C Reactive protein is important, that has to be checked, not just Cholesteral etc. Inflammation has to be checked.

Exactly!! It's inflammation that can make the cholesterol so dangerous. Those with autoimmune disease are at extremely high risk, so even moderately high cholesterol can be problematic.

Yes, and you work naturally to get the numbers better on the C reactive if needed.

The rub here is that ANY cholesterol, even low levels, will be used to patch inflammation damage. Because cholesterol is ubiquitous, it is always around.

So if you reach the arbritrary levels set by the drug companies, you can still have enough cholesterol to patch the inflammation.
They don't tell you this, but it happens.

This link explains the data very well.
http://trusted.md/blog/vreni_gurd/20...#axzz1nqQVXCDF

Also some provocative links to consider at the end of the
article.

edit: I just found this link on our PD forum, and it is about stress and inflammation:
http://www.sciencenewsdigital.org/sc...25/?pg=11#pg11

--that can be Googled, that cholesterol levels by themselves have little correlation with bad coronary events, and that yes, the C-reactive protein levels (and other inflammatory markers) are more prognostic. Moreover, triglyceride levels seem to be more important than cholesterol levels. And, within cholesterol analysis, there are several kinds of both high-density (HDL) AND low density (LDL), and not all subtypes of LDL are apt to cause plaques.

The situation is really much more complex than is reported generally, and still under investigation.

The problem has been that statins, which ARE effective in lowering cholesterol, are a big money maker out there. And, as with any pharmacuetical profit center, they will tend to be prescribed more often than they should be. But, as Mrs. D points out, the question is still open as to whether it is the cholesterol lowering effects of statins that are the real mechanism for reduced coronary events. I suspect, from some preliminary stuff that's been published, it may actually be the anit-inflammatory effects of some statins that are more helpful. (The Brian Lehrer show had a segment on this on public radio just yesterday, interviewing several doctors/researchers to get their takes on this--it can be found by going to the WNYC station website and looking up the shows archives by date--2/29/12--if anyone is interested.)

And, of course, statins do have side effects, as do all medications, and a risk/benefit analysis should always be done before people start taking them. There are alternatives for reducing cholesterol--niacin, fiber, etc.--and for reducing inflammation--fish/flax oil, vitamin D, etc.--that have lower side effect profiles.

Thanks Glenn....

Also it is interesting to note, that the pipeline of HDL raising drugs that were supposed to replace statins failed. We don't hear about them anymore...And Pfizer is left without its BlockBuster too.

Pfizer chose to mix theirs with Lipitor, and it killed people.
So it is gone.

http://seekingalpha.com/article/6391...olesterol-drug

This is quite interesting.

Especially since my 'cholesterol' levels are not that bad (just barley over normal). Yet I have known "extensive" (word used on scan results) calcification throughout my arteries. They have no doubt that the bigger culprit is the inflammation from Sjogren's. As explained to me the inflammation makes possible for the cholesterol to attach (I would guess like you mentioned, 'patch'). This continuous process though causes the layers of endothium (I think this is the word he used) tissue to thicken and calcify. Does this make any sense??

The logic the doctor used for short term statin treatment (hoping to limit it to two months) was based upon a completely different test, not standard lipids. It was Apo B (apolipoprotein B), which is supposed be more reliable in determining the risk for plaque in the arteries. I have tried to read about this lipprotein, but really don't understand it. If you've heard of this, I'd love to hear your comments (in laymen terms).

This may help:

http://www.medicinenet.com/your_chol...pth/page12.htm

Seems statins are not indicated for lipo B problems.

You'll be interested to know that quality curcumin (that is well absorbed) went head to head with Lipitor in testing, and was found as good for reducing inflammation as Lipitor.
http://www.ncbi.nlm.nih.gov/pubmed?t...20atvorastatin

This was a specific product with better absorption used in the study. Not all curcumin products are well absorbed.

And as usual this is a foreign paper. Not many US papers on this subject.

Edit to add: here is a story on Roche and Merck's HDL drugs:
http://www.foxbusiness.com/industrie...-for-hdl-drug/

You know one can raise HDLs and lower triglycerides with fish oil. ( or Krill oil).

I don't think (but could be wrong) that LDL particle A & B is the same thing as Apo A & Apo B. The Apo A was addressed at the bottom portion of the article you listed, but not Apo B.

Unless I'm reading the article wrong...but then why would they specifically list Apo A if it was the same thing as LDL particle A?

Statins are still used for Apo A (with limited effectiveness) and also estrogen. I don't think estrogen would be indicated for someone with clotting/stroke history.

Here is interesting stuff:

Taurine!

http://qualitycounts.com/fpapob.htm

Taurine keeps coming up lately. I guess not just for kitties anymore!

http://qualitycounts.com/fpapob.htm

http://www.ncbi.nlm.nih.gov/pubmed/18242615

http://www.ncbi.nlm.nih.gov/pubmed/18925970

Alot of the taurine studies are in animals still.