Re: (Oxydized) LDL not Mr. Bad Guy?



M

MattLB

Guest
Susan wrote:
> Enrico C wrote:
> > A new 8-year-long research says:
> > "there was no relation between level of antibodies to oxidized LDL and
> > the development of CHD or CVD."
>
> In this case, the question is whether antibody formation is an accurate
> indicator, since it's not direct measure?

Also oxidised LDL in circulation isn't the problem, it's oxidised LDL
in the artery wall. Since the macrophages in the artery wall tend to
get stuck there and then die (so never present to the rest of the
immune system) it's possible that any antibodies are unrelated (or only
weakly related) to actual plaque formation.

MattLB
 
Arachidonic is much more biochemically active than Mead acid, which is
why some like Enig say that it is a "filler" and ineffective. Those
who attack me want it both ways. If it is so much less biochemically
active (as all agree with, including myself, except, apparently
MattLB), then it will not cause the kinds of problems AA does.
Moreover, I am suggesting that the body should produce Mead acid on its
own, rather than getting it from the diet. In this way, you rely on
the intelligence of cells to refrain from producing something dangerous
to themselves. The only way you are going to get AA in your cells is
if you eat a lot of PUFAs, which the evidence suggests is a terrible
idea.

I don't know how MattLB thinks the oxLDL is going to get to the artery
wall if it is not in ciruculation first, though it's true that the
antibodies could very well be a red herring here. What MattLB is
talking about is not the first stage of "coronary heart disease" -
inflammation will occur first, and the oxLDL is acting as an irritant
that stresses cells, which then signal for the "immune system." Then
the macrophages come in and are rendered dysfunctional, creating what
one scientist called "death zones" in the artery walls. This is when
plaque formation begins.

It is important to point out that to have so much oxLDL as to cause
this problem, your diet has to be really bad: full of PUFAs, meat
cooked while exposed to air, and few antioxidant-rich foods. The
"heart disease epidemic" began when more food items were refined to a
point that destroyed much of the antioxidants. People were also eating
food like fried meats in large amounts, without antioxidant-rich foods
(meat and potatoes do not contain much in the way of antioxidants, for
example). Such an "epidemic" happened in England in the late 1900s,
when they began using powdered dairy, which is very rich in oxidized
cholesterol. In the USA, it happened after WW II, for similar reasons.
Refined oils, high in PUFAs, then became common by the 1960s, and the
"epidemic" reached a peak, though it's very high now, considering how
few people died of "heart disease" in the USA prior to 1940 or
thereabouts. Since the "epidemic" killed many men in "middle age,"
this should have also happened prior to 1940, and thus the only
explanation that makes sense in this dietary one.
 
montygram wrote:
> Arachidonic is much more biochemically active than Mead acid, which is
> why some like Enig say that it is a "filler" and ineffective. Those
> who attack me want it both ways. If it is so much less biochemically
> active (as all agree with,

Unlikely since you've never said what you mean by biochemically active.

> including myself, except, apparently
> MattLB), then it will not cause the kinds of problems AA does.

In an LDL particle it's irrelevant whether it's AA or Mead. They're
both PUFA and both do nothing biochemical, because they have to be in
cells to do that.

> Moreover, I am suggesting that the body should produce Mead acid on its
> own, rather than getting it from the diet. In this way, you rely on
> the intelligence of cells to refrain from producing something dangerous
> to themselves.

What an impressive example of your ignorance. Ever hear of lactic acid?

> I don't know how MattLB thinks the oxLDL is going to get to the artery
> wall if it is not in ciruculation first,

It's unlikely to be oxidized in circulation, but as soon as it gets
lodged outside the bloodstream it's more prone to attack since there's
less vitamin C to recycle the vitamin E in the particle.

> though it's true that the
> antibodies could very well be a red herring here. What MattLB is
> talking about is not the first stage of "coronary heart disease" -

Yes it is. The initial insult requires that LDL be accumulated at a
specific point. There's a reason that plaques occur in particular
places in particular arteries and not at random, you know.

> inflammation will occur first, and the oxLDL is acting as an irritant
> that stresses cells, which then signal for the "immune system."

So inflammation is second, then. Or do you have your own definition of
inflammation too in which the immune system isn't involved?

>Then
> the macrophages come in and are rendered dysfunctional, creating what
> one scientist called "death zones" in the artery walls. This is when
> plaque formation begins.

This is when it becomes visually detectable.

> It is important to point out that to have so much oxLDL as to cause
> this problem, your diet has to be really bad: full of PUFAs, meat
> cooked while exposed to air, and few antioxidant-rich foods.

Not true. All the above makes it more likely, but you still have to
recognise that it is a local phenomenon and that there are many
contributing factors other than those you mention.

MattLB
 
On 24 Feb 2006 06:18:10 -0800, "MattLB" <[email protected]> wrote:

>In an LDL particle it's irrelevant whether it's AA or Mead. They're
>both PUFA and both do nothing biochemical, because they have to be in
>cells to do that.

Nah, not quite correct. Isoketals may still be formed and do harm even
outside a cell, and chances are even increased that arachidonic acid
will meet such a non-enzymatically fate outside the cell, where oxygen
molecules may react with the cyclic form of it.

Most probably, many physiological/biochemical effects of arachidonate
not explainable by eicosanoids are due to the forming of isoketals and
alike :-(

(See isoketals, isoneurals and isofurans on PubMed, or do search for
isolevuglandins and levuglandins.
 
Alf Christophersen wrote:
> On 24 Feb 2006 06:18:10 -0800, "MattLB" <[email protected]> wrote:
>
> >In an LDL particle it's irrelevant whether it's AA or Mead. They're
> >both PUFA and both do nothing biochemical, because they have to be in
> >cells to do that.

> Nah, not quite correct. Isoketals may still be formed and do harm even
> outside a cell, and chances are even increased that arachidonic acid
> will meet such a non-enzymatically fate outside the cell, where oxygen
> molecules may react with the cyclic form of it.

Yes, but I'd call that chemistry rather than biochemistry. The
biochemical function of AA is as a second messenger in cells. In
lipoproteins it can't do that. Granted it's a slightly fuzzy use of
biochemical, but montygram never defines what he means by it -
presumably it's something different than "chemical".

MattLB
 
On 27 Feb 2006 03:55:54 -0800, "MattLB" <[email protected]> wrote:

>Yes, but I'd call that chemistry rather than biochemistry. The
>biochemical function of AA is as a second messenger in cells. In
>lipoproteins it can't do that. Granted it's a slightly fuzzy use of
>biochemical, but montygram never defines what he means by it -
>presumably it's something different than "chemical".

The detection of them in beginning was a chemistry thing, but, since
it is proven to be a daily episode in many cells in body, it is
biochemistry too. But, of course not only enzymologically.

Check literature for the levuglandins (derived from PGH) and
isolevuglanins (formed by oxygen attack and speeded up by
myeloperoxidase)

(See more in chapter of Laboratory examinations in
http://focosi.immunesig.org/immunityinnate.html or do a search on
either Pubmed or Google on the keywords isolevuglandins and
levuglandins, evt. also isoprostanes.
 
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