Did you know…

The mevalonate pathway that statins block to lower cholesterol also produces coenzyme Q10, the electron carrier at the heart of mitochondrial energy production. Statin-induced CoQ10 depletion is documented in animal and human trials. Whether every patient on a statin should co-supplement CoQ10 remains debated. The mechanism itself is not.

The claim, in the reference of pharmacology

Statins are HMG-CoA reductase inhibitors. HMG-CoA reductase is the rate-limiting enzyme of the mevalonate pathway. The mevalonate pathway produces cholesterol, and it also produces ubiquinone (coenzyme Q10), dolichol, and the prenyl groups that anchor several signaling proteins to cell membranes. Blocking the pathway upstream, as statins do, reduces production of all its downstream products, not only cholesterol. A 2005 review put the biochemistry directly:

“Statins inhibit hydroxy-methylglutaryl-coenzyme A (HMG-CoA) reductase leading to reduced production of mevalonate pathway metabolites including ubiquinone or Coenzyme Q10. Ubiquinone is an essential coenzyme in the process of mitochondrial respiration facilitating the transfer of electrons between complex I and II of the respiratory chain.”

— Hargreaves et al., European Journal of Pharmacology, 2005 (and subsequent literature)

What has been observed clinically

Published animal and human trials indicate that statin-induced blood and tissue CoQ10 depletion is real, with adverse effects noted particularly in settings of pre-existing CoQ10 deficiency, as seen in the elderly and in those with pre-existing heart failure. Whether routine CoQ10 co-supplementation prevents statin-induced myalgia is where the clinical debate sits. The physiological cause is not.

What the ordinary prescription does not say

The vast majority of statin prescriptions in ordinary primary care are issued without a discussion of CoQ10 status, without a baseline CoQ10 measurement, and without co-prescription of ubiquinol or ubiquinone. Patients experiencing muscle symptoms are typically switched to another statin or told to persist. The upstream mechanism that a first-year pharmacology textbook explains is not part of the standard conversation.

This entry is a companion to Right to Optimal Coenzyme Q10 Status.