As many of you know, I have hundreds of reports from statin victims stating that on apprising their doctor of their symptoms of weakness and unsteadiness, along with fuzzy thinking since starting their statin, the reaction almost invariably was, "You have to expect this type of thing now, you are over fifty." In other words the doctor was unknowingly equating statin symptoms with premature aging, which, incidentally, is the same conclusion I have reached from my past eight years of studying statin drug side effects.
I was seeking an explanation for why so many of the statin side effects such as muscle pain and weakness, the varied neuropathies and the ALS-like neuromuscular degenerations appear permanent. If the problem was due to deficiency of CoQ10, why do they not respond to full replacement of CoQ10? The common denominator in many of these cases appeared to be premature aging. In only a year or so after starting the statin drug, a vibrant, energetic person has become a querulous, tottering elder with a cane. Only one thing can cause that, I deduced - mitochondrial mutations. Finally I had an assessment of statin damage that made sense - a logical end product of CoQ10 and dolichol inhibition.
As I reviewed the research literature for aging the picture gradually emerged of mitochondrial mutations (MtDNA), a slow accumulation of molecular events with age that appear to be responsible for the age-dependent decline in mitochondrial respiratory functions. The natural result of this is lack of energy. Along with this is an increase in the generation of reactive oxygen species, energetic by-products of oxygen exposure, having the ability to seriously damage adjacent proteins, lipids and DNA strands, thereby increasing the rate of aging.
Protein degradation appears to be a key mechanism in cellular aging. The proteases, enzymes critical for protein turnover and degradation, are particularly susceptible to free radical damage. Many researchers feel that defective mitochondrial turnover is a cause of accumulation of defective mitochondrial constituents and an important contributory factor to human aging.
The start of this decline is inhibition of CoQ10 synthesis. One of the principal functions of CoQ10 is that of anti-oxidation. It is in complex I and II of each of our mitochondria that CoQ10 functions as a vital electron carrier as part of its anti-oxidation role. Imagine the consequences of insufficient CoQ10. Although there are other anti-oxidant substances in our bodies, none are so critically located in complexes I and II. Nothing can effectively substitute for CoQ10 lack. Abruptly, oxidative damage begins and lethal reactive oxygen species spring out at unprotected DNA strands. In only moments the damage is done. It is not reversible. All the CoQ10 in the world cannot turn back the clock once the DNA strand is damaged.
But, we say, doesn't our body have an ongoing detection and correction system for DNA damage? Don't we have thousands of these nucleotide deletions or substitutions every day that must be located and fixed? Yes, we do but there is one other factor - glycoprotein synthesis. You have heard me talk of dolichols - inhibited just like CoQ10, part of statins' collateral damage. Our entire detection and correction program depends upon specific glycohydrolases and guess what - they are all glycoproteins. Not only do we create more mutations, we cannot repair them. But there is more, much more to come.
A woman of child-bearing age with MtDNA mutations caused by her trial of statins must pass this on to her progeny. I am not concerned about men, for their Mt DNA characteristics are not transmitted but women's are. Statin damage in a woman will be passed along to her children, so they begin life with an inability to properly produce energy. How is that for a hidden side effect of the statin class of drugs that many want to put in our drinking water, but it gets far worse. They want to give this stuff to kids directly!
Now it is apparent that the mechanism of action of statin drugs is that of causing premature aging and chronic illness by accelerating natural mechanisms of aging, thereby escaping early detection efforts. Can you think of anything worse than giving statins to a child, capable not only of causing mutations in their respiratory chain of mitochondrial energy production but also of causing premature aging. What a gift we are passing on to our innocent.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor