"The conflict between maternal and fetus genes is one of the weirdest ideas in the modern theory of evolution."* According to evolutionary logic, the fetus "wants" to milk the mother for all it can get; the mother "wants" to restrict the fetus to what it needs to survive and save something for future offspring. The reason is that the fetus benefits from every bit of help the mother gives, while the mother's return on her investment diminishes with increasing investment, (i.e. ever greater investment won't necessarily increase her fitness).
One example of this struggle is the regulation of the mother's blood sugar, which is much than normal higher during pregnancy. Well this makes sense, you might think, because the mother is now feeding a growing fetus. But look at the mother's insulin level, it also is much higher than normal, and insulin is used to down-regulate blood sugar levels. Huh, that's weird, she is secreting more insulin, yet her blood sugar level is ever higher. She must be responding less to insulin. Why should that be?
David Haig suggested that the fetus is trying to increase blood sugar levels by releasing human placental lactogen (hPL, a hormone that reduces the effects of insulin) into the mother's bloodstream and the mother is trying to reduce blood sugar levels by increasing more insulin. The amount of hPL in the mother's blood is astonishing, on the order of 1000-2000x the level of comparable hormones, and the amazing thing is that hPL is entirely unnecessary because babies with nonfunctional hPL genes are completely normal at birth.
So the mother and fetus are battling over the allocation of resources by pumping out more and more hormones.
But wait that's not the weird part! The weird part is, strictly speaking, the conflict is not between mother and fetus, but rather between genes within the same individual. The fetus that contains a gene causing it to release more hPL will someday, provided it is a female, grow up to be a mother whose offspring may contain that very same gene and will be trying to suck every bit of nourishment out of her. The gene is then, within the very same individual, advantageous during fetus-hood and disadvantageous during mother-hood. The net result is that the fetus loses out by possessing the hPL gene, its lifetime reproductive output is reduced, but it doesn't matter.
The gene spreads anyway because the gene increases its representation in the gene pool. There is then an inherent inefficiency in life. The intragenomic conflict leads to reduced reproductive output, through less efficient use of resources and, more importantly, in the hPL case, through increases in the onset of diabetes. 10% of pregnancies result in gestational diabetes; and 50% of the cases of gestational diabetes results in full diabetes later on in life. Would that be object of an intelligent designer?
*Ridley, M. 2001. The Cooperative Gene. The Free Press.