The meta-analysis showed a significant reduction in plasma CoQ10 concentrations following treatment with statins.

Regardless of its definition, statin intolerance is an important phenomenon, leading to a poorer control of the LDL cholesterol levels among high-risk Japanese patients. We need to understand the risk factors, as well as the potential nocebo effect, so that we can accurately discriminate the pseudo statin intolerance from true statin intolerance and reduce their LDL cholesterol more effectively using the golden standard drug. Alternatively, we could consider using other LDL-lowering therapies, such as ezetimibe, PCSK9 inhibitors and fibrates, or some agents that have been shown as add-on/alternative therapies to statins, such as certain nutraceuticals, or coenzyme Q107–9).

Several trials demonstrate coenzyme Q10 depletion subsequent to statin initiation.42,43 There is conjecture about this depletion as the cause of statin–associated adverse effects (e.g., myopathy) with exogenous coenzyme Q10 supplementation as a possible mediating treatment. This assertion is refuted by a more recent crossover trial44 that found no significant coenzyme Q10 drop after initiation of selected statins. Several doxorubicin (Adriamycin) trials, mostly in animal models, have noted a reduction in cardiac coenzyme Q10 depletion and cardiotoxicity associated with coadministration of coenzyme Q10. The clinical implications on disease state and adverse reaction profile with coenzyme Q10 supplementation in depleted states requires further evaluation.