The burden of proof in science always lies with those who propose a theory - Curtis

Evidence Against Cholesterol Causing Atherosclerosis

by Ernest N. Curtis M.D. (Internal Medicine and Cardiology)

The burden of proof in science always lies with those who propose a theory. In this case the claim is that cholesterol is one of the chief causative agents for atherosclerosis.

Since the burden of proof is on those making the claim, we need only rebut their arguments. We don’t have to prove anything or advance an alternative theory.
The claim that cholesterol causes atherosclerosis can be rebutted on many levels. I don’t give much credence to epidemiologic evidence, but even that doesn’t pass scientific muster when it comes to cholesterol.

The correlations between cholesterol and heart attacks (the chief complication of atherosclerosis) cited in the medical literature are not even high enough to suggest an association between the two, much less a significant correlation. Even a high degree of correlation would not prove causation but the figures are nowhere near that level.

Another fly in the epidemiological soup is the fact that the incidence of heart attacks is fairly evenly distributed throughout the entire range of blood cholesterol levels. In fact more than half occur in those with cholesterol levels in the low normal range.

Many people with very high cholesterol levels live long healthy lives with no signs of complications from atherosclerosis. Conversely, many people with relatively low levels of cholesterol suffer from severe atherosclerosis and its complications. Add to that the fact that women have, on average, significantly higher cholesterol levels than men yet suffer far fewer heart attacks and I think we can conclude that the so-called evidence from epidemiology is nonexistent.

Many proponents of the cholesterol theory cite some of the statin drug trials as proof of the significance of cholesterol as an important factor by showing that reduction of its blood level provides a small degree of protection against heart attacks.

But these studies all showed a lack of normal response/exposure. There was a total disconnection between the small degree of outcome improvement and both the initial cholesterol level and the degree of cholesterol lowering attained. That is, the same small amount of benefit (which was so small as to be of no practical significance) was seen in subjects whose cholesterol declined only slightly and those in whom it declined a lot.

The benefit was also the same for those with low initial cholesterol levels and those with high initial levels. In scientific studies, this disconnection means that the factor being studied is not a cause of the outcome in question and that some other factor is at work. In this case it is possible that the anti-thrombotic action of the drug is the cause since the degree of protection against heart attack was almost identical to that seen in similar studies using aspirin or other anti-platelet drugs.

On the pathophysiologic level there are many reasons to doubt that cholesterol plays a causative role. Researchers have shown that some of the initial signs of atherosclerosis can be seen in the arteries of infants. These changes are seen in the same areas of the arteries where atherosclerotic lesions tend to occur later in life and consist of subintimal thickening with no sign of cholesterol infiltration or inflammatory reaction.

While the significance of these early changes can be debated, it is hard to deny the significance of the fact that atherosclerosis is a very focal disease process. It is found in the large and medium sized arteries and almost never in the smaller arterioles, capillaries, and veins.

Moreover, within the large and medium sized arteries there is a marked predilection for lesions to occur at branching points and along the lesser curvatures of arteries. These are areas of maximum shear stress on the arterial wall. Often one side of an arterial segment may be severely affected while the opposite wall shows no evidence of atherosclerosis whatsoever.

Atherosclerosis is often found in the arteries of the lower extremities but rarely in the arteries of the upper extremities. Atherosclerosis is never found in the veins of the body. However, veins that are subjected to arterial pressures when used as bypass grafts or arterovenous fistulas constructed for dialysis shunts often show rapid development of atherosclerosis.

These and other facts would seem to negate the possibility that atherosclerosis was caused by a chemical circulating in the blood since that should bring about a more generalized and/or random distribution of atherosclerotic lesions.

The blood flow through the larger arteries where atherosclerosis is typically found is much more rapid and laminar than it is in the smaller blood vessels. One would think that a slower flow would allow a noxious chemical to do more damage rather than less if it were a causative agent.
Einstein said that an elegant theory could be completely refuted by one inconvenient contradictory fact. In the case of cholesterol and atherosclerosis, there is a cornucopia of such facts.
Dr. Ernest N. Curtis, M.D
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Preventing Glucose-Induced Cardiovascular Damage - Michaels

Preventing Glucose-Induced Cardiovascular Damage

Conditions Associated With Elevated Blood Glucose and Advanced Glycation End Products

Elevated cholesterol and atherosclerosis49,50 Symptoms of carotid artery atherosclerosis (major risk for stroke)51 Risk of developing high risk cardiac rhythm disturbances following heart attack52 Cataracts of the eye35 Overall risk of developing cancer53 Risk of developing fatal cancer54 Increased prostate size in benign prostatic hyperplasia (BPH)55 Abnormal elevation in liver enzymes, markers of liver damage56 Incidence and severity of obstructive sleep apnea57

Blood vessels are lined by a thin layer of cells called the endothelium which constantly regulates blood pressure and flow. Damage to the endothelium, which occurs in response to elevated glucose levels, is an important first step in producing heart attacks, heart failure, and stroke.

Studies now show that benfotiamine can prevent endothelial dysfunction and substantially improve blood vessel and heart muscle function, even in the face of glucose-induced tissue damage.

The process of healthy endothelial cell replication is vital to maintaining healthy arteries. Excess levels of glucose can reduce endothelial cell replication. The addition of benfotiamine to endothelial cells grown in a high-glucose environment corrects the defective replication. Benfotiamine accomplishes this through normalization of advanced glycation end product production.

High glucose levels also trigger early death of endothelial cells through the process called apoptosis; benfotiamine supplementation reverses increased apoptosis in cultures of endothelial cells by several mechanisms.

The body produces toxic alcohol-like compounds called polyols during periods of high blood sugar. Polyols disrupt endothelial and cardiovascular cell function. Benfotiamine reduces production of polyols, accelerates the rate of glucose breakdown, and reduces free glucose levels within cells. All of these effects further contribute to protection of endothelial cell function.

After a heart attack, or as a result of persistently high blood pressure, heart muscle cells beat more weakly than they should, resulting in heart failure. High glucose levels and advanced glycation end products substantially contribute to this diminished heart muscle function. Studies show that benfotiamine abolishes many of the abnormalities in heart muscle cell contractility, which may "rescue" impaired heart muscle and improve its ability to pump blood effectively. Benfotiamine activates important cell survival signaling pathways in heart muscle cells failing under the effects of elevated glucose.

Atherosclerosis

Not all advanced glycation end products (AGEs) are produced internally in the body. Consuming a meal rich in AGEs (such as one abundant in browned meats or caramelized sugars) can increase blood levels of AGEs and impair endothelial function. Supplementation with benfotiamine, 1,050 mg/day for 3 days, completely prevented the changes in endothelial function and blood flow produced by such a meal in a group of human subjects.

In addition to its effective control of AGE-related endothelial dysfunction, benfotiamine exerts powerful direct antioxidant effects. In rats with experimentally induced vascular endothelial dysfunction, benfotiamine reduced oxidative stress and enhanced favorable generation of nitric oxide, a compound that contributes to blood vessel relaxation.33,34 The result was an improvement in endothelial integrity and function.

All of these endothelium-protecting effects make benfotiamine an essential nutrient in your fight against the devastating effects of elevated blood glucose on your cardiovascular system.
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Are We Over-Treating High Blood Pressure? - Peter Lipson

Forbes is not my usual go-to for my medical posts here but I thought this was an article worthy of note. Here is a small quote from the article. Please read the complete

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Are We Over-Treating High Blood Pressure?
By: Peter Lipson,

Heath argues that this is too aggressive, and that we over-treat people whose BPs run in the 140-160/90s range. She bases her opinion on a recent review published by the Cochrane Collaboration, an evidence-based medicine group that keeps an eye on such things. The review included data from four studies (they use fairly strict selection criteria).

Cochrane’s conclusions were fairly clear: when data from the four studies were analyzed,  the treatment of mild hypertension did not prevent important outcomes such as heart attack and stroke, but did cause side-effects.

At what level to treat high blood pressure is a hugely important question, given it’s impact on the nation’s health. As I said above, we’re talking about people who don’t already have other heart risks, and we’re talking about whether or not to commit them to long-term treatment. We’re also talking about patients who have not been able to bring their pressures down through proper diet and exercise (which, unfortunately, is a whole lot of people).

So what evidence is there to treat so-called low risk people with mild high blood pressure?

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Cholesterol Does Not Cause Heart Disease or Any Disease - McEvoy

 

Cholesterol Does Not Cause Heart Disease or Any Disease

Michael McEvoy CNC, CMTA MARCH 31, 2010

Contrary to most people’s understanding, cholesterol is one of the most vitally important substances in the body. Cholesterol has been accused of being the culprit in many diseases, including heart disease. However, without cholesterol the body simply cannot function.

 

Cholesterol is a waxy substance in the blood that is synthesized in the liver as a necessary agent for many significant bodily functions. Cholesterol has two forms: HDL (high density lipo-protein) and LDL (low density lipo-protein). HDL cholesterol is cholesterol that is en-route back to the liver, while LDL cholesterol is cholesterol that is en-route from the liver to the bloodstream to perform its functions. LDL cholesterol is commonly called ”bad” cholesterol because it has been found inside of the arteries of the body and has been pegged as causing heart disease.

 

However as we see in bullet number four below, cholesterol serves as a metabolic nutrient. One of the many functions of cholesterol is to provide repair to damaged tissues such as the arteries. The fact that cholesterol is found in the arteries does not correlate LDL cholesterol as being “bad” or causative in any disease. It indicates, rather that LDL cholesterol is repairing damage to an area of the body.

 

The damage done to the body is linked to several patterns of degenerative processes such as: substance abuse, certain lifestyle choices, and the improper dietary habits. These patterns are causative to disease, cholesterol is not.

 

As Dr. Natasha Cambell McBride states: “Calling LDL cholesterol “bad” and HDL cholesterol “good” is like calling an ambulance travelling from the hospital to the patient a "bad ambulance," and the one travelling from the patient back to the hospital a "good ambulance."*

 

“But the situation has gotten even more ridiculous. The latest thing that our science has "discovered" is that not all LDL-cholesterol is so bad. Most of it is actually good. So, now we are told to call that part of LDL the "good bad cholesterol" and the rest of it the "bad bad cholesterol."

 

It is a fact that lower cholesterol levels correlate with an increased risk of heart attacks and memory loss more than high cholesterol levels. In fact, high cholesterol levels correlate with an increased resistance to infections, memory retention and overall better health.*

 

Another misunderstanding is that cholesterol containing foods will cause your body’s cholesterol levels to elevate. Foods that contain cholesterol, such as eggs, account for only 15-20% of your body’s total cholesterol count. For most people, cholesterol levels will actually decrease when eating cholesterol containing foods and increase when restricting cholesterol containing foods.* Many health professionals who recommend a decrease in red meats because of cholesterol content, often recommend fish. Yet fish contains on average twice as much cholesterol than red meat! Apparently these health professionals are misunderstood.

 

Cholesterol has many vital functions in the body. One of which is to repair damaged tissue such as those that exist in the arteries.

 

Foods containing fats that have been oxidized from overheating may cause LDL cholesterol levels to elevate. But this problem can be resolved by eating the right type and quantity of fat for your individual metabolism, and by heating your fats at lower temperatures, or by not heating them at all. Regardless, the potential inflammation that may be caused by oxidized fats are nothing compared to the potential damage that can be done by the sugar molecule, trans fats (hydrogenated), alcohol and excessive grain and flour intake.

 

Here is a list of the major functions of cholesterol in the body:

 

•Cholesterol is used in all cell membrane integrity. Each and every cell of the body is comprised of cholesterol. Low cholesterol levels may correlate with enhanced cellular degeneration. Cells will literally fall apart in the blood without cholesterol.

 

•Myelin sheath development. The sheath or covering of nerve tissue is comprised of cholesterol and other fatty substances.

 

•Cholesterol is a building block for all hormone development, including the adrenal hormones and the sex hormones. Women who suffer from infertility often have very low cholesterol levels.

 

•Cholesterol is a metabolic nutrient, which repairs damaged tissues. This is why LDL cholesterol levels may rise after surgery, tooth procedures, and injuries.

 

•Cholesterol is necessary for the production of bile and bile acids. The body is not able to digest and assimilate fats without bile and bile acids. Bile is required for the absorption of vitamins A, D, K and E, all of which are vital, fat-soluble nutrients.

 

•Cholesterol is necessary to properly utilize Vitamin D. This is particularly true for the conversion of Vitamin D from sunlight. Cholesterol under the skin allows for this.

 

•Cholesterol is an anti-oxidant and scavenges free radicals. Cholesterol is required for immune system health. Being an anti-oxidant, cholesterol helps to fight infection.

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