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Getting Pregnant: Why Can’t Everyone Just Get Along?

Write By: Valentin Rosca on


How easy is it to get pregnant? Apparently, it is too easy for some but very difficult for others. In studies conducted in health-rich countries, the average amount of time it takes to get pregnant (called ‘‘waiting time to conception’’) is seven to eight months. At maximum fertility, in her early 20s, a woman has only about a 25% chance of getting pregnant per unprotected cycle, and it has been estimated that it takes about 100 acts of intercourse per pregnancy.  Why should it be so difficult? As we will see later, highly frequent sexual activity for a couple may play an important role in making sure her immune system does not attack the fertilized egg. But beyond that, other factors that seem to affect fertility include age, health (such as presence of sexually transmitted diseases [STDs] , or diseases like malaria), genetic incompatibilities, exposure to ubiquitous biochemicals in our environment, and lifestyle factors like smoking and alcohol and drug use. In this article I will focus primarily on aspects of evolved biology that impact pregnancy, although the other proximate factors, including sociocultural variables, play equally important roles.


Polycystic Ovaries as a Cause of Infertility

pregnant-woman-with-baby-shoesOne frequent cause of female infertility is polycystic ovarian disease or syndrome (PCOD or PCOS), which seems to have a genetic basis and is associated with obesity and a variety of hormone imbalances, including those that underlie conditions that predispose a person to heart disease and diabetes (known collectively as ‘‘metabolic syndrome X’’). Given that these seem to be on the increase worldwide, it is likely that PCOD will also increase in the future. Women with PCOD produce a large number of very small follicles that typically fail to ovulate. In many women it is not a permanent condition and in cases where it is accompanied by obesity, a small weight loss will often result in ovulation. Some scholars have suggested that it can be regarded as a ‘‘fertility storage condition’’ that allows fertility to be delayed until physical and environmental circumstances are more supportive of reproduction. Other researchers have noted that increased rates of PCOS parallel rates of obesity and insulin resistance and are particularly common in populations that are undergoing lifestyle transition or ‘‘Westernization,’’ and suggest that the syndrome is a result of entering into an evolutionarily novel environment.  According to this argument, this sort of transition puts women at risk for a number of challenges to reproduction and overall health, suggesting that we may begin to see increases in rates of reproductive failure as more and more people migrate to areas of relatively greater resource abundance and lower levels of physical labour. Another view proposes that the elaboration of the endometrium necessary to support a large-brained fetus has left humans vulnerable to disorders such as PCOS.  In particular, humans have unusually long follicular phases, presumably required to provide time and sufficient hormone production to form the more complex endometrium into which the placenta will implant if conception occurs. But this prolonged follicular phase makes humans vulnerable to excessive hormone production and to ovulation failure. Cell turnover rates are also higher in women with PCOS, which may explain their greater vulnerability to endometrial cancers. This proposal is in agreement with the argument that PCOS may have been adaptive at one time when caloric intake was lower but that today, in richer environments, it is a liability. Evidence that women with PCOD have delayed menopause suggests that not only do their more numerous follicles last longer, but they may be able to make up for lost fertility early in life by reproducing later than usual if conditions improve.  This concept has been linked with the fatal origins hypothesis, which argues that conditions during fatal development have long-term impacts on later life fertility and health. Women with metabolic syndrome X and other hormone imbalances during pregnancy may have foetuses that are ‘‘programmed’’ toward similar problems later in life, including insulin resistance, obesity, and PCOS. Whether these actually develop depends on the conditions under which growth and subsequent reproduction occur. Thus, PCOS can be seen as an example of a phenomenon that is problematic under certain circumstances (a ‘‘defect’’) and adaptive (a ‘‘defence’’) under others. This warrants referring to the condition as simply PCO (which may be good) rather than PCOS or PCOD, both of which explicitly emphasize the defect concept.

Physiological Changes in Pregnancy

pregnant-coupleMany aspects of a woman’s physiology are altered when she becomes pregnant. One of the most important is that she metabolizes food more efficiently and gets more nutrients from foods she consumes than she does when she is not pregnant. This leads to weight gain even when food intake does not increase or when it decreases, as it often does early in pregnancy in association with morning sickness. The proximate mechanisms for changed metabolism are hormonal alterations that optimize digestion. Among the hormones that increase is one (cholecystokinin) that also makes a woman feel tired and listless after a meal—such decreased activity also contributes to weight gain,  in addition to enhancing energy conservation. Now that she is ‘‘eating for two,’’ all of these changes can be seen as contributing to improve gestational environment. This increased ability to put on weight and store energy as fat was clearly adaptive for our ancestors, but in today’s world, where food availability is sometimes excessive, this ability raises concerns for women and their health care providers. Fatal and maternal developmental changes during pregnancy are so complex that it is amazing that any of us get born. If you read enough about what can go wrong, it seems a miracle that any pregnancy makes it to the end without a damaged fetus or a maternal system that can never conceive again. In fact, so much of the medical literature emphasizes the things that can go wrong that women often experience as much anxiety as joy over their pregnancies. An evolutionary perspective recognizes that when things do go wrong, there are often good evolutionary reasons behind it.  When reproductive maturity is reached and conception occurs, the mother’s system must be able to recognize that fact and work to maintain the pregnancy for the next nine months. Recall that when ovulation occurs, the corpus luteum produces estrogens and progesterone for several days so that if the egg is fertilized, it can be ‘‘rescued’’ and can continue to produce hormones required in early pregnancy, especially progesterone, until production is taken over by the placenta several weeks later. The term rescue is frequently used in biology and medical texts because the assumption is that the ‘‘normal’’ (most common) occurrence is for the corpus luteum to deteriorate in women who spend more time having menstrual cycles than not. It assumes that termination of the corpus luteum is the normal and expected occurrence at the end of the menstrual cycle, whereas in the ancestral past, its persistence (due to pregnancy) may have been more common than its demise, given that highly frequent menstrual cycling was relatively rare. 


From the time that the corpus luteum is rescued until the baby is born, so many interrelated systems must develop and function right that to describe them is to emphasize what can go wrong. Here are just a few of the things that happen from fertilization onward: rescue of the corpus luteum, implantation of the zygote, burrowing of the trophoblast into the uterine lining, development and proper functioning of the placenta, establishment of communication between mother and fetus through the circulatory systems, adequate nutrition for the mother so that nutrients can pass to the fetus, adequate oxygen transport, hormonal regulation of fatal growth, and keeping the uterus from having contractions until labour begins at term. To move forward in our discussion of pregnancy, we need to describe some of the hormones that orchestrate the process. The placenta produces a hormone similar to growth hormone, the production of which increases throughout pregnancy. It functions to make glucose more readily available to the fetus and, later, enhances milk production. Levels are proportionate to placental size and both have an influence on how large the fetus becomes. Estrogens, also produced by the placenta during pregnancy, stimulates uterine growth and development of the mammary glands in preparation for later breastfeeding. Progesterone from the placenta is secreted to both mother and fetus and helps to maintain the uterus and breasts and inhibits ovulation. It also affects thirst, appetite, and fat deposition. Clinical guidelines suggest that ‘‘normal’’ progesterone levels in pregnancy are those reported for well-nourished women in Chicago or Boston and that when the levels are too low, complications may result. But anthropologists who study populations that are not as well nourished (overly nourished?) report much lower levels, levels that would, in fact, be deemed problematic in Boston. In fact, pregnancy loss is no greater in women in populations with lower progesterone than in those with high levels, again calling into question the medical understanding of normal. Pregnancy is usually described in thirds (trimesters) because very different actions are taking place in each and the timing of growth and development events is somewhat constrained. The first trimester is one of growth and differentiation of the embryo, the second is when total length of the fetus increases, and the third is when the developing fetus is putting on weight as fat. Our discussion will examine what goes on in each of these trimesters and how our evolutionary history reflects the changes and impacts the successes or failures. 


First Trimester: The Story of the Egg, Part II

mother-holding-childThe egg from its embryonic stage until fertilization and implantation, or, more commonly today, menstruation. Here we will back up a bit and focus on what happens when the zygote prepares to implant into the uterine lining as a blastocyst. Part of the blastocyst (the inner cell mass) becomes the embryo and part (the trophoblast) becomes the placenta. From the view of clinical medicine, a failure to implant is a problem and a common cause of what seems to be infertility in women. Clearly some cases of failure to implant are pathological and can benefit from medical or pharmacologic assistance, but there are numerous situations in which failure of a pregnancy at this stage is a ‘‘good thing’’ from the perspective of evolutionary medicine. The zygote that results from the union of egg and sperm is unique and genetically different from both the mother and the father. Our immune systems are designed to deal harshly with organisms that are not familiar by damaging or outright rejecting them. This is fine when the invading organism is a pathogen, but when it is the beginnings of a hoped-for pregnancy, expulsion may not be desirable. The sperm that contributes to formation of the zygote has already successfully survived passage through the cervix, the vaginal mucus, and the fallopian tubes; at any point in its journey to the egg the mother’s system could have destroyed it. For a while the zygote can ‘‘hide’’ from the mother’s immune system, but eventually it is fully exposed and vulnerable. The luteal phase following ovulation is a time when the mother’s immune system is slightly dampened. This is a time when she might be more vulnerable to illnesses, but this dampening serves the zygote well because it is less likely to be detected and rejected. This is one of those trade-offs: a woman is a bit less protected from illness during the luteal phase and early in pregnancy, but if she does conceive, she is a bit less likely to reject the zygote. Implantation is the process whereby the embryo imbeds itself in the endometrial wall of the uterus. This is when HCG begins to be secreted by the trophoblast (a sort of pre-placenta) and a simple urine test can reveal the pregnancy.


Implantation is the process whereby the embryo imbeds itself in the endometrial wall of the uterus. This is when HCG begins to be secreted by the trophoblast (a sort of pre-placenta) and a simple urine test can reveal the pregnancy. It is probably appropriate to say that this is when pregnancy ‘‘officially’ ’begins and it is an important step in that a high percentage of fertilized eggs fail to implant.The ability to secrete HCG serves as a signal to the mother’s system that the embryo is viable, at least to this point.  The egg and the endometrium work together to coordinate implantation; if the timing is off on either side, the process will likely fail. But if all goes well, the embryo becomes successfully attached to the uterine wall and exchange of nutrients and oxygen begins. If things do not go well, or if implantation is delayed too long, the embryo is likely lost in what the mother perceives as a late, and perhaps especially heavy, menstrual flow. She may not even realize that she had conceived. It may seem surprising that so many fertilizations and conceptions are lost early in pregnancy. What a waste, and how sad the loss is for so many couples trying to get pregnant. But from an evolutionary perspective, it makes sense that embryos that may not have a good chance of surviving pregnancy to grow up and reproduce themselves are discarded before the mother invests too much time and energy in gestation. As Virginia Vitzthum says, rather than humans having a defective or inefficient reproductive system, it appears that we have one that ‘‘has been designed to be flexible, ruthlessly efficient, and, most importantly, strategic.’’  This will lead us to an evaluation of early pregnancy loss that differs from the clinical view,  as we will see later. Once pregnancy is well established, by the end of the second month, the percentage of embryos that are lost drops precipitously. A lot of that is up to the communication system between the mother and infant via the placenta, so before moving on in this pregnancy, let’s learn more about this amazing organ.

The Placenta

pregnant-woman-heartThe largest group of mammals is sometimes referred to as the ‘‘placental mammals,’’ illustrating the significance of the placenta in understanding characteristics of this subclass of mammals. There are several types of placentas, reflecting different demands of pregnancy among mammals. One way in which they are classified reflects the number of membrane layers between the maternal and fatal systems and how much of a barrier exists between the two circulatory systems. Humans have a type of placenta that enables fatal tissues to invade deeply into maternal tissues, so that there is only a thin layer between fatal and maternal blood vessels. Furthermore, the deeper invasion provides for a greater surface area over which nutrients and gases can be exchanged. This thin barrier between the maternal and fatal system also allows freer exchange, via diffusion, of molecules, both good (nutrients and oxygen) and bad (drugs, toxins, et cetera).  Other mammals with this type of placenta include monkeys, apes, tarsiers, rodents, and rabbits. Even within a group of mammals with the same type of placenta, there are a number of differences that relate to reproductive strategies of different species. For example, the mouse has the same general type of placenta that humans have but it gestates a dozen or more foetuses for only about three weeks, whereas the human usually carries only a single fetus for nearly 13 times that long. How can the same type of placenta handle such radically different gestational physiologies? One argument proposes that placental genes are differentially expressed in the first and second halves of pregnancy.  In the first half, the genes that are charged with getting the pregnancy started and with basic energy and gas exchange are similar in both mice and humans because the demands are similar at this stage. Once that has happened, more recently evolved (and mouse- or human-specific) genes kick in and allow for the short gestation in mice and the long gestation in humans and all of the associated differing physiological requirements and challenges. The fetus is sometimes referred to as a graft. Because mothers and foetuses share, on average, only about 50 percent of their genes, it is not surprising that just as skin grafts often fail, the fatal graft sometimes fails, leading to spontaneous abortion or miscarriage. This is an immune challenge that is faced by no other organ in the body but it is usually mediated adequately by the placenta.  What keeps the maternal system from rejecting all foetuses carrying genes and their proteins that would usually be recognized as foreign to the mother’s immune system? As noted, just as in the luteal phase of the menstrual cycle, the mother’s immune system is depressed early in pregnancy (under the influence of progesterone) so it is not as likely to reject the fatal graft as it might at other times. This phenomenon has been referred to as the ‘‘immunological inertia of viviparity,’’  and it is probably important for all animals that gestate internally and give birth to live young. 

Maternal-Fatal Incompatibilities: The MHC Gene Complex

In some cases the mother may reject a fetus that is too much like her. This is seen in the case of immune system genes that are part of the major histocompatibility complex, known as MHC. The MHC is found in all vertebrates and it is extraordinarily diverse, even in humans, who have hundreds of alleles.  This diversity partly reflects direct effects of pathogens on the human genome throughout history, but some of it may be influenced by mating patterns that increase the likelihood that offspring will have disease resistance. (In this case, selection favours greater differences between parents in MHC genes and offspring who are genetically different from the mother.) This phenomenon is referred to as ‘‘MHC-mediated mate choice’’ and it appears to be mediated by olfactory cues.  This has been amply demonstrated in rodents, but, as noted with regard to menstrual synchrony, the role of olfaction in human behaviour is still uncertain and highly controversial. In any event, even if olfaction is not influencing mate choice in humans, parental gene-sharing at the MHC locus is strongly linked to implantation failure and spontaneous abortion. In a study of a Hutterite population, couples who were similar in MHC genes took more than 2.5 times longer to achieve pregnancy and had far more pregnancy losses than couples who were genetically different. If a woman mates with a man whose histocompatibility genes are similar to hers, the resulting embryo will also be genetically similar to her. In this situation, she may not recognize the embryo when it begins to implant and may not depress her immune system to prevent rejection. One suggestion is that this is an ‘‘anti inbreeding’’ mechanism and it also may explain why women who have trouble conceiving with one man are easily able to get pregnant when they have a different partner.  The mechanism may be particularly important in small populations where genetic diversity would otherwise be low, a phenomenon that probably characterized most of human evolutionary history. 


Maternal-Fatal Incompatibilities: Blood Type Genes

pregnant-couple-holding-handsProbably more common are situations in which rejection occurs because the fetus is very different from the mother. But even if the pregnancy is maintained, maternal fatal differences may cause complications such as that seen when the mother is Rh negative and the fetus is Rh positive. In this case the fetus has antigens that are different from the mother’s and antibody production is triggered by her immune system, usually at the time of delivery. Unless these antibodies are neutralized within a few hours of delivery, they will remain in her system resulting in more severe immunological problems in subsequent incompatible pregnancies. The abortion and stillbirth rate is higher in these incompatible pregnancies, as is haemolytic disease of the new-born. ABO incompatibility is more common, although we do not hear much about it because it appears that many of the incompatible pregnancies may be lost before the mother even knows she is pregnant, perhaps before implantation. These occur most commonly when the mother is blood type O with a fetus of blood type A or B (also possible with mother type A and fetus type B and vice versa).  In this situation, the type O mother has antibodies against A and B antigens that circulate in her system at all times, even if there is not an immunological challenge. Thus, it is theoretically possible for these antibodies to cross the placenta and destroy the red blood cells of foetuses of type A or B, resulting in a number of complications and even miscarriage. Clinically recognized problems are not as common as would be expected, however, and although there are cases of elevated red blood cell counts in new-borns of ABO incompatible pregnancies,  this does not appear to affect the infant’s long-term health. 


As noted, one reason that ABO-incompatible pregnancies do not come to the attention of clinicians is that most are probably rejected before or soon after conception. In an early survey covering the years 127–1944, there was a net deficiency of 25% of A children in father A–mother O matings compared to the opposite configuration (father O–mother A). This meant a fatal death rate of 8% of all A children or 3% of all conceptions for the population they studied. These figures are much higher than the contemporary Rh incompatibility death rate of 0.5%. These researchers argued that the reason that ABO haemolytic disease of the new-born is so rare is that most of the pregnancies that would lead to the disease are aborted or miscarried before the disease is manifested.  Other studies confirmed the lower fertility in couples who were incompatible in genes of the ABO complex. Although these findings have been controversial, it is clear that the placenta is not a perfect barrier against fatal antigens that may trigger the mother’s immune response, just as it is not a very good barrier against noxious agents that may affect the fetus. Is there evidence that the human placenta with a thinner barrier is less protective than other types with thicker layers? A particularly tragic example of the problems that arise when drugs pass to the fetus through the placenta was the use of thalidomide in the 1950s and 1960s as a drug to suppress nausea of pregnancy. When the drug was tested on galagos, primates with thick-barrier placentas, it had no apparent effect on the developing fetus.  But when the drug was used by humans, serious limb malformations occurred in the fetus, crippling thousands of European children (fortunately, due to a particularly vigilant member of the U.S. FDA, Frances Oldham Kelsey, the drug was prohibited in the United States). One of the problems with testing drugs for use in pregnancy is that placenta types are so variable across species, even within taxonomic groups, that tests done on other species (like macaques and rats) may not be meaningful for understanding human pregnancies. Of course, it is obvious that testing drugs directly on pregnant women would not be ethically or morally acceptable, despite the potential benefits.


Early Pregnancy Loss and Maternal-Fatal Conflict

pregnant-woman-sunshineEvolutionary biologists often talk about pregnancy as a time for potential mother-fatal conflict because the interests of the mother and fetus do not always coincide.  If a pregnancy interferes with her own health or the health of her current and future offspring, it may be in the mother’s best interest to abort, but it is clearly in the interest of the fetus to maintain the pregnancy, no matter how bad the situation is. Based on studies in health-rich populations, it has been estimated that more than half of all conceptions are lost within the first five to six weeks, most of those occurring before implantation. Perhaps only a third of conceptions result in a healthy, full-term infant.  Preliminary studies of women in health-poor populations suggest that the failure rate is even higher.  If reproductive success is what it is all about, then how can there be benefits to early pregnancy loss? One way to examine this is to recall that for humans, quality of offspring overrides quantity because of the huge investment made by women and couples in each pregnancy and the subsequent years of parenting. An evolutionary perspective argues that gestating, giving birth to, breastfeeding, and raising an offspring that is not healthy and capable of reproducing would be energy that could be better allocated to future offspring who are healthier and more likely to reproduce. Indeed, in one study 77% of spontaneous abortions in the first trimester had chromosomal abnormalities,  although the portion of all lost conceptions due to genetic abnormalities is probably closer to 15%.  From the medical perspective, however, reproductive failure is often seen as pathological or at least unhealthy and preventing it is an overriding goal for physicians, women, and couples, serving as an example of where medicine and evolution might be at odds. Certainly there are examples of early pregnancy failure in which there are clear clinical explanations such as those caused by sexually transmitted diseases, other infectious agents, or uterine and placental abnormalities, but in many cases there are less obvious explanations, which may be effectively sought in evolutionary understanding of strategies for reproductive success. This might be seen as a ‘‘cut your losses’’ strategy whereby a pregnancy is terminated early if the fetus is not likely to be viable or healthy or otherwise jeopardizes future reproductive opportunities. As Vitzthum notes, in many cases of early pregnancy loss, ‘‘the woman is not necessarily broke, and there may not be any reason to fix her.’’ 


Timing in terms of resource availability may also play a role in early pregnancy loss. Vitzthum found that when Bolivian women engaged in particularly strenuous labour, such as during the planting and harvesting seasons, their rate of pregnancy loss was almost four times the risk during other seasons.  In general, women who work in the agricultural sector have higher losses than those who are not engaged in hard physical labour. Psychosocial stress may also have an impact on pregnancy loss,  most likely through elevations of the hormone cortisol.  This adds support to the evolutionary view that successfully bearing and raising offspring in humans benefits from social support to reduce stress at all stages. The risk of losing a pregnancy also rises with age, most likely associated with declining maternal health, and it is especially pronounced in women from health-poor populations.  If health status were equal, however, an evolutionary perspective would predict that older women would have a higher threshold for rejecting foetuses that were less-than-optimal if their future chances of reproducing were limited by age. In other words, the ‘‘cut your losses’’ concept would no longer work and would be replaced by ‘‘anything is better than nothing.’’ Perhaps in support of this, children with congenital defects are more common in births to older women. In fact, the rate of spontaneous abortion of foetuses with chromosomal abnormalities is much higher in women aged 25–29 than in those aged 30–39. Although the termination rate declines after the first trimester,  the potential for maternal-fatal conflict continues, especially if there is nutritional competition. The timing of nutritional stress may be important. Primate researcher Suzette Tardif and her colleagues demonstrated that if marmosets experience even modest food restriction in early to mid pregnancy, fatal loss frequently occurs.  The same degree of food restriction later in pregnancy, however, does not usually result in loss, although preterm deliveries are more common. From an evolutionary perspective, fatal loss in early pregnancy under conditions in which the infant may have compromised health makes sense in that it occurs before significant investment in the pregnancy has been made by the mother. Later, however, the mother’s reproductive success may be better served by maintaining the pregnancy until birth, at which time breastfeeding and other forms of maternal care may be able to make up for what was lost. In addition to pregnancy having the potential for mother-infant conflict, it is also a time of father-mother conflict in evolutionary terms. A particular pregnancy may be the only one the father will have with a given woman, so it may not be important to him (in an evolutionary sense) to compromise a current pregnancy for a better return in a later pregnancy. For the mother, however, she may be able to have more pregnancies, so if the current one seems compromised, terminating it and starting again later may be a reasonable strategy for her. 

Gestational Diabetes

Other clinical conditions that benefit from consideration from an evolutionary perspective and that may also result from maternal-fatal competition for nutrients include gestational diabetes and eclampsia/preeclampsia. In these cases, changes in maternal physiology that work to increase delivery of oxygen and nutrients to the fetus have passed from ‘‘normal’’ to problematic and usually warrant medical treatment. Furthermore, women who develop gestational diabetes are at higher risk for type 2 diabetes later in life. For women without diabetes, blood glucose levels rise after a meal and return to lower levels when counteracted by insulin. During pregnancy, however, both glucose andinsulinlevelsremainelevatedforalongertimetobenefitthefetus.Inevolutionary biologistDavidHaig’sview,thisisanexampleofthefetalinterestsworkingagainstthe maternal interests as the fetus obtains more and more glucose at the expense of the mother’s health. Because glucose elevation is also associated with excess nutrient intake in pregnancy, it is more common in health-rich countries. Women who develop gestational diabetes often give birth to large infants who are themselves predisposed to developing diabetes later in life.  This suggests that there is likely an optimal level of nutritional intake during pregnancy and that both reduction and excess of nutrients can cause pregnancy complications and lifelong health problems for both mother and infant. Thus we have another example of balancing selection, whereby both ends of the pregnancy food-intake scale result in reduced reproductive success.

Eclampsia and Preeclampsia

pregnant-womanPreeclampsia and its more severe form, eclampsia, is a complication of pregnancy worldwide, found in both health-rich and health-poor populations. Preeclampsia is associated with hypertension in the mother and is estimated to occur in as many as 10% of births. The only ‘‘cure’’ for preeclampsia is delivery of the fetus and placenta, so it is a common reason for premature birth. If the pregnancy is not terminated, the mother will experience damage to the kidney, liver, and brain, and maternal convulsions may result if it proceeds to eclampsia. Furthermore, even though the short-term effects may be improved with delivery, there is evidence that there may be lifelong effects on maternal health.  Unfortunately, there is no animal model for preeclampsia, which has inhibited research on causation and potential interventions. Some scholars  argue that the disorder is related to increased brain size in Homo sapiens and suggest that it may be uniquely found in our species. One notable effect of increased brain size in our species is increased need for oxygen and nutrients, as discussed earlier. At the time of implantation of the embryo, the trophoblast is imbedded in the uterine wall in such a way that it co-opts maternal blood vessels to provide for the needs of the developing embryo. This process of implantation of the trophoblast within a few days of conception is pretty much the same in all mammals. In humans, however, there is a second co-option of maternal blood vessels (known as a secondary invasion of the trophoblast) that occurs in the third month of gestation when brain development in the fetus takes off and nutrient and oxygen needs increase significantly. Sometimes this second invasion is incomplete or fails altogether. Among the reasons for this may be maternal fatal similarities in MHC genes  or the result of maternal-fatal conflict for nutrients that the infant ‘‘wins.’’  In this latter case, preeclampsia ‘‘makes sense’’ from an evolutionary perspective because it serves as a way for the fetus to divert resources from the mother to itself. In response to increasing nutrient and oxygen needs of the fetus and the limited vascular support provided by the incomplete invasion, the mother’s own blood flow system must compensate, with the resulting elevation of blood pressure. Slight elevations of blood pressure are common in pregnancy, but when it becomes excessive, the disorder of preeclampsia is diagnosed and women who are receiving prenatal care are monitored closely and usually delivered early. Where prenatal care is absent, death of the mother and infant often results: the World Health Organization estimates that as many as 70,000 women die each year from eclampsia/preeclampsia. This suggests that eclampsia/preeclampsia was likely a major agent of natural selection in the past when early induction of labour and delivery of the fetus was not an option.


Noting that preeclampsia is usually restricted to first pregnancies, immunologist P. Y. Robillard and his colleagues suggest ways of reducing the incidence of preeclampsia through understanding the evolutionary background and by relating the disorders to other aspects of human reproductive ecology including highly frequent and nonovulatory sexual activity. There are other interpretations and recommendations for treatment of preeclampsia,  but an evolutionary perspective offered by Robillard and his colleagues has a somewhat simple recommendation: delay pregnancy until after several months of sexual activity, preventing what they refer to as not just a disease of first pregnancy, but a ‘‘couple disease’’ resulting from exposure to novel sperm.  They argue that delaying pregnancy for a few months gives the woman’s immune system time to adjust to her partner’s antigens, decreasing the likelihood that her system will challenge the fatal ‘‘allograft’’ in the early months of pregnancy. So if a woman wants to try to prevent developing preeclampsia, Robillard and his colleagues would advise her to wait a while before attempting pregnancy with her partner. They may also suggest that she have sex with this partner frequently so that her system can adapt to his sperm and the associated antigens. In this rather speculative view, highly frequent sexual activity in human partnerships may be protective against the failure of the second deep invasion of the trophoblast. From an evolutionary perspective, women in the past who engaged in frequent nonovulatory sexual activity may have had more successful pregnancies than those who engaged in sex only when they were ovulating. Unfortunately, the evolutionary view of pregnancy is one of stress and conflict, rather than the unrestrained joy that many women feel when they first learn that they have conceived. Of course, the joy is understandable and appropriate in a wanted pregnancy, but the first few months are often not much fun for the mother because it is the time of morning sickness and physiological changes that may be strange and disconcerting. Once the pregnancy ‘‘takes,’’ however, it takes off and usually results in a healthy offspring. But as we will see in the next article, getting pregnant is not the whole story. We begin with a bit more commentary on the first trimester and then discuss the importance of nutrition throughout pregnancy, continuing the refrain that reproductive success is about food.

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