, too, go gunning when the survival of (bond with) their offspring is at stake.
Soap operas and reality shows are not the only other menaces that arise as a consequence of this potent brain mechanism. So is addiction. Odd as it seems, the impulse to fall in love (and mate to the point of habituation) may be behind the ease with which we hijack our brains using various risky excesses. Our delicate reward circuitry, which produces those all-consuming feelings when we fall in love, is the same pathway that produces the all-consuming feelings many users experience when they substitute drugs of abuse, alcohol, extreme porn, gambling, compelling video games, and so forth.
Obviously, this highly sensitive circuitry evolved to push us past any defensiveness and get us hooked on lovers—at least for long enough to fall in love with our children. It did not evolve to promote addiction to other activities and substances. Only humans can regularly exploit this mechanism with dicey surrogates.
It’s as if we pair bonders have an extra “little hole” in our brains whispering, “Fill me up.” It evolved in environments where our primary option for filling it was the occasional novel sexual partner (often followed by a “rest” as habituation set in). Artificial substitutes were absent. Sadly, this “hole” can never be filled by today’s blitz of brain-hammering indulgences. Too much stimulation dysregulates this part of the brain. It triggers subsequent neurochemical lows while our over-stimulated brains recover. The lows, in turn, can drive even more intense cravings to self-medicate. Voilà! Before we know it, we’re sharing our story in a 12-Step group.
This delicate feature of our brains may go far toward explaining why, as a society, we’re often looking for the next fix. More novelty. More stimulation. In fact, we don’t lack stimulation; we’re out of balance.
Our dilemma leads back to Part 1 of this article, which pointed out that bonding behaviors soothe stress at the same time they strengthen bonds. They appear to work because they produce comforting levels of oxytocin for the right receptors. Oxytocin has been shown to reduce cravings for sugar and drugs, and even to reduce withdrawal symptoms. Could this help explain why lovers notice daily bonding behaviors can ease sexual frustration (cravings) and forestall habituation between them in a way that pursuing ever more sexual stimulation cannot?
Even if humans can act like bonobos, we might be more content if we explored our unique options for creating balance as pair bonders.
Whether a particular human chooses to sidestep much of the mating drama by remaining single, unite for life, or pollinate many flowers without any stable bonds, s/he is generally stuck with a pair-bonder’s brain. This wiring could have major implications in areas of life that have nothing directly to do with romance. For example, in or out of relationship, too little daily affectionate interaction with others, and too much stimulation can increase distress without our conscious awareness.
The human brain has evolved to fall in love…repeatedly, should opportunity knock. The cycle of pair bonding, mating frenzy (excess), habituation, and pairing up again serves our genes, across populations, in many cultural variations—even when it creates chaos and taxes our capacity for forgiveness.
By becoming aware of our pair-bonding brain’s highly sensitive reward circuitry and its impact on our lives, we can more easily weigh the relative benefits of (1) yielding to our programmed impulses and (2) learning to ease them using natural techniques like meditation, exercise, yoga, bonding behaviors, and careful cultivation of sexual energy. Perhaps our pair-bonding program is a major impetus for humankind’s many “spiritual” practices that strengthen inner equilibrium.
* When vole researchers administer a dopamine-like substance that lights up D2 (craving) receptors, but not D1 (satiety) receptors, the voles hear rhapsodies and see stars—even if Pyramis Vole and Thisbe Vole do not have sex because they’re in different cages at the time. In contrast, when scientists prevent activation of D2 receptors (without affecting D1s), there are no valentines exchanged, just gametes. In short, dopamine-induced cravings, triggered by mechanisms within the brain, are critical to pair bonding. Without these mechanisms, even oxytocin, the “bonding hormone,” won’t cause voles to fall in love.