Of course not, but if you have high BP you are at greater risk for MI and stroke.

All the factors are indeed important but how you explain that ppl of a normal weight, slims with no diabetes or glucose tolerance problems still die of MI? IMHO, there are 2 factors that impact ouir health the most: GOOD GENES and STRESS, everything else is secondary. There is no reasonable explanation why one person can eat and drink whatsoever, smoke, never workout, not be in the best shape either, and live a long life and never get a heart attack, while another one- slim and health freak, will die from coronary at early age. If we assume that being slim=insulin sensitive body and low insulin, then it does not fit into your conclusion.
You may want to read more on connection to stress and genetics in regards to CHD and even cancer.
http://www.stress.org/topic-heart.h...dbd08e2af5f36#1
http://www.bhf.org.uk/questions/ind...level=1353#6299

Common ground among longest lived in different culture, are mostly folks who have great genes, are least ambitious, can handle physical and emptional stress, but not only those with low BGs and insulin.

Unless you are a cardiologist (not?), you know about cholesterol/heart desease connection as much as I do, that means ... not much. There is no proof that CHO causes heart desease, but the opposite is also questionable. Nothing to be sorry about. There is a lot of controversial info out there, and I too read all about sat. fat on Weston price and many other books and website, and still it is hypothesis.
http://www.cnn.com/FOOD/news/9905/28/france.wine/


I know 101 on the artherial inflamation and plaque formation, but thank you anyway for simplification.
The is major benefit of statins are due to reduction in inflamation, but infllamation can occur not only due to high insulin, but as I already mentioned, from many other factors.


Thanks, I will try to keep up. As for statins being Rx to children, have you ever seen pre-teen boys that weigh 300+ pounds? I have, and IMO, nothing wrong with Rx adult meds to the morbidly obese children, it may just safe their lives. No Dr. will Rx statins to a healthy, not obese child with normal CHO, BP, etc.
JMO

Maybe so, but the way statins reduce inflammation is to suppress the immune system. Do we really want to suppress the immune system on a long-term basis?

That would be a bad assumption since even normal weight people develop type 2 diabetes.




Riiiighhht...just like no doctor will rx statins to healthy, normal weight adults with normal cholesterol. (psst...between people I know at work and at church, I can count just off the top of my head no less than 6 people who fit that description and are taking statins at their doctor's suggestion)

Don't burn your fats!

The highly damaging oxycholesterols are found in foods in which cholesterol is subjected to heating and exposure to the oxygen of the air during either food processing, cooking or preservation. Such foods include dried egg yolk, dried milk powder and foods fried in heated oils. The oxycholesterol in these foods is absorbed into the blood after digestion and then becomes concentrated in the low density lipoprotein faction of the plasma. When lipoproteins are taken up by arterial wall cells, the cholesterol oxides that are released lead to damage to artery wall cells and tissues leading to arteriosclerosis.

As I understand, any dietary cholesterol which is heated to 100C (212F) is converted to oxycholesterols. Not a good thing!

Bo

Both GOOD GENES and STRESS are the doctor/god way of saying 'Hell, I don't know!'. They really aren't factors as such because (I know you love the science) there is no scientific relationship established for these factors for the most part. And when I say 'most part' I mean there is diddly squat. Crystal Therapy has as much validation as 'stress' and 'good genes' with respect to the rise of cancer (no disrespect to those using crystals)




Sounds more like it doesn't fit into YOUR paradigm. (I kinda hate that word 'paradigm' anymore ) Quite projecting! In any event, you tend to find or not find pretty much what you look for, including science. It may well be that whatever the 'real' reason for what we see has been looked for yet. Simple as that.



Speak for yourself... It really isn't that hard in most cases to become more educated and informed than the specialist. I'm confident that there are many here that have consulted professional nutritionists, bariatric doctors, endocrinologists, etc that can barely tell their ass from a hole in the ground... I try to resist being hard on doctors, however they have put themselves in the position as being all knowing and it has been legislated that only they can practice medicine, I think they deserve the abuse. Sure, there are some jewels out there, but as a group, they can *censored*



But that isn't the point. They are recommending statins to children as a general principal, not just the 300+ lb ones (god help them). Statins are just dumb in almost any case, and in the *few* cases that have been shown to have some, slight help, they are still a very poor solution. If you don't think so, back it up.

Kind regards

Well what about this?

http://www.theheart.org/article/767615.do

It seems statins don't do squat for women at all anyway.

Reply to anthony's paper http://www.jpands.org/vol11no1/correspondence.pdf

The recent paper by Anthony Colpo is
critically flawed from a scientific
standpoint.
The author states: “The belief that lowdensity
lipoprotein (LDL) cholesterol causes
atherosclerosis and subsequent heart disease is
a fundamental precept of modern medicine.”
Generally, normal levels of LDLcholesterol,
in and of themselves, do not
cause atherosclerosis; rather it is important
for normal physiological functions. There
is no disputing that hypercholesterolemia,
most commonly associated with an
elevation of plasma LDL, is an important
contributing factor in atherogenesis; its
correction can reduce the risk of coronary
heart disease (CHD).
Colpo states that “proliferation of
[atherosclerotic] plaques may occur, not
because of simple elevations in blood
cholesterol, but because of unfavorable
physiological conditions that damage or
weaken the structure of the arterial wall,” a
statement that is illogical and unscientific
because a high blood level of cholesterol
itself is one of the most unfavorable
physiological conditions that can lead to
damaging the structure of the arterial wall.
He then goes on to conclude that “all of
these factors have been shown to exert an
atherogenic effect unrelated to serum

cholesterol elevation.” Reaching such a
conclusion suggests a basic misunderstanding
of the pathogenesis of cardiovascular
diseases. The earliest recognizable
lesion of atherosclerosis is the fatty streaks
within the innermost layer of the artery
wall. They precede the development of
intermediate lesions, and develop into the
more complex occlusive lesions that may
impede blood flow by projecting into the
arterial lumen. The occlusive lesions of
atherosclerosis can be clinically reversed in
many cases after aggressive treatment with
various lipid-lowering drugs.
Colpo realized that “the number of
deaths from CHD has indeed decreased
since the late 1960s,” but argued that “total
incidence of CHD has not declined.” He
further blamed the medical community,
since it has “failed to help people avoid
CHD in the first place.” Strangely, Colpo
has ignored the fact that the world’s
population has doubled since 1960 and is
aging. The risk for CHD increases steeply
with advancing age. The claim that the
“war on cholesterol” has “delivered no
benefit to public health” is not only
irresponsible, but false.
Of further concern, Colpo has
repeatedly mixed up the terms LDL, highdensity
lipoprotein (HDL), and cholesterol.
He states that, “the concept that LDL is
‘bad’ cholesterol is a simplistic and
scientifically untenable hypothesis.” LDL
is not cholesterol. He also states that, “HDL
cholesterol, on the other hand, is the ‘heartfriendly
’lipoprotein.”
Cholesterol is not a lipoprotein.
Cholesterol is a lipid present in cell
membrane and travels in the blood in
distinct particles containing both lipid and
lipoproteins. LDL provides cholesterol to
cells through LDLreceptors, whereas HDL
removes excess cholesterol through reverse
cholesterol transport, thus maintaining
cholesterol homeostasis.
The link between lipids and CHD has
been firmly established by epidemiologic
studies and long-term outcomes trials.
Despite the emergence of new markers of CHD such as C-reactive protein, LDL
cholesterol currently should remain the
primary target for reduction of risk of CHD

associated with statins?

I have high cholesterol right now. My doctor gave me a form about a low fat diet. He wants me to come back in a few months. IF my cholesterol hasn't changed, he said he's going to "Pump me up with cholesterol-reducing drugs." He handed me a flyer for Lipitor.

I think it's mostly stress-related. I have had some major stresses in my life lately. Maybe I should take up yoga or something instead.

Let's assume you didn't actually read the article you cited otherwise you would have found Anthony Colpo's comprehensive demolition of Wu and Schauss which follows immediately after their letter ... and you would have posted both ... right?

"In Reply: Wu and Schauss insist that elevated total and LDL cholesterol levels are “an important contributing factor in atherogenesis,” but fail to address the numerous contradictions inherent in the lipid hypothesis that I raised in my article. Why have scores of studies found a complete lack of correlation between serum LDL and total cholesterol levels and extent of atherosclerosis? Why have numerous tightly controlled clinical dietary cholesterol-lowering trials failed to produce any reduction in CHD, despite the fact that cholesterol levels were indeed lowered in the treatment groups?1-6 Why have controlled clinical studies observed more atherosclerotic regression, less decrease in minimal luminal diameter, fewer cardiovascular events, and significant declines in mortality among patients taking fish oil, despite the fact that it raised serum LDL cholesterol levels? Where is their discussion of the fact that statins exert antiinflammatory, anti-atherogenic effects even when their cholesterol-lowering capabilities are disabled? To claim that elevated LDL or total cholesterol promotes atherosclerosis in the face of such observations defies logic.
Fatty streaks are considered to be an early manifestation in the development of atherosclerotic plaque. Fatty streaks are actually not fat, but congregations of cells under the endothelium, primarily made up of macrophages but possibly also containing lymphocytes, leukocytes, platelets, and smooth muscle cells.7 The macrophages have a foamy appearance due to high concentrations of cholesterol and phospholipids in their cytoplasm, but a high cellular lipid content does not prove that cholesterol is the causative factor. In fact, the extensive involvement of white blood cells reinforces the concept that atherosclerosis is not the product of simple blood cholesterol elevation, but an inflammatory immune response to arterial injury.
Lipid-lowering drugs can indeed impede and even reverse atherosclerosis, but there is a paucity of evidence for the claim that lipid-lowering is the responsible factor. As my article carefully detailed, an overwhelming body of evidence indicates that it is in fact the pleiotropic effects of statins that explain their beneficial cardiovascular effects. Wu and Schauss offer no discussion of this abundant evidence.
Had Wu and Schauss read the studies I cited, which highlight the glaring disparity between CHD mortality and CHD incidence, they would know that these studies used age-adjusted data, and thus already account for the increased proportion of the population aged over 65.
Wu and Schauss’s claim that I do not know the difference between cholesterol and its carrier lipoproteins is rather bizarre considering I clearly elucidate the difference in the first page of my article (see fifth paragraph). The terminology employed throughout the rest of my paper merely reflects popular use of the terms LDL and HDL as abbreviated references to LDLcholesterol and HDLcholesterol.
Apart from alluding to the simplistic and distinctly unscientific “passive osmosis” theory, Wu and Schauss offer no physiologically plausible mechanism by which elevated cholesterol can instigate atherosclerosis. Despite absence of evidence of a causative role for LDL cholesterol or total cholesterol in CHD, and the significant, clinically proven benefits of such interventions as omega-3 supplementation, antioxidant-rich diets based on unrefined foods, and exercise, Wu and Schauss nonetheless recommend that “LDL cholesterol currently should remain the primary target for reduction of risk of CHD.”

Such blind devotion to current dogma was the very stimulus for writing my paper in the first place.

Anthony Colpo"

Interesting study here on cholesterol intake and CHD and all cause mortality.

Dietary cholesterol and human coronary heart disease. The epidemiologic evidence.

Stamler J, Shekelle R.

Department of Community Health and Preventive Medicine, Northwestern University Medical School, Chicago, IL 60611.

For decades, dietary cholesterol has been recognized as the "materia peccans" (Anitschkow) for the induction of atherosclerosis in animals. In rabbits, chickens, and monkeys, long-term feeding of small amounts of cholesterol leads to atherosclerosis despite little or no rise in serum total cholesterol, indicating an independent contribution of dietary cholesterol to atherogenesis over-and-above its influence on serum cholesterol, possibly through effects on serum cholesterol fractions (eg, increased low-density lipoprotein-cholesterol and decreased high-density lipoprotein-cholesterol). In humans, ingestion of dietary cholesterol raises serum cholesterol, largely through its effect on low-density lipoprotein-cholesterol. Over the range of intake in usual American diets, this effect is substantial, eg, with 300 mg of cholesterol intake per 1000 kcal, rather than 100, serum cholesterol is on average about 6% to 7% higher, equivalent to a 12% to 14% greater risk of coronary heart disease (CHD). In international studies based on the Food and Agriculture Organization and the World Health Organization (Geneva) data, mean per capita dietary cholesterol levels are consistently related to CHD mortality rates. In addition, since 1981, four prospective within-population studies have shown that dietary cholesterol intake of individuals is significantly related to their long-term CHD risk, independent of and in addition to serum cholesterol, blood pressure, and cigarette use. On average, a 200-mg/1000 kcal higher intake of cholesterol at baseline was associated with a 30% higher CHD rate (95% confidence interval, 1.1 to 1.5). Conversely, lower intakes of cholesterol were associated with significantly lower risks of CHD, and of all causes mortality as well. For example, with 19 years of follow-up in the Chicago Western Electric Study, a 200-mg/1000 kcal habitual lower cholesterol intake was associated with a 37% lower risk of death from any cause, equivalent to a life expectancy longer by 3.4 years. The importance of a low-dietary cholesterol intake for prevention of CHD merits increased emphasis.

Not sure about monkeys, but rabbits are herbivores, and chickens eat a mix of seeds and insects. If left to their own devices, there is nothing in their natural diet that would contain significant amounts of cholesterol, so force-feeding them a substance foreign to their natural diet proves nothing.

Absinthe62, you read the bottom part of the abstract? It seems that it does translate well to humans.

"lower intakes of cholesterol were associated with significantly lower risks of CHD, and of all causes mortality as well."

With all due respect to the few that do seem to have a clue, most don't. Unless you happen to think only the really intelligent doctors would be prescribing statins to children, healthy, normal weight adults with normal BP and cholesterol and other demographic groups (ahem...WOMEN) who haven't been shown to benefit from such drugs. Why? Because the nice pharmaceutical rep said so.

Translation: those that ate less junk food died at a lower rate than everyone else from all causes of death.
There was nothing in that last part of the abstract that linked the lower all-cause mortality to lower serum cholesterol levels (and I suspect it was because there wasn't a link to actual serum levels) and lower CVD rates (they just cited all cause mortality, not just those deaths from MI or stroke) which begs the question, what was the lower death rate group eating besides less cholesterol that the other group was and were the CVD deaths among the lower cholesterol eating group actually lower?