This Is Your Brain on Sex (26 page)

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Authors: Kayt Sukel

Tags: #Psychology, #Cognitive Psychology, #Cognitive Psychology & Cognition, #Human Sexuality, #Neuropsychology, #Science, #General, #Philosophy & Social Aspects, #Life Sciences

BOOK: This Is Your Brain on Sex
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The Evolutionary Perspective

Let’s talk numbers. Your garden-variety human
male produces about two hundred million sperm per ejaculation after sexual maturity. It can be up to eight hundred million if he hasn’t seen any action in a while. There is no “waste not, want not” rule in effect here either. Men can ejaculate as much as they like and their body will just keep producing more sperm.

Women are born with all the eggs they are ever going to have. If you assume a woman starts menstruating around the age of fourteen and will release, on average, one egg each month until she becomes menopausal, you are looking at a rough calculation of twelve eggs per year over thirty-one years of fertility. That amounts to about 372 eggs in a lifetime.

Billions and billions of sperm can be ejaculated in a single month. About four hundred eggs are released over the course of a lifetime. That is a pretty sizable discrepancy.

Since evolutionary biologists argue that deep down we are completely and utterly enslaved by our genes. Human beings are essentially programmed for certain behaviors to help propagate the species. What do our genes want? To be passed down to offspring. Forget life, liberty, and the pursuit of happiness: genes are looking for procreation; they just want to out-reproduce other ancestral lines. Some scientists believe that men, possessors of that inexhaustible sperm arsenal, have been evolutionarily selected over the past 150,000 years to act just like the king of Siam’s proverbial honeybee from
The King and I,
fertilizing as many flowers as they can manage to land upon. In order to have the best chance of getting their genes out into the world, it is advantageous for them to spread that seed around and impregnate as many females as possible.

On the other side of the evolutionary gender coin, women are better served by being selective about sexual partners. After all, there is a run on eggs; a girl should not waste one on a bad bet. More important, a woman faces a serious commitment if one of those eggs is fertilized: nine months of pregnancy plus several years of child rearing. It is beneficial for a woman (and her genes) to take her time and find a mate with stellar genes as well as the resources and inclination to help raise a child. “As a basic principle, it’s kind of
inarguable,” said Marlene Zuk, professor of biology at the University of California, Riverside, and the author of
Sexual Selections: What We Can and Can’t Learn about Sex from Animals.
2
“It applies from gophers to dragonflies, and we see, as a general rule, that males are more likely to benefit from having multiple sexual partners while females are not.”

I am quite sure Roger would love it if it were this straightforward: Men simply have lots of sperm that need to be spread about the land and are therefore going to—nay,
need
to—cheat. Before any male readers try to use that line of thinking to explain what happened on last month’s business trip, Zuk cautions that human behavior is not that simple. Dragonflies have a few neurons to help facilitate behavior. Gophers have a little more going on upstairs, but they are certainly far from being the most complicated mammal in the animal kingdom. Roger may not be in the running for a Nobel Prize any time soon, but he is not a strict slave to his genes either. There’s more at work here.

The fairer sex, despite the evolutionary advantage of being selective when it comes to sexual partners, has been known to do no small amount of dirt too. That 14 percent female infidelity statistic? That is nothing to sneeze at. (Remember, that 14 percent consists solely of women
willing
to admit to cheating—the actual number is no doubt higher.) If women should be more selective about their sexual partners due to the scarcity of eggs, they should cheat far less than men. If they already have a good bet at home, cheating seems completely counterproductive from an evolutionary perspective. It would seem that infidelity encompasses more than just evolutionary imperative.

Besides natural selection, what else might factor into the infidelity debate? As it so happens, humans have complex neurobiological structures that underlie behaviors related to romantic love, attachment, and of course sex.

The Cheating Brain

Remember those three distinct brain systems found in neuroimaging studies? Helen Fisher postulates that there are three individual systems for sex, romantic love, and attachment. These systems activate many of the same brain regions, including key areas in the basal
ganglia and the frontal lobe. It is that old kaleidoscope again: same parts, different patterns. And that kaleidoscope means it is possible to be both attached to one partner, yet sexually attracted to or even romantically in love with another.

“The way you feel when you are madly in love is different than what you feel after casual sex,” Fisher told me. These systems use different neurochemical systems, resulting in different emotional states and behaviors. “Yet there is bound to be some interaction happening between these different brain areas. In a sense, the brain is very well built for both monogamy and cheating.”

And how. The frontal cortex likely plays a big role in fidelity. Although all mammals have forebrains, the human frontal lobe is the largest and most complex. Beyond DNA, it is what differentiates us from our primate relatives. The frontal lobe is the seat of what neuroscientists call “executive function”—the place where planning, decision making, metacognition, and other higher cognitive processing and behavior occurs—and it is also implicated in moral judgments and religious belief systems. Considering the fact that it is linked to the basal ganglia circuitry (and often lights up in love-related neuroimaging studies) and contains the most dopamine-sensitive neurons in the entire brain, one would think it also has a say in whether we cheat. It certainly has the right setup to be a candidate for the government of monogamous behaviors, with the frontal lobe processing signals from the romantic love and sex drive systems in the basal ganglia and then acting in an inhibitory fashion when behaviors have the potential to get in the way of long-term attachments.

There is also evidence that damage to this area can change social relationships. In 1848 a railroad worker named Phineas Gage sustained a severe injury to his left frontal lobe. In an explosion gone awry, a metal pole was launched through Gage’s eye socket and out through the top of his head. Given the extent of his injury, many were surprised that he lived. More shocking, however, were the changes this injury made to Gage’s personality. Before the injury he was considered a jovial and hardworking fellow. His physician, John Martyn Harlow, wrote the following about Gage after the accident:

He is fitful, irreverent, indulging at times in the grossest profanity (which was not previously his custom), manifesting but little deference for his fellows, impatient of restraint or advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operations, which are no sooner arranged than they are abandoned in turn for others appearing more feasible.
3

It was also rumored that this upstanding, moral guy became quite a skirt chaser after his accident. Though due to the state of science at the time—remember, phrenology was the brain science du jour back then—most of the evidence on Gage is anecdotal and somewhat unreliable.

Today clinicians can tell you that damage to the frontal lobe of the brain has been associated with sexual dysfunction, increased sex drive, and so-called sexually deviant behaviors. And recall that Lique Coolen’s lab linked damage to the frontal lobe with sexual addiction–type behaviors. Yet what do we know about the role of an
undamaged
frontal lobe in love and sexual behavior?

According to Lucy Brown, Fisher’s frequent collaborator at the Albert Einstein College of Medicine, the frontal cortex works with the VTA, ventral pallidum, and nucleus accumbens in the complex dance of love and attachment. It is difficult to tease them apart and definitively say which area is responsible for what. The likely scenario is that all these brain areas work together but perform slightly different functions. “The frontal lobe needs the support of the brain stem. Areas important for decision making are fed by dopamine released by the VTA, and the two areas communicate back and forth,” said Brown. “When you are talking about this level of complexity, it’s never just one part of the brain.”

I can’t help but think of Casanova, that poor, sexually unsatisfied rhesus monkey I observed when I visited the Yerkes National Primate Research Center’s field station. Even in the nonmonogamous culture of the rhesus monkeys, where he was free to love as he would, he used that forebrain of his to assess a potentially volatile social situation and avoid temptation. He knew what he could lose if he partook of easy sex: his status within the group. Even a monkey understood, despite ample opportunity for sex, that it was in his best interest to steer clear. If a monkey can use that kind of decision making
and judgment, it would seem your average human being could too.

This has led scientists to dig a little deeper—to examine the molecular pathways, or the interactions of neurochemicals, enzymes, proteins, and receptors at the level of the neuron, in these brain regions. Is there something about the way that dopamine, vasopressin, and oxytocin work on these parts of our brains that might result in a person’s being more or less monogamous? Enlisting the help of our friend the prairie vole, scientists investigate this question.

Your Cheating Voles

As we’ve already discussed in previous chapters, the basal ganglia provide the platform for monogamy in prairie voles. Vasopressin and oxytocin receptors help these animals learn to prefer sex with a pair-bonded partner rather than a stranger. When the gene that expresses these receptors is not working up to full capacity, as in the montane and meadow voles, it is more about the booty than any type of bonded relationship. If the difference is simply these receptors, finding a way to up them in naturally promiscuous voles should help the animals become more monogamous.

When researchers in Larry Young’s laboratory at the Yerkes National Primate Research Center increased the density of vasopressin receptors into the ventral pallidum of male meadow voles, their behavior changed dramatically. Suddenly these once-philandering rodents formed strong partner preferences for a single female. Even without having sex with them, males would bond to one special female—whichever one happened to be nearby. This is a major change for such a lone wolf species.

Similarly, when Young and his colleagues blocked the expression of vasopressin receptors in our faithful prairie vole males, they managed to finally let their inner Don Juans out. No longer able to associate a particular female with that overwhelming rush of dopamine, they became more promiscuous and noncommittal. For male voles, at least, it seems that a single gene, one that determines the density of these oxytocin receptors, may underlie monogamous behaviors.
4
Is it possible that a similar gene governs the same sorts of behaviors in humans?

It’s Never Quite That Simple, Is It?

Remember Hasse Walum’s
AVPR1A
gene study on relationship
satisfaction? When he and his colleagues at the Karolinska Institute examined the DNA of hundreds of individuals who had been in a committed relationship for at least five years, they found that those who had one variant of a vasopressin receptor gene,
AVPR1A,
were more likely to be unhappy in their relationship.
5
Between this study and Young’s work on vasopressin, many assumed
AVPR1A
must also have something to say about sexual fidelity. Headlines announcing Walum’s results ranged from “Why Men Cheat”
6
to “Infidelity: It’s All in the Genes.”
7
The assumption was that
AVPR1A
must be responsible if a guy strayed outside a committed relationship. The reporting of results by the media was more than just an oversimplification of Walum’s study—it was wrong. Walum did not try to correlate infidelity with
AVPR1A
. He couldn’t: the questionnaires did not directly ask the participants if they were unfaithful.

Before you ask the doctor to check your man’s blood for the
AVPR1A
variant as some sort of prenuptial test, look more closely. Despite these very interesting results, Walum would be the first to tell you that there is a lot more to a happy marriage than a single gene. He suggests there could be many other reasons these relationships were in trouble. First, there is another effect observed in voles that have had their vasopressin systems altered: aggression and anxiety. Perhaps the relationships surveyed in Walum’s study were less happy due to a domestic violence situation or some other kind of mental health issue. Second, some of the participants had children. We newer moms and dads know the extra strains that young children can put on the state of a relationship, ranging from differences in parenting philosophy to the division of responsibilities. It certainly played a role in the demise of my marriage. This variable was not examined by Walum’s group. Third, we cannot forget the women in this equation. As they say, it takes two to tango. Though we are more likely to point fingers at the guys when it comes to infidelity, the fact that 14 percent of women self-report having sex outside their marriage can’t be ignored. It is entirely possible that some of the relationship angst observed in Walum’s study had more to do with female infidelity than an exclusively male DNA variant. The group did look at variations
in the
AVPR1A
gene in females but found no significant link back to relationship satisfaction. The effect was found only in males. Without more data, it is difficult to pinpoint an exact cause for the observed interaction.

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