For the research-y people who want to see the theoretical underpinnings:
This disease is really a problem of evolutionary medicine, plus almost impossible to study in vivo. It's likely compromise between the mother and the father over the size of the neonate at delivery to get the head through the pelvis *and* maximize the odds of survival of the child: http://www.ncbi.nlm.nih.gov/pubmed/16344109
The idea is that the placenta generally embeds shallowly in preeclampsia because the communication between the maternal immune cells in the decidua and the paternal trophoblastic cells (they're epigenetically imprinted to silence maternal genes) goes awry during initial implantation, before you even know that you are pregnant:
http://humrep.oxfordjournals.org/cgi/co ... t/23/4/972
The soluble factors produced by the compromised placenta trigger symptoms when the fetus outgrows the blood supply:
http://ndt.oxfordjournals.org/cgi/conte ... 21/11/3052
and the researchers are currently working on a predictive test for the soluble factors, hopefully to be available later this year.
But the shallow placentation seems to be just in *some* cases of preeclampsia, because not all people with it have this defect of invasion. All women with it *do* seem to produce the same soluble factors. A lot of us seem to have "superimposed" preeclampsia, where there's an underlying condition like chronic hypertension that means we're more sensitive to some threshold level of the proteins produced by the placenta even if it's implanted normally:
So basically it boils down to: some sort of developmental issue with the placenta which results in shallow placentation which results in placental hypoxia which produces chemicals which cause the symptoms. And when the "it boils down to" sentence is *that* complex, you know the problem is an incredibly difficult thing to research. That's why I try to pop most of the current research up here; there's a lot of it, and looking at it briefly gives you a good idea of the scale of the problem...
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