Zocor and Mouse Stem Cells


Other trade names of Simvastatin are Lipex, Simcard, Simlup and Simcor ( Simvastatin with Niacin.)

Some readers might remember that I have specifically referenced Zocor in another page dealing with its effect on the mevalonate pathways of research mice.

Like all statins this one really interfered with the most basic aspects of the mevalonate structure including what is called normal phosphorylation. When you mess up this one the result is usually all bad.

That was certainly true in this earlier study when the result was excess tau protein production. Tau protein is the stuff of neurofibrillatory tangles (NFTs). When it enters the neurons of the brain the result is cell death.

Although this is being looked at in the cause of Alzheimers disease, little did we know this is likely the same process involved in the neuro-degeneration of ALS and even Parkinsonism, as well as Alzheimers. So when I saw the title of this next paper pointing at Zocor as the most disruptive of normal phosphorylation of the four statins studied, it caught my attention.

Simvastatin suppresses self-renewal of mouse embryonic stem cells by inhibiting RhoA geranylgeranylation by Lee MH and others from the Republic of Korea.

They start off by saying that although statins were originally developed to lower cholesterol, their pleiotrophic and cholesterol independent effects at the cellular and molecular level are highly related to numerous cell functions. This is what I have been talking about for the last six years. This is the collateral damage thing that the drug companies have ignored.

These researchers already knew about such statin associated effects on cell development as failure of proliferation and poor differentiation and now wanted to study the effects of statins on embryonic stem cells.

They compared the effects of Zocor, Mevacor, Lipitor and Pravachol on mouse embryonic stem cells (ESC) finding that Zocor was the most effective in inducing morphological change and decreased cell proliferation, resulting in marked failure of self-renewal of these stem cells.

Self-renewal is what these ECS do. These deleterious effects could be selectively reversed by adding mevalonate or its metabolite, geranylgeranyl pyrophosphate, demonstrating that Zocor's effect on ESC was based on depletion of mevalonate secondary to reductase inhibition. (This is what statins do. They are all reductase inhibitors.)

Now we have another major consequences of mevalonate inhibition by statins - the failure of self-renewal of stem cells. This is even worse than our somatic mitochondrial mutations associated with statin use. I suppose the drug company response will be that these are all mouse studies. To me this is a horror story developing. I have said before we have all been drug company guinea pigs these past 20 years. That puts us even closer to mice.

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


Books From Amazon

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


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