Deal in the womb: Fetal opiates, parent-offspring conflict, and the future of midwifery
Introduction
β-Endorphin (BE) is the human body’s feel good and analgesic peptide. It is mostly produced by the hypothalamus and pituitary, however, BE-like forms are also found in the placenta [1]. Placental BE (PBE) is produced since the third month of pregnancy and then its quantity in the maternal plasma increases steadily until parturition [2]. Its function is not well understood. Parasitic trematodes and nematodes (such as Schistosoma mansoni, Dracunculus medinensis, Ascaris suum and Trichinella spiralis) also excrete opiates into the hosts’ body to suppress host immune responses [3], suggesting an interpretation that foetuses might also use PBE to suppress maternal immune function [4]. Numan [5] suggested PBE to play a role either in modifying maternal behaviour or in analgesia. Here, we aim to interpret the function of PBE within the context maternal–fetal conflict.
This conflict is rooted in the difference between the adaptive interest of mother and foetus. Mothers face a negative trade-off between current and future breeding success; since the more nutrients they invest into nourishing a current foetus, the less they can spare for potential future ones. Thus, there must be a maternal optimum of resource-allocation between current and potential future embryos. A maternal optimum is not necessarily optimal for the foetus, or, more precisely, for the genes carried by the foetus. Foetuses might wish to gain more than predicted by their mothers’ optimal strategy [6]. Naturally, even the embryo has an interest in conserving some maternal resources for its mother’s future survival and reproduction; thus the fetal optimum is still less than the physiological maximum. The parent-offspring conflict simply arises since the fetal optimum of maternal nutrient supply is higher than the maternal optimum.
The adaptive interest of different fetal genes may also differ. Maternally derived alleles tend to share maternal optimum to a higher degree, since copies of the same alleles are more likely (say, 0.5) to be present in potential future siblings. However, paternally derived alleles are less interested in sparing resources for future offspring, since multiple paternity often reduces kinship between them and future half-sibs [7].
Section snippets
Hypothesis
Haig [8] already speculated about the likely nature of a hypothetical placental hormone involved in maternal–fetal conflict. Here, we propose the hypothesis that PBE is produced by foetuses to manipulate their mothers’ resource-allocation pattern. PBE, like other endogenous opiates, can probably cause addiction and dependency [9], [10]. We argue that foetuses make their mothers PBE-dependent and then trade PBE for extra quantities of nutrients. This hypothesis is testable in the sense that it
Hypothesis
Whatever the molecular mechanism of the conflict is, mother-foetus counter-interest regarding the allocation of maternal resources exerts a selective pressure upon human beings and other placental mammals. This is a more general – but partially overlapping – working hypothesis than the first one. Considering how selection pressure is modified by human health policies yields in the prediction that fetal aggressiveness – i.e., a particularly strong exploitation of maternal resources by the foetus
Concluding remarks
Naturally, we do agree that mothers and babies must receive the best possible health care and medical supply at the current state of science. However, we also point out here that this practice exerts a selective pressure upon our species that favours particularly high nutrient investment into foetuses and thus, indirectly, also favours complicative pregnancies. Mothers (maternal alleles) who supply more to their foetuses will outcompete those who supply less, and babies (fetal alleles) who
Acknowledgement
This work was supported by the Hungarian National Research Grant (T 049157).
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