Re: Homocysteine


"HeartZine" <vmurphy@xxxxxxxxxxxxx> wrote in message
news:1130412029.370086.23470@xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
> There has been a lot of publicity surrounding Homocysteine in recent
> months, raising crucial questions regarding the role of this factor.
>
> I would like to put the following questions to the group:
>
> 1./
> Does Homocysteine contribute to cardivascular disease, or is it
> inactive in itself but produced as part of abnormal cardiovascular
> pathophysiology.

That's a good question. They really don't know for sure. An association was
made in that those with high Homocysteine levels tend to have CAD as a risk
factor. It is used as a marker for risk of developing disease. The vast
majority of the homcysteins being performed now are for risk assessment.
That's where we are at now.
Homocysteine levels in the past were used in detecting folate or B12
deficiency. Folate or B12 deficiency is more common in the old as atrophic
gastritis becomes more prevelent.

>
> 2./
> Is their a health benefit in reducing levels of Homocysteine, or does
> this action only serve to reduce calculated risk factors by skewing the
> results. cf. reduction of rash by application of cosmetics.

You need to be careful about the context of homocysteine. If you have a
vitamin deficiency such as B12 you may suffer permanent damage if that
correction is not undertaken. In this case the correction of B12 deficiency
will reduce the homocysteine level.
The other context of risk reduction is more clouded with mixed results in
reduction of coronary risk.
A marker may not be directly responsible for the damage but another comorbid
factor that may be doing the damage.
You can reduce the marker but not the risk for heart disease if the latest
studies are valid. You then have to find a better marker for risk if your
homocysteine is reduced by taking folate and B vitamins. The new maker would
then be the gene that causes high homocysteine. The new hypothesis thus
becomes those with the specific genetic mutations have a high risk of CAD.
They will always have the mutation present and thus always have the risk
regardless if they reduce their homocysteine level.
One way to check for that is take those without mutations such as simple
vitamin deficiency states and the others to see if homocysteine is directly
responsible for damage.
My guess is that both groups have a high risk. One is correctable and the
other is not.
All speculation on my part.

>
> Thank you for your consideration of these issues,
>
> Vincent F Murphy
> Editor of HeartZine Magazine
> www.heartzine.com
>


.

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