IF FEMALE EJACULATE helps to keep women healthy, it may not be the only bodily fluid that lends a hidden helping hand. Semen may help to get women pregnant—which sounds obvious—but not just by supplying sperm. In 2003, an email circulated that included what appeared to be a CNN report discussing a study that linked women giving oral sex to a decrease in breast cancer. There was no such study—just a well-crafted college student joke. The email led to the embarrassment of some international media outlets that took it seriously and ran with it. Even though semen exposure through oral sex doesn’t decrease breast cancer risk, it may very well increase the chances of a successful pregnancy.
Here’s the idea in a nutshell. In women’s bodies, sperm are foreign entities, which means they should be treated like other foreign microbes—attacked and destroyed by the immune system. That doesn’t happen, at least not all the time—if it did, of course, we wouldn’t be here today. But it may be that a woman’s immune response to invading sperm is yet another hurdle sperm have to overcome in their race to fertilize an egg. It’s possible that repeated exposure to a partner’s semen (and a chemical called TGF-beta and the sperm within) may familiarize a woman’s body with it and make it more acceptable. If familiar sperm are treated more favorably than other sperm, it might provide another advantage as well: it would decrease the odds of pregnancy from a sexual encounter with a stranger, while increasing the odds for reproduction with a long-term mate. This theory is supported by new research that found that women who engaged in oral sex with their male partners were less likely to suffer from a rather dangerous pregnancy-related hypertensive crisis called preeclampsia. This condition can occur during pregnancy (family history, especially in sisters, is just one of the risk factors), in which blood pressure rises to potentially dangerous levels. Some women with preeclampsia can even deteriorate further, developing eclampsia, which is characterized by seizures and classified as a true obstetrical emergency. Providing even stronger evidence that the link between oral semen exposure reduced the risk of preeclampsia, the women who reported swallowing their partners’ semen had the most protection.
And, of course, the key may very well be overall semen exposure—not just oral sex. In all associative studies, while trying to tease out relationships between different factors, in this case semen exposure and preeclampsia, it’s difficult to know what is truly causal. For example, women who engage in oral sex and swallow semen have been found to be more likely to engage in other sexual behaviors more frequently than women who don’t, including unprotected vaginal sex and anal intercourse, both of which could increase their exposure to semen. And though this research looks interesting, so far the results are not confirmed. Suffice it to say, before doctors begin recommending oral sex and semen exposure to women trying to conceive, much more research still needs to be done.
But if you look at all the research from on high, the trend seems to confirm something humans have thought for millions of years—sex can be pretty darn good for you.
CHAPTER 5
come as you are
Nothing in evolution is free. Every adaptation is a tradeoff, a compromise of some sort: walking on two legs gave us the advantage of height but cost us in terms of speed; our bigger brains give us the advantage of higher intelligence, but much of that brain growth occurs after birth, which makes human newborns especially helpless. In that sense, nature is really a massive arbitrage that uses trial and error to arrive at certain biological traits through natural selection that, across a given species, confers more benefits than costs. And sexual reproduction is no exception—it comes with significant costs, although it clearly has benefits.
Here’s the general thinking about the overall benefit of sexual reproduction: sex makes a species more flexible by reshuffling the genetic deck with every generation, as well as purging parasites in parents instead of passing them on. Flexibility means that a species has better odds of finding the right adaptation to survive environmental changes that bring new threats in the form of microbes, climate changes, new predators, and so forth. In fact, some organisms, such as certain types of algae, can reproduce asexually and sexually. When it comes to “choosing” the type of reproduction, if there’s a serious enough change, they choose sex.
One of the best explications of this theory is the Red Queen hypothesis, which was popularized in the excellent book, The Red Queen: Sex and the Evolution of Human Nature, by Matt Ridley. The term was first coined by evolutionary biologist Leigh Van Valen of the University of Chicago to describe how species turn to sexual reproduction in order to survive in a changing environment in which other species are constantly evolving too. Van Valen got the name from Lewis Carroll’s book, Through the Looking Glass, the sequel to Alice’s Adventures in Wonderland. In the book, Alice is running in a race but getting nowhere, when the Red Queen explains to her, “It takes all the running you can do, to keep in the same place.” In other words, in a world where all manner of living things—from bacteria to plants to predators and prey—are evolving themselves, it takes a lot of evolution to keep up with the competition and thrive as a species. If a species stops evolving, it falls behind. Sexual reproduction gives a species the chance to undergo evolutionary experimentation every generation—it’s the running a species needs to do to keep in the same place.
But, as I said, sex is costly. Chemistry and biology are like every other process on Earth—the more complex a routine, the more room there is for error. The asexual reproduction of a single-cell creature through simple cell division is, at least on the surface, pretty straightforward, biologically speaking. It’s reproduction through carbon copy, very efficient and somewhat resistant to error. Sexual reproduction is the polar opposite—it uses enormous resources, requires two parents instead of just one, and is rife with possibilities for error as genes from two distinct organisms are blended together to make a third. In other words, sex is expensive.
So what exactly are the costs, especially to us? And if it’s so expensive, why is sexual reproduction so popular from an evolutionary perspective?
THE FIRST COST of sexual reproduction is the possibility that something can go wrong from the get-go, during development. Sexual and gender differentiation in humans is a massively complex choreography of chemistry and biology that transforms an undifferentiated seven-week-old embryo into a male or female fetus and ultimately, if everything goes according to normative development, a baby boy or a baby girl. The one thing you can always count on with a biological process as complicated as this one is that things don’t always go according to plan.
The truth is that developmental complications in sexual differentiation are far more common than most people realize. The Intersex Society of North America (ISNA), one of the major advocacy groups for people with sexual development disorders, put the rate of ambiguous genitalia at about one in two thousand—but that rate may far underestimate the true incidence of sexual development disorders that occur, especially if you include the number of naturally occurring aborted pregnancies that don’t continue (usually with a high number of genetic and physical abnormalities).
A controversial study in 2000 by Brown University researcher Anne Fausto-Sterling used a comprehensive examination of the medical literature from 1955 to 1998 to estimate the frequency of the complete range of sexual variation disorders. The report concluded that one out of every one hundred people has a body that differs somewhat from the standard male or female configuration.
A note on terminology, before we go any further. Sex can be defined in many ways. The most basic way is to use chromosomes. If you have a Y chromosome, then you are considered male, at least genetically. The traditional term for an individual with both male and female reproductive organs is hermaphrodite, but true hermaphrodites—people with both ovarian and testicular tissue—are extremely rare. Female pseudohermaphroditism occurs when a child is born with the normal 46 chromosomes and two X chromosomes (46-XX; i.e., genetically female) but with ambiguous or underdeveloped female ge
nitalia. Male pseudohermaphroditism occurs when a child is born with 46-XY (genetically male) but has the external physical appearance of a female, a lack of virilization usually resulting from insufficient testosterone production or insensitivity to testosterone. There is a third category of conditions that occurs when a child does not have the normal complement of chromosomes; from a medical perspective, these conditions are considered more in the realm of birth defects. We’ll discuss conditions in all three categories in this chapter.
As medical science has become more sensitive to and thoughtful about these conditions, the language used to discuss them has evolved as well, moving somewhat away from older terms, like hermaphrodite that are not particularly descriptive from a medical perspective and have become laden with pejorative connotation. At the 2005 Intersex Consensus Meeting, attendees agreed to adopt the term disorder of sexual development, or DSD, to cover the wide range of disorders that prevent an individual from being identified as typically male or typically female. The whole idea behind moving toward a clinical-sounding phrase was exactly that—to move toward a more scientific approach. Along those lines, the term intersex itself has given way for some to DSD as well, although groups like ISNA haven’t changed their names. Disagreement within the intersex community still exists about whether the name change is helpful. Cheryl Chase, executive director of ISNA, told Scientific American it’s her hope that the name change will encourage doctors to see DSDs as lifelong medical conditions. “Now that we’ve accomplished the name change, culture can accomplish a little magic for us.”
IN DECEMBER 2006, Santhi Soundarajan’s career as an elite athlete was about to really hit its stride. She had just won the silver medal in the women’s 800-meter race at the Asian Games in Doha, Qatar, and seemed destined for the 2008 Olympic Games in China. And then, just hours before she was supposed to be honored, her silver medal was taken from her, and she was barred from further competition as a member of the Indian team by the Athletics Federation of India. For doping? Some other form of cheating? No. She failed a sex test. Officials wouldn’t say exactly what the tests showed, but according to the online science magazine Inkling, some anonymous official told the Associated Press that Soundarajan had “more Y chromosomes than allowed.” Of course, one Y chromosome is all it usually takes to make someone genetically male. Here’s the thing, though: Soundarajan had apparently passed sex exams many times before. So what happened?
The exact nature of Soundarajan’s prior tests and the findings of the test that ultimately disqualified her aren’t publicly known, but we can hazard a few good guesses. First of all, it’s quite possible that Soundarajan’s initial exams were simply physical inspections of her genitals, and that she possesses genitals that look sufficiently female to pass such a test. Fears of men masquerading as women in athletic competition are not unfounded, although as far as anyone knows, they are extremely rare. One of the few times it’s actually thought to have occurred was during the 1936 Berlin Games when German Hermann Ratjen competed as Dora in the high jump. Funny thing is, he failed to place.
Soundarajan wouldn’t be the first athlete to pass a sex test and later run into trouble because of a genetic analysis of chromosome makeup that discovered a Y chromosome. The story of Spanish hurdler Maria José Martinez-Patiño became well known when she ran into problems in 1985 with the discovery that she carried a Y chromosome.
Here’s a quick primer on how sexual differentiation works. For seven weeks after conception, there’s really no observable difference between genetic male or genetic female embryos. Then, in a normal male fetus, one with a single X and a single Y chromosome, the gene on the Y chromosome, called the sex-determining region Y, flips on and produces a protein that causes the gonads of the fetus to transform into testicles. If SRY isn’t present at all, or the genetic sequence is damaged, then the gonads become ovaries. Of course, that’s what we know so far. The picture of sexual development is far from completely understood, and scientists believe many other genes are involved in orchestrating the process of testicular development alone.
Once the testicles are formed, they begin to produce testosterone. Testosterone and other sex hormones, such as dihydrotesterone (DHT), that spur the development of male sexual characteristics are collectively called androgens. In the womb, androgens trigger the development of the penis, the scrotum, and the descent of the testicles, along with the requisite cardiovascular connections of arteries and veins, from the abdominal cavity. At puberty, androgens are responsible for the growth of sperm and the development of male secondary sexual characteristics—male traits like dense pubic hair, facial hair, and increased muscle mass.
To trigger those developmental changes, androgens must bind with specialized receptors. Sometimes, even though an individual has what appears to be a standard genetic male chromosomal XY pattern, or karyotype, a genetic anomaly produces faulty androgen receptors. When that happens, the androgens can’t attach to their receptors and, as a result, they have little or no effect, depending on the exact nature of the anomaly. This is called androgen insensitivity syndrome, or AIS; it’s thought to occur as frequently as one in twenty thousand live births.
In a person with AIS, the SRY gene triggers the development of testicles as normal, but all the androgen-triggered changes just don’t happen. The genital ridge does not become a penis and scrotum and the testicles never descend. And, since the “default” configuration of an embryo is female, the baby is born with a clitoris, vaginal labia, and a vaginal opening. Although at the moment medical science considers the female configuration default, there may be other factors that we have yet to discover that determine the exact intricacies of differentiation. At the same time, at six to seven weeks, the testicles still produce anti-Mullerian hormone, that initiates the disintegration of the Mullerian ducts, the precursor to the rest of the female reproductive system. Anti-Mullerian hormone is not an androgen, so, like the testis-determining factor produced by the SRY gene which prompted the transformation of the gonads into testicles, its role in the developmental process is unaffected in these babies. The result is an infant who looks just like a normal baby girl on the outside; but internally the picture is very different. The vaginal canal is shorter than normal and can end in a blind pouch. There is no cervix or uterus, there are no Fallopian tubes, and instead of ovaries, there is an internal pair of undescended testicles.
At puberty, the testicles in such cases produce increased levels of testosterone as they normally would in a male. Some of that is transformed into estrogen, again, as it normally would be. But in a person with AIS, testosterone has limited or no effect, since cells don’t respond to it. It’s important to remember that development of some secondary female sexual characteristics does not always need ovaries and female sex hormones. The typical adult with AIS, despite being genetically male, has female breasts, wide hips in keeping with feminine fat distribution, no extensive facial hair, and sometimes less pubic hair. And because there is no uterus and no ovaries, there is no menarche. At the same time, the internal male organs, like the epididymis, vas deferens, and seminal vesicles, have not developed because they all depend on testosterone to do so.
Sometimes parents learn of AIS when a predelivery genetic test, like chorionic villus sampling (CVS) or amniocentesis, reveals a male chromosomal pattern that does not match images on the sonogram (sex characteristics can sometimes be observable as early as nine weeks). In the absence of such a genetic clue, AIS may not be diagnosed until a concerned teenager heads to the doctor as she begins to wonder why she hasn’t had her first period. And of course, sometimes AIS isn’t diagnosed at all.
In Maria José Martinez-Patiño’s case, her eventual diagnosis with AIS simultaneously explained how she could have a Y chromosome but otherwise have lived her life entirely as a female. Why didn’t anyone ever think twice about the fact that Maria didn’t menstruate? Remember, we discussed that menstruation is linked to body fat. If a woman’s body doesn’t have sufficient fat to suppo
rt a pregnancy, ovulation and, thus, menstruation are suppressed. This evolutionary mechanism prevents women from having children in times of famine or poor food supply, better to survive hard times and reproduce later than to lose both mother and child. Elite female athletes, especially runners, often have such low percentages of body fat that they experience menstrual suppression—so Maria may never have thought anything was out of the ordinary.
Humans normally have 23 pairs of chromosomes, for a total of 46. They are all matched pairs, each a copy of the other, except at times for the twenty-third pair, the sex chromosomes. When chromosomes come in pairs, it’s called disomy. Sometimes, because of a reproductive error, a human embryo might have three copies of a chromosome, or trisomy. Most embryos that have trisomy don’t survive, but sometimes they do. Down syndrome occurs when there is trisomy of chromosomes 21. A single copy of a chromosome is called monosomy. Most human embryos with full monosomy don’t survive; one exception is monosomy of the X-chromosome, when a woman is only born with one X-chromosome, resulting in Turner syndrome, a condition we’ll discuss shortly.
Women can also be born with an extra X chromosome; triple X syndrome is thought to occur in one out of a thousand newborn girls in the United States. Many women with triple X syndrome don’t have any symptoms, but when they do they can include above-average height or developmental delay. Klinefelter syndrome occurs in males (and males only) who have an extra X-chromosome, making them genetically XXY instead of XY. If a boy with Klinefelter syndrome has one extra X chromosome, he’ll have a total of 47 chromosomes instead of the normal 46. This is often referred to as 47-XXY, where 47 indicates the total number of chromosomes and XXY indicates the karyotype of chromosome 23. Genetic males can also have XYY syndrome; instead of having an extra X chromosome as in Klinefelter’s, men with this condition have an extra Y. As with triple X syndrome, they don’t usually exhibit symptoms except for increased height and are thought to be at higher risk for learning disabilities.
How Sex Works Page 13