The Cholesterol 'Paradox', page 1

Once it was established in health science that saturated fat, through it's effects on raising cholesterol, causes heart disease, it's been blindly accepted regardless of evidence to the contrary.

Claude Bernard, a French physiologist considered to be one of greatest of all men of science and possibly the pioneer of medical research, once said:

”When we meet a fact which contradicts a prevailing theory, we must accept the fact and abandon the theory, even when the theory is supported by great names and generally accepted”

Unfortunately, in the field of medical research the "great names" disregarded the evidence instead of abandoning the aforementioned theory. They confidently labeled any contradicting evidence as a 'paradox'. For instance:

The French Paradox: When epidemiologists noted that the French had a relatively low incidence of heart disease despite the high amounts of saturated fat consumed in the diet, they concluded that it's simply a paradox and that perhaps their red wine consumption was preventing CHD.

The Spanish Paradox, or Mediterranean Paradox: Though many Mediterranean countries consumed an almost identical fat profile as us diseased Americans, they seemed to be relatively CHD free, comparatively speaking. It was assumed that the perhaps the consumption of monounsaturated fats, such as Olive Oil, was protecting their hearts. (Olive oil is primarily Oleic acid, a monousaturated fat constitutes 50% of the fat found in red meat)

The Inuit Paradox: Pre-westernized eskimos had no incidence of CHD despite a diet that consisted of 90% fat/protein. The main staple of their diet? Whale blubber.....yummy.

The History? Two of the largest and most influencial studies on the prevalence and cause of heart disease were: The Seven Countries Study, Ancel Keys, et al.; The Frammingham Heart Study.

The Framingham Study never showed high cholesterol to be a risk factor in heart disease. And Ancel Key's purposefully dismissed those 'other' countries that did not comply with his preconcieved notion.

So you can understand my frustration when I stumbled across this article:

We know high cholesterol causes heart attacks, but does it also cause heart failure?

That's the title of the article. Do we really know that high cholesterol causes heart attacks? No. The data just aren't there to support this assumption.

Even today we're told that total cholesterol isn't as important as the "bad cholesterol" LDL (low-density lipoprotein). We're told that if LDL levels are elevated they can become oxidized and cause plaque formation along the arterial wall(atherosclerosis). But, is there any real, solid evidence to support the notion that elevated LDL levels are the cause of CHD?

Well, just recently JAMA released a study conducted by NHANES (National Health and Nutrition Examination Survey) that examined Trends in High Levels of Low-Density Lipoprotein Cholesterol in the United States, 1999-2006.

During this 6 year period LDL levels dropped significantly.

Conclusions Among the NHANES population aged 20 years or older, the prevalence of high LDL-C levels decreased from 1999-2000 to 2005-2006.

And since we all "know" that LDL cholesterol causes heart disease we would expect that the incidence of heart disease drop as well. Unfortunately, that wasn't the case. In fact, heart disease incidence increased, even if ever so slightly.

Now, getting back to what our good friend Claude Bernard said, we should assume that a true scientist would dismiss the conventional theory and accept the facts. Yeah, right.

What did the researchers suggest? Well, they suggested that those in the study be placed on lipid lowering drugs to help prevent CHD.

This, my friends, is the Cholesterol Paradox. These researchers consider their findings, once again, to be a simple paradox. They simply dismiss the facts and irrelavent, much like Ancel Keys did.

Oh....and to frustrate me even more....the first sentence in the article was:

High total blood cholesterol is recognized as a major contributing factor for the initiation and progression of atherosclerosis.

Is it really?

It's time to get back and find out where these "recognitions" originated and if the science is sound. Do some digging, research the nutritional research history and see where the current recommendations started. You'll be surprised how little evidence and how many bogus studies have been used to label saturated fat and cholesterol as "artery cloggers."

-Dev

[edit on 25-11-2009 by DevolutionEvolvd]

reply to post by DevolutionEvolvd

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Would you want the fulltext of the NHANES statistical survey you cited from JAMA?

Or you have access?

---

I have to sincerely say from observation and reading many stances on nutrition, that it can get like a religion discussion.

I haven't settled on a position yet, as new data gets published, it is bound to change eventually.

But, I can give you applause for discussing this openly and will discuss with my limited knowledge gained by reading, I'm not on college yet.

I agree with you in many points.

It is hypothesized that inflammation triggers the cholesterol oxidation and omega 3 fats help suppress the immune system reaction by reducing inflammation-promoting leukotrienes.

Cholesterol ONLY gets deposited IF oxidized. And WHAT gets oxidized is the LDL lipoprotein itself, cholesterol is not soluble in blood, therefore carried encapsulated inside these lipoproteins.

LDL carries to the cells, HDL retrieves it back to the liver, that is why they call HDL "good", it clears the blood.

Most cardiologists now know this, but don't feel comfortable talking with their patients about it.

Even Bayer itself silently acknowledged this. Where?

It its Vitamin E antioxidant product EPHYNAL technical sheet that comes with it. There it fully describes the deposit process. The selling point? Vitamin E prevents the oxidation and subsequent deposit, protecting against atherosclerosis.

Said this to explain the second point.

Saturated fat is not always bad. It depends on its source and micronutrients.

Palm Oil, despite having an unbalanced omega 3:6 ratio, contains the most powerful Vitamin E type: tocotrienols instead of tocopherols.

It a study, palm oil could reverse atherosclerosis if given time.

Plus, it was found to act EXACTLY like statins without side effects, blocking cholesterol synthesis using the same HMG CoA mechanism.

reply to post by Oldtimer2

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In the past Pfizer used the first artificial heart inventor to promote Lipitor with many untrue statements in a TV commercial.

When TV viewers caught on with the lies and started calling Pfizer, Pfizer suspended the commercial and cancelled the contract with the artificial heart inventor.

Statins are in a mixed gray area today.

In oncology, it is showing some signs of apoptosis-inducing and anti-proliferative properties in some animal studies.

On the other hand, the side effects keep rising. The most known side effect is muscle destroying, rhabdomyolysis.

But a shocking new side effect is being reported: Amyotrophic Lateral Sclerosis/Lou Gehrig!

I'm not joking, statins can cause ALS in some people, probably due to pharmacogenetic individual drug metabolism.

Those reports come from the WHO itself, published in a statistical report in a peer-reviewed journal.

Originally posted by jjjtir
reply to post by DevolutionEvolvd

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Would you want the fulltext of the NHANES statistical survey you cited from JAMA?

Or you have access?

I've got it, thanks.

I have to sincerely say from observation and reading many stances on nutrition, that it can get like a religion discussion.

I've said many times that a nutritional debate is as demanding and of equal conviction as any one of religous or political topic.

Cholesterol ONLY gets deposited IF oxidized. And WHAT gets oxidized is the LDL lipoprotein itself, cholesterol is not soluble in blood, therefore carried encapsulated inside these lipoproteins.

LDL carries to the cells, HDL retrieves it back to the liver, that is why they call HDL "good", it clears the blood.

Correct. And oxidation typically only occurs if the LDL particles aren't flowing freely. What researchers have found is LDL particles vary in size. The small, dense LDL particles have a greater tendency to stick between the cells that line the arterial wall and eventually oxidize, while the large, fluffy LDL flow freely.

Many biochemists will readily admit that the best markers for heart disease are LDL size, due to the reasons mentioned above, and the ratio of triglycerides to HDL.

Why triglycerides and HDL? VLDL (very low density lipoprotein) transports Triglycerides and then are converted into LDL. So, triglyceride levels, or VLDL, are usually a precursor to LDL and the amount that will be circulating.

Plus, it was found to act EXACTLY like statins without side effects, blocking cholesterol synthesis using the same HMG CoA mechanism.

That's nice to know. Also, while Insulin seems to stimulate HMG CoA reductase activity, either the presence of Glucagon or the negative stimulus of insulin is responsible for inhibiting it. So, avoiding high blood sugar will systematically provide the same mechanism as statins.

Great information. Thanks for posting.

-Dev

reply to post by Oldtimer2

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If, for whatever reason, you decide to take statins...make sure and supplement with CoEnzyme Q10. Otherwise, you'll feel muscle fatigue and even pain.

It's kind of ironic that statins inhibit CoEnzyme Q10 synthesis. CoQ10 defencies cause muscle fatigue.....and the muscle is a heart.

-Dev

Originally posted by jjjtir
reply to post by Oldtimer2

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In oncology, it is showing some signs of apoptosis-inducing and anti-proliferative properties in some animal studies.

Interesting. I wasn't aware of this. Is it specific to those cells that proliferate much quicker, cancer cells? Or is it a hit or miss?

reply to post by STFUPPERCUTTER

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Thank you for attempting to derail my thread while providing nothing of relevance to the conversation on the table.

Does acting like an hormonal, prebpubescent boy float your boat? Or are you actually a child?

Based on the structure, grammar, spelling and general attacking nature of your posts....it actually wouldn't surprise me.



[edit on 26-11-2009 by DevolutionEvolvd]

Originally posted by DevolutionEvolvd
reply to post by STFUPPERCUTTER

---

Thank you for attempting to derail my thread while providing nothing of relevance to the conversation on the table.

Does acting like an hormonal, prebpubescent boy float your boat? Or are you actually a child?

Based on the structure, grammar, spelling and general attacking nature of your posts....it actually wouldn't surprise me.



[edit on 26-11-2009 by DevolutionEvolvd]

sorry to dissapoiint you but i am 100% man.
and your welcome!

reply to post by DevolutionEvolvd

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I just found out about this. I can't give you more information at this moment in time.

But there is a paradox.

In some, but not all studies, some statins have been shown to promote VEGF, Vascular Endothelial Growth Factor, possibly contributing new artery angiogenesis to feed cancer tumours.

Also not all of the many statins on the market showed this, some statins lowered VEGF.

But then, statins appears to promote apoptosis and anti-proliferative activity.

Isn't this weird?

Could some statins be a trickster drug acting like a trojan horse?

PS: I learned about VEGF/statin link from Shane Ellison, another independent researcher like Uffe Ravnskov.

He was one of the first to warn about the whole cholesterol mess.

[edit on 1-12-2009 by jjjtir]

Wikipedia on Ancel Keys: en.wikipedia.org...

Then, as now, critics have rightfully pointed out that this "strong association" becomes weaker when data from other countries are added to the mix and there have been allegations that Keys "cherry picked" the data to support his hypothesis.

Ancel Keys was criticised by Uffe Ravnskov amongst others for falsifying his conclusions by selecting data. Ravnskov examined the data that Keys used and found no correlation to back up Keys findings. He concluded that Keys had deliberately excluded from his dataset any countries which did not support his hypothesis.

And it was Key's who pushed this lipid hypothesis into existance.

To answer your question. In most observational studies there is insufficient evidence to support the notion that elevated cholesterol levels cause CVD. Of course, except those with VERY high levels of cholesterol.

The studies typically have men and women devolping atherosclerosis with low levels and high levels of cholesterol.

-Dev

Perhaps coronary artery disease is an inflammatory disease ("TREG syndrome") and the effect of statins is to reduce the inflammatory response rather than simply to reduce the cholestrol number.
www.associatedcontent.com...
biovideos.zampbioworld.org...
Patents have been taken out for the use of statins to enhance TREG activity in order to reduce the inflammatory response.
www.wipo.int...
Statins are now being trialled in many other diseases e.g. multiple sclerosis, sepsis and Parkinson`s disease further suggesting the importance of the anti-inflammatory actions of statins.

reply to post by dr treg

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One "good" side effect of statins is as you said, reduce inflammation.

There is a growing number of cardiologists who now ask for and consider C Reactive Protein laboratory test more reliable and/or accurate than just cholesterol tests alone.

When I think about it, the more medicine becomes more "specialized" with narrower fields, they just seem to lose track of other body functions.

This is a good example.

Cardiology versus Neurology and Endocrinology.

Cholesterol is precursor to DHEA, which itself is a precursor to hormones.

And is the precursor of UltraViolet-B light generated Vitamin D(erroneously called a vitamin, now considered a steroidal hormone).

Also, cholesterol helps shield and improve conductivity of the nerves myelin sheath with as much as 20% of the myelin consisting of pure cholesterol.

Could cholesterol lowering be "helping/contributing" neurological disorders by making the myelin weak?

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