Parent-offspring conflict

Parent-offspring conflict is a term used to signify the evolutionary conflict arising from differences in optimal fitness of parents and their offspring. While parents tend to maximize the number of offspring, the offspring can increase their fitness by getting a greater share of parental investment often by competing with their siblings. The theory was proposed by Robert Trivers in 1974 and extends the more general selfish gene theory and has been used to explain many observed biological phenomena.

In plants
Studies have suggested that parent-offspring conflict may lead to the evolution of optimal seed numbers in plants and has been shown in pod bearing species.

In birds
Some of the earliest examples of parent-offspring conflict were seen in bird broods and especially in raptor species. While parent birds often lay two eggs and attempt to raise two or more young, the strongest fledgling takes a greater share of the food brought by parents and will often kill the weaker sibling (siblicide). Such conflicts have been suggested as a driving force in the evolution of optimal clutch size in birds.

In humans
An important illustration of such conflict is provided by David Haig’s (1993) work on genetic conflicts in pregnancy. Haig has argued that fetal genes would be selected to draw more resources from the mother than it would be optimal for the mother to give, an hypothesis that has received empirical support. The placenta, for example, secretes allocrine hormones that decrease the sensitivity of the mother to insulin and thus make a larger supply of blood sugar available to the fetus. The mother responds by increasing the level of insulin in her bloodstream, and to counteract this effect the placenta has insulin receptors that stimulate the production of insulin-degrading enzymes.

About 30 percent of human conceptions do not progress to full term (22 percent before becoming clinical pregnancies) and this creates a second arena for conflict between the mother and the fetus, because the fetus will have a lower quality cut off point for spontaneous abortion than the mother. The mother's quality cut-off point should also decline as she nears the end of her reproductive life and it may be significant that the offspring of older mothers have a higher incidence of genetic defects. Initially, the maintenance of pregnancy is controlled by the maternal hormone progesterone, but in later stages it is controlled by the fetal human chorionic gonadotrophin released into the maternal bloodstream, which causes the release of maternal progesterone. There is also conflict over blood supply to the placenta, with the fetus being prepared to demand a larger blood supply than is optimal for the mother. This results in hypertension and, significantly, high birth weight is positively correlated with maternal blood pressure.

After birth the young infant may demand more resources than the mother is prepared to provide and the presence of benzodiazepines in breast milk may be a counter to this strategy.

Within the offspring there will be sexual conflict between the genes from the father and those from the mother, with paternally derived genes activating to facilitate a demand for greater resources. Evidence for this comes from Prader-Willi syndrome in which infants with two copies of the maternal chromosomal region 15q11-13 have a poor sucking response and weak cry. Conversely, infants with Angelman syndrome have two paternal copies of 15q11-13 and are active and display strong, but poorly coordinated, sucking. This latter effect is an instance of genomic imprinting in which the effects of genes differ depending on whether they are contributed by the father or the mother.