chances of m/c

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m...
(Hillary Israeli) wrote in message
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(typing quickly because DS is sick)

*If it cheers you up at all, severe cases of pre-eclampsia and HELLP
*syndrome generally don't respond much to that sort of management. Our
*best guess at the moment is that a severe case means that your body
*didn't let the placenta implant properly right at the very beginning
*of your pregnancy. When the baby starts to put on weight, and starts
*demanding more blood, the spiral arteries of the placenta are unable
*to ferry a sufficient amount. So the placenta gets hypoxic and starts
*dumping a protein that destroys blood vessels, which gives you all the
*lovely sequelae you and I are so familiar with.

Whose best guess?

For the research on the hypoxic placenta and the protein it dumps in
response, see: http://www.jci.org/cgi/content/full/111/5/649


Read through some of this...it seems to say, "Placental damage seems to
cause an increase in a factor, which independantly, can cause preeclampsia
symptoms in rats." They make a hypothesis about what might cause that
placental damage.

But preeclampsia is incredibly complex...and I think any researcher trying
to narrow in on "one cause" is barking up the wrong tree.

Let's look at what can impair placental function:

Clotting disorders can lead to an increased tendency to clot. If some small
clots form in the placenta, they may tend to grow, gradually impairing
placental function. Impaired placental function is prone to cause fetal
hypoxia, which can trigger the cascade that leads to pe... What helps reduce
clotting? Increasing magnesium to calcium ratio. Getting enough protein,
fluids, vitamins and nutrients to keep blood vessels healthy, blood volume
well expanded, and homocystein levels down. Some herbs and foods tend to
reduce clotting. Medications can reduce clotting, including aspirin and
heparin, two medications commonly given to women with clotting disorders.

Okay, but some women get pre eclampsia without having a clotting disorder...
Well, other things that can decrease placental function include calcium
deposits in the placenta, which can be formed when poorly absorbed calcium
is taken in excess without sufficient magnesium to promote proper
absorbtion. Like, oh, TUMS... And even in women without clotting disorders,
increased estrogen can combine with a variety of nutritional factors to make
clotting more likely.

And sometimes the placenta just doesn't implant in an ideal place or ideal
way.

Some women already have high blood pressure and this reduces the placental
function, rather than reduced placental function causing the high blood
pressure.

Some times women are on medications which process through the liver, adding
stress to an already stressed system. One of the most "unlikely" cases of
PIH I've ever seen involved a strong, well-nourished mom who ate a ton of
protien, salted to taste, etc. But she also had heartburn and took a fairly
strong drug for it that processed through the liver. Now it is possible
there was some other hidden factor, or that the same thing that caused the
heartburn caused the blood pressure rise...

It's important to look at where causality is likely... sometimes the thing
we're pointing to may be a side effect, not a cause.... Does the placenta
have problems because the blood pressure is up or is the blood pressure up
because the placenta has problems?

Don't forget stress... being in a "stressed" state depletes the body of
vitamins and minerals, raises blood pressure and shunts blood away from less
critical areas toward the heart and lungs and brain. Unfortunately the body
considers the uterus to be "less critical"...but the placenta is pretty
pushy and demanding. Interestingly, both b-vitamins and magnesium help
mitigate the effects of stress...

But what we do know is that promoting healthy placental function and
reducing the effects of stress *does* help prolong pregnancies and reduce
problems.

I know that increasing protein and fluids had an immediate effect on my
swelling and blood pressure when pg with my dd. And there is a growing body
of research about how stress affects pregnancy. My best friend's blood
pressure dropped precipitously when she quit her teaching job...

So what can people do, not to eliminate risk (because there are no
guarantees), but to mitigate it?

1. Get enough essential nutrients. In this case, the B-vitamins, Vitamin E,
and Magnesium are the most critical of the "supplements", but vitamin C is
also important in moderation. An essential fatty acid supplement can also
promote healthy tissue growth and function--specifically a supplement high
in DHA and EPA, such as fish oil. Note that supplementing essential fatty
acids will work better if you're also avoiding trans fatty acids, such as
partially hydrogenated oils.

2. Eat sufficient food, particularly protien. Protein is necessary for
growth. The blood volume can't expand well without sufficient protein, nor
can the placenta grow as well. While most people are not undernourished,
when you've spent years getting by on 1500 calories on one diet or another,
it's sometimes surprisingly difficult to bump that up to a reasonable level
for pregnancy. I don't know about other people, but my resting body temp is
almost 2 degrees HOTTER when pregnant, and that means I need more fuel just
to *maintain* my weight, let alone grow a baby.

3. Drink sufficient fluids. Dehydration really screws with your blood
chemistry. It tends to increase nausea, inhibit blood volume expansion, and
make people feel really rotten. You don't have to flood yourself, but
drinking enough can help.

4. Exercise moderately. Reduces stress, improves pelvic circulation,
improves cardiovascular health...all good for placental function.

In addition to these things, because I have a *known* risk factor for
preeclampsia, namely a genetic clotting disorder, I also take measures
specifically aimed at reducing clotting. Most women in my situation will
take a form of heparin. I can't stand the idea, so I use foods like garlic
and purple grape juice, plus my vitamin and mineral supplements to reduce
clotting.

Interestingly, though I miscarried, there were no significant clots on the
placenta when it delivered, and I had very little clotting during the
miscarriage itself. The placenta had implanted strongly, but in a pretty
poor location for adequate blood flow. Sometimes life is like that... you do
everything you can, and things go wrong anyway. But I do know that it wasn't
my clotting disorder that caused my miscarriage. And I do know that I've
seen symptoms that could easily lead to preeclampsia disappear with dietary
changes.

I think that once it's full-blown, diet is usually inadequate to the task of
fixing pe. But most diseases are like that--if you can catch them really
early, diet may be enough. If you catch them a little farther, herbs and
simple medicines may help. But if they get really going, it takes full blown
medical intervention to cope with the aftermath. And sometimes, it really
won't matter what the hell you do.

Jenrose

"Jenrose" wrote in message ws.com...
wrote in message
m...

For the research on the hypoxic placenta and the protein it dumps in
response, see: http://www.jci.org/cgi/content/full/111/5/649

Read through some of this...it seems to say, "Placental damage seems to
cause an increase in a factor, which independantly, can cause preeclampsia
symptoms in rats." They make a hypothesis about what might cause that
placental damage.

It can also cause pre-eclampsia symptoms in humans. sFlt1 is also
marketed as VEGFTrap, and used to impair angiogenesis as part of a
treatment protocol for some types of cancer. The fact that those
patients then often developed proteinurea and high blood pressure led
them to investigate further.

They make the argument that it might be the case that an impaired
placenta becomes hypoxic, which causes it to generate this protein,
which causes further sequelae. But they do not speculate that this
protein has to do with the initial placental damage, though it can
further damage the placenta by impairing angiogenesis. And of course
it is all still speculation, which is why I always word this as "our
best guess at the moment."

But preeclampsia is incredibly complex...and I think any researcher trying
to narrow in on "one cause" is barking up the wrong tree.

Granted. That's why I posted a bunch of other links having to do with
initial placentation. :-) I have been doing a lot of looking at this,
and just picked through some of my bookmarks to answer Hillary's
question. And of course any number of other things can impair
placental function, cause hypoxia, etc. I was specifically addressing
the question of why it was I would say that we were speculating that
the initial placentation could be impaired in PE, and why it could
have to do with the immune system. This seems a fairly
uncontroversial thing to be saying, at this point, as even the
Department of Health and Human Services says it; see
http://www.ihs.gov/MedicalPrograms/MCH/M/HP01.cfm

"The inciting event is theorized to occur soon after conception and is
the result of defective placentation with poor vascularization of the
trophoblast. This may be the result of immune maladaptation between
the maternal host and the fetal partial allograft, genetic
predisposition, and vascular mediated factors."

And sometimes, it really won't matter what the hell you do.

Agreed.

--
C, mama to nineteen month old nursling

In ,
wrote:

*
*Granted. That's why I posted a bunch of other links having to do with
*initial placentation. :-) I have been doing a lot of looking at this,
*and just picked through some of my bookmarks to answer Hillary's
*question. And of course any number of other things can impair

Thanks for the links, by the way. I am going to need quite a while to go
through them

--
hillary israeli vmd http://www.hillary.net
"uber vaccae in quattuor partes divisum est."
not-so-newly minted veterinarian-at-large

(Hillary Israeli) wrote in message ...

Thanks for the links, by the way. I am going to need quite a while to go
through them

You're welcome. This one is also interesting:

http://www.jhypertension.com/pt/re/jhypertension/fulltext.00004872-200402000-00002.htm;jsessionid=ACjoLLBFUWiOPdRyEqcvLTSSaUdlq l0i22hyUWCfrOGi1DpmSiza!882045838!-949856031!9001!-1

(or http://tinyurl.com/2octz)

"It was not until 1996 [27] that sufficiently sensitive methods were
available to allow the demonstration of XOD in term human placenta.
Both protein and enzyme activity are localized in villous and
non-villous trophoblast. The blastocyst is exposed to low oxygen
tensions during implantation, as is the placenta during the first
trimester of pregnancy, a time of maximal trophoblast invasion.
Studies performed in vitro have shown that low oxygen tensions can
stimulate the invasiveness of first trimester trophoblast [28], and
thus may even be necessary for normal placentation. As placentation
procedes, with the erosion of the musculo-elastic walls of the spiral
arteries [29], the blood flow increases and placental oxygen tensions
rise. However, the placentae of pregnancies complicated by
pre-eclampsia and intrauterine growth restriction (IUGR) show impaired
remodelling of the spiral arterioles leading to vessels with reduced
diameters and reactive vessel walls and localized regions of placental
ischaemia/hypoxia [29]. Placental tissues may thus be exposed to
further periods of relative or absolute hypoxia. The expression of XOD
and the activity of XO have been shown to be increased in a
subpopulation of cytotrophoblasts from the placentae of women with
pre-eclampsia [30]."

--
C, mama to nineteen month old nursling