Statin Damage to the Mevalonate Pathway

By now many of you have read that all statins are reductase inhibitors. Unfortunately, the only reductase step in the entire 200 biochemical steps to the synthesis of cholesterol was right in the beginning of the mevalonate pathway, meaning that to get at cholesterol we had to interrupt many other vital functions sharing this same pathway such as CoQ10, dolichols, etc.

Nowadays even doctors are beginning to understand the need for CoQ10 supplementation (statin victims knew of this long before). This report focuses on dolichols and why we must be particularly concerned about the consequences of statin damage to this poorly understood, yet extremely important, biochemical function.

Most doctors got an introduction to this in medical school biochemistry classes but by the time of graduation most had forgotten dolichols and their important roles in glycolysis, neuropeptide formation, cell identification and immuno-resistance, if we were ever taught. Now, Drieu and others of the Karolinska Institute in Sweden, have reported in Glycobiology the mechanism by which statins adversely affect our mevalonate pathway.

To really understand what these researchers did we must return to basics. I have written previously of the tiny micro-factories in each of our cells known as the endoplasmic reticulum and Golgi apparatus. It is in this assembly line-like operation that these factories produce the neuropeptides that make us the emotional creatures we are. Imagine, every thought, every sensation and every emotion we have ever experienced, guided by the nature and sequence of the amino acids that make up these peptide strands and the entire process is orchestrated by dolichols.

To study the effect of statins, sufficient Mevacor was used to inhibit the mevalonate pathway of a melanoma cell line thereby arresting the usual DNA mandated cell growth for a period of 24 hours. This is now a routine laboratory procedure, telling us that researchers have long known of the effect of statins on cell growth.

By any clinical interpretation this "arresting cell growth" sounds harmful but this awareness of an important statin side effect seems restricted to laboratory personnel. By comparing the various possible mechanisms of how cell growth could be arrested, they found that 95% of this effect of statins was mediated by the dolichol route. In other words dolichol inhibition by statins stops cell growth. The results provide direct evidence of the important role of dolichols not only in the process of neuropeptide formation but, by inference, in glycolysis, cell identification and immuno-resistance as well.

"A product so safe it can be put in the drinking water," they say about statins. Obviously those that make these statements have completely forgotten their medical school biochemistry and if non-physicians are making such statements, they need much better training before publicly talking about how harmless the statins are.

After years of studying this subject I now have research documentation for the hundreds of case reports of unusual behavioral manifestations associated with statin use. There are now compelling explanations for the many reports of aggressiveness, hostility, sensitivity, paranoia, homicidal ideation, road rage like reactions, profound depression, suicidal ideation and even suicides associated with the use of statin drugs. And there is no doubt in my mind that many more statin associated problems may be involved with this dolichol function as we gain more knowledge.

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


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Cholesterol is Not the Culprit
The Statin Damage Crisis
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