Originally posted by djsnjones
--My "facts" are not your "facts", and so therefore I have nothing to offer you that fits your definition.
I would say that facts, true knowledge, consist of beliefs that are true and justified by reference to reality.
You are offering beliefs, not facts. We have no reason to believe that they're true; there's no good sound evidence to back them up.
In other words, the Cochrane review is evidence-based; your personal experiences are not.
Yes, I was on the final Brewer version of the diet. Yes, my midwife was careful to ask about my activity level etc. and encouraged me to add additional calories to my diet. Yes, I ate the eggs. No, it didn't work.
I am very interested to hear what about the diet you think we have mischaracterized. As I understand him, Brewer's proposed mechanism is that the blood volume is inadequately expanded as a result of poor dietary protein, calorie, salt, and fluid intake to support a pregnancy. He also suggests, as do you, that it would be possible to reverse preeclampsia via dietary changes.
Here's a link to a brief explanation of the mechanism as currently understood by researchers, as elucidated just by the women on this site: http://www.preeclampsia.org/forum/viewtopic.php?t=16607
I would like an explanation for how modifying diet in the third trimester is supposed to reverse the shallow implantation which occured in the first trimester. We know, insofar as we know anything, that the placentas in preeclamptic pregnancies are often shallowly implanted -- we have scientific studies showing this, and elucidating the mechanism.
But we have no reason to suspect that adding albumin to the bloodstream will reverse this process -- I cannot find a single study in PubMed suggesting that it serves any purpose other than having some predictive value. sFlt-1 also has some predictive value. sEng also has some predictive value. Lots and lots of plasma values are off in preeclamptics; albumin is just one.
This study, dating from 1998, is illustrative with respect to albumin values:
Quoting the abstract:
A decrease in serum albumin concentrations is an almost inevitable finding in disease states, and is primarily mediated in the acute phase by alterations in vascular permeability and redistribution. This change is not disease specific but marked changes that persist are generally associated with a poorer prognosis. Critical appraisal of long-standing practices and the availability of alternative colloid solutions have led to a reduction in albumin replacement therapy, and a widespread tolerance of lower albumin concentrations in patients. The factors determining serum albumin concentrations, their measurement and the implications of hypoalbuminaemia are reviewed. The clinical value of serum albumin measurement is discussed.