by caryn » Sun Nov 18, 2007 12:03 am
Because I'm actually on a 24-hour vacation with my ILs at the moment the original portions of this post will be brief and then I will cut and paste from older posts, but:
Brewer claims that preeclamptic women aren't eating enough protein to grow a baby. Specifically, he claims that a shortage of dietary protein causes insufficient albumin in the bloodstream, leading to leaky vessels, leading to the downstream symptoms of preeclampsia. He is quite explicit about this as the causal mechanism.
But we have no peer-reviewed data which supports this as the mechanism, and a very, very large amount of data supporting a different mechanism.
The current Cochrane Review on this subject found no change in preeclampsia rates when women were advised to increase their protein and calorie intake, and no change in preeclampsia rates when women were advised to a high-protein diet. It did, however, find an increase in SGA births in the high-protein diet group. It concludes: "Dietary advice appears effective in increasing pregnant women's energy and protein intakes but is unlikely to confer major benefits on infant or maternal health."
Here's a link or two to the abstract: http://www.update-software.com/abstracts/AB000032.htm
http://tinyurl.com/3837ht
In addition, you may be aware of the results of two recent large studies: one examined supplementation with the antioxidants C and E, and found that they did not reduce risk, and the other examined supplementation with calcium, and found that it did not reduce risk of occurrence of preeclampsia, but did reduce the frequency of severe outcomes like eclampsia.
Here's a link to the PubMed abstract:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16641396&query_hl=5&itool=pubmed_docsum
Another recent large study published in the American Journal of Obstetrics and Gynecology analyzed almost 30 nutritional factors and found no relation between intake and the development of the hypertensive diseases of pregnancy.
Here's a link to the PubMed abstract:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=11262466&query_hl=7&itool=pubmed_DocSum
The current model for the development of these diseases implicates immune system involvement during initial placental implantation which results in a poorly implanted placenta with inadequately remodeled spiral arteries, and the release of two proteins (sFlt-1, a VEGF antagonist, and sEng, which improves the invasive capability of trophoblastic cells by compromising the maternal immune system) by the placenta.
The entire syndrome is thought to be driven by maternal-fetal conflict. Human babies have large heads and pack on a lot of subcutaneous fat to fuel brain growth; human mothers have small pelvises because they walk upright. The maternal immune system negotiates with the placenta throughout pregnancy to grow a baby the right size to a) thrive and b) fit out. The best evidence we have suggests that when the mother's body has to shut down the placenta before the placenta is interested in triggering labor, a process very similar to graft rejection happens.
Graft rejection is when a foreign organ (and the placenta is foreign; the father's genes shut off the mother's genes via epigenetic imprinting) is rejected by the immune system of the host.
No one would seriously suggest to a patient undergoing kidney transplant failure that the problem was that they were eating insufficient protein.
Here are links to the publicly available paper on this from the Journal of Clinical Investigation:
http://www.jci.org/cgi/content/full/111/5/649
and a PubMed abstract of a Nature Medicine article:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16751767&query_hl=10&itool=pubmed_docsum
In addition, an article appeared in the New Yorker last year discussing this research further:
http://www.newyorker.com/fact/content/articles/060724fa_fact
The maternal-fetal conflict papers are also available in PubMed -- search on David Haig (at Harvard.) I don't have time to do that right now; I have to check out of the hotel. I can do it later if necessary.
I would be very interested to hear of any recent peer-reviewed research showing a causal link between nutrition and hypertensive outcomes, and would welcome any information supporting such a link. And actually, these discussions are quite popular -- in that they attract a lot of viewings and postings. It's just that there's no reason to think a high-protein diet can actually affect hypertensive pregnancies positively, so we don't tend to see much positive comment about this particular diet.