Deal in the womb: Fetal opiates, parent-offspring conflict, and the future of midwifery

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Summary

This paper argues that parent-offspring conflict is mediated by placental β-endorphins in placental mammals, i.e., foetuses make their mothers endorphin-dependent then manipulate them to increase nutrient allocation to the placenta. This hypothesis predicts that: (1) anatomic position of endorphin production should mirror its presumed role in fetal-maternal conflict; (2) endorphin levels should co-vary positively with nutrient carrying capacity of maternal blood system; (3) postpartum psychological symptoms (postpartum blues, depression and psychosis) in humans are side-effects of this mechanism that can be interpreted as endorphin-deprivation symptoms; (4) shortly after parturition, placentophagia could play an adaptive role in decreasing the negative side-effects of fetal manipulation; (5) later, breast-feeding induced endorphin excretion of the maternal pituitary saves mother from further deprivation symptoms. Finally, whatever the molecular mechanism of fetal manipulation is, widespread and intense medical care (such as caesarean section and use of antidepressants) affects the present and future evolution of mother-foetus conflict in the human species (and also in domestic animals) to increase ‘fetal aggressiveness’ and thus technology-dependency of reproduction.

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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