Mechanism of Statin Benefit


dr_duane_graveline_m.d._134By Dr. Duane Graveline, M.D., M.P.H.

I have written several books about the adverse effects of statin drugs. My first book Lipitor®, Thief of Memory was published after my personal experience with transient global amnesia associated with the use of Lipitor®. Further study of the statin drugs made me realize that the statin side effect problem was not limited to Lipitor® and the adverse reactions were not limited to cognition. That was when I wrote my second book, Statin Drugs Side Effects and the Misguided War on Cholesterol.

In looking for the reason why so many of the myopathy and peripheral neuropathy cases reported were permanent despite CoQ10 supplementation, I realized mitochondria must be involved and wrote my third book, The Statin Damage Crisis. Now, just two years ago, I came to realize that statins are causing premature aging, using the same biochemical pathways as our natural aging, that of CoQ10 inhibition and mitochondrial mutations. I called this The Dark Side of Statins.

During all this time I realized that statins appeared to help many people despite these serious shortcomings. This is because of the anti-inflammatory effects of statins, not even suspected when they were first marketed. Cholesterol reduction had nothing to do with this benefit.

A recent study of 112 high-risk men ( Ref. 1 ) did much to reveal, at least in part, the mechanism of action of statin drugs in cardiovascular disease control. The primary mechanism appears to be that of thromboxane inhibition, although much more study remains to be done. Thromboxane means nothing to most of us yet we all are very familiar with it. Anyone who has noticed a tendency for black and blue marks to appear much more easily while on aspirin knows a bit about thromboxane. So do those folks taking a small dose of aspirin for heart attack or stroke control with the understanding that it will lower the likelihood of clot formation.

This is another attribute of thromboxane. Synthesized in our blood platelets, thromboxane contributes to platelet aggregation and clot formation. Aspirin acts by inhibiting the precursers of thromboxane such as arachidonic acid in our blood platelets thereby reducing the risk of clotting. Low-dose, long-term aspirin use irreversibly blocks the formation of  thromboxane in platelets, producing an anti-coagulant effect making aspirin useful for reducing the incidence of heart attacks.

In this study, 112 individuals already on aspirin were given Zocor® 40 mg daily with close follow-up of selected inflammatory and coagulation markers. Zocor® decreased serum thromboxane by 20% - from 1.32 to 1.06 ng/ml. Zocor® decreased hsCRP ( high sensitivity C-reactive protein ) very substantially from 2.06 to 1.39 inflammatory units. Zocor® addition decreased platelet arachidonic acid from 9.6 to 5.4 units. The investigators in this study were quick to point out that the changes noted were unrelated to the cholesterol lowering properties of statins and appear to be associated with reduced inflammation and tendency for coagulation.

In the early days of statin therapy some were quick to come up with the name "super aspirin" for this new class of drugs. This study gives solid justification for this title although for marketing purposes the drug companies were not supportive of the somewhat demeaning "super aspirin" title. The primary effects of statins on platelet aggregation and clotting in this study were precisely those of aspirin. The only difference is in strength of effect. Three months of aspirin pretreatment produced the usually expected changes in thromboxane, hsCRP and arachidonic acid but the addition of statins substantially enhanced these effects.

There may be other ways in which statins benefit humans but they are few and far between. Originally these drugs were formulated to inhibit the synthesis of cholesterol but since the JUPITER study ( Justification for the Use of Statins in Primary Prevention: An Intervention Trial Evaluating Rosuvastatin ) ( Ref. 2 ) the evidence is clear that cholesterol has no role in atherosclerosis. Instead of being public health's greatest enemy as we have been brainwashed to believe these past 35 years, cholesterol is probably the most important biochemical in our bodies.

Not only is the cognitive function of our brains absolutely dependent upon ample supplies of cholesterol but cholesterol is the reservoir from which many of our most important hormones such as estrogen, testosterone and cortical are derived. Additionally every cell in our body is dependent upon cholesterol for myriads of vital cellular processes such as lipid rafting and  exo/endocytosis, most of which have been delineated only within the past few years, long after statins were first marketed.

Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
 
November 2010

Ref. 1: http://www.internationaljournalofcardiology.com/article/S0167-5273(10)00808-9/abstract
Ref. 2: http://www.ncbi.nlm.nih.gov/pubmed/16442935
 

Books From Amazon

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


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