By Duane Graveline MD, MPH
Statins and Mitochondrial Damage Part 8 of 11
For those statin victims desiring background information on their statin associated myopathy, neuropathy, ALS-like condition and even cognitive dysfunction, what I present here should suffice, for this condition can occur in any tissue: muscle, nerve, or brain.
The diminished bioavailability of intracellular CoQ10 and dolichols associated with the use of statins has the potential for seriously increasing oxidative damage and DNA mutations. The logical consequence of this is premature aging and the progressive development of such chronic conditions of aging as muscle weakness, burning pain and in-coordination and faulty memory - exactly the clinical picture we are seeing in tens of thousands of statin users.
The clinical responses we are seeing from this process of progressive mitochondrial damage is highly variable, more of a spectrum than any predictable, precise display of symptoms.
We first have to accept that most statin users appear to do quite well on statins. This tells me that in some people our mevalonate pathway must take several different forms, by-pass channels, if you will, that allow sufficient CoQ10, dolichols, selenoproteins etc to be available despite blockade of the basic mevalonate pathway.
We also find that some persons are completely unresponsive to statins, strongly supporting this possible presence of alternative pathways. In my 23 years of clinical medicine I soon discovered that doctors are fortunate if five out of every ten patients gave the expected response to a given medicine. We soon learn that "That's the way we are made!" There are many ways we biologic organisms evolve to get from A to B.
We also can say that premature aging and the earliest forms of neuropathy and myopathy may not yet be clinically apparent. Dull aches, slight numbness, senior moments and personality change all can be so minor as to escape recognition as possibly significant, so at least some of those who appear to be tolerant may actually have sub-clinical decrement.
Just as we have to accept the fact that many, even most patients appear tolerant to statins, many thousands of people have been disabled by statins and for them, their prescribing doctor directly contributed to their problem and, in their eyes, no longer wears a completely white jacket.
I have generally categorized the symptoms as cognitive, emotional, neuropathic, myopathic and neurodegenerative but in reality there is much overlap. Hovering above all of these categories is the frequent presentation of tiredness and easy fatigability, pointing directly at deficient energy. Fatigue is the end result of ATP lack, so with sufficient mitochondrial damage, fatigue becomes inevitable.
The cognitive manifestations of statins may be just episodes of transient global amnesia, or increasing confusion, disorientation and forgetfulness or progressive dementia, which could be called Alzheimers-like, differing only in underlying pathology. Only when one stops the statins and sees regression of symptoms can the true cause be inferred.
So an individual can present with any one or all of these symptoms. It all depends upon what kind of body tissue is the most involved with mitochondrial deterioration. Every cell comes equipped with mitochondria, the energy producers of the cell.
The cells of slowly metabolizing tissue may be composed of only a few mitochondria because its energy needs are minimal. Muscle, heart and brain cells come equipped with hundreds of mitochondria because of the urgency of their metabolic demand.
There is no way to predict how any one person will respond to this progressive mitochondrial deterioration triggered by statins. Therefore, a cognitively impaired victim may also present with emotional symptoms, painful neuropathy, disabling myopathy or an ALS-like manifestation or with just cognitive dysfunction alone. It all depends on the roll of the dice.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor