A statin's enduring legacy

A horrific result of statin use is insidious effects that may express long after quitting the drug. Such effects can, and do increase, for reasons well understood. By shutting off the enzyme required for cholesterol synthesis in the liver (HMG-CoA reductase*), biosynthesis of Co-enzyme Q10 in all cells is also unavoidably shut off – and there goes the ballgame. Without adequate CoQ10 as potent antioxidant shielding mitochondrial DNA from oxidative damage, mutations accumulate and increase over time, reducing energy (ATP) production and availability in all cells, muscles and neurons, leading to any/all possible neuro- and myo-pathic disease, such as heart disease (ironic, no?), myositis, ALS, Parkinson’s, Altzheimer’s, what have you (and don’t want to have), walker? wheelchair? nursing home?

*[en.wikipedia.org].

Read here a few accounts by Dr. Duane Graveline: [www.afibbers.org], e.g.:

"On the basis of my repository of several thousand reports from statin "victims", the first evidence of permanence came from reports of cognitive problems associated with statin use. Michael Hope was one of the first to receive widespread media attention - a former CEO reduced to unemployable status due to persistent loss of short-term memory. Today, four years after the onset, Michael is still grossly impaired. He is one of many hundreds who have persistent cognitive deficits long after stopping their statin."

And concluding with: "Not only have statin drug companies failed to adequately warn prescribing physicians of permanent cognitive loss associated with statin use, they have failed to warn about permanent neuromuscular and neurodegenerative consequences. Thousands of unsuspecting people have become victims and in most of these cases their doctors, having had no advance warning from the pharmaceutical industry, have tended to disregard patient complaints, offering almost any explanation other than the correct one."

This is the good doctor’s personal sad story: [www.spacedoc.net]

"When I first wrote of my personal reaction to Lipitor seven years ago, I considered myself to be lucky to have had only transient amnesia episodes, for when it was over, I was back to normal - or so it seemed to me for the next several years. During this time my statin damage research gradually was revealing hundreds of cases of permanent disabling peripheral neuropathy, permanent myopathy and progressive neuro-muscular degeneration and I wondered, for suddenly, in the past two and one-half years, I have grown old, with weakness and easy fatigability and the posture and gait of an old man.

My exposure to Lipitor had been minimal - a total of three and a half months at 10mg or less. My awareness of possible statin causation came to me slowly as years passed and I read report after report from statin damaged victims. Many of them exactly described my story with a gap from beginning of drug intake to onset of symptoms often measured in many years. The feeling of weakness and easily fatigability of legs and low back made me cringe at the idea of exercise. A chair became my preferred refuge. I am now a doddering old man with withered limbs, a stranger in the mirror.

If my transition to this state had been gradual, the natural result of getting old I might have missed the relationship but to transition thusly in just a few years was clearly not normal and hundreds of other people, all statin users, were experiencing the same thing. My rheumatologist considered a possible ALS-like condition. My neurologist said he strongly suspected mitochondrial mutation secondary to statin use. Only muscle biopsy would refine this presumptive diagnosis but he had been seeing this syndrome for several years and strongly suspected a statin causation. He said that there is no treatment. This ALS-like condition is slowly progressive and eventually disabling.

What about this presumptive mitochondrial mutation etiology? Does this have merit? Mitochondria are organelles that provide most of the energy our cells need for the work they do. It is in the mitochondria where CoQ10 and the reduced forms of niacin and riboflavin enter into that ingenious process of moving electrons from hydrogen molecules to one side of a mitochondrial leaf while storing the remaining protons on the other side creating an energy gradient - the magic energy resource of every cell in our bodies. It is here that oxidative phosphorylation takes place to create ATP.

As with any form of DNA, mitochondrial DNA (mtDNA) sequences are susceptible to mutation In fact, there is evidence that mitochondrial sequences may mutate at rates 3 to 5 times greater than nuclear sequences. This may be because of the front-line position of these tiny warriors in their battle to utilize oxygen without themselves being oxidized. Constantly at risk they ordinarily are well supplied with anti-oxidants.

Enter statin drugs, capable of halving your CoQ10 in just a few weeks through the inevitable process of mevalonate blockade while inhibiting cholesterol synthesis. Gone is the fuel of the mitochondrial engines and gone is one of the most important anti-oxidants, with the ****of inactivation of free radicals. Abruptly the mutation rate increases at the same time the mitochondrial engines are running low on fuel. Is this something to consider as a cause of statin-altered physiology?

Statin associated chronic neuropathy and chronic progressive myopathy may well be examples of this process in action. It seems likely that a side effect of statin drugs in some people is to trigger just this process - mitochondrial mutations of sufficient frequency and severity to express as a chronic, even progressive condition. Indeed, it is known that accumulating mitochondrial mutations contribute significantly to aging. This appears to be what we are seeing in the cases of permanent muscle wasting, weakness and neuropathies seen usually only in advanced age.

Variability of expression may well explain why some people seem extraordinarily sensitive, showing symptoms early, while others show no apparent effect but may well be victims of low-grade, accelerated aging type of presentation, taking years to become evident. This may also help to explain why some people may be on a statin at an unchanged dose for years before abruptly manifesting symptoms."

An excellent Scientific American article for understanding mitochondrial DNA, its mutations in aging and disease: [www.nslc.wustl.edu]. This was important in my attempt to comprehend AF etiology, when published just 2 years into my "career". It bears directly on this topic as it explains in depth and clarity the process whereby 'statin' caused mtDNA mutations may accumulate and increase over time.

Erling