The intimate connection between a human mother and a fetus developing in her womb has traditionally been viewed as the ultimate example of cooperative effort and even self- sacrifice on the part of the mother. However, Haig (1993) has pointed out that the genetic interests of the fetus are not in total alignment with the genetic interests of the mother. This is because the fetus carries only one-half of the genes carried by its mother. The mother-fetus situation can be thought of in terms of three separate genes with somewhat different interests. The genes of the mother constitute one set. The genes of the fetus that are derived from the mother (maternal) constitute a second set. And the genes of the fetus that are derived from the father (paternal) constitute a third set.
From the perspective of the motherís genes, investment in the current fetus must be weighed against investment in existing children or in future children. If conditions are such that investment in the current fetus will severely compromise the probability of survival of existing children or future offspring, then it is in the motherís interest not to invest in the fetus. However, even if the situation is such that future offspring are more likely to survive than the current fetus, from the perspective of the maternal genes in the fetus a greater weight is given to the fetus than to future offspring. This is because only a certain percentage of the genes present in the fetus that are derived from the mother will also be present in future offspring. The genetic interests of the genes derived from the father are even more divergent from those of the mother. Because the paternal genes could come from different fathers in future offspring, there could potentially be even less representation of the paternal genes in future offspring. The maternal and paternal sets of genes in the fetus can exert their respective self-interests because of a phenomenon called gene imprinting. Imprinted genes have different expressions depending on whether they are inherited via an egg or a sperm.
The differing interests of these different sets of genes have led to a process of constantly evolving escalation. This sort of evolved arms race is sometimes referred to as the Red Queen Hypothesis. The Red Queen of Lewis Carrolís fantasy runs in place all day long but never gets anywhere. Similarly, in evolutionary competition, predators get faster and their prey also gets faster, with the net result that the balance remains the same. Examples of the mother-fetus arms race range from the basic issue of sustaining the pregnancy to the struggle for fuel resources if the pregnancy is maintained. One consequence of placental gestation is that the fetus is able to release substances into a motherís blood that have distant effects on her physiology (Haig, 1993). Among these substances are placental hormones that act on maternal receptors. One example of a placental hormone is human chorionic gonadotropin (hCG). One action of the placental hCG is to usurp the role of the motherís pituitary in the production of hCG. This makes it much more difficult for the mother to spontaneously abort the fetus if it is of genetically low quality or if there is a shortage of nutrients in the current situation or some other stressful factor. Human chorionic gonadotropin indirectly results in the stimulation of the release of progesterone that is essential to maintaining the pregnancy. After the eighth week following conception, the placenta starts to manufacture its own supply of progesterone making it impossible for the mother to spontaneously abort through this particular physiological mechanism.
Maternal blood sugar levels typically drop during the early pregnancy and stabilize at a consistently low level throughout gestation (Haig, 1993). The early drop in blood sugar level is not a result of the fetal utilization of glucose because the demands of the fetus in these very early stages are relatively minor. The lowered glucose levels in the motherís blood appear to be an adaptation that has resulted in her resetting her homeostatic controls during pregnancy, as if in anticipation of off-setting the future demands of the fetus. The mother initially reduces her blood sugar levels to limit fetal uptake throughout the pregnancy.
Prior to the pregnancy, when the mother ingested a carbohydrate meal, her blood glucose levels would rise but then quickly return to normal levels in response to the release of insulin from the pancreas. When the mother eats the same type of meal in the advanced stages of pregnancy, her blood glucose levels and her insulin levels both go to higher levels and they remain elevated for much longer periods of time. These phenomena make sense from the perspective of an evolved arms race motivated by the conflicting genetic interests of the fetus and the genetic interests of the mother. The mother and her fetus are in competition for nutrients following every meal. The longer the mother has elevated levels of blood sugar the greater the amount of glucose that can be gained by the fetus. It appears that the maternal insulin resistance displayed in late pregnancy is caused by the placental release of human placental lactogen (hPL). Human placental lactogen is the most abundant peptide hormone produced by primates and its concentrations rise throughout the pregnancy. The human secretions of hPL are largely independent of maternal regulation or maternal levels of glucose or amino acids. Interestingly, the absence of hPL does not appear to have any effect on the pregnancy. Babies born from pregnancies where there has been a total lack of hPL fall within the normal range of expected birth weights. The placenta also produces enzymes that rapidly break down insulin and thus may counter the maternal insulin production. The pancreatic cells that produce insulin become greatly enlarged during pregnancy and women who experience impaired glucose tolerance during pregnancy have a greatly increased risk of developing gestational diabetes.