One thing that cervical cancer awareness overlooks is that HPV causes not only that cancer but also can play a role in penile, vaginal, urethral, anal, and head and neck cancers. In fact, a recent study found that about 1 in 10 men and almost 4 in 100 women are orally infected with HPV, the most common sexually transmitted virus in the United States, and HPV-related head and neck cancer rates are higher among men. Further, HPV-related oral cancers have been on the rise for about two decades now, and HPV is now responsible for about 50% of oral cancers today.
Research also shows that about 50% of college age women acquire an HPV infection within four years of becoming sexually active. In addition, an infected mother can pass HPV to her baby during childbirth, and the virus can populate the child’s larynx, causing recurrent growths that block the respiratory tract and require surgical removal.
The remainder of this post appeared initially on the Parents of Kids with Infectious Diseasesite, which provides information for preventing infectious disease in addition to supporting parents whose children have them. As insidious as HPV is, the vast majority of HPV infections can be prevented now with a vaccine.
Have you or a loved one ever had an abnormal Pap test result? If precancerous cells were identified, the cause was almost undoubtedly infection with human papillomavirus (HPV).Almost all cases of cervical cancerarise because of infection with this virus. Yet a vaccine can prevent infection with the strains that most commonly cause cervical cancer.
A vaccine against cancer. It’s true.
For the vaccine to work, though, a woman must have it before HPV infects her. You may find it difficult to look at your daughter, especially a pre-teen daughter, and think of that scenario. But the fact is that even if your daughter avoids all sexual contact until, say, her wedding night, she can still contract HPV from her partner. As we noted above, it happens to bethe most common sexually transmitted infection.
About 20 million Americans have an HPV infection, and 6 million people become newly infected every year. Half of the people who are ever sexually active pick up an HPV infection in a lifetime. That means your daughter, even if she waits until her wedding night, has a 1 in 2 chance of contracting the virus. Unless it’s a strain that causes genital warts, HPV usually produces no symptoms, and the infected person doesn’t even know they’ve been infected.
Until the cancer shows up.
And it can show up in more places than the cervix. This virus, you see, favors a certain kind of tissue, one that happens to be present in several parts of you. This tissue, a type of epithelium, is a thin layer of the skin and mucous membranes. It’s available for viral invasion in the cervix, vagina, vulva, anus, and the mouth and pharynx. In fact, HPV is poised to replace tobacco as the major cause of oral cancers in the United States.
The virus can even sometimes pass from mother to child, causingrecurrent respiratory papillomatosis, the recurrent growths in the throat that must be removed periodically and can sometimes become cancerous. It strikes about 2000 children each year in the United States.
How does a virus cause cancer? To understand that, you must first understand cancer. You may know that cells reproduce by dividing, and that cancer occurs when cells divide out of control. Behind most cancers is a malfunction in the molecules that tell cells to stop dividing. These molecules operate in a chain reaction of signaling, like a series of well-timed stoplights along a boulevard. If one starts sending an inappropriate “go” signal or fails to send a “stop” signal, the cell divides, making more cells just like it that also lack the right signals. If your body’s immune system doesn’t halt this inappropriate growth, we call it cancer.
The blueprint for building these “stop” molecules is in your genes, in your DNA sequences. As a virus, HPV also requires a blueprint to make more viruses. Viruses use the division machinery of the host cell—in you—to achieve reproduction by stealthily inserting their own DNA blueprint into the host DNA.
Sometimes, when it’s finished with the host, a virus leaves a little bit of its DNA behind. If that leftover DNA is in the middle of the blueprint for a “stop” molecule, the cell won’t even notice. It will use the contaminated instructions to build a molecule, one that no longer functions in stopping cell division. The result can be cancer.
Of the 150 HPV types or strains, about 40 of which pass through sexual contact, two in particular are associated with cancer,types 16 and 18. They are the ones that may persist for years and eventually change the cellular blueprint. The vaccines developed against those two strains are, therefore, anti-cancer vaccines.
Without a successful viral infection, viral DNA can’t disrupt your DNA. That’s what the HPV vaccine achieves against the two strains responsible forabout 70% of cervical cancers. Recent high-profile people have made claims about negative effects of this vaccine, claims that have beenthoroughly debunked. The Centers for Disease Control and Prevention as always offersaccurate informationabout the side effects associated with available HPV vaccines.
This achievement against cancer, including prevention of almost 100% of precancerous cervical changes related to types 16 and 18, is important.
Worldwide, a half million women receive a cervical cancer diagnosis each year, and 250,000 women die from it. These women are somebody’s daughter, wife, sister, friend. Women from all kinds of backgrounds, with all kinds of sexual histories.
Women whose precancerous cervical changes are identified in time often still must undergo uncomfortable and sometimes painful procedures to get rid of the precancerous cells. These invasive procedures includecone biopsiesthat require shots to numb the cervix and removal of a chunk of tissue from it. Cone biopsies carry a risk of causing infertility or miscarriage or preterm delivery. A vaccine for your daughter could prevent it all.
HPV doesn’t care if your daughter has had sex before. It’s equally oblivious to whether the epithelium it infects is in the cervix or in the mouth or pharynx or in an adult or a child. What it does respond to is antibodies that a body makes in response to the vaccine stimulus.
Even if your daughter’s first and only sex partner passes along one of the cancer-associated strains, if she’s been vaccinated, her antibodies will take that virus out cold. It’s a straightforward prevention against a lifetime of worry—and a premature death.
For more info: Facts about theHPV vaccinefrom the National Cancer Institute.
Today’s guest post (originally posted here) is from Katie Hinde, an Assistant Professor in Human Evolutionary Biology at Harvard University. Katie studies how variation in mother’s milk influences infant development in rhesus monkeys. You can learn more about Katie and mammalian lactation by visiting her blog, Mammals Suck… Milk!. Follow Katie on Twitter @Mammals_Suck.
Milk is everywhere. From the dairy aisle at the grocery store to the explosive cover of the Mother’s Day issue of Time magazine, the ubiquity of milk makes it easy to take for granted. But surprisingly, milk synthesis is evolutionarily older than mammals. Milk is even older than dinosaurs. Moreover, milk contains constituents that infants don’t digest, namely oligosaccharides, which are the preferred diet of the neonate’s intestinal bacteria (nom nom nom!) And milk doesn’t just feed the infant, and the infant’s microbiome; the symbiotic bacteria are IN mother’s milk.
Evolutionary Origins of Lactation
The fossil record, unfortunately, leaves little direct evidence of the soft-tissue structures that first secreted milk. Despite this, paleontologists can scrutinize morphological features of fossils, such as the presence or absence of milk teeth (diphyodonty), to infer clues about the emergence of “milk.” Genome-wide surveys of the expression and function of mammary genes across divergent taxa, and experimental evo-devo manipulations of particular genes also yield critical insights. As scientists begin to integrate information from complementary approaches, a clearer understanding of the evolution of lactation emerges.
In his recent paper, leading lactation theorist Dr. Olav Oftedal discusses the ancient origins of milk secretion (2012). He contends the first milk secretions originated ~310 million years ago (MYA) in synapsids, a lineage ancestral to mammals and contemporaries with sauropsids, the ancestors of reptiles, birds, and dinosaurs. Synapsids and sauropsids produced eggs with multiple membrane layers, known as amniote eggs. Such eggs could be laid on land. However, synapsid eggs had permeable, parchment-like shells and were vulnerable to water loss. Burying these eggs in damp soil or sand near water resources- like sea turtles do- wasn’t an option, posits Oftedal. The buried temperatures would have likely been too cold for the higher metabolism of synapsids. But incubating eggs in a nest would have evaporated water from the egg. The synapsid egg was proverbially between a rock and a hard place: too warm to bury, too permeable to incubate.
Ophiacodon by Dmitri Bogdanov
Luckily for us, a mutation gave rise to secretions from glandular skin on the belly of the synapsid parent. This mechanism replenished water lost during incubation, allowing synapsids to lay eggs in a variety of terrestrial environments. As other mutations randomly arose and were favored by selection, milk composition became increasingly complex, incorporating nutritive, protective, and hormonal factors (Oftedal 2012). Some of these milk constituents are shunted into milk from maternal blood, some- although also present in the maternal blood stream- are regulated locally in the mammary gland, and some very special constituents are unique to milk. Lactose and oligosaccharides (a sugar with lactose at the reducing end) are two constituents unique to mammalian milk, but are interestingly divergent among mammals living today.
Illustration by Carl Buell
Mammalian and Primate Divergences: Milk Composition
Among all mammals studied to date, lactose and oligosaccharides are the primary sugars in milk. Lactose is synthesized in mammary glands only. Urashima and colleagues explain that lactose synthesis is contingent on the mammalian-specific protein alpha-lactalbumin (2012). Alpha-lactalbumin is very similar in amino-acid structure to C-type lysozyme, a more ancient protein found throughout vertebrates and insects. C-type lysozyme acts as an anti-bacterial agent. Oligosaccharides are predominant in the milks of marsupials and egg-laying monotremes (i.e. the platypus), but lactose is the most prevalent sugar in the milk of most placental (aka eutherian) mammals. Interestingly, the oligosaccharides in the milk of placental mammals are most similar to the oligosaccharides in the milk of monotremes. Unique oligosaccharides in marsupial milk emerged after the divergence of placental mammals.
Marsupial and monotreme young seemingly digest oligosaccharides. Among placental mammals, however, young do not have the requisite enzymes in their stomach and small intestine to utilize oligosaccharides themselves. Why do eutherian mothers synthesize oligosaccharides in milk, if infants don’t digest them?
In May, Anna Petherick’s post “Multi-tasking Milk Oligosaccharides” revealed that oligosaccharides serve a number of critical roles for supporting the healthy colonization and maintenance of the infant’s intestinal microbiome. Beneficial bacterial symbionts contribute to the digestion of nutrients from our food. Just as importantly, they are an essential component of the immune system, defending their host against many ingested pathogens. The structures of milk oligosaccharides have been described for a number of primates, including humans, and data are now available from all major primate clades; strepsirrhines (i.e. lemurs), New World monkey (i.e. capuchin), Old World monkey (i.e. rhesus), and apes (i.e. chimpanzee).
Among all non-human primates studied to date, Type II oligosaccharides are most prevalent (Type II oligosaccharides contain lacto-N-biose I). Type I oligosaccharides (containing N-acetyllactosamine) are absent, or in much lower concentrations than Type II(Taufik et al. 2012).
In human milk, there is a much greater diversity and higher abundance of milk oligosaccharides than found in the milk of other primates. Most primate taxa have between 5-30 milk oligosaccharides; humans have ~200. Even more astonishingly, humans predominantly produce Type I oligosaccharides, the preferred food of the most prevalent bacterium in the healthy human infant gut- Bifidobacteria (Urashima et al 2012, Taufik et al. 2012).
Human infants have bigger brains and an earlier age at weaning than do our closest ape relatives. Many anthropologists have hypothesized that constituents in mother’s milk, such as higher fat concentrations or unique fatty acids, underlie these differences in human development. But only oligosaccharides, a constituent that the human infant does not itself utilize, are demonstrably derived from our primate relatives (Hinde and Milligan 2011). At some point in human evolution there must have been strong selective pressure to optimize the symbiotic relationship between the infant microbiome and the milk mothers synthesize to support it. The human and Bifidobacteria genomes show signatures of co-evolution, but the selective pressures and their timing remain to be understood.
Vertical Transmission of Bacteria via Milk
In the womb, the infant is largely protected from maternal bacteria due to the placental barrier. But upon birth, the infant is confronted by a teeming microbial milieu that is both a challenge and an opportunity. The first inoculation of commensal bacteria occurs during delivery as the infant passes through the birth canal and is exposed to a broad array of maternal microbes. Infants born via C-section are instead, and unfortunately, colonized by the microbes “running around” the hospital. But exposure to the mother’s microbiome continues long after birth. Evidence for vertical transmission of maternal bacteria via milk has been shown in rodents, monkeys(Jin et al. 2011), humans(Martin et al. 2012), and… insects.
A number of insects have evolved the ability to rely on nutritionally incomplete food sources. They are able to do so because bacteria that live inside their cells provide what the food does not. These bacteria are known as endosymbionts and the specialized cells the host provides for them to live in are called bacteriocytes. For example, the tsetse fly has a bacterium, Wigglesworthia glossinidia,* that provides B vitamins not available from blood meals. Um, if you are squeamish, don’t read the previous sentence.
*I submit the tsetse fly and its bacterial symbiont (Wigglesworthia glossinidia) for consideration as the number one mutualism in which the common name of the host and the Latin name of the bacteria are awesome to say out loud! Bring on your challenger teams.
Hosokawa and colleagues recently revealed the Russian nesting dolls that are bats (Miniopterus fuliginosus), bat flies (Nycteribiidae), and endosymbiotic bacteria (proposed name Aschnera chenzii)(2012). Bat flies are the obligate ectoparasites of bats (Peterson et al. 2007). They feed on the blood of their bat hosts, and for nearly their entire lifespan, bat flies live in the fur of their bat hosts. Females briefly leave their host to deposit pupae on stationary surfaces within the bat roost.
Bat flies are even more crazy amazing because they have a uterus and provide MILK internally through the uterus to larva! Male and female bat flies have endosymbiotic bacteria living in bacteriocytes along the sides of their abdominal segments (revealed by 16S rRNA). Additionally, females host bacteria inside the milk gland tubules, “indicating the presence of endosymbiont cells in milk gland secretion”.
The authors are not yet certain of the specific nutritional role that these bacterial endosymbionts play in the bat fly host. The bacteria may provide B vitamins, as other bacterial symbionts of blood-consuming insects are known to do. My main question is what is the exact role of the bacteria in the milk gland tubules? Are they there to add nutritional value to the milk for the larva, to stowaway in milk for vertical transmission to larva, or both?
The studies described above represent new frontiers in lactation research. The capacity to secrete “milk” has been evolving since before the age of dinosaurs, but we still know relatively little about the diversity of milks produced by mammals today. Even less understood are the consequences and functions of various milk constituents in the developing neonate. Despite the many unknowns, it is increasingly evident that mother’s milk cultivates the infant’s gut bacterial communities in fascinating ways. A microbiome milk-ultivation, if you will, that has far reaching implications for human development, nutrition, and health. Integrating an evolutionary perspective into these newly discovered complexities of milk dynamics allows us to reimagine the world of “dairy” science.
Hosokawa et al. 2012. Reductive genome evolution, host-symbiont co-speciation, and uterine transmission of endosymbiotic bacteria in bat flies. ISME Journal. 6: 577-587
Jin et al. 2011. Species diversity and abundance of lactic acid bacteria in the milk of rhesus monkeys (Macaca mulatta). J Med Primatol. 40: 52-58
Martin et al. 2012. Sharing of Bacterial Strains Between Breast Milk and Infant Feces. J Hum Lact. 28: 36-44
Oftedal 2012. The evolution of milk secretion and its ancient origins. Animal. 6: 355-368.
Peterson et al. 2007. The phylogeny and evolution of hostchoice in the Hippoboscoidea(Diptera) as reconstructed using fourmolecularmarkers. Mol Phylogenet Evol. 45 :111-22
Taufik et al. 2012. Structural characterization of neutral and acidic oligosaccharides in the milks of strepsirrhine primates: greater galago, aye-aye, Coquerel’s sifaka, and mongoose lemur. Glycoconj J. 29: 119-134.
Urashima, Fukuda, & Messer. 2012. Evolution of milk oligosaccharides and lactose: a hypothesis. Animal. 6: 369-374.
Human ovum (egg). The zona pellucida is a thick clear girdle surrounded by the cells of the corona radiata (radiant crown). Via Wikimedia Commons.
It was September of 2006. Due to certain events taking place on a certain evening after a certain bottle (or two) of wine, my body was transformed into a human incubator. While I will not describe the events leading up to that very moment, I will dissect the way in which we propagate our species through a magnificent process called fertilization.
During the fertilization play, there are two stars: the sperm cell and the egg cell. The sperm cell hails from a male and is the end product of a series of developmental stages occurring in the testes. The egg cell (or ovum), which is produced by a female, is the largest cell in the human body and becomes a fertilizable entity as a result of the ovulatory process. But to truly understand what is happening at the moment of fertilization, it is important to know more about the cells from which all human life is derived.
Act I: Of sperm and eggs
A sperm cell is described as having a “head” section and a “tail” section. The head, which is shaped like a flattened oval, contains most of the cellular components, including DNA. The head also contains an important structure called an acrosome, which is basically a sac containing enzymes that will help the sperm fuse with an egg (more about the acrosome below). The role of the tail portion of sperm is to act as a propeller, allowing these cells to “swim.” At the top of the tail, near where it meets the head, are a ton of tiny structures called mitochondria. These kidney-shaped components are the powerhouses of all cells, and they generate the energy required for the sperm tail to move the sperm toward its target: the egg.
The egg is a spherical cell containing the usual components, including DNA and mitochondria. However, it differs from other human cells thanks to the presence of a protective shell called the zona pellucida. The egg cell also contains millions of tiny sacs, termed cortical granules, that serve a similar function to the acrosome in sperm cells (more on the granules below).
Act II: A sperm cell’s journey to the center of the universefemale reproductive system
Given the cyclical nature of the female menstrual cycle, the window for fertilization during each cycle is finite. However, the precise number of days per month a women is fertile remains unclear. On the low end, the window of opportunity lasts for an estimated two days, based on the survival time of the sperm and egg. On the high end, the World Health Organization estimates a fertility window of 10 days. Somewhere in the middle lies a study published in the New England Journal of Medicine, which suggests that six is the magic number of days.
Assuming the fertility window is open, getting pregnant depends on a sperm cell making it to where the egg is located. Achieving that goal is not an easy feat. To help overcome the odds, we have evolved a number of biological tactics. For instance, the volume of a typical male human ejaculate is about a half-teaspoon or more and is estimated to contain about 300 million sperm cells. To become fully active, sperm cells require modification. The acidic environment of the vagina helps with that modification, allowing sperm to gain what is called hyperactive motility, in which its whip-like tail motors it along toward the egg.
Once active, sperm cells begin their long journey through the female reproductive system. To help guide the way, the cells around the female egg emit a chemical substance that attracts sperm cells. The orientation toward these chemicals is called chemotaxis and helps the sperm cells swim in the right direction (after all, they don’t have eyes). Furthermore, sperm get a little extra boost by the contraction of the muscles lining the female reproductive tract, which aid in pushing the little guys along. But, despite all of these efforts, sperm cell death rates are quite high, and only about 200 sperm cells actually make it to the oviduct (also called the fallopian tube), where the egg awaits.
Act III: Egg marks the spot
With the target in sight, the sperm cells make a beeline for the egg. However, for successful fertilization, only a single sperm cell can fuse with the egg. If an egg fuses with more than one sperm, the outcome can be anything from a failure of fertilization to the development of an embryo and fetus, known as a partial hydatidiform mole, that has a complete extra set of chromosomes and will not survive. Luckily, the egg has ways to help ensure only one sperm fuses with it.
When it reaches the egg, the sperm cell attaches to the surface of the zona pellucida, a protective shell for the egg. For the sperm to fuse with the egg, it must first break through this shell. Enter the sperm cell’s acrosome, which acts as an enzymatic drill. This “drilling,” in combination with the propeller movement of the sperm’s tail, helps to create a hole so that the sperm cell can access the juicy bits of the egg.
This breach of the zona pellucida and fusion of the sperm and egg sets off a rapid cascade of events to block other sperm cells from penetrating the egg’s protective shell. The first response is a shift in the charge of the egg’s cell membrane from negative to positive. This change in charge creates a sort of electrical force field, repelling other sperm cells.
Though this response is lightning fast, it is a temporary measure. A more permanent solution involves the cortical granuleswithin the egg. These tiny sacs release their contents, causing the zona pellucida to harden like the setting of concrete. In effect, the egg–sperm fusion induces the egg to construct a virtually impenetrable wall. Left outside in the cold, the other, unsuccessful sperm cells die within 48 hours.
Now that the sperm–egg fusion has gone down, the egg start the maturation required for embryo-fetal development. The fertilized egg, now called a zygote, begins its journey into the womb and immediately begins round after round of cell division, over a few weeks resulting in a multicellular organism with a heart, lungs, brain, blood, bones, muscles, and hair. It’s an amazing phenomenon that I’m honored to have experienced (although I didn’t know I was until several weeks later).
The Afterword: A note on genetics
A normal human cell that is not a sperm or an egg will contain 23 pairs of chromosomes, for a total of 46 chromosomes. Any deviation from this number of chromosomes will lead to developmental misfires that in most cases results in a non-viable embryo. However, in some instances, a deviation from 46 chromosomes allows for fetal development and birth. The most well-known example is Trisomy 21(having three copies of the 21st chromosome per cell instead of two), also called Down’s Syndrome.
The egg and sperm cells are unlike any other cell in our body. They’re special enough to have a special name, gametes, and they each contain one set of chromosomes, or 23 chromosomes. Because they have half the typical number per cell, when the egg and sperm cell fuse, the resulting zygote contains the typical chromosome number of 46. Now you know how we get half of our genes from our father (who made the sperm cell) and half from our mother (who made the egg cell). Did I just put in your head an image of your parents having sex? It’s the birds and the bees, folks—it applies to everyone!
All text and art except as otherwise noted: Jeanne Garbarino, Double X Science Editor
World Health Organization. “A prospective multicentre trial of the ovulation method of natural family planning. III. Characteristics of the menstrual cycle and of the fertile phase,” Fertil Steril(1983);40:773-778
Allen J. Wilcox, et al. “Timing of Sexual Intercourse in Relation to Ovulation — Effects on the Probability of Conception, Survival of the Pregnancy, and Sex of the Baby,” New England Journal of Medicine, (1995); 333:1517-1521
Poland ML, Moghisse KS, Giblin PT, Ager JW,Olson JM. “Variation of semen measures within normal men,” Fertil Steril (1985);44:396-400
Alberts B, Johnson A, Lewis J, et al. “Fertilization,” Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002.
[Trigger warning: frank language about sexual assault]
By Emily Willingham
By now, you’ve probably heard the phrase: legitimate rape. As oxymoronic and moronic as it seems, a Missouri congressman and member of the House Science, Space, and Technology committee used this term to argue that women who experience “legitimate rape” likely can’t become pregnant because their bodies “shut that whole thing down.”
If his words and ideas sound archaic, it’s because they are.Welcome to the 13th century, Congressman Todd Akin. It’s possible that this idea that a woman couldn’t become pregnant because of rape arose around that time, at least as part of the UK legal code. People once thought that a woman couldn’t conceive unless she enjoyed herself during the conception–i.e., had an orgasm–so if a rape resulted in pregnancy, the woman must somehow have been having a good time. Ergo, ’twas not a rape. This Guardian piece expands on that history but doesn’t get into why such a concept lingers into the 21st century. A lot of that lingering has to do with a strong desire on the part of some in US political circles to make a rape-related pregnancy the woman’s fault so that she must suffer the consequences. Those consequences, of course, are to be denied abortion access, to carry a pregnancy to term, and to bring a child of rape into the world.
This idea that pregnancy could determine whether or not a rape occurred was still alive and kicking in 20th century US politics, so Akin’s comments, as remarkably magic-based and unscientific as they are, are still not that shocking to some groups. In 1995, another Republican member of the House, Henry Aldridge, made a very similar observation, saying that women can’t get pregnant from rape because “the juices don’t flow, the body functions don’t work.” A year after Aldridge made those comments, a paper published in a US gynecology journal reported that pregnancies from rape occur “with significant frequency.” That frequency at the time was an estimated 32,101 pregnancies resulting from rape in a single year. In other words, the “body functions” did work, and “that whole thing” did not shut down in 32,000 cases in one year alone.
Consider that current estimates are that 1 out of every 6 women in the United States will be a victim of completed or attempted rape in her lifetime and that by the close of the 20th century, almost 18 million women were walking around having experienced either an attempted or a completed rape. The standard expectation for pregnancy rates, whether from an act of violence (rape) or mutually agreed, unprotected intercourse, is about 5%.
In his comments, Akin used the phrase “legitimate rape.” He joins with his colleague of 17 years ago in ignorance about human reproduction. But he also joins legions of people with a history stretching back hundreds of years, people who blamed women for everything having to do with sex and human reproduction. In the medieval world, if a woman bore a daughter and not a son, that was her fault. If she made a man so hot blooded that he forced himself on her, that was her fault for being so attractive, not his for being a rapist. In Akin’s world, in Aldridge’s world, a woman doesn’t need abortion access or a morning after pill to prevent a pregnancy following rape because the determinant of whether or not the rape was “legitimate” is whether or not she becomes pregnant. And the woman, you see, in the Akin/Aldridge cosmos, can “shut that whole thing down” and keep “bodily functions” from working if the rape was, you know, a real, legit-type rape.
In addition to quick primer on human reproduction, I’m offering here a couple of quick points about rape.
Rape is usually an act of violence or power. It is not just an act of sex. It uses sex as a weapon, as though it were a gun or a billy club. It is an act of violence or power against another person without that person’s consent. Nine out of ten rape victims are female. There is not a category of “not legitimate” rape. Sexual violence inflicted without consent is rape. Period.
The thing is, sperm don’t care how they get inside a vagina. They may arrive by turkey baster, catheter, penile delivery, or other creative mechanisms. Any rancher involved in livestock reproduction can tell you that violating a mammal with an object that delivers sperm is no obstacle to impregnating said mammal, no matter how stressed or unwilling the mammal may be.
Akin and Aldridge aren’t the first politicians to manifest a sad lack of understanding of the female body and of human reproduction. Mitt Romney himself has provoked a few howls thanks to his ignorance about birth control, leading Rachel Maddow to offer up a primer on female anatomy for the fellas out there.
Here’s my own quick primer. About the female: The human female takes some time producing a ready egg for fertilization. That time is often quoted as 28 days, but it varies quite a bit. When the egg is ready, it leaves the ovary and begins a journey down the fallopian tube (also called the oviduct) to the uterus. During its brief sojourn in the fallopian tube, if the egg encounters sperm, fertilization likely will take place. If the egg shows up in the fallopian tube and sperm are already there, hanging out, fertilization is also a strong possibility. In other words, if the egg is around at the same time as the sperm, regardless of how the sperm got there, fertilization can–and often will–happen. The fertilized egg will then continue the journey to the uterus, where implantation into the wall of the uterus happens. Again, if a fertilized egg shows up, the uterine wall doesn’t care how it got fertilized in the first place.
Now to the human male. With ejaculation, a man releases between 40 and 150 million sperm. If ejaculated into the vagina, these sperm immediately begin their short lifetime journey toward the fallopian tube. Some can arrive there in as little as 30 minutes. A woman who has been raped could well already be carrying a fertilized egg by the time authorities begin taking her report. Sperm can live up to three days, at least, possibly as long as five days, hanging out around the fallopian tube. So if an egg isn’t there at the time a rape occurs, if the woman releases one in the days following, she can still become pregnant. Again, the fallopian tubes and ovaries do not care how the sperm got there, legitimately or otherwise.
Although Akin talks about “legitimate rape,” what he and Aldridge and so many other men truly are seeking to do is a twofold burdening of women for having the temerity to experience and report rape. If a woman becomes pregnant because of a rape, you see, then it was not rape. Point one. Point two, because of point one, a woman who reports a rape but becomes pregnant was really engaged in a willing sexual act and therefore must bear–literally–the consequences and, yes, punishment of engaging in that act. She must carry a pregnancy to term. She cannot have access to morning after pills or abortion to prevent or end a rape-related pregnancy because if she’s pregnant, it wasn’t rape, and if she’s pregnant, well, that’s totally her fault for not having her body “stop juices” and “shut that whole thing down.” Got that?
Get this: If you’re a woman who has just been raped, among the many other considerations you deserve, you deserve a morning after pill as part of your rape treatment, if you so desire. Because the hormones in the pills can prevent the impending release of an egg, among other things, create an inhospitable uterine environment for pregnancy, this series of pills can block the implantation of a fertilized egg in the uterine wall** they can save you the added pain, burden, and anguish of a pregnancy resulting from a rape. That, Srs. Akin and Aldridge, is the only established way to “shut that whole thing down,” and it’s a right that every single woman should have. **A commenter has alerted us (thank you!) to information that came out in June regarding FDA claims about implantation prevention with the morning after pill, which may not be accurate. More on that hereand here(NYT). Planned Parenthood cites the IUD as a form of emergency contraception that presumably would prevent implantation.
These views are the opinion of the author and do not necessarily reflect or disagree with those of the DXS editorial team. Related links worth reading (updated 8/21/12)
io9 breaks down more of the data about rapes and pregnancies, including information about why mammals don’t tend to engage in sperm selection