I'm sorry, I don't see where this article even suggests that high cholesterol levels influences the rate of atherosclerosis. Could you highlight it for me?

Kind regards

Simplified:

Inflammation ---> Attempts at repair ---> blockage/ruptures/angina/etc.

It's not the cholesterol causing the atherosclerosis, but the inflammatory response sending cholesterol to sites in need of repair --- so the solution, we're told is lower cholesterol?

How about resolving the cause of the inflammation so the body doesn't need to make repairs that result in plaque formation?

Exactly.......

It doesn't suggest it at all.

Too simple and does not explain why some ppl can handle all the known risk factors: smoking, high BP, high CHO and still never get a MI, while others do everything right and still die of CHD. It is not only inflamation that causes cholesterole to stick and form plaque, it is also aging that makes artheries less flexible/more rigid so they do not contract and expand as in some one of younger age. Women for instance, have very low risk of heart desease while estrogen is high, so it keep artheries flexible and capable of accumulating more plaque (they just expland more). Once estrogen is gone, artheries no longer expand, and the existing plaque becomes problem.
Having high LDL is greater chance that some of the plaque will indeed get stuck and may become inflamed under many circumstances: simply by high stress level, depression, anxiety, virus, bacteria. Diet is one of the variables in heart desease equation.
This article has some interesting points.
http://www.emaxhealth.com/39/1874.html
So, they offer statins for HIGH RISK GROUP: diabetics (inflamtion already present), ppl with strong family history of heart desease (genetics), etc. Who will Rx statins to a 25 yo male or female just to lower CHO?

It hasn't been proven that high cholesterol is benign either. It's funny how the article uses masai tribes to demonstrate abundance of saturated fat not causing heart disease, yet they maintain healthy low total cholesterol from 90mg/dl - 120mg/dl (will provide link when I find it). The link below describes them as having the lowest cholesterol in the world (similar to that of certain areas in japan, where btw heart disease is rare). No wonder why they haven't got heart disease! Because heart disease steadily rises from 150mg/dl onwards.

http://www.ravnskov.nu/myth3.htm

This statement from the paper is incomplete and inaccurate. It fails to distinguish between LDL profiles. LDL type A is a larger particle that does not enter the endothelium. LDL type B is the smaller, denser particle that causes this problem. By missing this distinction, that article leaves the erroneous impression that LDL levels by themselves cause the problem. But LDL is not the issue. The LDL profile is the issue.

And the title of the myth you linked to?


In other words, the Masai and several other tribes consume a diet high in saturated fat which should, according to currently accepted theory, send their serum cholesterol sky high. Does it? Nope.
Gosh....if eating lots of saturated fat doesn't give you high cholesterol, could it possibly be something else???

Right, small dense LDL levels are more important than total LDL. Plus sdLDL gets oxidized first, before it enters the vessel wall. But why is it oxidized? Free radicals will be present to oxidize it. Why are they there? The state of the organism and endothelium is inflammatory. What causes that? Over-efficient activity in mitochondria with overproduction of free radicals. Why is that? Too little activity of uncoupling proteins in the mitochondrial inner membrane, and too high of a proton gradient across that membrane. What causes that? A macronutrient ratio in the diet with too many carbs and too little fat and protein blah, blah, lah, blah, blah, blah, blah, blah, blah.

All this theory is just speculation with some evidence to back it up, and it could all change with more research in the basic science.

But the point is -- IT DOESN'T MATTER...

The evidence to answer our question is already all there in the ridiculously expensive 5 year studies of 50,000 people, paid for by the only organizations with enough spare cash to do the studies, Pfizer et al.

The evidence is there, presumably, in the 8 studies. The CTT group could analyze them appropriately, and we'd know. After all, that's what they are supposed to be doing.

for some reason, it hasn't happened.

The simplification was from the abstract posted, not CVD in general.

Can you define what "doing everything right" is?



Cholesterol, specifically LDL, the so-called "bad" cholesterol, doesn't "stick" to anything - it collects, along with other things, within the wall structure of the artery.



See, you're of the belief the cholesterol gets "stuck" and that is what causes inflammation. Secondly, you seem to be under the assumption that all LDL is somehow bad? vLDL can be bad, but the large "fluffy" LDL isn't....that's why simply using the estimated LDL number on the standard cholesterol lab test isn't really helpful - particle size of LDL definitely in important.




Maybe you've missed the push to have anyone, male or female, with or without high risks, prescribed statins if their LDL is higher than "desired"?

That's because, in logical terms, you can't really prove that *anything* is benign. And that's why the burden of proof is on those who claim that something isn't benign.

Interesting discussion, keep it coming!

normal BP, not smoking, not being obese, not eating sugar and junk, being active, this is doing right in my book.


I used "stuck" just "to simplify" not because I think it is literally gets stuck.Other thing that is present is fibrinogen and is linked to atherosclerosis amongs other factors.
http://atvb.ahajournals.org/cgi/con...tract/15/9/1263
Frankly, I just think that getting older somehow is responsible for atherosclerosis and artherial inflamation. Not all older folks have it, but some can repair microtears in artherial wall structure, while others - can't. Insulin sensitive body can even grow natural by-pass around blocked arthery, so I have read, but one must be sensitive to insulin. But in general, tiny, hair like blood vessels, start closing after 40, while it does not lead to heart attack immediately (only when major artheries are blocked), it does deprive heart from much needed oxygen and nutrients, so heart muscle is somewhat starving, and heart desease develops.

I prefer that you don't assume things, and no, I don't believe, as I stated it already. I do believe that if there is inflamation, plaque will get inflamed and cholesterol is not helping in this matter.

Again, I prefer you not assume anything, but I do know differnce between Lipoprotein A and B, as well as VLDL, thank you, but this is beyond the point. I can think whatever I want, it does not change anything. I do think it is better to have lipoprotein A on a lower side, especially if there are other risk factors present, but it is JMO.


I did miss it, because I've never been pushed by any doctor to take statins to lower my CHO, and neither was my DH even his CHO is on the higher side (around 240) but with good HDL and low TRG. If a doctor"pushes" you to take statins, it is easy to say :NO. I never heard of drs Rx statins to young ppl either. Not in my experience at least.
From what I have read they recommend to keep CHO low for those in high risk group: existing CHD, those who already had one heart attack ( helps to prevent another one), diabetics, etc. I don't see anything wrong with this approach, I also don't think any heart patient will benefit from high cholesterol of any kind.

Dr. Kendrick, whose new book was the catalyst for this thread:

All those things are only markers of potential cardiovascular risks; not one is a guarantee you'll not have CVD or other health problem. From everything I've read, the three things that matter at the end of the day are insulin, blood glucose and triglycerides....that is the only common ground amongst the longest lived across different societies/cultures.

Yet, we here in the US perpetuate a myth that LDL causes heart disease. Sorry, but it doesn't.

If you step-back from the lipid-hypothesis and return to basic physiology and metabolism you'll start to see it's something BEFORE cholesterol gets outta whack, not the high cholesterol itself.....many contend it is the inflammatory processes that are causing dyslipidemia; and the improvements seen in those with CVD taking statins is due to it's effect on inflammation, not the lowering of LDL.



You need to read more about the issue then - statins are being recommended for more and more of the population, including children!