The greatest obstacle I have encountered in presenting the facts about statin drug side effects has been the prevailing attitude that "Statins do not do that!" Again and again I heard this refrain when I suggested that my strange encounters with transient global amnesia might have been related to my use of Lipitor, started by NASA doctors only six weeks before, for my slightly elevated cholesterol.
After 40 years of brainwashing by the ‘powers that be,' no one was more dedicated than I to the concept of cholesterol causation of atherosclerosis.
After writing thousands of prescriptions for whatever cholesterol busters were available I lauded the development of the statin class of drugs.
According to the sketchy details of the drug ‘reps,' statins were reductase inhibitors, directly interfering with the synthesis of cholesterol . Of course, at that time we had not the slightest awareness of the special needs in our brains for glial cell cholesterol synthesis for memory processing. This knowledge was not to come until 2001 by which time reports of statin associated amnesias and other forms of cognitive dysfunction were rapidly accumulating.
This earlier article - 662 cases of Cognitive loss reported to Medwatch - has much relevance
Nor did we realize that reductase inhibition, located at the very beginning of the vital mevalonate pathway, really meant mevalonate blockade.
The consequence of blocking cholesterol synthesis, then, was the inevitable inhibition of the synthesis of CoQ10, dolichols, selenoprotein, Rho and normal phosphorylation as well. Side effects came to no surprise to those of us familiar with the vital role of the mevalonate pathway.
The result has been thousands of statin ADRs ( Adverse Drug Reports ) for peripheral neuropathies, permanent myopathies and chronic, disabling neurodegenerative conditions, as well as raising concerns about mitochondrial mutations from depleted CoQ10 reserves.
Ralph Edwards, director of the W.H.O.'s Vigibase drug monitoring system, reported last year of their concerns about excess peripheral neuropathies and ALS-like conditions associated with statin use worldwide.
And now my neurologist has decided that my statin associated chronic neuromuscular degenerative process is really primary lateral sclerosis and a very close relative of ALS. I have hundreds more ALS-like cases like mine in my repository.
I wonder what next? I suspect increased cancer incidence with statins plus the irreversible nerve and muscle damage now appearing.
And now, four decades after it all began, the Enhance and Jupiter/Crestor/CRP study suggest the complete irrelevance of cholesterol to atherosclerosis!
Jupiter researchers suggested that CRP (C-reactive protein) was the best available marker of underlying cardiovascular risk, supporting the earlier Enhance study finding that cholesterol reduction was irrelevant.
When Uffe Ravnskov first reported in his book, ‘The Cholesterol Myths' that over half of first attacks of myocardial infarction occurred in those with completely normal cholesterols level, I knew something was seriously wrong with the cholesterol causation theory.
Recent studies have only served to confirm what I have known for over a decade about the irrelevancy of cholesterol to the atherosclerotic process.
All of these disabling side effects from the excessive use of a statin drug to reduce cholesterol, which has no relationship to the problem! Now they are saying that inflammation is the problem and we must use statins to fight inflammation!
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor