December 26, 2013 | 3
If you’re desperate for a child but have been having trouble in this area, semen may be the solution to your reproductive woes. That may sound like the most obvious sentence ever written in the history of the English language, but sometimes beneath the most ancient truisms lie remarkable secrets. People have known semen to be a required element in human reproduction ever since that metaphorical Adam first ejaculated into Eve, but it’s only now, in 2013, that we are beginning to fully realize just how, and more importantly why it all really works the way it does.
Actually, it was seven years ago that the theory I’m about to describe first saw the light of day, or at least a dim, filtered light through the pages of an obscure academic volume. In that specialist book, psychologists Jennifer Davis and Gordon Gallup from SUNY-Albany articulated a groundbreaking evolutionary theory—seminal priming theory—that ever since has been criminally unread (and thus unshared) by scientists and fertility doctors alike. Just off the top of my head, I can think of two still fruitless couples that undoubtedly would have benefited by having this information years ago.
The key to understanding seminal priming theory, and the part that is likely to be the most difficult for many people to accept—particularly those people who suffer the illusion that they are not animals—is the observation that certain cases of spontaneous abortion are biologically adaptive for the mother. One helpful hint is always to remember that “adaptive” in an evolutionary sense has an entirely different meaning from “adaptive” in a contemporary mental health sense. Very bad things, such as violence, depression, perhaps even suicide, may also be biologically adaptive while being outrageously maladaptive in the more everyday sense of the word. This is because the former implies simply a mindless, net genetic fitness advantage to the organism, whereas the latter centers on a person’s subjective wellbeing. So while it may sound especially bizarre, and perhaps somewhat insensitive, to say that losing a child (even if that child is still a fetus) could ever be adaptive, context is everything.
Now, the theory. I should start by pointing out that pregnancy in human beings and the African great apes appears to be different from that of every other known mammal in one crucial way. Only in our species, chimpanzees and gorillas are there two distinct stages of implantation, not just one. For all mammals, the fertilized egg migrates to the uterine wall shortly after conception and implants there. But only for human embryos and those of our closest living relatives is there another implantation at the end of the first trimester, in which the uterine spiral arteries are deeply “invaded” by the trophoblast, which digs into the wall to siphon off a greater blood flow to the placenta. The natural history of this unique second stage of implantation is thought to be related to large brain evolution; basically, our prenatal cortices required considerably more nutritional supplies than those of other animals. Unfortunately, a leading cause of prenatal infant mortality, called preeclampsia, may also be unique to the African great apes—and substantially most common in human beings—since it is believed to stem from problems associated with this crucial second stage.
The most prominent symptoms of preeclampsia are maternal hypertension and proteinuria (significant protein in the mother’s urine), and it can arise at any point during the second or third trimesters. Because it often correlates with spontaneous abortions—the only “cure” is immediate delivery of the child—the earlier it occurs in the pregnancy the more likely it is that the infant will not survive a premature birth. This was especially true, of course, during the yawning expanse of human history in which modern medical technology could not intervene to save the preterm infant. There are a host of ancillary risk factors for developing preeclampsia, including such things as obesity, maternal age, exercise, vitamin deficiency and maternal genetics, but the most astonishing common denominator is related to the father’s genetic profile. More often than not, preeclampsia is the result of a hostile immunological maternal response to the paternal genome in the developing conceptus. In other words, the mother’s body is unwittingly terminating a pregnancy that has arisen with a man for whom she has an incompatible biochemistry.
What makes this biochemistry incompatible? Its unfamiliarity, mainly. And this is the essence of the “seminal priming” construct: the risk of preeclampsia is substantially reduced when the woman has been exposed for an extended period of time to the father’s semen prior to conception—and perhaps even after conception. Davis and Gallup, in fact, were not the first to discover this curious priming effect. By the early 1980s, scientists had started to notice that preeclampsia was more likely to occur in pregnancies resulting from “one-night stands,” artificial insemination, and rape than in pregnancies that were the product of long-term sexual cohabitation. That it was the woman’s prior exposure to the male’s semen that was responsible for this pattern was evident by the fact that couples who’d been using barrier contraceptives (such as condoms), or who practiced coitus interruptus (in which the man withdraws prior to ejaculation) before they began trying to conceive also had higher rates of preeclampsia than those who’d been engaging in unprotected sex for some time. And you’re going to love me for this, my heterosexual male friends: several studies even found that women who regularly performed oral sex were dramatically less likely to develop preeclampsia than were those who shied away from this sex act.
Yet while these causative effects of unfamiliar semen on preeclampsia had been known for some time, Davis and Gallup were the first to interpret these peculiar semen-related facts within a theoretically meaningful evolutionary framework. “It may be useful to think about preeclampsia not simply as a medical anomaly,” reason the authors, “but as an adaptation that may have evolved to terminate pregnancies where future paternal investment was questionable or unlikely.” Their argument, which is admittedly speculative, is predicated on the basic parental investment theory in evolutionary biology. While males could impregnate a potentially limitless number of females and spread their genes far and wide without any cost but a euphoric 90-second time investment, ancestral women’s genetic interests were compromised by having sex with a man who had no intention of helping her to raise any resulting offspring. Yet, if she did, and conceived as a consequence of that intercourse, preeclampsia was a second line of adaptive defence that would terminate this “costly” pregnancy—a sort of Darwinian morning after pill, as Gallup explained it to me.
The authors are aware that, in rare cases, preeclampsia is fatal not only to the infant, but to the mother as well. “In our view, however,” they reason, “the costs associated with preeclampsia for the mother would typically by outweighed by the benefits that derive from terminating a costly pregnancy before the child has been born.”
A problem for many women today is that because this hypothesized preeclampsia adaptation predates modern technologies such as condoms and in vitro fertilization, and since natural selection could not have anticipated such recent cultural innovations, female physiology remains biased toward harboring fetuses that contain genetic material that their bodies have become intimately familiar with by way of a particular partner’s seminal infusions. “Frequent insemination would be a relatively good biochemical index of the existence of a committed pair bond,” write the authors:
… and, therefore, semen familiarity would predict the likelihood of long-term provisioning, protection, and care of the mother and the child during pregnancy and following parturition.
Clinical data are an embarrassment of riches supporting this model. Even after controlling for maternal age and parity (whether the mother has given birth before), the incidence of preeclampsia is still higher in donor-inseminated pregnancies than normally conceived pregnancies. And when looking exclusively at artificial inseminations, it is more common in women who became pregnant from a donor’s sperm than those artificially inseminated by their partner’s sperm. Studies with “multiparous” women—those who have given birth to more than one child—in regions as diverse as Nigeria and the Caribbean reveal that a change in paternity, from one pregnancy to the next, is also correlated with an increased risk of preeclampsia.
Davis and Gallup surmise that there would have been three “categories of unfamiliar semen” in the ancestral past that likely exerted selective pressure on this preeclampsia mechanism. Rape is the most obvious of these, and also the most theoretically important, because very often it would have meant a single instance of exposure to foreign semen. Prior to bottle-feeding, conception and childbirth meant that a woman foreclosed on any other reproductive opportunities for at least 2-4 years, so pregnancies arising through single acts of coercive sex, in which paternal investment was improbable, would have meant an enormous gamble for her genetic fitness. Although preeclampsia was once a strategic adaptation adjusting for these prospective losses, however, today novel scenarios such as artificial insemination of a donor’s sperm invoke the exact same mechanism. From the mindless perspective of the evolved woman’s proactive womb, there’s simply no way to tell this apart from rape.
The second category of unfamiliar semen, according to the authors, falls under the heading of “dishonest mating strategies.” “It is not uncommon for males to feign good intentions and commitment to females,” they point out, “as a means of attempting to gain sexual access.” But female physiology may have worked out a way to thwart this age-old love-‘em-and-leave-‘em tactic. Familiar semen continues to promote pregnancy retention (or to reduce the chances of preeclampsia) for a period of time after conception. This is an important point, because remember, preeclampsia traces back to problems with the second implantation occurring at the end of the first trimester. Frequent, continuing insemination of a woman during at least the initial duration of the pregnancy would have signalled a man’s ongoing commitment.
This same principle of recurrent insemination in the already-pregnant woman applies also to Davis and Gallup’s last category of unfamiliar semen. This involves honest mating strategies—the male genuinely feels committed upon having sex—but because conception happens to occur very early in the relationship, when the romantic bond is still tenuous, the chances of his abandoning her and the child are in fact quite high.
Now, if you’ll excuse me, I’m off to share the seminal priming theory with a lovely lesbian couple I know that soon will begin trying to conceive through laboratory methods. I suspect that their physician is unlikely to instruct them to do so, but they will be delighted to hear that simply gargling with the chosen donor’s semen each night, or perhaps gently dabbing some of this substance against one of their vaginal walls before bedtime, may very well work wonders for them. I jest. But this isn’t such a ludicrous idea, in fact. Some scientists have already recognized the potential of developing sublingual sprays or vaginal gels that are liquid concatenations of various immune factors mixed with the male’s protein—essentially, it’s a gay and singles-friendly, modern pharmaceutical proxy of good old-fashioned seminal priming.
[Author's note: A version of this article originally appeared in the Swiss magazine Das Magazin and was published in the German language on July 21, 2012.]