http://www.spacedoc.com/statins-mitochondrial-side-effects
Since glycohydrolase is one of our ubiquitous glycoproteins, requiring dolichols for synthesis, one must consider the possibility of altered glycohydrolase availability with statin use because of the well-known tendency of statins to inhibit dolichols along with CoQ10.
Please understand that the effect I am writing about is not some rare, remotely possible event. Mevalonate blockade of varying degrees is inevitable when statins are used. Although every cell in our bodies is affected by reductase inhibition those cells having greater need of energy such as muscle and heart cells, kidney and liver will be affected more.
The only escape from the consequences of this inhibition is the presence of pathway alternatives to the usual mevalonate one for synthesis of CoQ10, dolichols or even cholesterol. Serum cholesterol occasionally does not respond to statin use, suggesting the presence of alternative pathways for synthesis. If this is true for cholesterol, it is true for all other biochemicals equally dependent upon the mevalonate pathway.
Other than for these considerations, mevalonate blockade is inevitable with statin use and is the cause of the overwhelming majority of adverse reactions. The consequence of CoQ10 and dolichol inhibition is mitochondrial damage. It is inescapable and every MD using or recommending these drugs needs to understand this.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor
Since glycohydrolase is one of our ubiquitous glycoproteins, requiring dolichols for synthesis, one must consider the possibility of altered glycohydrolase availability with statin use because of the well-known tendency of statins to inhibit dolichols along with CoQ10.
Please understand that the effect I am writing about is not some rare, remotely possible event. Mevalonate blockade of varying degrees is inevitable when statins are used. Although every cell in our bodies is affected by reductase inhibition those cells having greater need of energy such as muscle and heart cells, kidney and liver will be affected more.
The only escape from the consequences of this inhibition is the presence of pathway alternatives to the usual mevalonate one for synthesis of CoQ10, dolichols or even cholesterol. Serum cholesterol occasionally does not respond to statin use, suggesting the presence of alternative pathways for synthesis. If this is true for cholesterol, it is true for all other biochemicals equally dependent upon the mevalonate pathway.
Other than for these considerations, mevalonate blockade is inevitable with statin use and is the cause of the overwhelming majority of adverse reactions. The consequence of CoQ10 and dolichol inhibition is mitochondrial damage. It is inescapable and every MD using or recommending these drugs needs to understand this.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor