Statins, Cholesterol and Stroke

You have repeatedly heard me say that cholesterol is irrelevant to heart disease and I now wish to extend this observation to strokes as well. We have known for years that any association between cholesterol level and stroke risk is minimal at best and benefit for strokes from statin use appeared to be due to some other factor than lowering of LDL cholesterol.

It is now well established by researchers that inflammation suppression appears to be the principal factor involved in explaining the benefit from statins.

If we think of atherosclerosis as a progressive inflammatory response to endothelial damage from whatever trigger or combination of inflammatory triggers, including high blood pressure, smoking, homocysteine elevation, lack of proper balance between omega 6 and 3, excess oxycholesterol intake, transfats, hidden focus of infection in the body and inherited coagulation and platelet defects, it becomes very easy to understand the stroke benefit from statin drugs.

Ora Shovman proved, only in 2002, this previously unknown effect of all statins in his paper titled, The Anti-inflammatory and Immunomodulatory Effects of statin drugs.

He proved that the four major components of any inflammatory reaction, platelet activation, monocyte adhesion, macrophage attraction and smooth muscle migration all were inhibited by statins through their ability to inhibit the ubiquitous transcriptase known as nuclear factor kappa B.

It is of considerable interest to researchers that this substance is another product of the mevalonate pathway and as such a collaterally damaged victim of mevalonate blockade along with CoQ10, dolichols and normal phosphorylation. Until revealed by Shovman, the medical community was completely unaware of this effect.

Although one might have expected that either the FDA or the drug companies would have picked up on this and informed doctors of the true reason for statin benefit in heart disease and strokes, this was not to happen.

What did happen was a stream of studies documenting the irrelevance of cholesterol lowering and, more recently, documentation that elevated CRP was the only blood test that seemed to correlate well with the underlying level of atherosclerosis.

To understand this, one must know that for the past 40 years we have all been bombarded with cholesterol causality of heart disease and strokes.

National organizations in the U.S. such as the FDA ( Food and Drug Administration) the AMA (American Medical Association ) and the AHA (American Heart Association ) are finding it difficult to accept the reality that they have been wrong for four decades, forcing several generations of doctors to follow the wrong path to prevention and treatment.
Cholesterol is not our enemy, it is perhaps our most important biochemical, with vital roles throughout the body, helping greatly to explain why the adverse effects of statin drugs are so diverse.

Simply put, one cannot block the critical mevalonate pathway with these reductase inhibitors without incurring very serious side effects up to and including actual DNA damage.

That is where we are today and that is why I stress that if statins must be used for heart disease and stroke prevention, they should not be dosed at the now traditional cholesterol lowering doses of 20-80mg. There is no way the human body can tolerate doses at this level without risking serious side effects. We now have legions of statin victims, disabled to varying degrees from statins and their doctors have yet to be officially informed.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor

Books From Amazon

The Dark Side of Statins
The Statin Damage Crisis
Cholesterol is Not the Culprit
Statin Drugs Side Effects
Lipitor, Thief of Memory

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